Gattarman
Etlnedby
Meridell. GanePlllan, MA, DC Research Faculty, New York Chiropractic College, Seneca Falls, New York; Former Director, Chiropractic Scien ces, Canadian Memorial Chi ropractic Col lege, Toronto, OntariO, Canada; Former Director, Chiropractic Scien ces , wester n States Chiropractic College, Portlan d , Oregon
with 150 il lustration s
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Editor: Martha Sasser Developmental Editor: Kellie White Project Marlager: Dana Peick Productiorl Editor: sravra Demerrulias Desig.ler: Amy Buxton Interior Design: Liz Fert Manufacturing Supervisor: Karen Lewis
Copyright © 1995 by Mosby-Year Book, Inc. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without prior written permission from the publisher. Permission to photocopy or reproduce solely for internal or personal use is permitted for libraries or other users registered with the Copyright Clearance Center, provided that the base fee of $4.00 per chapter plus $.10 per page is paid directly to the Copyright Clearance Center, 27 Congress Street, Salem, MA 01970. This consent does not extend to other kinds of copying, such as copying for general distribution, for advertising or promotional purposes, for creating new collected works, or for resale. Printed in the United States of America Composition by Black Dot Graphics, Inc. Printing/binding by Von Hoffmann Press, Inc Mosby-Year Book, Inc. 11830 Westline Industrial Drive St. Louis, Missouri 63146
The authors have made every eHon to ensure the accuracy of the information herein, parricularly with regard to technique and procedure. However, appropriate informa tion sources should be consuhed. especially for new or unfamiliar procedures. h is the responsibiliry of every practitioner to evaluate the appropriateness of a particular opinion in the conrext of actual clinical situations and with due consideration
[Q
new
developments. Authors, editors, and the publisher cannOt be held responsible for any rypographical or other errors found in this book.
Library of Congress Cataloging in Publication Data Foundations of chiropractic: subluxation/edited by Meridell. Ganerman p.
cm.
Includes bibliographical references and index. ISBN 0-8151-3543·2
I. Spinal adjustment. I. Ganerman. Meridel I. RZ 265.S64F68 1995
95-9902 CIP
615.5·34-<1c20
95 96 97 98 99
I
9 8 7 6 5 4 3 2
1
Contributors Kevin Bartol, DC
Susan A. Darby, PhD
Associate Professor, Northwestern College of Chiropractic,
Associate Professor, Department of Anatomy,
Bloomington, Minnesota
T he National College of Chiropractic, Lombard, Illinois
David E. Bereznick, MSc, DC Research Assistant
Glen R. Engel, DC, FCCS(C)
Canadian Memorial Chiropractic College Toronto, Ontario, Canada
Professor, Division of Clinical Education, Canadian Memorial Chiropractic
Thomas F. Bergmann, BS, DC
College, Toronto, Ontario, Canada
Professor Northwestern College of Chiropractic,
Donald Fitz-Ritzon, BA, DC
Bloomington, Minnesota
Vice-President, Physical Rehabilitation,
Kelli L. Blunt, DC
International Managed Health Care, Toronto, Ontario, Canada
Private Practice Brockville, Ontario, Canada
Richard G. GiUette, MS, PhD
Patricia C. Brennan, BA, MS, PhD
Visiting Scientist, R.S. Dow Neurological Sciences Institute of Good Samaritan Hospital and
Dean of Research, The National College of Chiropractic, Lombard, Illinois Peter Cauwenbergs, PhD Chairman, Department of Anatomy Canadian Memorial Chiropractic College Toronto, Ontario, Canada Gregory D. Cramer, DC, PhD Associate Professor and Chairman, Department of Anatomy, The National College of Chiropractic, Lombard, Illinois
Medical Center Portland, Oregon; Associate Professor of Physiology, Division of Basic Sciences, Western States Chiropractic College , Portland, Oregon Adrian Grice, DC, FCCS(C) Professor, Division of Chiropractic Sciences, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada
v
VI
Mitchell H aas, MA, DC Associate Professor of Research,
Cynthia K. Peterson, Rn, DC, DACBR,
Western States Chiropractic College, Portland, Oregon
Senior Lecturer,
Charles N. R. Henderson, DC, PhD Assistant Professor and Fellow, Institute of Graduate Studies and Research, Palmer College of Chiropractic, Davenport, Iowa Michael J . Hubka, DC Department of Clinics, Los Angeles College of Chiropractic, W hittier, Californja Charles A. Lantz, DC, PhD Director of Research, Life Chiropractic College West, San Lorenzo, California Robert D. Mootz, DC, DAB CO Associate Medical Director for Chiropractic, State of Washington, Department of Labor and Industries,
Dip Med Ed Radiology Residency Preceptor, Department of Radiology, Anglo-European College of Chiropractic, Bournemouth, England Zoltan T. Szaraz, DC, FLACA Associate Professor, Division of Chiropractic Sciences, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada John A. M. Taylor, DC, DACBR Associate Professor, Department of Radiology, Western States Chiropractic College, Portland, Oregon Allan G. J . Terrett, DipAppSc (Human Biology), BAppSc (Chiropractic), DAc, MAppSc (Chiropractic),
Tumwater, Washington
GradDipTertEd, MACE, FACCS, FlCC Senior Lecturer, Faculty of Biomedical
John P. Mrozek, BA, DC, FCCS(C)
and Health Sciences, Royal Melbourne Institute of
Dean, Academic Affairs, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada David M. Panzer, DC, DABCO Assistant Professor, Department of Chiropractic Science, Western States Chiropractic College, Portland, Oregon
Technology, Melbourne, Australia Howard Vernon, DC, FCCS(C) Associate Dean, Director, Center for rhe Study of Spinal Health, Research Department, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada
This book is dedicated to the memory of
A. Earl Homewood
A
respected friend whose vision of the neurodynamics of the vertebral subluxation predicted much of the work reported in this book.
VII
Foreword Foulldations of Chiropractic: SlIbluxatioll may be the first scholarly response ro focus on a definitive analysis of the enigmatic vertebral subluxation. Largely based on scientific research by chitOprac tic investigators, the text moves through the pri mary articular lesion, to the subluxation com plex-the theoretical teaching and research model, and concludes with the subluxation syn dromes, linking articular lesions to clinical syn dromes.
This text is a remarkable achievement indeed, and is destined ro become the authoritative work on the vertebral subluxation until such rime as it is revised to include new research or refute mater ial that is questioned by new investigative study. But this is the way of scholatship, critical think ing, and [he monitoring of scientific claim. Bertrand Russell, philosopher/mathematician, summarized it all in the New York Times Maga zille in 1950, when he said,
Science by itself, cannot supply us with an ethic. It can show us how ro achieve a given end, and it may show us that some ends cannot be achieved. Herbert J. Year, DC, FCCS(C)
IX
Preface The idea for this book originated from a confer ence titled "Subluxation Revisited", held in the fall of 1992 at Canadian Memorial Chiropractic College in Toronto. It has evolved since that time to become a foundations textbook for the chiro practic profession. The continuing debate in chi ropractic literature with regard to naming the pri mary lesion treated by chiropractors for the past 100 years has sparked much controversy. Failure to resolve this controversy has been a barrier to communication of chiropractors both with each other and with those outside the chiropractic pro fession. A terminology study directed by the Stan dards of Care Committee of the Consortium For Chiropractic Research was undertaken for the purpose of developing chiropractic nomenclature through consensus, in the hope that clearer com munication would be fostered. To facilitate the advancement of chiropractic nomenclature a model in the form of an algo rithm was developed. Moving from a small work ing group that agreed upon contentious terms, nominal and Delphi panels were struck involving increasingly larger numbers and wide political and geographic representation. It is paramount that these terms and definitions not be viewed as cast in stone but rather as a platform for dis course and study of the issues important to the chiropractic profession. In time some terms and definitions will no doubt evolve further, but it is equally important that the standardized terms and definitions be adopted and utilized as part of the daily dialogue of chiropractic practitioners, chiropractic educators, and chiropractic students.
The glaring lack of standardized terms within chi ropractic education became apparent as the study proceeded, and through discussion with student representatives to the World Congress of Chiro practic Students, and students and faculty of col leges in both North America and Australia. This three-year terminology project has resulted in agreement for 10 terms fundamental to the understanding of the foundations of the chiro practic profession. The ideas, concepts, theories, and issues discussed in depth in this text Stem from the 10 terms put forth to develop chiroprac tic nomenclature. In addition to the original presentation topics at the. "Subluxation Revisited" conference, addi tional material has been incorporated into vari ous chapters. For example, the material in Part Three examines syndromes related to subluxation of the spine and pelvis. Recognized through case studies and in some cases as entities of larger studies, these syndromes have been viewed as ourcomes of articular lesions known to chiroprac tors as subluxation. We must address the issues surrounding the term slIbluxation, nOt delude ourselves that they will disappear if we change the name to one of the many synonyms presented in Chapter 1. The reader is encouraged to keep an open mind, to objectively examine the issues and theories pre sented in an unemorional fashion, so that the foundations of the chiropractic profession can move progressively in the patient'S interest. Meridel I. Catterman Xl
Acknowledgments I wish to acknowledge with thanks the assistance of many people who have aided in the production of this book, particularly Alan Adams, William Meeker, Daniel Hansen, Henry Morrison, and Herbert Vear, all of whom participated in facili tating the terminology study that led to the initia tion of this work. This study was greatly helped by the generous cooperation of the members of the Consortium for Chiropractic Research, the Advisory Council to the Technic Committee of the American Chiropractic Association, and the varied panel members who participated in the multiple panel rounds that led to consensus. I am grateful to the many people who con tributed to the editing of this text and made sug gestions that clarified the overall content, includ ing Peter Cauwenburgs, Ian Fraser, Stephan Injeyan, Charles Henderson, Carolyn Malik, Jane Mannington, Igor Steiman, and Stephan Zylich. I
am indebted to Marilyn Schafer, director of the Canadian Memorial Chiropractic College library; reference librarians Mary Boite and Valda Svede; and the library staff, including Jane McLaughlin and Deanne Collier, for their assistance. Thanks also ro Dan McGinty and Aden Staring for pro viding illustrations. I particularly acknowledge the important con tributions of the staff at Mosby, especially Martha Sasser, Kellie White, and Stavra Demetru lias. Appreciation is also gratefully expressed to Anita Locke, Veronica Nass, and Beverly Fuller, who facilitated manuscript preparation and whose many favors eased the frustr.tion of the details that are encountered in the preparation of any book. Most importantly I wish to thank my hus band, Mike Jamison, whose patient support is unending.
XlII
Table of Contents Par tON E SUIiIxaIIon 1118 ArtIeR lesion 1
What's in a Word?
Defining Subluxalion
Cervical Intervertebral Discs
6
The Perception of Pain
10
Historical lssues
2
Region
14
29
Pain Generators Unique to the Thoracic
14
Region
29
The Dorsal Root Ganglia and Radicular
16
Pain
16
29
Somatic Referred Pain
Anatomy Related to Spinal Subluxation
30
Central Transmission of Pain 30 The Neospinothalamic Tract 31
18
Gregory D. Cramer
The Paleospinothalamic and
Susan A. Darby
Spinorecticular Tracts
The Zygapophyseal Joints General Description Articular Capsules
19
Supraspinal Control
19
3
19
The Zygapophyseal Joint Synovial Folds
Zygapophyseal Joints
Innervation of the Z·Joints The Intervertebral Disc
22
22
Nucleus Pulposus Vertebral End Plate
23 24
21
Basic Scientific Evidence for Chiropractic Subluxation 35
Review of Studies
21
Cervical Zygapophyseal Joint Synovial Folds 21
31
32
Howard Vernon
19 Unique Characteristics of the Cervical
Anulus Fibrosus
29
Pain Generators Unique to the Cervical
15
Economic Issues Conclusion
Nervous System
13
14
The Political Issue Clinical Issues
28
28
Pain of Somatic Origin 28 Nerves Associated wilh the Sympathetic
Defining Chiropractic Trealment Methods
The Philosophical Issue
27
Pain (Nociception) of Spinal Origin
Manipulable and Nonmanipulable
11 Opposilional Thinking
24
The Intervertebral Foramen 25 Accessory ligaments of the IVF
6
Origin of the Word Subluxalion Subluxations
24
Innervation of Intervertebral Discs
5
Meridel l. Gallerman
Discussion
4
38
53
Palpatory Diagnosis of Subluxation
56
Mllchell Haas David M. Panzer History of Palpation in Chiropractic Palpatory Indicators for Manipulation
57 58
xv
XVI
Test Reliability
59
Contact Points
Background
59
Line of Drive
Soft Tissue Therapy
Assessment
59 Reliability Indices
60
Strength of Concordance
7
60
Reliability of Chiropractic Spinal Palpatory Procedures
60
Specificity Assumption Motion Palpation
62
63
64 65
79 80
Conclusion
6
110
Sympathetic Neurons
111
111
Visceral Disease Reflexes
87
Kevin M. Bartol
112
113
Nimmo technique (Ischemic Compression)
113 113
Chapman (Neuro) Lymphatic Reflexes
88
115
90
BenneU's (Neuru) Vascular Reflexes
91
115
94
Choosing the Best Procedure Patients Needs
113
113
Connective Tissue Massage
Classification
Acupressure Point Stimulation
94
Muscle Energy Techniques
95
Thrust Procedure Components Thrusting
Facilitation
Massage
Historical Perspective
110
Nociceptors Reflexively Activate
Specific Technique Procedures
Osseous Manual Thrust Techniques
Subluxation
110
Manual Therapy and Somatoautonomic
84
Terminology
Disease
Musculoskeletal Manifestations of
Functional Radiography and Spinal
Cervical Spine
110 Reflex Muscle Spasm frum Visceral
Disease
70
Lumbar Spine
109
Musculoskeletal Dysfunction and Visceral
Static Radiography and Spinographic
73
109
Reflexive (Autonomic) Effects
Evidence of Chronic Segmental
John A.M. Taylor
Dysfunction
Effects on Metabolism
Somatoautonomic Reflex Theory
The Role of Radiography in Evaluating Subluxation 68
Analysis
108
Reflex Muscle Spasm from Spinal Injury
What We Can Do 63 Challenging the Specificity Assumption
5
105
Thomas F. Bergmann
109
Improving the Reliability of Palpation
Future Research
Chiropractic Reflex Techniques
Effects on Blood Flow and Temperature
62
Why Bother? 62 Sources of Inconsistency
103
Effects of Immobilization
61
61
Static Palpation
102 103
97
98
Long and Short Lever Arm Procedures 98 Force of the Thrust
99
Logan Basic
117
117
117
Spondylotherapy Activator Methods
118 118
Sacrooccipital Technique (SOT) Manual Cranial Theraphy Distraction Techniques
118 119
118
Conclusions
8
119
Diagnostic Tests
The Nonmanipulable Subluxation
123
Cynthia K. Peterson
of the Cervical Spine
Connective Tissue
124
Instability in the Cervical Spine
Inflammation
124
Causes of Cervical Spine Hypermobility and
Discussion
10
126
Degenerative Arthritis
132
Biomechanical Models Neurologic Models
134
Trophic Models
Hypermobility and Instability in the lumbar
Conclusions
135
Causes of lumbar Spine Hypermobility 137
Clinical Manifestations of Hypermobility and Instability in the lumbar Spine 141 Chiropractic Management of lumbar Intersegmental Hypermobility/
Part TWO
143
I I
Kelill. Blunt Meridel I. Gatterman David E. Bereznick Characteristics of Normal Motion
The Subluxation Complex
The Vertebral Subluxation Comptex
149
Charles A. Lantz History
Regional and Intersegmental Range of Motion
196 196
Abnormal Joint Motion Hypomobility
Kinesiologic Component Neurologic Component
207
207
Hypermobility
208 209
Compensatory Hypermobility
151
209
Mechanism of Intervertebral Joint
153
Restriction
155
Connective Tissue Component
191
193
Aberrant Motion
151
Overview of the Model
184
Kinesiology: An Essential Approach Toward Understanding the Chiropractic Subluxation 190
Cervical Spine
9
180
185
Analysis of Motion
144
178
178
183
Psychosocial Models
135
Radiographic Evaluation
177
Models of Chiropractic Subluxation
and Unstable Cervical Segments
Conclusion
Theoretic Models of Chiropractic Subluxation 175
for Model Classification
130
Chiropractic Management of Hypermobile
Instability
166
166
Clinical Rational Provides logical Method
127
and Instability
166
Robert D. Mootz
126
Inflammatory Arthropathies
Spine
165
165
Pharmacologic Considerations
and Instability in the Cervical Spine 125
163
165
Endocrinology
Radiographic Evaluation of Hypermobility
Anomalies
162
Inflammatory Component
Clinical Manifestations of Hypermobility and
Instability
160
Vascular Component
Biochemical Aspects ol the Model
Definitions of Instability and Hypermobility
Acute Trauma
159
Myologic Component
158
210
The Muscle Spindle: Structure
210
The Muscle Spindle: Function
211 XVII
XVLU
Korr's Theory of Joint Fixation Assessment of Abnormal Motion
212
Methods 269 Setting 269
214
Interventions
Biomechanical Effects of the Chiropractic Kinesiology Aspect of the Manipulable Subluxation
269 Outcome Measures
215
The Klnesiopathology of Spinal Joint Degeneration
217
15
219
12
Altered Somatic Afferent Input Theory
280
Clinical Phenomenology of Pain Originating from the Lumbar Spine
281
Pain Referral from Deep Tissue Injury
Intervertebral Encroachment Theory
226
280
Clinical Phenomenology of Pain Originating
229
from the Lumbar Spine
Dentate ligament, Cord Distortion Theory
Explanatory Hypotheses
231
281
281
Neurophysiologic Evidence for Central Convergence-Projection 284 The Contribution of Central Neuronal
Vertebral Subluxation and the Anatomic Relationships of the Autonomic Nervous System 234
Plasticity to Referred Pain Low-Back Pain
295
Neurophysiology of Paraspinal
Overview of the Autonomic Nervous System
Antinociceptive Systems
236 238
Sympathetic Division Enteric Division
Part THREE
238
Parasympathetic Division 260
261
Hypothalamic Control of Autonomic 261
Reflex Regulation of Autonomic Activity 263 Autonomics in Chiropractic
264
Review of the Systemic Effects of Spinal Manipulation 267 Patricia C. Brennan
299
I Sy••• TilIIIIIIIIII
253
Central Processing In the Control of Autonomic Function
295
Recapitulation and Conclusions
Peripheral Components of the Autonomic Nervous System
288
Sympathetic Nervous System Involvement in
Peter Cauwenbergs
14
Spinal Cord Mechanisms of Referred Pain and Related Neuroplasticity 279
Pain Referral from Deep Tissue Injury
Three Neurophysiologic Theories o n the Chiropractic Subluxation 225
Function
270
Richard G. Gillette
219
Charles N. R. Henderson
13
269
Results and Discussion
Pathologic Effects of Joint Immobilization Conclusion
269
Measurement of Manipulation Forces
Adjustment as It Relates to the
16
Cervicogenic Headache
306
Howard Vernon Headache and Spinal Manipulation
307
Mechanisms of Pain in Cervicogenic Headache
309
Implications for Headache of Cervical Origin 312 Cervicogenic Dysfunction in Headache Hypomobility
313
Craniovertebral Tender Points
313
Radiologic Findings of Cervicogenic
312
Dysfunction
315
Narrow Passages Traversed by the
Cervical Posture, Muscular Weakness,
Neurovascular Bundle
and Range of Motion Summary
360
Physiologic Factors Compromising the 315
Narrow Passages
316
362
Structured Anomalies Compromising the Narrow Passages Further
17
Cervicogenic Sympathetic Syndromes: Etiology, Treatment, and Rehabilitation 319
Functional Cause
Sympathetic Nervous System Age
320
Changes
Horner's Syndrome
331
Meniere's Disease
332
Barre-Lieou Syndrome Cervicogenic Vertigo
325
Radiography
Conclusion 340
341
343
Examples of Brain Hibernation
343
Brain Hibernation and Spinal Manipulation 346 Testing the Theory
19
349
370
370
21
370
371 372
Thoracic and Costovertebral Subluxation Syndromes 378 Adrian Grice Clinically Relevant Anatomy
379
Biomechanics of the Thoracic Spine Static Concepts 384 Dynamics of the Thoracic Spine Kinematics of the Thoracic Spine
350
Biomechanics of the Rib Cage
384 385
388
391
Accessory Muscles of Respiration and the Cervicogenic Dorsalgia
353
Glenn R. Engel
Treatment
354
358
392
and Ribs
393
Classification of Pain in the Thoracic Spine 394
The Thoracic Outlet Syndrome: First Rib Subluxation Syndrome 359 lollan T. Szaral Anatomic Features
Biomechanical Effects
Biomechanical Diagnosis of Thoracic Spine
History and Examination
20
369
Functional Evaluation Management
336
Brain Hibernation
Conclusion
Provocative Tests
332
368
369
Electrodiagnostics
Allan G_ J_ Terrett
Diaschisis
Diagnosis
333
The Cerebral Dysfunction Theory
366 367
367
Vascular Disturbances
324
Trauma to the Cervical Spine
364
Vasomotor Disturbances and Trophic
323
Intervertebral Discs
18
Motor Signs and Symptoms
324
Conclusion
363
Clinical Features 364 Sensory Signs and Symptoms
320
Biomechanics
363
Traumatic and Occupational Causes
Donald Fitz-Ritson Anatomy
363
Biomechanical Considerations
Medical Model of Pain: Emphasis on Pathologic Factors
394
Chiropractic Model of Pain
395
Functional Factors: Mechanical Disorders 360
395 XIX
xx
Sources 01 Pain in the Thoracic Spine
Diagnostic Imaging 01 Intervertebral Disc
396
Dynamic Palpation 01 the Thoracic Spine
Syndrome
436
DiNerentlal Diagnosis 01 Intervertebral
398
Disc Syndrome
General Principles Related to Palpation
438
Natural History 01 Intervertebral Disc
398
Syndrome
Dynamic Motion Palpation Findings and Suggested Adjustive Correction Concluding Remarks
439
Treatment 01 Intervertebral Disc Syndrome
404
440
409
Medical and Surgical Consultations
22
Facet Subluxation Syndrome
414
David M. Panzer
24
Facet Syndrome Delined
Tropism
Facet Versus Disc Degenerative Joint
Manipulation
419
Exercise
23
456
Straight Leg Raise (SLR, Lasegues' Sign) 460
425
Thigh Hyperextension (Yeomann's Test) 460
425
Radiographic Findings
460
Mechanics 01 Sacroiliac Subluxation and Dyslunction
Chiropractic Management 01 Intervertebral Disc Syndrome 427 Terminology 01 Intervertebral Disc Syndrome 429 Symptoms and Signs 01 Intervertebral Disc 430
Discogenlc Back Pain and Dlscogenlc Back and Leg Pain
430
Sciatica without Neurological Delicit and Sciatica with Neurological Delicit
Syndrome
25
432
464
Coccygeal Subluxation Syndrome Joh n P. Mrozek
466
Anatomic Considerations Levator Ani Coccygeus
467 467
Diagnosis
469
Treatment
469
431 Examination 01 Intervertebral Disc
461
Treatment 01 Sacroiliac Subluxation
Michael J. Hubka
Syndrome
456
456
Figure 01 Four (FABRE) Test
424
426
Syndrome
454
454
Pelvic Compression
Predisposing Factors and Therapeutic Conclusion
454
Tests lor Sacroiliac Dyslunction
424
Facet Injection
453
Sacroiliac Subluxation Pain PaHern
Ctinical Features 01 the Facet Syndrome 421 Treatment 01 Facet Syndrome
Sacroiliac Joint Motion Clinical Considerations
418
Facet Joint as a Source 01 Pain
452
Meridel l. GaHerman
415
415
416
Disease
Sacroiliac Subluxation Syndrome David M. Panzer
415
Facet Clinical Anatomy and Function Meniscoids
446
Conclusion
Glossary Index
473
477
467
Subluxation The Articular Lesion
C
emral to the philosophy, science, and practice of chiropractic is the vertebral subluxation. Part 1 of this book discusses the fundamentals of subluxation, the primary articular lesion treated by chiropractors. Long one of the most controversial concepts of chiropractic principles, the enigmatic subluxation will be discussed in Part 1 through the reductionistic model of mechanical joim dysfunction. Palmer's early concept of the subluxation applied a mechanical model whereby the body part, that is, the spinal articulation, is not working, and the chiropractor fixes Ot adjusts it. The subluxation as a mechanical breakdown is like a carburetor that must be adjusted. A reductionistic practitioner might be satisfied with this analysis and send the car out of the shop after an adjustment. Following this model, Part 1 presents evidence of subluxation as mechanical joint dysfunction and establishes the foundation for the more complex theories presented in Part 2 and the clinical manifestations of subluxation discussed in Part 3.
4
Chapter 1
What's in a Word presents the terms and definitions related to subluxation, based on the nomenclature agreed on through nominal and Delphi consensus methods. These rerms have been adopted by the Consortium for Chiropractic Research and the American Chiropractic Association house of delegates. Issues related to subluxation that have generated semantic confusion and much heated debate during the past century are discussed.
Chapter 2
Anatomy Related to Subluxation describes the structural relationships associated with subluxation. This chapter describes the components of the spinal motion segment, the threejoint complex that forms the functional unit of the spine. An understanding of the structural relationship of the intervertebral disc with the two posterior facet joints is necessary for understanding of the mechanical interaction of the spina l joints. Pain that accompanies loss of aqicular function characteristic of subluxation is only comprehended with a thorough knowledge of the anatOmic relationships of the spinal joints.
Chapter 3
Basic Scientific Evidence for Chiropractic Subluxation presents studies of animal models with experimentally induced vertebral misalignments, a component of subluxation. The methodology and findings of these studies are reviewed individually with comments on their methodology and findings. The models then are examined collectively, and their implications are synthesized inw a coherent set of conclusions.
Chapter 4
Palpatory Diagnosis of Subluxation examines palpatOry diagnostic criteria used to identify subluxation. PalpatOry techniques have been used to diagnose and differentiate subluxations since the beginning of the art of manipulation. From the Renaissance and later, emphasized by Flexner, medicine has scorned the use of touch
as being less reliable than visual and auditOry procedures. Chiropractors have refined palpatory techniques, the diagnostic mainstay of manual therapy, along with the development of therapeutic manual procedures.
Chapter 5
Radiographic Evidence of Subluxa· tion, evaluates radiographic procedures used by the chiropractic profession to diagnose and differ· entiate spina l subluxation. Predominantly used by the medical profession to detect pathologic conditions, radiography has been used by chiropractors to detect mechanical as well as pathologic lesions. Methods used by the chiropractic profession to differentiate mechanical lesions are presented.
Chapter 8
Treatment of Subluxation by Osseus Manual Thrust Techniques provides an outline of manipulative techniques used by chiropractOrs in the treatment of manipulable subluxations. Per· fected to a sophisticated level, these procedures have been demonstrated to be safe and effective and serve as the primary therapeutic procedures used by chiropractOrs.
Chapter 7
Treatment of Subluxation by Reflex Nonthrust Methods describes chiropractic techniques designed to affect physiologic changes through nonthrust procedures. Also classified as ch iropractic adjustive techniques, reflex therapeutic methods are used to treat subluxations through reflex mechanisms.
Chapter 8
The Nonmanipulable Subluxation discusses the diagnosis and treatment of subluxa· tions that are not amenable
[0
manipulative pro-
cedures. Motion segments that are unstable or ankylosed are nOt appropriately treated by thrust procedures, and in these cases spinal manipulation is contraindicated. Radiographic evidence of nonmanipulable subluxations is stressed.
A
wwtlil nat I cryltll, b,.......t ...
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may vary rallY In CIIIar ... C8IdIIIt ..............
to l1li drcIII.. r.1Cii ... the III WbIcIIIt II UIId. 1IInr_ .............
What's in a Word? Merldell. Gatterman Kay WuI'III
Adjustment, manipulable subluxation, manipulation, manual therapy, mobilization, subluxation, subluxation complex, subluxation syndrome
After reading this chapter you should be able to answer the following questions:
Quutlon #1
Did the term subluxation originally come from the chiropractic profession?
Quutlon#2
What is the definition of the word subluxation?
Quutlon#3
Explain the following issues surrounding the use of the word subluxation: A) Historical B) Philosophical C) Political D) Clinical E) Economic
6
T
he word subluxation has been daubed in a kaleidoscope of colors and embodied with a multitude of meanings by chiropractors during the past 100 years. To some it has become a holy word(l); to others, an albatross to be discarded(2). Currently, subluxation is the most loved and hated, hotly debated, and consecrated term used by chiropractors. To add to the confusion, more than 100 synonyms for subluxation have been used (Table 1-1). Why then do we persist in using the term subluxation when it has become so "overburdened with clinical, political, and philosophical meaning and significance for chiropractors, that the concept that once helped to hold a young besieged profession together"(l) now divides and keeps it quarreling over basic semantics? The obvious answer is provided by Terren(3): The concept of vertebral subluxation is central to chiropractic. The notion that by changing the word s,ibluxation to another term we will somehow change the clinical, political, and philosophical connotations of the concept is simply nOt rational. Changing the term used for the articular lesion treated by chiropractors (subluxation) does not eradicate the clinical, political, and philosophical issues that surround the construct; it obviously evades the issues(2,3). We have found it expedient to clearly and simply define the term subluxation and to anempt to objectively address the issues that surround the conStruct. The conceptual definition of subluxation has been the foundation on which chiropractic science has stood . It is now
time to operationally define subluxation by identifying the testable components of misalignment, aberrant motion, and dysfunction included in the definition. With these components delineated, we can examine current data and further study the topic of our discourse.
DefIning SUbluxation The definitions of subluxation and related terms used in this book are those developed through
consensus methods, using the algorithm developed by Ganerman and Hansen (Figure 1-1). These terms have been agreed on through both nominal and Delphi methods that included broad geographic, philosophical, and political representation. The field of terms includes subluxation, used for the articular lesion that is less than a dislocation; manipulable subluxation, subluxation that is amenable ro chiropractic manipulation; subluxation complex, the theoretical model that describes the widespread effects of subluxation; and subluxation syndrome, the clinical manifestations, including the associated symptoms and
physical signs of a subluxation. Each term is expanded on as it relates to the principles of chiropractic, and support for these principles is the subject matter of this text. Essential for the definition of subluxation has been clarification of the term molion segment. Definitions of therapeutic procedures used by chiropractots includes the terms manual therapy, manipulation, mobilization, and most importantly, adjustment. To arrive at consensus for terms commonly used by chiropractors, the origin of each term is examined relative to the concepts that underlie the profession.
OrIgIn of Ihe Word SUbluxation The rOOt words for the term subluxation come from a combination of the Gteek sub and lux, meaning " less than a dislocation. " In 1746, Hieronymus described a subluxation, identifying the following characteristics(4): .. . subluxation of joints is recognized by lessened morion of the joines, by slight change in posirion of the articulating bones and pain . ..
This does not differ significantly from the consensus definition agreed on by the nominal and Delphi panels of the Consortium for Chiropractic Research, which defined subluxation as follows:
IIMIxIlllOn
a motion segment in which align-
ment, movement integrity, and/or physiologic
function are altered although contact between the joint surfaces remains intact.
1 What'l ln a word
7
Subluxation Synonyms Synonym
Author
Vllr
Aberrant motion Abnormal joint motion
Garrerman
1992 1989 1992 1992 1993 1831 1989 1936 1985 1993 1965 1965 1985 1992 1954 1988 1993 1985 1988 1993 1960 1960 1985 1993
Acute cervical joint lock Acute locked back Apphyseal subluxation Articular derangement Articular dyskinesia Blockage Blocking Cervical joint dysfunction Chiropractic subluxation
Chiropractic sublux. complex Delayed instability Derangement Dysarthritic lesion Dysarthrosis Dysfunctional joint Dystopia Erratic movement
Facet joint dysfunction Facet syndrome Facer synovial impingement Facilitated segment Fanning of interspinous space Fixation Functional block Functional spinal lesion
Hyperemic subluxation Hypermobility Hypomobility
Lantz Ganerman Haas, Peterson DeBoer, Hansen Wark Lantz Hadley Dishman Slosberg Kunert Kunert Good Salem Indust. Biedermann Brantingham Chapman-Smith Dishman Brantingham Pate Collings Dalgleish Dishman Siosberg Gongal'skii, Kufryreva Watkins Darrer Mooney, Robertson Collins Dishman Pate Homewood Dishman Crawford Siosberg Hill Gatterman Brantington
Garrerman
1992 1968 1993 1976 1951 1985 1993 1963 1985 1992 1993 1949 1992 1988 1992
8
Sublux81lon
>
The ArtIcular lesion
Subluxation Synonyms
dl Synonym
Author
Year
Incomplete articular dislocation
Hubka Pate (Cheshire) Pate Brantingham Watkins Hubka Good Northrup Haldeman Watkins Watkins Watkins (Smith) Wood Brantingham Haldeman Brantingbam Hubka D.ishman (Suh) Boissonaulr, Bass Lohse-Busch Haas, Peterson Sinh Vance, Gamburg Hubka
1990 1992 1993 1988 1968 1990 1985 1975 1975 1968 1968 1968 1984 1988 1979 1988 1990 1985
Dishman
D.algleish D.algleish
1985 1960 1960
Watkins
1968
Siosberg D.algleish Collins Halliday Brantingham Collins Haldeman Watkins
1993 1960
Instability of the posterior ligament complex Intersegmental instability
Intervertebral blocking Intervertebral disrelationship Joint aberration
Joint bind Joint dysfunction Kinetic intersegmental subluxation Kinetic subluxation
Less than a locked dislocation Ligatights Locked facet Locking Manipulable lesion Manipulable joint lesion Manipulable lesion Mechanical disorder Mechanical musculoskeletal dysfunction Metameric dysfunction
Misalignment Motor unit derangement complex Motion restriction Neuroarticular dysfunction Neuroarricular subluxation
NeuroarticuJar syndrome Neurobiomechanical (lesion) Neurodysarthritic (lesion) Neurodysarthrodynic (lesion)
1990 1989 1992 1993 1992 1990
Neurofunctinal subluxation
Neurologic dysfunction Neuromechanicallesion
Neuromuscular dysfaciLitation Orthospondylodysarthritics Osteologic lesion Osteopathic articular lesion Osteopa thic lesion Osteopathic spinal lesion Paravertebral subluxation
Partial fixation
?
1936 1988 1975 1968
1 WhIt'IIn a WDrd
>
9
Subluxation Synonyms "
-..
>
"'~u-.'7"" •• ".--,...
\;.
Synonym
Autho,
Year
Posterior facer dysfunction Primary chiropractic lesion Pseudosubluxation Reflex dysfunction Restriction
Haldeman Gatterman Pate Salem Indust. Good Slosberg Haldeman Pate Dishman Mootz Trostler Watkins Northrup Keating Innes Wark Good Dalgleish Bourdillon Johnson Haldeman Dalgleish Palmer Pate (Harris) Ha ldeman Watkins Hieronymus Faye
1975 1990 1990 1992 1985 1993 1975 1993 1985 1993 1938 1968 1975 1992 1993 1831 1985 1960 1982 1985 1975 1960 1910 1993 1975 1968 1746 1986 1993 1992 1968 1965 1992 1985 1969 1976 1989
Sectional subluxation Segmental dysfunction Segmental vertebral hypomobility Simple joint and muscle dysfunction without tissue damage Slipping sacroiliac joints Soft tissue ankylosis Somatic dysfunction Spinal boo boo Spinal hypomobilities Spinal irritation Spinal joint blocking Spinal joint complex Spinal joint stiffening Spinal kinesiopathology Spinal subluxation Spondylodysarthritic lesions Sprain Stable cervical injury of the spine Static intersegmental subluxation Structural disrelationship Subluxation Subluxation complex Subluxation complex myopathy Subluxation syndrome Total fixation Vertebral displacement Vertebral dysfunction Vertebral dyskinesia Verrebrallocking Vertebral subluxation complex Vertebral subluxation syndrome Modi fied from Rome P, Terrett A. The names in brackers are o riginal autho rs cited by others.
Peterson
Gatterman Watkins Kunert Lirtlejohn Dishman Stoddard Faye Lantz
10 Terminology assessment model
AtIII'8 1-1 The definition allows for physiologic dysfunction, which was described as follows by Harr ison(3) in 1821: When any of the vertebrae become displaced or [00 prominenr, the patient experiences inconvenience
from a local derangement in the nerves of the parr. He, in consequence, is ro rmented with a train of nervous symprol11s, which are as obscu re in their origin as they are stubborn in their nature . ...
Harrison also considered a lignment a nd motion when describing subluxations, and in 1824 he wrote: The articu lating extremities are only partially sepa· rated , nor imperfectly disjoined . ..
and ... the articula r motions arc imperfectly per-
In case of a simple vertebral subluxation, the vertebra is not lodged in a fixed and permanent abnormal position li ke a displaced brick in the wall; (0 consider it so is preposterous for it is a moveable bone in a flexible and moveable co lumn. A simple subluxared vertebra differs from a norma l verrebra on ly in its field of motion, bur because of its being subluxated, its va rio us positions of rest are differently located than when it was a normal vertebra. . . its field of mocion may be roo great in some directions and too sma ll in others.
Within a decade of its inception, the chiropractic profession was arguing over the definition of su bluxation, the primary focus of chiropracric treatment. Was it misalignment, alteted motion, or joint dysfunction? Why not anyone, two, or all three?
formed, because the surfaces of the bones do nO[
fully correspond(3). Although Palmer himself foc used on misalignment in his ea rl y definition of chiropracric, he a lso wrote extensively on the neurologic effects produced by subluxa ri on. In perhaps rhe earliest published chirop ractic text, Modernized Chiropractic(S), autho rs Smith, Langsworthy, and Paxson wrote:
Manipulable and Nonmanlpulable SubluxaUons Not all subluxations respond CO manipulation; in fact, those subluxations most often seen on radiograp hs are often nonmaniplJlable or parhologic subluxa tions that are not reversible or that
11 require surgical repair (see Chapter 8). It is important that when defining subluxation the definition be broad enough ro include the medical concept of subluxation that is severe enough ro be visible on radiograph, as well as the more subrle manipulable subluxation detected by palpation. The manipulable subluxation is further defined as: IIIIIipuIIbIe IIMIxa1Ion a subluxation in which altered alignment, movement, or function can be
The terms subluxation complex and subluxation sy"drome are used as a means of broadening the idea of the effects of subluxation without attaching untested theories to the description of the articular lesion that responds ro manipulation. In any definition, words or phrases that need clarifying mUSt be clearly stated. So it is with the term motio" segment. The need for a term that can be applied ro peripheral joints as well as to spinal joints fostered the following definition:
improved by manual thrust procedures. Moving beyond subluxation as exclusively a joint phenomenon and addressing the complex of neurologic effects theorized to be caused by articular subluxation, the term subluxatio" complex is used. This has been defined as: IIMIxa1Ion _ _ x a theoretical model of motion segment dysfunction (subluxation) that incorporates the complex interaction of pathologic changes in nerve, muscle, ligamentous, vascular, and connective tissues.
The subluxation complex was first described by Faye in the mid 1970s(6). Building on the work of Gillet, IIIi, Homewood, and janse, Faye(6) formulated a theory that the chiropractic spinal adjustment (manipulation) restores normal joint motion, which in turn normalizes physiologic
function. The subluxation complex has been developed further by Lantz(7) and is discussed in Chapter 9. Subluxatioll SYlldrome is the term used ro describe the clinical manifestations of subluxation (articular lesion). Most widely recognized among these syndromes are mechanical back pain, neck pain, and vertebrogenic headaches. Subluxation syndrome is defined as:
.y.......
IIMIxa1Ion an aggregate of signs and symptoms that relate to pathophysiology or dysfunction of spinal and pelvic motion segments or ro peripheral joints. The clinical manifestarions of subluxation syndromes are discussed in Part 3 of this text.
III01IIIn .......1 a functional unit made up of two adjacent articulating surfaces and the connecting tissues binding them to each other. The following definition is mote specifically related ro the joints of the spine:
.... 1IIOIIan .......1 twO adjacent vertebrae and the connecting tissues binding them ro each other. The origin of the functional unjt of the three-joint spinal motion segment comes from junghanns, who coined the term bewegungssegment. The inaccurate translation(8,9) of bewegungssegme"t to "motor segment" by Besemann in 1971(10) was clouded further when the term was modified to "moror unir" and popularized through the proceedings of the NrNCDs monograph, "The Research Status of Spinal Manipulative Therapy," published in 1975(11). The prior use of "motor unit" by physiologisrs ro refer ro a single motor neuron and the group of muscle fibers that it innervares has precipitated the need for clarification of the concept with standardization of the term.
Denning Chiropractic lreatment Methods Chiropractic treatment has been directed traditionally ro the resroration of function and has not been designed solely to relieve pain. just as the primary lesion treared by chiropractors has been subluxation, the primary chiropractic technique has used manual procedures ro treat the body. As with the term subluxation, much confusion and
12 controversy has surrounded the use of terms and
definitions used to describe chiropractic treatment methods. To clarify the procedures used by chiropractors, the terms manual therapy, manipulafion mobilization, and adjustment were subjected to the consensus process. The definitions arrived at are as follows:
niilllllllllllil1 movement applied singularly or repetitively within or at the physiologic range of joint motion, without imparting a thrust or impulse, with the goa l of restoring joint mobility.
J
manuallherapy procedures by which the hands directly COntact the body to treat the articulations or soft tissues .
The term manllal therapy generated little controversy, but it is included because of the lise by some of the terms mallip"latioll and spinal manipulative therapy synonymously with mal1ltal therapy. By using these terms inclusive of manual procedures, mobilization becomes a form of
manipulation. It is necessary CO differentiate manipulation from mobilization because recem studies have indicated the greater effectiveness of thrust procedures (manipu lation ), for example, in the treatment of back pain. Early studies did not make this distinction when producing equivocal data as ro the effectiveness of manipulation. As mo re studies are undertaken, many more may
show different effects from thrust versus nonthrust procedures, making this distinction even more critical. Unknowing patients may assume that they have received manipulation when indeed they have not when mobilization is considered a form of manipulative therapy, thus denying them the possible benefits of thrust techniques. Based on the 1991 RAND study(12) that looked at the appropriateness of spinal manipulation for low-back pain that defined manipulation as a thrust procedure, the following definition reached consensus :
IIIIIIIpIDtIon a manual procedure that involves a ditected thrust to move a joint past the physiologic range of motion without exceeding the anaromic limit. To differentiate manipulation from nonthrust mobilization, the following definition was ag reed on:
Next to the term slIblllxatioll, the use of the word adillstment has sparked the most heated debate. It was agreed that chiropractOrs applying the adjustment intend [0 influence morc than joint mechanics and related pain. The resultant definition that reached consensus therefore includes reference to changes in neurophysiologic function. Although some believed that the adjustment should be restricted to specific short-lever, highvelocity, low-amplitude thrust techniques, it was agreed to define the term broadly enough to not exclude those procedures routinely used by chiropractOrs that fall outside of this narrow category. The resultant definition is as follows:
IItIItment
any chiropractic therapeutic procedure that uses controlled force, leverage, ditection, amplitude, and velocity directed at specific joints or anaromic regions. Chiropracrors commonly use such procedures to influence joint
and neurophysiologic function. The reference to neurophysiologic function in the definition of adjustment and nOt in that for manipulation is not intended to imply that such neurophysiologic effects do not occur with manipulation, that is, thrust procedures. On the contrary, it may be demonstrated that manual thrust procedures through reflex mechanisms produce widespread effects. These mechanisms are the subject of Part 2, in which data are discussed that support Palmer's later contention that [he
body is not a sim ple machine but rather a complex interaction of systems mediated by the nervous system(12) . To those traditionalists who want chiropractOrs to use on ly the term adiustmellt as opposed to manipulatioll, it is noted that D. D. Palmer used the term mallipulatioll to describe his early techniques, and nor until later in the twentieth century was the term adjustment lIsed for Palmer's unique style of manipulation(13 ).
CIIapter 1
What's In • Word
13
Issues 01 Chlropracdc Terminology Unfortunately, when it comes to the word subluxation, too many chiropractors act quite like Humpty Dumpty in Lewis Carroll's Through the Looking Glass: "' . . . When I use a word,' Humpty Dumpty said, in rather a scornful tone, 'it means just what I choose it to mean-neither
more nor less . ... ", Such an attitude toward the use of the word subluxation, as with any term, does nor facilitate communication; as Lawrence(14) has stated that " ... one of the greatest challenges facing the chiropractic profession today is simply to learn how to communicate with one another." He emphasizes the seriousness for the chiropractic profession of miscommunication from semantic confusion, stating, "Semantic difficulties
have hampered our overall development.»
Oppositional TlIinking As with many issues, much of the controversy surrounding the use of the term subluxation has
involved dualism or oppositional thinking by which the phenomenon is either/or but not both . If a subluxation is A, it therefore cannot be B. If I am right, you must be wrong. Examples include those who view a subluxation as an alteration of motion in which the misalignmem component is
nonexistent or at best unlikely, or as a medical term used to describe displacement without joint dysfunction(15) . It seems probable that sublu xation refers to impaired mobility with or without positional alteration. In many cases the misalignment component is not discernible by current technological methods and cannot be used as the sole criteria for subluxation detection. Slighr misalignment cannot be accu ratel y ascertained by analyzing radiographs, and in those cases where misalignment is gross enough to be detectable by plain film radiographs, manipulation may be contraindicated because of excessive motion . As Howe and Phillips(16) have both noted: Any method of spinographic interpreta tion which
utilizes millimetric mensurations from any set of preselected points is very likely ro be faulty, because structurally asymmetry is universal in all vertebrae .
Does this mean that a subluxation must be gross enough to be detectable on radiographs to be identifiable? Some consider that the term sublllxatio" should be reserved for radiographically measurable positional disrelationships of joint surfaces. Others suggest that subluxation should be reserved for static positional relationships measured in in vitro investigations(17). For 100 years have chiropractors been treating a lesion detectable on ly in vitro? Yet others claim that subluxation has not been measured in any case. At the extreme, if a subluxation is a misalignment, then it is not motion restriction but rather a vertebra out of place. Alternatively, the subluxation is viewed as a motiory restriction, and no component of malposition should be considered. This is attractive to some, given the current lack of sophistication of methods available to consistently detect spacial disrelationships radiographically; logic leads us to conclude that we are dealing with a functional entity involving restricted vertebral movement. Rationally, it is the movement restriction component of the manipulable subluxation that responds to thrust procedures, yer reliable measurement of motion remains as elusive as radiographic detection of subtle misalignment. Does this mean that pain is the sole reliable criterion for detection of subluxation? What of nonmanipulable subluxation with excess motion and instability? Is it not painful? This brings us full circle and leads to a definition of subluxation in which all three components of the subluxation should be considered:
1. Misalignment or spatial relationship 2. Excessive or restricted motion 3. Dysfunction with or without pain
14
Subluxation
Tbe AI'tIcuIar Laslon
One component should not be used to describe or de tect a subluxation to the exclusion of any other, nor must all three components be present. Similarly, we saw that the prechiropractic use of the word subluxatioll included slight change in posi-
tion of the articulating bones, lessened motion of the joints, and pain . Why then must we now relegate the term subluxatioll to a lesion with only one of the early distinguishing features?
Issues Surrounding the Use 01 the Word Subluxation Historical Issues Early chiropractic terminology became distinctive to differentiate the new profession from both osteopathy and medicine. Whereas the osteopath manipulated the osteopathic lesion, the chiropractor manipulated (and later adjusted) the subluxation. D. D. Pa lmer sought to differentiate chiropractic from osteopathy, probably in response to charges of having stolen ideas from the founder, Still(18). The distinction that chiropractors do nor diagnose symptoms and trear d.isease,
rather they analyze the spine and adjust subluxations, although a successful legal defense, has led to much isolation and great misunderstanding of the chiropractic profession.
The Philosophical Issue T he use of the word subluxation as a metaphor has created a phi losophic issue whereby subluxatioll becomes like the medical use of the word disease, the eradication of which resto res the homeostasis of the body and eliminates all human ailments(19) . Although it remains to be conclusively demonstrated that, as
Harrison wrote in 1820, "an almost infinite variety and endless complication of nervous symptoms" may be the effects of subluxation, this theory must be kept in perspective, examined, and tested. Criticism of the va lidity of this basic premise must nOt be auromacically rejected as an attack on the chiropractic profession but viewed as a cha llenge to be met. Evidence that supports the va lidity of the theory espoused by Palmer(20) that subluxations cause functional changes in the
nervous system is presented in the following chapters. Emotional and unbending adherence to this construct by some without crideal evaluation
has polarized the profession. The notion that subluxation is the cause of all disease is not rationa ll y defensible and has caused much derision of the chiropractic profession to be brought on by dogmatic proponents of this theory(21). Evidence must be evaluated and integrated where rational to support the principles of chiropractic theory.
The Political Issue The political controversy surrounding the use of the word subluxatioll stems from the medical influence that adds the qualification that visual evidence of subluxation must be demonstrated on radiographs(22). This is nOt stated, however, in the following dictionary definitions of subluxation:
1. Subluxation: A partial dislocation(23 ) 2. Subluxation: Partial dislocation (as of one of the bones in a joint)(24) 3. Subluxation: An incomplete or partial dislocation(25) 4. Subluxation: A partial or incomplete dislocation(26) 5 . Subluxation: An incomplete luxation or dislocation; though a relationship is altered, contact between joint surface remains(27)
Yet radiographic visualization of a subluxation is the criteria for reimbursement of the treatment of
subluxations by chiropractors under the United
1 WhaflIn a WOI'd States Medicare and Medicaid Acts. Because the reliability of radiographic detection of manipulable subluxations has been questioned, some believe that by abandoning the term this issue can be sidestepped . What then of Medicare and Medicaid coverage of chiropractic patients? The emotional response of some with regard to this politica l issue again stems from the derision of chiropractic that comes from those who deny the existence of manipulable lesions on the grounds that they are nor consistently seen on radiographs. Rather than falling prey to this political ploy, we must clearly determine and agree on the crireria used to detect manipulable subluxations, which is the primary issue surrounding the subluxation as
a clinical entity. We are once again polarized by those who wish to abandon the term on the basis of medical territoriality that requires radiographic detection and those who cling to dogmatic philosophic beliefs. Medical use of the rerm subluxation for the lesion that responds to manipulation, as we have
noted, existed before the advent of radiographs(3) and continues to be used in this manner. Examples are: "Sacroiliac subluxation " implies that ligamentous stretching has been sufficiem to permit the ilium to slip o n the sacrum. An irregu lar prominence on
one articu lar surface becomes wedged upon another prominence of the other articular surface, the ligaments are taut, reflex muscle spasm is inten se, and pain is severe and conrinuous uneil reduction is effected. The displacement is so slight that it cannot be recognized in roentgenograms ... . The pain of subluxation is often relieved dramati-
cally and suddenly by manipulation(28). and Subluxated Facet Joint: The facet syndrome, which can cause severe back pain, consists of a subluxarion or partial dislocation of a lumbar vertebral facet joint. This is rhe condirion most likely to be relieved when a chiropractor manipulates [he
spine(29). It is apparent that medical use of the term subluxation when referring to the lesion treated by
15
manipulation does not require radiographic evi-
dence to support the existence of this clinical entity. A more reasonable solution seems to be a
classification of subluxation in which the most severe are seen on radiographs and are nOt
a lways amenable ro manipulation. The less extreme lesions, which are sti ll subluxations of a lessor degree, are nonetheless articular lesions, but less so than dislocations and, in many cases,
manipulable subluxations.
Clinical Issues As previously noted, rhe method of detection is the primary clinical issue su rrounding the sublu xation concept. It is ironic that an effective method of treatment has existed for centuries, yet there is no common agreement on the criteria
used to detecr the lesion ro be treated. Various palpation procedures have been developed, which has been the traditional method used to detect subluxation; yet these merhods are under crirical attack for poor interrater reliability. Difficulty arises i;' describing palparory procedures because we use one-d imensional language to conceptualize a three-dimensional abstraction. Diagnosis of
the manipulable subluxation is dependent on the kinestheric perception of the palpating chiropractor, which is more akin to reading braille: threedimensional and difficult to translate verbally. This phenomenon, which may account for the greater intra rater reliability than interrater relia bility, must be better understood if we are to further improve rhe chiropracror's diagnostic predictability. This issue is addressed further in Chapter 4. The dogma and irrationa li ty exhibited by some regarding the derection of subluxation is embodied in the following quote: «A chiropractic case is one with a sublu xation . . . . We take a case even though ou r insr.rumentation doesn't show a
subluxation because we know it's there"(30) It is reasonable and rational to objectively determine the most reliable method of detection of subluxations rather than to continue to argue over which
16 method of detection is most effective. The detection of subluxations has given tise to a multitude of technique systems that apply a cookbook approach to diagnosis of chiropractic disorders. These include muscle testing, leg length checks, and finite radiographic marking procedures. The medical criterion of using pain syndromes as the criteria for manipulative therapy is an abandonment of the specificity that chiropractic diagnosis has employed in analyzing mechanical disorders of the spine. It does not rationally account for the pain produced by nonmanipulable subluxations, which cannOt be differentiated by using pain as the primary diagnostic criteria.
Economic Issues Perhaps the most damaging of all issues, considering today's economy and the escalating cost of health care, is the overtreatment of subluxations charged to third-party payers. Ongoing treatment of subluxations attributable to work-related and personal injuries, which in most cases have long
since healed, strains the credibility of the chiropractic profession. It is imperative that chiropractors differentiate between the subluxation leading ro joint dysfunction and tissue abnormalities. Simple subluxations, exhibiting restricted motion only, respond rapidly, in one or rwo treatments, to manipulation. More seriously injured joints,
with injured holding elements and accompanying surrounding soft tissue damage, take much longer to heal. It is essential that the chiropractor make two types of assessment. The first is a biomechanical analysis to determine the site and nature of the subluxation . This determines where and whether manipulation and other adjustments are appropriate. The second form of assessment is a diagnosis necessary to ascertain the extent of pathologic damage and ro determine the type of adjunctive thetapy that will hasten the healing process. The first diagnosis (biomechanical analysis) is necessary to determine the functional component of the patient's coodinon, whereas the second diagnosis gives the patient's prognosis with regard to healing time. Both the functional
and pathologic diagnoses must be considered and recorded as parr of ethical and legal records and are necessary when seeking insurance reimburse-
ment(31 ).
Conclusion The establishment of any profession requires terminology unique to that profession. Unless chiropractic would become ancillary to medicine as is physical therapy; or co-opted and included in medical practice as is osteopathy, it is imperative
that the chiropractic profession continue to develop and maintain its distinctive nomenclature. This is nOt to say that chiropracrors should cling to outdated concepts and ambiguous terms. It is incumbent on the chiropractic profession to come to consensus whereby key terms used to describe chiropractic procedures and practices are used universally. The chiropractic profession has long enjoyed clinical legitimacy. If we are to move into the realm of scientific legitimacy, we must operationally define the terms we use for the methods we employ. Chiropractors do not have to be adversarial to medicine. Practically speaking, the chiropractic profession is not an alternative form of medicine,
but, like acupuncture, homeopathy, and naturopathy, is complementary to current medical practice. Chiropractic science is considered a poorly organized science by many. The first step in the organization of any science is the establishment of nomenclature that is widely recognized and accepted . What is in the word subluxatloll? The chiropractic subluxation is a more subtle lesion than the radiographically recognized medical subluxation. For thousands of years before the advent of x-rays, manipulation was employed to alleviate pain and loss of function from joint lesions less than a luxation or complete dislocation. For 100 years chiropracrors have been successfully diagnosing and treating manipulable subluxations, relieving much human suffering. A foundation of the chiropractic profession is the primary lesion treated with manual therapy: the subluxation.
1 WIIIt'1In • WUI'd
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22. 23. 24. 25. 26. 27. 28. 29. 30. 3 1.
17
behavior, pathology, etiology, and nomenclature of the chiropractic lesion. ACA J Chiropractic 1985; 19:8. Phillips RB. The use of x-rays in spinal manipulative ther· apy. In: Ha ldeman S, ed. Modern developments in the principles and practice of chiropractic. East Norwalk, Connecticut: Appleton-Century-Crofrs, 1979: 189-208. Hubka MJ. Another critical look at the subluxation hypothesis. Chiro Technjque 1990; 2:27-9. Brantingham JW. Stili and Palmer: the impact of the first osteopa th and (he first chiropractor. Chiro History 1986; 6,19-22. Keating Jc. The evolution of Palmer's metaphors and hypotheses. Philosophical Constructs for the Chiropractic Profession, National College of Chiropractic, 1992. Palmer DO. The chiropractor's adjuster: the scie nce, art and philosophy of chiropractic. Portland, Oregon: POrt· land Printing House, 191 0:57. Keating Jc. Toward a philosophy of the science of chiropractic. Stockton CA: Stockton Foundation for Chiropractic Research, 1992:25-49. Watkins RJ. Subluxation terminology smce 1746. JCCA 1968; 4,2H. Urdan L, ed. Mosby's medical and nursing dictionary. St loU"" Mosby, 1983, I 032. Pease RW, ed. Webster's medical desk dictionary. Springfield, Massachusetts: Merriam-Webster, 1986:685. Taylor EJ, ed. Jl\ustrated medical dictionary. 27th ed. Philadelphia: WB Saunders, 1986: 1599. Davis CL, ed. Tabor's cyclopedic medical dictionary. 16th ed. Philadelphia: FA Davis, 1989: 1772. Hensyl WR, ed. Stedman's medical dictionary. 25th ed. Baltimore: Williams & Wilkins, 1990:1494. Turek SL. Orthopaedics principles and their application. 3rd cd. Philadelphia,JBlippincot, 1977, p1469. Keirn HA, Kirkaldy·Wiliis WHo Low back pain. CIBA Cli nical Symposia 1980; 32:6. Wardwell WI. Chiropractic: history & evolution of a new profession . St. Lo uis: M osby, 1992:27 1. Gatterman MI . Chiropractic management of spine related disorders. Baltimore: Williams & Wilkins, 1990:397.
........ Anatomy Related to Spinal Subluxation Gregory D. Cramer
SUsan A. Darby
KeyWOrds
Zygapophyseal joint, intervertebral disc, intervertebral foramen, radicular pain
After reading this chapter yOIt should be able to answer the following questions:
Quesllon #1
What structures form the boundaries of the intervertebral foramen (IVF)?
Question #2
What is radicular pain?
QueSUIII #3
How might treatment of a subluxation decrease somatic referred pain?
19 a vascular central layer made lip of areolar cissue and loose connective tissue, and an inner layer
T
he relationship between the anatomic com-
ponents of the spinal motion segment is criti-
cal to understanding the spinal subluxation model. This three-joint complex consisrs of the two zygapophyseal (posterior) joints and the (anterior) intervertebral disc. These structures interact to
form the funcrional unit of the spine. The position of the intervertebral foramen provides a significant boundary between the central nervous system and the peripheral nervous system, and in some cases it may
be
structurally important to nociceprion aris-
ing from the spinal motion segment (subluxariongenerated pain). Pain of spinal origin is transmitted through peripheral and central neural structures and is modulated at various sites.
consisting of a synovia l membrane (3). The anterior and medial aspect of the Z-joint is covered by the ligamentum flavum. The synovial membrane lines the articular capsule, the ligamentum flavum (4), and the synovial joint folds (see following discussion), but not the articular cartilages of the joint surfaces (1). The Z-joint capsules throughout the vertebral column are thin and loose and are attached to the margins of the opposed superior and inferior articular facets of the adjacent vertebrae (5). Superior and inferior protrusions of the joint capsules, known as recesses, bulge out from the tOP and bottom of the joint. These recesses are filled with adipose tissue, and the inferior recess is
The Zygapophyseal Joints
larger than the superior recess (6). The capsules are longer and looser in the cervical region than in the lumbar and thoracic regions. This is to
General DescMpUon
compensate for the greater amount of movement that occurs in this region. As mentioned previ-
The junction between the superior and inferior articular faccts of the articular process
(zygapophyses) on one side of two adjacent vertebrae is known as a zygapophyseal joint (Z-joint). These joints are also referred to as facet joints or inter/aminar joints (I). The Z-joints are classified as synovial (diarthrodial) planar joints. Of course, there is a left and right Z-joint between each pair of vertebrae. They are rather small joints, and although they allow motion to occur, they are perhaps more important because of their ability to determine the direction and limitations
ously, the anteromedial aspect of the joint is formed by the ligamentum flavum (4), and hyaline cartilage covers the surface of each facet.
Tbe Zygapophyseal Joint Synovial Folds
The Z-joint is of added interest to those who
Zygapophyseal joint synovial folds are synoviallined extensions of the capsule that protrude into the joint space to cover part of the hyaline cartilage. The synovial folds vary in size and shape in the different regions of the spine. Engle and Bogduk in 1982 (7) reported on a study of 82 lumbar Z-joints (cervical folds are discussed later). They found at least one intraarticular fold (meniscus) within each joint. The
treat spinal conditions because, as is the case in any joint, loss of motion or aberrant motion may
three types: The first was described as a connec-
be a primary source of pain (2).
tive tissue rim found running along the most
ArtIcuI.. capsules
tive tissue rim was lined by a synovial membrane.
Each Z-joint is surrounded by a capsule posterolaterally (Figure 2-1). The capsule consists of an
The second type of "meniscus" was described as an adipose tissue pad, and the third type was identified as a distinct, well-defined, fibroadipose meniscoid. This latter type of meniscus was usually found entering the joint from the superior or inferior pole of the joint (or both).
of movement that can occur between vertebrae.
intraarticular Structures were categorized into
peripheral edge of the entire joint. This connec-
outer layer of dense fibroelastic connective tissue, Adapted from Cramer C, Darby S. Basic and clinical anammy of (he spine, spinal cord, and ANS. St. Louis: Mosby, 1995.
20
Z joint
A
Z joint
--- -
--- lumbar
fIIIpe 2·1 The zygapophyseal joint showing the layers of the articular capsule. A, Typical zygapophysea l joints of each vertebral region. B,
Typical zygapophyseal joint. The layers of the Z·Joint as seen in parasagirtal section (inset) are color coded as follows: light blue, joinr space; dark blue, articular cartilage; brown, subchondral bone; red, synovial lining of articular cartilage; pink, vascularized, middle layer of the articular capsule; violet, fibrous outer layer of the articu lar capsule. (From Cramer, Darby. Basic and dinical anatomy of the spine, spinal cord, alld ANS. St. LOllis: Mosby, 1995.)
.=.--+--
s..bchondoal
bone
• Giles and Taylor (3) studied 30 zygapophyseal joints, all of which were found to have "menisci." The "menisci" were renamed zygapophyseal joint
synovial folds because of their histologic makeup. Free nerve endings were found within the folds, and the nerve endings met the criteria for pain
21 receptOrs (nociceptOrs). That is, they were distant from blood vessels and were of proper diameter (6 to 12 ~ms) . Therefore, the synovial folds or menisci themselves were thought to be pain sensitive. This meant that if the Z-joint synovial fold became compressed by or trapped between the articular facets making up the Z-joint, back pain could resulr.
IJnIque Characteristics 01 the cervical Zygapopltysaal J«*rts The cervical Z-joints lie approximately 45° to the horizontal plane (8). More specificaliy, the facet joints of the upper cervical spine lie at approximately a 35° angle to the horizontal plane, and the lower cervical Z-joints form a 65° angle to the horizontal plane (9). The superior articular processes and their hyaline cartilage-lined facets face posteriorly, superiorly, and slightly medialiy. The appearance of rhe cervical Z-joints changes significantly with age. Before the age of 20 years the articular cartilage is smooth and approximately 1 to 3 mm thick, and the subarricular bone is regular in thickness. The articular cartilage thins with age, and most adult cervical Z-joints possess an extremely thin layer of carrilage wirh irregularly thickened subarricular cortical bone. These changes of articular cartilage and the subchondral bone usually go underected on magneric resonance imaging and computed tOmography scans. Osteophytes (bony spurs) projecting from the arrieular processes and sclerosis (thickening) of the bone within the arricular processes are quite common in adult cervical Z-joints.
Cervical ZygapophY8ea1 Joint Synovial Folds Zygapophyseal joint synovial folds (menisci) project into the Z-joints at all levels of the cervical spine. Yu et al. (10) found four distinct types of cervical Z-joint menisci, ranging from thin rims to thick protruding folds. Yu et al. demonstrated several types of folds on magnetic resonance imaging scans.
marvallon 01 the Z-JoInt8 The Z-joint capsule receives a rich supply of sen-
sory innervation. The sensory supply is derived from the medial branch of the posterior primary division (dorsal ramus) at the level of the joint, and each joint also receives a branch from the posterior primary division of the level above (Figure 2-2). In addition, Wyke (11) states that there are three types of sensory receptors in the joint capsule of the Z-joints. These are as follows :·
type I very sensitive static and dynamic mechanoreceptOrs, which fire continua ll y to some extent even when the joint is not moving
type I
less sensitive and fire only during move-
ment
Mixed spino I nerve Posterior primary
division (dorsal ramus) Anterior primor'( division (ventra ramus)
lateral branch of PPO Medial branch of PPO
Ascending division Descending division
Agtre 2-2 Innervation of the zygapophyseal joints. Notice each posterior primary division (dorsal ramus)
divides into 3 medial and lateral branch. The medial branch has an ascending division which supplies the Zjoint at the same level and a descending division which supplies the Z·joint immediately below. (From Cramer, Darby. Basic and clinical anatomy of the spine, spinal cord, and ANS. 51. LOllis: Mosby, 1995.) ·Note char type Ulare nociceptive fibers found in joints of (he extremities, and Wyke (10) did nOt find these in the Z·jolnts.
22
SublUXallon
The Ar1IcuIr 18110n
type IV slow conducting nociceptive mechanoreceprors
The Intervertebral Disc The intervertebral disc (!VO) is composed of water, cells (primarily chondrocytelike cells and fibrob lasts), proteoglycan aggregates, and collagen fibers. The proteoglycan aggregates are composed of many proteoglycan monomers attached to a hyaluronic acid core. Howeve~ the proteoglycans of the lVD are of a sma ller size and are of a different composition than the proteoglycans of cartilage found in other regions of the body (articu lar cartilage, nasal carti lage, cartilage of growth plates) ( 12) . The lVO is a dynamic structure that has been shown to be able to repait itself and is capable of "considerable" regeneration (13). The !VO is composed of three regions known as the anulus fibrosus, the nucleus pu lposus, and the vertebral (cartilage) end plate (Figure 2-3). Together they make up the anterior interbody joint or intervertebral symphysis. Each of these regions consists of different proportions of the pri mary materials that make up the disc (see previous discussion) .
Anulus Abrosus The a nulus fibrosus is made up of several fibrocarti laginous lamellae or rings, which are convex
externally. The lamellae are formed by closely arranged collagen fibers and a smaller percentage (10% of the dry weight) of elastic fibers (14). Most of the fibers of each lamella run parallel with one another at approximately a 65° angle from the vertica l plane. The fibers of adjacent lamellae overlie each other, forming approximately a 130° angle between the fibers of adjacent lamellae. The most superficial lamellae send thick bundles of collagen into the bone of the vertebral rims in the region of the ring apophysis. These bundles are known as Sharpey's fibers. They form firm attachments between the intervertebral discs and the vertebral body. The inner lamellae of the anulus fibrosus attach ro the cartilaginous vertebral end plate. The direction of the
..... 2-8 MRl of a sagittal section of the intervertebral disc with adjacenr vertebral bodies. The parts of the intervertebral disc are labeled (Photograph by Ron Mens ching, illustration by Dino Juarez. The National College of Chiropractic. (From Cramer. Darby. Basic and clinical spinal anatomy o f the spine,
spillal cord, alld ANS. St. LOllis: Mosby, 1995)
lamellae varies considerably from individual ro individual and from one vertebra ro the next (15 ). The lamellae of the anulus fibrosus are subject ro tear. These rears occur in two directions, cit-
cumferentially and radially. Many investigators believe that ci rcumferential tears are the most
common. This type of tear represents a separation of adjacent lamell ae of the anu lus. The separation may cause the lamellae involved to tear
away from their vertebra l attachments. The sec-
23 ond rype of rears are radial in direcrion. These run from rhe deep lamellae to the superficial layers. Mosr aurhors (16) believe rhar rhese types of rears develop after circumferenrial rears and rhar the presence of circumferential tears make it easier for radial tears ro occur because radial rears are able to connect severa ) adjacent circumferen-
tial rears. When this occurs the inner nucleus pulposus may be allowed to bulge or even extrude into rhe ve rtebral canal. This is known as intervertebral disc protrusion (bulging) or herniarion (extrusion ). However, this scenario probably occurs much less frequently rhan was once believed.
Ib:Ieua P..... The nucleus pu lposus is a rounded region located wirhin rhe center of rhe IVD. Ir develops from rhe embryologic notochord. The nucleus pulposus is gelatinous and relatively large just after birth, and several mulrinucleared notochordal cells can still be found within irs subsrance (5). Except for the most peripheral region of the anu lus fibrosus, the disc is an avascular structure, and the nucleus pulposus is responsible for absorbing most of rhe fluid received by rhe disc. The process by which a disc abso rbs its fluid from rhe vertebral bodies above and below has been rermed imbibition. When a load is applied to the spine, an IVD loses water but retains sodium and potassium. This increase in electrolyte concentration creates an osmotic gradient that resu lts in
rapid rehydrarion when rhe loading of the disc is stopped (17). The disc appa rently benefits from borh activity during the day and the rest it receives during rhe hours of sleep. As a resulr, rhe disc is thicker (from superior ro inferior) after rest than after a typical day of sitting, standing, and walking. Too much rest may nor be beneficial, however. A decrease in the amount of fluid (hydration) of the intervertebral discs has been noted on magnetic resonance imaging scans after
5 weeks' bed rest (18) . The disc reaches its peak hydration at app roximately the age of 30 years, and the process of degeneration begins shortl y thereafter (19). As rhe disc ages it becomes less gelatinous in consistency, and its ability to absorb
fluid diminishes. The aging changes in composition and structure, which are common to all sources of cartilage, occur ea rlier and to a
grearer extent in rhe rYD (20) . Breakdown of the proteoglycan aggregates and monomers is thought to contribure to rhis process of degeneration . Breakdown of proteoglycan resu lts in a decreased ability of rhe disc to absorb fluid, which, in rurn, leads to a decrease in rhe abil ity of rhe disc to resist loads placed on it. The degenerarion associated with rhe decrease in ability to absorb fluid (water) has been identified with computed romography (2 1) and magneric resonance imaging, and has been correlated wirh histologic strucrure and fluid con rent. As the disc degenerates, it narrows in the superior to inferior dimensions, and the adjacent vertebral bodies may become scleroric (rhickened and opaque o n radiographs). Much of the disc thinning seen with age may also be the result of the disc "sinking into" rhe adjacent vertebral bod ies over the course of many years (15). Pathology of the intervertebral disc is seen rarher frequent ly in clinical practice. As mentioned previously, the nucleus pulposus may cause bulging of the outer anular fibers or may prorrude (herniare) rhrough the a nulus. This was first described by Mixter and Barr (22). Bulging o r herniation of the disc may be a primary source of pain, or pain may resu lt from pressure on the exiting nerve roots within the vertebral or
inrervertebra l foramen. Such bulging is usua ll y associated with trauma, although a history of rrauma may be absen t in as many as 28% of patients with confirmed disc protrusion (23) . Some investigarors believe thar proreoglycan leaking o ut of a tear in the anu lus also may cause pain by creating a chemical irriration of the exiting nerve roots. Pain caused by pressure on or irritation of a nerve root radiates in a dermaromal pattern. Such pain is termed radicular
pail! because of its origin from the dorsal root (radix) or dorsal root ganglion. Treatment for hern iation of the nucleus ranges from conserva-
rive methods (24 ) to excision of the disc (discectomy) to chemica l degradation of rhe disc (chymopapain chemonucleolysis) (25, 26).
24
Vertebral End Plata Vertebral end plates are carrilaginous plates that limit the disc (with the exception of the mOSt peripheral rim) superiorly and inferiorly and are artached to the nucleus pulposus, anulus fibrosus, and ro the adjacent verrebral body. Although a few authors consider the verrebral end plate to be a parr of the verrebral body, most authorities consider it to be an integral porrion of the disc (18, 26). The end plates are approximately 1 mm thick peripherally and are thicker centrally. They are composed of both hyaline carri lage and fibrocartilage. The hyaline carrilage is located against the vertebral body and the fibrocartilage is found adjacent ro the remainder of the intervertebral disc. The end plates help to prevent the verrebral bodies from undergoing pressure atrophy and, at the same time, contain the anulus fibrosus and nucleus pulposus within their normal anatomic borders. Occasionally the nucleus pulposus ruptures through the verrebral end plate, causing a lesion known as a Schmorl's node. These nodes cause the verrebrae surrounding the lesion ro move closer together. This movement is thought ro increase pressure on the anterior joints between the verrebrae, speeding the degenerative process of the anterior inter body joint (by means of internal disc disruption). In addition, the disc thinning or narrowing that results from these end plate herniations leads to more force being borne by the Z-joints, which may result in more rapid degeneration of these structures as well . The vertebral end plates begin to calcify and thin with advancing years. This leaves them more brittle. The central tegion of the end plate in some verrebrae of cerrain individuals may be completely lost in the later years of life.
innervation
0' Intervertebral lilacs
The outer third of the anulus fibrosus of the interverrebral discs has been found ro receive both sensory and vasomoror innervation (28). The sensory fibers are probably both nociceptive (pain sensitive) and proprioceptive in nature, and the vasomoror fibers are associated with the small vessels located along the superficial aspect of rhe anulus fibrosus. The posterior aspeer of the disc
receives its innervation from the recurrent meningeal nerve (sinuverrebral nerve). The posterolateral aspect of the anulus receives both direct branches from the anterior primary division and also branches from the gray communicating rami of the sympathetic chain. The lateral and anterior aspects of [he disc primarily receive their innervation from branches of the gray communicating rami and also from branches from the sympathetic chain (Figure 2-4). The fact that the disc has direct nociceptive innervation is very clinically relevant. The intervertebral disc itself is probably able to generate pain. Therefore, disorders affecting the intervertebral discs alone, such as internal disc disruption and tears of the ourer rhird of the anulus fibrosus, can be the sole cause of back pain. The disc also can generate pain by compressing (entrapping) an exiting dorsal root. Also, leakage of nerve-irritating (histaminelike) molecules from disrupted intervertebral discs has been found to be a cause of irritation ro the exiting dorsal root. These larter conditions cause a sharp, stabbing pain that radiates along a dermaromal pattern. This type of pain is known as radicular pain because it results from irritation of a nerve rOOt (radix).
CarvlcallntarvlrtebrallHscs The basic anaromy of the cervical interverrebral discs is similar to that of interverrebral discs throughout the spine. The discs of this region make up more than 25 % of the superior to inferior length of the cervical spine and help ro allow for the large amount of motion that occurs in this region. The intervertebral discs in the cervical region thin as one ages, while at the same rime, the uncinate processes continue to enlarge. As a result, by the age of 40 years the uncinate processes create a substantia l barrier that prevents lateral and posterolateral herniation of rhe intervertebral disc. Therefore, Bland (29) believes that the cervical discs dehydrate earlier in life than do the discs in the thoracic and lumbar regions. In fact, he states that there is no nucleus pulposus in the cervical spine beyond the age of 45 years, and therefore he believes that intervertebral disc protrusion has been overdiagnosed in
2 Anatomy RaIIted to SpInal SUbluxation
25
f1111'12-4 The innervation of the intervertebral disc in horizontal section . The neural elements have been drawn onto a horizontal magnetic resonance imaging scan. The tOP of the illustration is anterior and the bottom is posterior. Numbers indicate the following: 1, sympathetic ganglion; 2, gray ramus communicantes; 3, branch of the gray ramus coursing toward the inrervertehral foramen (JVF) ro contribute to the
recurrent meningeal (sinuverrebral) nerve; 4. anterior
primary division (ventral ramus); 5, medial branch of posterior primary division (the lateral branch is seen coursing ro the right of the medial branch in this illustration); 6, dorsal root (spinal) ganglion and dural root sleeve (red) within the IVFi 7, recurrent meningeal (sinuverrebral) nerve; 8, cauda equina (yellow) within
the cerebrospinal fluid (blue) of the lumbar cistern of the subarachnoid space; 9, zygapophyseal joint. Notice the intervertebral disc is receiving innervation from branches of the sympathetic ganglion (anteriorly), gray communicating ramus (laterally and posterolaterally), and the recurrent meningeal nerve (posteriorly). Also notice that the zygapophyseal joint is receiving innervation from the medial branch of the posterior primary division. (From Cramer, Darby. Basic and clinical anatorny of the spine, spinal cord. and ANS. St. Louis: Mosby, 1995. Photograph by ROil Mellschillg, illustration by Dina Juarez. The National College of
Chiropractic.)
the cervical region . Recall that there are no intervertebral discs between the occiput and the atlas or between the atlas and the axis. The C2-C3 interbody joint is the first such joint to possess an intervertebral disc. Therefore, the C3 spina l nerve is the most superior nerve that is able to be affected by possible disc protrusion. Mendel et al. (13) studied the innervation of the cervical intervertebra l discs and found sensory nerve fibers throughout the anu lus fibrosus. These fibers were mOSt numerous in the middle (from superior to inferior) third of the disc. The structure of many of the nerve fibers and their end receptors was consistent with those that transmit pain. In addition, pacinian corpuscles and Golgi tendon organs were found in the posterolateral aspect of the disc. These findings help to confirm
that the anu lus fibrosus is a pain-sensitive structure and further indicate that the cervica l discs are involved in proprioception, enabling the central nervous system to moniwr the mechanical status of the interverrebral disc. Mendel et al. (13) hypothesized that the arrangement of the nerve fiber bundles may a llow for the IVD to sense periphera l compression o r deformation as well as alignment. No nerves were found in the nucleus pulposus (13).
The Intervertebral ForaRlen The intervertebra l foramen (fVF) is a very important "hole" of the spine. T he fVF is an area of great biomechanical, functional, and clinical significance (5). Much of its imporrance stems from
26
Subluxation The ArtIcU' LIIIIon
the fact that the IVF provides an osteol igamentous boundary between the central nervous system and the peripheral nervous system. Therefore, knowledge of the specific anatomy of this clinically important area is important in the differential diagnosis of back and extremity pain and can help with the proper management of individuals with compromise of this region. A pair (left and right) of intervertebral foramina are located between all of the adjacent vertebrae from C2 to the sacrum . There are no [VFs between C1 and C2. When present, the lYFs lie posterio r to the vertebral bodies and between the superior and inferior vertebra l notches of adjacent vertebrae. Therefore, the pedicles of adjacent
The [VFs are smallest in the cervical regIon, and generally there is a gradual increase in IVF dimensions to the fourth lumbar vertebra . The lYFs between L5 and 51 are unique in size and shape. As mentioned previously, the lYFs are actually canals, varying in width from approximately 5 mm (31) in the cervical region to 18 mm (32) at the L5-51 level. Many structures (surrounded by adipose tissue) traverse the lVF (Figure 2-5). They are as fo llows:
vertebrae form the " roof" and "floor" of this region. The width of the pedicles gives depth to
mental arrery---one to the posterior aspect of
these openings, making them actually neural canals (30) rather than foramina, but the name remams.
5ix structures form the boundaries of the lVF (Figure 2-5). Beginning from the most superior border (" roof") and continuing anterio rl y in a circular fashion, the boundaries are as follows :
1. 2. 3. 4.
The mixed spinal nerve The dural roor sleeve Lymphatic cha nnel(s) Three branches of rhe spinal ramus of a seg-
Epidural adipose Intervertebral ti ssue
vein
Spinal branch of lumbar segmental artery
Tronsforaminal ligament
1. The pedicle of the vertebra above (more specifically, its periosteum ) 2. The vertebral body of the vertebra above (again, its periosteum) 3. The intervertebral disc (posterolateral aspect of the anulus fibrosus ) 4. The vertebral body of the vertebra below, and in the cervical region, the uncinate process
(periosteum) 5. The pedicle of the vertebra below forms the "floor" of the lYF (periosteum ). A sma ll part of the sacral base (between the superiot articular process and the body of the 51 segment) forms the floor of the L5-51 lYE 6. The zygapophyseal joint (forms the " posterior wall" ). Recall that the Z-joint is made up of (1) the inferior articular process (a nd facet) of the vertebra above, (2) the superior articular process (and facet) of the vertebra below, and
Ventral and dorsal
lymphatic
Recurrent
nerve roots within dural root sleeve
channel
meningeal nerve
figure 2-5 The inrervertebral foramen (IVF). Notice the structures that normally traverse the IVE The most
(3) the an terior "articular capsule", which is
common locations of the rransforaminalligamenrs are also shown on this illustration. (From Cramer. Darby. Basic and clinical anatomy of the spine, spinal cord, and AN5. St. Louis: Mosby, 1995. Photograph by Ron Mensching, illustration by Dino Juarez, The National
composed of the ligamentum fla vum (1, 4).
College of Chiropractic.)
2 Anatomy Related to SptnaIlIIII*IxaUon rhe vertebral body, one to the posterior arch, and one ro rhe mixed spinal nerve (neural branch) 5. Communicating veins between the internal and externa l vertebral venous plexuses 6. Two ro four recurrent meningeal (sinuverrebral ) nerves The dorsal and ventra l roOts unite to form the mixed spina l nerve in the region of rh e lYE The mixed spinal nerve is surrounded by the dural roOt sleeve, and the dural rOOt sleeve is attached to the borders of the IYF by a series of fibrous bands. T he dural rOOt sleeve becomes continuous with the epineurium of the mixed spina l nerve at the latera l border of the lYE The a rac hnoid blends with the con nective tissue of the nerve root proximal to the dorsal root ganglion and at an eq uiva-
lent region of the ventral root. Occasiona ll y the arachnoid extends more distally, and in such cases the subarachnoid space extends to the lateral third of the lYE Each recurrent meningeal nerve (sinuve rtebra l nerve of Yon Luschka) origi nates from the mOSt proximal portion of the ventral ramus. It receives
a branch from rhe nearest gray communicating ramus of rhe sympathetic chai n before traversing the lYF. This nerve provides sensory innervation (including nociception) to the posterior aspect of the a nul us fib rosus, the posterior longitudina l ligament, anterior epidu ral veins, periosteum of rhe posterior aspect of the vertebral bodies, and the anterior aspect of the spi na l dura mater. Usually severa l recurrent meningeal nerves enter the same lYE
Accessory Ugaments 01 Ute IVF Golub and Silve rman (33) first used the term Iralls(oramil1a i ligamellt (TFL) when describing a ligamentous band seen to cross the IVF at any level of the spine. These ligaments vary considerably in size, shape, and location from one IYF to anothe r. They found that the spinal arteries and veins ran above this structure and the anterio r primary division ran underneath it. Bachop and Janse (33) reported that the
27
higher the ligament is placed, the less space remains for the spinal vessels, which cou ld conceivably lead [0 ischemia or venous congestion . The lower the ligament is placed, the greater the possi bility of sensory and/or mOtor deficits. Bacho p and Hilgendo rf (35) studied 15 spines and from these they dissected the lum bar lYFs on both the left and the ri ght sides, making a total of 150 lYFs. From these dissections they found the foll owi ng: 26 (17.3%) lYFs had TFLs 13 (50%) of TFLs were at LS-Sl and 11 (73.3%) of the 15 spines had 1 to 2 TFLs at LS-S l 2 (13 %) had 1 to 2 TFLs at LS-Sl
The term corporotransverse liga men t is used when referring to a ligament that runs between the ve rtebral body and the transverse process at the LS-Sl junction (34). Bachop and Hilgendorf (35) found that the corporotransve rse liga ments were of rwo basic types: (1) broad and flat, and (2) rod like. The rodlike liga ments were usually to ugher (firmer ) than the flat type. Golub and Silverman (33) reported that these could calcify and be seen on radiographs. Bachop and Ro (36) fo und the gray communicating sympathetic ramus running through the opening above the corporotransverse liga ment. Bachop and Janse (34) believed that the corporotransverse liga ment could have a constricting effect on the anterior primary division (ventral ramus). That is, in patients with sciatica, as the leg is raised, the anterior primary division could be stretched across the liga ment, possibly mimicking the thigh and leg pain of a disc protrusion. Amonoo-Kuoffi et al. (37) have recentl y d iscussed accessory ligaments of the lYE They consistently found them throughout the lumbar regio n a nd mapped out the relationship of the spinal nerve, segmenta l veins and arteries, and the recurrent meningeal nerve through the openings between the ligaments. They concluded that the accessory liga ments tend to ho ld the above-mentioned structures in their proper place. Bakkum and Mesran (38) also found several ligaments at each level that decreased functional superior-
28 inferior diameter of the IVF by approximately one third .
Pain (Noclceptlon) of Spinal Origin The Perception of PaIn All pain should be considered as real and as having both physical and psychological components, one of which may predominate. Further, all pain alters the personality of the individual (39) . This personality usually terurns to the prepain state when the physical cause of the discomfort has sufficiently healed. In addition, pain is always subjective and is perceived by the patient in relation to experiences they have had with pain in their early years (40) .
Pain
the dorsal rOOt ganglia (DRG), which, with the exception of Cl and C2, are located within the intervertebral foramina of the spine. The sensory fibers that are associated with the recurrent meningeal nerve and the sympathetic nervous system provide a rOute for the transmission of pain arising from somatic structures of the anterior
aspect of the vertebral column. Fibers arising from these sources pass through the anterior primary division for a short distance before reaching the mixed spinal nerve. The Structures innervated by the ventral ramus, dorsal ramus, and recurrent meningeal nerve are listed in the boxes below.
>
Spine-Related Structures Innervated by the Ventral Ramus Possible Pain Generators
d. somadc Origin
Once a nociceptor has depolarized, it changes its properties, frequently becoming more sensitive to subsequent noxious stimu li. This increased 'sensi-
tivity to pain is known as hyperalgesia. The central nervous system also has several mechanisms
by which it, too, may create hyperalgesia in an area of injury. Therefore, after rissue is damaged it is usually more sensitive to pain until healing has occurred. After development of a pathologic condition or injury, hyperalgesia also may be present in the healthy tissues surrounding the site of the lesion. Frequently pain of spinal origin is the result of damage to severa l structures, and the effecrs of hyperalgesia allow for pain to be felt from tissues that, if injured to the same degree independently, may have gone unnoticed (41) . Most pain of spinal origin has a physical cause. One way to organize possible pain generators is by listing them according to the four main sources of neural innervation to spinal structures.
These sources are as follows: (1) the anterior primary division (ventral ramus), (2) the posterior primary division (dorsa l ramus), (3) the recurrent meningeal nerve, and (4) sensory fibers that course with the sympathetic nervous system (including fibers that run with the sympathetic trunk and also the gray communicating rami). All of these afferent nerves have their cell bodies in
• Referred pain from structures innervated by plexuses • Psoas muscle • Quadratus lumborum muscle • lntertransversarii muscles
>
Structures Innervated by the Dorsal Ramus Possible Pain Generators
• • • •
Deep back muscles Zygapophyseal joints Periosreum of posterior vertebral arch Interspinous, supraspinous, and intertransverse ligaments, ligamentum flavum
• Skin (upper cervical, middle cervical, and thoracic) lI............. 01 .... doni. n ........mtn:
• Erector spinae muscles • Splenius capitis and cervicis muscles (cervical
region) • Skin
2 Anatomy Ralated to Splnll SUbluXaUon
>
Structures Innervated by the Recurrent Meningeal Nerve Possible Pain Generators
29
Pain Generators Unique to the Cervical RegIon Pain generators unique to the cervical region include irritation of the nerves surrounding the
vertebra l artery and also pain arising from uncovertebral "joints" (joints between the uncinate
o Periosteum of posterior vertebral bodies o Internal vertebral (epidural) veins and basivertebral veins o Epidural adipose tissue • Posterior intervertebral disc o Posterior longitudinal ligament o Anterior spinal dura mater
Nerves Associated wtth the Sympathetic Nervous System Several structures are innervated by nerves that
arise from the sympathetic trunk and the gray communicating ram i. The sensory fibers of these nerves follow the gray rami to the anterior primary division, where rhey enrer the mixed spinal nerve and then reach rhe spina l cord by coursing through the dorsal roots. Pathology of the periosteum of the anterior and lateral vertebral body, which are innervated by sensory fibers traveling with gray rami, may lead to pain. Some of the most common causes of this type of pathologic condition
include
fracture,
neoplasm,
and
osteomyelitis (42). Sprain of the anterior longitudinal ligament or the outer layers of the anterior or larcral anulus also may resu lt in pain conducted by fibers that cou rse with the gray communicating rami. The structures innervated
by nerves
associated with the sympathetic trunk and gray communicating rami are listed in the box below.
>
Structures In nervated by Nerves Associated with the Sympathetic Trunk and the Gray Rami Communicantes Possible Pain Generators
processes and the vertebra l body immediately above). In addition, pain arising from pathology or dysfunction of the cervical Z-joints can refer to regions quite distant from the affected joint (43) . The two most common types of pain referral are (1) neck pain and head pain (headache) arising from the C2-C3 Z-joinrs, and (2) neck pain and shoulder pain arising from the C5-C6 Z-joints (44) . However, pain arising from almost any structure innervated by the upper four cervical nerves may refer to the head, resulting in head pains and headaches (43, 45-47). Pain originating from the region of the basiocciput and occipital condyles frequently refers to the orbital and frontal regions. Sweating, pallor, nausea, alterations of pulse, and other autonomic disturbances
have frequently been observed in association with disturb.ances of the suboccipital and upper cervical spine. The intensity of autonomic reactions seems
to be proportional to the stimulus, and the proximity of the stimulus to the suboccipital region. The autonomic responses range from mild subjective discomforts to measurable objective signs (45).
Pain Generators Unique to the Tboraclc Region Pain generators unique to the thoracic region
include pain arising from the costocorporea l and costotransverse anicuiarions. Compression frac-
ture of the vertebral bodies is also an important source of acute pain arising from the thoracic
region .
The Dorsal Root Ganglia and RalMcular Pain • Periosteum of the anterior and lateral vertebral bodies o Lateral intervertebral disc o Anterior intervertebral disc o Anterior longitudinal ligament
The dorsal root ganglia serve as modulators of spinal pain. They contain many neutopeptides associated with the transmission of pain (substance P, calcitonin gene-related peptide, vasoac-
tive intestinal peptide) (40). These substances may be released from the peripheral terminals of
30
Subluxallon
The ArtIcular Lesion
the sensory nerves that transmit pain, and the neuropeptides ma y reach these peripheral terminals (receptors) by axona l transport mechan isms. The presence of neurope ptides in and around the receptors may "prime" them by maki ng them more susceptible to depolarization (40). Direcr pressure or irritation of the dorsal roots or dorsal
root ganglia results in radicular pain. Radicu1ar pain is sharp and stabbing in nature and radia res a long a narrow band, and is accom panied by other sensory or mOlOr deficits. Some of the ca uses of radicular pain include intervertebral disc protrusio n, spinal (vertebral) cana l stenosis, and other space-occupyi ng lesions.
>
Radicular Pain
• Pain arising from the dorsal root or the
dorsal rool ganglion. Usually causes pain to be referred along a portion of the course of the nerve or nerves formed from the affected dorsal root. • This is known as a dermatornat pattern.
Somatic Referred Pain There a re several possible mechanisms of pain referral from a somatic structure. Perhaps one of
the m OSt importa nt is attributable to the internal organ ization of the spinal cord . The nociceptive
to the postcentral gy rus of the cerebra l cortex. The back and neck have ve ry small regions allotted 10 them on the postcentral gyr us (sensory homu nculus), a nd this also may contribute to the poor loca lization of spinal pain. In addition, the tract neurons for ascending pain pathways most frequently ca rry nociceptive information from cutaneous areas. Therefore, when the tract neurons are sti mulated to nre, the cerebral cortex (where conscious awareness of pain occurs) may interpret the impu lse as coming from a cutaneous region or from another, morc recently injured, region. Either of these areas may be distant to the structure that is currently damaged or inflamed. This phenomenon is sometimes referred to as "pain memory" (48,49) . Somatic referred pain is characterized as being a dull achi ng pain that is difficulr to localize a nd rather conStant in nature. Activity of the muscles and the Z-joints, as well as spinal manipularion of the Z-joints, tends to decrease pain through a "gate contro l" type of mechanism (39). Therefo re, if pain is of somatic origi n, the patient may benefit mOSt by treatment that promotes ac tivity and movement (39). Of course, ca re must be taken not to comp romise the da maged tissue in any way (see box) .
>
Distinguishing Features of Somatic Referred Pain
informa ti on coming in from a pain generator is
dispersed by ascending or descending with in the tract of Lissauer for several cord segments before synapsing on tract neurons of several cord levels.
Therefore, nociceptive information entering from several vertebral levels may converge in the sa me interneuronal pool. The dispersal of incoming afferents onto different tract neurons, in combination with the convergence of several different afferents onto single-tract neurons, may decrease the ability of the central nervous system to loca lize pain. This type of dispersal a nd convergence also may be found at the second synapse along the pain pathway, which is in the ve ntra l posterior lateral nucleus of the thalamus. Finally the vent ral posterior latera l thalamic nucleus projects
• Dull ache • Difficult to localize • Rather constant in nature
Central Transmission of Pain The afferent fibers that cOllvey nociception a re group A-delta and gro up C fibers. These fibers enter the dorsolateral tract of Lissauer located at rh e tip of the dorsal horn . Within this region, collateral branches of those fibers rhat continue directl y into [he gray marrer ascend or descend numerous cord segment levels before they, too, enter the dorsal horn. The A-delta fibe rs, which
31 convey pain quickly and rapidly, terminate in lamina I and laminas rv through VI. The group C fibers, which convey a dull sensation of pain at a slow ratc, terminate in lamina II. The neurons, which transmit the information to higher centers, are located in various laminae of the gray marrero Surgical cordotOmy procedures that relieve pain have shown that the major fibers that transmit nociceprion to higher centers decussate in the ventral white commissure and then ascend in the
anterolateral quadrant of the white matter of the spinal cord (50). Alternative pathways also may be involved, although their course and function in humans remains unclear.
The Neasplnothalamic Tract One of the tracts in the anterolateral quadrant is the neospinothalamic tract (Figure 2-6). This rract ascends through the brainstem to the ventral lateral nucleus (posterior part) and also to the posterior nucleus of the thalamus with little or no input to the brainstem. From the thalamus, axons course
[0
the somesrheric region of the correx,
that is, the postcentral gyrus and the posterior part of the paracentral lobu le of the parietal lobe. As the axons ascend, body parts are represented in specific regions of the tract, and in the cerebral cortex a parrern is retained such that a specific area of cortex corresponds to the region of the body from which the sensory fibers originate.
-.!~
The primary pathway for transmittal of nociceprion-the neospinorhalamic tract. (Illustration by Dina Juarez. The National College of Chiropractic.)
This cortical representation is referred to as the
sensory homunculus. The size of the body part represented on the homunculus reflects the amount of sensory innervation devoted to that
body area. As previously mentioned, this unequa l neuronal representation may explain why localization of sensations, such as pain, is morc difficult in one region (such as the back) than in another. The neospinorhalamic tract synapses in
the region of the sensory homunculus and provides the basis for the discriminatory qua lities of pain sensation, such as stimulus intensity and spatial localization.
lateral quadrant are the paleospinothalamic and spinoreticular tractS (Figure 2-7). The paleospinothalamic tract, which ascends through the brainstem and likely contributes collateral branches to the reticular formation, terminates in
the midline and intralaminar tha lamic nuclei. From these nuciei, thalamic fibers travel to regions associated with the limbic system and to widespread areas of cerebra l cortex such as the orbitofrontal region. The spinoreticular tract ascends
[0
the reticu-
The PaIeospinothalamlc and SpInoreticulll' Tracts
lar formation of the brainstem. The reticular for· mation is a complex network of neurons located throughout the core of the brainstem. It has
Two additional tracts that ascend in the anrero-
numerous functions and is a major component,
32
SUl*lXatIon TIle ArtIcular Lellon is that they both terminate in the same region of the thalamus, which in turn projects to nonspecific areas of cerebral cortex. Another similarity is that neither of them is somatotopically organized. Both the spinoreticular and paleospinothalamic tracts may be involved with the generation of chronic pain and the qualities associated with that sensation . The response of the brain to painful stimuli is quite involved. The perception of pain takes place in the thalamus, postcentral gyrus, frontal cortex (affective component), and temporal cortex (memoty of previous pain component) (39). The unpleasant emotional response associated with pain, however, seems to be associ-
ated with the limbic system. The limbic system allows one to perceive a sensation as being
uncomfortable, aching, or hurting (41 ). The focusing of one's attention on the painful area is likely a function of the ascending reticular activating system.
SUpraspinal Control
FIgIre 2:·7 The paleospinothalamic tract and the spinoreticular tract. (illustration by Dino Juarez. The National College of Chiropractic.)
Evidence from studies in which electrical stimu lation of regions of the brainstem produced analgesia (51) indicates that there are descending pathways that can modulate nociceptive signals. One of the components of this endogenous pain control system is the periaqueductal gray matter (PAG) of the midbrain. This region has a major projection to the nucleus raphe magnus, which is located in the midline of the rostroventral medulla. This nucleus is rich in the neurotransmitter serotonin. From [his region, serotonergic
along with the thalamus and the cerebral cortex, of the ascending reticular activating system . The ascending reticular activating system provides the
circuitry rhrough which arousal and attentiveness are maintained. The tract neurons synapsing in th e reticular formation form complex connections
within this region and subsequently project to brainstem nuclei, the hypothalamus, and the midline and intralaminar nucleus of the thalamus. Subsequent thalamic projections course to widespread areas of cerebral cortex. The paleospinothalamic and spinoreticu lar tracts possess sim ilar characteristics. One of these
fibers course into the dorsolateral funiculus of the spinal cord (raphe-spi na l tract) and synapse heavily on neurons in the superficial dorsal horn (laminae I and U) . The superficial dorsal horn is a lso the region that receives input from afferent fibers conveying nociception . In addition, it is the location of the origin of the spinothalamic tracts (51, 52) and is the area involved with the segmental modu lation of nociception (see previous discus-
sion). Descending fibers synapse on neurons, which include enkephalin (an opioid peptide), containing inhibitory interneurons and also on the nociceptive projection neurons (tract neu-
33 rons). The opioid-containing inhibirory interneurons arc in close proximity to both primary nociceptive afferents and the tran neurons. In fact, the afferent endings and the dendrites of the tract neurons both contain opioid receprors (55). Pharmacologic studies have shown that the release of opioid peptides from the inhibitory interneurons block transmission of nociception by two mechanisms. One mechanism is by binding ro receprors and blocking the release of neurotransmitters, such as subsrance P, from the primary afferent fibers . Although direct axoaxonic synapses between enkephalin neurons and the primary afferent fibers have not yet been found, enkephalins may possibly bind ro receptors by diffusing from their site of release to the presynaptic membrane of the afferent fiber (52-54). The second mechanism by which inhibitory inrerneurons can mediate spinal neurotransmission of nociception is by directly synapsing with the postsynaptic membrane of the tract neuron. This occurrence has been well documented (5254). Through these connections, nociceptive transmission is prevented. As mentioned previously, analgesia can be produced by neural stimulation. Analgesia can be produced also by the administration of opiates into the central nervous system. The areas that are activated by the opiates are the same as those
that produce analgesia when electrically stimulated, that is, the PAG and the rostroventral medulla. This lends credence ro the theory that endogenous opioid peptides, which have been found in the brain, can activate the descending system (52). In addition to the seroronergic descending pathway, there are other fibers descending from the pons (50, 53) that appear to be involved with control of the nociceptive system. These descending fibers camain norepinephrine and appear to
inhibit nociception at the dorsal horn level. At the same time, however, collateral branches of these fibers synapse on the seroronergic neurons of the raphe nuclei. The subsequent release of norepinephrine at this level results in "tonic inhibition" of the raphe-spinal neurons (53). Thus both sys-
terns provide a descending component ro the mechanism for controlling pain. Feeding into these systems is the nociceptive information transmitted through ascending pathways (41), possibly the spinomesencephalic tract and input from the reticular formation, and possibly Stressinduced input channeled through the limbic system and hypothalamus (52) .
Acknowledgments The authors thank Mr. James McKay, Ms. Sheila Meadows, and Dr. Michael Kiely for invaluable assistance during the preparation of this chapter.
References 1. Giles LG. The surface lamina of the articular cartilage of human zygapophyseal joinrs. Anat Roc t 992;
233,350-356. 2. Paris S. AnalOrny as related (0 function and pain. Orthopedic clinics of Norch America 1983; 14:475-489. 3. Giles LG, Taylor JR. Human zygapophyseal joint capsule and synovial fold innervarion. Sr J Rhcumarol 1987;
26,93-8. 4. Xu G, ct al.: Normal variations of the lumbar facet loint capsules. Clin Anat 1991; 4: 1 17-22. 5. Williams PL, et al.: Grays' anatomy. 37th ed., New York: Churchill Livingstone, 1989. 6. Jeffries B. Facet joint injections. Spine: State of the Art Reviews 1988; 2:409-17. 7. Engle R, Bogduk N. The menisci of the lumbar zygapophysia1loints. J Anat 1982; 135:795-809. 8. Panjabi M, Oxland T, Parks E. Quanmative anatomy of cervical spine ligamenrs. Part II. Middle and lower ccrvical spine. J Spinal Dis 1991; 4:277-85. 9. Oliver J, Middledltch A. Functional anatomy of the spine. Oxford: Bunerworth Heinemann, 1991. 10. Yu S, Sether L, Haughton VM. Facet jOint menisci of the cervical spine: Correlative MR imaging and cryomicrotomy study. Radiology 1987; 164:79-82. II. Wyke B. The neurology of low back pain. In: Jayson M. The lumbar spine and back pain. 3rd ed. New York: Churchill Livingstone, 1987. 12. Buckwalter, et al. Articular cartilage and intervertebral disc proteoglycans differ in structure: An electron microSCOpiC study. J Orthop Res 1989; 7: 146-51. 13. Mendel, et al. Neural e1emenrs in human cervical intervertebral diSCS. Spine 1992; 17: 132-5. 14. Bogduk N, Twomey LT. Clinical anatomy of the lumbar spine. London: Churchill Livingstone, 1991. 15. Humzah MD, Soames RW. Human intervertebral disc: Structure and function. Anar Rec 1988; 220:337-56.
34 16. Ito S, er al. An o bservation of ruptured annulus fibrosus in lumbar discs. J Spinal Dis 1991 ; 4:462-6. 17. Kraemer J. et at. Water and electrolyte coment o f human intervertebral di scs under variable load. Spine 1985; 0,69-71. 18. leBlanc, er al. The spine: C hanges in T2 relaxation times from disuse. Radiology 1988; 169: I 05-7. 19. Coventry MS. Anato my o f the intervertebral d isc. Clin Orthop 1969; 67 ,9- 15. 20. Bayliss, et al. Proreoglycan synthesis in the human imervertebral disc: Variation with age, region and pathology. Spine 1988; 13,972-8 1. 21. Ba hk YW, Lee JM. Measure-set computed tomographic analysis of inferna l architectures of lumbar disc: Clinical and histologic srud ies. Invest Radiol 1988; 23: 17-23. 22. Mix ter WJ. Barr j5. Rupture of the intervertebral disc w ith involvement of the spina l cana l. N Eng J Med 1934; 211,210-15. 23. Martin G. The role o f trauma in disc protrusion, N Z Med J 1978; M . "h, 208-211. 24. Sanders M, Stein K. Conservati ve management of herniated nucleus pulposes: treatment approaches. J Ma nipula tive Physiol Ther 1988; 11 :309-13. 25. Alcalay M , et al. Traitement par nuclcolyse ala chymopapaine des hernies discales a forme purement lomba lgique. Revue du Rhumatisme 1988; 55:741-5. 26. Dabezies, et al. Safety a nd efficacy of chymo papain (disease) in the treatment of sciatica due to a herniated nucleus pulposus: results of a double-blind study. Spine 1988; 13,561-5. 27. Bogduk N. Cli nica l a natomy of the lumbar spine. London : C hurchill Livingsto ne, 199 1. 28. Bogd uk N, Tynan W, Wil son A. The nerve supply to the human lumbar intervertebral discs. J Anat 198 1; 132,39-56. 29. Bland J. The cervica l spine: from a natomy to clinical care. Medical Times 1989; 11 7:15-33. 30. Czervionke L, er al. Cervical neu ral fora mina: Correlative analOmic and MR imaging study. Radiology 1988; 169,753-9. 3 t. Hewi tt W. The intervertebral foram en. Physiotherapy 1970; 56,332-6. 32. Pfaundler S. Pedicle origin and intervertebral compartment in the lumbar and upper sacral spine. Acta Neurochir 1989; 97, 158-65. 33. Golub B, Siverman B. Transforaminalligaments of the lumbar spine. J Bone Joint Surg 1969; 51 :947-56. 34. Bacho p W, Janse J. The corporotransverse ligament at the L5 intervertebral foramen (Abstract). Anar Rec 1983; 205. 35. Sachop W, a nd H ilgendo rf C. Transforaminalligamcnrs of the human lumbar spine (Abstract). Anar Rec 198 1; 199.
36. Bachop WE, Ro CS. A ligament sepa rating rhe nerve from the blood vessels at the L5 intervertebral foramen. J Bone Joint Surg 1984; 8:437. 37. Amo noo-Kuofi HS, er al. Ligaments associated with lumbar intervertebra l foramina. 1. LI to L4. J Anar 1988; 156, 177-83. 38. Bakkum BW, Mesra n M . The effects of transformatio na l ligaments on the sizes o fTI I to L5 human intervertebra l foramina.J Manipulative Physiol Ther 1994; 17(8): (in press). 39. Kirkaldy-Willis WHo The mediation of pain. In : Kirkald)'Willis W, ed. Managing low back pain. 2nd ed. New Yo rk : C hurchill Li vingstone, 1988. 40. Weinstein WHo The perception o f pa in. In : KirkaldyWillis W, cd. Managing low back pa in. 2nd ed. New Yo rk: Churchill Livingstone, 1988. 41. Haldeman S. The neurophysiology of spinal pain. In : H a ldeman S, ed. Principles and practice of chiropractic. 2nd ed. Eas[ Norwa lk, Connecticut: Appleton a nd Lange, 1992. 42. Bogduk N. The innervation of the lumbar spine. Spine 1983; 8,286-93. 43. Dwyer A, Aprill C, Bogduk N. Ce rvica l zygapophyseal joint pain pancrns. I. A stud y in normal volu nteers, Spi ne 1990; 15,453-7. 44 . Bogduk N, Marsland A. The cervical zygapophysea l joints as a source of neck pain. Spine 1988; 13:6 10-17. 45. Campbell, Parsons. J Nerv Menta l Dis 1944; 99:544-5 1. 46. Bogduk N, Engel R. The menisci of the lumbar zygapophysea l joints. Spine 1984; 9:45~0. 47. Aprill C, Dwyer A, Bogduk N. Ce rvica l zygapophysea l joint pa in panerns. 1I. A clinical evalu ation . Spine 1990; 15(6),458-6 1. 48 . Carpenter MB, Suti n J . H uma n neuroanatomy. 8th ed. Ba ltimore: Williams & Wilkins, 1983. 49. Nolte J . The human brain. 2nd cd. Sr. Lo uis: Mosby, 1988. 50. Hofferr MJ. The neurophysiology of pain. Neurol Clin J 989; 7(2), 183-203. 5 1. Basba um AI, Fields Hi. Endogenous pain control mechanisms: review and hypothesis. Ann Neurol 1978; 4,451 -62. 52. Jessell TM, Kelly DD. !'ain and a nalgesia . In : Kandel ER, Schwartz JH, Jessell TM, eds. Principles of neu ral science. 3 rd ed. New York: Elsevier; 1991. 53. Basbaum AI. Cytochemica l S{udics of the neural circuitry underlying pain and pain conrro l. Acta Neurochir 1987; 38 (,uppl),5-lS. 5 4. Besson JM . The physiological basis of pain pathways and the segmemal controls of pain. Acta Anaesth Belg 1988; 39 (,uppl 2),47-51.
Basic Scientific Evidence for Chiropractic Subluxation Howard Vernon
Key words
Subluxation, animal model, basic science, neuroscience
After reading this chapter you should be able to answer the following questions:
QuesUoo #1
Has chiropractic's subluxation theory been explored by basic science research within the profession?
QuesUon #2
Has it been verified by studies using animal models?
QuesUon #3
Have the predicted aspects of subluxation theory been verified?
36
C
hiropractors have traditionally viewed spinal subluxation from twO points of view. First, it has been regarded as the set of symptoms experienced by the patient, typically consisting of pain, both local to the spine and referred to distal sites, stiffness, and, less frequently, sensory disturbances. Recently, this aspect of subluxation has been termed the subluxation syndrome (1,2). Secondly, it has been regarded as a pathophysiologic disorder of the motion segment of the spine, complete with various categories of tissue damage and functional disturbances. This aspect has recently been described as the sllbluxation complex (3-5) . It is logical to view the latter, the actual disorder (the "complex"), as causative of, or at least strongly associated with, the former. This fulfils the mechanistic demand in medical nosology that all clinical symptoms must arise from some disturbance of biologic function (as opposed to being psychogenic in origin). Although this logic has been implicitly accepted by chiropractors and others with similar viewpoints, it has met with opposition in orthodox circles. In addition as a scientific hypothesis ("the disorder causes the symptoms") it has received negligible attention by chiropractic researchers, in some part because of the inherent difficulties in conducting studies to test it, a point that will be elaborated on further. Opposition from orthodoxy arises in no small measure from the fact that the empirical data available to support the premise are so scanty. In addition, in the medical model, the same set of symptomatology just described has been attributed to quite different explanations, none of them requiring the characteristics of the chiropractor's subluxation. Curiously, one of the most prevalent medical explanations for much of this sort of symptomatology (wh ich, by the way, is among the most prevalent in general medicine [6]), is that the cause is unknown, giving rise to the term idio-
pathic back pain.
Many chiropractors, however, might take issue with the premise that there is very little substantive evidence that the subluxation complex actually exists or is the causative agent of much of the subluxation syndrome. Until recently, they might have argued that the vaSt cumulative experience of the many practitioners, especially those who took the time to publish, some in reputable journals, was prima faciae evidence that when the subluxation is adjusted, the symptoms resolve, and therefore they must have been attributable to subluxation beforehand. More recently, the profession might argue that the many well-conducted clinical trials of manipulation for back and neck pain " prove the point" (7). Unfortunately, both arguments 3rc based on retrospective interpretation of clinical events. Year (8) and others have quite correctly termed this the fallacy of "post hoc ergo propter hoc" (after the fact, therefore because of it). There may be many other valid and rival explanations for the clinical improvements in patients who have their spines manipu-
lated by a chiropractor. Substantiating a pathophysiologic theory with clinical evidence is risky business, especially in the absence of any prospectively obtained evidence from basic scientific studies. In fact, no study exists in which subluxation of the spine has been operationally defined (fo r example, as a misalignment of two spinous processes of 3 mm or more) and then induced in a human patient. It is doubtful that such a study could ever pass an Institutional Review Board in the first place. There is a small body of work in which one of the aspects of the theoretical model-in this case, painful irritation of the deep articular and muscular tissues-has been induced in humans (by injections of hypertonic saline into the facet joints, sacroiliac joints, and the deep suboccipital muscles). These studies (9- 11 ) provide what is known in experimental science as a
model of the theory. In these studies, the prediction from the model-that a painful disorder of the posterior motion segment tissues would provoke diffuse
3 BasIc ScIentIIIc Evidence lor CfIIroprICllc SlII*Ixatlon patterns of spinal pain that often would be referred to dista l ateas of the body-has been verified. This qualifies as the sort of prospectively obtained data that wou ld be necessary to substantiate the more generic theory described above. Given the ethical limitations of conducting
37
Model linkage: the hard way
subluxation research on normal humans, and
given the logical difficulties in interpreting da ta from clinica l stud ies, basic scientific studies employing anima l models offer an attractive alternative for chiropractic researchers and prac-
titioners alike. This chapter reviews anima l model studies that have been conducted to investigate the subluxation complex. The process of modeling in basic scientific research achieves a representation of the part of the empirical world undet investigation. De Bono defines a model as "a method of transferring some relarionship or process from its actua l setting to a setting where it is more conveniently
studied" (12) . The box below lists some of the advantages of using a nimal models in the study of
>
Animal Model Studies: Reasons for T heir Use
• • • • • •
• •
Test theories derived from conceptual models Provide data to support clinical experience High level of experimental control Prospecrive; therefore can explore cause and effect relationships Explore "treatment" effects when lesion is reversed Explore physiologic components of subluxation, but cannot explore behavioral components in acute experiments Chronic experiments may allow for exploration of behavioral effects Animallrudies are the "Holy Grail" of clinical science
spinal subluxation. There are essentially two approaches that can be (and have been) adopted to create a suitable
Rt111'13-1
Flow chart of animal modeling of the
su bluxarion-the hard way.
model of spinal subluxation. The first of these is depicted in Figure 3-1 and shows a process whereby the primary objecti ve of the exercise is to create the essential component of the human version of the problem, namely, vertebra l misalign ment. In this approach, the investigators
38 devote considerable time [Q devising innovarive methods of creating the kind of misalignment that is thought to exist in the human condition . After doing so, the effects of this modeled condition in whatever animal preparation has been selected then can be observed . This approach retains the highest fidelity to the natural circumstances and achieves the highest level of prospective validity, because, as was mentioned previously, the disorder was created first and its putative effects were studied thereafter. Unfortunately, as we will see latet, this approach is by far the more difficult, and possibly even less valid than is necessary. First, creating the minor degree of misalignment necessary to model the chiropractic version of a subluxation in an animal spine is surprisingly difficult, and many innovative attempts have been made to do just that. Second, after creating such a misalignment, it is necessary to actually verify its presence; that is, it must be determined how much force was used to effect the misalignment, and by how many millimeters or degrees the test vertebra is misaligned compared with its neighbors. These measurements are not easily performed and lack a critical level of reliability. Fina ll y, the conceptual model of subluxation posits that the vertebral misalignment causes some form of "nerve interference. " This has come to be understood as either (1) some element of compression of the spinal nerves in the environs of the intervertebral foramen or (2) the initiation of pain in the spinal joints that is capable of creating secondary aberrant reflex effects such as
requirements, and it will be shown that it has never been achieved in total in any of the reported studies. This prompts us to consider an alternative approach, which is depicted in Figure 3-2. It is much easier, both experimentally and logically, ro start by accepting the premise that the misalignment creates the nerve interference and to begin the experiment at that point, that is, by modeling the effects of either the nerve root compression or the spinal joint pain . Studies employing this approach have been far more productive than those employing the first approach. When sufficient data have been gathered from studies like this, then investigators can return to the problem of whether the misalignment really produces the proximate effects.
Review 01 Studies The following section consists of a structured review of published works, in chronological order, in which an animal model was employed to investigate some aspect of the behavior or nature of the spinal subluxation. With one exception, the first of these srudies, these studies appear in the chiropractic literature.
Study #1 No review of this body of work could begin without first examining the work of Louisa Burns and her osteopathic colleagues, which took place
increases in motoneuron or sympathetic neural
activity. In the misalignment approach to animal modeling, it is necessary for investigators to provide evidence that the misalignment has caused either of these two forms of nerve interference. In other words, nerve rOOt compression and joint pain become the proximate or first-order effects of the experimental misalignment. They must be adequately demonstrated before the distal or second-order effects, such as disturbances in reflexes or in nerve conduction, can be demonstrated and logically correlated with the misalignment. This is a difficult and unwieldy sequence of experimental
Model linkage; the eosy way
FIgII'e 3-2 Flow chart of anImal modeling-the easy way.
3 Balle ScIenIIIIc Ev1denc:8 , ... Chlrapracllc SUbluXation from 1917 ro 1948 at the A.T. Sti ll Reseatch Institute's Sunny Slope Laborarory in Chicago, Illinois.
TITlf: Pathogenesis of visceral disease following
39
loss of elasticity, increased contract ions, and
increased fa tiguability. As with the othet tissues, in the ea rl y stages, there was edema in the muscles, whe reas in the larer stages of the lesion, fibriotic changes and atrop hy were observed.
vertebral lesions
Nerve Uu.: In the early stages, spina l cord hype r-
AUTlIORS: Burns L, Chand ler, Rice, et al.
AfoWUJ.S USBI: Rabbit, gui nea pig, cat, dog, goat SUBlUXATION COMPOI'oINT MOOB.BI: "... A slight slipping or maladjustment of the articular surfaces"
METIIOOS: 1) Manual misal ignments 2) Misalignments confirmed by manua l palpation, radiographic evidence, and autopsy
3) Control lesions produced by deep pressure or other stimulations (for example, electrica l,
chemical, thermal, or mechanical) 4) Histologic exami nations were used in both the spina l area and the viscera. Morphologic
em ia was nored. In [he long-term experiments,
primary degeneration of the nerve fibers at the site of the lesion was observed as well as ch romarolysis of the spina l neurons. Burns et al. noted that Wallerian degeneration rarely occurred. ArtICIDr 1InuaI: Edema and changes in the synovia l fluid of the lesioned articular su rfaces were noted in the earl y stages. Later, reductions in the synovial fluid and increases in its viscosity were
noted, culminati ng in fib rotic changes. In the late r stages, "join[ mice" were observed and were
thought to be the product of fibrotic degeneration around the joint capsule, which itself was found ro be thickened and less elastic. The reporting of "joint mice" may be the fi rst mention of w hat has
come ro be known as joint meniscoids (13) .
examinations were also used.
5 ) Experiments were both short-term and longterm.
lntIrvertllllrll dIIc tIIIUe: Again, in the earl y stages, increased internal pressure within the disc as well
as loss of elasticity of the disc were noted. In the
FNRS: The findings of these experiments a re
later stages, fluid resorption, fibrotic invasion,
provided by Burns et al. in summary sections according to the different tissue types. These are repeated here:
and atrop hy of the disc cells we re noted. Burns et a l. proposed the following mechanism to explain how the minor misalignment of the intervertebral joint could have such profound effects on the
SlIm: In the early tages after misalignment, hyperemia was observed in the skin near the lesion. In the chronic stages, thickening and fibrotic changes were always noted.
intervertebral disc: the misalignment resulred in
asymmetry of pressure and reduced mobi li ry. As the posterior vertebralligamenrs thickened, compression of the surrounding circulatory vessels resulred, impairing loca l circu larion ro and from
PeItI: In the ch ron ic stages, desquamation and thinning of the fur was noted around the lesion.
the cancellous bone and resulting in loss of nutrition to the disc. Thus, both mechanical and metaboli c impairment occurred ro the tissues of the
SID:utaneouIIInuaI: As with the skin, in the early stages of the lesion, edema was always noted. Latet, fibrotic thickening was observed.
disc.
Deep 1!1i1a1111UIdeI: The following findings wete
ety of viscera were ana lyzed morphologically and histologically. The latter two thirds of Burns et
VllceralIInuaI: Usi ng short-term and long-term prepararions, postmortem findings in a grear va ri-
frequently noted once the lesion had settled in:
40
SUbluXation
The ArlIN.. lBIIon
al.'s text is devoted to a system-by-system presentation of the various results. For the purposes of this chapter, the featu res common to a l1 the viscera are noted. These findings were always reported to impair the function of the particular organ involved. In the ea rl y stages of the lesion, the viscera always demonstrated impairments of circulation, changes in smooth muscle function, and changes in secretory function of the various glands involved. In the later stages, circulatory congestion and edema were always observed, as well as denervation-related changes and diminished elasticity of the surrounding connective tissues. Burns et al. summarized their findings in the fol1owing generic mechanism, which was thought to result from the induction of the minor subluxationlike lesion: the lesion produced segmental1y organized somata-a utonomic reflex dysfunction, resulting first in disturbed regulation of the viscera. This was fol1owed developmental1y by disturbances of function and ultimately by protopathologic changes. [n many instances, actual pathologic changes were observed, such as the development of ulcerous lesions in the gastric mucosa and infarcts in the kidney tissue. This body of work is seminal in the history of basic scientific investigations of spinal subluxation (14-16). It was a vast and expansive body of work while at the same time being precise, methodical, fastidious, and focused. It is remarkable that, in the laner part of this century, modern investigators have not even come close to replicating the breadth of findings in these investigations. Unfortunately, that is the on ly downfal1 of the work left to us by Louisa Burns and her col1eagues. As time has passed, experimental techniques have adva nced so much that these studies have become outdated, a nd their findings are cal1ed into q uestion. It is hoped that current and future investigators in chiropractic and osteopathy can conduct the kind of modern investigations that will vindicate the enormous historic contribution made by the scientists at the Sunny Slope Laboratory.
Study #2 mu:
Researching the subluxation on the domestic rabbit
AUTHOII: Carl Cleveland, Jr., and col1eagues JOUIINAl.S: 1) Cleveland Col1ege of Chiropractic Monograph 1961 2) Science Rev Chir 1965; J (4):5-28 .
Al'AtU: Rabbit
S\JIII.UXATlON CIM'IIMNT MOO8BJ: Misalignment of the intervertebra l joint
PIIT1IOIIS: 1) Minimal surgical procedure using external metal splint attached to spinous processes of three vertebrae. Subluxation produced by tightening a screw on the frame of the splint, thereby lateral1y misaligning the middle vertebra
2) Degree of misalignment variable and easily rep licable 3) Procedure done under fluoroscopic assistance 4) Misalignment was verified by radiographs 5) Outcomes were physiologic measures such as heart rate, blood pressure, erc. 6) Pathologic and postmortem ana lyses conducted o n various tissues 7) Short-term and long-term experiments proposed; no controls reported
FHRS: Two case studies were reported of a successful induction of a T12 subluxation. In both cases, subsequent kidney abnorma lities were described. Mention is made of numerous other experiments in which "hearr diseases, valvular leakages, paralysis, arrhythmias, vasomotor paralysis, dropsy, kidney conditions, and the formation of tumours" were observed.
41
8 Balle Sc:Ien1IIIc Evld8nc8 IIII' Chiropractic BWluxatlon This study represents the first attempt by chiropractic investigators to employ an animal
model of spinal subluxation. The method used was quite innovative and relatively noninvasive. Unfortunately, no future investigators carried this method forward. This may have been because of rhe very limited dissemination of the Cleveland report.
quem years, orrhodox scientists came to reconsider their opposition to the notion of nerve pres-
sure, as witnessed by the work of Sunderland (1 7) , Rydevik et al. (18 ), and others. In this article, Haldeman reports on several features of compression-related nerve dysfunction . The first observation was the reduction of conduction ve locity associated with the constric-
Study #3 TTTlf: Changes in the structure and function of the sciatic nerve caused by constriction
tion ex periment. Secondly, Haldeman reported on blockage ofaxoplasmic flow along the nerve trunk, evidenced on histologic examination by
swelling of the nerve proximal to rhe consrriction site. These findings lent great support to the preva iling
notions
among
chiropractic
thinkers
regarding the importance of subluxogenic nerve
AUllIOII: Haldeman S (with Drum D)
compression.
JOUIINALS: 1) M.Sc. Thesis, 1969. 2) J Clin Chiro, 1969. ~ Frog
Study #4 TTTlf: Experimental induction of vertebra l subluxation in laboratory anima ls
SIIIluxmoN COM'OMI'IT MOOBBI: Subluxogenic compression of nerve root
AIITIIORS: Lin HL, Fujii A, Rebech ini-Zasadny H, Hartz DL
WTIIOIIS:
J Manipulative Physiol Ther 1978;
1) Surgical procedure/short-term experiment 2) Ligation of sciatic nerve 3) e1ectrophysiologic and histologic analysis of sciatic nerve Structures
JOIIINAl:
fRRS: This study represents the first attempt
SIIIlUXOGIMC COM'OMI'IT MOOBBI:
to use an animal experiment to model the purported compression-related effects of subluxation on nerve function. Traditional chiropractic theory placed a great deal of emphasis on the notion of subluxation creating interference on nerve function by creating direct bony pressure in the intervertebral foramen; this was the so-called " bone out of place/garden hose" theory. This idea was the object of much scorn in orthodox circles, and this study by Haldeman did much to counter this by showing the deleterious effects of even mild
1) Vertebral misalignment 2) Intervertebral fixation
levels of compression on a major nerve. In subse-
1:63-68. ~ Rat
.ntOIIS: 1) Surgica l procedure/se mi-short-term experiment
2) Misalignment and fixation produced by implantation of screws into rhe spinous processes of TID and Til 3) Screws joined and tightened by variable springs 4 ) Radiographic verification of alignment
42 5) Semichronic experiment lasting 14 days 6) Shams and controls used
FNIWGS: This experiment, co some degree, did follow up on rhe work of Cleveland and his colleagues by using an externa ll y implanted device co successfully create spinal misalignment. In this study, the on ly direction of misalignment was downwa rd, that is, the spinous processes were approximated, creating a backward extension of the intervertebral joint. Radiographic evidence (see Figure 3-3) showed that an average of 7 ~ 3 degrees of extension was induced. This was compared with no evident extension in the shams and the controls. This a rticle is certainly one of the strongest in its use of sham and control preparations and in its use of radiographic studies as an
~
objective outcome. Unfortunately, this group of investigacors did not report on any subsequent effects of the induced misalignment, nor did they publish any further work. It seems that this model was lost to future investigators.
Study #5 mu:
The present use of guinea pigs for chiropractic research
AI/11IORS: MacGregor M, Wiles M, Grice A JOUIINAl.: Canadian Chiro Assoc 1980; 24 (3):101-7.
8-8 Surgically induced misalignment of T10 and Til. (From Lin er 31. 1979.)
3 Basic Sclentllic Evidence lor Chiropractic Subluxation ANNAL: Guinea pig
43
nal area by implantation of loose Silastic ligatures surrounding the nerve
SUBLUXOGENIC COMPONENT MOOEUD: Misalignment FlllllNGS: This study established, for the first time, a workable and valid model of the kind of
METHODS: 1) Nonsurgica l procedure 2) External concussion over spinous processes, using a mechanical "adjusting" device
nerve compression and irritation that, as a pro-
posed mechanism, dominated the chiropractic paradigm. It is interesting to note that this model of chronic sciatic constriction predates by 8 years
IRInGS: This srudy was a reporr of preliminary findings of a proposed experiment to use a mechanical Uadjusting" device to concuss the
the model of neuropathic pain devised by prominent pain researchers at the National Institutes of Health (NIH) (19).
spinous process of a tcst vertebra into misalign-
ment. This study artempted to determine the feasibility of using this model by assessing normal animal parameters over an extended period and
by determining the reliability of palpation of the animal's spine for detection of the misalignment.
Unfortunately, no induction of the model was done, and no further reporrs were issued by this group. The use of an external concussion device
was explored in later papers, particularly by the group headed by Ken DeBoer.
Triano and Luttges reported a number of critical observations that are consistent with the chiropractic theory of subluxogenic nerve compression, including (1) inflammation demonstrated in the ep ineurium surrounding the Si lastic imp lantation; (2) diminished nerve conduction velocities, despite there being no complete circumferential constriction of the nerve; (3) faci litation effects noted in nerve refractory recovery rimes; and (4)
motor d isturbances observed as disturbances in gait as a result of dysfunction of the affected (that is, surgically treated) hind limb.
Study #8
Study #7
TITLE:
Subtle intermittent mechanical irritation of the sciatic nerves of mice
TITU: An attempt to induce vertebral lesions in rabbits by mechanica l irritation
AUTHORS: Triano J, Luttges M AUTHOR: DeBoer K JOURNAL: J Manipulative Physiol Ther 1980; 3 (2):75-80.
JOURNAL: J Manipulative Physiol Ther 1981; 4 (3):119-27.
ANI't'IAL: Mouse ANIMAL: Rabb it
SUBLUXATION COMPOM3VT MODRED: Subluxogenic nerve rOOt compression
SUBLUXOGENIC COMPOMNT MODRED: Misal ignment
METHODS:
METHODS:
1) Surgical procedure 2) Short-term and long-term experiments 3) Controls used
1) Nonsurgica l procedure in awake anima ls 2) Lesions (misa lignments) induced by means of an external concussive adjusting device (Figure
4) Constriction of sciatic nerve in the periforami-
3-4)
44
Rg&re 8-4
Subluxation
TIle ArtIcular LalOII
External concuss ion procedure. (From De Boer.) Manipulative Physio / Ther 4:122, 1981.}
3) Lesions confirmed by manual palpation 4) Long-term experiment (lasting 2.5 weeks) 5) Controls used
cessful induction of most misalignments. Unlike Lin et .I.'s report, radiographic findings were inconclusive.
fNIIIGS: This study, the first in a body of work by DeBoer and his colleagues at the Palmer College of Chiropractic, represents the first attempt to establish a workable, noninvasive, replicable method of inducing an intervertebral joint misalignment. The lesion was induced by [he use of
Study #8 TnU: Changes in nerve physiology in the rat after induced subluxation
an "activator-type" adjusting gun, and palpators were employed afterward to determine if a lesion had been induced, and if so to attempt to agree on its location. lnterpalpator agreement was
JOURNAl; M.Sc. Thesis; summarized in Articula-
reported as fairly high, probably indicating suc-
tions 1983; (Aug) :9-1 O.
AUT1IOR: Israel V
45 AI'At\l: Rat
SUIILlJXOGIMC COMI'IIMNT MOIJ8BI: Misalignment
3) Physiologic and e1ectrophysiologic measures made 4) Controls for surgery used
producing nerve root compression
FNIWGS: This report represents the most elegant fIlTHOIIS: 1) Lesion induced by graded external pressure applied to the spinous process of L6 by a mechanical "drill press-like" device 2) No controls used; short-term experiment 3) Electrophysiologic outcomes
and thorough experiment ever undertaken in the responses of the autonomic system to an induced subluxation. Expanding on the large body of work published by Sato and his colleagues, this "chiropractic version" of his experimenta l model still stands as the best of the animal model studIes.
FNIrIlS: Israel reported that H-wave latencies increased by an average of 15%. This was thought to be indicative of compressive disturbance of th e nerve roots resulting in decreased conductivity. This report showed great promise for a relatively simple model of subluxation-induced nerve disturbance. Unfortunately, no further work by Israel or with her model has been forthco ming.
Study #9 mu:
Sympathetic nervous system responses to mechanical stress of the spinal column in rats
AUTIIOIIS: Sato A, Swenson R JOURNAL: J Manipulative Physiol Ther 1984; 7(3):141-7.
Sato and Swenson reported that, after induction of the lateral flexion stress at TI0-Tll, there were significant reductions in blood pressure that were concomitant with decreases in renal nerve activity. By surgica ll y denervating neighboring joints, and by denervaring the carotid sinus, they showed that these changes were indeed induced by the experimental procedure of mechanically stressing the spine. They proposed that the autonomic disturbance was caused by sensory bombardment from the compressed spinal joint. This likely cook the form of nociceptive irritation of the spinal joint, alt hough the use of an anesthetic joint injection would have confirmed this. They concluded that these findings represented abnormal somatovisceral reflexes resulting from a brief spinal dysfunction. They wisely declined to speculate on whether such a mechanism could lead to "soma to-visceral disorders," but others have improperly extrapolated this conclusion from this srudy.
Study #10
AI'At\l: Ra t
SUBLUXOGIMC COMI'IIMNT MOIJ8BI: Misalignment producing nervous system dysfunction
mu:
Altered metabolic enzyme activities in fast and slow twitch muscles due to induced sciatic neuropathy in the rat
fIlTHOIIS: 1) Surgical procedure; short-term experiment 2) Misalignment produced segmentally by lateral flexion of vertebrae fixed by clamps into a bending rig
AUTIIIIRS: Christiansen J, Meyer J
JOIIINAL: J Manipulative Physiol Ther 1987; 10(5) :227-31.
46 SIIIlUXOGIMC CIM'INNT MOIII.BI: Misalignment
AI'A1Al: Rat
producing altered nerve activity
SIIIlUXOGIMC CIM'INNT MOIII.BI: Subluxogenic nerve compression
METHODS: 1) Manual manipulation (as per Burns et al. )
METHODS:
used to induce vertebral misalignment
1) Surgical procedure; long-term experiment (duration of 2 to 4 weeks). 2) Sciatic constriction model with loose ligatures 3) Physiologic and metabolic ourcomes
2) Surgical implantarion of gastric electromyo· graphic (EMG) monitor. 3) Controls used for surgery and for pain by sham manual stimu lation and cutaneous noci-
ceptive irritation
FNHS: This study expanded on the experiment of Triano and Luttges (see previous discussion).
FNHS: This is the second model employed by
Using the sciatic constriction model, these investi-
DeBoer and his colleagues and is highly reminis· cent of the methods of Burns et al. in the induction of the lesion. In rhis study, however, DeBoer et al. employ a modern approach to exploring the neurally based effects of such a vertebral lesion by monitoring changes in gastric myoelectric activiry with an indwelling EMG monitor. They found inhibitory effects on gastric smooth muscle activiry rhar appeared to be segmentally coordinated. They proposed a mechanism arising from subluxogenic somatovisceral reflex disturbance. This work is similar to the study by Sato and Swenson in that it is based on Sara's work on somarovisceral reflexes, and, in particular, that it
gators studied the end-organ effects of neural compression, which is thought to be caused by foraminal compression. They observed the fol· lowing: (1) changes in the gait of the animals, which they measured using an ingenious method employing dipping the rat's paws in developing solution and having them walk across x-ray film. The resulting footprint analysis allowed the investigators to determine that the experimental limb was protected during gait; (2) changes in nerve conduction velocity sim ilar to that found by Triano and Lunges; (3) enzymatic changes in the denervated muscles, which indicated a shift from fast-twitch to slow-twitch fibers. This latter change is reminiscent of the work of Haldeman (see previous discussion), in that it implicates an alteration in orthograde axoplasmic flow, which would alter the biochemical and metabolic environment of the muscle end organ.
Study #11 TTTlf: Acute effects of spinal manipulation on
demonstrates which organ systems depend more
on spinally mediated responses, and which, like the cardiac system, depend more on supraspinally mediated responses.
Study #12 TTTlf: Surgical model of chronic subluxation in rabbits
AUTHORS: DeBoer KF, McKnight ME
gastrointestinal myoelectric activity in conscious
rabbits
JIIIIWAl: J Manip Physiol Ther 1988; 11 (5):366-72.
AUTHORS: DeBoer KF, Schutz M, McKnight ME AI'A1Al: Rabbit
JIIIIWAl: Manual Med 1988; 3:85-94. AI'A1Al: Rabbit
SlllLUXOGlMC CIM'INNT MOOB.BI: Vertebral misalignment and fixation
47
3 Balle Sc:Ien1IIIc Evidence lor ChIropractic SUbluXation
- ;;..-.-
-.
Flgll'83-5 Surgically induced misalignment (From De Boer, McKnighr. J Manipularive Physio l Ther 1988; II :368.)
1'tE1IOIIS: I ) Surgica l implantation of a metal bar between three thoracic spinous processes, ro misalign the middle one (Figure 3-5) 2) Long-term experiment 3) Controls used
IRMS: This is the third in the series of stud ies reported by DeBoer et a l. In this study, a novel method of inducing a chronic, sustained subluxa-
rion with minimal surgical trauma was devised. This study reported on the method of surgical
induction as well as on its durability in maintaining the misalignment. In addition, observations made of the misa lignment after the surgery also were reported. The conclusion of this report was that a misalignment could be induced and verified
on visual inspection, manual palpation, radiograph ic analysis, and autopsy study. Unfortunately, no outCome effects of this lesion were studied, a lthough the aut hor was made aware, by personal communication with DeBoer, that one of the intended applications of this model was to stud y its effects on the lactation reflex in mothering rabbits. It was theorized that if a lesion could be induced in the TS-T6 segment in one group of mothering rabbits, and compared with a control group, there might be a significant disturbance of lactating behavior, given that the senso ry component of the lactati ng reflex is carried by cutaneous nerves from skin innervated by this dorsal segment. This represents an ingenious test of the theory of central faci litation and disturbed somatovisceral reflexes.
48
Study #13 mu:
Thermographic evaluarion of rars wirh complete sciatic nerve transection
AUTIIORS: Gerow G, Callron M, Meyer JJ, Demchak JJ, Chrisriansen J
JOURNAL: (Abstract). Proc FCER ICSM 199 I; 272-4. AfAQL: Dog
SUIIlIIIIATD\I CIJIIoIIOMNT MOOflBI: Intervertebral joint fixation
r.HlIOOS: JOUIINAl; J Manipularive Physiol Ther 1990;
1) Surgical procedure
13(5):257-61.
2) Dental adhesive glue injected into bilateral
apophyseal joints in the upper lumbar spine
AMMA1.: Rar SUBLUXOGfMC CIJIIoIIOMNT MOOflBI: Sciaric rran-
fI\IKS: These investigators employed a novel
section models severe nerve compression
method of modeling an intervertebral joint fixation. Radiographic and biomechanical stiffness testing demonstrated an increase in the segmenral stiffness, verifying that a segmental fixation was, indeed, induced. This form of fixation, in contrasr to that of the models of Cleveland and DeBoer et aI., involved significantly less invasive procedures and probably could qualify as a valid candidate for a workable long-term experiment. Although increased stiffness was found at the experimental segment, these investigators could nor demonstrate increased stiffness in the entire lumbar spme.
METHODS: 1) Surgical procedure transecting the sciatic
nerve unilaterally 2) Controls used 3) Thermographic evaluation of the hind limbs,
comparing operated with nonoperated
fI\IKS: Thi study attempted ro extend the model of milder, transient nerve irritation to the upper limit of complete transection. In that regard, it is arguable that it was even designed ro study subluxogenic effects, as opposed to those that might arise from a discogenic mechanism, or
onc involving significant nerve rOOt injury. Nonetheless, these authors report that transection did result in increased temperature on the affected side, a resu lt that prompts us to consider the possible autonomic effects of these sciatic irritation models.
Study #15 mu:
Immunologic correlates of reduced spinal mobility: preliminary observations in a dog model
AUTIIORS: Brennan PC, Kokjohn K, Triano JJ,
Study #14 mu:
Spine stiffness measures in a dog model of restricted joint motion
Fritz TE, Wardrip CL, Hondras MA
JOURNAL: (Abstract). FCER ICSM 1991: 118-21. AfAQL: Dog
AUTHORS: Papakyriakou MJ, Triano JJ, Brennan
SUBlUXOGfMC cor.I'OI'BT MOO8fD: Fixarion;
PC
somatovisceral effects
3
BasIc SclIII1IIIc Evidence I... CfIII'OII'lCtIc SUbluxation
METHODS:
49
1) Same as Srudy 14 2) Controls used 3) Long-term experiment (up to 12 weeks)
3) Chronic experiment. 4) Muscle enzymes assayed after killing of animal 5) Contralateral side used as control
ffII\IGS: This study, from the same group as
fI'tM'flS: This srudy is a modification of the ear-
Study 14, employed the dog fixation model to explore immunologic outcomes of a long-term upper lumbar fixation . The reported results were preliminary, but did show evidence of, in the
lier one by Christiansen er aI., with much the same results. In this srudy, rhe results of five preparations were reported, and included "significant decrease of enzyme activiry of both aldolase and lactate dehydrogenase in the flexor digitorum longus muscle and a decrease in lactate dehydrogenase in the gastrocnemius on rhe side with the compressed nerve" as compared with the control side. Other enzyme assays showed trends toward significant alteration, bur the small sample size prevented statistical significance of these findings. As the authors state, "these results suggest that mild, chronic nerve compression, within the physiological range, will produce significant alrerations in end-organ metabolism."
aurhors' own word s, "functional impairment of
the immune system," mOSt likely related to impairment of natural killer lymphocytes. This study provides the first, if only fleeting, evidence to support the notion that the spine plays an important role in the immunologic health of humans. However, before we can accept some of the anecdotal observations regarding clinical improvemenrs in immune-related conditions by chiropractic treatment, a great deal morc work
like this study will have to be done.
Study #18
Study #17
TITU: Enzyme changes in rabbit muscles due to
1TI1.E: Characterization of spinal somatosensory
chronic compressive nerve irritation
neurons having receptive fields on lumbar [issues of cats
AUTlIOIIS: Christiansen JA, Beals S, Burnham G, Magnani M, Urbanek S
AUTlIOIIS: Gillette RG, Kramis RC, Roberts WJ
JOIIINAl: Proceedings of the World Federation of Ch IropractIc Congress, Toronto, Ontario, 1991
JOURNAL: Pain 1993; 54(1 ):85-98. Af&'tW.; Ca t
SUBl.UXOGENIC CIJMIIOMNT MOIIBBI: Motion segSUBlUXOGENIC CIJMIIOMNT MOIIBBI: Chronic, low-
ment tissue pain; central sensitization
level foramina! nerve compression
METHOIIS: .ntOOS: I) Surgical procedures used 2) Miniature compression cuff around one sciarice nerve u~cd to model foraminal compresSIon. Inflated to 40 to 50 Torr for 8 hours daily for 30 days
I ) Surgical preparations 2) Labeli ng and tracing of dorsal horn neurons using standa rd electro physiologic and histochemical techniques to determine the response characteristics of each neuron, its location in the dorsal horn, its receptiveness to deep or
50 superficial stimuli, and its receptive fields in skin and deep tissues 3) Percutaneous injections of algogenic subStances such as bradykinin and hypertonic saline into a variety of motion segment tissues in the lumbar spina l area . These tissues included : Multifidus muscles Facet joint capsules Discs
Dura mater Sympathetic ganglia 4) Characterization of changes in response properties attributable to noxious stimuli of the various lumbar tissues. These changes take the form of expanded receptive fields, unmasking of latent receptive fields, and other manifestations of central sensitization (see following discussion).
FNRS: The work of Gillette, Roberts, and their colleagues represents a major departure from the traditional work reviewed previously. The foremost reason is the sophistication of neurophysiologic investigative technjques, which include peripheral afferent tracing with radiolabeled substances, single-unit electrophysiologic recordings in the dorsal horn, and other e1ectrophysiologic techniques of spinal cord monitOring. Secondly, this investigation (which is made up of a large number of studies, many of which were reported in conference proceedings) takes the form of an attempt to model the pain-inducing effects of the spinal subluxation without resorting to the difficult and cumbersome step of actually misaligning the intervertebral joims themselves. In fact, this study's objective is really the phenomenon of deep somatic pain in the paraspinal area, a topic that has yet to be explo red by any investigators from neurophysiology or any of the other basic clinical sciences. Whereas many of the previo us subluxation studies may have induced pain in the paraspinal tissues, none has done so in a controlled fashion. In some instances, the pain that may have been induced by one experimental maneuver might have been accompanied by other,
more significant, tissue injury. In other instances, compression-related effects of nerve constriction and other manipulations may actually have been pain inducing, creating an unclear picture of experimenta l cause and effect relationships. In this stud y, carefu l a lgogen ic stimu lations were conducted as the primary objective of the experiments, resulting in much new knowledge about the afferent neuronal connections subserving deep spinal pain and of the modifications in response characteristics of the central nervous system to deep somatic pain. Most of the dorsal horn neurons studied by Gillette et al. that received nociceptive input from deep paraspinal tissues were located in the lateral portions of the superficial dorsal horn. Many of these connections were bilateral in the cord. The receptive fields of many of these neurones were comparatively larger than those that innervate less proximal tissues and were certainly much larger than those that innervate truly dista l tissues of the hind foot. Most of these neurons (72%) received input from a large number of sources, including skin, deep somatic tissues, dura mater, and visceral inputs. Gillette et al. have termed these cells "hyperconvergent neurones."
As for modifications of the response properties of these neurons to the various algogenic stimuli, a typical pattern emerged from their studies that is reminiscent of previous work involving tissues from the extremities (20), and that includes slowly increasing after stimulus exciratory discharges, expansion of the receptive fie lds to incorporare further distal tissues, not only ipsilateral but also contralateral to the side of injection, and hyper responsiveness to subsequent noxious and non noxious stimulations. All of these findings are consistent with the current model known as central sensitization, a term proposed by Woolf (21), but that is really reminiscent of the concept advanced by Korr in the late 1940s known as central facilitation (22 ). As Gillette and his colleagues point out, these neurophysiologic findings are the most likely mechanisms that underly a great variety of c1ini-
3 Balle SCIentIIIc Evldencllor ClI......·1CtIc SUbmaIlon cal phenomena associated with deep somatic pain. These findings provide an explanation for the diffuse and poorly localized character of spinal pain, and for the phenomenon of referred pain. They provide a basis for understanding why spinal pain might be exacerbated by subsequent pain arising from nonspinal sites, and, possibly, the reverse situation. In other words, these findings provide for a great advance in our understanding of subluxogenic pain, which is the basis for understanding of the great variery of spinal pain syndromes so commonly treated by chiropractors.
Study #18 mu:
Excitatory effects on neck and jaw muscle activity of inflammarory irritant applied ro cervical paraspinal tissues
AIITIIOIIS: Hu JW, Yu X-M, Vernon H, Sessle 8J
JOUIINAl.: Pain, 1993.
51
4) EMG monitoring using unipolar leads placed in the following muscles: (1) ipsilateral masseter, (2) ipsilateral digastric, (3) ipsilateral trapezius, (4) ipsilateral deep paraspinal, (5) contralateral deep paraspinal.
1ItI'CS: This study takes an approach similar to that of Gillette et aI., in that the proposed paininducing effects of the subluxation are modeled directly using an inflammatory algogenic substance, mustard oil, which is a known C-fiber irri-
tant (23). Although Gillette et al. employ more direct measures of the nociceptive effects (that is, by investigating response properties of dorsal horn neutons), we employed an indirect method based on the pain-spasm theory (24). This is the first study, to our knowledge, that demonstrates the very commonly observed clinical phenomenon of deep paraspinal somatic pain eliciting muscular excitation. Of great interest in this study was the finding of excitatory effects in muscles that were not only local (for example, the ipsilateral deep paraspinal muscle, which showed the largest initial response and the most prominent second-phase response), but also distant, in several ways. First, excitatory effects were seen in
AM't'IAl: Ra t
SUIIlUXOGIMC CIM'INNT MOOEUD: Intervertebral joint pain
Pt'ITIIOOS: 1) Surgical procedure 2) Injection of inflammatory irritant (mustard oil) into the pararticular space around the C2-C3 joint on the left, and into the deep sub-
the contralateral deep paraspinal muscle, which were almost identical to those in the ipsilateral muscle, with the exception of the slightly smaller magnitude of the increased EMG output. Secondly, excitatory effects were observed also in a superficial muscle (the trapezius) and in distal muscles thac surround another articulation (the
temporomandibular joint), but that are related by their shared nociceptive innervation by the trigeminal nucleus subcaudalis (25) .
occipital muscle-rectus capicus posticus
major--
tions with no mustard oil following. The latter experiment was to determine if volumetric
trauma produced any effects, as opposed to the inflammatory irritant itself.
Of further interest is the finding of a biphasic response in the spinal muscles. The first, and larger, response startS immediately and lasts for an average of 1.6 minutes. A period of suppressed response, which lasts for up to 10 minutes, is then followed by a second excitatory phase that can continue for up to 20 minutes. In general, all of these excitatory responses were reversible by 120 minutes (Figure 3-6).
52 . _ . , . ... 1.,1"1 Iftln,,.1 011.
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ItI'n 011 O"'O r,ul,lng ,"In "o' 011 onlr
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& "=& ,' &' ~'H~!Ii_",'~'~~~&,&,,&~:~ 10 IIIln
Rgure a..a Average changes in EMG activity induced by injections of mineral and mustard oil into deep parasp inal tissues sur round ing the Cl-3 vertebrae. The means (:5.0.) data shown are norma lized values relative to the mea n va lue of the pre-i njection EMC activity (= 100 %) in each rat . The solid line shows the changes in EMG activity of one group of rats receiving mustard oil at 20 min after the vehicle (mineral oil) injection (n: number of rats tested by the injection of mustard oil). The dashed line shows the changes in EMG activity of the control group of 4 rats receiving the vehicle, instead of mustard oi l, again 20 min after the first vehicle injection. # and ##: P < 0.5 and P < 0.01 (Wilcoxon test) indicate significant difference between pre-injection and postinjection level of EMG activity. ... and ... : P < 0.05 and P < 0.0] not only indicate significant difference between the preinjection and the posrinjection level of EMG activiry (Wilcoxon test), but also between the animals receiving mineral then mustard oil and the a nim als receiving mineral oil injection twice (Mann-Whirney test).
3 Basic SclentIIIc Evidence lor Clt*WIC1Ic SUbluxation The control experiments confirmed that the mineral oil injections, both singly and in paired series, did not elicit any appreciable excitation beyond baseline levels. This confirms, for the first time, that the pain thought to result from an intervertebral subluxation is capable of eliciting local and possibly widespread excitation of spinal musculature.
These last two studies demonstrate that it is relatively easy to model, in an experimenta l preparation, the pain-inducing effects of intervertebral subluxation. These models (both the singleunit recording and the EMG-based) shou ld provide for fruitful research into the clinical and neurophysiologic effects of subluxation.
Discussion The lists of the various components of the subluxation that have collectively been modeled in the literature just reviewed. Only the studies by Burns et aI., Cleveland, Lin et aI., Israel, Sato and Swenson, and DeBoer et al. have involved attempts to actually misalign an intervertebral segment. This misalignment is accomplished in either a passive or an active fashion . In the former case, external or internal methods have been used . External methods involve either manual misalignment or the use of some form of surgi-
cally implanted device to achieve a fixed misalignment. Active misalignment refers to procedures such as those used by Israel and by Sato and Swenson. In these procedures the segments are caused to be actively displaced (either into backward extension or latera l flexion). The displacement is typically reversible. In a ll of the studies mentioned in (his group, intervertebral misalignment has produced a set of typical and predictable findings . These effects range from decreases in nerve conductivity (Israel) to increases in autonomic discharge and changes in visceral function (Sato and Swenson, DeBoer et al.). Although these findings have been relatively small in magnitude and in their duration, they are, as a group, consistent with the theory of sub· luxation and hence justify continued investigation .
53
>
Components of Subluxation Modeled By Animal Studies
• Facet compression • Paraspinal deep somatic pain • !ntervenebral foraminal nerve root compres· sian • Fixation
• Hypermobility
Other studies have attempted to actua ll y model the components of the subluxa ti o n itself: compression in the intervertebral foramen, paraspinal pain, or fixation of the motion segment. In the former case, sciatic liga tion has been the chief method employed, although Christiansen et al.'s most recent work em ployi ng a miniature pressure cuff is quite innovative. In every case, the compressio n-related effects predicted by the subluxation theory have been demonstrated, including reductions in conduction velocity and in axoplasmic flow, as well as enzyme changes in muscle end o rgans. In the case of pain-related effects, both mechanical a nd chemical methods have been employed. Mechanical methods include facet compression and misal ignment, whereas chemical/infl ammatory methods have employed a lgogenic injections of bradykinin, mustard o il, and hypertonic saline. In these models, deep spi nal pain has been shown to have profo und effects on neurophysioiogically based pheno mena such as response characteristics of dorsal horn cells and muscle activity. In the one case in which fixation was induced without accom panying misalignment (by Brennan, Triano, an d their colleagues), interesting systemic effects of the induced hypomobility were demonstrated, which certainl y prompt further in vestigation. The box at the top of p. 54 lists the different outCome measures used in this set of studies. When
54
>
Animal Model Studies: Measures and Outcomes Used
!MIl
Histology of joints and nerves Radiographs of the spine Pathologic function of nerves o EMG of paraspinal muscles Dlltall o o o
• Autonomic nerve function
Homeostatic rellexes Organ pathologic effects Changes in cutaneous receptive fields H-Reflexes Conduction velocity Axoplasmic flow Trophic changes in muscles Motor behavior
o o o
o o o
o o
combined with the great variety of techniques used to experimentally induce or model a subluxation, one can only be impressed by the breadth of technical innovation and sophistication that has been employed by the profession's basic scientists. Their efforts have been rewarded by the accumulation of a database that is remarkable for its theoretical and experimental consistency. in virtually every instance, some aspect that has been predicted by the subluxation theory has been verified. The box below lists some of the strengths and weaknesses of this body of work.
>
Animal Models in Chiropractic Science
• Numerous investigative groups o Innovative methodologies devised o Conceptual consistency in experimental approaches o Theoretical consistency in experimental findings ".pU. . • No sustained lines of investigation • No comprehensive line of investigation
o No replications o No clinical implications o Very few conferences/no "body of literature" o Growing concern over animal welfare may make long-term experiments difficult
Unfortunately, as this box shows, there are some compelling concerns that exist after some eighty years of investigation. The chief among these is that this body of work has not been crystallized in the collective consciousness of the profession. The profession, it seems, is either still "fixated on" or feels more satisfied with its conceptual models and its elaborate speculative pictures than with the pursuits of morc basic scientists, who seek to depict or study subluxation as it really occurs. The profession's research agenda (which, thankfully, has finally come into existence) seems far more preoccupied with clinical matters than with those of its basic science. This may suffice for the musculoskeletal domain, because, as of the writing of this chapter, the pathologic model of low-back pain is in poor repute, with the functional, patient-oriented model predominating. In this kind of atmosphere, chiropractic therapy can flourish because demonstrating the efficacy of a treatment is more important than elucidating the mechanism that underlies it. However, for nonmusculoskeletal conditions, the opposite situation pertains. It is my opinion that dozens of clinical trials can occur in such areas as the chiropractic treatment of asthma, dysmennorhea, hypertension, etc., but they will all be relegated to insignificance and be dismissed as large-scale exercises in the placebo effect if a credible, va lid biologic mechanism that links dysfunction in the spinal column with dysfunction in organ systems cannor be provided. This is the task that only the profession's basic scientists, in their pursuit of the scientific basis of subluxation, can accomplish.
References I. Ganerman MJ . Chiroprac1ic management of spme related disorders. Baltimore: Williams and Wilkins, 1990.
2. Brantingham jW. A survey of the luerarurc regardmg the
a
3.
4.
5.
6.
7.
8.
9.
10. II.
12. 13. 14.
BaaIc ScIen1IIIc Evidence
behaviour, pathology, etiology and nomenclature of the chiropractic lesion. J Ch iro 1985; 22(8):65- 70. Lanrz CA. The vertebra l subluxation complex. Part 1 t The neuropathological and myoparhoiogica i components. Ch;
'II' CI*opi'8CIIc Blmluxatlon
55
15. Burns LA. Effects of upper cervical and upper thoracic lesio ns. J Am Osteopath Assoc 1923; 22:266. 16. Surns LA. Laboratory proofs of the osteopathic lesion . J Am Osteopath Assoc 1931 ; 31:123. 17. Sunderland S. The anatomy of the intervertebral fo ramen and the mechanisms of compression and nretch of nerve roots. In: Haldeman S, ed. Modern developments in the principles and practice of chiropractic. New York: Appleton-Cenrury-Crofrs. 1979. 18. Rydevik B. Brown M, Lundborg C. Parhoanatomy and pathoph ysiology of nerve compression. Spine 1984; 9,7-15. 19. Bennett G, Xie Y-K. A peripheral mono-neuropathy in rat that produces disorders o f pain sensation seen in man. Pain 1988; 3:87-107. 20. Mense S. Nociceprion from skeletal muscle in relation to clinica l muscle pain. Pain 1993; 54:241-89. 21. Woolf Cj. Recent advances in the pathophysiology o f acute pain. Sr J Anaesth 1989; 63:139-46. 22. Denslo w jS, Korr LM, Krems AD. Quantitative studies of ch ronic facilitation in human motoneuron pools. Am J Phys;ol 1947; 150(2),229-38. 23. Wool f Cj, Wall PD. Relative effectiv eness of C-primary afferent fibres of different origins in evoking prolonged facilitation o f the flexo r reflex in the rat. J Neurosci 1986; 6, 1433-42. 24. Denslow JS, Hassett Cc. Spontaneous and induced spasm in structural abnormalities. J Am OSteopa[h Assoc 1943; 42,207-10. 25. Sessle 8J , Hu jW, Yu X4M. Srainsrem mechanisms of referred pain and hyperalgesia in the orofacial and temperoma ndibular regions. In: Yecchiet L, AJbe-Fessard 0, Linbloom U, Giamberardino MA, eds. New trends in referred pain and hyperalgesia. London: Elsevier, 1993,59-7 1.
• Palpatory Diagnosis 01 Subluxation r.ItcheII Haas David M. panzer
Key Words
Palpation, motion palpation, joint play, end feel, reliability
After reading this chapter you should be able to answer the fol/owing questions:
Question #1
What are the three most frequently cited adjustive indicators evaluated by palpation?
Question #2
What is the reliability of spinal palpation?
Question #3
What strategies can be used to improve the reliability of palpatory procedures?
4 Pllpal...y _ _ _ DI Slauxatlon
T
he hands are rhe primary rool of rhe chiro-
practor and are of utmOSt imponance in
identifying subluxarion. The onglO of rhe rerm
chiropractic is the Greek cheiroprattiell (done by hand), and current texts used in chiropractic education are replete with comprehensive palparory techniques (1-4). Manual therapies are, however, not unique to chiropractic.
Historically, manual therapies can be traced to Eastern and Western cultures rhousands of years before the advent of chiropractic (5). Hippocrates was a notable proponent of manual treatment, particularly for spinal conditions such as scoliosis and subluxarion (5,6). In light of modern advances in diagnostic imaging and other procedures, it may seem that the tedious process of palpation to evaluare rhe neuromusculoskeletal system is outdated . However, palpation remains recognized as an essential
skill by disciplines such as osteopathy (7) and physical therapy (8, 9), which employ many techniques quite similar to those used by chiropractors. Beal (7), an osteopath, notes rhat "palpation is of prime imponance in diagnosis, manipulative
treatment, and prognosis" of musculoskeletal conditions. Magee (9) describes numerous static and dynamic palpatory procedures for spinal and extremity articulations.
In quite another realm, Goble (10) offers practical advice for purchasing a horse. He states that "with reccnt advances in diagnostic techniques . . . there is a tendency to reduce our
reliance on the most important part of purchase evaluation of rhe horse, the hands-on physical examination." Human parallels are obvious in our age of cost-conscious health care, in which a thorough physical examination may render more useful information than do expensive diagnostic tests.
History of Palpation In Chiropractic Because the use of diagnostic palpation has stood (he rest of time, it is of interest to briefly review
57
its history in the chiropractic profession. In 1912, Gregory (11) defined palpation as "the gentle application of the hand or fingers to rhe surface of the body for the purpose of determining the condirion of the surface and adjacent parrs of a certain localiry or organ of the body." He described palpable characterisrics of the "spinal lesion" as:
1. Pain 2. Tender nerves 3. Thermic alterations
4. 5. 6. 7.
Congested neural cords Contracrured or contracred muscle Spinous process malposition Transverse process malposition
A contemporary study by Keating et al. (12) to evaluate interexaminer reliability of currently used palpation procedures showed remarkable similariry ro indicarors listed in 1912, with the addition of a dynamic component: I. 2. 3. 4. 5. 6. 7. 8.
Osseous pain Soft tissue pain Temperature difference Visual observation Passive motion palpation Muscle tension palpation Active motion palpation Misalignment palpation Among the earliest chiropractic palpation
techniques was nerve tracing, defined as "the art
of following, by pa lpation, a tender nerve from its spinal origin to some inflammatory or pathological lesion or zone, or the act of tracing a tender spinal nerve from an inflammatory zone back
to its spinal exit. "(11) D. D. Palmer (13) identifies himself as the originator of nerve tracing, but B. J. Palmer (14) also wrOte extensively on the subject. In fact, according ro B. J., methodologic consistency and reliabiliry appear to have been recognized as a problem even in his day (early twentieth century): "so far all of the nerve tracing in chiropractic, while it has been excellent, has produced excellent results,-has been used by many chiropracrors with a large degree of suc-
58 cess,-has still shown a remarkable divergence of method and accuracy" (14). It is interesting that early nerve tracing was nor unique to chiropractic. Cyriax, a medical doctor, published a paper on "nerve palpation" in
1914 (15). Nerve tracing is no longer emphasized in chiropractic education.
In addition to the aforementioned static palpation techniques, various dynamic forms of palpation have developed within the chiropractic profession. Gillet (16-18) developed and systematized motion palpation techniques that have been expanded and disseminated by Faye (2, 19, 20) and Schafer (20). Palpation is currently defined as the application of manual pressures, through the surface of the body, to determine the shape, size, consistency, posicion, and inherent motiliry of the tissues beneath (21).
Palpatory Indicators lor Manipulation Contemporary palpation techniques can be divided into static and motion procedures used in the adjusrment decision-making process (1,4):
2. Accessory motions a. joint play b. end play or end feel c. joint challengeltenderness
Of the aforementioned palpatory techniques, some seem to be emphasized more than others. Bryner (22) surveyed 27 manuals and texts from chiropractic, osteopathic, physical therapy, and medical sources. He reported the frequency of citation of 15 different indicators for knee manipulation. He found the three mOSt frequently cited indicators to be: (1) joint play abnormaliry, fixation, adhesion, tissue tension; (2) misalignment, displacement, prominence; and (3) tenderness, swelling. He concluded that "more consensus between professional groups exists than is suggested in most professional forums." A survey of chiropractic colleges (23) found that all of the respondents (9 of 18 colleges surveyed) reported using joint play assessment and motion palpation as important indicators for joint manipulation . It was further concluded that improved standardization of procedures is needed, a concern also
A. Static Palpation 1. Soft tissue a. tenderness b. edema c. temperature
d. moisture e. muscle [One f. hyperemia response g. motility h. trophic changes 2. Bony a. tenderness b. malposition c. anomalies B. Motion Palpation I. Active/passive segmental range of motion
a. tenderness b. quantiry c. qualiry
noted by others (8, 24-27). Previous mention was made of selection of
palpatory techniques that identify manipulable subluxation or manipulable lesion . lull, Bogduk, and Marsland (28) looked at this issue, as well as the accuracy of manual diagnostic techniques for specific localization of cervical zygapophyseal pain and dysfunction. The three palpatory criteria selected were: (1) abnormal end feel, (2) abnormal qualiry of resistance to movement, and (3) local pain on palpation. This study was unique in many respects. First,
its subjects were 20 patients with chronic (more than one year) neck pain. Second, they were evaluated with diagnostic nerve blocks to establish with certainry the vertebral level of their symptoms and that the zygapophyseal (facet) joints were indeed the source of pain . Third, the examiner blindly examined the subjects either before or after the diagnostic nerve block (I) to
59
4 p.tory IlIIgIIOIIs of SUllluxalIaII establish if the pain was the result of facet joint dysfunction; (2) if so, to identify the precise level of pain; and (3) to identify patients with nonfacet pain. The results were as follows: 1. The examiner correctly identified 15 of 20 patients with confirmed facet pain or dysfunction.
2. The correct segmental level was identified in all 15 patients. 3. Five patients with confirmed non facet pain were correctly identified. 4. It was concluded that "manual diagnosis by a trained manipulative therapist can be as accurate as can radiologically-controlled diagnostic nerve blocks in the diagnosis of cervical zygapophyseal syndrome." 5. The three diagnostic indicators chosen were "highly specific for symptomatic zygapophyseal joints."
Although these results seem quite impressive, they have yet to be replicated and cannOt be generalized to other areas of the spine. Still they invite a closer look at the issue of reliability as it relates to palpation procedures.
Test Reliability
adjusrive indicators has remained elusive because
of rhe absence of a "gold standard" for identifying manipulable subluxation. Reliability assessmeor thus continues to be the primary research
being conducted on the clinical usefulness of palpation. Although strong consistency of measures does nOt ensure validity, reliability assessment is extremely important because it estimates the con-
tribution of a tesr irself to the clinical decisionmaking process beyond what would be expected
by examiner guessing or random measurement error (34).
Assessment Reliability is evaluated by mulriple blinded measurementS performed on a sample of subjects. There are several types of reliability relevant to palpation (Table 4-1). Intraexaminer reliability evaluares the consistency of different examiners and is determined through repeated assessment
by two or more raters. Intraexaminer reliability is a measure of self-consistency; each rater must perform at least two measurements. Inrraexaminer reliability is susceptible to overestimation because of difficulty of blinding the rater (35) and a tendency toward consistency of measurement error (36) . Interinstrument reliability evaluates the agreement between rwo diagnostic techniques or two
Background Reliability is the reproducibility or consistency of measurement or diagnosis (29-3 1). It is the extent to which a test can produce the same result on repeared evaluation of an unchanged charac-
instruments (same type or different kinds). For example, the reproducibility of pain thresholds by two different types of pressure algometer can be evaluated. Interrechnique reliability can be assessed only if both instruments use the same units
teristic. When a rest result is categorical in nature,
of measurement.
such as the decision on whether to perform an adjustment, reliability is also called chancecorrected agreement or concordance.
Reliability evaluation is only one step in the determination of the clinical usefulness of a diagnostic or evaluative procedure (32,33). The accuracy or validity of a procedure-to what degree the test is on rhe mark and to what degree it actually evaluates what is intended-is of paramount imporrance. Direct assessment of the validity of
Types of Reliability
':;'..,. - '. ~
~
:.
•
Typo
Evaluation
Lnterexaminer lntraexaminer lnterinstrument Test-retest
~
2 raters ~2 times ~ 2 instruments ~ occasions
60 Test-retest reliability seeks to determine if examiners or instruments are consistent over
time. Measurement of this type of reliability is problematic because the stabiJity of manipulable subluxation and other palpatory entities is largely unknown. Biomechanical changes may be responsible for any apparent lack of consistency over time.
pie. The reliability of ordinal dara is evaluated with the weighted kappa statistic. When the data are continuous (interval or ratio), as for the force required to cross the patient'S pain threshold, the
statistic of choice is the inrraclass correlation
coefficient (ICC). When applied appropriately, the ICC also can be used to evaluate concordance for ordinal and two-category nominal data (37, 38 ).
R8IIabII1ty indica.
SIreIIgth of COncordance
The choice of the most appropriate reliability sta· tis tic depends on the type of measurement being made (Table 4-2). Although other statistical measurements have been used, they tend to give ambiguous results; in-depth discussions of reliability statistics may be found elsewhere (29-31). The most common data collected on patients through palpation are nominal. A prime example is the yes-or-no decision on the site of a manipulable subluxation. Another, with a four-categoty
The indices of reliability, for all practical purposes, are measured on a zero to one scale. Zero
implies no relationship between ratings and that agreement berween examiners can be attributed to chance alone; one represents perfect consis-
tency. Although possible, negative values, like zero, are taken to mean that the procedure itself contributes nothing to the measuring process beyond
guessing
and
measurement
error.
Although interpretation of values in between zero
outcome, is motion restriction on the left, on the
and one are somewhar arbitrary, there appears to
right, both, or neither. The reliability statistic of choice in the case of a clinical decision based on such categorical data is kappa. Kappa is often described as a chance-corrected measure of examiner agreement (6, 30, 31, 33).
be consensus that values less than 0.4 represent inadequate reliability (39-41). Just what repre· sents good reliability depends on the nature of the test performed; clearly a test for acute myocardial infarction would require a greater level of consistency than a test for manipulable subluxation. Table 4-2 provides a rule of thumb for the interpretation of reliability for palpatOry procedures.
When the measurement categories are ordered
in some way, the data are called ordinal. A clinical decision of degree, such as mild, moderate, or severe joint play restriction, is a common exam-
Reliability 01 Chiropractic Spinal Palpatory Procedures
Reliability Statistics
There have been close ro 90 articles published in the peer-reviewed chiropractic literature on the
Scales and Indices
Nominal Ordinal Interval
Kappa Weighted kappa lntraclass correlation
Strength of Agreement
0.00 0.00-0.39 0.40-0.59 0.60-1.00 1.00
Chance Poor-fair Moderate Good-
subject of reliability; 28 address palpation. Beca use it is beyond the scope of this text to do an exhaustive review of the literature, average
study findings are reported here in summary form only for those studies reporting the statistics just discussed. However, there are in-depth review
articles (Table 4-3) available that explore the original research on the reliability of palpatory procedures and several articles that carefully examine reliability study design, analysis, and
61
Review Articles
Author Alley (57) Russell (58) Dishman (59) Keating (60) Haas (35) Breen (24) Panzer (27)
Motion Palpation Rel iability Studies
Vlar 1983 1983 1988 1989 1991 1992 1992
Suble"· MP, MP,SP MP,SP MP
MP,SP MP,SP MP
.. MP, motion palpation; SP, static palpation.
interpretation in general (30,35,42,68). Further studies may be found in the physical therapy and medical literature. These have not been included here because of their questionable generalization to chiropractors; other professionals may have different training in these procedures and may apply and interpret them in a different manner.
Specfficlty Assumption The assessment of the reliability of palpatOry procedures in the chiropractic literature has been guided by a fundamental chiropractic precept, the assumption that spinal manipulation must be and can be performed at specific spinal segments or motion segments to engender the appropriate therapeutic effect (44). It then follows that palpatOry procedures mUSt be equally specific and it would seem reasonable that investigatOrs have focused on the examiner consistency of identifying individual segments with manipulable subluxation. What must be kept in mind in reviewing study findings is that the specificity assumption has compelled the profession to accept a stringent standard for determining reliability; this precept still awaits clinical verification.
MotIon Palpation Fifteen srudies report original data on the reliability of motion palpation in various regions of the spine and pelvis (Table 4-4): five cervical, two thoracic, six lumbar, and six sacroiliac. The interexaminer reliability of identifying motion or
Author Wiles (61) DeBoer et al. (56) Mior et al. (47) Bergstrom and Courtis (62) Love and Brodeur (25) Carmichael (46) Boline et al. (45) Rhudy et al. (63) Nansei and Jansen (64) Herzog et al. (65) Leboeuf et al. (66) Nansel et al. (49) Mootz et al. (26) Mior et al. (48) Keating et al. (12)
Region· SI C C L L SI L C,T,L C,T,L,SI SI L,SI C L SI L
Year
1980 1985 1985 1986 1987 1987 1988 1988 1988 1989 1989 1989 1989 1990 1990
·C, cervical; T, thoracic; L, lumbar; 51, sacroiliac.
end-feel restriction at specific segmental levels was poor, averaging 0.00 to 0.15 (Table 4-5) (12, 26, 45-49). Raters agree little more than would be expected by chance. Intraexaminer reliability was considerably better, averaging 0.45 to 0.53 (26, 46-48). However, the latter findings must be viewed with caution . Within the context of the specificity assumption, if two
Average Reliability of Palpatory Procedures
Motion Palpation
Interrater Intrarater
0.00-0.15 0.45-0.53
Poor
0.00 0.07-0.20 0.20-0.69
Poor Poor Fair-good
Moderate
Static Palpotiol'
Interrater Ma lposition Muscle tension Pain provocation Inrrarater
62
SUbluxation
TIle ArtIcular LesIon
exam in ers are self-consistent but cannot agree, then at least one rater must be consistently in
error. Also, a ny clinica l findings that cannot be replicated by others are always considered suspect.
actually depend on individual palpatory procedures? How do chiropractors weigh the evidence from a variety of adjustive indicators? Are palpatory rests morc valuable in certain patient popula-
tions than in others? Do chiropractors effect successful adjustments and patients show clinical
StaUc PalpaUon
improvement in spite of the diagnostic tests per-
Ten studies appear in the literature addressing static palpatory procedures (Table 4-6): three on
formed? Finally, we must ask ourselves if the
the cervical region, one on the thoracic spine,
eight on the lumbar region, and three on the sacroi liac joints. Inrerexaminer concordance of
specificity assumption led us astray from investi-
gating the reliability of palpation in a context relevant to the actual biomechanical and clinical effects of manipulation on the body.
vertebral malposition (0.00) and muscle tension (0.07 to 0.20) have been found to be little more than happenstance (Table 4-5) (12,45,50). How-
Improving the Reliability 01 Palpation
ever, some results for provocative pain over the spinous processes and paravertebral soft rissue
There is a rich supply of literature on the need for en hancing the reliability of diagnostic tests,
have been encouraging (0.20 to 0 .69) (12, 45, 50). There have been no intraexaminer reliabiliry studies on static palpation.
sources of inconsistency, and recommendations
for reliability improvemenr (Table 4-7). This lirerature is as valuable to the practicing clinician as it is to clinical researchers.
Conclusion
Why Bother?
Although the reliability of palpation appears discouraging, a ll is far from lost, as will be seen
We must first ask ourselves why improving
in
the
next section.
Many
interesting
and
consisrency is so important. After all, experience
provocative questions have arisen from more
tells us that we ca n successfully identify manipulable subluxations and make our patients better.
than a decade of research. For example, to what degree does the clinical decision-making process
Unfortunarely, even accurate recollection of our experience can lead us to wrong conclusions
about the effect of diagnostic tests on patient outStatic Palpation Reliability Studies
Author DeBoer et al. (56) Boline et al. (45) Nanse! and Jansen (64) Owens (67) Leboeuf et al. (66) Jansen et al. (68) Keating et.1. (12) Byfield et al. (69) Byfield et al. (70) Boline et al. (50)
Year
1985 1988 1988 1988 1989 1990 1990 1992a 1992b 1993
Reglo.' C L C,T,L,SI ~ ~
L L,SI L L,SI SI L
·C, cervical; T, rhoracic; l, lumbar; 51, sacroiliac.
Clinical Judgment and Reliability Literature '..
, •
.~.
",:I'
'J._.
,
--~.
.'
Author Deparunent (52)" Department (53) " Feinstein (71) Feinstein and Kramer (72) Feinstein (73) Sackett et aJ. (33 ) Wright and Feinstein (51)
.-
'
. . •
"'7
Year
1980 1980 1964 1980 1987 1991 1992
· Departmenl of Clinical Epidemiology and Biostatislics, McMaster UniverSity. Iinmiiton. Ontario, C.1nnda.
4 Palpatary DtalilOlla 01 SUbluxation come (33), and there are several good reasons why it is imperative that reliability of palpatory procedures be improved (51). Our first motivation is the justification of
using palpatory procedures in the first place. A test in which the findings cannot be replicated will always be called into question. How can we be sure that we can identify a manipulable subluxation; how can we be sure that a patient really has a motion restriction o r malposition and that it responded to treatment? Furthermore, poor
reliability implies that a test performs little better than guesswork and as such contributes on ly marginally to the decision-making process (34); why bother wasting the time and effort? An unreliable test can hardly be justified as cost-effective. Improving reliability can also enhance the accuracy of a rest; an unreliable test can never be
accurate (51). Improvi ng accuracy can lead to increased efficiency of care because false-negative findings can lead to underadjusting, and falsepositive findings can lead co excessive intervention. Finally, better consistency increases our con-
fidence in finding manipulable subluxations and monitoring changes in clinical status.
SOII'C8I 01 n:onslstancy Three sources of test inconsistency are discussed in the literature: the exam ined, the examination, and the examiner (51, 521. Different clinical findings may be attributable to variability in the procedure. For exa mple, imersegmenral orientation and motion characteristics may vary greatly in the various patient positions used to perform the examination: sitting, supine, prone, or side posture. Physicians also use different landmarks to locate malposition and sites of provocative pain and use different methods for evaluating quality of motion, joint play, and end feel. Even when the same procedure is used, there is variability in its performance. Physicians hold patients in slightl y different positions or palpate with varying degrees of force. Procedure and performance being equal, inconsistency still arises from variability in interpretation: differences in
63
principle and perception. Where do individual clinicians draw the line in identifying manipulable subluxa tions from hard end feel or joint play restriction; what constitutes a malposition? Perception also can vary with physician expectation, alertness, and mood. After an adjustment, what chiropractor is not confident that a manipulable subluxa tion has been rectified?
What we Can Do Standardization There are several important trategies for improving the reliability of palpatOry procedures (Box below) (53). Probably the most difficult to implement is standardization of test procedure, performance, and interpretation. Chiropractic colleges need to make a concerted effort to research and develop instructional methodologies that foster consistent terminology and palpation outcomes. Ir has been suggested that improved standardization of techniques and enhanced ability to evaluate psychomotor ski lls may be faci litated by the use of mechanical devices to assist in quantitative feedback by the quant.ification of manual forces (8,54,55). Examples include bathroom scales (8), pressure plate with osci lloscope (55), and a mechanical spina l model with simulated fixations (54). IntructOrs a lso must emphasize to their students the potential influences of perception a nd expectation on clinical findings. Ambiguity not o nl y affects measurement consistency but also undermines the ability of chiropractors wit h diverse ideologies and treatment strategies to communicate with each other.
>
Steps To Be Taken to Improve Reliability
1. Standardization of test procedures 2. Repetition of test findings 3. Corroboration of test findings 4. Identification of suitable patient subpopulations
5. Reevaluation of specificity assumption
64
Subluxation TIle Articular lesion
Repeated Tests It is well known that for a teSt with nonzero reliability, the reliability of the average finding of test repetitions is greater than the reliability of a single evaluation (29-31). For example, when repeated tests are conducted independently (examiner blinded to previous results ), if the ICC = 0.50 for a single measurement, the reliability of two evaluations would be ICC = 0.67, and for three assessments, ICC = 0.75. Although repeated palpations are not blinded in clinical practice, they shou ld reduce diagnostic error. However, because of the likel ihood of some consistent error, the physician should regard high self-consistency with caution (36). Corroboration Another strategy for strengthening rhe reliability of manipulable subluxation detection is the use of diagnostic test regimens (42). Reliabiliry mighr be increased by using multiple tests for the evaluation of a si ngle palpatory dimension' of the subluxation (for example, motion, alignment, or palpatory pain ). The evaluation of mulriple pal patory dimensions as well as the inclusion of other clinical information is also strongly recom-
mended to avoid false-negative results. Research into the value of multitesr regiments is in irs early stages ('12, 45, 50). Further investigation is required to clearly identify individual dimensions of the subluxation and to establ ish regiments of related tests for evaluation of rhese
dimensions. Identification of Suitable Patients It is possible that various palpation techniques are more su itable fo r certa in subpopulations of patients than for others. These subpopulations could be identified through studies of carefully defined homogeneous groups of patients : probably parients with more severe and extensive problems. It also must be pointed our that, in genera l, concordance depends on the prevalence of the entiry being assessed (3 0, 34). For patient populations wit h a dearth of manipulable subluxation, it
is difficult for any test to perform better than guessing that the patient is normal at any particular segmental level. Reliability will inevitably be low in this case, and the contribution of palpation to the cl inical evaluation of the patient will be minimal.
Challenging the specmclty AssumptIOn With two exceptions (26, 56), reliability has been exclusively evaluated within the context of the specificity assumption. Whar we muSt ask ourselves is whether this precept is clinically valid: are we really investigating the re liability of detecting what we actually treat, and if not, are we underestimating the reliabi lity of our adjusrive indicators (44)? The specificity of the vertebral conracr rna y nor be necessary for correction of the "truc" underlying manipulable subluxation. Alternatively, the specific adjustment of different manipulable subluxations may have the same clinical effects; two chiropracrors may rightfu ll y treat different segments. If contact specificity is nor valid, examiners would not have to agree on specific segments bur only on a specific region to have the same clinical outcome. In this case, "regional " rather than "segmental" concordance in the site of an adjustment might be a sufficient condition to establish acceptable interexaminer reliabiliry of palpatory procedures. If adjustment specificity is not required to treat a clinical condition, however, self-consistency may be paramount and intraexaminer concordance the key to the reliability of pa lpation (the concerns listed previously norwithstanding) . Clearly it is easier to find agreement over a wider range of vertebral segments and with oneself than it is to find interexaminer agreement segment by segment. However, enhancing reliability is no justification for abandoning rhe specificiry assumption a priori . There is no biomechanical model or clinical evidence to suggesr how big the zone of agreement might be or how it might vary for different regions of the spine or different clinica l conditions.
4 Palpatory 0iagI1OIIs of Uluxa1lon
Future Research The goal of investigators must be to represent the adjustive decision-making process as realistically as possible in measurement evaluation research. Clinically relevant reliability assessment must include the study of de facto test regimens as well as the eva luation of indi vidua l procedures. The viability of the specificity assumption will be investigated in part through studies of the biomechanical relationship of the spinal contact with the motion segments being affected. Further research mUSt be conducted ro establish the clinical usefulness of palpatory procedures (32, 33) . The validity of palpation ro detect manipulable subluxations will be measured indirectly in the short term through the assessment of its theoretical properties (construct validity); these include the correlation of palparory findings with patient symptomatology, other diagnostic findings, ndjustive intervention, and treatment ourcomes. Ultimately, the utility of palpation must be evaluated: is the patient better off for having had the procedures performed'
References I. Bergman TF, Peterso n DII. Lawrence OJ. Chlropracric technique. New York: Churchill Livingstone, 1993. 2. Faye LJ. Wiles MR . Manual cxanunation of the spine. In: J laldcman S; cd. PrinCiples and practice of chIropractic. 2nd ed. San Matco, Gtlifornia: ApplclOl1 and Lange.
1992: .101-18. l. Gatterm.ln MI. Chiropractic management of spine relared disorders. Baltimore: Williams & Wilkins, 1990: 118-122, 142-146, 187- 197,222-229. 4. Plaugher G, Lopes MA , cds. Textbook of clinical chiropractic, Baltimore: Williams & Wilkins. 1993:
86-91.
10.
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5. Schiotz Ell, Cyriax J. Manipulation past and present.
London: Willi:tm Ilclnemann Medical Books, 1975: 6.
7. 8.
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.\-27. Anderson R. Spinal mampulation before chiropractic. In : IialdcI113n S, ed. Principles .md practice of chiropractic. 2nd cd. San Mateo. C... hfornia: AppiNon and Lange, 1992. Seal MC Perception through palpation. J Am Osteopath A"oc 1989; 89(10): 1334-1352. KeaungJ, Matyas TA, Bach TM . The effect of training on phYSical therapists' ablliry to appl), specified forces of pal · pallon. Ph ys Ther 1993: 73 ( I): 45-53. Magee OJ: Onhopedic physical assessmcni. Philadelphia:
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27. 28.
29.
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WBSaunders, 1987: 14-15,38-40,83-87,101-3, 131-7, 160-<>, 196, 197,231-7,256-9,30 1-7,343-52. Goble DO. Medical evaluation of the musculoskeletal sy~ (eln and common integument relevanr to purchase. Vct elln North Am Equme Pract 1992; 8(2): 285-302. Gregory AA. Spmal treatment science and technique. Oklahoma Cit): The Palmer-Gregor) Conege, 1912: 345-6. KeaungJC, Jacobs GO, Bergmann T~, et al.lnrerexamIller reliability of eight evaluative dimensions of lumbar ~egmental abnormality. J Mampulatlve Physiol Ther 1~90; 13:46.1 -70. Palmer DO. The science an and philosophy of chiroprac£Ie. Portland, Oregon: Portland Prmnng I-Iouse, 1910: 10. Palmer BJ. The Philosophy science and art of ncrve nacing. In: thc science o f chiropractic. Vol. 6. Davenport, Iowa: Palmer School of Chiropractic, 191 J: I 1-18. C),riax E. On the rechnique of nerve palpation by nerve "friction." Review of Neurology & PS)'chlatry (G B) 1914; 12:148-51. Gillet H. Vertebral fixations, an mtroducnon to movement palpation. Ann Swiss Chlro Assoc 1960; 1:30. Gillet H, Llckens M. A further study of spmal fixation s. Ann Swiss Chiro Assoc 1969; 4:41. Gillet H. Liekens M. Belgian chiropractic research note!>. HuntingtOn Beach, California: Motion Palpation Instilutc; 1981 . Faye LJ. Motion palpation of the spine. From MPI notes and review of literature. Huntington Beach, Caltforma: Motion Palpation Institute, 1981. Schafer RC, Faye LJ. Motion palpanon and chiropractic technique: prinCiples of dynamic chiropractic. Huntingwn Beach, Caltforma: Motton Palpation Insmute, 1989. ACA Council on Technique. Chiropractic terminology: A report. JAm Choro Assoc 1~88; 25110):46. Bryner P. A survey of indications: knee manipulation. ChiroTcch 1~89; 114): 140-145. Bryner P, Bruin J. Extremity jOint technique: Survey of the status of technique teaching in chiropracric colleges. Chito Tech 1991; 311 ):30-32. Breen A. The reliability of palpation and orher diagnostic methods. J Manipulative Physiol Thcr 1992; 15:.14-56 . Love RM, Brodeur RR. Inter- and mrra-examiner reliability of marion palparion for rhe thoracolumbar spme. J Manipulative Ph)'siol Ther 1987; 10: 1-4. Moorz RD, Keating JC, Kantz HP. Intra · and Inter-exa mmer reliability of passive morion palparlon of the lumbar spine. J Manipulative Physiol Ther 1989: 12:440-5. Panzer D. The reliability of lumbar motion palpation. J Manipulative Ph)'siol Ther 1992; 15:518-24. Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophyseal Joint pain syndromes. MedJ Aust 1988; 148:133-6. s.... rrko JJ, Carpenter Wf. On the methods and theory of reliability. J Nerv Ment DIS 1976: 163:307-1 7. t
66 30. Haas M. Sransrical methodology for reliability studies. J Manipulative Physiol Ther 1991; 14:119-32. 31. Kramer MS, Feinstein AR. Clinical biostaristics. L1V. The biostatistics of concordance. Clin Pharmacal Ther 1981 j 29,111-23. 32. Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilron, Ontario. How to read clmical journals. II. To learn about a diagnostic teSt. Can Med AssocJ 1981; 124,703-9. 33. Sackett DL, Haynes RB, GuyaH GH, Tugwell P. Clinical epidemiology: A basic science for clinical medicine. 2nd ed. Boston: Little Brown, 1991. 34. Feinstein AR, Ciccheni DV. High agreemem but low kappa. I. The problem of two paradoxes. J Clin Epidemiol 1990; 41 (6P43-49. 35. Haas M. The reliability of reliability. J Manipularive Physiol Ther 1991; 14,199-208. 36. Rosner S, Willen WC, Spiegelman D. Correlation of logistic regression relative risk estimates and confidence intervals for systematic within-person measuremem error. AMJ Ep,demiol1989; 8,1051-1069. 37. Fleiss JL. Estimating the accuracy of dichotomous judgments. Psychometrika 1965; 30(4):469-79. 38. Fleiss JL. Cohen J. The equivalence of weighted kappa and the intraclass correlation coefficient as measures of reliabihry. Ed Psychol Meas 1973; 33:613-19. 39. Fieiss JL. Statistical methods for rares and proportions. New York: John Wiley & Sons; 1981 :212-36. 40. Landis JR, Koch GG. The measurement of observer agreement for categorical data. Biometrics 1977; 33,159-74. 41. Rosner B. Fundamemals of biostaristlcs. 2nd ed. Boston: Duxbury Press, 1986. 42. Haas M. Interexaminer reliabiliry for multiple diagnostic test regimens. J Mampulative Physiol Ther 1991; 14,95-103. 43. Reference deleted. 44. Haas M, Peterson D, Hoyer D, Ross G. The reliability of muscle testing response to a pro\'oca tive venebral challenge. Chiro Tech 1993; 5(3),95-100. 45. Boline PO, KearingJC, Srist J, Denver G.lnterexaminer reliability of palpatory evaluation of the lumbar spine. Am J Choro Med 1988; U-II. 46. Carmichael JP. Inter- and intra-examiner reliability of palpation for sacroiliac joint dysfunction. J Manipulative PhYSlol Ther 1987; 10,164-171. 47. Mlor SA, King RS, McGregor M, Bernard M. Intra and interexaminer reliablhry of motion palpation in the cervical spine. J Can Chiro Assoc 1985; 29: 195-8. 48. Mior SA, McGregor M, SchUl AB. The role of experience m clinical accuracy. J Manipulative Physiol Ther 1990; 13,68-71. 49. Nansel 0, Peneff AL, Jansen RD, et al.: Interexaminer concordance in detecting joint-play asymmetries In the cen'lcaJ spmes of othenvise asymptomatic sublects.
J Manipulative Physiol Ther 1989; 12:428-433. 50. BollOe PD. Haas M, MeyersJJ. Kassak K, Nelson C, Keating J. Interexaminer reliability of a multi-dimensional index of lumbar segmental abnormality. Part II. J Manipulative Physiol Ther 1993; 16 (6) :363-74. 51. Wright JG, Feinstein AR. Improving the reliabilLty of orthopaedic measurements. J Bone JOint Surg 1992; 74S,287-91. 52. Departmenl of Clinical Epidemiology and Biostatistics, McMaster Unlversiry, Hamilton, Onrario. Clinical disagreement. 1. How often It occurs and why. Can Med Assoe J 1980; 123,499-504. 53. Departmenl of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario. Clinical dis· agreement. II. How to avoid it and how to learn from one's mistakes. Can Med AssocJ 1980; 123613-1 7. 54. Harvey 0, Byfield D. Preliminary studies with a mechanical model for the evaluation of spinal motion palpation. Clin S,omech 1991; 6(2P9-82. 55. Lee M, Moseley A, Refshauge K. Effect of feedback on learning a vertebral jOint mobilization skill. Phys Ther 1990; 70(2),97-104. 56. DeBoer KF, Harmon R, Tunle CD, Wallac~ H. Rehabillty study of detection of somatic dysfunctions m the cerVical spine.J Mampulatlve Physiol Ther 1985; 8:9-16. 57. Alley JR. The clinical value of motion palpation as a diagnostic tOol: a review. J Can Chiro Assoc 1983; 27,97-100. 58. Russell R. Diagnostic palpation of the spine: a review of procedures and assessment of their reliability. J Mampularive PhYSlol Thor 1983; 6,181-183. 59. Dishman RW: Static and dynamiC components of the chiropractic subluxalion complex: a literature review. J Mampulatlve Physiol Ther 1988; 11 :98-1 07. 60. Keatmg Jc. Interexaminer reliability of motion palpation of (he lumbar spine: a review of the chiropractic hterawre. AmJ Chiro Med 1989; 2,107-110. 61. Wiles MR. Reproducibility and II1terexaminer correlation of motion palpation findings of the sacroiliac Joints. J Can Chiro Assoc 1980; 24,59-69. 62. Bergstrom E, Courtis G. An inrer- and intra-examiner reliability study of motion palpation of the lumbar spine In lateral nexion in the seated position. Eur J Chiro 1986; 34,121-141. 63. Rhudy TR, Sandefur MR, Burk JM. Interexamlncr/ inrertechnlque reliability in spinal subluxation assessment: a multifactorial approach. Am J Chlro Med 1988; 1,111-14. 64. Nansel DO, Jansen RD. Concordance between gaivalllc skin response and spinal palpation findLngs In pain-free males. J Mampulative Physiol Ther 1988; 11:267-272. 65. Herzog W, Read LJ, Conway PJ, et al. Reliability of motion palpation to detect sacrOIliac loint fixations. J ManipulatIVe Physiol Ther 1989; 12:86-92. 66. Leboeuf C, Gardner V, Carter AL, Scott TA. Chiropractic
4 palpatory ___ 01 SUbluxlllon
67. 68.
69.
70.
exa minatio n procedures: :J. reliability a nd consistency srudy. J Au .. Chi ro Assoc 1989; 19, I 0 I- I 04. Owens E An objective measuremem of muscle tone. Chiro Res J 1988; \,34-42. Ja nsen RD, Nansel DO, Slosherg M. Normal parasp inal tissue com pliance: the reliabi liry of a new cl inical a nd experi menta l instrument. J Manipul ative Physiol Ther 1990; 13,243-246. Byfield D, Hu mphreys K. Inrer- and inter-examiner reliability of bony landmark identifica tion in the lumbar spi ne. Eur J Chiro 1992; 40:13-17. Byfield DC, Mathiasen J. Sangren C. The reliability of osseous la ndmark palpation in the lumbar spine and
67
pelvis. Eur J Chiro 1992; 40,83-88. 7 1. Feinstei n AR Scientific methodology in clin ica l medicine. IV. Acquisition of clinical da ta. Ann intern Med 1964; 6 1(61, 1 162-93. 72. Feinstein AR, Kramer MS Clinica l biostatistics. L1L1. The architectu re of o bserver/method va ria bility and other types of process resea rch . Clin Pharmacol Ther 1980; 28(41,551"';;3 . 73. Feinsten AR Clinimetrics. New H aven, Connecticut: Yale University Press, 1987. 74. Jansen RD, Nansel DO. Diagnostic illusions: the reliabi liry of rando m chance. J Manipulative Physio \ Ther 1988; 1\,355"';;5.
The Role 01 Radiography in Evaluating Subluxation John A. M. Taylor
KeyWords
Static radiography, spinographic analysis, functional radiographs
After reading this chapter you should be able to answer the following questions:
Question #1
What are the common clinical reasons for taking radiographs?
Question #2
What are the clinical findings that indicate functional radiography may be useful?
Question #3
What is the procedure for identifying cervical flexion-extension motion abnormalities?
5 The Role 01 Radography In Evaluating Subluxatloo
>
T
he role of radiography in the evaluation of the chiropractic spinal vertebral subluxation has evolved considerably over the years (1,2). Both static and functional radiographs are used in chiropractic to eva luate posture and biomechanics. In clinical practice, emphasis on one
method or the other appears to depend largely on the individual practitioner's concept of a subluxation. Although some chi ropractors view subluxation as a purely static phenomenon of vertebral misalignment, more recently an increasing num-
ber of chiropractors have begun to view the subluxation as a more dynamic, functiona l concept encompassing abnormalities of articu lar motion (3-5) .
Today, chiropractors use radiography for several reasons. Shennan (6) identifies the following clinical reasons for taking radiographs: 1. 2. 3. 4.
To establish a clinical (pathologic) diagnosis To evaluate biomechanics and posture To identify anomalies To screen for conrraindications
5. To monitor degenerative processes Nonclinica l reasons for taking radiographs are inappropriate and include (6,7) : 1. Financial ga in for the practitioner
2. Force of habit 3. Medicolega l advantage 4. Patient education Current epidemiologic studies examining the role of lumbar spine radiography question the value of taking radiographs for many clinical situations. Howard and Rowe (8) and Deyo and Diehl (9) recommend severa l criteria for selecting low-back pain patients for radiography (see box above). Some chiropracrors argue that chese recommendations ignore factors unique to the ch iro-
practic approach to stead Clinic Staff. spme radiography. 1-8). For instance,
69
patient care (6,10, and GonGonstead concepts on fu ll Unpublished position paper, Gatterman (11) identifies 31
Spine Radiography: C linical Indications for Patient Selection
• • • • • • • • • • •
Patients older than 50 years Significant trauma Neuromotor deficits Unexplained weight loss Suspicion of ankylosing spondylitis Drug or alcohol abuse History of cancer Corticosteroid use Increased temperarure, above 100°F Diabetes or hypenension Recent visit for same problem and not improved • Patients seeking compensation for back pain Pllyllcal FItIdIIp
• • • • • • • • • • • •
Dermopathy (psoriasis, melanoma) Cachexia Deformiry and immobiliry Scars (surgical, accidental) Lymphadenopathy Localized pain, tenderness, spasm Motor or sensory deficit Elevated erythrocyte sedimentation rate Elevated acid or alkaline phosphatase Positive rheumatoid faeror Positive HLA 827 Serum gammopathy
Adapted from Dcyo and Diehl 1986 (9) and Howatd and Rowe 1992 (8).
conditions that contraindicate or require modifi-
cation of spina l manipulation and suggests that, in at leaSt 20 of those conditions, radiographic examjnarion is pan of the standard of practice for establishing the diagnosis. The fact remains that radiography should never be used as a general screening procedure without specific clinical indication (9,12) . Howe (13) stresses that routine o r stereoryped methods of radiographic examination do not serve the best interests of the patient.
70 The following discussion focuses on rhe indications and limitations of some of the more com-
monly employed sraric and funcrional radiographic procedures employed in rhe evaluarion of posture, biomechanics, and misalignment.
Static Radiography and Spinographic Analysis Spinography, the procedure of analyzing spine radiographs for postural and structural abnorma lities, dares from 1910, when ir was firsr introduced ar Palmer School of Chiropracric by Dr. B. J. Palmer (1). Marking radiographs ro identify misalignments was a natural extension of the
popular sraric concepr of subluxarion in rhe early 1900s. From 1918 until 1936, full-spine radiographic techniques were developed (1,2,14) . Texts on chiropracric spinography have been published by Thompson (15), Hildebrandr (16), and Winterstein (17). [n addition, technique systems using spinographic analysis have been developed by several chiropractors, including Clarence C. Gonstead (10,18) and Hugh B. Logan (14,19). The validity, reliabiliry, and clinical relevance of many spinographic methods have been srudied . The fundamental criticism of measuring misalignments on radiographs is rhe ptoblem of anatomic asymmetry. Asymmetric developmental anomalies are common and can simulate [rue misalignments
(20) . The role of full-spine radiographs in chiropracric analysis remains conrroversial (2). Opinions held by chiropractors vary widely and include those who consider full-spine radiography a routine procedure to those who consider it an overused procedure that never should be used. The lirerarure suggesrs, however, rhar wirh proper patient selection, careful attention to technical derail, and use of several rechnologic advancements, full-spine radiography is a diagnosric and analytic procedure wirh an acceptable risk/benefit ratio (2) . The circumstances in which full-spine radiographs might be preferred over sectional radiographs are as follows: (1) cases in which
clinical examination discloses the need for radiography of several spinal secrions; (2) cases in which severe postural distortion is evident; (3) for scoliosis evaluation after clinical assessment; (4) cases in which a mechanical problem in one spinal area adversely affects other spinal regions; (5) to specifically evaluare complex biomechanicalor postural disorders of the spine and pelvis under weight-bearing conditions (2,16,21,22). Many chiropracrors agree that full-spine radiography should be reserved for evaluating scoliosis after a thorough clinical evaluation . Scoliosis measurement using the Cobb merhod is well established (Figure 5-1) . This measurement is reported to be accurate to within 2.8 0 to 11 0 (2325). Mehta concluded thar rotation of up to IS' is necessary for clearcut identification of vertebral rotation on scoliosis radiographs (26). This observation calls into question many of rhe methods used to measure millimetric changes in vercebral rotation. A high correlation has been demonstrated between Cobb angles measured on posteroanterior (PA) and anteroposterior (AP) radiographs (27) . Conflicting evidence regarding the reliability of pelvic spinographic analysis has been reported. Plaugher and Hendricks (28) found excellent interobserver and inrraobserver reliability, and Phillips (29) found very little consistency berween the various methods used. Many errors arise from faulty patient positioning (30). Leg-length inequality (LLl) can be measured reliably from spine radiographs (31), but most authors agree that specialized orthoradiography or clinical examination is morc accurate in the
assessment of LLl (Figure 5-2) (31-34). Some chiropracric analytical procedures are based on the premise that static misalignments can be confirmed by radiography and rhat these misalignments can be corrected by chiropractic adjusrments. In one large study (35), rhe only demonstrable postmanipulation change was a 340/0 reduction in retrolisthesis. No posttreatment change was observed in cervical lordosis, sacral
base angle, lumbar lordosis, scapular angle, or Cobb's angle.
Ii 1118 Role 01 Radiography In Evaluating SUbluXation
~
5-1 Scoliosis Measurement: Cobb's Angle. Cobb's angle is obtained from frontal (AP or PAl spine radiographs by constructing lines along the end plates of the end vercebra located at the superior and inferior
extremes of the scoliosis. Perpendicular lines are then
constructed and the intersecting angle is then measured. This angle is used ro assist in managemenr
71
~ 5-2 Scoliosis Secondary ro Leg Length Inequality. This 35-year-old woman sustained a severe femur fracture when she was 12 years old, resulting in significanc growth retardation of one lower extremiry. This has resulted in obvious disparity in [he heights of the femoral heads and iliac crests as well as scoli osis.
decisions and as a comparison to previous and future
studies to monitOr scoliosis progress. This measurement is accurate to within 2.80 to 11 °.
This study (35) raises the question of the clinical validity of spinographic ana lys is. Phillips et a l. (36) concluded that spine radiographs, analyzed
by measurements, have minimal value in predicting the presence or absence of low-back pain compla ints. Mootz and Meeker (37) and Phillips agree that the use of rad iography for biomechanica l (postural) eva luation req uires further c1arifica-
tion and research. Evidence is lacking that these parameters demonstrate any clinical significance. Owens' review of the literature and summary of the role of line drawing ana lyses of static cervical radiographs used in chiropractic (38) is consistent with those of Phillips et al. (36) and Mootz a nd Meeker (37). Owens concludes that, although some studies demonstrate reliabi lity of some of these procedures, the accuracy and clin ic significance remain in question. "The major questi o n should no longer be if x- ra y ana lysis can be
Subluxation
72
The
Artl~
lesion
>
Commonly Used Radiographic Lines, Angles, and Measurements
line, Angle , Measurement
Figure
Proposed Clinical Significance
Lumbar gravitational line Lumbar lordosis angle
5
Anrerior or posterior weight-bearing on lumbosacral disc
Lumbosacral base angle
7
Determines shearing or compressive forces on discs and facets Can be increased in facet syndrome
7
Can be increased in hyperlordosis
Lumbar Spine
Hyperlordosis or hypo lordosis determines stress on discs or facets
Lumbosacral disc angle Lumbar intervertebral disc angles
McNab's line Flexion-extension analysis Hadley's US" curve
Ullman's line Meyerding's grading Eisenstein's method Interpediculate distance Canal/body ratio
George's line
12
4
6
Unreliable method of assessing facet impingement or imbrication Measure of instability on lumbar flexion--extension views Method of assessing facet impingement or imbrication For assessing presence of LS-Sl anterolisthesis Method of grading spondylolisthesis (Grades 1-5) Lumbar sagittal canal diameter: stenosis or widening Lumbar co ronal canal diameter: stenosis or widening Combined sagittal and coronal canal diameter Disrupted in anterolisthesis or retrolisthesis
Cervical Spine and Skull Base
Chamberlain's line McGregor's line George's line Posterior cervical line
jackson's lines Angle of cervical lordosis Cervical gravity line
11 10
Cervical range of modon
Atlantodental imerval (ADI)
Basilar invagination, cranial settling, basilar impression Basilar invagination, cranial settling, basilar impression Cervical or lumbar, anterolisthesis or retrolisthesis Anterolisthesis or retrolisthesis or neural arch fracture Alterations in physiologic stress lines on flexion-extension views Hypolordosis or hyperlordosis measurement Anrerior or posterior weight-bearing Measurement performed on flexion-extension views Indicates atlantoaxial instability from transverse ligament
damage Sagittal canal diameter Pre vertebral soft tissue spaces
8 9
Stenosis or widening from intraspinal mass Inflammation, hemorrhage, or mass in soft tissues
used as a too l in th e sc ie nt ific in vest iga ti on o f c hi-
occ iput can be a ca usa tive facto r in the c hi roprac-
rop racti c subluxa ti o n. Ra ther, studies sho uld be designed, using x- ray a na lys is, to test rhe fund amenta l hypothesis of rhe ana lys is techniq ues, tha t
ric subluxa ti o n " (38) .
static stru ctu ra l [m is Jal ig nmenr in th e nec k an d
"systems" ta ug ht primaril y th ro ug h entrepreneur-
In his rev iew, Owens lists 15 named chiro-
practic rad iograph ic analys is tec hniques that a re
73
5 The Role of Radloraphy In Evalll8tmg SUbluxation ial postgraduate weekend seminars. Of the 15 techniq ues, onl y twO (Go nstead a nd upper cervica l specific-hole in one [HIO] ), are taught as parr of the curriculum at more than one accred-
ited chi ropractic college (38). Lo add ition to the many "systems approaches" to marking radiographs, severa l lines and angles of measurement have been developed in the fields of radiology and ch iropractic for assessing staric and functional radiographs (39,40). Table 5-1 ou tl ines some of the more common proce-
du res and rheir clinical significa nce, and rhe box below lists the classification fo r intersegmental subluxations that sometimes can be seen on static
>
Radiographic C lassification of Subluxation
SIIU.I.............I MIuIII.mI'"
• • • • • • • • •
Flexion malposition Extension malposition Lateral flexion malposition Rotational malposition Anterolisthesis Spondylolisthesis Retrolisthesis Lareralisrhesis Decreased interosseous spacing
• Foraminal encroachments
KlneU. InII....m.nIIlllylfuncll...
• Hypomobility • Hypermobility
and functional radiographs (Figure 5-3) (41 ). Figures 5-4 to 5-10 illustrate some of the more commonly used lines, angles, and measurements. It shou ld be emphasized, however, that the clinical significance of static misalignment subl uxations has never been clearly established. Many of the patterns listed in the box on this page actuall y only occur as a result of articu lar derangements
such as severe inflammatory or degenerative disc a nd apophysea l joint disease, o r long-stand ing developmental articu lar changes. One area of radiographic ana lysis rhar has received conside rable anemian is the cervical curve and its degree of lordotic configuration (Figure 5- l1 ). Over rhe years, chiropractors have attributed various degrees of sign ifica nce to the presence of hype rlo rdosis, hypolordosis, fl attened lordosis, and kyphosis . After his review of the literature on the curve of the cervical spine, Gay (43) conclu ded that there is a wide ra nge of normal, th at many traumatic and nonrraumaric fac-
tors influence the curve, and that there is little evidence-based support of the contention that altered cervical curva ture has any prognostic sig-
nificance (42). He fou nd, based on the literature, thar lo rdotic straighte ning or reversal could result from muscle spasm, but that more specific interprerarion is speculative. He emphasized that, altho ugh acute angu lar kyp hosis cou ld represent an unstable ligamentous injury sllch as is seen in hyperflexion sprains, it could represent a norma l variant in the absence of clinica l a nd further radio ographic corroboration (42).
• Aberrant motion
Secllo.. 1Sebluull...
• • • •
Scoliosis secondary ro muscle imbalance Scoliosis secondary to structural asymmetry Decompensation of adaptational curvatures Abnormalities of global motion
Pa....rt.bral S. bluull...
• Costovertebral • Costotransverse • Sacroiliac
Functional Radiography and Spinal Dysfunction Gi llet and Leikens (4) and Schafer and Faye (5) are responsible for raising chiropractic awareness of the importance of spine function and placing more emphasis on dynamic concepts such as fixa tion ana lysis and movement palpation. This paradigm sh ift, from a static ro a dynamic approach to spine analysis, initiated an increase in the lise Tex( cominued on p. 78
74
Rgare ~8 Static Intersegmental Misalignments. Top, Lateral flexion malposition. Bonam, Larerallisthesis. Although an extensive classification of static intersegmental misalignments exists (Table 5-3), it is unusual ro observe genuine malpositions on radiographs in the absence of seve re degene rative or inflammatory joint changes. Note in both Top and Bottom the advanced discovertebral and apophysea l degenerative changes a ll owing rhese non physiologic mal positions to occur. Most nondegenerarive or noninflammatory misalignments seen on radiographs actually represent asymmetry of vertebral structures.
flIIre 6-4
Lumbosacral Spondylolisrhesis. Myerding's method of measuring slippage in spondylolisthesis involves dividing the sacrum inro four equal quadrants on the lateral lumbosacral radiograph. The degree of slippage is graded based on the alignmenr of the posterior aspect of the L5 vertebral body with one of the quadranrs. The illustration above demonstrates a grade 2 spondy lolisthesis.
5 Tbe Hole 01 HMilography In Evaluating SUbUXallon
..... 5-5 Lumbar Gravitational Line. This line is constructed by identifying the central portion of the L3 vertebral body on a weight-bearing larerallumbar
radiograph. A vertical line is constructed inferiorly from this center paine. In the "ideal" weight-bearing pOSTure, this line should intersect the anterior portion of the sacrum. In anterior weight bea ring, the line falls anterior to the sacrum; in posterior weight bearing, frequendy associated with hypcrlordosis, the line falls posterior to the anterior portion of the sacrum.
75
Rgare H George's Line. George's line is drawn to detect evidence of anrerolisrhesis or retro lisrhesis. On a lateral rad iograph of either the lumbar o r cervica l spine, a conrinuous verrica ll ine is drawn along rhe posre rior margins of rhe verreb ra l bodies. In the norma l situation, this li ne shou ld be smooth, curvi linear, and uninterrupred.
FlgLre6-7 Lumbosacral base angle a nd lumbar interverteb ra l disc a ngles. Ferguson's angle or the lumbosacral base angle is obtai ned on the late ral lumba r radiograph by constructing a line along the
superior aspect of the sac ral base. The angle formed between th is line and an intersecting horizontal line is then measured (curved arrows). On upright radiographs, this measurement ranges from 26° (0 57°, An increase in this angle has been associated with an inc reased incidence of spondylo lytic spondylo li sthesis. In measuring the lumba r imerverrebral disc angles,
lines are constructed along the vertebra l end plates of the lumba r vertebrae. The intersecring angles indicate the configuration of the inrerve rreb ral disc (open arrows). The norma l range is 10° ro 15°. Excessive angulation is seen in hyperextension or hyperlordosis, and diminished angulation is seen in patients with hypolordosis or acu te flexion anta lgia.
FIIIn 6-8 Sagirral ca nal diameter: cervical spine. The sagitta l cana l di a meter is measured on a neutra l latera l cervical radiograph taken at 72-inch target-film distance. Measurements less than 12 mm suggest canal stenosis, and excessive measurementS (more than 22 to 3 1 mm ) suggest a space-occupying lesion expanding the sp ina l ca na l.
5 11HI Role 01 RadIography In Evaluating 8u1*1xallon
77
~
D
6
c::' c;:'J
~I
C'-
c:: Ag&re 5-9
a
/
Preverteb ra l soft tissue meas urements. The prevertebral soft tissues can be meas ured on a neutral lateral cervica l radiograph taken at 72-inch target- fi lm distance. The measurement at C2 sho uld not exceed 5 ro 6 mm and at C6 sho uld not exceed 20 mm. These measurements are wider in cases of rerrorrachea l, rerropharyngeal, o r rerrolaryngea l abscess, neoplasm, or posttraumatic hemaroma.
f9n 5-10
Ce rvica l sp ine ce nter of gravity. The cervica l gravity lin e is measured by constructing a vertica l line from the superio r tip of the odonto id process. Th is line sho uld intersect th e C7 vertebra l body. When the line passes anterior to the C7 body such as in the schematic diagram a bove, the patient is said to have anterior head ca rriage or anterior weight bearing.
78 Functional radiography typically is used to esta blish the presence of: 1. 2. 3. 4. 5. 6.
Segmental or global hypomobility or fixation Segmental or global hypermobility Segmental instability Aberrant segmental or global motion Paradoxical motion Postsurgical arthrodesis evaluation
Considerable disagreement persists regarding the indication for functional radiography. The chief concern revolves around the issue of radiation exposure (64-68). In all cases, the anticipated benefit of the study must outweigh the potential risk of ionizing radiation. Although some practitioners use functional radiography routinely, most aut horities agree that it should be reserved as a supplementary procedure. The following guidelines are suggested for the use of functional radiography based on clinical findings :
1. Persistent signs and sympcoms or unsatisfac-
A111'15-11 Cervical lordosis measurement. The cervical lordosis is measured by constructing lines along the atlas plane line and the inferior end plate of C7 on a neurcallateral radiograph. Perpendicular lines then are constructed and the intersecting angle is
measured. Although 30° ro 45° is generally considered "normal," a wider range of normal exists. Several factors, including muscle spasm, influence the degree of curve, but there appea rs to be no prognostic
significance of altered curvature.
of functional radiography in chiropractic. Many authors, both ch iropractic and nonchiropracric, have addressed the issue of functional radiography of the lumbar (43-5 1) and cervical (52-63) spine.
tory response to a conservative trial of chiropractic care 2. Suggested persistent segmental dysfunction 3. Suggested segmenta l instability 4. When other approp riate imaging studies are inconclusive in establishing joint dysfunction Meticulous attention to patient positioning is essential in functional radiography. Because of the difficu lty of precise, standardized positioning in each patient, quantitative measurements derived from these films are subject to inaccuracies (55). Therefore, functional radiographs should be used more as qualitative indicators of spine motion rather than as a precise quantitative assessment. Another significant limitation of functional radiography is that the range of "norma l" segmental motion in the genera l population has never been established. Wide variations of spina l motion exist in the normal population, and there is no evidence to confirm that too much or too little motion correlates with pain or disability, except in some cases of obvious instability (59) .
5 Tbe Role of RMilography iI Evaluatilg SUl*ixalloo
Lumbar Spine Functional radiographs of the lumbar spine include flexion-extension and latera l bending studies. Flexion-extension radiogra phs are used mOSt often to evaluate translational movements between segments. Excessive translational move-
ments indicate the possibility of instability and must be correlated with the clinical examination. Most authors agree that more than 3 to 5 mm translation from flexion to extension must raise
79
the possibility of ligamentous instability (Fig ure 5-12) (47,50) . Tanz (49) has identified the ave rage ranges of segmental lumbar flexion at various ages as indi-
cated in Table 5-2 . Tanz's study showed that segmental flexion increases at each successive level descending from L2-L3 through L5-S1 in the young healthy spine. With increasing age, motion decreases throughout the spine. With increasing age, motion decreases throughout the spine such that only minima l differences in segmental morio'n are observed at successive leve ls.
Flexion
Extension
Hgare 5-12 Flexion-extension analysis of the lum bar spine. Several methods have been developed to analyze functional radiographs of the lumbar spine for evidence of insrabilir)'. The schematic diagrams above illustrate tracings of the L4-S and LS-S I levels from flexion (A) and extension (BJ radiographs. Many aurhors comend that excessive translational movemems measuring above 3 (Q 5 mOl suggests ligamemous in scabi li r)',
80 Range of Lumbar Flexion at Various Ages' Age (ye ... ) 511-64
2- 13
35-49
10° 13° 17° 24°
5° 8° 9° 12° 8°
65-77
level
Ll-L2 L2-L3 L3-L4 L4-LS LS-SI
4° 5° 8° 8° 8°
2° 5° 3° 7° 7°
.. Adapted from Tanz 55. Motion of the lumbar spme. AJR 1953; 69,399.
Latera) bending radiographs have attracted significant interest within the chiropractic profes-
sion since the articles by Cassidy (43) and Grice (44) appeared in the 1970s. They recommended using lateral bending radiographs for several assessments, including:
l. 2. 3. 4.
Global range of motion Segmental body rotation Segmental disc wedging Aberrant lateral flexion analysis
They developed a method for studying lateral bending radiographs to evaluate the coupled lumbar motions of rotation and lateral flexion. They identified four types of segmental coupling motions and have attempted to correlate these aberrant patterns to various muscular imbalances
and joint dysfunctions (43,44). A more recent study by Hass and Cassidy and others questions the use of lateral bending radiographs for categorization of the lumbar spine in clinical practice (69) . It shou ld be emphasized that all radiographic findings must be correlated with clinical findings to be considered significant (Figure 5-13) . Table 5-3 lists the average ranges of segmental lumbar lateral flexion at various ages (49). The values indicate maximum lateral flexion occurring at the L3-L4 and L4-L5 levels with very min imal motion occurring at LS-Sl. Significant
reduction in lateral flexion occurs at all levels with increasing age.
Figll'85-13 Lateral Aexion analysis of the lumbar spine. Left lateral Aexion (A), Neutral AP (8), and right lateral nexion (C) radiographs of the lumbar spine in a 30-year-old man with acure low-back pain. The ana lysis of coup led Illotion on lateral flexion radiographs was advocated in the 1970s and 19805. Recent studies, however, suggest that these analyses are of little value in categorization of the lumbar spine in clinica l practice. Information from all radiographs must be correlated with clinical findings .
Cervical Spine Flexion and extenSion views of the cervical spine form an integral part of the cervical Davis
series. Coupled with routine views of the cervical spine, flexion-extension views can provide important information about the osseous and soft tis-
sues of the cervical spine (52,53,58). Coupled
81
5 TIle Role O'RadIography In Evaluating SUbluxation
"-" 5-13 continued
~
5-13 continued
motions of rotation and lateral flexion are difficult ro analyze in the lower cervical spine because
of the complexity of motions involved, and radiographic evaluation in these planes is nor recom -
mended.
)
Range of Lumbar Lateral Flexion at Various Ages
The flexion-extension examination is used
extensively in assessing the effects of trauma on the cervical spine (Figure 5-14, A-C). Excessive (mo re than 3 mm) translational segmental movements can signify instability. Atlantoaxial instability is recognized radiographically as an increase in the atlantodenta l interval measuring
more than 3 mOl in adults and 5 mm in children on the neutral lateral or flexion views (39) . Similarly, hypermobility, hypomobility, and aberra nt and paradoxical motion can be identified, according to some authors (52-54 ).
Ap. (y •• rs) 2-13
35-49
50-&4
65-77
12° 12° 16° 15° 7°
5°
5° 7°
4° 7° 6° 5° 0°
level
Ll-L2 L2-L3 L3- L4 L4-LS L5-S1
go go go
2°
go
7° 1°
Adapred from Tanz 55. Motion of the lumbar spine. AJR 1953; 69,399.
82
SUbluXation
The ArtIcular lesion
Agars 5-14 Cervical flexio n-extension o verl ay stud y. Extens ion (A), neu tral (8 ), and flex ion (e ) radiographs ca n be analyzed for inrersegmenral morion
by trac ing
the anato mi c ourl ines from the neutral radi ograph
(soUd line in D and E) and compa ring these with the extension (D ) and fl ex ion (E) trac in gs (do tted a"e in D and E), whic h are su perimposed on the neutral trac ings. This procedure is performed most frequently in patients after sp ine trauma and is used to detect excessive or abnorma l moti on.
Cervica l overlay studies are useful in idenrifying fl ex ion-extension moti on abnorm alities (5 1-
53). In this proced ure, o utlines of rhe ve rtebral bodies from the radiogra phs a re traced on acetate tra nspa rencies with colo red fi ne-tip pens. [n this way, a depic tio n of segmemal mo tio n can be com pared berween flexion, neutral, and extensio n positions (Figure 5- 14, D-E) .
83
•
/'
. .. •
c;::.
.. D .. ••
•• '
.........,.......
~
'
----D
E
Exte . N;~:~
fIIin fH40
........ ....
For legend see o pposite page.
J
Flexion ...................... . Neulrol - --
RIIN fi.14f For lege nd see OpposIte . page.
84 Another method of evaluating motion on cervical flexion-extension radiographs is to identify the instantaneous axis of rotation (lAR) at each vertebra l level. The LARs are then compared with well-established normal values (55-57). Although this method appears reliable and va lid, it has yet to gain widespread clinical use. Open-mouth views taken in lateral flexion can demonstrate excessive lateral translation of the arias lateral masses In relation to axis 10 atlantoaxial instability and abnormal motion in rotary atlantoaxial subluxation (61) .
ConclUSion The role of radiography in chiropractic is well established. Several clinical indications for radiography, based on patient history and physical finding;, have been identified. In addition to using radiographs for identifying pathologic processes, chiropractors often use both static and ,'ynamic radiographs to derive postural and biomechanical information. Many radiographic lines, angles, and measurements have been demonstrated to be reliable indicators of postural and biomechanical abnormalities. These indicators help identify static a nd dynamic subluxation , dysfunction, and abnormal or excessive motion. Further research is necessary, however, to determine the precise clinical significance of many of these procedures.
Acknowledgments Special thanks to Drs. R. Sherman and T. Bergmann for reviewing the manuscript for this chapter and offering many helpful suggestions.
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Med 1989; 4, 17-21. 59. lmd B, Slhlbom H, Nodwall A, Malchau H. Normal range of motion of the cervical spme. Arch Phys Med
Rehabol 1989; 70,692-5. 60. Monu J, Bohrer SP, Howard G. Some upper cervical spine norms. Spine 1987; 12:515-19. 61. Reich C, Dvorak J. The functional evaluation of craOlocervical ligaments m sidebending using x-rays. Manual
Med 1986; 2,108-13. 62. Sigler DC, Howe JW. Inter- and mtraexaminer reliability of the upper cervical x-ray marking system. J Manipulative Physiol Ther 1985; 8:75-80.
86 63, Vorra J. Johnston WL. Hubbard RP. Clinical biomechanic correlates for cervical function. Ullnrermittent secondary movemems. JAOA 1991; 2:145-55. 64. Sherman R. Optimal kilovolrage technique for spinogra-
phy. ACAJ Chit 1990; (Oec),41-4. 65. Andersen PE, Andersen Poule E, Van dec Kooy P. Dose reduction in radiography of the spine in scoliosis. Acta
Radiol Oiag 1982; 2],251-3. 66, Hardman LA, Henderson OJ. Comparative dosimetric evaluation of current techniques in chiropractic full-spine and sectional radiography, J Can Chico Assoc 1981;
25,141-5.
67. Field TJ. Buehler MT. improvements in chiropractic full spine radiography. J Manipulative Physiol Ther 1981;
4,21-5. 68. Buehler MT, Hrejsa AF. Application of lead-acrylic compensating filters in chiropractic fuJI spine radiography: a technical report. J Manipulative Physiol Ther 1985;
8,175-80. 69. Hass M, Nyiendo J, Peterson C, et al. lnterrater reliabiliry of roentgenological eva luation of the lumbar spine in lateral bending. J Manipulative Physiol Ther 1990;
U,179-89.
Osseous Manual Thrust Techniques Kevin M. Bartol
Kay WOI'da
Subluxation, mobilization, manipulation, adjustment, long lever arm, short lever arm, force, thrust
After reading Ihis chapter you should be able to answer Ihe fo llowing questions:
QuaatIOn #1
What has led to the multiplicity of chiropractic techniques?
QuestIon #2
What causes cavitation? Is it a necessary outcome of manipulation?
Quullon #3
What distinguishes manipulation from mobilization?
QIl8lIIon #4
How can the amount of force be minimized in manipulative procedures?
88
Subluxation
The ArtIcuI.. I.8aIon
Historical Perspective Osseous manual thrust techniques have been used to trear various conditions since early recorded
hismry. Records of 4000-year-old artwork from Thailand depict the use of manual therapy, as do artifacts from early Egyptian, Polynesian, Japanesc, C hinese, and Native American cultures. It
appears that many ancient civilizations developed various forms of manipulation for the treatment
Ot even place a foot over the hump. If even more force was indica red, a board was used. Wirh one end anchored m rhe wall and rhe middle of rhe board resring over rhe hump, rhe physician cou ld push down on rhe free end of rhe board, using rhe board as a lever to induce a posterior to anterior
force onm rhe hump (3). Ga len, Celisies, and Orbsius a ll used spinal manipularion techniques for various spinal deformities, neurologic defi-
of various disease processes ( 1,2). In the Corpus Hippocratum, Hippocrates (The Father of Medicine, 460-370 B.C.) described a form of spina l manipulation assisted by long
ciencies, and disease processes.
axis distraction . The patient was lying prone and
therapy was seen. In the early 1800s Docmr Edward Harrison was renowned in London for his expertise in manual procedures. Like many
stretched by applying long axis distracrion. When sufficient long axis distracrion was app lied, the physician would make a palmar contacr over the "h ump, " reinforced by his or her other hand. In rhis manner the docmr could deliver a straight thrust in a posterior to anterior direction, or if indicared, change rhe line of correcrion superiorly or inferiorly (Figure 6-1) . Hippocrares a lso described variations of this manipularive rechnique: instead of contacting rhe hump wirh a palmar contact, the physician cou ld sit on the hump
Rgan 8~1
During the Middle Ages there exists a void in writings describing manual procedures. By the nineteenth century, a renewed interest in manual
others in the nineteenth ce ntury, he was sh unned
by his colleagues, who were more interested in practicing pharmacology and surgery. "Bonesetrers" became popular in borh Europe and rhe Unired Srares in rhe ninereenth century. English boneserrers, including Hurron, Pager, Hood, Sweet, Mapp, and Barker, became famous . Herbert Barker developed sllch eminence as a boneserrer rhar in 1922 he was knlghred by rhe crown.
Spinal manipularion as described by Hippocrates. (From f.H Scholtz. Mompulalioll treatment of the sputal column from the medical-historical standpomt. Pari I. Journal of the Norwegian Medical AssociatIon 1958; 78,)59-372. Norske Laegeforelllug.)
89 The nineteenth century was a time of turmoil and controversy in the hea lth care world. It was this dissatisfaction with current medical practice that produced Daniel David Palmer and Andrew Taylor Still, the founders of chiropractic and osteopathy. Palmer and Still organized the knowledge of the bonesetter and manual medicine into health care systems. Palmer believed in the "innate intelligence" of the brain and the central nervous system and thought that alterations in the spinal column (subluxations) altered neural function, causing disease. Removal of the subluxation by a chiropractic adjustment was viewed to be the treatment of choice. Still endorsed the osteopathic lesion, emphasizing hypomobility of the motion segment and its effect on the vascular and lymphatic systems. Unlike Palmer's model, Still's model was more inclusive, taking into consideration the soft tissues as well as the primary role of the circulatory system . Still's model is similar to the "vertebral subluxation complex" subscribed to by many chiropractors today. Another major difference between Still's early osteopathy and Palmer's early chiropractic is that Still employed long lever arm techniques with nonspecific contacts; Palmer's system of chiropractic consisted of short lever arm adjustments to verrebrae using specific contacts on spinous and transverse processes. Many historians believe that Palmer organized his chiropractic theory after studying and modifying Still's techniques. Palmer emphatically denies borrowing any concepts from Still, stating that he learned the basis of chiropractic from Jim Atkinson (I). In the days of the bonesetters, knowledge and techniques were passed down from generation to generation without formal training. After Palmer organized chiropractic into a system, he opened the first chiropractic college in J 896 (4). Many of his early students went on to establish schools of chiropractic that in turn produced students who opened other schools. Carver, who graduated from a school opened by Parker, an early student of Palmer's, expanded Palmer's idea of nerve pressure as the cause of disease. Believing that,
instead of removing nerve pressure, the adjustment relieved "interference with nerve conduction," Carver opened a school of his own in Oklahoma City. Among the many differences between Carver and Palmer was the relative efficacy of "tratco thrusts" and "recoil thrusts" (1). Among the many who differed with the Palmers was John Howard, who opened a college in Chicago (the National College of Chiropractic). B. J. Palmer had his differences with his father, Daniel David Pa lmer, and in 1906 took over his father's college. B. J. Palmer examined the scientific literature, using that which supported his beliefs and discarding that which did not fit his needs or contradicted his beliefs. From these early differences stem a lack of communication or intra professional cooperation and an attitude of "Mine is the only way to do it." In the next century, more than 1 00 "named techniques" were developed, many professing to be "the best," "the most scientific," or "the only system necessary." Most of these "named techniques" had their origins in devoted and inquir· ing practitioners. These practitioners may have modified a particular technique to fit their own physical needs or to fit the needs of their subluxation conceptual model. Some observed a phenomenon of patients' improving, and developed a technique around this phenomenon. Regardless, many of the named techniques were developed out of the desire to improve the practitioners' abi lity to deliver health care. Innovative concepts have evolved in chiropractic over the past 100 years. B. J. Palmer began as a "diversified" practitioner, evolved into a "meric" practitioner, and eventually became an upper cervical or hole in one (HlO) practitioner (5). As Palmer's practice evolved, he left in his wake practitioners that continued to follow and bui ld on his teachings. From Pa lmer's H IO technique sprang other upper cervical techniques. Wernsung, Grostic, and Gregory believed that Palmer's atlas toggle technique was toO forceful and attempted to develop a corrective adjustment with a more gentle thrust. The effort of these three doctors led to
90 the formation of the National Upper Cervica l Chiropractors' Association (NUCCA). Petti bon adopted the upper cervical technique from NUCCA and added it to his method for full spine adjusting. Harrison expanded on the Petti bon model and developed ch iropractic biophysics. The G rostic technique, Pierce technique, Kale
ital technique, and network. Major Dejarnette expanded on Logan's model of the spine as an organ and developed the sacro-occipital technique (SOT) . Dejarnette, expanding on osteopathic reflex technique, developed CMRT, the
technique, Blair technique, and many others were
chiropractic manipulation reflex technique. From
extrapolations, mod ifications, or just simply evo-
SOT came othet reflex techniques, including applied kinesiology and neurovascular dynamics. The history of osseous manual thrust procedures is more than 4000 years o ld. After Still and
lutionary phenomenons of Palmer's HIO. Clarence Gonstead and Hugh Logan were philosophically simi lar, Gonstead preferring a more dynamic osseous adjustment than Logan's soft contact. Gonstead was basically a diversified adjuster, whose theories centered on disc invo lvement. He modified early techniques utilizing an engi neering background. He also built on Logan's philosophy of the sacrum being the centrum of the body and proposed a "level base" phi losophy. Thompson end point terminal adjusting also employs diversified techniques with the use of a d rop piece table ro augme nt the thrust. Over the yeats the followers of the diversified technique have fallen into two main schools of thought: those primarily looking for restriction of joint
Much of Logan's treatment technique is found in rhe neural organization technique, sacro-occip-
Palmer organized it into distinct professions, a
turbulent hisrory of changing and maturing philosophies, modified and evolving techniques, misconceptions, misunderstandings, and simplis-
tic viewpoints fo llowed. These different named techniques developed because individuals perceived a need. They interwove philosophy, diagnostic procedures, [rcarmen[ procedures, and often office management tactics into their named
technique, and developed a system of patient management. Th is was a time of technique rivalries, intraprofessiona l jealousy, mistrust, and con demnation . It was a time of lack of communica-
motion, and those looking for static or kinetic misa li gnment. Many practicing chiropractors do
tion berween doctors within different technique schools. As these named techniques sprang up, it
not completely endorse one philosophy over the other but have developed more of an ecclectic approach. Logan developed the Logan basic technique, in which basic refers to the base of the sacrum a nd should nor be interpreted as a principle or fundamental law. Logan extrapolated Lovett's theory of the spi ne as an o rgan, developing a system of analyzing the architecture of the spine from x- ray markings. He promoted a system of correcting subluxation with light touch contacts to sacral areas and the application of heel lifts (6). Logan's model, based on spinal biomechanics, laid the groundwork for other named techniques such as Gonstead, Petti bon, and chiropractic biophysics. These three "named techniques" borrowed from Logan, extrapolated their own theories, and developed their own systems of
was evident that many of them were creating their own language, redefining terms, and creat-
diagnosis and treatment.
ing new words. This lack of a common language fanned the flames of miscommunication.
Terminology As the chiropractic profession developed into the second largest health care delivery system outside of medicine it also developed in many directions. With the lack of communication between the practitioners of different chiropractic techniques,
each school of thought evolved a an independent entiry. They expanded philosophies, refined techniques, and redefined terms. Although communication was a necessity for su rvival, there existed a
severe communication gap. After the 1975 Nationa l Institute of Neurological Communicative Disorders and Stroke (NINCDS) Conference
91 that evaluated the resea rch status of spina l manipulative therapy, manual procedures we re no
whereas others believed that manipulations are a more accomplished form of treatment. Most of these practitioners basically perform simi lar types of osseous manual thrust procedutes but call them by different names. To foster consistency, the following terms will be used:
longer considered invalid and became the object of study of a number of professions besides chiropractic. Medicine, naturopathy, and physical therapy, in addition to osteopathy, began to study and employ manipulation and other manual techniques. The chiropractic profession was facing a serious dilemma. It was being forced to communicate with other branches of medicine, but a common la nguage no longer existed to allow successful dia logue. Out of this dilemma, a subcommittee of the standards of care committee of the Consortium for Chiropractic Research began to develop nomenclature through consensus (See Chapter I ). Using the following terms outlined in Cha pter 1, we can discuss osseous thrust techniques using the definitions developed: subluxation, manual therapy, manipulation, mo bilizatio n, and adjustment.
lIIoblizalIoIl "movement applied singu larly or repetitively within o r at the physiological range of
SUbluxation
with the goal of restoring joint mobility" (7).
~
"a ny chiropractic therapeutic
procedure that utilizes controlled force, leverage, direction, amplitude, and velocity which is directed at specific joints or anatomica l regions.
Chiropractors commonly use such procedures to influence joint and neurophysiological function " (7).
IIIIIIIIUII1Ian "a manual procedure that involves a directed thrust to move a joint past the physiological range of motion, without exceedi ng the anatomical limit " (7).
joint motion, without imparting a thrust or impulse,
Ever since D. D. Palmer's time, chiropractors have been attempting to find and "correct" subluxarions. Bur what is a subluxation? How can one detect a subluxation ? And how can a subluxation be "corrected"? A subluxation is "0 motio n segment, in which alignment, movement integrity, and/or physiological (unction are altered although contact between joint surfaces remains intact." (7). This definition is precise, concise,
and inclusive of the philosophies of different techniques. It is not limiting. It states that on ly one of [he three parameters must be presem for a condi-
tion to be called a subluxation. It does not define what tissues may be affected or how these tissues are affected. It does not describe how to diagnose a subluxa tion but places this clinical decisionmaking process in the hands of the clinician, rea lizing that each patient and condition is different, necessitating the use of different diagnostic procedures, as well as treatment procedures. The terms ma"ipu!atiol1 and adjustment have created much friction among chiropractors. Some practitioners believed that adjustments are a more
skilled form o f osseous manual thrust techniques,
Characteristics of Joint Motion Motion in diarthrodial joints can be described in four stages (Figure 6-2): active motion, passive motion, motion within the paraphysiologic space, and motion past the para physiologic space. There exist three barriers or end points to movement
separating these four stages of motion. The first end point occurs when an individual has maximally moved the joint through the use of active muscular contraction . At the end point of active
motion, with the muscles relaxed, the joinr can be passively moved to the next end point or barrier. For diarthrodial joints to achieve full normal active range of motion, there must exist this small
buffer zone of passive motion just beyond the end point of active motion. If the joint is moved
through the passive range of barrier is reached. Movement within the physiologic range exceeds this second (elastic)
motion, the second up to this point lies of movement. If it barrier, the move-
ment occurs in what is termed the paraphysio-
logic space. As movement extends past the second barrier it may be associated with an audible pop
92 Neutral position
)} ",,-
7'---
---
Elastic barrier of resistance (crock) Paraphysiologic I spoce f'.., /
~~VV
anatomic ~.......... Limit ofintegrity
VV
'-.. Hypermobility
Active ROM Mobilization Manioulation Joint sorain
n.n 8-2
Sandoz charr: Four stages of range of
movement in diarthrodial joints: 1, Active range of movement (motion produced
by
muscular action),
2, Passive range of movement (motion produced by traction or springing the joint-joint play, up [0 the
elastic barrier of resistance). Characterizes mobilization. 3, Para physiologic range of movement
(morion beyond the elastic barrier of resistance up the limit of anatomic integrity produced
CO
by
manipulation and accompanied by an audible release ), 4, Pathologic movement (morion beyond the limit of
normal anatomic integrity, which damages ligaments and capsule, resulting in joinr hypermobility). Manipulation that is roo forceful may move the joint beyond the limit of anatomic integrity, creating or perpetuating joinr instabiliry.
or a click . This audible pop or click is believed to be caused by a gapping or a cavitation of the joint, causing a sudden liberation of dissolved synovial gases. The third barrier is the anatomic barrier; it lies at the end of the para physiologic joint space. Movement past the anatomic barrier results in rupturing of capsular and ligamentous fibers, causing a compromise to the integrity of the joint (1,8,9). Mobilization techniqlles are those procedures in which movement is introduced within the physiologic joint space and is not taken beyond the second (elastic) barrier. Joint gapping or cavirarion does nor occur. However, this does not nec-
essarily mean that cracking sounds, audible pops, or clicks do not occur during mobilization techniques. The "audible" portion of the definition should not be used to distinguish mobilization techniques from manipulation or adjustment techniques. Cracking sounds, pops, and clicks (audibles) can come from other sources, such as a connective tissue band popping over a bony prominence, breaking of adhesions, or realignment of the normal tracking mechanism within a joint. According to the consensus definition of mobilization, motion is created without imparting a thrust or an impulse. Strictly speaking, the terms thrust or impulse means an impelling or a directed force in which force is a function of velocity and amplitude (Velocity and amplitude lie on a continuum, ranging from very high to very low.) (10). The terms thrust or impulse, used in the context of this definition , should convey the connotation of a directed high-velocity force. Mobilization techniques such as gentle, slow, passive continuous motion (within the physiologic space) denote a very low-velocity force. " Muscle energy techniques " that cause submaximal muscle contraction, followed by a gentle passive stretch of the muscle, denote a low-velocity force, a force that keeps the motion within the physiologic space (11). Manipulative procedures involve a thrust that forces the joint beyond the elastic barrier into the paraphysiologic space, but does not go beyond the third barrier, which exceeds the anaromic limit. Manipulation is characterized by movement of short amplitude and a high-velocity thruSt, which moves a joint into the para physiologic space. However, any thrust, whether it is of a high velocity-low amplitude, or a low velocityhigh amplitude, that carries the movement past the second (elastic) barrier into the paraphysiologic space is a form of manipulation . Many manipulative procedures are associated with a cavitarion or a gapping of rhe joint, wirh a usual resulting audible pop or crack. This audible pop or crack is a result of creating sudden negarive pressure wirhin the joint space, causing a liberation of synovial gases (12). The audible should
8
oa.lI Manual TlII'UIt T~
nor be used as an Outcome measure for the deliv-
93
Manual therapy procedures
ery of a successfu l manipulation procedure, because thete are other causes of an audible, and the procedure may achieve irs intended outcome without an audible. Following an audible release (cavitation), rhe articular crack cannot be repro-
duced for approximately 20 minutes and the joint has a tendency toward instabi lity. This has been termed the refractory period. Attempts at remanipulation during this period will not reproduce rhe familiar crack and are not recommended.
II,lanipulation of the joint should be forceful enough to produce the articular crack sound, but nor so great as to separate the joint surfaces beyond their limit of anatomica l integriry (l).
Thus the major difference berween manipulation and mobilization techniques is that manipulation techniques carry the joint past the elastic barrier into the para physiologic space, and mobilization techniques are confined to the physiologic joint space. Adjustments refer to a wide variety of man-
ual interventions that may range from a highto a low-amplitude thrust and from a high- to a low-velociry thrust. They may employ a short or a long lever arm (or a comblllation of both), a recoil thrust, or a straight-line thrust. They may be mechanically assisted or nonmechanically assisted, performed in the closed-pack or open-pack position, and may occur within the physiologic joint space or carry the joint into the para physiologic joint space. Adjustments that occur within the physiologic Joint space are a specialized form of joint mobilization, and when carrying the joint motion into the paraphysiologic space are a specialized form of joint manipulation. The major difference between adjusrmem and mobilization techniques is that adjustment techniques involve " . . . controlled force, leverage, direction, amplirude and veloc-
iry .. . " (7). When examining adjustment, manipulation, or mobilization techniques, an overlap between
the diffetent manual therapy techniques exists (Figure 6-3). All three are forms of manual therapy procedures.
f1111'18-8 Model depicting the overlapping between manipulation, mobilization, and adjustment, all of which are manual therapy procedures.
Clinical Application The chiropractic osseous manual thrust technique (manipulation) is the primary consideration of this chapter. When a chiropractor examines a
patient, a conceptua l model of the patient's condition is developed. If this condition is one in which a subluxation exists, the doctor should develop a conceptua l model of the existing subluxation: which tissues or functions are affected (muscles, nerves, con nective, cerebrospinal fluid, circula-
tion, gla nds, orga ns, or the kinematics of the motion segment), and how they a re affected. Only after a conceptua l model of the causative factors (pathop hysiology or pathobiomechanics) has been developed can the doctor attempt to establish a n optima l treatment program. In establishing an optima l treatment program, the doctor
must answer the following questions: 1. What conditions are responsible for the dysfunction?
2. Are these conditions reversible? 3. What forms of intervention will affect the reversible pathology?
94 4. What can be done to optimize residual function if the condition is irreversible? 5. What can be done to prevent recurrences, secondary problems, and progression of the existing disorders? Wirh such an approach, the treatment becomes patient oriented rather than symptom oriented. The primary goal of management becomes restoration of an optimal level of functioning rather than simply resolution of symptoms. Treatment must be individualized for each parienr, according ro the narure and extent of rhe pathologic processes. The tendency to incorporate "standardized" programs or systems of treat-
ment should be avoided . The rrearment obviously depends on the diagnosis. The cause of many conditions is subluxation and joint dysfunction,
and the end result of many condirions is, likewise, subluxation and joint dysfunction. What tissues are causing the subluxa tion, what tissues are being affected by the subluxation, and how are these tissues being affecred? Only the answers to these questions will determine which osseous manual thrust procedure is the best for a particular patient with a particular condition, at a par-
be driven by the therapeutic intention of the procedure. This six-tiered flow chart attempts to classify rreatment procedures based on the following physical characteristics: 1. Manual and non manual procedures: Manual procedures are those procedures in which direct physical contact is necessary between the doctor and rhe patient. 2. Area primarily being affected: Anatomic joint, physiologic joint, or viscera . «Anatomical joint: The space between two or more adjacent bones and the connective tissues which define it. Physiological joint: A functional unit comprising the anatomical joint as well as those structures which are responsible for the funcrioning of th e joint such as ligaments, muscles,
nerves and vessels. Visceral: Of or relating to any internal organ in any of rhe four great body cavities" (14). 3. Type of COntact employed: Specific, nonspecific, or mechanical. 4. Type of lever arm used: Short lever arm, long lever arrn, or a combination.
5. Type of force used.
ticular time of their recovery.
This model is a first step; many orher physical
Clantftcatloo
characteristics of osseous manual thrust proce-
In an attempt to study the intent of osseous manual thrusr ptocedures, the Panel of Advisors to the ACA Council on Technic developed a generic classification system of treatment ptocedures based on a mechanistic approach (Bartol 's model). This model (Figures 6-4 and 6-5) was used to organize modules for the evaluation of chiropractic treatment procedures at the Sixth and Seventh Annual Conference on Research and Education. Used by the Mercy Conference to establish categories for standards of care, it is now recognized by a number of authors in Chiropractic Technique (2), Textbook of Clinical Chiropractic (15), and Chiropractic: An Illustrated History (16). The theory behind this model is that the physical characteristics of rhe trearment procedure are direcrly related and consequently should
dures that can affect the intent of applying the procedure. As this model evolves, it will certainly be expanded to encompass other physical characteristics.
Choosing the Best Procedure Once the doctor has made the clinical decision that an osseous manual thrust is indicated, the
next step is to determine which procedure is best for the patient. This decision should be influenced by the inherent needs of the patient and rhe intended outcome of the thrust procedure. The procedure should be chosen based on the conceptual model of the pathophysiology and pathobiomechanics of the tissues involved in the condition.
8 0 _ ManualTbrust TecIIiques
FigIre IH
95
Barrol's model.
Patients Needs Patients needs vary, and it is the responsibiliry of the doctor to fully assess these needs. A primary concern of the doctor should be how the parient will tolerate the rhrust procedure. The golden rule
is Hippocrates': prirnum non lIoeere (first do no harm). The patient's age, gender, body build, general physical condition, area of complaint, flexibility, chronicity, location of subluxation, and possible
eo.lhis
procodu-o ompIay
No -+
• tpeci/ic: "'""'"
Y..
16 Is 0 short & lang "'- ann ~ ~ Y..
Shon & lang "'nanspocific """"" procodu-o
No -+
19
h. slat & No -+ lang "'- ann ~ ~ Y.. 14 Shon & lang "'-
h.1ang " ' - ann
~
~ Y.. nan",",;f;c
"'""'" procodu-o 17 b • slat
""""" procodu-o
" ' - ann
Long "'-
nampoc;f;c """"" procodu-o
15
Shon"'-
nan",",;f;c
~ ~ Y..
No -+
18 No -+
Long "'- specific
20
Shon "'-
nanspoc;f;c
"'""'" procodu-o
.....IitJJA
FIgIre 8-5 Algorithm: Bartol's mode l.
'"..
97 contraindicarions shou ld always be considered when choosing a rhrusr procedure. For example, for a parient who has stretched capsular and ligamentous fibers at the C5-C6 motion segment from previous injuries, and is now presenting with restriction of motion, static misalignment, and neurologic deficit, repeated or vigorous thrust procedures are contraindicated. A gentle thrust or mobilization may be necessary to restore function, with restriction of excess motion
app ropriate. A female patient in her third trimester of pregnancy may not be comfortable lying prone. Supine or sitting procedures may be a better choice. Many side-lying techniques are also uncomfortable for pregnant patients, making relaxation difficult or even impossible. Because of hormonal changes causing ligamentous and capsular fiber laxity, the force of the thrust should be greatly reduced, decreasing any risk to the
patient'S normal daily actjvities. Some considera-
tions for choosing a clinically appropriate thrust procedure for patients diagnosed with either vertebrobasilar insufficiency or aneurysms are (1) specific short lever procedures rather than the use of long levers, (2) nonthrust procedures, and (3) limitation of rotation techniques (16B).
Thrust Procedure Components A full understanding of the anatomy and kinematics of a motion segment is paramount in
deciding which thrust procedure will result in the desired outcome. The chiropractic examination
should be thorough enough for the chiropractor to develop a conceptua l model relative to the patient's condition . The chiropractor shou ld take into consideration the patient'S unique needs and
patient. Again, restriction of any excess motion is
develop a treatment protocol based on this conceptual model, including the tissues and functions affected. Empirica ll y, chiropractOrs and a growing
desirable. Techn iques that use low-velocity forms of
number of studies substantiate that osseous manual thrust procedures are effective in patient care.
force such as continuous passive motion, proprioceptive neurofacilitation, and muscle energy tech-
Many times patient improvement can be directly attributed ro the thrust procedure. Currently, understanding the mechanism of how the procedure develops the desired effect is specu lative at best (See Chapters 10 and 11. ). There is a tremendous need for further research to give us a better appreciation of rhe potential benefits of thrust procedures. Keeping this in perspective, the fol-
niques should be considered over high-velocity thrusts when treating people with osteoporosis, aneurysms, bone infections, or acme painful joints. Certain mechanical devices can decrease
the amount of force necessary, for example, drop piece rabies, thrusting when the patient is under long axis distraction such as with the Jenson table, Leander table, or Cox flexion and distraction tables. According to Kleynhans (14 ), vertebrobasilar insufficiency and aneurysms are absolute contraindications to manipulation, requiring referral to a vascu lar specialist (14 ). Man y patients with
vertebrobasi lar insufficiency, however, can greatly benefit from receiving appropriate mobi lization and less vigorous adjustive procedures. Even though vertebrobasilar insufficiency and aneurysms are thought to be absolute contraindications to high-velocity manipulative thrust procedures, appropriate mobilization and adjustive procedures should carry no more risk than the
lowing discussion on the various components of
thrust procedures is offered with the theoretical conceptualization of intent of the various components.
Manipulation Versus Mobilization Procedures The term manipulation refers to long lever or short lever thrust procedures, whereas mobilization employs repeated oscillation and slow passive stretches. More forceful ptocedures are chosen when the intent is to break adhesions in the capsular fibers, restore normal tracking, reduce capsular entrapment., stimulate articular nerve
ending, or relieve mechanical blockage. Mobilization procedures are used when the intent is to
98 stretch shortened ligaments to restore globa l range of motion.
range of motion. In assessing joint play, the doc· tor usually checks the following accessory mocions: long axis distraction, translarory glide,
Three-Point Tension Essential to pain-free manipulation is traction of
the joint to tension in all three planes (th ree-point tension ). Without tension, the force of the thrust is absorbed by the capsule and surroundi ng soft tissues. In add ition, the su rrounding muscles absorb substantial force if the patient is tense and the muscles are contracted.
The successful manipulation employs sufficient force to overcome the resistance of capsular and ligamentous fibers (the elastic barrier). The thrust induces a rapid separation of the a rticular surfaces (joint gapping) . Audible release of synovial gases (joint cavitation) indicates that joint separation has occurred. The separation of the joint surfaces may stimulate mechanoreceprors or
nociceptors and is thought to produce reflex and pain modulation. The capsular and ligamentous fibers are sufficiently stretched to allow this separation of the joint surfaces. This has a therapeutic affect of resraring normal motion to a restricted
motion segment, if the restriction was caused by a shortening or loss of elasticity in the capsu lar or ligamentous fibers or mechanical blockage. The direction of thrust shou ld follow the normal arc of motion of the motion segment. There exists little margin for error in the direction of thrust. If the thru t does nOt follow the arc of motion of the motion segment (a pproximately the plane of the articu lar surface), the a rticular surfaces jam against each other, possibly traumatizing the articular cartilage.
J oint Play and End Feel Joint play is a n accessory motion necessary for normal active and passive range of motion. Joint
play represents the amount of capsular laxity within a joint. If joint play is reduced, active motion will be decreased, restricted, or abnormal,
and may be painful. The muscles that move a joint do not function efficiently with decreased joint play and become hypertonic, resulting in muscle spasm, trigger points, myotogenous pain, articular pain, or decreased or abno rmal active
and axia l spin (9). Joint play shou ld not be confused with end feel (end play), which is assess· ment of the resistance supplied by the elastic bar· rier. End feel is assessed at the end of passive range of motion and tests the integrity of the cap· sular and ligamentous fibers . Voluntary motion or exercise cannot restore
joint play. Joint play can be restored only by manipulation or adjustment. When it is found that normal joint play is decreased, the joint IS tractioned to tension followed by a thrust (7).
Thrusting It is important for the doctor to ascertain how
much thrust is to be employed . The amount and type of thrust should be determined based on the desired intended effect (Figure 6-6) . If the restricti on of motion is from "mistracking" of the artic-
ular surfaces, a very high-velocity, very lowamplitude thrust is recommended to restore the normal alignment with very little to no effect on the capsular fibers. The capsu lar fibers are nOt stretched sufficiently to cause a gapping or cavitation of the joint surfaces (adjustment). Many times, when the tracking mechanism is restored, a
cracking sound is produced. This cracking sound should nOt be misinterpreted as the cracking sound of passing through the elastic barrier. If the doctor a pplies more thrust than is necessary to restore the normal tracking mechanism, another
pop or crack is usually heard, indicating passing through the elastic barrier and cavitation of the joint (ma nipulation) . If even more thrust is used, the joint passes through the para physiologic space, causing a joint sprain . Whether to employ manipulation or mobilization should be decided based on which tissues or functions are to be affected.
Long MIl Short Lever Arm Procedures A lever is "a rigid body that transmits a modified force or motion when forces are applied at twO
points and it turns about a third [fulcrumJ. " A
8
oa-II ManuII TIIrUIt TecIInIqua
lever arm is " the perpendicular distance of the axis of rotation from the line of action of the force.'" A long lever arm "is created when a force is applied distal to the axis of rotation," and a short lever arm "is created when a force is applied proximal to the axis of rotation" (13). When performing an osseous manual thrust procedure, lever arm(s) are used to deliver a force into the motion segment. Some procedures involve a short lever arm, a long lever arm, or a
combination of the two to deliver the thrust. The length of the lever arm should be chosen according to what tissues or functions are to be affected by the thrust. Some use short lever arm procedures to prevent absorption of force by soft tissues (17). With thrust procedures the capsu lar and ligamentous fibers on one side of the joint become lax as their counterparts on the other side of the joint are becoming taut. If a long lever arm procedure is employed, the thrust has a tendency ro first stretch and tear the ligamentous fibers, then the capsula r fibers on the side that is being separated. The thrust has its initial effect on the tight ligamentous fibers. As these fibers are being stretched they develop more resistance to the force. Eventually the force is transmitted to the opposite side of the joint, causing the arricularing surfaces to
abut against each other. This abutment causes a jamming of the articu lar surfaces. When the articulating surfaces are jammed as tightly as possible, the effect of the force is transferred back to the other side. With more force, the ligamentous fibers continue to stretch, and the capsular fibers stretch until the capsular and ligamentous fibers are overwhelmed and the joint instantaneously separates, causing a cavication of the joint
(manipulation). Shorr lever procedures, depending on the vecror force of the thrust, have the potential of causing the same mechanical effect as a long lever arm procedure, or they can create more of a translatory glide or an axia l spin affect. The sharrer the lever arm, the more likely that the force will create a translatory glide or an axial spin . When the vector force of a short lever arm procedure creates a translarory g lid e or an axia l spin, the thrust
99
has a tendency ro primarily affect the capsu lar fibers before the ligamentous fibers are affected. Short lever arm procedures are used when the intended effect is ro increase the elasticity ro the capsular fibers. Long lever arm procedures should be employed when the intent is to increase the elasticity of the ligamentous fibers. Usually, the sharrer the lever arm, the more controlled and specific the thrust will be. Long lever arm procedures have the mechanical advantage of developing a larger thrust at the expense of control.
Force
d. the Thrust
Force is a function of velocity and amplitude and can be categorized as either high or low. However, force is a continuum . The veloc ity and
amplitude of the thrust should be chosen based on the intended outcome of the procedure. Controlled velocity and controlled amplitude thrusts are attributes of adjustments. Thrusts of any velocity or any amplitude that carry the joint into the paraphysiologic space are manipulations. Consideration must be given to the effect that different ty.pes of force have on the joint structures. Most of the components of the physiologic joint are connective tissue, and mOSt osseous thrust pro-
cedures are directed at affecting these connective tissues (that is, capsu lar fibers, ligamentous fibers, articular carti lage, tendons, interverrebral discs). All connective tissues have viscoelastic prop-
erties, that is, they all have both elastic and plastic qualities. The elastic stretch quality of connective tissue refers to its springlike behavior. Elongation occurs when it is placed under tensile loading, and when the loading is removed the normal length of the tissue is recovered. This is a temporary or recoverable elongation of the connective tissue. The viscous or plastic property of connective tissue consists of linear deformation of the connective tissue when placed under tensile loading, and when this loading is removed, the deformation or stretching stays the same. This is a nonrecoverable or permanent elongation, a "plastic deformation" (18). The amount of the applied force and the duration of the applied force determine whether the elastic or the plastic properties are affected . A high force over a short period
100
A -t-------'r-
Fibrous alp 01 menilClOid
ArticuIar~ ;)!DfJii'J~'P'''----+ Fibooaclip _ ti_
cell base
•
c Normal position FIgII'I B-1 Position and postu lated incarceration of synovial joint meniscoids. A, Diagrammatic representation of the structural components of a meniscoid in a lumbar facct. B, Meniscoids entrapment in cervical facet joints restricting extension and flexion movements. C, Entrapment of meniscoids is postulated to produce deformation of the articular cartilage surface; after reduction and over time the articular cartilage will remodel. (Modified from Churchill Livingstone.)
101 results in elastic deformation. A low force over a
ation. Some patients are nOt comfortable in cerrain
long period results in plastic deformation. When connective tissue is stretched, the relative proportion of elastic and plastic deformation can vary widely, depending on how and under what conditions the stretching is performed. The time required to stretch the tissue a specific
adjusting positions. The doctor should be cog-
amount varies inversely with the forces used.
Therefore, a low-force stretching method requires more time to produce the same amount of elon -
gation than a higher-force method. The proportion of tissue lengthening that remains after the tensile stress is removed is greater for the low-
force, long-duration method . It has been demonstrated that when connective tissue structures are
permanently elongated, some degree of mechanical weakening is present, even though rupture has not occurred (J 9). The amount of weakening depends on the method and degree of stretch. For the same amount of tissue elongation, howevet, a
fast, high-force stretch method produces more structural weakening than a slower, low-force method. Thus, if the intention of the procedure is to stretch ligaments, a low-amplitude, low·velocity thrust with a long lever arm is indicated. If the intention is to break up adhesions in the capsular fibers, a high-velocity, low-amplitude thrust with a short lever is indicated. If the intention is to break up fibers that do not align along the normal lines of stress within the capsular fibers, a high-velocity low-amplitude type of thrust with a short lever is indicated. If the intention is to restore normal joint play without affecting the capsular or ligamentous fibers, or if the intention is to stimulate the nerve endings within the joint capsular fibers, a procedure of high velocity and very low amplitude with a short lever is needed. If more thrust is employed than is necessary to achieve the desired results, the force of the thrust is abso rbed by other Structures . This may result in affecting normal tissues o r additional motion segments. With thrust techniques it is important to use no more thrust than necessary.
The more relaxed the patient, the less the muscles resist or attenuate the thrust. Patient positioning is very important in patient relax-
nizant of in which position the patient is most
relaxed. The patient'S position should be chosen nOt to fit the doctor's whims and preferences but to fit the patient'S needs. Most patients tighten their muscles when the thrust procedure induces pain, indicating that this may not be the best setup or procedure for that patient. Patients usually tense their muscles if the doctor uses a heavy contact. Some doctors use a pause technique: they move the motion segment to the position just
before the thrust is to be delivered, then pause and sample the amount of resistance. By sampling the amOunt of resistance, they attempt to calculate how much force is necessary to overcome the resistance. The problem with pause techniques is that they allow the patient a chance to anticipate the thrust and "tighten up." To minimize this response, other doctors employ non pause techniques: They take the motion segment to the point of resistance and, without pausing, give the
thrust; the patient'S muscles do not have a chance to tighten up. Nonpause techniques focus on patient relaxation rather than calculation of the minimum amou nt of thrust necessary. Others
believe that having the patient take a deep breath in and then letting the breath Out (with the doctor thrusting at close to full expiration) creates patient relaxation. In some patients this breathing technique causes the muscles to relax, but some-
times, having the patient breathe allows time to anticipate the thrust. The doctor should use those procedures that augment patient relaxation and
shou ld not attempt to adjust or manipulate all patients the same way. Table selection is very important in minimiz-
ing the thrust. If the table has toO much padding, the padding itself will attenuate the thrust. Soft padding tends to decrease the velocity of the thrust,
necessitating a
morc
forceful
thru~t
(i ncrease velocity a nd increase amplitude). A table with too little padding decreases patient comfort and thus relaxation. Drop piece tables can be used to augment the thrust. Theoretically, when using a drop piece table, the drop piece
102 tends to increase the velocity of the thrust. By increasing the velocity of the thrust, less amplitude is necessary. Distraction tables (for example, Cox tables, McMannis tables, Leander tables, Jenson tables) create long axis distraction in the motion segment (20) . If the motion segment is placed under long axis distraction, the joint surfaces separate, rather than lock; consequently, less force is required. Stabilizing the segment above (or the segment below) tends to localize the thrust to the intended motion segment. If the thrust is nOt absorbed by other motion segments, less force is necessary. Counterthrust techniques, in which a thrust is
delivered to both components of the motion segment but in opposite directions, also help localize the thrust to the intended motion segment. With counterthrust techniques, the force necessary to
affect the motion segment is divided between the twO portions of the motion segment, allowing less thrust on the lower or upper portion of the motion segment. Performing soft tissue work on the patient to comrol pain, relax constricted muscles, decrease swelling, etc., decreases the amount
have a more specific effect than a broad, general contact over not only the transverse process of
the vertebra to be affected but also the transverse process of the verrebra above and the transverse process of the vertebra below. A contact on the patient, made as close to the
joint space as possible, tends to have a short lever arm affect. Depending on the line of drive, a contact very close ro the joint space creates either a separation of the articular surfaces on one side
and an approximation of the articular surfaces on the other or the force causes a translatory glide or an axial spin. Short lever arm contacts are pri-
marily made to create the translatory glide or axia l spin forces. The farther the contact is made from the articulating surface, the more likely it is to cause a long lever arm effect, primarily causing
the effect of the thrust to be absorbed by ligamentous fibers. A contact made over an osseous landmark,
close to the surface of the body, tends to transmit the force from the effector to the motion segment without attenuating a measurable amount of the
thrust. An example is an osseous thrust procedure
of force attenuated by the soft tissues. Choosing
in wh ich the contact is made over the spinous
the optimal contact points and the correct vector
process of the lumbar verrebra. Most of the force of the thrust is transmitted ro rhe spinous process of the vertebra to cause the intended effect. When the thrust is given, the force is transferred to the spinous process with very little of the force of the thrust being absorbed by the soft tissue in the
of the thrust can also reduce the amount of force necessary for the procedure.
Contact POints The contact between the doctor and the patient is usually referred to as being specific or nonspecific. A specific cOntact is defined as "a precise focal contact between the doctor and the patient, " and a nonspecific contact is defined as
"a broad genera lized contact between the doctor and the patient" (13) . The contact point on the patient determines whether a general technique or a specific technique, a long lever arm technique, or a short lever arm technique is desired. The contact point determines how much of the thrust is absorbed by the area of contact.
Logically, the smaller the contact point on the patient, the more localized the effect of the thrust. If a vertebra is rotated posteriorly, contact over just the transverse process of that vertebra should
region. A contact made over an osseous landmark
that is covered by a substantial amount of soft tissue, however, tends to transmit a measurable
amount of the thrust to the soft tissue. An example is a lumbar osseous thrust procedure in which the contact is made over the mammillary process
of the lumbar vertebra. As the force of the thrust is transmirred from the effector to the osseous landmark, a proportion of the force is absorbed by the soft tissues, tending to reduce the velocity of the thrust, necessitating increasing the overall
force . The closer the osseous landmark (to be contacted) is to the surface of the body, the less force is needed. The contact point on the doctor's body also affects rhe outcome of the th rust procedure. A
8 OSSeous Manual TbruIt Techniques pisiform contact is much more specific than a palmar con tact. A pisiform contact does not absorb
as much of the force of the thrust as a soft hypothenar or thenar contact. When performing a rotatory cervical maneuver, a distal interphalangeal joint COntact may absorb more of the thrust than a metacarpophalangeal joint contact. A metacarpophalangeal joint contact delivers a more forceful thrust than a distal interpha langeal joint cOntact. Depending on the thrust procedure, some contacts may create a higher-velocity type of thrust. Extension types of thrust are usually of a higher velocity than flexion types of thrusts.
Une of Drive There is a dichotOmy of opinion as to the correct path of the thrust. Some believe that the thrust should be delivered through the plane of the disc, and others believe that the thrust should be delivered along the plane of the arriculating surfaces. Some describe an "arc of motion " for the correc-
tive force and others describe a "line of drive." The path of the correcting force should be determined by the intended outcome of the procedure, based on the conceptual model of the pathophysiology and the pathobiomechanics of the condition. If the subluxation is caused by inelasticity of the ca psular fibers, the appropriate thrust may be a translatOry glide or an axial spin type of force, depending on the direction of restriction . If the subluxation is caused by a mistracking of the articulating surfaces, the path of correction may be more appropriately made along the arc of motion of that segment. If the joint subluxation is caused by restriction in the ligamentous fibers, the appropriate thrust may be more of a valgus, varus, hype rflexion, o r hyperextension type of force.
son lIssue Therapy Addressing the needs of the soft tissue before or after manipulation augments the manipulative procedure. Therapy to soft tissues helps reduce pain, decrease muscle spasm, decrease swell ing, and improve parienr relaxation. If the patient is in pain during a manipulation, or the procedure itself is the cause of the discomfort, the patient will not be able to relax. If the patient is not
103
relaxed, the force of the thrust is less localized, necessitating a larger amount of force. In resisting the force, tight muscles absorb some of the force, causing a stretching, separation, and tearing of the muscle fibers. Even if the manipulation is successfu l, muscle tension and spasm perpetuate subluxations. There are many soft tissue therapy procedures, ranging from techniques attempting to have a mechanical, circulatory, or neurologic effect. They are useful in acute as well as chronic conditions. Depending on the desired effect, soft tissue techniques are prudently performed as a prelude to more aggressive manipulative procedures, after manipulation (to reinforce the manipulation), o r both .
Reflll'tlllC8S 1. Garterman M. Chiropractic management of spine related disorders. 1st ed. Baltimore: Williams & Wilkins,
1990. 2. Bergmann T, Peterson D, L..,wrence D. Chiropractic tech nique. 1st ed. New York: Churchill Liv ingstone, 1993. 3. Hippocratcs. Hippocr:nes, with an English translation by Dr. E. T. Withington. 3rd ed. Cambridge: Howard University Press, 1959. 4. Greenman P. Principlcs of manual medicine. 1st ed. Baltimore: Williams & Wilkins, 1989. 5 . Gibbons RW. The evolution of chi ropractic: medical and socia l protest in America. In : Halderman 5, ed. Modern developments in the principles and practice of chi ropractic. East Norwalk, Connecticut: Appleton Cenrury Crofts,
1980. 6. Filson R, Johnson G. Logan system of body mechanics asscssmenr. Proceedings of the First National Symposium on the Comparison of Chiropractic Treatment Procedures, 1993; 1:67-72. 7. Gatterman M, Hansen D. The development of chiropractic nomenclature through consensus, June 1993. 8. Haldeman S, Chapm:1O-5mith D, Petersen D. Guidelines for chi ropractic quality assurance and practice parameters. 1st ed. Gaithersburg, Maryland: Aspen, 1993. 9. Kessler R, Herding D. Management of common musculoskeletal disorders: physical therapy principles and methods. 1st ed. Philadelph ia : Harper, 1983. 10. Barrol KM. Proceedings of the 1991 Consensus Conference on Validation of Chiropractic Technique, Monterey.
J Ch;coTcch 199 1;4( 1). II . Wadsworrh C. Manual examination and treatmem of the spine and extremities. 1st ed. Baltimore: Williams & Wilkins, 1988: 25. 12. Unsworth A, Dowson P, Wright V. Cracking joints: A bioengineering of cavitation of the metacarpophalangeal joint. Ann Rheum Dis 197 1; 30:348-58.
104
Subluxation The Ar1IcuI.. lesion
13. Barrol K. The use of generic nomenclature of chiropractic frcaunem procedures in chiropractic publications. Chico Edue 1993; 7,1 . 14. Kleynhans AM. Complications of and contra indications to spina l manipulative therapy. In Haldeman 5, ed. Modern dcvelopmenrs in the principles and practice of chiropractic. East Norwalk, Connecticut : Appieton Cenrury C,ofts, 1980, 539. 15. Plaugher G. Textbook o f clinical chiropractic: A specific biomechanical app roach. 1st ed. Baltimore: Williams & Wilkins, 1993. 16. Peterson D, Wiese G. Chiropractic: An illustrated history. 1st ed. Sr. Louis: Mosby, 1994. 168. Year H. Chiropractic standards of practice and qua liry of carc. 1st ed. Gaithersburg, Maryland: Aspen, 1992.
17. Schafer RC. Clinica l biomechanics, musculoskeletal actions and reactions. 2nd ed. Baltimore: Williams & Wilkins, 1987. 17 B. Bartol KM. Long and short lever-specifidnonspecific comact procedures. Proceedings of the 7th Annual Confe rence on Research and Education 1992; 260-63. 18. Stromberg D, Wiederhielm CA. Viscoelastic description of a collagenous tissue in simple elonga tion. J Appl Physiology 1969; 26,857-862. 19. laBan MM. Collagen tissue: Im plications of its response to Stress in vitro. Arch Phys Med Rehabil1959; 43,265-283. 20. Bergmann T, Peterson D, Lawrence D. Chiropractic technique, 1st ed. New York: Churchill Livingstone, 1993.
Chiropractic Reflex Techniques Thomas F. Bergmann
Key WDrds
Facilitation, nociceptors, somatic dysfunction, trigger points, spondylotherapy
After reading this chapter you should be able to answer the following qllestions:
Question #1
What are the common mechanical, soft tissue, neurologic, and psychologic effects of manual therapy?
Question #2
What is the proposed effect of chronic segmental facilitation?
Question #3
What is the rationale for the use of manual therapy to ameliorate negative somatoautonomic reflexes?
106
SUbluxation
The ArtIcuI.. lesion
C
hiropractic has maintained that the mOSt specialized and significant therapy employed involves the adjustment of the articulations of the human body, especia lly the spinal column. This may be done manually or mechanically, actively or passively, with the purpose of restoring normal articular relationship and function as well as reestablishing neurologic integrity and thereby influencing physiologic processes. Although mOSt chiropractic techniques impart a thrust, many techniques are designed to affect physiologic processes without involving the use of a thrust procedure. These techniques are nonetheless considered chiropractic adjustments. This chapter discusses the theory and evidence supporting these nonthrust procedures. The role of the soft tissues and reflex mechanisms of the body in terms of health and disease deserves specific consideration. The ways in which dysfunction in the soft tissue mirrors deeper pathology of both the mind and body, and the ways in which it influences such pathology, directly or reflexively, are profoundly important (1) . There seems to be a trait characteristic of ch iropractors-perhaps of humans in genera l-that keeps us searching for therapeutic specifics in the management of human ills (2). Various and numerous forms of manual therapy are used by the profession of chiropractic (3). The originality of and difference between systems of chiropractic technique is generally found in the underlying rationale and philosophy rather than in the techniq ues themselves. Typically, the underlying ph ilosophy and originatot's hypothesis dictates the sequencing of the technique and attemp ts to explain the proposed mechanism of action and results. Furthermore, an individual's reaction to
internal and external stimuli are so complex and varied that no compendium of specific forms of treatment for specific dysfunctions cou ld possibly be complete and usable. The goals of manual rherapy include a combination of mechanical effects, soft tissue effects, neurologic effects, and psychologic effects.
Although these effects are usually considered or discussed separately, the division is purely academic because the effects of manual therapy cannOt be specifically directed or limited. In other words, one cannOt apply a manual procedure and consistently achieve a single or specified effect. For exa mple, when using a thrust technique to create a motion or alignment change (mechanical
effect), input to the joint receptors (neurologic effect) occurs, muscles and ligaments (soft rissue effect) are compressed, stretched, or lengthened, and the patient is aware that something was done (psychologic effect). The chiropractic adjustment is a unique form of manual therapy that uses controlled force, leverage, direction, amplitude, and velocity directed at specific joims or anatomic regions. It
>
Goals of Manual Therapy
Manual Therapy is thought 10 pmdllCl! maltges i ..: • Joint alignment • Dysfunction of motion • Spinal curvature dynamics • Entrapment or extrapment of a synovial fold
(15)
Soft na.. EIII*
• Changes in the tone and strength of suppotting musculature • Influencing the dynamics of suppottive capsuloligamentous connective tissue (viscoelastic properties of collagen)
_"10111 EIIIcII • Reduction in pain • Altering motor and sensory function • Influencing autonomic nervous system regulation ...,.Ioglc EfII* • Laying on of hands • Placebo factor • Patient satisfaction
7 ctnpractlc RIIIIx TIIChnIqua is necessa ry to understand, however, that because a wide variety of methods exists, the assumpcion that all manual therapy, adjustments, or manipu -
lations are equivalent must be avoided (4). Factors that influence the selection of manual procedures (5) include: I. 2. 3. 4. 5.
Age of the patient Acuteness or chronicity of the problem General physical condition of the patient Clinician's size and ability Effectiveness of previous or current therapy
Manual procedures can be specifically directed to the soft tissues. Even though all manual
107
Mechanica l devices have been used with manua l therapy to provide light force contacts and to produce purportedly controlled, repeatable percussion forces. Although some evidence exists to support that these procedures move joints, there is seldom an audible release or cavitation response (8). A factor that seems to be common to the body-wall reflex technique procedures is that the irritable "lesion" resides in fascial tissue. Therefore it is necessary to explore the structure and function of connective rissue, because it is a sig-
nificant component of the fascia as well as of all the soft tissues.
techniques have some effect on the soft tissues,
Connective tissue contributes to kinetic joint
the justification for a separate classification is to
stability and integrity by resisting the rotatory moments of force developed by forces acting at each joint. When these rotatory moments of force
draw attention to the prime importance of includ-
ing techniques that have the specific purpose of improving the vascularity and extensibility of the soft tissues (6) as well as to reflexively influence neurologic elements and physiologic processes. Furthermore, soft tissue manipulation tends to
relax hypertonic muscles so that, when other forms of manual therapy are applied, equal tensions are exerted across the joint. Soft tissue manipulation includes massage (stroking or effleurage, kneading or petrissage, vibration or tapotement, transverse friction massage), trigger point therapy, connective tissue
massage, body wall reflex techniques (Chapman lymphatic reflexes, Bennert vascular reflexes, acu-
are large, considerable connective tissue power is
required to produce the needed joint stability and integrity. Within the past several decades a great deal of scientific investigation has been directed at defining the physical properties of connective tissue. Connective tissue is made up of various densities
and spacia l arrangements of collagen fibers embedded in a protein-polysaccharide matrix, which is commonly called ground substance. Collagen is a fibrous protein that has a very high tensile strength . Collagenous tissue is organized into many different higher-order structures, including
pressure point stimulation), and muscle energy
tendons, ligaments, joint capsu les, aponeuroses,
techniques. [n addition, some methods of chiropractic adjustment apparently have a greater direct affect on the soft tissues or have a greater effect on the homeostasis of the body through
and fascial sheaths. Therefore, under normal and pathologic conditions, the range of motion in most body joints is predominately limited by one
reflex mechanisms.
or more connective tissue structures. The relative contribution of each to the total resistance varies
Meeker (7) identifies chiropractic soft tissue techniques as those physical methods applied to
with the specific area of the body.
muscles, ligaments, tendons, fascia, and other
involved in the body's reparative process frequently impedes function because it may abnormally limit the joint range of motion. Scar tissue,
connective tissues with the goal of therapeutica ll y affecting the body. He also defines non force techniques as very light force methods sometimes applied to the soft tissues but most often to the bony parts of the spine and pelvis with the goal of improving the hea lth of the patient.
After trauma or surgery, the connective tissue
adhesions, and fibrotic cont ractures are common
types of pathologic connective tissue that must be dealt with during chiropractic manipulative procedures. Understanding the physica l factors influ-
108 cocing mechanical behavior of connective tissue under tensile stress is therefore essential for deter-
mining the optimal means through manipulation to restore normal function.
All connective tissue has a combination of two qualities, elastic stretch and plastic (viscous) stretch. The term stretch refers to elongation of a linear deformation that increases in length. Stretching, then, is the process of elongation . Elastic stretch represents springlike behavior. Elongation produced by tensile loading is recovered after the load is removed. It is therefore also described as temporary or recoverable elongation. Plastic (viscous) stretch refers to puttylike behavior, in which the linear deformation produced by tensile
tress remains even after the stress is
removed. This i described as nonrecoverable or as a permanent elongation. The term viscoelastic
is used to describe tissue that represents both viscous and elasric properries (9). There are different factors that influence whether the plastic or elastic component of connective tissue is predominately affected. These include the amount of applied force and the duration of the applied force. Therefore the major facrors effecting connective tissue deformation are
force and time. A high force over a short period results in elastic deformation . A lower amount of force sustained over a longer period produces plastic deformation. When connective tissue is stretched, the rela-
Trauma generally occurs as a result of a high force of shorr duration that influences the elastic deformation of the connective tissue. If the force is beyond the plastic range of the connecrive tissue, it enters the plastic range. If the force is beyond the plastic range, tissue rupture occurs. Commonly encountered is the microtrauma seen
in postural distortions, muscle imbalance, and joint dysfunction as a result of low gravitational forces occurring over a long period, thus creating
plastic deformation.
Enects 01 Immobilization Connective tissue elements lose their extensibiliry when their related joints are immobilized (10). With immobilization, water is released from the proteoglycan molecule, allowing connective tissue fibers
[Q
contact one another, encouraging abnor-
mal cross-linking and resulting in a loss of extensibil ity (11). It is hypothesized that manual therapy can break the cross-linking and any intraarticular capsular fiber fatty adhesions, thereby providing free motion and allowing water inhibition to occur. Furthermore, procedures can stretch
segmental muscles, stimu lating spindle reflexes that may decrease the state of hypertoniciry ( 12). Muscle tightness or shortness develops after periods of immobilization as well. Length changes in muscle are associated with changes in sarcomere number, and reorganization of the con-
tive proportion of elastic and plastic deformation can vary widely, depending on how and under what conditions the stretching is performed . When tensile forces are continuously applied to
nective tissue elements within the muscle (13). Muscle immobilized in a shortened position develops less force and tears at a shorter length
connective tissue, the time required to stretch the tissue a specific amount varies inversely with rhe
ing length ( 14 ). For this reason vigorous muscle stretching has been recommended for mu c1e tightness (15). For the stretch to be effective, however, the underlying joints should be freely mobile. Patients often tequire manipulation before muscle stretching. Cantu and Grodin (16) reviewed the literature on the effects of manual therapy on fascia, which include circulatory changes, blood flow changes,
forced used . Therefore, a low-force stretch ing method requires more time to produce the same amount of elongation as that produced by a higher-force method. However, the proportion of tissue lengthening that remains after the tensile stress is removed is greater for the low-force,
long-duration method. Of course, high force and long duration also cause stretch and possibly rupture of the connective tissue.
than nonimmobilized muscle with a normal rest-
cap illary
dilatation,
cutaneous
temperature
changes, metabolic changes, and reflexive auto-
7 Chi'opractIc Rallex TecI1nIquea nomic changes. However, most of the citations were quite old .
Enects on Blood How InI Temperature Deep stroking and kneading of the soft tissues in the extremities of normal subjects, patients with rheumatoid arthritis, and subjects with spasmatic paralysis create a consistent and clinically significant increase in total blood flow and cutaneous temperature (17). These findings are supported by other studies (18-20); however, it must be emphasized that the clinical procedure being tested in all of these reports was a deep or heavy massage application. Therefore, conclusions on the effects of light-force stimulation of the body wall cannOt be drawn from these data.
Enects on MetaboHsm Cuthbertson (21) performed a literature review on the effects of massage on metabolic processes, including vital signs and waste products of the body. He reported that, in normal subjects, there was no increase in basal consumption of oxygen, pulse rate, or blood pressure, although an increase in urine output was observed . To effect a change in the vital signs, however, a systemic affect must be achieved. Localized changes in basal consumption may occur but this has yet to be studied. Schneider and Havens (22) did find an increase in red blood cells needed to bring oxygen to the tissues being influenced with massage. This provides some suppOrt, then, for soft tissue procedures being able to increase circulation and nutrition to desired areas. Again, these were vigorous massage procedures that were described; caution is necessary when trying to apply these principles to other procedures.
109
may be activared rhrough connecrions with the lareral horn cells in the cord to produce vasomotOr, trophic, visceral, or metabolic changes. The impulse-based paradigm of neurodysfunction that has been developed from the work of Homewood (23) and Korr (24), suggests that somatic dysfunction or joint dysfunction induce persistent nociceptive and altered proprioceptive input. This persistent afferent input triggers a segmental cord response, which in turn induces the development of pathologic somatosomatic or somatovisceral reflexes (25-27). If these reflexes persist, they are hypothesized to induce altered function in segmentally supplied somatic or visceral structures. Manual therapy, including soft tissue techniques and other forms of adjustive therapy, would have the hypothetical potential for arresting both the local and distant somatic and visceral effects by terminating the a ltered neurogenic reflexes that are associated with somatidjoint dysfunction. Reflex pathways exist such that when a stimulus (see box below) is applied to a somatic structure of the body, a resulting response occurs in another somatic structure of the body. These are referred to as somatosomatic reflexes. Although they are considered the mOSt primitive reflexes in the human body, somatosomatic reflexes are essential to the control of normal physiologic activities and may become involved in abnorma l reactions. The somatosomatic reflex has a direct application to the problem of muscle alterations in the paravertebral region. When conditions are such that the stimulus elicits and abnormally prolongs a muscle contraction in this area, the tissues become a secondary source of irritation with the
>
Stimuli for Evoking a Somatosomatic Reflex Response
Renexive (Autonomic) EHects Reflexive or autonomic effects relate to evidence
• Variation in temperature
of change in tissues or structures distal to or distant from the site of therapeutic application. Lesions in the soft tissue can initiate sensory irritation, which produces referred pain and tenderness. Moreover, aumnomic nervous involvement
• Mechanical stress
• Chemical irritation • Environmental stress • Structural stress
110 potentia l of disturbing bomeostatic balance. If the
Somatoautonomlc Renax Theory
individual's inherent resistance cannot compen-
Korr (24) proposed that spinal muscles, when
sate for the imbalance, clinically recognizable symproms may result (28). One of the signs of somatic dysfunction is the presence of muscle hypertonicity. Localized increased paraspinal muscle [One can be detected with palpation and in some cases with electromyography. Janda recognizes five different types of increased muscle rone: limbic dysfunc-
under strain or tension, caused the firing of pro-
tion, segmental spasm,
reflex spasm, trigger
points, and muscle tightness (15). Liebenson has discussed the treatment of these five types using active muscle contraction and relaxation procedures (29).
I1811ex Muscle Spasm from SplnallI$I'y Reflex muscle spasm or splinting follows trauma or injury ro any of the pain-sensitive structures of the spine. The pain-sensitive spinal tissues include the zygapophyseal joints, posterior ligaments, paravertebral musc.les, dura mater, the anterior and posterior longitudinal ligaments, and the intervenebral discs (30). Mechanical deformation o r chemical irritation of any of these tissues
causes restricted motion by way of muscle spasm. Treatment directed at the rissue source of pain
reduces the reflex muscle spasm and increases the range of motion; however, if the muscle spasm has been present for some time it requires direct treatment as well.
Renax Muscle Spasm from VllCerIi Dlseasa Visceral disease also can cause reflex muscle splinting. T he diagnosis of a viscerosomatic reflex is based on a history of visceral disease, or current visceral disease sympromarology, and objective palpation findings (31). Objective palpation findings include: twO or more adjacent spinal segments that show evidence of fixarion located within a specific auconomic reflex area; a deep
prioceptive nerve receptors embedded in the muscles. Korr believed that this proprioceptive information, which synapses with second-order neu-
rons located in the spinal cord, facilitated or lowered the firing threshold of the second-order neurons. When second-order neurons are facili-
tated, they act as a "neurologic lens" and are hyperresponsive to impulses reaching them from any source in the body. He termed this hyperirritability chrollic segmelltal {acilitatioll (24) . Second-order neurons synapse with a variety of cell in the nervous system; however, Karr focused primarily on the local segmental connections in the spina l cord. In the spinal cord, second-order neurons synapse with amerior horn ceils, which innervate muscle, and with latera l horn cells, which are pan of the sympathetic nervous system. Karr proposed that continuous irritation of the lateral horn cells caused these (sympathetic) neurons ro become faci litated. A facili tated or hyperirritable sympathetic nervous system is considered by Korr to be a major contributing factOr in perpetuating musculoskeletal dysfunction and visceral organ exhaustion and disease (24) . Numerous conditions have been linked to hyperactivity of the sympathetic nervous system, including various rypes of cardiovascular, gastrointestinal, and genitourinary disorders, and certain musculoskeletal disorders such as reflex sympathetic dystrophy.
Evidence or Chronic SBtIIIIBIdII Faclltallon Korr and his osteopath ic colleagues performed several elaborate srudies that supported his theory of chronic segmemal facilitation (32). The presence of segmental muscle spasm at the site of spinal dysfunction supported the reflex connection to the anterior horn cells. The presence of
[Q
vasomotor changes (vasoconstriction or di lata-
segmenta l joint motion; and skin and subcutaneous tissue changes that are consistent with the acureness or chronicity of the reflex (3 1).
rion), sudomoror changes (sweating or dryness), and pilomotOr changes (hair follicle elevation) at the site of spina l dysfunction supported the reflex
paraspinal muscle splinting reaction; resistance
7 CIIII"IIPI'aclic Rellex TIICbnIquea connection (0 the sympathetic nervous system. Korr proposed that, because hyperactivity was demonstrated in the sympathetic fibers innervat109 the skin, the sympathetic fibers innervating the viscera would also be hyperactive and possibly contribute to visceral disease. The clinical evidence supporting this theory is primarily indirecr and based on rhe correlation of physical symptOms with spinal lesions. Because the spinal soft tissues are loaded with receptOrs, it seems plausible that any acute injury would resu lt in increased sensory input to the spinal cord, which in turn could result in segmental faci li tation .
The segmental facilitation theory is also called the Impulse-based theory because ir depends on impulses from the proprioceptive nerve receptors located in rhe spinal muscles. Nerve compression is nor a factor in this theory; in fact, facilitated nerves are functioning as they are designed: to carry information. Facilitated nerves become sensitized by the vast amount of stimulation they receive from strained muscles. Korr also postulated that when facilitated nerves become overburdened with activiry, their axoplasmic flow rate may become reduced. However, the primary lesion stressed in the segmental facilitation theory is sympathetic nervous system hyperactivity.
NocIceptors Reflexlvety Activate Sympathetic
NeII'ona Recent advances in the understanding of muscle spindle physiology question the ability of muscle spindles to activate sympathetic fibers (32). In response to this discrepancy in Korr's theory, Van Buskirk has ptoposed that nociceptors are the primary receptOrs causing chronic segmental facilitation and sustained sympatheticotOnia (32). SatO has recently reviewed the experimental studies of somatOvisceral reflexes (33). He and his colleagues have been able to alrer the heart rare, blood pressure, and renal and adrenal sympathetic nerve activity by applying mechanical pressure to the rat spine (34). In addition, it has been
111
discovered that stimulation of periarticular nociceprors causes a significant reflex activation of sympathetic neurons, whereas, in contrast, stimulation of nonnociceptive receptors has a minimal
influence on sympathetic activity (35). Unfortunately, the stimulation threshold required to cause nociceptor activity and subsequent symparhetic facilitation in the living human is unknown. In addition, the extent [Q which spinal dysfunction in patients mimics experimental animal lesions is unknown. Korr has recendy discussed some of the limitations of the segmental facilitation theory and points out the need for clinical outcome research that tests manipulative therapy as it is practiced (36).
Musculoskeletal Dysfunction and Visceral Disease Whether musculoskeletal dysfunction causes visceral disease appears ro depend on many facrors, such as the amount of nociceptive input from the musculoskeletal tissues, the previous threshold of the sympathetic neurons, in part determined by the central nervous system's ability ro reduce (or enhance) sympathetic activity, and the previous condition of the viscera. For this reason, musculoskeletal dysfunction is considered to be one of many potentiating factors that can lead to visceral dysfunction and disease. It is rhought that altered or impaired function of components of the musculoskeletal system either may cause or may be presympromatic signs of disease. There is, however, little more than anecdote or personal opinion ro support these ideas. Basic science information does exist to supPOrt the occurrence of somatovisceral and viscerosomatic reflexes (24-27, 31). This informarion does not, however, support a clinical utility for intervention. Although theory and clinical practice suggest that events affecting the musculoskeletal structures may influence visceral function and that disturbances of visceral function may be reflected as altered musculoskeletal func-
112 tion, the chiropractic profession has done nothing to adequately show the relationship between manipulative therapy and visceral disease. The hypothesis is, of course, that the musculoskeletal component may be treated with chiropractic procedures (adju tments and other modalities), altering the course of both the musculoskeletal and visceral disturbances, thereby allowing the physiologic process to return to optimal function .
Musculoskeletal ManHestations of VIsceral
DIsease
It has been suggested that the body wall manifestations of visceral disease are an integral part of the disease process, rather than just physical signs and symptoms (37). However, the definitive causative factors and the characrerisric response of the individual are still unknown. Early signs of most disease stares are manifested as symptoms and signs that are part of a common reaction pattern to injury or streSs. Pain in the somatic tissues is a frequent presenting symptom in acute conditions related to visceral dysfunction. PalpatOry cues of transient muscle hyperroniciry
and
irritation
or
subcutaneous
edema may be accompaniments of ill-defined subclinical states (31) . Moreover, subtle changes in tissue texture, joint position, and joint mobility identified by discerning palpatory ski lls appear to be latent manifestations of the somatic component of visceral disease (see box) . In a study (38) petformed on cardiac patients in an intensive carc unit, the following was noted
in the 3uronomic spinal reference site for the
involved viscus: Vasomotor reaction: increase in skin temperature Sudomotor reaction: increase in skin moisture Increase in muscle rone/contraction Skin texture changes: thickening Increased subcutaneous fluid In studies by Kelso (39) and Beal (40), it was noted that, as the visceral condition progresses, the omatic Stress pattern subsides, and the rypical visceral reflex pattern is seen. Therefore, the
>
Abnorma l Pa lpa to r y Findings Associa ted w ith the Application of Soft Tissue M a n ipula tion (7)
• Tenderness • Indurations
• Edema • Skin texture changes • Skin temperature chang•• • Muscl. hypertonicity • Joint hypermobility or hypomobility
chronic phase of reflex activity is characterized by trophic changes in the skin and subcutaneous ti sues, as well as by local muscle contraction. This typically results in a joint misalignment and decreased segmental mobility. It is not known, however, whether the continuation of reflex somatic dysfunction is related to the initial impact of the visceral disease, or whether it is a result of long-term segmental facilitation. In a blind study of 25 patients, Bea l (40) was able to differentiate patients with cardiac disease from those with gastrointestinal disease, with a reported accuracy of 76 0/0, using a compression test to examine for soft tissue texture changes and resistance to segmenta l motion. Similarly, Beal and Dvorak examined 50 patients in a physicianblind format and were able to identify characteristics specific for patients with cardiovascular, pulmonary, gastrointestinal, or musculo keletal diseases (41). The use of spinal manual therapy in the treatment of visceral conditions has been advocated on the hypothetical basis that ir is designed to reduce somatic dysfunction, to interrupt the viscerosomatic reflex arc, and ro influence the viscus through stimu lation of the somatoviscera l reflex. However, the effectiveness of manipulative procedures for the muscu loskeletal manifestations of organic disease has not been clearly established. There is a definite need for further data on the incidence of viscerosomatic reflexes and the relationship to manipulative therapy.
113
1 ChIroprIlC1lc l\ellex T~
Manual T1Ierapy and Somatoautonomlc
Renexes Manual therapies, and specifically chiropractic adjustments, are thought to disrupt harmful somatoautonomic reflexes by reducing the noxious input into the spinal cord. For example, a panell[
with
<1
strained posterior jOll1t capsule
that is accompal1led by reflex muscle spasm may have nociceptive bombardment of the spIIlal cord. If the nociceptive bombardment is of suffi-
muscular system as well as on the local and gen-
eral circulation of the hlood and lymph (43). The vari ..Hion~ of ma~sage movemenrs include emeurage,
petrissage,
roulemont,
tapotemant,
and friction. Effleurage, or stroking, is app lied over a large area, uSlllg broad contacts. It may be deep or very superficial, creating general relaxation as a superficial warming caused by a mild erythema . Petrissage involves the grasping of the skin and lifting it while applying a pinching action to the held tissue and a stroking or stretch-
cient strength and duration, it can cause segmen-
ing action to the tj~sue beneath. Rouiomont, or
tal facilimtion. If a manipulative procedure can reduce the
.kin rolling, lifts the skill away from fascial surfaces beneath; when adheSive areas are encountered, a pull is app lied to the skin to allow freer movement. Tapotemont is described as a tapping or vibratory action applied to the soft tissue in a rapid fashion, creating a stimu latory effect. fric-
strain on the joint capsule or reduce muscle
spasm, nociceprion from these tissues into the spinal cord may be ameliorated or reduced. At the
same rime, because mantla l techniques stimulate many different types of neuroreceptors, the result is a degradation of a negarive somar03utonomic
reflex.
SpecIfIc Teet._ ProcedIreI What follows is a brief description of some manual therapies used to some degree by chiropractic physicians and other health care providers. Although this IS nOt meant to be an "II-inclusive treatise on soft tissue and reflex Techniques, It is deSigned to present the concepts or foundations app1tcable to m
docs exclusion sigl1lfy ineffectiveness but rather oversight.
Massage Classical or traditional massage procedures form the baMs for many other procedures. Simply defined, massage consists of hand motions prac-
ticed on the surface of the body with a therapeutiC goal (42). A more clinical or practica l definirion is a rerm used
[0
tion
IS
done with a slow and deep circu lar
~troking
with the ball of the thumb to move the underlying tissue.
ffmmo Technique (Ischemic Compression) Raymond Nimmo was one of the first chiropractiCS
to incorporate the trigger point work of IIldi-
viduals such as Travell and Simon into chiropractic practice. He termed the procedure the ReceptorTOI1I1S Techlllqlle, to emph"size his theory that this is a reflex technique and nOt a form of mass~lge
therapy. Emphasis is placed on posture and muscular II1volvement, involvements that are pa lpated fo r poims, with each
as well as on the neurologic then may occur. The soft tissues tenderness, spasm, and trigger muscle exhibiting it unique and
characteristic pattern of referred pain (Figures 7- 1, 7-2, and 7-3). Nimmo technique uses deep pressure applied directly over the irri13ble leSIOn to produce an ischemic compression effect (44-46). Travell advocates the use of vapocoolant spray while the irritable tissue IS oelllg stretched, as well as the II1jection of an anriinflammatory medication
(procaine) into the trigger point (47) (Figure 7-4).
describe cerra in manipula-
tions of the soft tissues of the body; these manipulations are most effectively performed by the hands and are administered for the purpose of
Connective TIssue Massage
prouucing e(fecr\) on rhe nervous ,,)'~rcm anu rhe
connective ti!)sue on the hody .,urfnee. The patient
Ebner (48) defines connective tissue massage as a form of manipu lation carried out in the layers of
114
SUbluxation
The ArtIcuIr lesion
Rgare 7·1 Cross·sccriona l schema tic drawing showing fl at palpation of a taU[ band (b lack ring) and irs trigger paine Flat pa lpation is used for muscles that are access ibl e o nl y fro m one direction, such as the infraspinatus. A, Skin pushed to onc side to begin palpation. B, Fingertip slid across muscle fibers to feel the cord like texture of the taut ba nd rolling beneat h it. C, Skin pus hed to other side at comp letion o f snapping pa lpatio n. (From Travell l C. Simons DC. Myofacial pain and dysfunction: The trigger point manlla/. Baltimore: William s & Wi/kiltS.)
c R111'17-2 C ross-secti onal schema tic d raw ing show ing pincer palpation of a taut band (black ring) at a trigger poinr. Pincer palpatio n is used for muscles that can be picked up between the digits, such as the sternocl eid omasto id, pectoralis major a nd lacissimus dorsi. A, Muscle fibers surround ed by the rhumb and fingers in a pincer grip. B, H a rdn ess of rhe taut band felt clearly as it is rolled between the d igits. The c hange in the a ngle of the dista l ph a langes produces a rocki ng motion that improves discri mi natio n of fine deta il. C, Edge of th e [aut band sharply defined, as it escapes from between the fin ge rtips, o ften with a local twitch res ponse.
7 ClIII'OIII'1CtIc lllllex TIICIInkIIIa
115
A ~ 7·8 Referred pain patterns (shows essential zones and stippling shows (he spillover areas) with location of corresponding trigger points (Xs) in the right sternocleidomastoid muscle. A, The sternal (superficial) division. B. The clavicular (deep) di vision. (From Travell lG, Simons DC. Myofascial pain and dysfunction: The trigger point manual. Baltimore: Williams & \Vilkim.)
is usually treated in the sitting position with a long or short stroking action carried our using the
econd and third fingertips of the relaxed hand to draw the skin slack (Figure 7-5) . The effects include a marked hyperemia and sweat gland stimulation.
Bruising
sometimes
occurs
after
treatment, depending on the degree of capillary fragility. This proced ure is purported to cause a release of a histaminelike substance that acts on the autonomic nervous system.
Chapman's (Neuro) lNmphallc Renexes Frank Chapman, an osteopath, was of the opinion that body wall reflexes are clinically useful for diagnosis, for influencing the motion of fluids (mostl y lymph), and for influencing visceral function through the nervous system. The surface changes of a Chapman's reflex are palpable, which are thought to be from changes found in the deep fascia such as gangliform contractions located at specific points and consistently associated with the same viscera . The amount of tenderness is an important consideration in differen -
tiating the gangliform contraction from subcutaneous fat globu les. After the surface locus has been contacted by the pad of the middle finger, a firm, gende contact is maintained and a rotary
motion imparted to the finger through the arm and hand so as to express the fluid content of the locus into the surrounding tissues. The actual application of attention to a given reflex is expressed in terms of seconds, but in practice it is
actually determined by a response to palpation. The actual time of treatment may vary from 20 seconds to 2 minutes or more (1).
BeIii... tr. (NeIro) V8scuIar Renaxes Terrence Bennett, a chiropractor, described reflex
points mainly on the skull but also on other body parts. He believed that an irritable reflex reflected the vascular condition of organs and other structures. Bennen developed the Neurovascular Dynamics Technique, which he proposed alters and restOres autonomic homeostasis. Treatment
involves the stretch of a long muscle [0 initiate a palpable arteriole pulse at a specific location. A
116
f1g1r17~ Trigger poine therapy (Q pelvic muscles. (From Ca"tu RT, Grodi" AI MyofasClal mampulatlon: Theory and clmicaf application. Maryla"d: Aspen, 1992.)
7 CIIIropracUc Rellex TII&hnIque8 light but steady ptessute is applied fat at least 1 minute (49, 50).
117
Cervical section
Acupressure Point Stimulation Acuptessure is a method of massage ro acupunctute points for the usual purpose of analgesia. Much has been wrinen on the clinical aspects of acupuncture, acupressure, and meridian therapy. ACupul1crure points are organized along meridians that have no known neurologic or vascular
panern. There appeats to be a measurable change in electrical potential in irtitable points, and they can be tteated by electtical stimulation, needle application, or manual pressure. Theoretically, blockage at othet dysfunction in the meridian causes a departure from health (7). Acuptessure can be applied with the fingertip with a magnitude sufficient ro cause pain. A possible explanation for the mechanism of pa in relief is, therefore, in the modulation of endorphin levels (51).
Muscle Energy Techniques Described by Fted Mitchell, this technique uses specific muscle activity to tesrore physiologic joint function. Active muscle contractions are
Figure 7.-5 The approximate direction and position of CfM strokes applied to basic, thoracic, and cervical sections. (Modified from Grieve Gp, ed. Modem Manual Therapy of the Vertebral Column. New York: Churchill Livingstone, 1986, p. 831, Figure 80.4.)
used at varying intensities from a precisely con-
trolled position in a specific direction against a distinctly executed counterforce. The patient is therefore active in the corrective process, which encourages the patient ro assume responsibility for self-care (51).
Logan Basic Basic technique was developed by Hugh B. Logan, who noted that the body must have normal structure to have normal function. In part,
this system takes inro account the effects of gtavity on the spine and its related structure. Logan hypothesized that the body of the lowest freely movable vertebra will rotate toward the low side of the sacrum (or the vertebra on which it tests), that is, that the body of that vette bra totates toward the side of least support. This is usually the low side of the sacrum. Logan believed that the sacrum was the biomechanical keystone of the body, because it supported the spine and also
allowed fat locomotion, and he believed that the spine would respond to changes in the sacrum. Thus, returning the sacrum to notmal relations with its articulating bones was essenr.ia1 to reduce spinal involvements. He thought this required little force to accomplish with specific types of contacts on and around the sacrum. Pressure is applied steadily to these contacts, with no ttue thrust delivered. One of the most common contacts involves approximately 2 to 10 ounces of pressure applied to the junction of the sacrotuberOtiS and &acrospinalis ligaments. Somatic changes in muscle tone, skin and core body temperature, respiration, and perspiration are not uncommon (52,53).
Spondylotllerapy Spondylotherapy is defined by Janse (54) as a method of tteating visceral disease through the stimulation of the involved sluggish reflexes by
118 the application of a mechanical or electrical force in properly judged fashion on rhe vertebra overlying the reflex center. The principle of interrupted percussion or vibration is usually employed. A light, continuous contact held beyond the initial stimulation time is thought to produce relaxation
throush sedation, whereas a heavy conrinuous contact eventually produces inhibition because of actual nerve blockage. Continuous percussion, concussion, or vibration eventually inhibits
because of fatiguing of the reflexes involved. Interrupted
moderate
percussion,
concussion,
vibration, or sinusoidalization prolongs the initia l stimulation of the reflexes involved .
ActIvator Methods Activator technique was developed by chiropractors w. C. Lee and Arlan W. Fuhr. Their emphasis from the start was on body mechanics and how to use light-force contacts to effect changes in those mechanics. The roots for the principles of activator methods can be traced to Logan. The analysis is centered around isolation testing,
which involves specific patient positioning, causing changes in leg length. Therefore, the prone leg check is the main evaluative tool used to identify specific segmenta l levels of joint dysfunction. Activator methods is known for its use of a handheld mechanical adj usting device called the Activator Adjusting Instrument (AAI), or Activator for short. The device is purported to produce a controlled and repeatable percussion force whe n it is triggered, and thus it ind uces a known force into the human body. It was developed to simulate a light-force thumb thrust (Logan Basic). This device has now begun to be examined with more rigorous research. In addition, there have been efforts to place it into a basic science model. Evidence exists to support the idea that the Activator thrust moves a spinal joint; however, there
is seldom
an
audible release or cavitation
response. Mechanoreceptor coactivation is theo-
ri zed as the mechanism for the observed effects (8).
8acr1lOCCIpI'taI TacImIque (SOl) Major Bertrand Dejarnette is the developer of the sacrooccipiral technique (SOT) system, which is purported to restore normal functioning to the central and peripheral nervous systems through the effects on the meninges by the mechanical
relationship between rhe cranium and pelvis. Padded wedges called "blocks" are placed between the patient'S pelvis and the table, with the patient in either the prone or supine position,
and gtavity is allowed to affect the relationship of the innominates to the sacrum . Occipital fibers that apparently tepresent texture changes in the upper trapezius muscles are evaluated and treated. Cranial manipulative procedures based on the work of osteopaths Sutherland and Upledger are also used . Evaluation is based on posrucal assessment as well as on some reflex
phenomenon (the arm fossa test, dollar sign, and heel tensions). The evaluative process places the patient in one of three categories, and blocks then are placed under the pelvis in a specific manner, with the patient in either the prone or supine position. Category I involves slipping of the synovial part of the sacroiliac joint, placing a stress
into the dura and primary respiratory cycle. Category 2 is the most common distortion parrern and involves a slip in the weight-bearing, hyaline portion of the sacroiliac joint caused by trauma. Category 3 usuaUy involves a lumbar disc or vertebral subluxation and is characterized by sciatica, anta lgia, and possible neurologic signs (55 ).
Manual Crllllal Therapy Manual cranial therapy, directed to the intrinsic joints of the skull, has been described by Cottam (56) in chiropractic and Vrederoogd and Upledger (57) in osteopathic literature. It is reasoned that the sutures of the sku ll are intricately fashioned for maintenance of motion. The sutures are pre-
sent throughout life, have consistent areas of bevel edge, and consistently separate when the skull is "exploded" (filled with beans and immersed in water) (58). It is further hypothesized that the skull has normal mobility during
7 CIiroprICtlc Rellex TechnIquea healrh and will show resrrictlons in response ro trauma or disease. The perception of a widening
and narrowing of rhe skull of relarively low amplitude can be made in association with respirarion. This response is rheomed to be rhe mechanism of cerebrospinal fluid flow. Evaluarion consists of observation and palparion of rhe skull for symmetry, followed by surural palparion for widening,
narrowing, and
tenderness.
Sacral
movements are also evaluated. Treatment involves various direct and indirect manual proce-
dures as well as molding and disengagement procedures. All involve a relarively lighr force or susrained pressure applied in conjunction with rhe primary respiratory mechanism.
Distraction Techniques Mechanical assisrance ro manual therapy procedures is produced by an adjusring rable rhar has a movable pelvic secrion. Cox developed rhis type of rable in the early 1970s, blending osreopathic and chiropractic principles based on the early McManis rable (59-62). The mobile pelvic piece uses a long lever acrion ro place rhe lumbar spine rhrough rhe normal individual ranges of morion
119
lordotic position, reduces pressure in the motion segment, as well as reducing venous engorgement
in the spinal veins. Both of these characreristics would be desirable in cases of low-back pain of mechanical origin. Data supporting these claims have not been published, and the theory remains unsubstantiated.
Markey has also described a distraction technique using flex;onldistracrion (64). His use of the Lloyd distraction table allows the possibility of both flexion and extension posirions. An apparent contradiction exists between the theories of Cox and Markey and those of Eckard. One advocares flexionldistraction; the other, extension/distraction. The procedures are used for the same condirions but are based on different hypotheses abour rhe mechanisms involving traction forces on the three-joint complex of the spinal motion segment.
In each procedure, however, rhe docror places a specific contact on a spinous process (short lever) and applies headward pressure, while the distal end of the pelvic section is moved roward rhe floor (long lever). Therefore, each technique uses a specific short-lever contact that is mechani~
of nexion, extension, lateral bending, and rota-
cally assisted by a long lever (65). Schneider notes
tion, as well as rhe combined movement of circumduction. Cox has developed a protocol for rhe use of flexionldistracrion in the rrearment of lumbar disc protrusion, spondylolisthesis, facer
cal compression of nerve roots by extruded disc material is nor rhe only source of low-back pain, nor irs reducrion the sole relief of such pain. He
syndrome, subluxation, and scoliotic curves of a
nonsurgical nature. His contention is that the axial traction of rhe vertebral motion segmenr
while in flexion creares a force rhar rends ro reduce extrusion of dISC marerial (59). Eckard bas also developed a mechanized distraction table that differs from rhe Cox rable in
that even with an acute disc herniation, mechanj~
identifies other mechanisms such as chemical irritation of the nerve roots, facet synovitis, and
intrinsic lumbar muscles (especially the multifidus) as sources of low-back pain thar mayor may nor accompany disc hern;ation (66). Schneider discusses the different effects of the two tracrion methods on rhe possible mechanisms.
that the axial traction of the Illotion segment is
done in slighr extension. The drop-away abdominal piece maintains the neutral or lordotic pos-
Conclusions
ture and is thoughr ro mechanically separate the facer joints during ttaction, thereby requiring
Evidence supports rhe existence of irritable lesions in soft tissues, including muscles, liga-
much less force than a conventional manipulative
ments, and fascia. These lesions can produce nox-
procedure (63). Eckard further contends that the exrended posirion, which IS actually the normal
ious effects in various parrs of rhe body, remote from themselves, and cause pain or dysfunction.
120
SUbluxalloo The ArtIcular l.eIIon
cu.
Specific techniques have been theorized and designed to affect and eliminate the Irritable lesion uSing sofr tissue and reflex mechanisms. Various forms of soft tissue and reflex therapy have been described. Although many of these procedures have some overlap with rhe location of treated areas, there has been no acceptance or indication (har they could be rreated in the same fashIon. The one thing that all of these pathologic reflexes seem to have In common is that they are a ll orga nismic responses to various types and degrees of tissue injury, thar is, physical trauma, infection, degeneration, and chemica l irritation ( I). Rational use of manual stimu lation of the skin and soft tissues of the body places the physiologic starus of the ski n at an optimum, invigorates rhe circularion of rhe blood and lymph, and alerrs rhe central and peripheral nervous system (72). Little evidence exists to validate the greater efficacy of anyone therapy for a specific dysfunction. Although a few case reporrs have been p ublished, no comparative studies have been conducted. Is It necessary to have validIty or even an u ndersranding of somerhing before it is used clinically? If a procedure IS observed ro have a clinica l effect, s hould ir not be used? Full understanding a nd abso lure validarion may not be attainable with the technology a nd knowledge of today. C linica l success may carry weight for a rime, but nor as a ge neral rule. The notion of clinical success is relarive and fragile. It is necessary rhat practitioners further substantiate the principles and procedures of clinical practice (73).
18. Wolfson H. Srurlics on effcct rhysic.lltherapeutll.: procedures un funcrton and ~tructurc. JA.\1A 19.,1; 96:2020. 19. Currier FB. Studies on physloioS)' of capillam-s: Re;1I.:uon of human skin 1.:.lpiJiaries ro drugs and other stimuli. Am J
Reflll'8llC8S
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I. ChaltOw L. Soft - Il!io~uC manipulation. Roche.Mcr. Vermom: Ht.''''I0~ Arr'i Press, 1988:9. 2. V:mncr<.,on JF, [\ln10U1 RI. Spenticlt)' .lIld the la\\ of far.:ll -
6. GriCH' ( ,I'. Common \·ertehra! Jomt prohlems.lnd Edinburgh: Churchill-LIVingstone 1988 . ., ~teeker Wc. Soft tl"!>UC and nonfon;e tt'r.:hniqllell. In: 1-I.lklcman S. ed. Principle:, ilnd Jlraltice of lhlropral.:llc. Easl t'nrw.1Ik. Connenil.:lIt: AppletOn and l.ange. 1992:
120. 8. Osterhauer PJ. Fuhr A\'(I. The current .!.I.nus of acnV.lIor methodl> chlropraltic [C\:hnique. thear)" Jno tr:ul1Ing.
ChoroTech 1991,3( 11,19-2.1. 9. Bergmann TF, I}eu:rson OH, Lawrence DJ. ChiropractK Technique. New York: Churchill LIVingstone, 1993:34-5. 10. Akeson WH, Amlel D, Woo SLY. Cartilage and ligament: physiology and repair processes. In: Nicholas JA, Hershman EB, eds. The lower extn:nury and Splnt' In sports medldnc. St. LoUIS! Mosby, 1986:3-41. II. Akeson \VH. Amici 0, Mechanic Gl., \'(.'00 S. Harwood Fl. Hamer ML. Collagen cross linking alleranons In jOint Conrr:lCfures: changt."S in reducible cross Imks 10 perianicular connective tissue colJ:tgen 'lfter 9 weeks of Immobl117a[ioll. Connl'C[ Tissue Res J 977; 5:5. 12. Burger AA. [xperllnenral neuromu')(.:ular model~ uf spmal manual techniques. Manual ~Ied 1983; 1: 10. 13. Garren W, TIdball J. Myotendtnous juncrion: structure, funcrion, .lnd failure. In: Woo SI Y. BUlkwalrcr JA. cds. Inlury ano repair of the musculoskeletal soft rissues. Park Ridge, Illinois: Americ,1O Academy of OrthopaedIC Sur-
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ennal dlagnow;. ~l;lIlu.J1 Med 1991; 6: 136-9. M)·ofa~dal nl.1mpulatton theor)" and dinu:al application. Galthl'f\hurg, M.Jryi.lnd: Aspen.
1992;.1.1 -". 17. Wakim K(i. The "ftelrs of ma~sagt' on the I.:trI.:uiatinn In normal and paralp.ed extremities. Arch Phys ~Ied 1949;
30,13.1.
ClUff) Ttxh 1993; .5{lJ:5J-J.5.
4. Haldeman S. Spm::" manipulative therap), .1nd SPOrtS mcd· iUlIe. elm Sport.. .\It·d 1986; .5{lJ:2-:-7-29J. S. Cireenman P. PfIIKlpal ... of manual medlr.:me. Baltimore: William!> & Wilkins, 1989.
Physiol 1021, 6U28--47. (,M, Roth (.!\1. er al. Cutaneous remperarure ot
~1artln
the extrell1uiel> of norm.1i l>uh]e4.:tl> .lIld pallents with rheumatcud arthritIS. Arch Php Mcd Rehahd 1946: 2":"":66., . 21. CuthOertSon DP. Effect of massage on metJh()li~m: a ~ur
J
~Icd 1931,2,200-13. ~hnelder lC. Havcns Changes m the wntems of
vey. GIa'gow
22. V~n()us form" of r.:hiropranlr.: (C(:hmque.
different lengths. Trans
16. C:tntu RI, Grodin AJ.
ltation 111 rhe ncrvous system. ACA J Chim 1973; 7(S):
17-25.
:It
Orthop Res Soc 1985; 10,6. IS. Janda V. MuS(.·le spasm: A propo'>Cd procedure for differ-
loc.
haemoglohln and rcd corpuscles in the hlood of men .It high a/tirudes. Ant J Pllr~lol 191J; 36:360. 23. Homewood AE. Neurod}'nami<.:~ of [he \o't·rtehral mhlu\:arion. 51. Perersburg. Flurida: Valkyrie Press. 19-7. 24. Korr 1M, cd. The neurohiologic mechani"ms In mJllIpu/aII\'C thcr.lp)'. i cw York: Plenum. 19~~L
7
CliI'OjIi'1C1Ic llellex TIICIInIIpIa
25. S:uo A. The \omalosympathrtlc reflexes: their phYSiOlogic
and dmu.:.11 significance. In: Goldstein M. ed. The research ~lalUS of ~ptnal mampulatH'c Ihcrap)", WashmglOn. DC: U.S. Governmcni Priming Offif.:e. 1975.
26. Leach RA. Chaplcr 11 . In: The chlropracflc theones. 2nd ed. 8ahUllnrc: Wllhams & Wilkins. 1986. 27. ~;HO A. Spll131 reflex physlolog)', Chapler In: Iialdeman S, cd. Principles and practice of chiropractic. 2nd cd. East Norwalk, ConnecncUI: Appleton & bnge, 1992. 28. HoagJM. Cole "\f!V, Bradford SG. cds. Osteopathic medl' cine. New York: McGraw-lilli, 1969:89. 29. liebenson C. ActIVe muscular relaxation techniques. Part I. BaSIC pnnclpit's and methods. J Mampulative" Physiol The< 1989; 12(6):446-.54. 30. Bogduk N, Twomey LT. Clinical an:Horny of the lumbar spine. 2nd ed. Melbourne: Churchill Llvmgstone, 1991:152. 31. Beal MC ViS(erosomauc reflexe5: A review. J Am Osteopath A>soc 1985: 85( 12):53-<>8. 32. Van Buskirk RL. Nociceptive reflexes and the somatic dysfunction: A model. J Am O$tcopath Assoc 1990; 90(9):792-809 . .13. SatO A. The reflex effects of spmal somatic nerve stimula· tlon on visceral function. Proceedmgs o( the sclenufic symposium of the World Chiropractic Congress. Toronto. Canada; May 4-.S, 1991. 34. Saw A, Swelbon RS. Sympathetic nen'ous system response to mechanical stress of the spmal column In r;us. J MampulJtlve Physull Thcr 1984; 7(3): 141-7. 35. 5,1[0 Y, Sch;uble IIG, Schmidt RF. Reactions o( cardiac postganglioOll.: ~ympathetic neurons to movements of nor· mal and mflammed knee 10m{s. J Auton Ncrv Sysr 1985; 1l:1-1l. 36. Korr 1~1. Osteopathic rcsearl.:h: Tht' nceded par~ldlgm shih. J Am OHeoparh Assoc 1991; 91 (2): 156-7 1. 37. Gramger fiG. The somatic component in Visceral disease. In: Academy of Applit'd Osteopathy 1958 Yearbook. Newark. OhiO: American Academy o( OMeopathy, 1958. 38. L1rson NJ. Summary of Slfe and occurrem.:e of parasplnal soft tissue Lhang~!I 01 pancms III the mtenslve care umt. JAm OstcopJlh A"DC 1976: 75:840-2. 39. Kelso AF. A double blind dlnKal siudy of ustcopathll.: nnJlng~ In hosplrJI patients. J Am Osteopath Assoc 1971; 70:170-92. 40. neal Me. Palpatory finding!. for somanc dysfunction 10 rauents wllh cardiovascular disease. J Am Osteopath Ihsex 1983; fl2:822-.lI. 41. Beal Me. Dvorak J. Palpator~' examinauon of ,he spme: .1 comparilOon o( the re~uhs. o( two methods and their relationship to vlscerolll.hscJse. Manual Mcd 1984: 1:25-3l. 41. Iloll:osh J~1. (JJ~~lcal massage. In: BasmaJi:m JV. cd. MampulJllon, tr;u.;tion :md massage . .3rd ed. Baltimore: Williams & Wilkins, 1985:26.1.
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43. Beard G. Wood EC. Massage: PrinCiples and tl'1.·luuqucs. I'hiladclphia: WB Saunders. 1964. 44. Nunmo RL. Thc receptor and tonus control method defined. Receptor. sclf.puhllshed (undated) I: 1-4. 45. Schneider MJ, Cohen JII. Nimmo receptor tonu,> techmque: A chiropracric approach to trigger point therapy, In: Swecrc JJ. ed. Chiropractic (amily pracncc. Ganhers· burg. Maryland: Aspen Publishers, 1992;3-3: 1-18. 46. Cohen JI-I, Schnclder MJ . ReceptONOnus technique: An overvIew. Chiro Tech 1990; 2( 1): 13-6. 47. Travell JG, Simons DG. M)'o(ascial palO and dysfunction: The trigger point manual. Bailimore: Williams & Wilkins, 1983. 48. Ebner M. Connccm'e (issue massage. PhysiOther:tpy 1978; 64(7):208-10. 49. Bennett TJ. DynamiCs of corrcctlon of abnormal function. Sierra Madres, California: RalphJ. Manm, 1977. 50. Nelson WA. Diabttes mellirus: Two case reports. Chlro Tt:Ch 1989; 1(2):37-40. 51. Basmajian JV. Nyberg R. eds. Rarional manual therapies. Baltimore: Williams & WilklOs. 1993:21-47. 52, Logan HB. Textbook o( Logan hasic methods, St. Louis, 1950. B. Lawson DA. Logan baSIC technique: short and long lever, mechanical J~sisted. In: Proceeding.';. 61h Annual CORE, Monterey, 1991 :336-9. H. To(rness IN. Researching the chiropractIc adJustment. Cumberland. \'('\sconsm: stU-published. 1961. 55. Jent'S6 ~IE, Tofrness IN. Vahdanon of the Toftness/Jeness s),stem 10 chlropracnc. Dig Chlro Econ 1981; 24(2}:22-6. 56. Gemmell HG, Heng 8J. Correction o( sacrOiliac fixation by a low (orce sust:lIned prC'isurc method. Am Chlro 1987: (Nov):22-<>. 57. Ilawkmson EJ, Snyder 8J, Sanders CE. Evaluanon of the Ton-ness system o( chlropr,lcrtc adJus[1ng (or the relid of a{lIte pam o( musculoskeletal ong1l1. Chlro Tech 1992; 4(21:57-<>0. 58. Van Rumpt R. Directional nun·force technique. In: K(our)' PW. et!. CalOloglle of chiropractic te~hll1ql1es. 59. lanse JJ. Pnnciples and practice of chiropractic. l.ombard, Illinois: National College of Chiropractic. 1947. 60. Dejarnette MB. Sacro-«cipual technique. Nebraika (Ity, Nehraska: Malor Bertrand DcJarnene. 1984. 61. Cottam C. Cranl,ll and (aclal aJlustll1g. Sdf·puhlishcd. Los Angeles, 1987. 62. Uplcdgcr JE. Vredervoogd JO. Craniosacral therapy. Chicago: Eastland Press, 198.1. 63. Greenman PE. Pr11lciples of manual medicine. Baltimore: Willtams & Wilkins. 1989. 64. COX JM. ~ l echJnism. diagnosl~ and treatment 01 low baLk pam. 5th ed. Baltimore: Williams & Wilkms. 1990. 65. COX JM. Chiropractic mall1puiatlon 10 sciatica: ~taflStical data on the diagnosis, treatment and response of r'6 con· secum-e cases. J Mall1pulauve Ph)'slo\ Ther 1984; 7( I): I-II.
122 66. Lawrence I, Macrioni S. A flu o roscopic study of lumbar spine biomechanics during passive motion in (he prone position. Anglo·European College of Chiropractic doc·
roral thesis, November 1987. 67. Dcutro CL, Meeker we, Menke JM, Keene K. The effi· caey of nexioo-traction manipulation and inverted graviry traction for treatment of idiopathic low back pain. Transactions of the Pacific Consorrium for Chiropractic Research, First Annual Conference on Research and Education, june 1986. Sunnyvale, California: Palmer College of Chiropractic West. 68. Eckard L. Literature packet and training manua l fo r use with the Leander table. Leander Research, 12300 Sidney Road, POrt Orchard, Washington.
69. Markey LP. Markey distraction rccnnique: new prorocol for doctor's and paticm's safery: A pragmatic approach) parr 1. Dig Chiro Econ I 985;1uVAug:66-9. 70. Bergmann TF. Manual forcl!:: Mechanically assistcd articular chiropractic technique lIsing long andlor short level comacts: a literature review. J Manipulative Physiol Ther 1993; 16(1),33-<>. 7 J. Schneider MJ . The traction methods of Cox and Leander: The neglected role of the multifidus muscle in low back pain. J Chiro Tech 1991; 3(3), 109- 15. 72. Wakim KG. Physiologic effects of massage. In: Basmajian JV, ed. Manipulation, tracrion and massage. 3rd ed. Baltimore: Williams & Wilkins, 1985:256. 73. Zucker A. Chapman's reflexes: Medicine or metaphysics? JAm Osteoparh Assoc 1993; 93(3),346-52.
The Nonm Keywords
ulable Subluxation
Hypermobility, instability, nonmanipulative subluxation
After reading this chapter you should be able to answer the following questions:
Question #1
Are there any contra indications to manipulation noted on these radiogra phs?
QuatJon #2
What procedural error did the practitioner make when taking this x-ray series?
124 Some think that hypermobility is " ... a dis-
T
tinct category along a continuum from normal
he first problem confronting the clinician in the evaluation of a nonmanipulable subluxation is consistency of terminology; the second problem is recognizing the associated clinical and radiologic signs. A nonmanipulable subluxation is a vertebral motion segment with radiologic or clinical features indicating that an adjustive force or osseous manipulation to this motion segment
would be harmful or dangerous and is therefore contraindicated. Although it is well recognized that many pathologic processes affecting the skeletal system, such as malignant tumors and infections, are absolute contra indications to manipulation of the effected area, this chapter focuses on those conditions that may result in hypermobility, instability, or osseous fusion of the
joint motion to pathological movement" (5). Chiropractic principles emphasize the importance of manipulating those motion segments that are fixed or hypomobile, with the goal of restOring normal motion (7,8), while avoiding motion segments that are already hypermobile or unstable (8 ,9) . With this goal in mind, how ate nonmanipulable subluxations recognized? Excessive intersegmental motion to the point where damage to the spinal cord or nerve roOtS becomes a potential hazard has several causes. These include acute trauma, repetitive microtraumas, congenital anomalies, both degenerative and
inflammatory arthropathies, surgical fusions and laminectomies, and compensatory phenomena
vertebral motion segment.
caused by loss of motion in adjacent segments (6,10-12).
Definitions of Instability and Hypermobility 01 the Cervical Spine
Clinical Manifestations of Hypermobility and Instability in the Cervical Spine
Clinical instability of the spine is defined as:
Segmental hypermobility in children may simulate the symptOms of chronic rheumatic disease, making it difficult to properly diagnose (5). Adult patients may complain of a variety of symptoms that seem to be slowly progressive, building over a period of years. The complaints include recurrent episodes of neck pain with or without muscle spasm, which is often described as "dull" or "aching"(5). The pain is either unilateral or bilateral, more commonly located in the area of C5-C6. There may be associated crepitus in the neck at the end ranges of motion, and the patient often complains of "tight, tired, stressed" feeling throughout the neck. Headaches may be associated (5). These clinical features are very nonspecific and alone would not necessarily make the clinician think of excessive segmental motion. Some authors claim that cervical instability (they do not differentiate hypermobility from instability) is related to loss of the lordosis (11 ). This finding alone, howcve~ is insignificant because many factors may produce loss of cervical lordosis, including the fact that it can be tOtally normal
Loss of the ability of the spine under physiologic
loads
(0
maintain relationships between vercebrae
in such a way that there is neither damage nor subsequent irritation (0 the spinal cord or nerve roots, and in addition, there is no development of incapacitating deformities or pain due to structural
changes (I). The terms instability and hypennobility are often confused both in practice and in the literature (25). It is important to try to differentiare berween these rwo conditions as they relate to the spine because the clinical significance and thus the therapeutic approaches ro the these rwo entities are nOt the same. Segmetttai hypermobility has been defined as: The mobility of a given motion unit which is excessive but not so extreme as to be life-threatening or require surgery (5).
Several authors claim that hypermobility may be a precursor to the development of instability at a later date if not properly managed (2,3,6).
125
8 TIle NaI............ SIMIXIIIon and asymptomatic. Additional physical examination findings include hypertrophy of the anterior neck and anterior chest musculature with protraction of the scapula and elevation of the clavicles. Active and passive ranges of motion are usu-
ally limited. Segmental palpation may show hypermobility of the involved segments with restrictions above and below the affected levels (5,11). Patients with segmental hypermobility are more likely to exhibit symptomatic degenerative joint disease (DJD) than those patients with DJD with no hypermobility (5). Actual segmental instability may demonstrate similar clinical findings to hypermobility, with the additional potential for neurologic signs and symptoms and progressive deterioration (6,10).
Radiographic EvaluaUon of Hypermobility and Instability In the Cervical Spine The definitive diagnosis of intersegmental hypermobility and instability has relied on the evaluation of kinematic radiographic studies of the cervical spine in the sagittal plane (5,6,10,12-15). The chiropractic profession has used these radiographs for decades to assess global range of motion and intersegmental range of motion and ro artempt to objectify the effects of manipulation (15,16). Neutral, flexion, and extension lateral radiographs are taken with various methods devised for assessing normal and abnormal motion (6,7,12,14-17). These studies have traditionally been performed actively by the patient. Dvorak et al. (12), however, emphasize the value of obtaining functional radiographic srudies of the cervical spine both actively and passively. They claim that many more hyper mobile segments are discovered on the passive kinematic
studies as compared with evaluating active flexion/extension radiographs only. The radiographs can be analyzed by hand, using templating procedures (see Chapter 5) or with the aid of computer digitizing. Other researchers are investigating the efficacy of digital
video fluoroscopy
CO
assess the entire interseg-
mental motion (13,14). The various assessment methods emphasize measuring translation in the sagirtal plane, analyzing intervertebral angles, and calculating the axes of rotation (6,17,18). There is a consensus that the quantity of normal intersegmental motion varies considerably between the various motion segments of the cer-
vical spine and that this intersegmental motion decreases with increasing age (6,13,14,16). Some authors state that the "amount" of motion at an intervertebral segment is not as important as the
"path" of the motion (13). Although computer digitization and digital video fluoroscopy are important research tools, it is currently impractical to expect clinicians to be evaluating kinematic studies of the neck using these procedures. Henderson and Dormon (6) developed a method of assessing intersegmental motion in the sagittal plane that can easily be applied to flexion and extension radiographs in clinical practice. Normal and abnormal intetsegmental motion is defined in terms of a percentage of the sagirtal body diameter (SBD). Absolute hypermobility is defined as intersegmental motion that falls between 61 % and 72% of the sagittal body diameter,
whereas
instability
is
any
motion
exceeding 72% of the SBD. This is one of the only studies to attempt to objectively differentiate hypermobility from instability. It is useful as a guideline as long as the clinician keeps in mind the range of normal between subjects and within subjects. Other studies have defined instability as a translation in the sagirtal plane of one vertebra on another in excess of 3.5 mm during flexion to extension (18). This again is a useful and simple method of evaluation of excessive joint motion. Figure 8-1 demonstrates neutral and flexion and extension lateral radiographs in a patient with an
anterolisthesis of C3 on the neutral film along with facet arthrosis between C2 and C3. Notice that the anterolisthesis increased during flexion and completely reduced during extension, giving an overall excursion of approximately 4 mm. This figure is consistent with a diagnosis of intersegmental instability, and this motion segment should not be manipulated.
126
FIgIre 8-1
The slight anrerolisrhesis of C4 noted on the neutral radiograph the sagittal plane during flexion and extension.
Causes of CerVical Spine Hypermobility and instability Acute ll'IIIna Figure 8-2 represents the flexion and extension lateral radiographs of a teenage girl who fell OntO her head while doing handstands at school. She complained of neck pain and stiffness immediately after the incident. The flexion-extension radiographs of the young woman in Figure 8-2 demonstrate several of the classic signs of posttraumatic instability caused by ligamentous and discal injury at C4-S. There is an acute kyphotic angulation berween C4 and CS w ith an antero listhesis of C4,
dcmOnSrf3(CS
excessive translation in
fanning of the spinous processes, gapping and overriding of the articular facets, and a loss of disc height at this level. The findings do not completely reduce on the extension film and would have been evident on the neutral latera l radiograp h. The dangerous error made by the clinician responsible for this radiographic series was to have taken flexion-extension films in the first place, because of the histOry of recent trauma. In cases of acute cervical trauma, the neurra) lateral radiograph must be taken first and scrutinized thoroughly for any signs of instability and ligamentous damage before subjecting the patient to motion srudies ( IO,12,19). If any signs of
instabiliry are noted, f1 ex ion ~exten s ion radiographs, as well as manipulation, 3rc conrraindi-
127 a displaced ve rtebra, or hyperextensionlhyperflexion dislocations that spontaneously reduce on recoil of the neck (10, 19 ). In such cases, ca reful analysis of the neutral lateral radiograph ma y show the wa rning signs of prevertebral soft tissue swelling and displacement of the prevertebral soft tissue stripe. An upright neutral lateral radiograph must be taken because subtle signs of posttraumatic instabiliry may not be visible on supine cross-table lateral radiographs (19). This discussion focused on soft tissue injuries of the cervical spine associated with acute trauma. The myriad of fractures and fracture/dislocations of the cervical spine that also may be unstable are not covered, and the reader is referred to standard skeletal radio logic texts for this information. It must be noted that chiropractors do not manipulate new or recent fractures.
- . . &-1 CIIII'. For legend see opposite page.
cated . The patient should be placed carefull y into a cervical collar a nd taken to the hospital. Halo bracing and surgical fusion are the appropriate treatments for acme traumatic instability.
In addition to these signs, prevertebral swell ing, displacement of the prevertebral fat stripe, and an increase in the ADI (atlantodental interva l) may be noted in patients wi th acute
posttraumatic instabi liry (19). Late nt or occult posmaumatic instability of the cervica l spine is the physician's nightmare because the initial neutral lateral cervical radiograph is " normal. " Reasons for this include technica ll y inadequate radiograp hs; for example, perhaps the lower cervical spine is obscured by the shoulders, muscle spasm temporarily reducing
Look at the radiographs of the 60-year-old woman in Figure 8-3, A and 8-3, B. This patient complained of neck pain and stiffness after an automobile accident. Was her automobile accident responsible for the radiographic changes seen? This rype of question plagues clinicians daily and is one that usually has no definite answer. If you said that this patient has a dens fracture caused by her recent trauma, yo u are 100% wrong! There is definitely instabiliry of C1 on C2 as noted by the marked translation in the sagittal plane during fl exion and extension. Perhaps the accident ca used her to rupture her transverse ligament? Wrong again. Posttraumatic rupture o f the transverse ligament is very rare, and the patient is
more likely to fracture the dens than to rupture this ligament (19,20) . The clue on the lateral views lies in the shape o f the anterior tubercle of Cl. Rather than the classic "0" shape with a straight posterio r margin, this patient'S an te rior tubercle is rounded and hype rtrophied . This important radiographic sign indicates an anomaly of the upper cervical complex (20). You may have noticed that the dens was not visualized on the lateral view, and the open-mouth pro jection provides the evidence that the dens is absent (Figure
128
A.... 8-2
SUbluxation
The ArtIcular Lesion
Teenage fema le with neck pain and stiffness after fallin g
8-3, C). Other anomalies of the upper ce rvica l spine that may resu lt in instability include the os odontoideum and odontoid hypoplasia (20) . Flexion-extcn ion views are indicated when anoma lies are suggested to determine rhe presence or absence of insrability. Translation in the sagittal plane of more than 3.5 mOl ( 18) is considered unstable, and these patients shou ld be referred for surgical consu ltation.
Blocked Vertebrae Figure 8-4 depicts the classic congenita l blocked ve rtebra at C5-C6 with normal bone density,
ontO
her head during gymnastics class.
normal vertebral body height, wasp waist, and remnant disc. Congenita l blocked vertebrae are common anomalies whose clinical significance
relates to the effect that this fusion has on adjacent mobile segments and nOt to the fact that two segments are fused together (6,20) . Obviously chiropractors
do
not
attempt
[Q
manipulate
blocked vertebra. What must be remembered, however, is that blocked vertebrae, whether they are congenital or surgical (Figure 8-5), can result in increased motion and potential instability at
adjacent motion segments (6,20). The patient in Figure 8-4 has large osteophytes at the adjacent
129
B
A
c figIre 8-3 A and B, Eld erly woman with neck pain and stiffness after a road traffic accidem. In add itio n to rhe degenerarive disc disease of the lower cervica l spi ne, instability of C i on C2 is present. The al tered shape of the anterior tubercle of C I is the clue to the cause. C, Agenesis of rhe dens is the cause of the instabi lity of C I on C2. This was nor rhe result of the road traffic accidenr.
130
FIgII'e 8-4
SUbluxation The ArtIcular lesion
Classic congenital blocked vertebrae C5-6.
Rall'88-5 Surgically fused C5-7.
anterior body margins berween C6 and C7, indi caring probable instability at some time. Whether this motion segment or the upper cervical motion
segments are currently unstable cannot be determined on this neutral lateral film alone. Clinicians must be cognizant that the fused segments can cause adjacent hypermobiiiries or instabilit ies and must thoroughly eva luate these patients before manipu lation. Absence o f the T ra nsverse Ligament in Down Synd rome Down syndrome, or mongolism, is a common congen ital abnormality caused by trisomy of the 21st chromosome. The significance of this syndrome to chiropractors is that up to 20% of these people are born without a transverse ligament
and are therefore prone to instability of C i on C2. Every patient with Down syndrome must be eva luated for this potentially life-threatening condition by taking a flexion lateral radiograph before manipulation of the upper cervical spine to evaluate the AD I (20). A measurement of greater than 5 mm in the child or 3 mm in the adult is abnorma l (20,21).
Innammatory Arthropathies Now look at the flexion lateral fi lm in Figure 8-6, B. The neutral lateral radiograph (Figure 8-6, A) demonstrates mild degenerative disc disease in the mid and lower cervical spine (C7 is not included on the film). The ADI is within norma l limits. This is not the casc, however, on the
8 TIle NaI.I..III...... SUblllXItIon
131
fIIIre B-1 A, Neutral lateral radiograph of a middlc·aged woman with a long history of rheumatoid arthritis. 8, Spot flexion lateral upper cervical radiograph demonstrates an increased arlanrodenral interval consistent with ruprure of the transverse ligamem caused by rheumatoid arthritis.
flexion latera l film of the same patient! The ADI now measures 6 mm, well above the maximum normal value of 3 mOl. Note also the anterior displacement of the posterior spinal line, another indicator of Cl-2 instability. Without the flexion lateral view, the clinician would not have realized that this patient with a history of rheumatoid arthritis (RA) has ruptured her transverse ligament and now has a potentially life-threatening instability. Obviously manipulation is contraindicated in her upper cervical spine. Rheumatoid arthritis is notorious for affecting the upper cervical complex. Up to 40% of RA patients develop atlantoaxial subluxation in the course of their
disease (21). Other causes of instability wit h RA include erosion of the dens, posterior arch, and destruction of the alar ligaments (21). Although rheumatoid arthritis is the most common of the inflammatory arthropathies to cause rupture of the transverse ligament, it must be remembered that any of the inflammatory arthropathies, (or example, ankylosing spondylitis, psoriatic arthritis, Reiter's syndrome, systemic
lupus erythematosis, and juvenile rheumatoid arthritis, also can rupture this ligament, with
resultant instability (20,22). Ankylosing spondylitis, as its name implies, can lead to osseous spinal fusion. Spinal manipu-
132 ment of the uppet cetvical spine. Thete is also marked prevertebral swelling noted. Amazingly, he suffered no neurologic deficits but is now at high risk for a spinal cord injury. He should be immediately transported by ambulance to the hospital with his neck carefully immobilized. Flexion-extension radiographs are obviously con-
traindicated, as is spinal manipulation. DegeneraUveA~s
AtIIre 8-7 Severe ankylosing spondylitis of the cervical spine. The patient can suddenly move his neck
and he is thrilled! lative therapy is nOt of benefit once these segments have become fused. Howevet, as described under congenital and surgical blocked vertebrae, motion segments that are fused predispose nonfused segments to become hypermobile or unstable (6,20). Figure 8-7 depicts the lateral cervical radiograph of a man with longstanding anky losing spondyl itis with the typical appearance of the "bamboo spine." He suffered a minimal trauma recently and can suddenly move his neck better than he has been able to in years. He is thrilled and believes that the accident has helped his ankylosing spondylitis. Do you agree? Certainly not. This man has a "carrot stick fracture" at C3 with marked posterior displace-
Degenerative joint disease (DJD) is the most common arthropathy seen by chiropractOrs and is certainly nor in itself a contraindication ro manipulation . In fact, many patients with this disorder benefit tremendously from spinal manipulation when it is app lied judiciously. It is important, however, for the clinician treating the patient with DJD to recognize the association between degenerative changes in the spine and segmental hypermobilities at instabilities. Remember that hypermobility reptesents increased intetsegmental motion, does not pose a threat to the nervous system, and is not considered a presurgical stare, compared with instability, which is more severe, does threaten the neural elements, and requires surgical intervention . JUSt how is degenerative ioint disease associated with segmental hypermobi lity and instability? There appear to be twO main theories regarding this problem. The first suggests that hypermo-
bility, caused by repetitive microrraumas from occupationa l or sporting activities or a hereditary predisposition, is the precutsor to DJD (3,5,6,101. The other purports that degenerative disc disease results in posterior capsular and ligamentous laxity, which then allows excessive intersegmental motion (6,23). The importance to clinical practice, however, is [Q remember the association between these twO entities rather than debating the actual causes after the fact. Look at the radiographs of an elderly woman in Figure 8-8 A, B, and C. The neutral lateral film shows an anterolisthesis of C4 on C5 of approximately 5 mm and a slight retrolisthesis of C3 on C4. Moderate to marked degenerarive disc disease is present throughout the cervical spine.
fllll'e1Hl Degenerative hypermobility/instabiliry of the C3-S motion segments.
134 Flexion and extension radiographs were taken based on the findings noted on the neutral film. There is a slight increase in the forward translation of C4 during flexion and incomplete reduction in this subluxation during extension . The retrolisthesis of C3 is completely teduced duting flexion and increases slightly during extension. Both of these motion segments demonstrate signs of intersegmental hypermobility on these kinematic studies. A chiropractic technique that emphasizes the use of spinal manipulation to restore proper ver-
tebral alignment from plain film radiographs without considering aberrant morion can prove detrimental co patients such as the woman in Figure 8-8 (5,7,10). A practitioner who adheres to the simplistic philosophy of replacing the "bone out of place " would adjusr the spine, atrempting to correct the anterolisthesis of C4 and retrolisrhesis of C5, and in effecr would be manipulating areas of hypermobility. Not only does this fail to correct the patient's problem, it may delay healing and create instability in already hypermobile articulations (7, I 0 ). Pain alone is also not a sufficient criterion to
justify a manipulative thrust into a motion segment. Hypermobile arriculations are often painful (5,7), with the symproms frequently temporarily relieved by manipulation (7). This relief is thought ro be attributable ro the reduction in local muscle spasm. Motion palpation of the involved segments is also often unrewarding, with difficulty arising in differentiating a "normal" motion segment from one rhat is hypermobile (3,7). Flexion-extension lateral radiographs are also the method employed ro diagnose hypermobility associated with OJO. Should every patient with OJO of the cervical spine receive kinematic radiographic studies? Although there may be no clues on the neutral radiographs ro differentiate patients with hypermobility (5), the presence of an intersegmental anterolisthesis or a rerrolisthesis, especially if associated with mild degenerative changes at the involved level, or significant degenerative changes at the adjacent spinal levels, indi-
cates inclusion of flexion -extension studies before manipulation (3). Hypermobile or unstable motion segments related ro degenerative joint disease frequently stabilize themselves through the formation of osteophytes (5,23), but this process can take years. Severely degenerated motion segments that demonstrate hypomobility on kinematic radiographs may result in hypermobility in adjacent motion segments.
Chiropractic Management 01 Hypermobile and Unstable Cervical Segments The treatment of the patient with hypermobile cervical motion segments is complex (5). Chiropractors use many therapeutic approaches in addition to various manual procedures when treating their patients. As stated previously, manipulative thrusts into unstable articulations are contraindicated. However, it is possible that hypermobility and hypomobility or fixation may coexist in the same motion segment. Remembering that an intervertebral motion segment is a three-joint complex consisting of the intervertebral disc and the two facet articulations, a fixa tion in one facet articulation might result in a compensatory hypermobility of the contralateral articular facet (7) . In such cases, adjusting the restricted side while leaving the hypermobile side alone would be logical as well as adjusting adjacent restricted motion segments. Additionally, hypermobility in one plane, fot instance, the sagittal plane, might be accompanied by restricted motion in another plane, such as lateroflexion or rotation (3), requiring ca reful analysis and application of specific manipulative procedures. Various physical therapeutics can be employed, including electrical modalities. Specific exercise programs to stretch tight muscles and strengthen weak muscles should be incorporated. Trigger point therapy is also often beneficial (7) . Management of patients with unstable cervical motion segments requires conservative care and nonthrust procedures because of the danger of
135 neurologic complicarions. Referral for neurologic
Radographlc Evaluatloo
and surgical consultation is recommended when the holding elements of the segment are damaged to the point of instability because of the threat of neurologIC damage.
Static plain film radiographs cannot reliably detect lumbar intersegmental instability or hypermobiliry. The presence of an anterolisthesis, laterolisthesis, or retrolisthesis alone, although suggesting that hypermobility was most likely present at one time, does not indicate that the motion segment is currently unstable (4,26) . Degenerative and potentially unstable retrolistheses are more common at L5, with L4 being the most common level for this rype of anterolisthesis (28) (Figure 8-9) . The presence of the small trac-
Hypermobility and instability In the Lumbar Spine The terms hypermobility and illstability are also used inconsistently and interchangeably when referring to the lumbar spine (2,24,25). Several authors define lumbar segmental instability simply as an increase or an abnormal motion (2,25), without differentiating between hypermobility and instability. Grieve (26) is clear in his definition of the two entities by stating that" hypermobiliry" represems "3 little tOO much motion," and need not be painful, be clinically significant, or lead to instability, whereas "instability" occurs in a degenerating lumbar motion segmenr that is functionally incompetent because of insufficient soft tissue control. Paris (27) tends to agree with Grieve's differentiation of the two conditions,
adding that "instability exists only when, during the performance of an active motion, there is a
sudden aberranr motion, such as a visible slip, catch, or shaking of the section" (27). In all of the definitions submitted for "instability" specifically rel,"ing to the lumbar spine, none include the likelihood of resultant neurologic deficits as was so clearly the case for the cervical spine. This is most likely because acute posttraumatic instability caused by rupture of the ligaments of the lumbar spine, although occurring especially in the thoracolumbar junction, is not nearly as common as in the cervical spine ( 19,28). Most unstable acute traumatic injuries to rhe lumbar spine also show evidence of fracture (19). The terms hypermobility and illstability should not be used interchangeably when referring to spinal mechanical lesions. Instability should be reserved for motion segments that produce neurologic effects, incapacitating deformities, or pain caused by structural defects.
AIII'I 8-8 Degenerarive anrerolisrhesis of L4 wirh decreased inrervertebral disc space and sclerosis of the L4-5 facet articulations. It is nor possible on this static neutral radiograph to determine the stability of this morion segment.
136 tion spur is rhoughr ro be associared wirh insrability, whereas rhe larger osteophyre indica res rhar rhe segment has srabilized irself (24,26). This finding actua ll y may be significant because rhe tracrion spur is one of the few radiographic findings ro have a posirive correlarion wirh low-back symproms (29), jusr as segmenral insrability is known ro be sympromaric (2,3,25,26,27). As in rhe cervical spine, dynamic (kinematic) radiographic srudies are rhe methods used ro diagnose hypermobility and insrability in rhe lumbar spine. The earliest procedure used flexion and exrension lareral lumbar views raken afrer rhe patients acrively posirioned rhemselves at rhe extreme of rhese ranges of morion (2-4,8,2426,28,30-34). This merhod is sri ll w idely used and, alrhough incomplere in the assessment of inrersegmenta l motion, gives valuable information as to intersegmental instability, along with being relarively easy ro perform and interprer in rhe clinical serring (2,26,30,34). Most proponents of fl exion-extension radiographs have rhe' parient perform the maneuvers actively in the standing position (2,3,33,34). Han ley er al. (30) and Dupuis er a l. (25), however, recommend rhar flexion-extension views be performed with the parienr recumbent in the lareral decubitus position. They state that recumbency increases the global range of morion by decreasing rhe effecrs of low-back pain on rhe roral excursion. Sirring flexion-exrension radiographs also have been used, adding rhe effecrs of gravity whi le providing pelvic stabilizarion (32). Dvorak er al. (3n a re strong proponents of "passive" rather than "active" standing flexion-extension radiographs of rhe lumbar spine. They claim rhat rhe passive examination shows more intersegmencal hyper-
mobiliries and insrabiliries rhan rhe acrive procedure because rhe parient wirh back pain will "nor bend as far as rhe spine will permir." Ir is well recognized rhar rhe presence of low-back pain influences rhe reliability of rhe findings obrained wirh fl exion-exrension radiography (25,30,31,33). Ora Friberg (4) in 1986 pioneered a new approach ro diagnosing lumbar inrersegmental instability. His srudy found rhar rracrion-com-
pression lareral lumbar radiographs were superior ro flexion-exrension lareral radiographs for rhe diagnosis of insrability in parients wirh anrerolisthesis or rerrolisrhesis diagnosed on rhe neurral lareral films (Figure 8-10). Furthermore, he found rhar rhe severity of low-back pain had no correlation wirh rhe severity of rhe listhesi nored on rhe neutral films bur correia red significantly ro rhe quantity of translatory movement found with
tracrion-compression. This has been further subsrantiared by Sandoz (3) . Friberg's radiographic mer hod appears ro have specific advantages over flexion-extension radiographs, specifically: (1) Parienrs wirh back pain tolerare rhe procedure better, wirh less morion artifacr. (2) The reproducibility and comparabi lity of traction-compression radiography in regard ro posirioning of rhe patient and reading the measurements seems to be significantly better (4). Flexion-extension and traction-compression kinematic studies remain the primary methods used ro diagnose intersegmental insrabiliries because of rheir accessibi li ty and ease of inrerprerarion. Several srudies have srared rhar a rranslari on of >3 ro 4 mm in rhe sagirra l plane from full Aexion to full extension is indicative of intersegmental insrabi li ty (24,26,28). When using rhese figures, however, one must remember that they are on ly a "ru le of rhumb" and rhar rhere remains a wide range of "normal" intersegmental motion within subjects and between su bjects (25,30,32). Researchers are now using digiral videofluoroscopy (24,35), which is much berrer rhan plain film for rhe derecrion of segmental insrabiliry. Digiral videofluoroscopy (DVF) nor only derecrs intersegmental translation and angular measurement, bur it is also used to calculate the instantaneous cenrers of rorarion (ICRs) for each morion segment. Alrhough rhe radiarion dose is considerably les rhan for plain film radiology of rhe lumbar spine, rhe expense for rhe procedure and inaccessibi liry make ir impracrical for use by rhe clinician in daily practice. Lareral bending lumbar radiographs have been used in rhe past ro derect aberranr and
8 Tbe Nonmanlpulable SUbluXation
137
Rgare 8-10 Traction and compression larerallumbar radiographs. Note the vacuu m phenomenon visible on the traction radiograph onl y. The sagittal plane translati on of LS measured app rox imarel y 3 111111 from traction ro compression.
excessive intersegmental morio n (36-38). This radiographic procedure has fa llen o ut of favor recently because of poor interrater reliability in interpretation of the intersegmental motion, in
addicion to rhe fact that "a bnorma l" motion patterns were shown to have no correl ation with
low-back pain (36,37) .
Causes 01 Lumbar Spine Hypermobility and Instability As previollsly mentioned, acure severe trauma is o ne possible, although fa irl y rare, ca use of instability in a lumbar motion segment. Other causes
include repetitive microtraumas, either work related o r spo rrs related, hereditary predisposition to hyper1110bility, spondylolytic spondylolisthesis, ho rmonal influences (estrogen ), adjacent hypomobi lities or blocked verrebrae, spina l fu sions, and wide laminectomies. However, the most common cause of lumbar spina l instability is undo ubtedly degeneration of the intervertebra l joints (2,4,8,25-28). Degenerative Disc Disease Kirkald y- Wi ll is and Cassid y (2,8) identify three phases of the degenerati ve process a ffecting IU111-
138 bar morion segments. The first phase is characterized by segmental dysfunction and decompensation presenting as a posterior joint syndrome or diminished functional capability of the back musculature. They claim that, although in this first phase there may be early pathologic changes in the intervertebral disc and facet joints, these changes are not readily apparent radiographically. It is nOt until the second stage, referred to as the unstable phase of the degenerative process, that these radiographic changes become evident. They further state that the patient's symptoms are directly related to this abnormal increased intersegmental movement. Kinematic radiographic studies at this stage often show the increased intersegmental mobility (2,28), suggesting that forceful manipulative procedures are contraindicated (8) . Sandoz (3) describes an additional phase characterized by episodic fixations of spinal motion segments. He notes that the unstable phase and the episodic joint locking phase often coexist with much overlap. After the 'unstable phase, the spine stabilizes itself through the formation of osteophytes and pericapsular and intradiscal fibrosis (stage 3). This process may take many years, with the end result being a fixed deformity and complete loss of intersegmental motion (2,28) . The clinical significance of this third phase of degeneration is that it alters the spinal canal dimensions because of the osteophytic formation resulting in potential lateral recess entrapment or spinal stenosis (2,28). Look at Figure 8-11 and evaluate the radiogtaphic findings in the lumbar spine of this elderly man with longstanding low-back pain. There is significant degenerative disc disease and facet arthrosis of the lower lumbar spine. Disc space narrowing is noted between L2 and L4 with anterolistheses at these levels. Additional findings include loss of the lumbar lordosis, flexion between L3 and L4, and calcification in the abdominal aorta and common i.liac arteries.
Which if any of these findings are tesponsible for his low-back pain? Although it may be hard to accept, the fact remains that there is little correlation between
low-back pain and the severity of degenerative
RIIIrIB-11 Marked degenerative disc disease and facet arthrosis of the lower lumbar spine resulting in anrerolisrheses of L2 and L3. Arteriosclerosis of the abdominal aorta and common iliac arteries is present.
arthritis seen radiographically (29,39). The unsta· ble phase of the degenerative process as just noted is usually symptomatic (2,25) but is associ· ated with minimal radiographic findings of DJD. Therefore, none of the findings found in the elderly gentleman's radiographs shown in Figute 8-11 may account for his symptoms. The third phase of degeneration, that of "fixed deformity," may be occurring in this patient, as evidenced by the significant anterior and posterior osteophyto· sis. Potential sequelae of this phase may be spinal stenosis of his lower lumbat spine and secondary hypermobi lities or instabilities of the upper lum-
8 TIle ................ IIMIxatIon bar segments (3,28) . Clinical correlation is obviously indicated to detect lateral recess entrapment, central stenosis, or findings associated with hypermobility of L2 or L3. Based on the clinical findings in combination with the radiographic findings, flexion -extension or traction-compression radiographs may be indicated. However, these add itiona l radiographs shou ld onl y be taken with sufficient clinical justification and not as a routine procedure. If the patient does demonstrate evidence of nerve root entrapment or centra l stenosis, computed tomography (CT) or magnetic resonance imaging (MRI) images would be indicated. Spondylolytic Spondylolisthesis Defects in the pars interarticularis (spondylolysis) are present in approximately 5% to 7% of the population and involve the L5 verteb ra in approximately 90% of cases (20). The cause of these defects is now recognized to be stress fractures related to the upright posture. Much has been claimed about the clinical significance of spondylolysis and the often-resulting spondylolisthesis, with many chiropractic and medical physicians offering inappropriate treatment and restricting the activities of these patients unnecessarily (20) . Pars interarticularis stress fractures usually occur in childhood and are an incidenta l discovery on radiographs taken years later for other reasons (4,20) . They usua ll y on ly slip during the first .J 8 months to 2 ycars after occurrence and are therefore usually not unsrable when discovered and most likely are not the cause of the patient's low-back pain (26). Friberg found that the severity of slippage of the verrebral body noted on neutral lateral lumbar radiographs had absolutely no correlation to low-back pain (4 ). Rather, back pain was signi ficantly associated with the amoum of translation in the sagittal plane found dur ing rracrion-compression radiographs. Does this mean that every patient with radiographic evidence of spondylolysis should have flexion -extension or traction-compression radiographs done? Absolutely not! Most cases of spondylolytic spondylolisthesis are stable and of minimal clinical significance. If the patient
139
does not respond to conservative treatment and the clinician believes that instability may be present, traction-compression or flexion-extension radiographs are indicated . Excessive translation or angu lar motion in the sagittal plane is evidence of instability. Figure 8-12 shows flexion and extension latera l lumba r radiograp hs of a parient with pars defects noted at L2. T his is a rather unusual level for spondylolysis and correlated to the patient's area of complai nt. The motion studies demonstrate translation of approx imately 3 mm from full flexion to full extension and markedly increased intersegmenta l tilt (angular rotation) as compared with the adjacent levels. In this patient, forceful manipulative ptocedures to this motion segment would be contraindicated, and the clinician could claim that the spondylolytic spondylolisthesis was most likely the ca use of the back pain. Contrast this with the patient in Figure 8-13, who has pars defects at the common level of L5 but without any evidence of anterolisthesis. Flexion-extension radiographs were taken, and no evidence of instability is noted. These pars defects in this ad ult patient a re therefore most likely nOt the cause of the low-back pain, and no contraindications to adjusting are noted on these radiographs.
Postsurgical lnstability The mOSt common cause of postsurgical instabi lity is the excessive removal of the supporting structures during decompression surgeries for nerve root entrapments (28). The surgical removal of 30% to 50% of the articular facets may lead to instability. Plain film findings often show an anterolisthesis at the affected level, wh ich was nOt evident on the preoperative radiographs (28). Even less radical spina l operations may lead to instability. Frymoyer and Selby (28) State that "20 % of women who have undergone lumba r disc excision without removal of facet joints demonstrate signs of instability, usually at L4--5. " Look at the radiographs (Fig ure 8-14) of the middle-aged woman who presented to a chiropractor with a long history of low-back pain. The
140
Subluxation TIle ArtIcular I.8IIon
fIIIrt 8-12 Spondylolysis with spondylolistheses of L2 showing evidence of instability on flexion-extension radiographs.
most obvious findings are the absences of the spinous processes and laminae from L1 through L4 with no evidence of fusion. Additionally noted is the moderate loss of disc height between L3 and L4 with a rerrolisthesis and left lateral listhesis at this level. The levoscoliosis also has its apex at the L3-4 level. All of these findings strongly suggest instability, particularly at L3-4. You should have also noticed the diffuse marked increase in bone density. If you missed t~is significant finding, look at the "normal" L5 vertebra, which still possesses its posterior arch. This
first consideration. Osteopetrosis results in brittle bones that fracture easily, a factor very significant
Blocked Vertebrae Surgically fused segments as well as congenitall y blocked vertebrae also may result in hypermobility or instability at the un fused motion segments above or below the block (6,20). It has long been tecognized that surgical fusion of one lumbar
patient has osteopetrosis. Without this history, however, osteoblastic metastasis would be the
motion segment often causes eventual disc lesions at the adjacent superior motion segment caused
to the treating chiropractor. This case is a nice
demonstration of the principle " the patienr has the right to more than one condition."
141
FIgIre 8-13 Flexion and extension lateral lumbar radiographs in a patient with spondylolysis of L5 but no evidence of instability.
by the excessive motion at that level induced by the surgical fusion. Not all surgical fusions, however, are succe sful at immobilizing the intended segments. Therefore, assumptions cannot substitute for a careful clinical and radiologic examination of the area . Similarly, congenitally blocked vertebrae (Figure 8-15) lead to early degenerative disc disease at the adjacent levels, with these unfu ed motion segments passing through the unstable phase before osteophytic stabilization (2,3,8). JUSt as in the cervical spine, there is no point in attempting to manipulate fused motion segments.
d.
Clinical MM/fastatlons Hypermobllty and Instability In tile Lumbar Spine The clinical descriptions of patients presenting with hypermobility and instability are blurred and confusing, again because of [he inconsistency in the use of the terminology. Those who do differentiate between these two condir.ions stare that hypermobility is not necessarily symptOmatic, it may be insignificant or reversible, and although it may lead to instability, this is not necessarily the case (11,27). In the early stages of the unstable phase symptoms are often minor, with the patient cornplain-
142
Rgure 8-14
Laminecromy of L 1 through L4 with no evidence of fusion. Loss of disc height is nored, along with
borh a lateral lisrhcsis and rerrolisrhesis of L3. The levoscolios is has its apex at the L3 level. Also noted is the diffuse bone sclerosis consistent with the patient's known osteopetrosis.
ing of chronic, nagging, episodic low-back pain (2,25). This pain is often aggravated during specific movements such as extension or twisting motions, anything that places strain on previously
srretched ligamenrs (25,28,40). However, move-
"catching" sensation during specific spinal move-
ments (11,26,27). According to Dupuis et aI., this is not a reliable or consistent finding (25). Grieve (26) lists several clinical criteria that if present suggest lumbar instabiliry. These include:
ments in genera) may bring some temporary
relief, and these patients may have difficulty sitting still (27,4 1). As the condition progresses, the interval between aggravating spinal movements
1. A history of much conservative treatment for
low-back pain and early morning stiffness 2. The presence of bilateral loin creases on
and back pain becomes shorter and shorrer, to the
observation from behind in nonobese or
point where any activity requiring axial pressure
elderly patients 3. In earlier stages, surprisingly free, full, and
on the spine becomes symptomatic (27,40) . Several authors describe patient complaints of a
painless movement, including straight leg
143 testing accessory movement with provocation of the lumbosacral ache or pain 10. Excessive movement on passive physiologic movement resting by comparison with adjacent segments
It is difficult for palpation alone to detect hypermobility (3) . A "boggy" end feel and overlying soft tissue edema are indicative of instabi lity (26,40). Palpation also may detect excessive segmental anteroposterior' mobility by applying a posterior to anterior force ro extend the patient's
lumbar spine with the dorsum of the hand (8). Uncoordinated muscle contractions or spasms
during active forward flexion or localized deviations of motion may signify instability (27). Lumbar segmental hype rmobility is tOO often overlooked, with incorrect interpretation of the
clinical features leading to inappropriate therapeutic maneuvers. If the condition is nor sug-
gested, the confirming radiographic studies will nOt be done and the patient may receive a series
of manipulative thrusts to the region. Although inappropriate, surprisingly, these adjustments may actua ll y · provide some temporary relief for the first few treatments (26,41 ), after which they do nOt help and can actually worsen the condition. ~
11-15 Classic congenital blocked vertebra L3-4.
ChlropracUc Management of lJInlNl' Intersegmental HypermobllttyINtabIIIy Conservative treatment begins by manipulating
ralsmg (however, lumbar spine appears to "hinge" at one segment on extension)
4. In some patients, a steadily increasing lumbosacral ache when extremes of spinal movement are sustained for 15 to 20 seconds 5. In later stages, cautiolls active movements,
which often look rather precarious 6. A momentary catch or twinge distorting one or more lumbar movements-usually flexion,
but sometimes others 7. A tendency to grasp the thighs for support when returning from flexion, with lordosis often maintained during flexion 8. Undue tenderness localized to one segment 9 . A slight but unmistakable "boggy" feel on
the adjacent fixed or hypomobile segments while avoiding hypermobile and unstable ones (8) . Sandoz (3) notes that dynamic instability is usually in the sagittal plane with concomitant fixation in lateroflexion and rotation. He emphasizes that the planes and directions of abnorma l motion should always be mentioned. This should affect the types of manipulative procedures chosen. Muehlemann (41 ) emphasizes the importance of using "locking mechanisms " fat adjacent hyper-
mobile areas when adjusting fixation s. He goes on to state that "movement should be induced
from the part of the spine that is nOt affected by hypermobilities, i.e., if a hypomobile L4-5 adjacent to a hypermobile L5-S1 is to be moved,
144 movement should be induced from the supetior part of the spine." Furthetmore, long-lever manipulative procedures should be avoided (41). Grieve (26) recommends "mobilization" of hypermobile (not unstable) segments within the normal range of accessory movement. He claims
that this relieves the pain associated with the hypermobility and that in some cases no more need be done than ro teach stabilization exercises. Stretching of the tight large muscles groups (iliopsoas, quadriceps, hamstrings, piriformis, quadratus lumborum) along with trigger-point therapy in the sma ller intersegmental muscles is helpful (40). Both Muehlemann (41) and Grieve (11,26) are strong proponents of progressive stabilization techniques, which require much dedication from both the patient and the physician. These stabilization techniques begin with short-lever isometric conrractions, moving to continuously longer
levers while avoiding trunk movements. These are srarted after 4 to 6 weeks of treatment of adjacent hypomobile segments. After 8 to 12 weeks of rherapy, Muehlemann recommends guided and oprimally measurable resisrance exercises (4 1). Posture should be improved by attempring ro correct the tendency to hyperlordosis and by reducing obesity (26,27) . Activities that produce both compression and shear should be avoided. These include shoveling; lifting; playing handball, squash, racquetball, or tennis; cycling; and gardening (27). Walking and swimming the backstroke or crawl are encouraged to increase overall
firness (40). It may be of comfort to both the patient and the doctor to remember that rime alone will reduce hypermobility (26,27). However, this may take years. Lumbosacral supportS may be prescribed, but o nly if the doctor has a treatment plan intended to eliminate this support (26). Frymoyer and Selby (28) claim that although most standard conservacive treatment programs are effective, there are some patients who have
persistent symptoms. If the symptoms are exacerbated in extension and relieved by flexion, the patient may be helped by facet injection. If spinal
fusion is contemplated, the specific area of segmental instability must be identified based on knowledge of coupled motion patterns, and the surgical procedure must be tailored to it. By doing this, one may reduce the unacceptably high failure rate in the surgical management of degenerative spinal instability (28). Grieve summarizes the indications for surgical referral in those cases of lumbar segmental instability in those whose condition fails to respond to appropriate conservative therapy (26). These include: 1. The severity of symptoms 2. Lack of response to simple measures 3. The passage of time 4. Significant restriction of the patient's activities
5. Confidence as to the true origin of the pain
Conclusion Lumbar segmental hypermobility is common and often is a transient stage affecting the lumbar spine, frequently occurring as part of the degenerative process. Awareness of the frequency of this condition and the associated clinical features increases the diagnosric accuracy and thereby the appropriateness of therapeutic choices for these patients.
References 1. White AA, PanJabi MM. Clinical biomechanics of the spine. Philadelphia: JB Lippmcort, 1978: 192. 2. Kirkaidy-Willis WH, Cassidy JD. Toward a more precise diagnosis of low back pain. In: Spme update 1984. San Francisco: Radiology Research and Education Foundation, 1983:5-16. 3. Sandoz R. The narural history of a spinal degenerative lesion. Ann SWISS Chiro Assoc 1989; 9:149-92. 4. Friberg O. Lumbar instability: A dynamic approach by traction-compression radiography. Spine 1987; 12,119-29. 5. McGregor M, Mior SA. Anatomical and functional per· spectives of the cervical spine. Parr II. The "hypermob.le>t cervical spine. JCan Chlro Assoc 1989; 33: 177-183. 6. Henderson OJ, Dormon TM. Functional roemgenomcrric evaluation of the cervical spme m the sagittal plane. J Manipulative Physiol Ther 1985; 8:2 t 9-27. 7. Garrerman MI. Indications for spinal manipulation in the treatmem of back pain. ACA JChiro 1982; 16:51-66.
145 8. Cassidy JD, Poner CE. Motion examination of the lumbar spine. J Manipulative Physiol Ther 1979; 2: 151-8. 9. Lewit K. Malllpuiation: reflex therapy and/or restitution of impaired locomotor function. Manual Medicine 1986; 2,99-100. 10. McGregor M. Mlor S. Anatomical and functional perspectives of the cervical spme. Part III . The "unstable" cervica l spine. J Can Chiro Assoc 1990; 34:145- 152. I 1. Henling D. Kessler RM. Managemcm of common musculoskeletal disorders: Physical therapy principles and methods. 2nd ed. Philadelphia: J8 lippincott. 1990:522-23, 556-9. 12. Dvorak J, Froehlich D. Penning l, Baumgartner H, PanJab. MM. Functional radiographic diagnosis of the cervical spine: flexion/extension. Spine 1988; 13:748-55. 13. Dvorak J. Panjabi MM, Grob D, Novotny JE, Antinnes JA. Clinical validation of fu nctional flexion/extension radiographs of the cervica l spine. Spine 1993; 18: 120--7. 14. Lind B, Sihlbom H, Nordwall A, Malchau H. Normal range of motion of the cervical spine. Arch Phys Med Rehabi! 1989; 70,692-5. 15. Hviid H: Functional radiography of the cervical spine. Ann Swiss Chiro Assoc 1965; 3:37-65. 16. McGregor M, Mior S. Anatomical and functional perspectives of the cervical spine. Part I. The "normal" cervical spine. J Can Chlro Assoc 1989; 33:123-9. 17. Amebo B. Wonh D, Bogduk N.lnsrantaneous axis of rotation of the typical cervical motion segments. II. Optimization of technical errors. Clin Biomech 6:38-46, 1991. 18. Whue AA, Johnson RM, Panjabi MM, Southwick WOo Biomechanical analysis of clinical stabi li ty in the cervical spine. CIIn Onhop Rei Res 1975; 109:85-96. 19. Gehweiler JA, Osborne RL, Becker RF. The radiology of vertebral trauma. Philadelphia: WB Saunders, 1980,99-100,215-7,229,236,267,273. 20. Yochum TR, Rowe LJ. Essentials of skeleta l radiology. Vols I and 2. Baltimore: Williams & Wilkins. 1987:100, 103-5,176,244-5,269,431,434. 2 I. Reich C, Dvorak J. The functional evaluation of craniocervical ligaments In sidebcndmg USing x-rays. Manual Medicine 1986; 2,108-13. 22. Chapman S, Naklelny R. Aids to radiological differential diagnosis. London: 8ailliere linda II , 1984:53. 23. Resnick 0, Niwayama G. Diagnosis of bone and joint disorders. Vol 2. Philadelphia: WB Saunders, 1981: 1370-82. 24. Mick T, Phillips RB, Breen A. Spinal imaging and spinal biomechanics. In: Haldeman S, ed. Principles and practice of chiropractic. 2nd ed. East Norwalk, Connecticut: Appleton and Lange, 1992:402-12.
25. Dupuis PR, Yong-Hing K, Cassidy JD, Kirkaldy-Willis WHo Radiological diagnosis of degenerative lumbar spinal instabiliry. Spine 1985; 10:262-76. 26. Grieve GP. lumbar instabiliry. Physiotherapy 1982; 68,2-9. 27. Paris SV. Physical signs of instabiliry. Spine 1985; 10,277-9. 28. Frymoyer JW, Selby OK. Segmental instabiliry: rationa le fo r treatment. Spine 1985; 10:28G-6. 29. Frymoyer JW, Newberg A, Pope MH, Wilder DG, Clements J, MacPherson B. Spine radiographs in patients with low-back pain. J Bone Joint Surg 1984; 66A, 1048-55. 30. Hanley EN, Matteri RE, Frymoyer JW. Accurate roentgenographic deternunation of lumbar flexion-extension. Clin Orthop 1976; 115,145-8. 3 I. Dvorak J, Panjabi MM, Chang DG, Theiler R, Gross D. Functional radiographic diagnosis of the lumbar spine: Flexion-extension and lateral bending. Spine 1991; 16,562-71. 32. Hayes MA, Howard TC, Gruel CR, Kopea JA. Roentgenographic evaluation of lumbar spine flexion-extension in asymptomatic mdividuals. Spine 1989; 14:327-31. 33. Pearcy M, Ponek I, Shapherd J. The effect of low·back pain on lumbar spinal movements measured by threedimensional x-ray analysis. Spine 1985; 10:150--3. 34. Sandoz R. Technique and Interpretation of functional radiography of the lumbar spine. Ann Swiss Chiro Assoc 1965; 3,66-110. 35. Sha len PRo Radiological techniques for diagnosis of lum· bar disc degeneration. Spine: State of the Art Reviews; 3 ( 1),27-48. 36. Haas M, Nyiendo J, Peterson C, et a!. Lumbar motion trends and correlation with low back pain. Pan 1. A roentgenological evaluation of coupled lumbar motion in lateral bending. J Mampulative Physiol Ther 1992; 15,145-58. 37. Haas M. Nyiendo J, Peterson C, et al. Inter-rater reliabiliry of roentgenological eva luation of the lumbar spine in lateral bending. J Manipulative Physiol Ther 1990; 13,179-89. 38. Weitz EM. The lateral bending sign. Spine 1981; 6,388-97. 39. Magera A, Schwam A. Relation berween the low·back pain syndrome and x-ray findings. J. Degenerative osteoarthritis. Scand J Rehabil Med 1976; 8:115-25. 40. Catterman Ml. Chiropractic management of spine related disorders. Baltimore; Williams & Wilkins, 1990:170--1. 41. Muehlemann D, Zahnd F. Die lumbale segmentale hypermobilitaet. Manuelle Mediz.in (Ger) 1993; 31:47-54.
The S
T
xation Complex
he subluxation complex is a theoretical model of morion segment dysfunction (subluxation) that incorporates the complex interactions of pathologic changes in nerve, muscle, ligamentous, vascular, and connective tissues. First described by Faye as a paradigm shift from the static misalignment or "bone out of place" concept of subluxation, the vertebral subluxation complex has served as a more dynamic and inclusive teaching and research model for the chiropractic profession. According to Kuhn, a paradigm prepares students for membership in the scientific community with which they will later practice. By joining a group who learned the bases of their field from the same model, subsequent practice provides a basis for agreement over fundamentals. An accepted paradigm mUSt seem better than alternatives but does not necessarily explain all the facts with which it can be confronted . It suggests which experiments are worth performing and selects phenomena in more detail for more rigorous study. Supporting Palmer's concept that the neurologic component of the subluxation is the cornerstone of chiropractic theoty, the subluxation complex provides a structure for better understanding the foundation
148
11Ie Subluxation Complex
principles of chiropractic theory and provides a paradigm for chiropractic education and research.
Chapter 8 The Vertebral
Subluxation Complex presents an overview of the subluxation complex paradigm, outlining the ateas affected by the
articular subluxation. The interaction of the
pathologic changes of the nerve, muscle, ligamentous, vascular, and connective tissue components
is discussed. Taking the subluxation concept beyond that of a biomechanical lesion, this chapter explores the functional manifestations associated with the articular lesion.
Chapter 10
The Theoretical Causes of Subluxa-
tion discusses the proposed causative agents put
luxation on rhe nervous system. Used to visualize
the abstract principles involved, models of intervertebral encroachment, altered somatic afferent
input, and dentate ligament and cord distortion are discussed. These theories present the neurologic foundations of chiropractic theory in light of current supporting evidence.
Chapter 13
Vertebral Subluxation and the Anatomic Relationships of the Autonomic Nervous System emphasizes the impottant associa-
tion of the autonomic nervous system with the
effects of the subluxation complex. The potential for widespread changes in the parasympathetic and sympathetic nervous systems caused by vertebral subluxation is a controversial topic fundamental to the foundations of chiropractic princi-
forth to explain the misalignment, aberrant
ples. The anatomic relationships relative to this
movement, and dysfunction characteristic of the
debate are documented, with the physiologic implications for somatic dysfunction outlined.
subluxation. Articular adhesions, ligamentous shortening, meniscoid entrapment and extrap-
roeor, muscle spasm, and mechanical . Iocking have all been implicated as causative agents of the subluxation. The rationale and supporting evidence for these suggested causes are presented.
Chapter 11
Chapter 14
The neuroimmunologic implica-
tions of spinal manipulation are presented in
Chapter 14. Observed changes in the immune system after manipulation support the theory that improved neurologic function has beneficial effects on overall health. The possible role of
The Kinesiopathology of the Vertebral Subluxation emphasizes the aberrant movement component of the subluxation. Considered the primary element in the hierarchy of the subluxation complex, the kinesiopathology that both
Chapter 15
causes and results from altered movement in the spinal motion segment is examined. Both normal
dence that convergent input onto spinal neurons
and abnormal motion are considered, and the role the muscle spindle plays in each is presented .
Chapter 12
The Neurophysiologic Theories of the Chiropractic Subluxation reviews three theories that explain the proposed effects of the sub-
manipulation in modulating neuroimmunologic function is discussed.
Spinal Cord Plasticity and Mechanisms of Referred Pain explores the scientific evi-
produces widespread neurologic activiry. Studies evaluating the nociceptive "traffic flow" involved in spinal pain are discussed. Theories of somatosensory input with neuronal responses to
mechanical and sympathetic stimuli produced by manipulation are proposed.
J
The Vertebral Subluxation Complex Charles A. Lantz
Key Words
Vertebral subluxation complex, immobilization degeneration, dorsal root ganglia
After reading this chapter you should be able to answer the fo llowing questions:
QuestIOn #1
Of what benefit to the chiropractic profession is the vertebral subluxation complex?
QueatIon#2
How does minimal acute compression affect the dorsal root ganglion?
QuestIon#3
What effect does immobilization have on a spinal joint?
150
T
he Vertebral subluxation complex (VSC) is a model of spinal dysfunction from a chiropractic clinical perspective. In this model we describe the common and essential elements of spinal degeneration and dysfunction in an attempt ro make them more understandable in the context of chiropractic adjustive procedures. Classically, subluxations have been viewed as osseous impingement on nerves that interfered
with the proper functioning of those nerves. Hisrocically, this "bone on nerve " concept was seen ro be in direct conflict with the original osteopathic model of "muscle on vessel" shutting off the vital life-sustaining blood supply to the tissues. Current concepts have taken us beyond these limiting views, and we have grown to appreciate that when a spine is dysfunctional, all tissues arc involved in such an interconnected way that it is impossible ro discern where one tissue involvement ends and another begins. The VSC model attempts ro organize this new awareness of the fundamentally holistic nature of the human body machine into a conceptual framework that allows chiropracto rs and other hea lth cate providers ro gain a better insight inro the processes involved. The purpose of this chapter is ro present a model of changes in nerve muscle, connective, and vascular tissues that accompany the kinesiologic aberrations of spinal articulations. The development of the VSC is distinctively chiropractic and reflects in a unique way the clinica l practice of chiropractic. Common to all concepts of subluxation are some form of kinesiologic dysfunction and some form of neurologic involvement. The primary form of kinesiopathology that is addressed in chiropractic clinical practice is hypomobiliry, ofren referred ro as fixation. Immobilization degeneration (1) is a term that refers to a consistenr pattern of degeneration in
all tissues associated with an immobilized joint. There is considerable discussion as ro whether partial immobilization can lead ro significant degenerative changes, and such issues can be
appropriately addressed through this model. Another significant facror that can contribute ro subluxation degeneration is trauma, both severe and moderate. Repetitive stress is seen more fre-
quently as contributing ro degenerative changes and dysfunctional states, and continual exposure to vibration, as is common in the workplace or while commuting, are also seen as contriburing ro
degenerative states of the musculoskeletal system. All of these aspects can be adequately treated within the context of the VSc. At least as important as the internal consis-
tency and va lidiry of the descriptive information that constitutes the model is the impact that the model has had and continues ro have on the chiropractic profession itself. The model has provided a common conceptual context in which ro discuss relevant aspects of rhe subluxation con-
cept in a logical and ordered fashion. The model has been the focus of at least one scientific conference and has been a guiding force in the development of technique assessment prorocols by the American Chiropractic Association (ACA) Council on Technique. The model is seen as a natural extension of rhe origina l "bone on nerve" concept, just as rhe quantum mechanical arom is seen
as an extension of the original Bohr atom. It provides a common language for chiropractors ro discuss the many and varied approaches to manipulative and adjustive procedures found in modern chiropractic today, from osseous adjustive procedures, to trigget-point therapies, to
reflex techniques. The VSC addresses the issues of chiropractic in a uniquely chiropractic way but is
also understandable ro any other interested parry. It is a model that can grow and adapt ro new information in areas of neurology and kinesiology and any other relevant ropic. It provides a contextual framework in which students of chiropractic can organize and understand the man y
aspects of the basic clinical sciences relative to adjustive procedures. As an outgrowth of the original subluxation model, the VSC is familiar ro most practicing chiropracrors, who mOSt often
understand the implications and significance of the model implicitly. Finally, the VSC creates a
151 bridge between basic and clinical aspects of spinal degeneration and dysfunction from a distinctively chiropractic perspective. Each diagnostic procedure has a correlate with one or more of the components of the VSC, and clinical outcome measures can, for the most part, be mapped onto the components of the VSc. The VSC as presented in this text deals exclusively with the neuromusculoskeletal components of spinal degeneration and dysfunction as they relate to the chiropractic concept of subluxation. The subtle aspects of psychology relating to the doctor/patient relationship are not addressed, nor do we discuss the socioeconomic factors involved in health and well-being. We shall also avoid the issue of patient satisfaction and quality of life in the context of this model. Although addressing subluxations on a clinical level can have profound effects on an individual's psychological state or sense of self, these ate issues better left to clinical psychology. Our purpose is to desctibe the fundamental natute of spinal subluxation and how the body responds to chiropractic adjustive procedures.
History The VSC model as originally developed by Faye consisted of five components (Table 9-1) . Dishman (2,3) was the first to publish an account of the original five-component model, limiting the histopathology component to a description of cartilage degeneration. Faye, (4) confined the histopathology component to a description of the
OriginalS-Component Model of the VSC
1. 2. 3. 4. 5.
Kinesiopathology Neuropathology Myopathology Histopathology Biochemical abnormalities
The 5-component model originally developed by Faye and first published by DIshman (21.
Neoromuscuiosketetal Components
01 the Verlobrol Suhl.x""" Complex
Biochemical obnormoJitiM
fIgIre 8-1
Organizational model of the vertebral subluxation complex originally published by Lantz (5).
This model includes three components nor specified in the original model and shows [he hierarchic rei arion· ship of the various components. (Lantz CA. The vene-
bra I subluxation complex. leA Review 1989; (Sepl Oct); 37-61.) inflammatory process. A more extensive and substantial formulation of the model (Figure 9-1) included connective tissue pathology, vascular abnormalities, and inflammatory response (5). Since that time, the model has been further refined; pathoanatomy was substituted for histopathology, and pathophysiology was included as a basic component. In this chapter, the pathology terminology has been dropped and a more generic terminology adopted in which the neurologic component is used instead of neuropathology, kinesiologic component for kinesiopathology, and so forth (Figure 9-2). This evolution of the model is shown in Table 9-2.
Overview 01 the Model Figute 9-2 illustrates the hierarchic organization of the VSC in which the components ate seen in relation to one another. The kinesiologic compo-
152
vsc
Neuropathology
InAammatory response
Pathoonotomy
Pathophysiology
Pathobiochemistry
AllIn 8-2 Updated version of the VSC model shown in Figure 9-1. Hi stopathology ha s been re placed by the more generic parhoanaromy. and patho physiology has been added. nenr is represented as rhe apex of our mode l because resroration of marion is rhe central goal in the clinical pracrice of chiropractic. This is in effect the functional end poinr of the combined efforts of rhe tissue components. Movement is affecred by the muscles (myologic component); guided, limired, and stabilized by connecrive rissue; and controlled largely by the nervous system . The vascular system serves the essential nutritive and cleansing role for all tissues and is rhe conduir for rhe immediare srages of the inflammatory response (ar least in vascularized rissues ). These
constitute the tissue-level componenrs of the VSC, and each works in coordinarion wirh the orhers to permit and sustain proper movement. Interference with any single componenr affecrs all others (6). Each tissue component musr be understood rhoroughly to appreciate irs role in spinal parhomechanics and rhe pathologic processes associated with subluxation degenerarion. Each component consists of identifiable elements: rhe interverrebral discs (IVD), articular cartilage, and interspinous ligaments are examples of elements of the connective tissue component; the nerve roots,
153
8 1118 Vertebral 8IMol11lon Complex
Three p hases of evolu tion of the VSC m odel sh owing refinem ent o f th e con cepts a nd terminology
Original
Kinesiopathology Neuropathology Myopathology
Histopathology Biochemical abnorma lities
Updated
Reviled
Kinesiopathology Neuropathology Myopathology Connective tissue path. Vascu lar abnormalities lnflammatory response Histopathology Biochemical abnormalities
dorsal root ganglia, and recurrent meningeal nerves are elements of the neurologic compo-
nent-which can be subdivided further as to segmentallevel: the L5 IYO, the C5 facets, or the Cl nerve roOlS, for example. Changes in these elements are described in terms of anatomic, biochemical, and physiologic alterations, which are called pathologic when they are involved in
Kinesiology Neurology Myology C.T. physiology Angiology Inflam. resp. Anatomy Physiology Biochemistry
discuss kinesiology of joints withour discussing ligaments, capsules, and muscle-tendon systems. In addition, in the spine, the dural sac, along with its contents, must be considered in the kinetics of movement (14,15). The spine is further complicated in its kinesiology in that it responds as an integral unit in which restrictions of movement at
one level can lead to compensatory changes in
degenerative processes, and restorative or thera-
peutic when associated with healing processes. Although the basic components and their specific elements form the foundation of the Y5C, these would be of little value if they did nOt correlate with clinical practice. The model is therefore seen as having three levels of organization (Table 9-3): the basic structural-functional level as illustrated in Figure 9-2, the level of diagnostic evaluation in which each diagnostic procedure maps OntO the basic components, and the thera-
Levels of applica tio n of a compo nent o f the VSC using the kinesiologic com pon ent as a n example
Tx
peutic outcomes that represent the outcome of therapeutic intervention.
Ox
KInesiologic Component
Sx
The fundamentals of kinesiology form the foundation of the kinesiologic component (6-13) . Cerrain features, however, are morc significant when viewed from a chiropracric adjustive perspective.
The most significant details are presented here as a guide for further development. It is difficult to
Adjusting Procedures Traction Thrust Torsion ROM Muscle StrengthIFunction Rheumatology Biomechanics Kinesiology Biochemistry, etc.
Sx, Basic science aspects that form the basis of our under· standing of the component. Ox, Diagnostic procedure associated with the component in question. Tx, Treatment procedures associated with the component.
154
TIle S_luxltlon COIIIpIex
other areas (15,16). No disorder of a single major component of a motion segment can exist without affecting fitst the functions of the other components of the same unit and then the functions of other levels of the spine (6). The basic unit of spinal mobility is the motion segment (7), a three-joint complex (9). Functionally it may be considered to be a single, compound joint with three articulations (10), analogous to the wrist. A typical motion segment consists of two ad;acent vertebrae joined by an lVO, two posterior articulations with their capsu les, and several intrinsic ligaments (8) . Parke (6) includes the muscles and segmenta l contents of the spinal canal and the intervertebral canal (lYC). Atypical spinal motion segments include the occiput-atlas (CO-C1) and the atlas-axis (C1-C2) articulations. The pelvic ring with the two posterior sacroiliac joints and the disclike symphysis pubis a lso has been considered an atypical three-joint motion segment (11). Chiropractic eva luative procedures are often directed at determining specific intersegmental motion or positional abnormalities and correcting
these through specific adjustive procedures directed to those segments (see Chapter 6). Joint movement is a complex phenomenon, more so in
the spine than in any other organ system (12). In addition to the three planes of physiologic movement, flexion-extension, lateral flexion, and roration, there is also long axis traction. Joint play, a springiness in the joint when it is taken to tension, represents the elastic barrier of resistance to
joint motion (see Chapter 6) . In addition to specific intersegmental movement, tegional or gross range of motion (ROM) must be considered, which is far easier to objectively evaluate than segmental motion. It is restriction of spinal ROM that is clinically most notable and most readily monitored as a clinical outcome (15,16) (see Chapter 11). More complex motion, such as gait and dynamic posture, fall into the domain of the kinesiologic component and within the purview of chiropractic.
lmmobilization Degeneration (ID) One of the most prevalent ideas in chiropractic is the notion that restricted motion of the
manipulable subluxation central to spinal degeneration. From the scientific literature it is clear
that all siruations that lead to immobilization cause some degree of degenerative change in the musculoskeletal system, and early mobilization, traction, and continuous passive motion
overcome these harmful effects (17). Lack of movement in a joint leads initially to stiffness (18) and associated pain (19) followed by joint degeneration (1,20) and ultimately fusion by bony ankylosis. The idea that Jomt restriction or
"fixation"
is
an
integra l component of
manipu lable subluxation was first proposed by Smith, Langworthy, and Paxson in 1906 (21 ). More recently, spinal fixations by motion palpation of the spine were formalized by Gillet and Liekens (22 ) and organized by Faye (4) into a system of spinal joint palpation (see Chapter 4). In a study of the effect of interna l fixation on the zygapophyseal joi nts in dogs, degeneration occurred within 2 months of immobilization (23). Human patients with tuberculosis of the spine underwent
ventra l
fusion
with
discecromy,
thereby effectively eliminating movement between the two vertebrae (24). After 6 months it was observed that, in these same patients, fusion of the zygapophyseal joints had also occurred. In the lumbar spines of cadavers, intraarricular adhesions, ranging from thin threadlike filaments to dense mats that preclude any articular movement
(25), were observed in all adult specimens. Restoring motion to a previously immobilized joint leads to normal joint function and physiology. Although the degenerative effects of immobilization may be completely reversed on remobilization (26-28), the extent of and time for maximal recovery are dependent on the duration of immobilization (29) . In extreme cases of immobilization to the point of fibrofatty consolidation of the synovial fluid, remobilization results in the formation of a new joint cleft with articular carti-
155
8 TIle vertebral SUl*lxltlon COIIIpIex lage having normal histologic architecture (26) . This constitutes some of the strongest evidence available supporting a physiologic basis for the effectiveness of chiropractic adjustive procedures. Early mobilization is gaining a foothold in medical programs fot treatment of whiplash (30) and after knee surgery (31). Forced motion causes physical disruption of adhesions between gross structures, such as capsule to cartilage, and leads to a disruption of the intermolecular cross-bridging of collagen (32).
NeIroIogIc Component In the original "bone on nerve" model of subluxation, the nervous system played a centra l role as the mediator of all of the effects of subluxation and, conversely, of the therapeutic benefits of adjustive procedures (33). The neurologic component of rhe VSC has tradirionally been the cornerstone of chiropracric theory (34). Beyond the application of chiropractic and other manipulative procedures as a means
of relieving headache and low-back pain, rhe nervous system has been viewed as the mediator of vitality and health to the individual organs and rissues (35). Increasingly, scientific research supports this fundamental concept of chiropractic (36-39). It is also c1ea~ however, that rhe role the
primary
indicators
of
neurologic
function
observed in the physical examination (43). Spinal Nerves Spina l nerves formed by the dorsal and ventral nerve roots may be impinged by herniated discs (44,45) or by spurs and osteophytes around the joints of Luschka (46) . Nerve impingement from hypertrophy of the zygapophyseal joints also has been documented. Studies now show evidence of successful c hiropra ct ic management of such cases
(47,48). Within the last two decades it has become apparent that not a ll back pain is caused by herniated intervertebral discs, nor do all patients with disc herniation suffer with clinical symptoms (10,49,50). Although patients with herniated discs and nerve impingement may show dramatic
evidence of the effectiveness of chiropractic management
programs,
other
mechanisms
that
expla in the positive results obtained by chiropractic care mUSt be studied.
Dorsal Root Ganglia The integral relationship between the dorsal root ganglia (DRG) and the spina l articulations necessitates that we evaluate the role of these struc-
tures in the subluxation complex (51). DRG lie
nervous system plays in the subluxation comp lex
within the intervertebral canal in close associa -
is far from understood and that fundamental changes in the concept of neurologic involvement in subluxation need to be made. Many aspects of the nervous system's organization and function are relevant to the theory and practice of chiropractic, and many levels of neurologic involvement are reflected in the subluxation complex (40-42). Although compression of
tion with the articular capsule (52,53), except for the first and second cervical segments. DRG contain the cell bodies of all sensory neurons, except for those found in the cranial nerves. Their strate-
the cord, nerve roots, or segmemal nerves may
play a major and often dramatic role in this process, other aspects of the nervous system arc involved as well, from sensory receprofs to inter-
nuncial cells. Pain is by far the most significant factor in a patient's seeking chiropractic carc. In the diagnostic evaluation, motor function, reflexes, altered sensation, and pain responses are
gic location between adjacen t vertebrae make
them prime targets in the causation of subluxation, induced dysfunction, and the focus of chiropractic adjustive procedures. Dorsal rOOt ganglia are far more sensitive to mechanical stimulation than are nerve roots, spina l nerves, or peripheral nerves. When
inflamed, the ganglia become hyperexcitable and give rise to spontaneous discharges (54,55) . Minimal acute compression or chronic irritation lead
to long periods of repetitive firing that last longer than the stimu lus itself; acute compression of
156 peripheral nerves or nerve roots, however, does
not. Aberrant impulses could lead to clinical and pathologic signs and symptoms. The ganglia are richly vascularized (56) and have not been shown to have a blood-nerve barrier. The permeabiliry of ganglionic capillaries is far greater than that of the central nervous system (eNS) or the peripheral nerve (57), and rhis has been implicated as a route of infection by virus
and bacteria (58-61), as a site for the development of chemical irritation and inflammation by bloodborne agents (62), and as a porral of entry for anesthetics injected into the epidural space (63). Any compression or sclerosis that might compromise the arterial supply to or venous drainage from the ganglia is likely to promote irritabiliry, as with peripheral nerves (64). Articular eurology Articular neurology is germane to the theory of chiropractic. Wyke (65) has classified the spinal joint receptors into four rypes-three types of mechanoreceptors and the nocicepwrs. The role
that each plays in degenerative processes, and particularly in pain (66) , is the subject of intensive research. It is known that rhe spinal joints can produce patterns of pain referral (somatosomaric reflex), bur the neurologic mechanisms are nOt well understood (10,67) . Gillette (40) has proposed that coactivation of the articular receptor system and other somatic receptors constitutes a major component of rhe chiropractic
adjustment. The afferent discharges derived from articular mechanoreceptors have a threefold impact when they enter the neuraxis (66,68): reflexogenic effects, perceptual effects, and pain suppression. There is a significant correlation between propri-
oceptive input from the cervical spine and coordination of the extremities (68). There is a discharge of afferent fibers of the knee joint after passive movements of the leg (69). Joint inflammation sensitizes articu lar nociceptors to fire at rest
and
during
normally
nonnoxious
joint
movements (70). The proportion of neurons displaying resting discharges is higher and the
receptive fields are larger in inflamed joints. In humans (7 1), distension of the joint capsule of the knee led to reflex weakening of the quadriceps muscles. Injection of saline into the lumbar facets resulted in pain and significanr increases in the myoelectric activity of the quadriceps (10) or the hamstrings (72), depending on the levels injected. These responses were abolished by intracapsular injection of local anesthetic.
Pain The most common clinical characteristic of patients entering chiropractic offices is pain. Pain is known to be a significant aspect of cervical spinal degeneration (58) as well as of lumbar and pelvic degeneration (66). The mechanism for such pain is related to mechanical or chemical irritation of the DRG, spinal nerves or their roots (58), or specific articular nerves (49,66). Because of the largely subjective nature of pain, its evaluation by clinical methods and objective measures is a challenge to clinicians of all professions (66,73) . For the patient, the experience of pain is real, regardless of whether there are objective clinical findings and, as in the case of phantom pain (74), whether the body part is present. There have been numerous theories proposed that attempt to explain pain (75). One of the more widely discussed is the gate theory of pain (76), in which specific internuncial neurons of the spina l cord control the perception of pain. The transmission of pain sensation through the gate is dependent on the relative input of large (A-beta) and small (A-delta and C) fibers converging on the gate (75). This is one of the major mechanisms evoked in modern theories of manipulative therapies to explain how adjustive procedures relieve pain (41,77,78). Pain assessment is a major undertaking in clinical practice. Numerous methods have been developed to assess pain or to confirm its presence; visual analogue scales (VAS) and other forms of pain scales are widely used in all clinical practice. Evaluation of the pulse rate while pain is elicited is a way of confirming the presence of pain. But despite all of these attempts at quantifi-
157 cation, pain remains a subjective experience, influenced by culture, gender, social status, mood, attitude, and a host of other parameters.
shown that chiropractic adjustments exert a definite influence on pupillary diameter.
Viscerosomatic Relationships
The neurodystrophic hypothesis proposes that neura l dysfunction is stressful to the viscera and other body Structures and leads to "lowered tissue resistance," which can modify the nonspecific and specific immune responses and alrer rhe trophic function of the involved nerves. This has often been evoked by chiropractors to explain the positive results obtained in patients suffering from conditions of a more genera l nature than musculoskeletal pain, such as chronic obstructive pulmonary disease (81), bronchia l asthma, dysmenorrhea, and hypertension (82). Currenr research provides growing evidence of rhe presence of a dynamic interaction between the nervous and immune systems. Histologic studies have shown that mast ce lls are innervated directly by symparhetic nerve fibers, and that this relationship appears to serve a regu latory role in immunologic response (83). These observations are con~istent with those showing a reduction of norepinephrine in lymphoid tissue after an immunologic challenge (84). The evidence supportS the hypothesis rhar sympathetic innervation exerts an inhibitory effect on the immune system and rhat changes in tissue levels of norepinephrine can affect immunologic responsiveness. In animals, sympathecromy of one side of the body leads ro an increase in the development of tumors on thar side (85) . This suggests that interference with the sympathetic nervous system can compromise rhe body's immune system (86,87).
The Nel/rodystrophic Hy pothesis Viscerosomaric relarionships are widely recognized as patterns of referred pain (79). For example, pain associared wirh heart attack is often felr in the left shoulder and radiating down the left arm. Kidney degeneration refers pain to the lowback, and pancreatic degeneration refers pain to the right shoulder and back. Ir has been further demonstrated that skilled examiners can palpate spinal soft rissue changes associared with ischemic heart disease, and can diffetentiate those from changes associared wirh other heart conditions (79). There is little question as to the validity of viscerosomatic reflexes, and the asture diagnostician is aware that somatic pain can herald more serious underfying visceral conditions. The converse process, by contrast, is a hotly debated issue and appears ro be ar rhe heatr of the chiropractic controversy.
So motoallt01lOmic Relationships Somatovisceral relarionships are perhaps rhe key concept of chiropractic theory. The central issues can be divided intO twO complemenrary aspects: (1) Can spinal or paraspinal neurologic dysfunction lead to degeneration in rhe organs supplied by rhe involved nerves? (2) Can chiropracric intervention prevent degeneration and restore vitality to degenerating visceral rissues? This is, perhaps, the mOSt conrroversial issue in chiropractic theory. The evidence, however, tends to support such a concepr. Sato and Swenson (37) have demonstrated that the nerves to the kidneys and adrenals respond wirh reflex impulses when spinal motion segments are larerally flexed passively; the sympathetic response observed was correlated wirh alterarions in heart rate and blood pressure. Clinical studies tend to support these observations. In a randomized, controlled trial (39), it was shown rhat chiropractic adjustments were effecrive in reducing blood pressure in humans. In another human study (80), ir was
Trophic Infll/ences The trophic influences on nerve function have been discussed by a number of authors (89-91) . Severa l compounds are implicated as mediarors of trophic influences (trophic substances) (92,93), wirh acetylcholine being most ofren cited (94,95) . Trophic influences stimu lare more subtle responses in tissues than do neurotransmitters, such as a lrered growth rate (96). Ir is suggested rhar proper vita lity, morphology, and function of
158
TIle . . . .1Ion COmplex
the target tissues are dependent on an adequate degree of trophic stimulation. In muscle, for example, exchanging nerves between "white" and " red" muscle led to white muscle transforming to red and vice versa (97). This line of research gives considerable impetus to the compression models of subluxation . Trophic substances are synthesized in the cell body and transported to the synapse by axoplasmic transport (98) . By compressing the nerve and shutting off the flow of these vital supportive substances, one could explain how the tissues might suffer from degeneration for lack of the chemical stimulation . The amount of force required to cut offaxoplasmic flow, however, leads to serious neurologic deficits that would far overshadow any subtle trophic changes predicted by subluxation models. It remains to be seen, however, whether chronic irritation might lead to excessive trophic stimulation that could lead to tissue hypertrophy or even pathologic degeneration.
Neurodiagnosis In general, neurodiagnostic procedures are not very quantitative, relying on patient complaints such as pain, numbness, or loss of smell or hearing, for the determination of the presence or absence of neurologic involvement (43). Other neurologic tests, such as the visual acuity test or sound discrimination eva luations, can produce quantitative data, provided some amount of sensibility is present, for example, the patient is nOt totally blind or deaf. From a chiropractic clinical perspective, pain, either ongoing or elicited by the doctor during diagnostic tests, is the most readily accessible test of neurologic involvement. Quasiquantitative assessment with instruments such as the VAS are more useful than the purely qualitative assessments, because they permit a more precise tracking of outcome. By noting the specific areas involved in pain, the chiropractor often can derive a refined understanding of segmental levels of involvement of subluxa rion-induced dysfunction, and this is useful in directing the practitioner to the areas to be adjusted.
Neurologic Effects of Adjustive Procedures The most dramatic effects of adjustive procedures are related to the reduction or elimination of back pain (47,48) . Decreased pain appears to be associated with increased range of motion, supporting the dynamic focus of rhe vertebral subluxation complex. Mechanical spinal challenge has been demonstrated also to produce decreased reflex activity in adrenal and renal sympathetic nerves, followed by a rebound increase of activity of the adrenal sympathetic nerves caused by a baroreceptor response. The neurologic as well as the kinesiologic components of the vertebral subluxation complex paradigm offer a rich and varied arena for further study of this model.
ConnectIve lInue Component The major impact of connective tissue changes in the vertebral subluxation complex model is seen with joint immobilization. Joint stiffness (99) or contracture (J 00,101), which is known to increase with age, has been the subject of intensive research because of the use of casting in orthopedic procedures (101) . All connecrive rissue elements are affected by immobilization, each with its own unique pattern of change (20,101 ). Synovial fluid undergoes fibrofatty consolidarion, progressing to more adherent fibrous tissue and ultimately providing a marrix for the deposition of bone salts (26) in the final stages of ankylosis. After joint immobilization, articular cartilage shrinks because of the loss of proteoglycans (102). Its cellular e1emenrs exhibit a reorganization (103), rhe surface develops ulcerations that connect the synovial space with the subchondral bone, and ultimately it shares the same fate as the synovial fluid by ossifying (104). Shrinkage leads to softening of the cartilage, which renders it more susceptible to damage by minor rrauma (105 ). When joints are immobilized, adhesions form between adjacent connective tissue StruCtures (26,103). Forced motion leads to a physical disruption of rhese adhesions as well as a disruption of inrermolecular cross-linkages (32). Adhesions also may form between the nerve root sleeve and
9 llHI Vertallral SlMlxIllon Camplex
159
the adjacent osseous and capsular structures in
bling changes in hypermobile joints. If the discs
the interverrebral canal (106), berween rendons
are analyzed as a unit, the two effects cancel, giving the appearance of no change in the ND.
and articular capsules, or between any two cooneccive tissue structures that come into COntact
and do not move relative to each other. The effect
DIagnostIc Tests
on articular connective tissue depends on the
Virtually all tests for connective tissue integrity are subjective in nature. The standard orthopedic tests are the most accessible and are widely used in clinical practice (43). Passive versus active
position of the joint when it is immobilized (20, 107), a reflection of the forces placed on the respective tissues (1 05,108 ). Age is also important in determining the response to altered forces
motion can give insight into the nature of inju.ries
(109, 110). [n developing bone, excessive pressure inhibits bone growth, whereas a reduction of pressure may accelerate bone growth (111 ). In mature skeletons, abnormal distribution of stresses leads to altered mineral deposition and osteophyte formation (112). Weight-bearing and
and help differentiate berween muscular and connective tissue problems. Palpation is a powerful
motion appear to exert separate influences on the
maintenance of connective tissue (113 ). Ligamentous contracture is widely discussed
as a mechanism for joint stiffness (32) . This may well apply to later stages of immobilization, but in the earlier stages of immobilization degeneration, ligaments become more pliable and compli-
procedure for eva luating connective tissue. Static palpation can provide information relating to specific connective tissue involvement in joint
dysfunction, and motion palpation can give a skilled clinician an indication of segmental stiffness and loss of "joint play" (43) (see Chapter 4) . History and presenting symptoms can also be revealing with regard to connective tissue involvement. Age is a significant factor in connective tis-
sue integrity, and a history of prior surgery or trauma to a joint or region can suggest connective
ant, a condition referred to as ligamentous laxity
tissue involvement. A history or diagnosis of
(100,113-115 ). Alrerations of the point of attachment of ligament to bone after immobilization are also well described (100,116), and this is a signiEcant faeror in the ligament's response to Stress.
osteoarthritis or other arthritides can provide sig-
Most research on joint immobilization has
been performed on extremities, especially knees and elbows (1) and on experimental animals such as rats (103 ), rabbits (11 7), and dogs (109). Studies with humans have suggested that the animal findings are applicable to human spinal degeneration (24,118-120); however, very little research has actually been conducted on the effects of immobilization on the spine itself in either animals or humans. Most of the studies that have been done on the spine are related to scoliosis (112) or lumbar discectom y (24). [n scoliotic
nificant insight. Radiographic analysis is most helpful in deter-
mining the involvement of osseous elements in spinal dysfunction and degeneration (43), but is relatively useless for soft tissue, such as ligaments and articu lar cartilage unless they are ossified. MRl , however, holds great promise for the determination of soft tissue involvement in the subluxation complex and spinal degenerative processes (see Chapter 5). Range of motion analysis is very revealing with regard to connective tissue in volvement,
especially when performed passively. When muscle contraction is not involved in the motion, restrictions mOSt likely indicate connective tissue involvement.
spines, changes on the concave side of the curve
differed from those on the convex side (121 ), the former resembling ligamentous and cartilaginous changes in immobilized joints, the latter resem-
Therapeutic Benefits Little research, if any, exists that directly evaluates the effect of adjustive procedures on connec-
160
1111 Subluxation CGmIIIIx
rive tissue. Results of animal studies, however, are revealing, as are results of medical research using continuous passive motion in promoting healing in injured knees. Restriction of motion of a joint
leads to profound degenerative changes in connective tissue. Return of motion can prevent or
reverse these changes (1). Clearly, if knee joints are allowed to remain motionless after surgery,
they will develop internal adhesions, which will limit mot io n in the future, hence the use of con-
tinuous passive motion immediately after knee surgery. Claims abou nd that regula r adj ustments prevent the development of disc degeneration and, a ltho ugh this sounds plausible, there is no evidence to support this claim. It would be anticipated that simi lar benefits would be bestowed on
degenerative process known as disuse atrophy (122-124). The precise role this plays in joint degeneration is not well understood. Although the changes in muscle function a re often completely reversible (124-127), the time required for complete restoration of muscle function depends on the duration of immobilization ( J24,125). These findings are complicated by the different responses to immobilization by different muscle types ( 124,128-130), as well as by differences in degenerative response related to the position of the joint, and thereby the length of the muscle in the immobilized state (125,131-133). In some cases, the muscle c hanges
3fC
secondary to immo-
bilization, but in turn contribute ro joint degeneration (103). In other instances, such as trauma,
ligaments , tendons , and capsules, but confirma-
congenital anomalies, or diseases that affect mus-
tion of this awaits the appropriate research.
with neuromuscular problems. Historically, chiro-
cles (s uch as polio and muscular dystrophy ), muscle degeneration or pathology can be primary and also might contribute to joint degeneration. It is not always possible to discern the role of muscle in joint pathology, especially of the spine. In particular, scoliosis poses an enigma. Although muscles tend to differ on the concave versus convex
practic
nerve"
sides of the scoliotic cu rve, their contribution to
app roach to managi ng health care problems, and osteopathy, one of the early rivals of chiropractic, espoused the "muscle on vessel" concept. The two schools of thought were dogmatically
the development of the cu rve is nOt understood in most cases ( (34). Current trends in scoliosis theory lean tOward the idea that there is a loss of unilateral regional control of muscle tone or loss of coordination of the righting (postural ) response in the spina l musculature (135, 136). Virtually every significant aspect of muscle structure and function has been eva luated in the context of degenerative changes after immobilization. In studies of induced immobilization of the knee, it was shown that in the early stages of
Myologic Component It is perhaps trivial to state that muscles maintain osseous relationships as we ll as move bones, but such a realization is profound to one who works represented
the
"bone
on
entrenched, and any inclination of one toward the other was anathema. Some in rhe chiropractic
profession sti ll hold to this narrow perspective, but most realize the importance of muscles in the overall function of the human body and are willing to incorporate muscular activity and dysfunc-
tion into their clinical practice. Evidence of this is the close association of chiropractic practitioners with massage therapists and the development of schools of thought within chiropractic itself that address the muscular component as the primary focus of patient management (11 ). O ne of rhe most sign ifi cant aspects of muscular activity from a chiropractic clinical perspective is the fact that, when joints are immobilized, the muscles associated with them undergo a
joint degeneration, restricted joint mobility was
caused almost exclusively by the muscleltendon unit (26); curting the muscle away restored movement ro normal ranges. In later stages, mobility appears to be restricted by capsula r and ligamentouS stricture (118,137) followed by intraa rticular adhesions (132). Muscle tension might lead to excessive degeneration of cartilage by compressing the joint surfaces tOgether (103), thereby con-
9 The VeI'IaIII'1I SUlllllXatIon Complex
161
tributing ro the development of osteoarthritis. A vicious cycle has been described (72) in which muscle spasticity leads to joint contracture, which
immobilized limbs between the tendon and its sheath (138).
leads ro morc spasticity and muscular contrac-
Evalua tive Procedures Evaluation of muscle function and integrity, like that of connecrive tissue, remains largely a clini-
ture. The specified treatment for this condition is ro rerum the joints to their full ROM and maintain that range through the healing stages. Muscle spind les are adversely affected by immobilization, showing significant morphologic, physiologic, and biochemical changes, including shortening and thickening, degeneration of the primary spindle endings, swollen capsules, and loss of cross-striations (138,139) . Physiologic alterarions include increased sensitiviry to stretch and elevation of resting rate of discharge (138,140). One consequence of such an increase in spindle activity would be ro feed excessive stimuli into the central reflex pathways, resulting
in altered efferent activity. This could lead ro the overstimulation of muscle groups that respond to
the stretch reflex leading, in the end stare, to muscle spasm and tender trigger points. Alternatively, such input could lead ro reflex inhibition or failure of joint musculature on challenge (141) . When a joint is immobilized, the effect on muscles depends on their length in the immobilized state ( 133,142) or the angle at which a joint is fixed ( 122). Such changes have been reported for gross morphologic appearance (143) as well as biochemical (144-146) and ultrastructural ( 122 ) characteristics. Shortened muscles show a
cal art. Palpation is used to determine tautness
and tenderness of the muscle mass. Elicitation of pain during active or attempted movement can
indicate muscle injury (43) . Of course, a knowledge of anatomic relationships of muscles ro the relevant osseous structu res is implicit in being
able to diagnose muscle injury and dysfunction. Stretching a muscle by moving its associated joint in an appropriate direction can be revealing as to
the state of the stretched muscle. Muscle testing has long been used to evaluate specific muscles or groups (43). An attempt is made to isolate a specific muscle or group and challenge its strength by manually applying pressu re. In some instances, attempts have been made
to objectify this process by using an intervening air bladder (sphygmomanometer), but the uncertainties .in positioning and cooperation make this
reduction in tension -producing capacity, whereas
approach largely subjective as well. Severa l systems have been developed to determine muscle strength by developing standard reference frames and protocols for determining applied force, using either inflatable bags or pressure plates. With these, as with the handheld pneumatic sensors, problems with reproducibility seriously impair the interpretation of results of such deter-
those chronically stretched retain their ability ro
minations. By contrast, dynamometry recordings
generate force in direct proportion to changes in
of handgrip strength have found wide acceptance in the analysis of upper extremity problems such as carpal tunnel syndrome. All muscle strength
cross-sectional area. Alteration of the distractive forces applied to the Achilles tendon induces extensive cellular and extracellular changes in the musculotendinous junction (146). The distribution of cell types and architecture of the extracellular matrix depend ro a large degree on the type of force applied ro the tissue (compressive versus distractive) (147). Early mobilization of previously immobilized limbs increased the rate of healing in lacerated flexor tendons (148 ), whereas adhesions form in
determinations rel y on relative muscle strength
of the individual's left side compared with the right. This has to be reconciled, to some degree, with the inherent differences in left and right sides relative ro normal handedness. Therapeutic Benefits Directed muscle work is unquestionably beneficial, and numerous reports have been published
162
The SUlllllXaIlon Complex
on the effects of trigger-point therapies, Nimmo receptor tonus procedure, shiatsu, and massage (11). It is often difficult to differentiate the benefits of simply touching someone from rhe benefits of massage, and no doubt both playa role when massage or other muscle work is performed. Cervical traction procedures have been shown ro reduce cervical muscle spasm, and similar
responses have been reported in the lumbar spine (11). Mobilization procedures are used in cervical whiplash injuries to reduce muscle inflammation and cervical pain. Ice is applied to injured and inflamed muscles to slow the inflammatory process and facilitate healing in the early stages of acute inflammation. This can be very beneficial to the patient and facilitates the doctor's task if the patient's pain is reduced (11).
vascular Component Each motion segment is supplied by a segmental artery that passes through the intervertebral canal into the spinal cana l and divides into dorsal and ventral radicular arteries (149), supplying, respectively, the dorsal and ventral nerve roots. These arteries course along with the rOOts and enter the spinal canal, piercing the dura and eventually anastomosing with the spina l arteries and contributing to the blood supply of the spinal cord. Occasionally, one of these carries most of the blood for that segment (56) and such asymmetries may contribute to radicular-type symptoms, possibly through insufficient anastomoses. These arteries are susceptible to the same mechanical forces as are the nerve roots, and if osseous displacement impinges on a nerve or root and leads to compression of that structure, the artery may be compressed as well. Each intervertebral cana l contains, as well, a
segmental vein that drains the spinal canal and vertebral column. The veins are the exit ports for the venous plexus of Batson (150), an extensive
vide a route whereby toxins or inflammatory agents from one area of the spine could influence more remote areas, as is believed to accoum for metastatic dissemination to the spine (150). It is unclear what role specific intersegmental motion plays in regional venous drainage, but it could contribute to clinical symptomatOlogy. In other parts of the body, movement is critical to proper venous circulation (152) . Blood flow increases on resisted rhythmic contraction of the calf and thigh muscles (153) . Immobilization likely leads to localized venous stasis, which effectively creates a negative relative pressure at the area of immobilization. Retrograde venous flow then can bring roxins into the area of immobilization. Whenever venous stasis occurs, there is a reduced
rate of removal of the toxins of metabolism, which, in turn, leads to inflammation and an accelerating degenerative process. Experimental arteria l or venous occlusion is
known to lead to joint stiffness (99), and recent studies have clearly demonstrated that venous occlusion is associated with spinal degeneration. Compression within the intervertebral canal by disc protusion, osteophytes, tumors, or hypertro-
phied bone potentially affects the vascular component before affecting the neurologic structures directly, (151) and veins, because of their thin walls, can easi ly be compressed and occluded. Lack of proper venous drainage may lead to inflammatory states. Diminished venous return leads to
alterations in capillary distribution around joints (154), and a similar mechan.ism has been suggested in immobilized joints (153,155 ). Vascular abnormalities are known ro be contributing or complicating facrors in a range of clinical conditions, including thoracic outlet syn· drome (156), trigeminal neuralgia (157), and ver· tigo (158). The vertebral arteries are known to occasionally develop asymmetrically, with one side making an insignificant contribution ro cra-
anastomosis of vertebra l veins containing no
nial blood flow (159). Similar patterns of devel-
valves to control the direction of blood flow (151). Because of this, venous drainage is dependent on posture and the forces of gravity, which allows for retrograde flow to occur. This can pro-
opment are seen in the segmenta l arteries as well. In addition, vertebral arteries are known to
form loops or kinks within the transverse canal (160), and this is believed to lead to signs and
9 The VII'llIIIrailullluxallon Complex
163
symptoms of cerebral ischemia. Vertebrobasilar
cular system in one of several ways . If srasis ex ists
insufficiency is a contraindication to rotatory
because of a lack of motion, then restoring motion allows the vessels to clear out inflamma-
adjustments to the upper cervical spine (161). Cases have been reported of paralysis, hemiparesis, Wallenberg's syndrome, or death resulting from extreme rotation and extension of the cervi-
cal spine, whether voluntarily (162) or through cervical manipulation (161). Stroke after manipulative procedures may be caused by dissection of the vertebral artery, thrombus formation, and embolic development (43) . Structural anomalies must be considered as well (160, 163). Evaluative Procedures There are virtually no evaluative procedures to determine the integrity of the small arteries and vein, such as the segmental arteries that pass
through
the
intervertebra l
cana l.
Although
tOry exudates. When postural distortions are present, which leads to arterial compression, then
restoring a more normal biomechanical integriry to the body can have a profound effect on the vessels invo lved. It has been postu lated that inflammation around the intervertebral cana l can
lead to compressive edema that cou ld occlude veins or arteries. Restoring motion to those seg-
ments leads to reduction of inflammation and restoration of normal vascu lar integrity. All of these hypotheses are purely speculative, however, because little effort has been put inro understanding the basic mechanisms of manipularive and chiropractic procedures.
angiography can provide such information, its
Innammatory Component
use is limited because of the invasiveness of the procedure, and such information is genera ll y nOt considered clinically relevant.
distinctive component has met with some discon-
Extension and rotation of the cervical spine
have been used to screen for predisposition to vertebral artery compromise, along with a series
of screening tests including eva luation of the patient'S history for vascular problems, blood pressure evaluation, and carotid artery palpation
(43). The effectiveness of these procedures, how-
Identification of the inflammatory response as a tent and conrroversy. Many believe that rhis aspect belongs in the vascular component, and Faye (4), in the five-component model, discusses inflammation under histopathology. The inflammatory response is a composite of cellular and biochemical processes that is largely mediated by rhe vascular sysrem (164), but ir is initiared by local events within the tissues themselves. Highly
ever, has nor been demonstrated.
vascula ri zed tissues, such as skin or muscle,
Venous inregriry is even harder to assess than that of arteries, especia ll y for those veins of inter-
express inflammation very differently than does fibrous connective tissue (165) . Lacerated tendons undergo a repair process controlled by intrinsic
est ro chiropractic and other manipulative proce-
dures. The presence of radicular pain could be indicative of venous obstruction, but such a diagnosis is pure speculation. Phlebography has been used to evaluate spina l venous obstruction (158), but again its use is limited because of the invasiveness of the procedure. For clinical pracrice in chiropractic, it is of lirrle value, but for research
into the mechanisms underlying that practice, the procedure holds promise.
mechanisms that involve recruitment of tissue
macrophages and proliferation of fibroblasts (148). This is more represenrative of a chronic inflammatory response (165,1 66), which a lso leads to an alterarion of collagen types (167, 168), resulting in fibrosis and long-term exposure to the destructive actions of macrophages (165). Immobilization of joints clearly leads to an inflammatory response (155), rhe end point of which is ossification (169) . Inflammatory spillover into
Therapeutic Benefits
surround ing tissue is a critical parameter to moni-
Restoring normal motion to a motion segment could have a direct influence on the intrinsic vas-
tor (170), as implied in the concept of chemical radiculitis (171). It represents one way in which
164 the degeneration of spinal joints may affect the neurologic components. The mOSt obvious clini-
cal manifestation of inflammation is pain, which is the major presenting complaint in chiropractic offices (39) . Arthritis Pain caused by rhe inflammarory processes in arthtitis is perhaps the most obvious atea of inflammation associated with the theory of chi ropractic. Arthritis means simply inflammation of a joint, and it can affect any joint of the body, including the spine (1 14,11 9). All forms of arthritis are associated with pain and decreased movement of the involved joints. When scientists wish to reproduce arthritis in experimental animals, the most common procedure is to immobilize rhe
joints (172-175) . Even in humans, situations that result in immobilization contribute to osteoarthritis (176), which is commonly associated with scoliosis caused by restticted motion of the spine ( 11 9). Restoration of movement can decrease the rate of degeneration or even restore rhe joint to its normal structure and function (177), as seen clinically (178,179) and in basic animal research (17, 180). Thete is a very close association between movement and the brea kdown of connective tissue and the development of the inflammatory processes associa ted with the development of arthritis. Although osteoarthritis, or degenerarive joint disease, is classically considered a noninflammatory condition (181), as many as 75% of cases of osteoatthritis show evidence of inflammation (182). Molecular fragments of collagen (183,184) and proteoglycans (185-187) are inflammarory stimuli and have been associ~ ated with rheumatoid arthritis (188-190), as well as polyarthritis in mice (191) and humans (192), osteoa rthritis (193), and other arthritic conditions (194). The details of this process a re dealt with more thorough ly when we discuss the biochemical compo nent. LnAammation of Nerves and Nerve R oots Inflamed nerves are hyperexcitable (54) and exh ibit behavior different from that of normal
nerves. The DR G of normal nerves respond ro mechanical stimulation by a discharge of action potentials, which stopS on cessation of the stimulus; when inflamed, however, they continue to fire long after the mechanical stimulus has ceased. It has been proposed that the ganglia and nerve roots are affected by inflammarory agents after disc herniation, a process that has been called "chemica l radicu litis" (171). Nerves become inflamed when venous obstruction leads to stasis and edema. Thus, compressive forces in the inrer~ vertebra l ca na l need not directly affect the nerves to impact neurologic func tion . Such processes appear plausible as mechanisms ro mediate the effects of subluxation degeneration. Assessing Inflammation The classic cardinal signs of inflammation are rubor, tumor, calor, and dolor (redness, swelling, heat, and pain, respectively). These characterize the classic acute inflammatory response. Evaluation of these is by observation, interview, and palpation. Heat can be objectively evaluated by thermographic methods and pain can be assessed by rating scales, such as the visual analogue scale (VAS) a nd batteries of que&tions such as the Oswestry pain disability questionnaire. Swelling, o r edema, can be eva luated by observation and palpation; turgor in the area suggests edema, and a pitting of the skin that returns slowly after digital pressure to express accumulated tissue fluids helps to confirm the diagnosis. Redness is readily seen if it i superficial. Assessing inflammation is more challenging if the injury is deep, such as a herniated IVD or zygapophyseal joint inflammation. Localized heat sti ll may be detected by manual palpation or thermographic procedures, and swelling of the deeper tissues often can be palpated. Rubor, in such cases, is impossible to detect. Pain is often considered to be pathognomonic for inflammation, particu larl y if trauma o r tissue damage is suggested . Radicu lar pain is frequently interpreted as a rising from inflammation of the nerves or their rOOts. Localized pain on passive movement is suggestive of joint inflammation, whereas pain on active
9 Tl18 Vlll'llIbrai SUbluxation Complex movement
may
indicate
muscle
or
tendon
involvement. rain elicited by touch is clearly an indication of an active inflammatory process, such as around the ankle joint that has been sprained. Chronic inflammation is much harder to evaluate, especially in the deeper tissues. In superficial tissues, chronic inflammation is identified as scar tissue. In joints and between connective tissue structures, it is characterized by fibrous adhesions. Late stages of inflammation manifest as osteophytes or ankylosis and at this point are not clinically manageable, although they may give rise to problems that continue to haunt the victim. Managing Inflammation Acute inflammation is managed by applying ice to slow the process. In joints, especially those of the spine and particularly the IYD, it is not possible to effectively cool the joint, so other methods mUSt be found to help resolve the situation (11). Of course, medicinally one can recommend the use of antiinflammarory agents, but such measures are outside the purview of chiropractic. Manual procedures, however, can be quite effective in reducing inflammatory srates. Pressure, either applied manually or by means of a bandage, can help to express edematous fluids and restore morc normal rissue integrity. Often a stroking motion with light to moderate pressure will effectively move or "milk» inflammatory fluids from a local edematous area into the general circulation, resulting in a "flushing" of the injured area with fresh extracellular fluid. Simply raising an extremity, such as an ankle or knee, higher than the rest of the body leads to a gravity-assisted flushing of the injured area. Mobilization is a powerful tool for reduction of inflammation. Because immobilization leads to inflammatory changes in the articular tissues, the converse leads to a reversal of that state. Indeed, passive mobilization is widely used to promote healing after knee surgery (179), and passive motion has been used successfully in the management of cervical flexion/extension injuries (30) .
165
Biochemical Aspects 01 the Model ConnecUve lIssue Mechanical failure of ligaments, discs, capsules, or other connective tissue can result from local variations in chemical composition (195). In addition, alterations of the biomechanical forces that Stress connective tissue lead to local changes in the biochemical composition of the tissue (l). We thus have a clearly delineated link between biomechanics and biochemistry as relates to connective tissue structure and function. Collagen forms chemical cross-linkages that hold adjacent collagen molecules tOgether and stabilize its overall structure (32). The numbers of these cross-linkages increase with advancing age (196) and in states of degeneration (197). This is involved in the formation of connective tissue adhesions as are known to form between the nerve root sheath and the articular capsule (26,103). The sulfated glycosaminoglycans draw water into the spaces between individual collagen fibrils. The water contributes to the space-filling properties of the proteoglycans but also provides for lubrication between adjacent collagen fibrils (32,198), especially in fibrous connective tissue. On immobilization of a joint, the first measurable biochemical change is a decrease in proteoglycan, a change that occurs in all connective tissue components of the joint (102). This allows the collagen fibers to approximate each other more closely and facilitates the formation of more collagen cross-linkages (196). The longer a joint is immobilized, the more collagen cross-linkages are formed . This appears to be a mechanism for stabilizing the joint in its new ROM . Remobilization of a previously immobilized joint leads to a disruption of collagen cross-linkages (197,198), as by the high-velocity, low-amplitude thrust that is characteristic of the chiropractic adjustment,
lnnammatlOn Another aspect of connective tissue biochemistry that is significant is the antigenic and inflammatory properties of fragments of collagen (183,184) and proteoglycans (199) . Fragments of
166
TIle SUbluXallon COIIIpIex
hyaluronic acid are potent angiogenic agents; that is, they stimulate the development of new capillaries (200). It has long been believed that rheumatoid arthritis is an autoimmune disease,
with the organism producing antibodies to its own collagen (183). Collagen plays a significant role not only in rheumatoid arthritis (207) but in osteoarthricis and other joint diseases as well
(193,194); antibodies to collagen are frequently found in patients suffering from nonrheumatoid arthritis. Antibodies to proteoglycans exist in rheumatic diseases such as polychondritis, osteoarthritis, and rheumatoid arthritis (191).
lation, but this is a generalized Stress response and not a specific effect of chiropractic adjustive procedures (207). Muscle disuse after immobilization leads to an insulin resistance altering glucose metabolism (208). No doubt other hormonal effects on neuromusculoskeletal tissues have a significant impact on biomechanical function or response, such as the effect of pregnancy in softening the ligaments of the female pelvis to facilitate delivery.
PharmacolOgIC COnSIderations Given the widespread use of drugs by the medical
Connective tissue is known to release specific
profession to treat a variety of diseases and con·
chemical mediators of the inflammatory response called autocoids (186), including a group called
ditions, including musculoskeletal disorders, the effects of drug usage on the course of chiropractic
connective tissue activating peptides. There is an
management programs must be considered. In addition, there is a growing movemenc in the chi·
inflammatory response to tissue injury, such as ligamentous or capsular tear (150), but the inflammatory response to simple immobilization
is less well understood. Evidence of such a response includes the development of pain (19) and the marked alterations of joint morphology seen on immobilization (26, 103). The products of connective tissue degradation could stimulate an inflammatory process as an initial step in tis-
sue remodeling and adaptation to new dynamic joint function, Stich as
limited
motion.
The role of histamines in inflammation must be understood, as well as the events that control their release from the mast cells and other immunologic components (202,203). Similar consideration also mUSt be given to the role of prostaglandins in the pain response (204,205).
ropractic profession toward the use of proprietary and nonproprietary drugs (209). Although it is not the purpose of this chapter to debate the use of drugs in chiropractic, the effects of drugs on human physiology and function cannot be ignored. As an example, the regular use of muscle relaxants might well alter the outcome of a chiropractic adjustment program. Conversely, it is well known that narcotic use leads to a type of muscular rigidity (2 I 0), and such an effect could have a dramatic impact on the patient'S response to care.
The use of injectable and topical steroids to treat inflammatory conditions can lead to adverse
effects (2 I I) that could interfere with effective chiropractic care.
Endocrinology
DIscussion
Serum aldosterone levels have been shown to
The VSC represents the current state of the evolution of the concept of subluxation. It does not identify any single event or process as the sole causative element in the complex process of sub-
decrease after chiropractic adjustments in patients
with hypertension (206). Spinal mobilization resulted in specific sympathetic input into the adrenal gland (36) . Although adrenal hormonal output was not monirored, one would expect a
change of circulating medullary hormones based on the neurophysiologic observations and observed changes in heart rate and blood pressure. Cortisol levels increase after spinal manipu-
luxation degeneration but rather places inco con-
text the various tissues and processes that playa role in this complex phenomenon. It is the author's belief that there is no single identifiable subluxation that accounts for all of the problems and conditions that respond to chiropractic and
9 1be Vllrl8bl'" lWIIuxatlon COmplex
167
other manual therapies, bur rather there are a
trigger-point therapy, etc. It is now time to begin
family or several families of processes. Any par-
of the patient. As an exa mple, patients with genetica lly linked connective tissue disorders would be expected to have a predominance of
to explore the implications of this vast body of procedures and understanding of human response to manual procedures and to tap into the wealth of knowledge of how and why these procedures affect human health. Only by understanding these processes can we hope to evolve further and
connective tissue involvement in degenerative
assume a role of preeminence in health care man-
ticular tissue component may predominate in subluxation degeneration, depending on the stare
processes. The extent to which these lead to biomechanical and kinesiologic dysfunctions that are manageable by adjustive and manipularive procedures defines the role thar chiropractic mighr play in such cases. Similarly, chronic alco holics suffer from neurologic and kinesiologic disorders that may bring them to a chiropractor. The extent to which these problems can be addressed by adjustive procedures is largely irrelevant unless the consumption of alcohol is curtailed. Knowledge of these aspects of human health are essential for the chiropractor as a primary care provider and a holistic practitioner. It is remarkable how human health changes with the changing of the environment in which we live. Today's major problems have shifted from infectious diseases of the turn of the century to degeneracive conditions, such as arteriosclerosis and arthritis of the more recent past, and
toward biomechanical problems, such as repetitive stress injuries, whiplash, and low-back pain in the current era. As health consciousness improves and diet and exercise become morc of a
priority in the daily lives of typical Americans, the biomechanical problems will take on even
agement. As society moves away from the obsession with chemical intervention, only a solid
understanding of the alternatives will provide guidance and comfort for the masses to aid them in the acceptance of new and different approaches to their health problems. The VSC lays the foundation for a solid understanding of the myriad processes involved in spinal degeneration and its effect on human health. By integrating all aspects of spinal structure and function into our understanding of sub-
luxation degeneration and its reversal by adjustive procedures, we can better understand the processes involved and how to correct them. We can approach the development of new techniques and procedures more rationally and with an underst~nding that will give us confidence in what we do. The VSC does nOt prove the existence of subluxations; rather, it provides a context in which
to discuss and understand the processes involved. It does not limit one to a single perception of subluxations but recognizes and describes the various
components and elements that may be involved, how these elements interrelate, and what their
more significance. Chiro practic, because of its
relative importance is in any given clinical situa -
role in managing such disordets, promises to provide a substantial portion of the care for and
sophisticated understanding of what we do and how we do it. Fundamental to chiropractic is the adjustive
tion . It allows each practitioner to identify where he or she fits into the grand scheme of things without compromising the integrity of anyone, regardless of their particular approach to patient management. It provides a common language for the development of dialogue, not only between chiropractors and other health care providers, but
procedure, which has undergone a dramatic evo-
among chiropractors themselves.
lution in the past century, from the excessively forceful procedures of early chiropractic pioneers to more refined osseous adjustive procedures and subtle reflex techniques, nonforce procedures,
Although the VSC dea ls only with the neuromusculoskeletal aspects of subluxation degeneration, one must not lose sight of the profound effect that correction of subluxations can have on
treatment of such conditions. It is essential, therefore, to develop more realistic models and more
168
1l1li s.mmllllon complex
a patient's life. When a person is dysfunctional because of pain and integrity is restored by adjustive procedures, what profound emotional and psychologic effects would that individual experience? The VSC allows for every aspect of chiropractic clinical management to be integrated into a single conceptual model, a sort of "unified field theory" of chiropractic. Each diagnostic procedure can be mapped into one or more of the components, and specific therapeuric effects of adjustive procedures can be assigned to specific tissue components or their elements. Each component can, in turn, be described in terms of precise details of anatomic, physiologic, and biochemica l alterations inherent in subluxation degeneration and parallel changes involved in norma lization of structure and function through adjustive procedures . Still, we have seen those who cling to the arcane ideas of a prior century use the VSC as a paradigm to promote their outdated ideas. We cannOt afford to let this distract us from the value in the mode l as it is presented in this chapter. Conversely, many who have denounced the concept of subluxation see the VSC as just another th inly vei led rationa lization of a cultist group using unproven procedures. These, too, have lost sight of rationa l enterprise, for their objections are based on past perceptions and nOt on the current State of knowledge. The VSC was designed [0 bring understanding to an area that was fraught with confusion; it was crafted to be consistent with known rationa l thought and valid information; it was designed to adapt to a growing body of information and understanding of the function of the human body and how the physical machi nations interrelate with what we call human health.
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Theoretic Models of Chiropractic Subluxation Robert D. Mootz KayWllrdl
Vertebra l ma lposition, joint fixation, men iscoid entrapment, somatic dysfunctiona l adhesion, nuclear fragmenta tion, facet tropism
After reading this chapter you should be able to answer the fo llowing questions:
Question #1
How does the early chiropractic subluxation differ from an osteopathic lesion?
QueItIon #2
How does asymmetry of the spinal articular facets predispose a patient to mechanical joint locking?
Question #3
How do chiropractors use the placebo effect to benefit their patients?
176
The SUbluxation Complex
T
his discussion offers a classification of the chiropractic concept of subluxation. The "chiropractic vertebral subluxation" remains one
>
Historical Development of Manipulable Spinal Lesion Concepts
of the most controversial concepts in chiroprac-
tic. Irs nature remains elusive, and its diagnostic and politica l va lue have been vigorously debated (1-3). Numerous reviews, discussions, definitions, and justifications abound (4-7), but the ability to discuss, support, critically evaluate, and differentiate between what is known, what is o nl y supported, and what is purely conjectu re regarding the subluxation remains an emotional issue withi n the profession. A lack of agreement on standardization in definitions and classifications has permeated discussions on adjusting and subluxation (8,9). This lack of agreement has stimulated a study for the development of chiroptactic nomenclature through consensus. In addition
[Q
chiropractors, other health care providers manipulate the spine, includ ing some osteopaths, physi-
ca l therapists, and medical manipulators. Each professional group has developed and perpetuated a phi losophica ll y trademarked "brand name" for the spi nal lesion they manipulate. Over the years, each has had its own explanations and rationa les describing their lesion and its physiologic implications. These are summarized in the box at right. The Palmers originally described and defined the chiropractic subluxation by a number of clinica ll y observable characteristics (10, ll). They proposed that subluxation was a structural disrelarion that resulted in altered or impeded neurologic function (12,13) . The American Chiropractic Association has established that a sublu xation represents an abnorma l physical relationship between adjacent anatomic structures whose contiguous tissues elicit neurologic responses (7) . Although the soph istication of hypothetical mechanisms has increased (5,14, 15), chiropracrors have continua ll y emphasized rhe proposed neurologic component of the subluxation. This emphasis on the neurologic components of the subluxation has led to development ( 16)
• Early conception (1910): Structural disre1ationship of spinal joints causing nerve impingement at the intervertebtal foramen. • Modem conception (1979): Abnormal physical relationship between adjacent articular structures eliciting neurologic responses. OIteopItIItc CGMIPII
• Early conception of osteopathic lesion (1899): Altered relationship of zygapophyseal joints affecting flow of vital body fluids (blood, lymph, nerve). • Modem conception of somatic dysfunction (1973): Impaired or altered function of related somatic components (musculoskeletal, arthrodial, and myofasciall and related vascular, lymphatic, and neural elements. lledlcll ....I'.llblt .,1tII11tIIlGII_IIII
• Early conceptions (1930s): Facet fixation due ro mechanical derangement of the posterior joints may cause pain; intervertebral disc dysfunction may cause pain and/or radiculopathy. • Modern conception (1978): Joint dysfunction contributes to complex neurologic reflexes that affect the neutomusculoskeletal system. From Mootz RD. Chiropractic models: currenl understanding of venebral subluxation and manipulable spinal lesions. In SW«'1't' J. (ed). Chiropractic famlly practice. Gaithersburg, Maryland: Aspen Publishers, 1992.
and refinement of the vertebra l subluxation complex (17) (see Chapter 9). Osteopathy describes a different lesion altogether. A. T. Still ( 18) coined the term osteopathic lesioll to describe an altered relationship of the zygapophysea l joints affecting the flow of "vita l body fluids," especially blood and lymph. In recent years the osteopath ic profession has agreed on a name change to somatic dysfUNction. This
10 Theoretic Models 01 Chiropractic SubluxaUon
177
Munual medicine also has recognized manipulable spinal lesions. However, medicine's termi-
physiologic explanations. It is worthwhile to characterize some clinical Issues in attempting ro dasslfy subluxation models. All practitioners tend [0 follow similar clinical processes III attempting to identify the site of a manipulable subluxation . The box lists some common clinical characteristics looked for by manipulators. After a thorough history and phYSIcal examination, practitioners perform a mechanical evaluation. The manipulator may look for contributing
nology has been based on strict anatomic diag-
mechanical causes (nature of injury, repetitive
noses. Mennell (21) wa, convinced that a mcch ..lOical posterior joint derangement was responsible for loss of joim play. Cyriax (22) emphasized the contribution of "intervertebral disc dysfunction." Other mantlal medicine practitioners and physical therapists have theorized an IInportant role for loss of soft tissue elasticity (23). Although medical manipulators' opinions differ as to what the manipulable lesion is, they have tended to be skeptical of any significant neu-
postural activities), static asymmetries (high shoulder, altered curves, externally rotated hip or
rologic componenr other than pain being associ-
terns provide hisroric cues. Palpating for tenderness and muscle spasm or altered tone also may
ha, been defined as "Impaired or altered function of related C()l11poncnt~ of the somatic system:
musculoskeletal, arthrodial and myofascial strucrurcs, and related vascular, lymphatic, and neural
elements" (19,20). Throughout its history, the osteopathic world has speculated on the ischemic and trophic qualities of spinal disrelation as well as neurologic aberration.
ated with it. With recent English-language works of East European neurologists such as Lewit (24) and Janda (25, 26), medical thought is beginning
foot, erc.), dynamic asymmetries (gait, other movements), as well as passive and active individual joint ranges of Illotion (sratic and motion palpation). Some practitioners try to image these
altered mechanics radiographically (29). Most practitioners also look for changes
111
neurologic activity. This is often identified by patient symptomatology. Pain distribution pat-
suggest neurologic activity. Some look for indirect indications of neurologic involvement
b}' assess-
to appreciate morc complex neurologic ramifica-
tions of SPll1alloim dysfunction. Organized mediCllle as a whole has only recemly begun to acknowledge benefits from spinal manipulation .
>
Evaluation for Manipulable Subluxations
01II1I'I1 ........ A11111111"
Clinical Rationale Provides Logical Method for Model ClassHication Models of pathophysiologic processes traditionally result from attempts to explain empirically observable clinical phenomenon. Such IS the case with mantpulable subluxatlons. The historical models represent isolated attempts to do so. Research in this arena has occurred primarily wlthtn the osteopathic profession (27,28). With morc interest heing generated in spinal manipula-
tion as a result of several clinical trials dcmonsrranng effectiveness in the treatment of back pain, more attention is again focusing on possible
• History • Physical examination
• Special studies (radiographic imaging. clinical laboratory tests, etc.) . lclllnlCll _ _
• History of mechanical etiologies • Static structural asymmetries • Dynamic structuraVmechanical asymmetries • Static palpation • Motion palpation
• Imaging of structural alterations (radiographic, functional capacity testing, motion analysis, etc.)
178 ing vasoconstnctlon or dilation (thermography), and sudomotor activity (galvanic skin response). Standard neurologic indicators including hyper-
>
Models of Chiropractic Subluxation
reflexia or hyporeflexia, sensory changes, and
motor changes also may suggest spinal dysfunctions. Some consider altered tissue texture and edema as indications of aberrant local tissue metabolism or vascularization (rubor, tumor,
dolor, calor, etc.). All healers recognize the role the patient's psyche and lifestyle plays in the function of the body's somatic structures. Mental attitude, social
interactions, lifestyle habits, and Stress may induce muscular tightness that leads to more anxiety and contributes to abnormal muscle tension. Attempting to break the cycle with a spinal adjustment has been a clinical option taken by many manipulators.
When assessing the purposes of manipulation,
it is clear that aberrant mechanics, neurologic activiry, trophic function, or psychosocial problems are addressed. The argument then is made that a classification system for models of manipulable spinal lesion and subluxation should be based on these commonalities of generic clinical practice rather than "brand-name" theories. Spe-
cific explanations of the vertebral subluxation within each of these four general categories of biomechanical, neurologic, trophic, and psychosocial models are presented and summarized in the box. Rationales, explanations, and brief reviews of relevant literature of these clinically derived models are presented in the following discussion.
• Vertebral malposition • Fixation caused by adhesion • Fixation caused
• • • •
by meniscoid entrapment
Fixation caused by nuclear fragmentation Disc deformation caused by tissue creep Hypennobility and ligamentous laxity Mechanical joint locking
IIItnItItIIc ........ • Nerve, root, DRG compression or traction • Spinal cord compression or traction • Somatosomatic reflexes • Somatovisceral and viscerosomaric reflexes • Motor system degeneration • Psychoneuroimmunology ,...Ic ........ • Aberrant axoplasmic transpon • Intraneural micrcx:irculation ischemias • Macrcx:irculation ischemias • Altered cerebrospinal fluid flow Payl ..... cl.......
• Placebo effeCt • Stress reduction • Lifestyle modification
regarding radiographically demonstrable articular disrelationships. Trauma, disc degeneration, ero-
sive arthritides, and congenital factors all have been shown to cause such radiographic changes. However, reduction of such mechanical alter-
Models of Chiropractic Subluxation lIIom8chanIcai Models Vertebral Malposition One of the oldest concepts of subluxation considers trauma to be a major cause of altered joint position. Palmer (12) and Still (30) both discussed this model, and Leach's (5) chapter on intervertebral subluxation reviews medical literature
ations has not been demonstrated with manipula· tion. More subtle mechanical alterations are probably what chiropractors adjust, which are difficult ro demonstrate radiographically (29). The clinical value of radiography for such assessments has been questioned (3 j ,32) (see Chapters 5 and 8). The concept of a static misalignment, although promising initially, seems difficult to support. Chiropractic studies have thus far shown interobserver and intraobserver agreement of
10
n-..1Ic Modell 01 CI.....·1CIIc Slauxallon
many technique-based x-ray markings ro be relatively poor (32). Some radiographic mensuration methods indicating disc wedging and overa ll articular contours can be evaluated consistent ly
and are sometimes used as indications for mechanical therapies. However, good quantitative outcome studies clearly identifying usefulness remain ro be done. Although this mechanical approach may potentially ind icate aberrant segmental position, it also may be representative of activity of surrounding muscularu_re. Discussion of the larrer lies within the domain of neurologic models, specifically somatosomatic reflexes. Mechanically, the "out-of-place bone" is not likely ro be the sole explanation for chiropractic subluxation . Fixation Caused by Adhesion Adhesion in and around synovial joints may arise in two ways. It may result from trauma resulting in extracellular accumu lation of inflammatory
exudate and blood (33). Platelets then release thrombin-converting fibrinogen inro fibrin, which organizes into collagenous scar tissue, resulting in
a variety of soft tissue and articular adhesions. A second type of adhesion results from the dehydration associated with immobilization. Extensibility of connective tissue is caused
by infusion of water
between layers of proteoglycan molecules. This provides lubrication, allowing for a more parallel configuration and greater stretch under longitudinal tension (34 ). Immobilization leads ro dehydration with resultant app roximation of the proteoglycans, which tend to stick rogether, creating movement restrictions (35,36) . Another by-product of prolonged immobilization can be intraarticular fatty ad hesion within synovia l joints (37). The relevance ro spinal lesion models is that both trauma and immobilization are frequently implicated causes in patients with subluxation.
Manipulation increases movement in dehydrated tissues, promoting the imbibition of fluid, or the actual mechanical shearing or breakdown of newly deposited adhesions. This model explains many clinical phenomena and is supportable based on the literature (38).
179
Fixation Caused by Meniscoid Entrapment Bogduk and Engel (39) and Giles and Taylor (40,41) have reported on the presence of intraarticular synovial tabs or meniscoids. These tabs may cause fixation when the fibrocartilaginous edge of a tab gets caught between the articular surfaces (42). The resultant deformation and restriction, especially at end range, is also thought ro stress the joint capsule from which the men iscaid originates. This may result in irritation of [he capsular nerve endings and may contribute to
pain and spasm . Meniscoids appear to be present throughout the spinal facet joints (42,43). However, problems with this model have been identified (36) : meniscoids may not be present in fixed joints, and most meniscoids may actually be softer than the joint carti lage and therefore may be more likely ro be deformed or cleaved by the joint (38). Disorders such as rheumaroid arthritis appear to have associated proliferation of synovia l tabs (42), yet there does not seem to be any reporting of increased likelihood of fixation in these kinds of individuals. Although the potential is promising for some kind of role of synovial tabs, particularly as instigarots of muscle spasm (39), or perhaps through extrapment where the meniscoid becomes trapped beyond the articular facets, they do not seem likely to be the primary cause of subluxarion. Fixation Caused by Nuclear Fragments This model suggests that, through movement, a portion of the disc's nucleus pulposus pushes through weakened sections of the anulus fibrosis. A sequestrati on may occur on subsequent movements, impeding normal movement between the
end plates. Such restriction (as well as resultant muscle spasm) may resu lt in fixation (44) . Disc derangements have been implicated in manipulable spinal lesions for some time (45-47). Sandoz (48) suggests that long axis manipulation coupled with rotation could suction the fragment centrally. It has been suggested by Farfan et a l. (49) that the layers of the anulus migrate, permitting the disc ro withstand large amounts of compression before a second ruprure. However, manipu-
180 lators report fixation in joints without discs (for examp le, the atlanooccipira l junction, or the
sacroiliac joints) (24,50). Fixations seem to occur in younger individuals in whom disc degeneration is not a likely contributing factor. Further contradicting this model are arguments pointing out
that the earliest degenerative anular changes begin at the periphery and work centrally (51). Additionally, there seems to be little evidence of nuclear fragmentation on autopsy (51) . Disc Deformity as a Manipulable Lesion Radiographically observable changes in intervertebral disc alignment have been used as an indicator of subluxation (52,53). Prolonged compressive loading of a disc has been shown to lead to tissue creep deformity (54) that results in degenerativelike changes in anular composition. Manipulation of such discs has nOt been shown to alter either configuration or composition of Structures having undergone such tissue creep. However, it is reasonable to suggest that mechanical stresses (manipu lation, stretch, exercise)
directed in an opposing manner may help slow progressive degenerative changes. In light of Weisel's report (55) of a significant incidence of disc herniation in asymptomatic patients, the role
such trophic and biomechanical changes play clinically remains speculative.
Mechanical Joint Locking From a purely mechanical point of view, Steindler (56) noted that tropism in the lumbar spine, in which one facet faces relatively coronally while the other faces more sagitally, can lead to the sagittal facets mutually locking on each other. Farfan and Sullivan (57) describe this locking as the "cam" effect of the facets when one facet is rotated against its "fellow." They contend that the more coronal-facing facet fails to resist torsion as sheer force, with strain of higher magnitude than usual falling directly on the disc corresponding to the level of disc pathology and the side of disc herniation. Cop lens (58) suggests that tropism or asymmetry of the apophyseal joint causes diminished mechanical efficiency, leading to limitation of motion that may be readily relieved by manipulation. A change in the axis of rotation allowed by the slight translation in the vertebra l motion segment can screw down the inferior facets, twisting
them like an eccentric cam, and jamming them against the cuplike superior facets (59). Gravity and muscle spasm then continue to hold the facets in a locked position. A mechanical locking from a slight shift in the axis of rotation of the sacroi liac joints has also been described by Turek (60) (see Chapter 26) . The immediate relief often experienced after manipulation makes this theory
appea ling. Hypermobility and Laxity as Manipulable Lesions It is obvious that a lax joint is not likely to be mechanically benefited by manipulation. It ca n be argued, however, that hypermobility and the resultant irritation may lead
[Q
muscle spasm and
symptomatology that cou ld respond to mechanical stimuli. Manipulation of an unstable segment seems unlikely to promote greater instability, provided such manipulation is properly appl ied wit hin the joint's physiologic range. However, this approach would probably be temporary and palliative. Some have suggested that hypermobile segments resu lt from fixed or fused segments at an adjacent level (51). Instabi lity then may be an
Nerve, Nerve Root, and Dorsal Root Ganglion Compression or Traction Nerve compression
is of historical
nOte as
Palmer's "foot on the hose" theory (12). He suggested that nerve energy cou ld be reduced or increased from pressure applied by the vertebra . Leach (5) summarizes the debate on this model in his chapter on nerve compression. Early work by Hadley (61,62) suggested that nerve root compression could result from radiographically demonstrated intervertebra l subluxation. However, CreJin (63) tried to refute this. He attempted
indicator for assessment of surrounding areas
to close an electric circuit between wires placed
(see Chapter 8) .
along the nerve and inside of the intervertebral
181
10 11Ieoretk: Modell 01 ChroprIC1lc SUl*lxallon foramen in cadavers. Manual forces applied along all ranges of motion were unable to close the circuit. Both his methodology and conclusions could hardly be considered unbiased and do nOt
spinal canal pathology (75). Cord and neura l ele-
accounr for structural variants such as the trans-
ment distortion caused by traction also provide a
foramina l ligaments or functional alterations such as edema (64).
rationale for craniosacral techniques (76). Breig et al. (77,78) have investigated the mechanical relationship of the meninges with the spinal cord and the osseous vertebra l column. Distortion of the cervical spina l cord caused by stabilizing attachments of the dentate ligaments has been observed with normal cervical flexion (76,79) . The rationale for this hypothesis appears to be
Given that there 3 rc other structures within
the foramen (blood and lymphatic vessels, far, connective tissue, etc.), the possibiliry exists that
other kinds of mechanical stresses may affect the nervous sy tern. Luttges et al. (65,66), Triano and Luttges (67), and MacGregor et al. (68) have demonstrated that mechanical pressures and tensions may create a myriad of subclinical neuro-
physiologic a lterations. These range from changes in intraneural protein composition to altered nerve conduction characteristics. The dorsal foot
trauma consequence leading to sudden infant
death (74). Additionally, cord and thecal sac compression are well recognized as a complications of
sou nd, but no evidence exists to show that mechanical vertebral or cranial restriction is
capable of placing the kinds of force on cord structu res that creates a ltered neurophysiology.
seems to be more sensitive to sma ll amo unts of pressure and tension than the efferent anter ior
Somatosomaric Reflexes
root or the nerve itself (69). The magnitude of tension on rhe posterior root required to effect a
hypothesis (14,80), the somatosomatic reflex model suggests that the highly innervated soft tis-
change may be within the scope of mechanical
sues around joints may become irritated, which
Sometimes referred to as the proprioceptive insult
edema
may lead to reflex modifications in postural tone
around the foramen or capsule, but this has not been experimentally verified. The dorsal roor ganglion (DRG) is a disrinct structure also in the vicinity of the intervertebral foramen. Lantz (70) points out the exquisite sensiriviry of rhe DRG ro mechanical stresses. DRG
and neural integration of posrura l accivities.
distortion
possible
from
traction
or
compression has been implicated as a cause of
pain in stenosis, disc bu lge, fibrosis, etc. The distinction berween nerve rOot and DRG is primarily anaromic, but Lantz notes that a sign ificant
aspect of DRG physiology is that the cell bodies of the DRG undergo trophic changes when the nerve is injured peripherally (71). Concerns regarding the kinds of mechanical forces needed to affect the DRG are the same as those outlined previously for nerve rOOt compression and traction.
Spinal Cord Compression or Traction B. J. Palmer was perhaps the first proponent of this model of subluxation (72). It has served as a basis for upper cervical chiropractic techniques (73) and has been implicated as a post-birth-
Wyke (81,82) has suggested that spinal manipulation stretches mechanoreceptors in the joint cap-
su le. This stimulus has an inhibitory effect (mediated through cord interneurons) on nociceptive activity of the type IV endings. This mechanism has been called the pain gate (83) . Gillette (84) has expanded on this model by providing a detailed
accounting
of
[he
various
somatic
mechanoreceptor populations in the lumbar fascia. Although Wyke (81) has documented that joint capsule stretch can inhibit pain, Gillette (84) specu lates that this phenomenon has the potential to be initiated by other nerve ending populations as well. Another example of a somatosoma ti c reAex
involves reflex muscle spasm (85,86) . This is a positive-feedback cycle mediated by the gammamOtor loop in which a spasmed muscle may result from and contribute to proprioceptive irri-
tation. This has been referred to as the "facilitated segment." It appears that spinal cord segments in [he vicinity of a spina l fixation have a
182 lower threshold for firing (27,28,85). There is some evidence for the reduction of muscle spasm as measured by electromyography after spinal adjusting (87,88). Perhaps one of the most promising models of the manipulable subluxa-
organic disorders, most patients that present to chiropractors self-select for neuromusculoskeletal conditions (98,99). The outcome literature for somatic interventions on organic problems has
been relatively limited, dated, or anecdotal.
tion, somatosomatic reflex pathways seem to
explain many of the clinical observations seen with spinal adjusting. In and of itself, this model does not represent any kind of pathologic lesion; rather it suggests a mechanism by which spinal adjusting and manipulation has an effect on reduction of pain and spasm in the absence of any specific spinal lesion. Somatovisceral and Viscerosomatic Reflexes This model attempts to explain effects manipulation might have with organic disorders. Early osteopathic research in this area concluded that vertebral lesions in a nimals may affect vascular supply to various glands and viscera (5). Sato and Swenson (89) demonstrated sympathetic discharge in rats by placing mechanical stresses into the spinal joints. Somatic stimulation by manipulation has been shown to affect gastric function (90) and angina pain (9 1). Early work by Speransky (92) suggested that somatic blockade injections at segmental spina l levels have a beneficial effect on the progression of lobar pneumonia. Spinal lesions have been clinically associated with deep visceral pain (93). In addirion, physiologic effects of somatic stimulation by mechanical means have some early experimenta l support (9497) . It is reasonable to consider that certain organic disorders may contribute to development
Motor System Degeneration The Eastern European manual medicine movement has theorized a model of peripheral and somatic "blockages" and their role in affecting integrated function of the motor system from cortex to periphery (24,26,100). This model offers a considerably different role for spinal or extremity dysfunction than other neurologic models. Two kinds of nervous system integration can be described. The first is termed "vertical integration," which refers to the relationship between
(1) the centra l nervous system (CNS) structures; (2) the spinal cord; (3) peripheral nerves; and (4) musculoskeletal structures. The second, " horizontal integration," refers to the relationship between anatomica ll y adjacent or related structures within any of the four vertical components
(for example, motor cortex and cerebellum from group 1, knee and hip from group 4, etc.) It is well known that in upper moror neuron lesions degeneration of function follows in both horizo ntal and vertical directions and that loss of function becomes morc permanent over time. For examp le, after a cerebrovascular accident, neuro-
of segmental somatic muscle tone changes. Some
logic firing patterns change in the vicinity of the lesion, leading to reorganization and changes in related CNS Structures (horizontal degeneration). In addition, there is a gradual cumulative functional change vertica lly in the cord and peripheral
early osteopathic animal research provides evi-
nerves, which eventually leads ro muscular atro-
dence that somatic interventions (a djustment,
phy in the affected peripheral structures. The motor system degeneration model argues that a lesion in any of the four vertical levels (including a peripheral joint lesion) leads to subtle and gradual functional alterations vertically and horizontally throughout the motor system. Treatment and rehabilitation programs by modern manual medicine and physical therapy practitioners have
injection, etc.) may influence the progression of a sma ll number of organic conditions. What is clearly speculative at this point is the role that spinal lesions have in the development of these organic disorders. Clear manipulative treatment
protocols and quantitative outcome studies for different kinds of conditions are also lacking. Although both chi ropractic and osteopathic prac-
centered on distinctions between acrive (patienr-
titioners report anecdota l successes with various
performed ) care and passive (doctor-performed)
183 care (101). It is thought that treatment of peripheral joint lesions (including spinal dysfunction) needs to be more than passive mechanical work (for example, spinal adjustment). Because of the holistic nature of the entire moror system, C3fe mUSt include exercise and retraining along lines similar to those involved in rehabilitation of other motor system pathologic conditions (such as upper motor neuton lesions). The longer the condition is left to progress, the greater the likelihood that recruitment (vertical and horizontal) of other areas of the motor system will occur, leading to recurrence of the peripheral lesion (22) . Psychoneuroimmunology Just as somatosomatic reflexes may be considered a component part of the motor system degenerarion model, somatoautonomic and viscerosomatic
reflexes may be considered a component part of psychoneuroimmunology. Attempts to quantify the relationship of psychological considerations with immune system function as mediated through the endocrine and nervous systems are
being made. Because of the intimate relationship berween [he nervous system and the endocrine
system, the specialty of behavioral medicine has taken a particular interest in psychoneuroimmunology (102). Ader's (103) text on the subject reviews literature and concepts that support the
role that various psychologic and behavioral factors play in physiologic function. The field, although controversial (104), has a rational basis and a large literature base that seems to correlate behavioral syndromes and interventions with clinical phenomena and outcomes (l05). In the previous discussion of the mOtor system, it was suggested that somatic injury can provide sensory input to the nervous
system, leading to horizontal and vertical integration with resultant long-term patterning. It is reasonable to speculate that a chiropractic adjustment, which might influence somatoauronomic activity, could also contribute input to higher CNS centers that may be important in psychoneuroimmunology relationships. With increasing interest in neuroimmunology research, this
model is likely to develop greatly. Exact neural pathways and neurophysiologic responses are not well identified nor understood, and chiropractic applications of this model remain speculative (see Chapter 14 ).
1rophIc Models Aberrant Axoplasmic Transport It is known that axonal transport can be affected chemica lly (106,107), and mechanical stresses have been shown to alter intracellular protein metabolism (69). This model suggests that mechanical or chemical stresses (from metabolism of traumatized tissue) may alter nervous system physiology. Singer (108) describes how nerves provide trophic sustenance for muscle growth and maintenance. He further states that axoplasmic flow can be affected without damage to nerve conduction. Manipulation'S role would be to free up mechanical pressure, perhaps in the soft tissues, which may impede axonal transport. However, no studies exist that demonstrate changes in axoplasmic flow with spinal or soft tissue manipulation. Also unclarified are the details regarding the extent and kinds of mechanical pressures possible with spinal or soft tissue lesions. lnrraneural Microcirculation Ischemias Because the blood vessels supplying nerve tissue are softer and more susceptible to compression than are the nerves, a likely candidate for a spinal lesion is localized neuroischemia. The symptOms of neurapraxia are understood clinically (109) and often manifest as paresthesias. This model is closely related to the axoplasmic transport model in that one of the major consequences of neura l ischemia is altered intracellular metabolism of the nerve and resultant aberrant axoplasmic flow. A detailed review of the experimenta l literature in this area has been provided by Sjosrrand et al. (110) . This model has been a favorite of the osteopathic profession, but suffers the same limitations as the previous model: absence of documentation regarding the kinds of pathoanatomic lesions that cou ld lead to ischemia.
184
TIle SUbluXation CCJmpIex
Macrocirculation Ischemia (Aberrant Vascular a nd Lymphatic Supply)
variety of head symptoms and postural disorders. Much of the literature surrounding the biome-
This model serves as an extension of microcirclI-
chanica l model of cord compression and traction
lation ischemia as applied to larger blood vessels and lymphatics. Many clinical syndromes involv-
is applicable here. This speculative rat ionale suggesrs that a condition of CSF stasis or aberrant Aow leads to decreased nutritional supply to those CNS components bathed by the Auid. Surgical case stud ies can be found showing that a complete obliterarion of the subarachnoid space can lead to obstructed CSF flow and resultant arrophy of neural elements ( I J 7). However, this
ing tissue contracture or space-occupying lesions can impede larger vessels. To what exrenr spinal dysfunctions can influence larger vessel flow is
debatable. Although mechanical stresse can impact on cerebral blood Aow, many documented cases of mechanical impingement are secondary to excessive trauma and may nor be manipulable.
Verrebrobasilar arterial insufficiency afrer cervical manipulation has been imp licated as a cause
of stroke ( 111 ). Therefore, predisposition to vascu lar insufficiency is a possible conrraindication
to certain kinds of cervica l adjusting (J 12).
IS
far
removed
from
minute,
manipulable
mechanical srresses allegedly cau ing subtle alterations in the nutritive capaciry of CSF. The exact mechanisms of this model are perhaps best discarded in favor of direct subtle mechanica l effects of meningeal traction on eNS components.
Because functional mechanical stresses associated
with spinal manipulation may significantly affect cephalic circulation, it is reasoned that manipula-
tion may have beneficial effects as well as negative ones. The significance of this model is that chiropractic adjusting has been implicated in the resolution of a wide variery of cepha lic symptomatology ( 113, J 14 ). Although neurologic expla-
Psychosocial Models Placebo Effect The placebo effect has often been cited as a source of the effectiveness of spinal manipulation
nations may account for some of these effects, possible vascu lar consequences have nOt been
by its detracrors ( I 18). Yet the therapeutic va lue of the placebo effect shou ld not be overlooked ( I 19). It is important for providers to recognize rhe mind-body relarionship and the role rhat the
adequarely considered. Although mOSt of the lit-
doctor-patient
erature regarding this mechanism centers on cervical vascu lature, thi s model might be extrapolated to other anatomic regions where mechanical inrr usions on vascular elements may occur.
Placebo has too often been used to explain away the unknown whi le confounding psychological
relationship
has
in
healing.
responses with sources of experimenta l design variabi lity, such a measurement error, sampling
error, etc. (l20 ). Cherkin and MacCornack ( 121) Altered Cerebrospinal Fluid Flow Improper circulation of the cerebrospinal fluid (CSF) has been suggested as a mechanism in spina l dysfunction that is amenable to manipulation (78, 11 5). Movement of the cranial bones secondary to pressure changes within the cranium
may be responsible for a pumping acrion that circu lates CSF (78, 11 6). Craniopelvic manipulation is thought by some to normalize aberrancies of
have compared patient satisfaction between family practitioners and chiropractors in back pain
patients and noted higher degrees of confidence and satisfaction with chiropractors. This was att ributed to the chiropractors' ability to commu -
nicate clearly and believably with their patients. Although Cherkin and MacCornack did not attribute any portion of patient satisfaction to adjustive care itself, the point is demonstrated
this movement. It is unclear what the exact clini-
that the patient'S belief in both the practitioner
cal consequences of impaired CSF flow would be, but specu lat ion based on clinical experience has
and the treatment plays an important role in the hea ling process. Interestingly, another report
suggesred the va lue of this approach for a wide
noted that almost half of the family practitioners
10
n-,,1Ic Modell 01 CllII'GIII'acllc saxallon
stated that they use the placebo effect therapeutically with their back pain patients (122). Fewer than 5% of the chiropractors stated rhat they did so. Part of a placebo's effectiveness may come
185
clinically by education on environmenta l and lifesryle modification. Although many of these problems may not always be considered as the primary instigators of joint dysfunction, chiro-
from the practitioner's lack of awareness of, or
practors have recognized the importance of
unwillingness to acknowledge, placebo effects. Placebo certainly constitutes a portion of the therapeutic effect of any health care approach (123). The extent to which it has an effect in chiropractic practice is nOt clearly quantified, bur it does serve as one of the possible models or explanations of the effectiveness of spinal manipulation . Practitioners need nOt be fearful or belittled
trauma, roxicity, and autosuggestion in health and disease since the time of D. D. Palmer (J 2).
by
elucidation
of its
extent
in
chiropractic.
Placebo is perhaps the most noninvasive of approaches, and its role should be maximized, because it truly lIses the patient's own recuperative ability. The only caveat is that this should not
Often the doctor's recommendations for changes in lifestyle ca n be the active ingredient in a therapeutic response. The chiropractor who casua ll y suggests a change in posture or activity at the
work station may very well give full therapeutic credit to the passive component (spi nal adjustment) while neglecting to consider the role played by the lifesryle modification.
Conclusions
serve as a Justification to avoid seeking under-
Whether it is ca lled manipulable subluxation,
standing of other possible physical mechanisms.
manipulable lesion, chiropractic subluxation, somatic dysfunction, fixation, or "bump in the
Stress Reduction Selye (124) articulated the role emotional stress plays with the endocrine system and muscle tension. High anxiety and stress levels have been implicated in a number of muscle tension and
other clinical syndromes (125). Spinal adjusting may help relax tense muscles as outl ined in the somarosomaric reflex model, yet many chiropractors go further with relaxation exercise, biofeedback, lifestyle counseling, nutritional guida nce, and related procedures. For the sake of completeness, stress needs to be considered as a possible mechanism in the mediation of spinal dysfunction, especially in cases in which muscle tension
and joint fixation fail to resolve with a reasonable
back," this clinical phenomenon brings millions of patients to doctors. Perhaps communication
and collaboration among various interested parties will advance our understanding in this area.
D. D. Palmer ( 126 ) first noted the problem of multifactOrial terminology when he wrOte the following: Too many manufacture rheir own definition of terms . .. . What would be the result if each banker and broker should invenr and persist in using his own devised addition and multiplication rahle. Herein arises the discordant. inharmonious jan· gling among chiropracrors regardmg what constl· tutes the principles of science . ...
Chi ropractors are ga inin g greater acceptance
3moum of carc.
into the mainstream of sociery's health ca re deliv-
Lifesryle Modification
ery systems . As such it is becoming imperative that our concepts, procedures, and professional
In addition to stress, many of the actlvl[lcs of
daily living are likely contributors to spina l and joint dysfunction. Repetitive and prolonged posrural activity, either static or dynamic, nutritional neglect, inadequate or improper exercise, and roxic exposure are examp les of numerous areas that manipulative practitioners might address
identiry be clarified not only for others, but for ourselves. Emphasis also IllUSt be placed on adopting meaningful and supportable terminology and classifications for subluxation models. Opinionated, histOrically and politically motivated definitions of subluxation (or other terms) are no longer adequate to explain the myriad of
186 effects spinal adjusting is thought to have (8). The chiropractic profession is being called on to quantify and describe both our effectiveness and our rationales. Without this, the barrIe for equal access to patients in an ever-decreasing supply of health care resources becomes even more difficult. Distinctiveness about chiropractic cannOt be centered on vague or outdated and inaccurate concepts. An understanding and appreciation of the state-of-theart about what is known, supported, and speculative on "manipulable subluxation" is essential for the future. Doctors of Chiropractic require a common starting point for interdisciplinary dialogue. Such investigation and collaboration can lead to input from our perspective into the health care delivery system along with clinical refinements and developments that result in better patient care.
Ra'1II'8I1C88 1. Brantmgham JW. A su rvey of the lIterature regarding the behavior, palhology, etiology, and nomenclature of the chiropractic lesion. ACA J Chiropractic 1985; 19(8H5-70. 2. Brantingham JW. A critical look at the subluxation hypothesis. In: Hodgson M cr aI., cds. Current lOpics In chiropraCTic: reviews of the literature. Sunnyvale, Cali· fornia: Palmer College of Chiropractic-West 1987; DU-6. 3. KeaungJc. Science and poillics and the subluxation. Am J Chiropractic Med 1988; 1(3),107-10. 4. Dishman RW. Review of the literature supporting a sciennfic basis for the chiropractic suhluxanon complex. J Mampulative Physiol Ther 1985; 8(3):163-74. 5. Leach RA. The chiropractic theories: A synopsis of scientific research, 3rd ed. Baltimore: Williams and WilkinS, 1994. 6. Moorz RD, CiRulio Bl, Haney PL. The existence of the manipulable spinal lesion. In: Coyle BA, ed. Current topics 111 chiropractic: Reviews of the literature. Sunnyvale, Califorma: Palmer College of Chiropractic-West, 1984; 1l
10. Ganerman MI, Hansen DT. The development of chLropractic nomenclarure through consensus. J Mampulative l>hysio) Therap 1994 Uune); 17(5),302-309. 11. Lomax FL. Manipulative therapy: An historical perspecrive from ancient rimes. In: Goldsrein M, cd. The research sratus of spinal mampulative [herap)". NINCDS Monograph 1975; 15,11-15. 12. Palmer DO. The science, art and philosophy of chiropractic. Portland, Oregon: Portland Printing House. 1910. 13. Palmer BJ. Fight to climb. Davenport. Iowa: Palmer School of Chiropractic, 1950. 14. Homewood AE. The neurodynamics of the vertebral subluxation. 3rd cd. St. Perersberg, Florida: Valkyrie Press, 1979. 15. Janse J. Principles and practice of chiropractic. lombard, illinois: Narion:ll CoUege of ChiropraCtic, 1976. 16. Faye LJ. Mmion palp::H1on of the spine. Huntington Sc:ach, Califorma: Motion Palpation Institute, 1983. 17. Lann CA. The vertebral subluxation complex.ICA ReVIew 1989; (SeprlOct),37-61. 18. Still AT. Philosophy of osteopathy. Kirksville,l\1issouri : The Author, 1899. 19. H-ICDA.llospital Version of ICDA. 2nd cd. Commission on Professional and Hospital Activities, 1973. 20. Greenman PE. PrinCiples of manual medicine. Balttmore: Williams & Wilkins, 1989. 21. Mennell JM. HIStory of the development of medical manipulation concepts: Medical ternunolog),. In: Goldstein M, cd. The research ~tatus of spmal mampulatlVe therapy. N1NCDS Monograph 1975; 15,19. 22. Cyriax J. Treatment of pam hy manipulation. In: Goldstein M, cd. The research status of spinal manipularj\'e therapy. N1NCDS Monograph 1975; 15,19. 23. Paris SV. Spmal malllpulative therapy. Clm Orthop 1983; 179,55. 24. Lewit K. Malllpulauve therapy 111 the rehabilitation of the motor system. 2nd cd. London: Butlerworths, 1991. 25. Janda V. Muscles, central nervous regulation and b<1ck problems. In: Korr 1M, ed. Neuroblologic mecham ... ms in manipulative therapy. New York: Plenum Press, 1978: 27-42. 26. Janda V. On the concept of postural muscles and posture. Aust J Physiothcr 1983; 29:83. 27. Korr 1M, cd. The neurobiologic mechanisms in manipulative therapy. New York: Plenum Press, 1978. 28. Korr 1M. The collected papers of Irvin M. Korr. Colorado Springs: American Academy of Osteopathy, 1979. 29. Meeker WC, Moor!. RD. Evaluatmg the validity, reliability and cilmcal role of spmal radiography. In: Coyle et aI., cds. Current topics In chLropractic: ReViews of the literature. Sunnyvale, California: Palmer College of Chiropractic-West, 1985; £5: 1-20.
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58A5-49. 4 1. Giles LGE Lum ba r apophyseal joint a rthrography. J Manipulative Physiol Ther 1984; 7:21-24. 42. Wo lf J. The reversible deforma tion of joi nt cartilage surface and its possible role in joint blockage. In: Lewit K, et a I., eds. Proceedings o f the 4th Congress International Federation of Manua l Medicine. Bratislava: Orbis, 1975: 30-3 4. 43. Rauschning W. Detailed sectional ana to my of the spine. In: Rothman S, et al. Multiplanar cr of the spine. Baltimore: University Park Press, 1985. 44. Sandoz R. Newer trends in the pat hogenesis of spinal disorders. Ann Swiss Chiropractic Assoc 1971; ;,93- 180. 45. Maigne R. Orthopaedic medicine: A new approach to vertebral manipu lations. Springfield, Illinois: Cha rles C Thomas, 1972.
187
46. Cy riax J . Textbook of ortho paedic medicine, Vol. 2, 9th cd. Ba lliere Tindall, 1974 . 47. COX JM. Low back pain: Mecha nism, diagnosis, and treatment. 4th ed. Baltimo re: Williams & Wilkins, 1985 . 48. Sa ndoz R. Some physical mechanisms and effects of spina l adjustments. Ann Swiss C hiropractic Assoc 1976; 6 ,91 - 141. 4 9. Farfan HF, Cossette JW, Robertson G H, Wells RY. The effects of torsion on the lumbar ineerverrebra l joines: The role of torsion in the production of di sc degeneratio n. j Bone joint Surg 1970j 52A: 468. 50. Good AB. Spinal joim blocking. j M anipula tive Physiol Ther 1985; 8+8. 5 1. Kirkaldy-Willis WHo Managing low back pain. 2 nd ed. New Yo rk : C hurchill Livi ngstone, 1988. 52. Sweere JJ. Predisposi ng fa cto rs to lower spi na l instabi lity: An illustra ted guide. Bloomington, Minnesota: Northwestern College o f Chiropractic, 1987. 53. Goldstein M. The research status o f spina l manipulative therapy. NINCDS Mo nograph 1975; 15. 54. White AA, Panjabe MM . Cl inical biomechanics of the spine. 2nd ed. Philadelph ia: JB Lippincott, 1990:3- 10. 55. Weisel SW, Tso urmas N, Feffer HL, C itrin C M , Pa tronas N. A study o f compu ter-assisted tomography. I. The incidence of positive CAT scans in an asymptomatic g ro up o f patients. Spine 1984; 9(6) :549-55 1. 56. Stei ndler A. Kinesiology of the human body under normal a nd pathological conditio ns. Springfiel d , Ill inois: Charles C. Tho mas, 1973. 57. Farfan N HF, Sullivan jB. The relation o f facer o rienta rio n to intervertebral disc fai lure. Ca n J Surg 1967; 10, 179-185. 58. Coplens CWo The conservative treatment o f low back pain, Helfer Aj, G rubel Lee OM , cds. Disorders of the lumbar spine. Philadelphia: JB Lippinco tt, 1978: 16 1. 59. Garrerman MI. Chiropractic managemem of spine rela ted disorders. Baltimore: Williams & Wilkins, 1990, 148- 152. 60. Turck SL. Orthopaedics principles and their application. 3rd cd. PhiladeJphi a: jB Lippincott, 1977: 1469. 6 1. H ad ley LA. Interve rtebral joint sublu xation, bony impingement and fo ramen encroachment with nerve rOOt cha nges. Am J Roentgenol Radiat Ther 195 1; 65,377-402. 62. Hadley LA. Anatomico-roentgenographic studies o f the spine. Springfield, Illino is: C harles C T homas, 1964. 63. Crdin ES. A scientific test of the chiro practic rheory. Am Sci 1973; 6 1,574-580. 64. Golub BS, Sil verma n B. Transfo ra mina lliga ments of the lumbar spine. j Bone Jo int Surg 1969; 5 IA:947-956. 65. Luttges MW, Kelly PT, Gerren RA. Degenerative cha nges in mouse sciatic nerves: electrophoretic and electr oph ysi~ ologic characterizations. Exp Neurol 1976; 50:706--733. 66. Luttges MW, Srod iek LS, Beel JA . Postinju ry changes in
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the biomechanics of nerves and rOOts in mice. J Manipu· Iori,e Physiol Ther 1986; 9(2),89-98. Triano JJ. Lunges MW. Nerve irrirarion: A possible model of sciatic neuritis. Spine 1982; 7: 129- 136. MacGregor RJ, Sharpless SK, Lunges MW. A p ressu re vessel model for nerve compression. J Neurol Sci 1975; 24,299-304. Sharpless SK. Suscepra biliry o f spinal rootS to com prcs· sian block. In: Goldstein M, ed. The research status of spinal manipulative therapy. NINCDS Monograph 1975; 15, 155. Lantz CA. The role of dorsa l roO( ganglia in the developmen! of chiropractic subl uxarions. In: Keene KJ, et a l. cds. C urrem lOpics in chi ropractic: Reviews of the literature. Sunnyvale, Ca lifornia: Palmer College of Chi ro-
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• Kinesiology: An Essential Approach Toward Understanding the Chiropractic Subluxation Kelll L. Blunt Meridell. Gatterman David E. Beremick KeyWords
Kinesiology, spinal motion segment, six degrees of freedom, coupling, hypomobility, hypermobility, aberrant mobility, paradoxical motion, instability, instantaneous axis of rotation
After reading this chapter you should be able to answer the following questions:
Quastloo #1
What contributes to coupled movement in spinal motion segments?
Quastloo #2
What is the function of muscle spindles?
Quastloo #3
What are the stages of spinal joint degeneration and how do they effect segmental spinal motion?
K
YZ
XY
inesiology is the science or study of movement and the active and passive structures
involved. This chapter focuses primarily on th e kinesiopatho logy of the sublu xation complex model by app lying the principles that govern motion to the spinal motion segment. The charac-
rcrisrics and ana lysis of normal dynamic regional and intersegmental motion a re explored to und erstand a deviance from these patterns that characrerizes the abnormal morion of a subluxari'on complex . A continuum of abnorma l motion is
described, from hypomobiliry to hypermobility and instabiliry. In addition, aberrant motion an d compensatory hypermobi liry are presented. Specifically, we examine a principle neurophysiologic receptor, namely, the muscle spindle,
,Z
1
xz
X
,, ,, ,, ,,
in its role in restricting spinal segmenta l motion . We review the studies that address a manipu lable subluxation's response to chiropractic adjustments. Finally, pathologic changes that occur with degeneration of the th ree-joint complex are discussed relative to the effecrs that this process
PLUMB'
UNE
has on segmental spina l movement.
Charactarlatlcs of Normal MotIon The standard position of reference or anaromic position has the erect body facing fo rwa rd, the elbows and fingers extended at the sides of th e body, with the palms and the feet facing forward (Figure 11-1). It is necessary from this position to establish cardi nal body planes and axes for the pu rpose of describing structura l position and directions of functiona l movement. The body planes are derived from dimensions in space and are arranged perpendicular to one another. The midsagittal or sagittal plane (YZ plane) divides the body into right and left ha lves . The corona l plane, also called the fronta l plane (XY plane), is at right angles to the midsagittal plane and divides the body into ante ri or and posterior portions. The transverse plane is a horizontal plane (XZ plane), dividing the body into upper a nd lower components (Figure 11-1).
-- -- --
-- -- --
FigIre 11-1 Central coord in ate system with irs origin between the cornua of the sac rum . The human body is shown in anatomic position. The planes are as shown : the sagirral plane is the YZ plane; the frontal plane is the YX plane; the horizonral plane is the XZ plane. The - y-axis is described by the plumb line dropped from the origin, and the + x-axis points to the left at 90 degrees to the y-axis. The + z-axis points forward at a 90-degree angle to both the y-axis and the x-axis. Movemenrs are described in relation to the origin of the coordinate system. (From While AA, Paniabi MM.
Clinical biomechanics of the spine. 2nd ed. Philadelphia, JB Lippincott, 1990,87.)
192
The SUbluxation Complex y
,, Posterior : Anterior
,, ,, ,
z fIg&n 11-2 The spatial orienrarion of the superior verte bra relative to the inferior ve rtebra can be plo rred
by placing the origin at the center of the superior vertebra. Motion then can be described in relation ro translation along any of the three axes or rotation around any of the th ree axes. These six components of vertebral morion give six degrees of freedom to the vertebra l motion segmen t. (Ca tterman MI. Chiropractic management of spine related disorders. Baltimore: Williams & Wilkins, 1990:25.)
The card inal axes system, namely, the X-, Y-, and z-axes, are oriented at right angles to one another
[0
generate a three -dimensional coo rdi -
nate system (Figures 11 - 1 a nd 11 ·2). This coordi· nate system is significant in defining or locating the extent of three types of movement possible at each joint: rotation, translation, and curvi linea r motion (I ). All movements that occur about an ax is are considered rotationa l, whereas linea r movements along an axis and through a plane are
ca lled translational (1). Cu rvilinear motion occurs when a rotatio nal movement is accompanied
by
,
,,
>----0"
A
: ()
F~
'E
Figure 11·3 Three-joint complex of the lower cervical spine. Anterior elements: A, anterior longitudinal ligamenrj B, anterior anulus fibrosus; C, posterior anulus fibrosus; D, posterior longirudinalligamenr. Posterior elements: E, coscotransversc liga mentj F. capsu lar ligament; G, articu lar facet; H, ligamentum
flavin; I, interspinous and su praspinous ligame nts. (White AA, j ohllsoll RM, Palljabi MM, SOl/thwick \\'l0. BiomecIJal1;cal analysis of clinical stability in the
cervical spille. elill Orthop 1975; 109:87.)
a
translational movement (1). The fundamenta l unit of spinal movement referred to as the motion segment (2) is a threejoint complex (3). This unit consists of an intervertebral disc surrounded by two adjacent vertebrae, the two posterior joints, and th e surrounding contiguous ligaments, including capsules (Figure 11 -3) . This forms the functional unit of spinal motion. The potentia l exists for a spina l joint to
exh ibit translational and rotational movements along and around each of the X·, yo, and z-axes. Thus we characterize a motion segment as a viscoelastic, energy-absorbing entity, possessing six degrees of motion (4·7) . Specific motions or resultant positions are defined by the axis around which movement takes place a nd the plane th rough which movement occurs. The Illmions of fl exion and exten-
11 Klneslolagy: An Essential Approach Toward UndeI'stlllllllng the ChIropractic SubluXation sian occur about the x-axis and through the sagit-
tal plane. Lateral Oexion occurs about the z-axis in the coronal plane. The longitudinal axis (yaxis) is vertical and allows axial rotation through the transverse plane. The origin of motion is the Intersection of the three planes and is convention-
ally placed in the center of the superior vertebral body in the spinal motion segment. Therefore, conventional segmental spinal motion is
described in terms relative
to
the subadjacenr
superior vertebrae.
The potential for six degrees of freedom originates frol11 the unique arrangement of the threejoint complex, with the separation of the verte-
bral bodies by the intervertebral disc allowing for
193
translation in all directions. Although the amounr of motion permitted in each segment is slight, pri-
marily restricted by the posterior facet joint anatomy and plane of the joint surface, this multilinked mechanical system of motion segments allows for a wide range of overall spinal motion. Coupling of more than one degree of freedom occurs when rotation or translation of the vercebrae about one axis is consistently associated wirh rorarion or translarion of rhat same vertebra
about another axis (8). Jofe et al. (9) state that coupling is primarily caused by the geometry of the regional facet articulations, and the connecting ligaments and curvature of the spine playa
secondary role. A rigid body's motion also can be described with reference to the instantaneous axes of rota-
tion (tAR) and hel ica l axis of motion (HAM) . At every instant in plane motion, there is a line in
the body or a hypothetica l extension of it that does nOt move. This line, which is perpendicular
Position 1 _ _ _ B,
to the motion plane, is the instantaneous axis of
rotation (Figure 11-4) (8). The helical axis of motion js defined as a unique axis in space that
completely defines a three-dimensional motion of a rigid body from position 1 to position 2 (10). It is analogous to the instantaneous axis of rotation
B.
for plane Illation . According to the laws of mechanics, a rigid body may always be moved from position 1 to position 2 by a rotation about a certain axis and a translarion along rhe same
axis ( 10). This constitutes helical motion . The motion of a screw is an example of helical motion. This concept has been introduced in the thoracic spine and investigated in the lumbar spine. A given Agare 11-4
Insranrancous axis of rorarion. Graphical
technique of determining the instanraneous axis of rotation when a hody moves from position I to
posicion 2. The axis is found to be ac the inrersection of the twO perpendicular bisectors of translation vectors AI·A z and 8 1,82 of any twO poinrs A and Bon rhe
instantaneous
axis
of
rotation
depends on the Structure as well as the type of loading. The calculation for a particu lar vertebra differs as a result of various combinations of force and movement (8).
body. (WIllie AA. Panjaln MM. Clmical biomechamcs
Analysis 01 Motion
of th" spme. 2/1d ed. Pln/adelplna: fB Lippmcott,
The analysis of normal and abnormal motion
1990:6S9-60.)
requires a system of measurement that can reli-
194 a bly produce high-quali ty, high-resolution images in a simple, accurate, and repeata ble manner. The ra nge of motion was studied initia lly in cadave rs (4,5, 11 ,12) before the advent of x- rays. This posed difficulties beca use of postmo rtem changes that occurred w ith cadaver specimens, thus not accurately reflecting spina l mobility. But in vitro studies co ntinue, attempting to simulate
motio n without the physiologic muscle forces present. In vivo procedures have been developed but a re too complex to perform in a practica l manne r.
Radiographic imaging of living subjects is ge nerall y the initial imagi ng modality of choice. Sta ndard radiograph ic series provide static information onJy, capturing the structural status of the
,
,,
,,
,,
, "...J Rgure 11-5 Movement di agra m o r tem plate analysis. The so lid lines represent extens ion of C2-C4, and [he interrupted lines depic t flex ion o f C2-C4 . These can be superimposed onto an image of C2-C4 in ne utral (nor shown ), Analysis of intersegmenral translation and rora tion can then be performed. (From Penning L. N ormal movements of the cervical spi,Je. Am J Roentgenoi 1978; 1]0:3 17-26.)
11 KiI8aIoIogy: An ElI8II1IaI Approach Toward Underllaldng the ClIII'1IjIi'ac1lc SUl*Ixatlllll spine in one plane. " Functional" tadiographs depict [he instantaneous positions of a vertebra at the extremes of global range of motion . Although individual segmental movement cannot be assessed, aberrant motion may be identified as
restricted or increased or as abnormal vertebral alignment at the end of a given range of motion. Various authors used template analysis (13) and "moror diagrams " from these radiographs to
quantify motion (Figure 11 -5) (14-17). Dimnet et al. (18,19 ) studied lateral cervical radiographs in full flexion, full extension, and three intermediate motions to detect angles and cemers of move-
ment for each vertebra (18). This same procedure was used earlier in the lumbar spine to observe lumbar sagittal plane motion (19 ). Coupled motions out of this plane, however, cannot be
observed . Dynamic evaluation of spina l motion has
been advocated by many authors (20) using stress
195
radiographs. Stress radiographs consist of fronta l rad iographic views of the spine whi le the patient is placed in maximum rig ht and left latera l bending, and late ral views of the spine whi le the patient is positioned in maximum lumbar flexion
and extension (20). More sophisticated and costly imagi ng techniques are now available, such as biplanar orthogonal radiography. Radiograp hs are taken simultaneously throug h two x-ray tubes arranged at right angles to one another (Figure 11-6). Movement in all three planes can be detected and quantified (21-26). A year after Roentgen's discovery of the x-ray in 1895, fluoroscopic screens were introduced, allowing for x-ray observation of dynamic events (27). In 1921, investigators began using cineradiography. This process documents fluoroscopic examinations by photographing a fluoroscopic screen with 16-mm or 35-0101 motion picture fi lm
lolerol
source
source
Agure 11-6 Biplanar radiographic technique. Geometric construct ion showing [he projection of points on a body onto (wo o rthogonal planes. (Pea rcy M. Burrough S. Assessment of bony union after interbody fusion of the lumbar spine using a hip/anar radiographic technique. J Bone Joint Surg 1982; 64B:228-3 2.)
196
The SUblUXation Complex
(27) . The film could later be viewed at real-time, slow motion, or freeze-frame speeds. By the late 1950s, several researchers began to apply cineradiography to the skeletal system to eva luate joint motion (28-30). This technique allows for the srudy of dynamic motion with the contribution of the joints, disc, ligaments, and muscles. Cineradiography requires increased radiation dosages and poses difficulty to the investigator in quantifying the enormous amount of data. The widespread availability of video recording systems in the 1970s and 1980s led to the inevitable replacement of cineradiography by videofluoroscopy. Serial x-ray images were digitized from an image intensifier and directly interfaced to a computerized image processor. This digitized and displayed selected fluoroscopic images on a computer monitOr. This spinal imaging modality is subject to observer variation in measuring angles and operator inconsistency
(31). It has potential in evaluating asymmetrical or paradoxical motion and intersegmental motion with low radiation exposures. Newer techniques such as dynamic computed tomography (CT) and magnetic resonance imaging (MRI) are being
~ 11·7
used to visualize three-dimensional moving images (27). [n conclusion, the cost, dose, and yield must be evaluated before choosing a method of imaging to assess spinal kinematics.
Regional and Intersegmental Range 01 Motion The physiologic range of translation and rotation of a vertebra for each of the six degrees of freedom are explored in the cervical, thorat.::ic, and lumbar spine. The reader should be aware that the literature spawns a wide range of techniques used to evaluate and describe ranges of motion . This will inherently cause conflicting data when quantifying and qualifying motion. In addition to this factor, biologic variation is always at play.
Cervical Spine Atlantooccipital Joints The atlantooccipital joint is formed from the articulation of convex occipital condyle and con-
Flexion and extension of the occiput on the atlas. During flexion the occipital condyles glide posteriorly and superiorly on the lateral masses of atlas, as the occipital bone separates from the posterior arch. During extension, the condyles slide anteriorly on the lateral masses of arias, while the occipital bone approximates the posterior arch of arias. (From Bergmann TF, Peterson DH, Lawre"ce DL. Chiropractic technique. New York:
Churchill Livingstone, 1993:219.)
11 Kinesiology: An EHen1IaI AppI'IIICh Toward IInderstald ng the ChIropractic SUbluXatIon cave atlas facet . This is a symmetrical and mechanically linked joint (32). These joints produce predominarely sagitta l plane movements of flexion and extension, as rhe condyles slide in rheir corresponding lareral masses of the atlas (Figure 11-7). Controve rsy exists as to the amount of movement, with as little as 13° reported by Werne (33) and White and Panjabi in rad iographic studies (7). Fielding, using cineroentgenography, evaluated sagitta l motion at 35° (29). Penning performed overlay studies on 20 healthy adults to find an average of 30° sagittal motion, with a range of 25 to 45° (34 ). Panjabi et aI., in later studies, concluded an average range of 24.5°, approximately 21° of extension and 3.5° flexion (35). In a stud y reported by Jones, two patterns of total cervical flexion exist (36). Cervical fl exion initiated with the chin retracted produces greater motion at the
CO-C1 segment than flexion sta rting with the head erect. Most authors agree that pure rotation cannot occur (S,9,33,36). However, Kapandji, in studying this unique joint believes that rotation
between CO and C1 (3 degrees) is seconda ry to rotation of the atlas a bout the odontoid, accompanied by secondary minimal linear displacement to the same side of roration, and lateral flexion on the opposite side (Fig ure l1-S) (32). Dvorak et aI., using Cf, eva luated the maxi mal rotational excursion of this joint as 10.25° (37). Penning and Wilmink reported a mean value of 1° rOtation at this level using CT sca ns (3S). Panjabi et a l. discovered as much as 7.2° axial rotation (o ne side) using stereophotogrammetry (measurements derived from three-dimensional photographs) (35). White and Panj abi report an approximate So lateral flexion determined by a review of the literatu re and their own a na lysis (S) . Werne in his ea rlier studies on cadave rs contended 11.9° lateral bending with slightl y less, 7.So on radiographs (33). Panj.bi et a l. found less lateral bending of 5.5° using stereophotogrammetry (35). It wou ld appea r that lateral flex ion of the atlanco-occipital articulation is limited not only by the osseous geometry but by the alar ligament attachment
197
~
11 ·8 ROtation at [he atlanrooccip iral joint. Rocarion of the occiput to the left is associa ted with an anteri or displacement of the right occipita l cond yle on
the right lateral mass of the adas (arro", 1). At the same rime tension develops in the adanrooccipiral ligament, pulling the right occipital condyle to the left (arrow 2). There rotation of the occiput to [he left is associated with a linear displacemem of 2 to 3 mm to [he left and lateral flexion to [he right. (From Kapandji IA . The rhysiology of the joints. Vol. 3. The trunk and the vertebral column. Edinburgh: Churchill
Livingstone, 1982,182-3. )
(Figu re 11-9) (10). Penning contends that lateral bending of the a rlantooccipital segment is always combined with the lateral bending and slight rotation of the C1-C2 joint (34 ). Coro nal plane rotation and transverse plane rotation occur in the opposite directions because
of the convex shape of the occipital condyles and concave shape of the arias articular surfaces. Thus ipsilateral latera l flexion is coupled with rotation of the head to the opposite side (10,29,39) . On lateral fl exion to the left, C1 translates to the left to adjust the position of the left lateral mass of C 1, which otherwise would prevent the left side flexion (Figure 11 -10). T he right a lar ligament is pulled tight by this movement, pulling on the dens, rotating the C2 spino us process to the right. Jirout contradicts this theory in his x-ray analysis of rotarional synkineses of occiput and
198 Alar ligaments from behind Occiput
A
len bending of head
Left latera l flexi on of the upper cervical
spine (solid arrow) with tran slarion of rhe arias (broken Q"ow) roward rhe lefr. (Bergmann TF. Peterson DH, Lawrence DL. Chiropractic technique.
New York: Churchill Livingstolle, 1993:223.)
B
f111t1'111-8 The role of the alar ligamentS in lateral flexion of atlanrooccipiral articulation: A, posterior
view in the neutral position; B, left lateral flexion. Motion is limited by the right upper portion and the left lower portion of the alar ligaments. (Bergmann TF. Peterson DH, Lawrence DL. Chiropractic technique.
New York: Churchill Livillgstone, 1993:220.)
atlas on lateral inclinarion (39) . He reports that in nearly half of his 322 cases the rotation of the atlas from the side of inclination cannOt be looked on as normal a nd constant, because it does nOt occur.
Translatory movements at the oceipitolatlanto complex are small, 0 to 1 mm (9, 10). The instantaneous axis of rotation for flexion-
extension is located in a sagittal axis 2 to 3 em above the apex of the dens (to). For lateral bending the axis appears to be located in the midline slightl y more distant from the tip of the dens (40) . Because there is very little or no axial rOtation at the occipiroarlantal articulation, the instantaneous axis of rotation for this plane is nor
considered (Fieure II-Ill.
Atlantoaxial Joints This mechanically linked four-joint complex lacks the disc of the typical vertebral motion segment (41 ). There are rwo paired atlantoaxial joints, one central atlantoodontoid joint, and one joint between the transverse ligament and the posterior
aspect of the odontoid process. Thus the pattern of motion is primarily controlled by the geometry of the osseous and ligamentous articu lations.
This joint exhibits predominately rotation of the atlas around the y-axis of the odontoid process. Werne evaluated the amOunt of move-
ment as 47°, constiruting 40 % to 50% of the axial roration of the neck (33). This is supported by Panjabi and White in their 1978 article (8). Penning and Wilmink discovered 40 .5° of motion to either side, with a range of 29 to 46° (38). Less motion is reported by Dvorek et aI., with an average of 32.2° (37). Panjabi et al. also found less axial rotation of 38.9° (35). Coupled motion exjsts during rotation, with a
"screwlike" mechanism allowing the atlas to drop 2 to 3 mm because of the biconvexity of the joint surfaces (Figure 11 -12). There is an associated ipsilateral lateral bending to a small degree (34). This vertical approximation was confirmed by Hohl in cineradiographs (42) . Werne concluded that the vertical displacement depends on
11 Kinesiology: An EnentIaI AppI'tIICb TOWII'd 1JI. .·.ta.... 1he CIIII .......:1Ic Subluxltlon
199
on the superior facets of C2. In flexion, the posterior joint capsule and posterior arches separate and the atlas articular surface glides forward. In extension the posterior joint capsule and posterior arches approximate and the arias articular
surface glides posteriorly (44). Panjabi er al. report 11.5° flexion and 10.9° extension at the atlanroaxia l joint (35). These similar measurements were confi rmed by Werne and Hohl, who demonstrated 10° of flexion a nd extension (33,42). Penning, using movement diagrams from functional radiographs to study flexion and extension, found on average 30 of motion with a range of 25 ro 45° (34). It is generally accepred that there is no measurable lateral flexion at the atlantoaxial joint (9) . Penning (34) reports a mean value of 10° to each side. Panjabi et al. report 6.7" of lateral flexion to one side at rhe atlantoaxial segment (35) . Q
B FiIIII'I1Hl The approximate location of the lAR (dot ) for rhe atlanrooccipital joint in the frontal plane, right and left lateral flexion (A). The location of the
lAR in the sagittal plane, nexion and extension (8 ). (From White AA. Panjahi MM. Clinical biomechanics
of the spine. 2nd ed. Philadelphia: ] B Lippincott, 1990:96.)
the extent to which the longitudina l axis of the dens correlates with the imaginary longitudina l axis of the body (33) . The more parallel the two are, the more distinctive the vertical displacement
(33). Jirout (43) used x-ray analysis ro formulate conclusions regarding rotation and linear displacement. In his model, rotation had two phases, with the initial phase involving a symmetrica l roration of C2 around rhe longitudinal axis of the cervica l spine (attributable ro the facet joints), followed by an asymmetrica l phase of further rotation (influenced by the addition of muscle traction), with pronounced lateral translation of the axis against the atl as. Flexion and extension require the anteri or
arch ro slide up and down on the odontoid process as the C I inferior facets ro ll and slide
Flexion and extension movements of the
atlantoaxial joint are associated
with small
translational movemems from 2 to 3 mm in
the adu lt and up to 4.5 mm in the ch ild (10). The atla ntodenta l interspace a lso diminishes during fl exion, creating a V-shaped appeara nce (29). Although there is still controversy as to whether lateral (x-axis) translation of the atlan toaxia l joint occurs, most of the literature
suggests that a displacement of 0 to 4 mm is normal (9). The instantaneous axis of rotation for the atlantoaxial joint is located by cineradiographic studies in the middle third of the dens for flexion and extension (Figure 11-13) (33) . For axial rOtation, the axis may be assumed to lie in the center portion of the axis (Figure 11-14 ) (9). Because lateral flexion at this joint is sma ll or nonexistent, the location of an axis for this motion may be deemed irrelevant (40) . Lower Cervical Spine The lower cervica l spine from the second to the seventh vertebra possesses six degrees of motion: flexion, extension, rotation, and lateral flexion . The range of morion is determined by osseous geometry and the stiffness of the disc (7) . Move-
200
The SubluxlUon Complex
Neutral
Rotation
fIgUre 11-12 The coupling of vertical translation of C 1 with axial translation of C i on C2. (Bergmann TF, Peterson DH, Lawrence DL. Chiropractic technique. New York: Churchill Livingstone, 1993:222.)
ment is not isolated to anyone segmental level but generally is accompanied
by simi lar motion at
ather levels (4S). Sagitta l plane motion (flexion and extens ion) predominately occurs in the lower cervica l spine and is accompan ied by translation and roration
(Table 11-1). The upper vertebrae in the motion segment tilt and glide on the arricu lar surfaces of the lower facet joints, producing the total motion required by the head and neck (Figure 11 - 15) . The coupled translation that occurs with flexion and extension has been measured at approximately 2 mm per segment, with an upper range of 2.7 mm (9,46). In the sagitta l plane the z-axis translation
occurs
in
decreasing
magnirude
approaching the C7 vertebra (8), producing a "stair-step" effecr. In addit ion, for every degree of sagittal plane rotation, morc translation occurs in
the upper cervical segments than in the lower cervical segments (44 ). This tran lation has been anribured [0 the inclination of the facet joints (29) . Conversely, the caudal segments tend to have a larger amount of tilt (14 ).
Younger individuals may possess a general physiologic ligamentous laxity, demonstrating disproportionately greater motion at C2-C3, unlike most adults, who show the greatest flexion sagittal motion at C4-CS or CS-C6 (47). On flexion, C2 appears to subluxate several millimeters anteriorly, bur maintains the integrity of th e spinolaminar junction line (3 4 ). Rotation in the lower cervical spine never occurs in isolation; it is accompanied by some degree of lateral flexion (Table 11 -1) (32). Ranges of motion for segmental axial rotation on average are slightly less than those for lateral flexion, with a similar tendency for decreased movement in th e lower cervical segments (4 4 ). Lateral flexion averages approximately 10' to each side in the midcervical segments, with decreasing flexibility in the caudal segments (Table II- I) (44). Lateral flexion in the lower cervical spine is coupled with rotation such that ipsilateral lateral bending is coupled with rotation of the spinous process to the contralateral side (or convexity of the curve) (Figure 11 - 16 ). The
201
11 Dlestology: An EssenUai Approach Toward lInderatandIng the ChIropracllc SUbluXadon
Rotation
ofe]
C2 Rgare 11-14
Rep resenrarion of the approx imate location of the IA R for axial rota ti on of C l an C2. (Wlhite A A, Palljabi MM . Clinica l biomechanics of the
spille. 211d ed. Philadelphia: JB Lipp illCOlI, 1990:96.) figure 11-13
A, Represemarion of sagittal plane morion of Cl an C2, wi th approx imate IAR also
indica ted. B, The anrerior curva ture of the dens may permit some degree of additio nal sagitta l plane morion in both rota tion and rrans larion. (White AA. Palljabi
MM. Clinical biomechanics of the spine. 2nd ed. Philadelphia: JB LippillCOlI, 1990:93.)
>
degree of coupled motio n decreases in a ca udad direction (44 ). At the second cervical ve rtebra, there is 20 of coupled axial rota tion fo r every 3 0 of lateral bending, a ra tio of 2:3 (9). At the seventh ve rtebra, there is l Oaf coupled ax ial rotation for every 7.5 0 of
Limits and Representative Values of Rotation of the Cervical Spine
Interspace
Comblnod Flllion/Eltonsion (..·.'i. rotation) lImill of R.ng .. Representative (dogr.es) Angl. (dogrees)
Ono Sido lateral Bonding (,·axi. rot.tlon) limit. of Rango. (dogree.)
Representative
Angle (dogrees)
Ono Side Allat Rotation (y·.,I. rot.tlon) lImlll of Ranges (dogrees)
Ropresentatlvo Anglo (dogrees)
0-10 3-10 1-12
3 7 7
2-12 2-10 0-7
7 6 2
Middle
C2-3 C3-4 C4-5
5-16 7-26 13-29
10 15 20
11-20 9-15 0-16
10
13-29 6-26 4-7
20 17 9
0-16 0-17 0-17
8
11 11
wwer
C5-6 C6-7 C7-Tl
7 4
Whi te AA III, Panjabi MM, cds. Clinical biomechanics of the spine. 2nd cd. Phila delphia : JB Lippincott, 1990.
202
C2
C4
Filll'ell-1B Movement of the facet surfaces in rhe lower
C7
fIIIII't 11-15 A diagrammatic approximation of the relative regional cephalocaudal variations in radii of curvature of the arches, defined by the cervical verrebrae as they rotare and translate in the sagitta l plane. (From White AA, Palliahi MM . Clillical biomechanics of the spine. 2nd ed. Phjladelphia:}8 Lippillcott, 1990:99.)
late ral bending, a ratio of 1 :7.5. Jofe theorizes that the gradua l change in coupling ratio may be related to the change in inclination of the facet JOIntS (9). The greatest obliquity of the facet joints is at C2-C3 (40° to 45°), progressively
lower cervical spine causes coupled rotarion with lateral nexion. (Bergmann TF, Peterson DH, Lawrence DL. Chiropractic technique. New York: Churchill Livillgstolle, 1993:233.)
decreasing to 10· at C7-T I (32). Kapandji also believes that during lateral fl exion some degree of extension occurs as a result of anatomic structure (32) . Penning and Wilmink, using CT, discovered that during latera l flexion, to avoid the uncinate process imbrication, the superior vertebra performs a translation in a con tralatera l direction (38) . Because the unciform process is located posteriorly on the edges of the vertebral bodies, this mechanism takes place only posteriorly (41). With posterior translation of the upper vertebra with respect to the lower verteb ra in rhe opposite direction during lateral flexion, simultaneous rotation must occur (4 1). Fielding adds that becallse of the inclination of the intervertebral joints, du ring lateral flexion, the in fe rior articular processes on the concave side glide downward and backward, whereas those on the convex side glide upward and forward, thus producing the mO'ion of rotation (29) .
11 Kinesiology: An &l1lil1li AppI'OICII Toward IDIerlllld nl the ClIII"IIPI'1Ctic SW*uIItion Viewing all of the available data, it would appear that the highest intersegmental movement is located in the midcervical spine level. There appear to be only a few studies that give indication of the location of instantaneous
axes of rotation in the cervical region. Lysell postulates these locations based on judgment from observations of patterns of motion rather than on quantitative assessment (48 ). The IAR for sagittal and horizontal plane motion is located in the anterior portions of the subadjacent vertebrae (48). The instantaneous ax is of rotation for lateral fl exion has not been determined (Figure 11- 17) (48).
Thoracic Spine The thoracic spine is an area of transition from
the transversely situated facets of the cervical spine to the sagitally orientated facets of the lumbar spine. The principal movements that take place in the thoracic region are flexion, extension, rotation, and late ral flexion. Nevertheless, motion
is limited in all planes because of the ribs, narrowed discs, and elongated spinous processes. Combined flexion and extension in the thoracic spine averages approximately 6° per motion segment and increases in a cephalocaudad
Flexion/ extension
lateral bending
203
direction (44). Movement averages 4° in the upper thoracic spine, 6° in the midsegments, and
finally 12° in the lower two motion segments (Table 11-2) (10). As in the lower cervical spine, sagittal plane motion is accompanied by rotation with slight sagittal plane translation . Translation is uniform but markedly less than that of the cervica l spine (10). Lateral flexion averages approximately 6° to each side, with the lower two segments averaging 7 to 9° (Table 11 -2) (44). Data on the coupled motion (rotation and lateral flexion ) in the thoracic spine are less convincing because the resu lts
have been somewhat varied, depending on the segments studied (7). In the upper thoracic region the pattern mimics the lower cervical spine. The coupling is such that ipsilateral latera l bending occurs with the vertebral body rotating into the concavity and spinous process deviation to the convexiry. The degree of lateral bending produces somewhat less axial rotation than it did in the cervical spine (8) . In the middle and lower thoracic spine, the coupling is less distinct and may occur in any direction, bur it is genera lly assumed that the lower thoracic segments have a tendency to follow the coupling pattern of the lumbar spine (44 ).
Axial rotation
E~F R~L
fIIII't 11 ·17 Th e approximate locatio ns of instantaneous axes of rotation in the lower cervical spine. F is the location in going from a neutral to a flexed position. E is the location of the lAR in going from a neutral to extended position. L shows the axes in left axial rotation, and R shows them in right axial rotation. The question mark indicates chat there are no convi ncing estimates of the lAR for lateral bending in the cervical spi ne. (White AA. l'aniabi MM. Clinical biomechanics of the spine. 2nd ed. Philadelphia: JB Lippincott, 1990: 102.)
204
The SUbluXation C8mp1ex
>
Limits a nd R ep resenta tive Valu es o f R o tatio n of th e T h oracic Spine
Comblnod FIOIlon/Ellon.lon (..-axl. rolallon)
Intenplea
lImli. of Rang .. (degree.)
Tl-T2 T2-T3 T3-T4 T4-T5 T5-T6 T6-T7 T7-T8 TS-T9 T9-TlO TlO-T11 Tll-T12 Tl2-Ll
3-5 3-5 2-5 2-5 3-5 2-7 3-8 3-8 3-8 4-14 6-20 6-20
Representative
Angle (dogroo.)
Ono Sldolllo .. 1Bending ('-IIi' rolallon) limits of Rangel Representative (dogroo.) Angl. (dog".')
4 4 4 4 4 5
5 5-7 3-7 5-6 5-6
6
3-8 4-7 4-7 3-10 4-13 5- 10
6 6 9 12 12
6
5 6 5 6 6 6 6 6 6
7 9 8
One Sido Axial Rolalion (Y-Ixl. rolallon) lImli. of Rangl. (dogrees)
Anglo (dogroo.)
14 4-12 5-11 5-11 5-11 4-11 4-11 6-7 3-5 2-3 2-3 2-3
9 8 8 8 8 7 7 6 4 2 2 2
Representative
From White AA III, Panjabi MM, eds. Clinical biomechanics of the spine. 2nd ed. Phi ladelphia: JB Lippincott, 1990: 103.
Axia l ro tati on of the th o racic spine is encouraged in the up per segments beca use of th e mo re tra nsve rse o rienta ti o n of th e face t jo ints. Segmenta l axia l ro tati o n averages 8 to 9° in the upper tho rac ic spine (10)_ Ro tati ona l movements decrease in th e cepha locaudad d irecti o n, a pproximating 2° in th e lower two o r three th o rac ic segments (Ta ble 11 -2) (10)_ ROtati o n is a lso limited by the a nteri o r attac hment of the ribs to th e stern um. The locati o ns of the instantaneo us axes of rota ti o n have been stu d ied by White (10)_ The res ults have been ave raged a nd a re presented in Figure 11 - 18_ Lumbar Spi ne The principa l movements exhibited by th e lumbar spine a nd its individua l jo ints a re ax ial compressio n, ax ia l distracti on, flexion, extension, ax ia l rota tio n, and latera l flexio n (49) _ Ax ial compressio n is the movement that occurs during weig ht bearing in the upr ight posture (49)_ T he a nulus fib rosus an d nucleus pulposus bear the load a nd tra nsmit it to the ve rtebra l
end plates_ T he zyga po ph ysea l joi nts pa rti cipate in the load bea ring if th e o rie ntatio n of th ei r surfaces is other than in the coronal plane_ The jo ints a lso ca n share the load by th e impaction of th e inferio r a rtic ul ar process with the superior a rti cul ar face t o r the la mina of the ve rtebra below w hen the ve rtebra l body is rocked (49)_ T he lo rdosis of th e lumba r spi ne and ante rio r ligame nts pa rticipates in the ax ia l load-bea ri ng mecha nis m. Ax ia l distracti on has bee n stud ied fa r less (49)_ The ca psules of th e zyga po ph ysea l joi nts are the most significant element res isting this motion. Lumbar segmenta l fl exio n and extension are the predomina nt moti o ns in th is region of the spine_ Combi ned sagittal plane mo tion averages 14 to 15° per segment, with mo ti on increasing towa rd the lu mbosac ra l juncti o n (Table 11 -3) (10,24 ). Increasing range of mobi liry in the lower lumba r segments is exhibited by onl y a mino ri ry of pati ents (50) . Flexio n an d ex tension req uire anterio r sagitta l rotati o n aro und the x (co ro n. I)-axis, w hich is located in the posterio r a nulus o f the intervening disc (5 1), alo ng wi th a small a mo unt of fo rwa rd tra nsla tio n_ Sagittal
extension
Laterol bending
rotation
E~F
R~L
R~L
Flexion/
Axia l
Thoracic
FIgUre 11-18 The approximate locations of the instantaneous axes of rotation in the tho racic spine. (From White AA, Panjabi MM. Clillical biomechanics of the spine. 2nd ed. Philadelphia:)8 Lippincott, 1990:105.)
plane translation averages 1 to 3 mm in each direction (25,49,52), whereas anterior sagittal rotation averages 8 to 13" (49). The facet joints guide rotation and resist translat.ion. Segmental lateral flexion averages approximately 6" to each side uniformly throughout the lumbar spine, with the exception of the L5-S1 motion segment (Tab le 11-3). The lumbosacral junction demonstrates hal f of this mo tion (10). Pearcy and Tibrewal found the sa me pattern of latera l flexion, with approximately 10" occurring in the upper three levels, but there was sign ificantly less movement, 6"
and 3" at L4-L5 and L5-S1, respectively (53). Lateral flexion may be acco mpanied by either flexion or extension of the same joint, but extension occurs more frequently and to a greater degree (49). Lumbar lateral flexion involves a complex coup led movement of latera l tilting and rotatory motio n that is open for much debate rega rding the precise biomechanical motion. During lateral bending, some authors describe the " normal " lumbar verteb ral bodies to rOtate toward the concavity, with the spinous process rotating towa rd the convexity (5 1,54,55 ). Unfortunatel y, this may not a lways be the case. Cassidy
>
Limits a nd R epresenta tive Values o f Ra n ges of M o tio n of the Lumbar Spine
Inle .. pa.e
Ll-L2 L2-L3 L3-L4 L4-LS LS-S1
Combined Flllion/Elt.nsion (
On. Sld.lat... 1B.ndlng (Hxls ,otaUon) limits of RanglS Representative Angl. (d'g,e .. ) (deg"lI) 3-8 6 3-10 6 4-12 8 3-9 6 2~ 3
One Sid. Axial RotaUon (Y-3Ils rollUon) limits 01 Rang.s Representative Anglo (deg,,") (d'g"") 1-3 2 1-3 2 1-3 2 1-3 2 0-2 1
White AA Ill, Panjabi MM, eds. Clinica l biomechanics of the spine. 2nd ed. Philadelphia: J8 Lippincott Company, 1990: 107.
206 and Grice were the first to classify three patterns of coupled motion with lateral flexion in the lumbar spine (56,57). These patterns included type I, lateral flexion associated with contralatera l vertebral body rotation (spinous processes rOtate toward the side of latetal flexion ); type 11, ipsilateral vertebral body tipping with ipsi lateral body
.::p Type I
~ ------~
-----~-------
~. Type II
(k --I)
~
Type III
~ - - .;;=:~ ---~--- --
~ Type IV
f1111'111 -18
The cl assi ficatio ns of moti on patterns during lumbar lateral flex ion. (From Grice AS. Radiographic, biomecha1lical and clinical {actors in lumbar lateral flexion. Part 1. J Manipulative Physio/
Ther 1979; 2(1}:26-34.}
rotation (s pinous process toward the convexity);
and type 1Il, reversal or lack of vertebral body tipping with contralateral body rotation (56). Grice later expanded on these classifications by adding a type lV, reversal of lack of segmental tilt and rotation of the vertebral body toward the side of trunk bending (Figure 11-19 ) (58) . These patterns are primarily determined by evaluation of lateral bending functional x-ray studies. Type I has been suggested to be the normal coupled movement of the lumbar spine with types II, III, IV indicating aberrant motion patterns (56,58) . Other authors took this a step further by stating that coupled motion mechanics at va rious regions
of the lumbar spine are different. That is, Lt , L2, and L3 demonstrate axial rotation accompan ied by lateral flexion to the contralatera l side (49,53,59). The L5-S1 joint, in contrast, demonstrates axia l rotation accompanied by lateral flexion to the same side. L4-L5 shows no particular preference; bo th coupling parrerns can exist
(49,53,59). Haas et al. have mo rc recently shown, in their
population under investigation, that 40% to 60% of both asymptomatic and symptomatic subjects demonstrate type II motion at various levels of the lumbar spine (Lt-L4) (60). It is possible that much of the type II motion is a consequence of norma l asymmetries in facetel anaromy, soft tis-
sue orientation, and normal variation in cooperarive muscle activity (61). More research is necessa ry to verify "norrnal " and "normal variant "
coupling mechanics in the lumbar spine. Axial rotation in the lumbar spine is extremely limited and arrested by the intervertebral joints (Figure 11 -20) . Segmental rotation is relatively uniform throughout the lumbar spine and averages between 2° a nd 3° (10,24,49) (Ta ble 11 -3). One author found more axial rota-
207
11 Kinesiology: An Essential Approach Toward IInd8rstandlng tile Chi'oprac1lc s....xatlon
tion at L3-L4 and L4-LS (53). Manua l axial rotation was determined from L2 unfixed cadav-
ers, \virh approximately 5
[0
6° of rotation being
achieved in each direction over rhe rhree mobi le
segmen ts (62). Axial rotation is variably coupled wirh flexion and exrension. Eirher flexion or extension may occur during left or righr rotation,
but neither occurs consistently (49). Consequently, the mean amounr of flexion and exten-
sion coupled with axial rotation is zero (49) . The instantaneous axis for axial rotarion and
lateral flexion is placed within the poste rior nucleus and anu lus of the subadjacent disc space ( JO ). The IAR for sagittal plane motion is most commonly placed wirhin rhe intervertebra l disc of
the subadjacent vertebra, with flexion located toward
the
anterior
portion
and
extension
roward the posterior portion (Figure 11 -21) (10) . Regardless of the spinal location, the quantity and qualiry of motion are determined by norma l
--,
variation in sagittal curvature and segmental ori-
emation (53,59), muscular control (56,58), facet orientation (63), and degenerative changes of the motion segments (64,65).
Abnormal Joint Motion Abnormal joint motion can be characterized inro
three categories: hypomobiliry, or restriction of norma l motion; hypermobi lity, or marion in excess of normal; and aberranr mobility, or motion in which there is a change in the axis or rotarion, including paradoxical or reversed motion.
Hypomobility Hypomobi lity ranges from a slight restriction of joinr motion to a total absence of morion or joint locking. This norion was introduced into rhe chi-
figure 11~20 The mechanism of left axial rotation of a lumbar inrervertebral joinr. Two conseclltive vertebrae, superimposed on one another, are viewed from above.
ropr.lctic literature in 1906 by Smith, Langworthy, .1I1d Pa xson (66). The intervertebra l joint was capable of a certain field of motion and had a cer-
The lower verteb ra is depicted by a dotted line. AJ
rain axis of morion. Other terms have been pro-
Initially, rotation occurs about an axis in the vertebral
posed ro describe hypomobiliry in more recent literature, including interarticular dyskinesia (67), spinal articular dysfunction (68), manipulable
body. B, As the posterior elements swing around, the right inferior articular process of lower vertebrae impacts the superio r articu lar process of the lower vertebra. (Bodguk N, Twomey LT. Clinical anatomy of the lumbar spine. Edinburgh: Churchill Livingstone, 1987,66,)
208 Flexion/
lateral
Axial
extension
bending
rotation
E~F
R~L
R~L
lumbar
Figll'811 -21 The approximate locations of the instantaneous axes of rotation in [he lumbar spine. (From \Vhite AA, Paniabi MM. Clinical biomechanics of the spine. 2nd ed. Philadelphia: JB LippincolI, 1990:112.)
lesion (68) , and joint fixation (69). Restriction or hypomobiliry of joint movement, which is a principle component of the manipulable subluxation, should be reversible for manipulation to be of benefit. An early chiropractic paradigm viewed the subluxation complex as a malalignmenr, restrained in an abno rmal position, thus disallowing normal joint motion. This model suggested that a vertebra was pulled out of its ideal neutral position by alterations in articular and periarticular soft tissues and restricted in its movements in the direction away from rhe malposition (70). This concept is not contained in the definition of hypomobility or restricted motion in current theory
and research. In a srudy by Howe in 1970, intervertebra l malposition as estimated from plain film radiographs did not correlate with morion studies indicating dysfuncrion in the form of hypomobiliry o r hypermobility, erratic movement, or even reversa l of normal motion (30) . Conversely, apparently well-aligned vertebrae may be present wirh abnormal morion. The premise that the direction of malposition can predict the direction of movement restrictions has been refuted by Haas and Peterson (70) . Vertebrae demonstrate greater tilt movement away from the direction of
malalignment, not diminished in the direction opposite the malposition. In this same study by Haas and Peterson, segmental malalignmenr was universal in the population studied (70) . In addition, Shram and Hosek could not demonstrate the effects (change in posirion) of chiropracric manipulation with prepoststatic radiographic technology (71) .
Hypermobility Hypermobiliry ranges from a slight increase in joint motion that is reversible, to instabiliry in which the holding elements of the spinal motion segment are no longer intact. Usually a traumatic or congenital anomaly alters the properties of the restraining tissue, permitting excessive joint com· pliance. Three main factors determine segmental hypermobility: congruency of the joint surfaces in close-packed position; structural integrity of the collagen that contributes to joint capsule, tendons, and overlying tissues; and neuromuscular tone that stabi lizes the spine under physiologic conditions. Segmenta l hypermobility has been defined by McGregor and Mior in the cervical spine as "the mobility of a given motion segment which is excessive and is accompanied by local and/or
11 1IiIesIoIogy: An EsIIIIItIaI ApproacI1 Toward Underltll..... the CI*'opracllc N*lxallon peripheral symptoms, but not so extreme as to be
life-threatening or require surgery (72)." Motion slightly in excess of normal is usually reversible and not an absolute contraindication to
manipulation. A manipulable subluxation may occur in a motion segmem in which the holding elements have been moderately stretched, producing hypermobility with a joint block that is reversible. Even with excess joint motion, there
can be a shift in the axis of rotation resu lting in an abnormal pattern of movement. Repeated thrusting into such a joint, however, may not produce optima l results and prolong the healing time of the stretched elements. Instability in cOntrast is extreme hypermobility whereby the holding elements of the threejoint complex have been permanently damaged in such a way that the pattern of abnormal motion is nOt reversible. In such cases the subluxation of the joint would be considered nonmanipulable and may require surgica l repair if neurologic deficits are apparen t.
andoz refers to thi s as a
surgical subluxation as opposed to a reversible fixation characterized by a vertebral body, a zygapophyseal joint, or both that have moved into a posicion that [hey can never occupy during
normal spinal movement (73) (see C hapter 8) . Clinal instability in the cervical spine has been defined as "the pathological state of motion at an intervertebral level in the cervical spine that results in clinically intolerable symptoms, as in cord or rOot damage, requiting prolonged bracing or surgery" (74). Centrode patterns have been used ro assess segmental instabi lity (75). A centrode is defined
209
Loss of normal end play resistance (em pty end feel ) is also clinica ll y significant, because it is a potemial manifestation of joint hypermobility or instability (44).
Aberr..t Motion Aberrant motion has been discussed as both motion in which a change in the axis of rotation has occurred or there is a reversal of normal
motion desctibed as paradoxical. Smith, langworthy, and Paxson describe it as a change in the field of vertebral motion; a subluxation is like a "wheel whose hub was off center" (eccentric in
contrast to concentric) (66). A normal change in the instantaneous axis of rotation has been
described by White and Panjabi when referring to the changing axis that occurs with coupled motion. For example, with flexion of a vertebra,
translation along the Z-axis coupled with rotation around the X-axis produces an instantaneous change in the axis of rotation as flexion proceeds. It is thought that a restriction at one joint in
three-joint complex can produce a change in the axis of rotation and an abnormal parrern of motion . . Physiologic consequences of abertant segmental mechanics can lead ro unnatural load distributions. It is postulated that manipulation can quite effectively change the instantaneous axis of rotation in a motion segment where move-
ment has been demonstrated to be pathologic in reference to the normal coupling mechanism (77) . Thus the quality of motion has changed, not the quantity. Paradoxical motion has been observed at the atlantooccipita l joint with the occiput moving
as a locus of successive positions of instantaneous
into extension on the atlas during cervical flexion
centers of rotation (75) . The position and variation of the centrode defines the motion at the segmental level. The greater the translation, the greater the centrode length (76). If the relative
(36). Lane considered this motion to be a normal variant (78) .
amounts of translation and rotation are inconsis-
tently distributed throughout the range of motion because of mechanical irregularity of the joint, the centers of rotation determined for adjacent motion arcs may shift and increase cenrrode
length appreciably (76).
Compensatory Hypermobillty Global motion of the spine is dependent on the combined movement of 24 spinal motion segments. It has been proposed that restriction of movement at one level will be compensated for by hypermobility in other area (13,79) . Compensatory hypermobility often occurs adjacent to a
210
The SubluxBUon Complex
restricted segment or surgically fused segment (80-84). Stokes et al. studied the behavior of spinal segments adjacent to surgical fusions, using
biplanar radiography, and discovered lower lumbar spine segments to be hypermobile in flexion and lateral bending (85). In addition, these primary motions were accompanied
by an involun-
mately 3 mm in length, lies in parallel within the skeletal muscle fibers, termed extrafusal fibers. Each spindle, surrounded by these extrafusal fibers, contains specialized fibers called intrafusal fibers. These intrafusal fibers are encapsulated by connective tissue that joins either with the fascia
of the skeletal muscle fibers or at the musculoten-
tary, increased coupling of motions rhat resulted
don junction.
in increased shear on the disc and posterior
Each spindle possesses six intrafusal fibers in total. Two specific types of intrafusal fibets exist: two nuclear bag fibers and four nuclear chain fibers . There are also rwo types of bag fibers, namely, the nuclear bag large fiber (NBL) and nuclear bag small fiber (NBS). Of key importance are the polar (end) regions of each intrafusal fiber.
facet joints (85). In dogs, immobilization of long spinal segments of the spine influences the remaining mobile segments by increasing the load and motion not only at the immediately adjacent segment but also at the distal segments (86). Not only may fusion result in increased motion above the involved segment, this also may occur above an unstable one (74). Gael et al. observed an increase in the relative motion of seg-
ments above the induced instability (87). These compensatory mechanical effects also have been observed across spinal regions. Sagittal lumbar movement was found to be significantly. reduced with increasing sacroiliac restriction (88). This
These regions are made up of contractile muscle
fibers similar to that of skeletal muscle. The contractile (polar) regions of the nuclear chain fibers reach farther into the central region than those of the contractile portions of the nuclear bag fibers. This has strong functional implications, as is discussed later. in terms of sensory outpm, there are two
mobility.
types of afferent fibers, namely la and 1I. Type la afferent endings (primary endings) innervate all of the intrafusal fibers, whereas the type 1I afferent endings (secondary endings) innervate mostly the nuclear chain fibers. Note rhar the la endings,
Mechanism 01 Intervertebral Joint Restriction
around the most central portion of the spindle, also known as the equatOrial region of the spindle. The type 1I endings, known as the f1owerspray endings, are found near the end of the sen-
relationship, however, reversed at a certain level of sacroiliac restriction. At this point, lumbar mobility increased with increasing sacroiliac restriction but never to "normal" sagittal lumbar
known
The cause of restricted segmental movement, a component of the chiropractic subluxation com-
plex, has been discussed in Chapter 10. Presented in this chapter is one theory of motion restriction, namely Korr's theory (89). The structure and function of the muscle spindle are discussed to better understand the mechanism of joint restriction.
The Muscle Spindle: Structure The muscle spindle is a proprioceptor found rhroughout all skeletal muscle that is used to generate lengrh and velocity sensitivity, thus guiding our movement. The muscle spindle, approxi-
as annulospiral
endings,
are wound
sory region, also known as the iuxtaequatorial
regions of the intrafusal fibers. The primary and secondary afferent endings of each spindle feedback into the dorsal root monosynaptically, to ultimately synapse on the alpha-motor neurons that supply the muscle from which the spindle is contained. These spindles also may feed back to alpha-motor neurons that supply the muscles in the vicinity of the activated spindle. Group la afferent fibers are velocity- and length-sensitive nerves. That is, they signal the rare to which a muscle lengrh is changing (velocity) and also signal changes in muscle length (absolute length). Group II signals length sensitivity primarily. In
reference to Korr's theory, only the primary type la afferent nerve endings are considered. The muscle spindle is the only receptor that can be controlled by inputs from the central nervous system. This is accomplished through the gamma neuron system, also known as the fusimo-
tor neurons. These gamma fibers originate alongside of the alpha-motor neurons in the anterior horn of the spinal gray marter. They descend directly to innervate the polar (contractile) regions of the inerafusal fibers so that, with
ents at a high frequency yields very little shortening of the polar regions of the large bag fibers . This is because of the poorly developed myofibrils in the bag fibers allowing for minimal contractile ability. When the bag fibers are contracted, only an approximate 5% increase in overall length of the middle region of the intrafusal fiber is possible. Thus, stimulation of the gamma dynamic efferents is primarily to make the end regions of the large bag fiber more "stiff" without bringing about much change in length of the middle
gamma activation, a contraction of both polar
region. If, however, you activate the gamma static
regions of each intrafusal fiber occurs. This in turn generates elongation of the central region of the intrafusal fibers, as the polar regions COntract. As the central region of the spindle becomes stretched, so do the membranes encasing the spiral endings of these la afferent nerve endings. This leads to an actual opening of the pores of
efferents, which supply mainly the nuclear chain fibers, a substantial shortening of the polar regions and significant lengthening of the central region of the spindle is generated, increasing the la afferent output. This is caused by the welldeveloped myofibrils at the polar regions of the chain fibers . In isolation, the purpose of the gamma system is to regulate the length or stiffness of the polar regions of specific types of intrafusal fibers . This in turn modifies the length or stretch characteristics of t.he central region where the sensory la afferent nerve endings are located . Furrhermore, because the muscle spindles lie in parallel with the extrafusal fibers, the spindles, and thus the central region, change in length as the whole muscle changes in length. Thus, the output of the spindle is dependent on the length of the muscle only when there is no gamma involvement. How-
these membranes, creating ionic exchanges, lead-
ing to an action potential that travels along the la afferent fibers. There are two ways to stretch the spindle's central region to increase its discharge: stretching
the overall muscle and contracting the polar regions of the spindle through the gamma system. Both methods increase the firing of the la afferent output. This introduces the final point regarding spindle structure, that being twO types of gamma innervations, namely gamma dynamic and gamma static efferent nerve endings. The gamma dynamic efferents generally supply only the larger bag fibers. The gamma static efferents generally innervate both the small bag fibers and all chain fibers. The gamma fibers have acquired their names from their funcrions. If you activate the gamma dynamic efferents, this affects only the sense of velocity or rate of muscle shortening. If the gamma static efferems are activated in isola-
tion, then only the sense of absolute muscle length is affected. The reasons for this observation are discussed in the next section.
ever, in vivo, this is not the case. Both the gamma
system and the overall muscle length work in concert to generate accurate proprioceptive sensa-
tions regarding rate of muscle length changes and absolute length. To furrher understand this, we look to the function of each gamma system, beginning with the gamma dynamics. If a muscle, and thus spindle, is stretched at a rate of 5 mmlsec, one sees an initial jump of la afferent output and a gradual increase in discharge frequency until the end of the stretch, where there is an adaptation down to a new
The Muscle SpIndle: function Understanding the function of the muscle spindle requires a full understanding of the gamma system. Activating only the gamma dynamic effer-
steady state level. The difference berween the peak discharge during the dynamic phase (stretch) and the following steady discharge during the static phase (rest) is known as the
212 dynamic index (01). If a spindle is stretched at a rate of 30 mm/sec, a proportionate increase in DI is observed. There is a fairly linear relationship between the size of the 01 and the tate at which the muscle changes length. The 01 is what the central nervous system (CNS) potentially takes into account to decipher and create our percep-
tion of rate of muscle length change. The dynamic index is the result of the morphology of the nuclear bag (NBL) fibers. When you stretch the spindle, the polar regions do nOt undergo stretch initially; only the middle region undergoes stretch . As the stretch is continued, the actin-myosin bonds in the polar contractile regions begin to break apart, which unloads the intrafusal equatorial region, decreasing the la affe rent output. This breakage is caused by the poor actin-myosin development in the nuclear
bag intrafusal fiber. This "backward creep" generates a gradual decrease in [a output to a new
steady-state level; the difference in la output ultimately creating the 01. The greater the rate of stretch, the greater the actin-myosin breakage of bonds and thus an increase in 01. If you stimulate on ly the gamma dynamic efferents, this increases the 01 during the appl ication of a stretch. As mentioned, the polar regions of the nuclear bag fiber contract, making the polar regions more resistant to being stretched (stiffer). Because they are stiffer, more of the stretch is applied to the middle (equatorial) region, where the group la afferent nerve endings a re located. Thus, the spind le output reaches a higher peak frequency, promoting a greater decrease during adaptation, creating a larger 01. This is interpreted by our CNS as an inc rease in the rate of muscle lengrh change. The gamma dynamic sysrem is most important in the maintenance of posture. Anytime a
limb is moved rapidly out of the intended posture, the muscle spindle would produce a very high discharge with a subsequent large downward creep of la afferent Output, thus a large 01. From higher centers, this large 01 would reflexively activate app ropriate alpha-motor neuron pools to restore adequate limb posture. If a situation arose in which one required a greater percep-
tion of muscle length change to perform a given task, the eNS would turn up the gamma dynamic effeceors, which in turn would increase the
dynamic index. With this in mind, the gamma dynamic effetents are somewhat like an amplifier, amplifying our perception of rate of stretch and respective reflexive responses. If, however, you stimu late the gamma static
efferents alone, you would see a significant increase in the steady-state output of the la afferent nerve endings. This is attributable to the shortening of the polar regions of the nuclear chain fibers where there are well-developed myofibrils allowing no cteep and, therefore, no dynamic index. The importance of the static system is to maintain the la afferent output (sens itiv-
iry) of the spindle during the course of muscle shortening. For example, bringing the elbow into flexion, shortening the biceps, shortens the muscle spindles. This potentially unloads the sensory region of the involved spindles if it were nOt for the gamma static efferents. Therefore, if you were to apply a resistance to the biceps in a shortened position, you a re likely to see less la output of the spindle, indicating the spind les are nOt operating optimally throughout the full range of muscle shortening or lengthening. During the initiation of limb movement, OU[put from higher centers simu ltaneously activates the gamma- and alpha-motor neurons eliciting both intrafusal and extrafusal fiber contraction . This alpha gamma coactivation is referred to as servo-assistance control (90). As the muscle shortens, the overall length of the spindle shortens bur the equatoria l region is maintained in
length because of the contraction of the polar reg ions from the gamma activation. Therefore, the ga mma static system is maintaining a con-
stant amount of stretch on the equatorial (sensory) region of the spind le as the muscle undergoes length change.
Korr's Theory
d. Jt*II Axallon
Korr's theory for the kinesiopathologic aspect of the "osteopathic lesion" or "somatic dysfunc-
tion" is based on the premise that muscle spindles can participate in the development of muscular
11
~:
An £sI8n1III W"" TOWII'd 111.... '1111.... the ClIi'lllll'actIc SUl*XIIIIon
resistance. From a mechanical viewpoint, the
osteopathic lesion can be synonymous with the chiropractic subluxation. Palpation of decreased mobility and increased resistance in one o r more
planes of motion is used to identify and evaluate the subluxation. Korr perceived this resisted motion to be caused by one or more hypertonic muscles that traverse a vertebra (89). As previously discussed, the gamma stacie
efferents in conjunction with the alpha neuron system can modulate the Ia afferent output. During muscle shortening, there is a "canceling
effect" berween the extrafusa l fiber shortening and the intrafusal fiber polar region shortening, creating a constant spindle equatorial length, and thus, a steady-state spindle la output throughout all ranges of muscle length. Korr termed this gamma gain. The greater the gain, the greater the steady-state spindle output at all muscle lengths. Now, let's apply this to the chiropractic subluxation.
Korr hypothesized that segmental muscles of the spine may have acquired an increased gamma
gain. During this high gamma activity, the spindles may be encouraging their homonymous muscle, which is in an already shortened state, to contract, creating restriction of the involved motion
segment. The spindle reports the extrafusal fiber length relative to the polar region length of the intrafusal fibers , nOt absolute extrafusal fiber length . This means that increased gamma gain is really an increased steady state in spindle discharge through all ranges in muscle length. The
213
dynamic effecenrs were increased, this generates an increased DI relative [0 [he actua l rate of mus-
cle lengthening if a stretch were applied. For example, any stretch applied to the right lumbar rotatores or multifidi muscles, as in right lumbar rotation, would signal an elevated muscle velocity feedback, potentially eliciting heightened reflexive pathways to generate right muscle contraction to
"break" this perceived increase in rate of rightsided muscle lengthening. However, there is evidence that the gamma dynamic and static efferents can be stimulated independently. This wou ld suggest the possibility that on ly one gamma system is responsible for this theory. Regardless of the specific gamma system involved, what would cause this maladapted increased gamma gain? Korr mentions two causes for this increased
setting in gamma gain: (1) an unanticipated "giving away" of a load during an isometric COntrac-
tion or (2) the abrupt approximation of two muscular attachments as with two vertebrae. Both of these situations yield a sudden slackening of the equatoria l region of the spind le, creating a spindle silencing. The CNS, in response, would demand feedback from the spindle by increasing the gamma discharge to the intrafusa l fibers and subsequently restore the spindle afferent output disc harge. After recovery from these external forces, the two muscular attachments would then be in opposition to regain their normal anatomic
relationship because of the continued gamma discharge exiting the alpha-motor neurons of the resisting muscle(s) . The more stretch applied to
greater this gamma gain, with irs increased spin-
the muscle, the greater the resistance to stretch
dle afferent output and corresponding facilitated alpha motor neurons, the greater the extrafusal
caused by the increased spindle afferent output. External forces passively approximating mus-
comraction in an attempt ro shorten the extra-
cular attachments or minor "accidents" and microtraumas inducing strong rapid voluntary contractions, as theorized by Korr, would induce
fusal fibers and silence the spindle output. When an external force, such as the palpating hand of a chiropractor, is applied to a spinous process stretching the hypertonic musculature, muscle spindles of the involved muscles increase their already heightened output, promoting more contraction and further resistance to stretch, crc-
ating a "blocked" end feel. Korr's theory also can be applied to the nuclear bag fibers . If the gain for the gamma
rapid intrafusal equatorial slackening. T his wou ld silence the spindle afferent output and subsequently order the CNS to increase the gamma gain. If such an event were to happen, how would the chiropractic adjustment help? The chiropractic adjustment, which involves a high-velocity low-amplitude thrust directly applied to restOre norma l physiologic motion of a
214 specific vertebra, in effect would be stretching the hypertonic muscles responsible for this restricted movement. Korr explained that rapid stretch of these extrafusal fibers generates a rapid stretch of the intrafusal fiber's equatorial region, which is already under significant tension as previously set by the gamma efferents. The subsequent spindle stretch would potentially generate such an immense barrage of afferent impulses that the CNS would apptopriately respond by "turning down" the gamma efferents. Normal gamma gain would, therefore, be reestablished with concomitant return of normal muscle tonus.
Eldred et aI., using an animal cat model, dissected out the ventral roots supplying the gastrocnemius in preparation for electrical stimulation
(91). The dorsal rOOts were used to record the la afferent output from the muscle spindles. The muscle was fixed at a set length and baseline la afferent output was recorded. A tetanic stimulation of the gamma motor neurons through the ventral root were elicited for 10 seconds at twice the twitch threshold. After the removal of this stimulus, the 13 output remained above resting levels. When the muscle was passively shortened, creating a shortened spindle, the la afferent output decreased. However, when the spindle is relengthened, the la afferent output increased above its pretetanized level. Only until a rapid stretch, potentially analogous to a chiropractic adjustment, was applied to the muscle would a permanent reduction in the la afferent firing be achieved to that of resting pretetanized levels. Edin and Vallbo have also shown in humans that only after rapid muscle stretching will elevated la firing decrease (92). They and others have suggested that stable attachments of actin-myosin crossbridges in intrafusal muscle fibers (after fusimococ stimulation) are formed, generating an
elevated level of la afferent output (93-95). A rapid stretch to the involved muscles would potentially break the "stuck" bonds of the actinmyosin filaments in the intrafusal fibers and consequently would permanently decrease the once elevated 13 afferent discharge. Grice and Shambaugh showed a decreased muscle activity after
manipulation (96,97). Whether this is a result of muscle spindle pathways remains controversial.
Assessment of Abnormal Motion Currently there is no singular gold standard for detecting primary joint subluxation. As chiropractors we rely on numerous measures to diag-
nose spinal dysfunction, beginning with regional and intersegmental joint range of motion. Although interobserver and intraob$erver reliabiliry studies have somewhat validated the use of passive and active gross or regional motion pro-
cedures (98-101), testing of intersegmental motion has resulted in contradictory findings (102,103). Intersegmental motion can be assessed using motion palpation. Motion palpation is defined as the palpatory diagnosis of the quality and quantity of passive and active intersegmental
joint ranges of motion. Keating completed a literature review of the inrerexaminer reliability of motion of the lumbar spine and concluded we2k evidence of reliability (104). Nansel et al. found poor interexaminer reliability detecting cervical spine asymmetries in asymptomatic subjects (lOS). On a more positive note, researchers have
found good sensitivity and specificity in manual detection of cervical joint dysfunction (106) and lumbar joint dysfunction (107) and good intraand imerexaminer agreement using motion palpa-
tion of the sactoiliac joint (108). The possible reasons for discrepancies between the studies are interpretation of the degree of fixation by the examiner, improper standardization of methodology, increase in spinal mobility after the first examination, improper statistical analysis, and
discrepancy in the definition of fixation. Thus the palpatory procedure used most by chiropractors cannot be substantiated by the research to date. To validate such a testing procedure, it is imperative that a known or "Gold Standard" be achieved, test/retest reliability be determined, and interpretation of degree and definition of fixation and palpatory procedures be standardized. In addition to the three planes of physiologic movement, flexion-extension, lateral flexion, rotation in the active and passive ranges of
11 Kinesiology: An Esaenllal Approach Toward lhIIratandIng tile CIIiroprac1lc StmIuxallon
215
motion of the Joint (as assessed by motion palpanon), there is also end play and joint play. End play is assessed by applying additional overpressure to the specified joint at the end range of passive movement (44). Each spinal region has characteristic end-play qualities that are determined by the local bony and soft tissue anatOmy (44). Evaluation of end feel encompasses detection of
should nOt be confused with radiographic proce-
the point at which resistance is encountered, quality of resistance, and associated tenderness.
iner reliability) and muscle tonus (little significant
Loss of anticipated end-play elasticity is thought to be indicative of disorders within rhe joint, its capsule, or periarticular soft tissue (44). Encountered end-play resistance is a significant finding in the determination of joint dysfunction and adjustive vector orientation (along the planes of encountered resistance) (44). In the J930s, John Mennell described another form of physiologic motion called joint play, which cannOt be produced by voluntary muscles (109). It IS a qualitanve evaluation of the joint's resistance to movement when it is in a neurral or loose-packed position (44). Joint play assessment is advantageous to differentiate articular-based pain and dysfunction ftOm nonarticular sofr tissue disorders. As with end play, you check for the presence or absence of pain, the quality of movement, and the degree of encountered resistance
(44). Joint play procedures attempt to isolate a parncular plane of increased or restricted glide. This procedure has been proposed as a method for determining the direction of appropriate adjustment (44). Algometry measures the patient'S perceived pressure-pain threshold. Fischer has documented the reliability, reproducibility, and validity of using algometry (110, III). Chiropractic researchers have used algometers to measure
pressure-pain thresholds to identify segmental dysfunction associated With a manipulable spinal lesion (112) and to document improvement (outcome measure) after a chiropractic adjustment ( 113).
Leg-length assessments for the detection of spinal motion segment mobility have demonstrated poor to satisfactOry reliability (I 14-116). Chiropractic functional leg-length tests, which
dures used to determine an anatomically short
leg. These tests are suspect in the area of validity and correlation with clinical findings. Palpation for bony and soft tissue tenderness (117) and postural assessment (118) have demonstrated satisfactOry reliability. Chiroptactors palpare for tissue texture changes (weak interexamagreement hetween examiners) ro csrahlish
.1
clin-
ical picture in the determination of segmental
dysfunction (117). More sophisticated measures of spinal segment motion abnormalities include: surface elec-
tromyography (1 19,120), infrared and liquid crystal thermography, videofluoroscopy, motion radiography (56,58), and physical performance evaluation (sttength testing). Triano summarizes the outcome measures used ro diagnose and treat the subluxation complex as (1) regional mobility, (2) pain reporting
instruments, (3) self-cate activities, and (4) limited petformance measures (12 1).
Biomechanlcal EHects of the ChlropracUc AdjuSbnent as It Relates to the Kinesiology Aspect of the Manipulable SubluxaUon It is the purpose of this section to review some of the research that studied the behavior of the spinal motion segment, specifica ll y its motion chatacteristics afrer the application of chiropractic manipulation.
In a recent study by Gal et aI., human unembalmed postrigor cadavers were used to study the subsequent segmental translational and rotational movements that occurred between the vertebrae
TIO, Til, and T12 afrer a posterior to anterior adjustment to the right transverse process of Til (122). The data were acquired with the usc of steel bone pins threaded into the respective verte-
bral bodies and high-speed cineradiographic cameras to measure vertebral movementS relative to
216
The SUbluXation C8mp1ex
each other. This direct approach on cadavers allowed for accurate measurements that cannot
be performed in living patients. During the adjustive thrust, the following rel ative movementS were recorded. Posterior to anterior translation was only slightly greater for Til, the contact vertebra, compa red with the adjacent venebra. Rotational movements were a lso found, even though the line of drive was from posterior to anterior. All three vertebrae rotated in a right axial direction; howeve r, the greatest significant rotation was measured at T12 . This is a peculiar finding because Tl2 possesses sagitally oriented inferior facets that shou ld limit axia l rotation and encourage sagittal rotation.
Right translation was shown to be greatest in TIl. The most striking data demonstrated sagittal rotation of T I 0 and Til inferiorly, while TI2 rotated in a superior direction.
Immediately at the completion of the adjustment, these changes recorded in the relative sagittal position of T il and TI2 remained, Implying some permanent or semipermanent changes in
relative verteb ral position with respect to its neighboring one. Sagitta l rotation was the on ly movement to show this type of mechanical behavior. For the mOSt part, TIO-TIl tended to react to the appl ied fo rces as a unit compared with TII-Tl2, w hich could be explai ned by the unique nature of the T I2 facet joints. This experimenr demonsrrares rhe porential for relative small movements among vertebrae after adju tments, but was not designed to make direct predictions about the mechanical responses of the vertebra l column in li ve parients. However, the author believes that simi lar trends in relative vertebral movemenrs would be observed in live patients following the sa me adjustive procedure. Herzog and his colleagues demonstrated indirectly rhat chiropractic manipulation has a biomechanical effect on spinal mechanics (123, 124). They demonstrated on 11 patients with unilateral sacroiliac syndrome thar six treatmenr sessions of spina l manip ulative therapy (over 12 days ) caused significant changes in the external ground reaction forces during walking (124). The effects were measured with a force platform . The
sacroiliac joint motion was tested using the Gillet motion palpation procedure and indicated improved mobility in all patients. This improvement remained without treatment for at least 14 to 17 days. Nansel and his colleagues in a series of studies investigated the effectiveness of cervical spine manipulation to amel iora te goniometrically verified cervica l lateral flexion passive end-range asymmet ries ( 125- 127). The results of the first experiment demonstrated that a single lower cervica l adjustment delivered to the most restricted side of end range, was capable of consistently and markedly amelio rati ng the magnitude of cervica l lateral flexion passive end-range asymmetries, at least for 30 minutes (125). They further clarified that the resultant reduced asymmetry was a consequence of improved (statistically significant) range of motion on the originally most restricted side and due to very little (s tatistically insignificant) reduction in range of motion on the originally least restricted side. In a followup study, this same group investigated the stability of the effects of a single cervica l adjustment (126). In this study, two groups with goni ometrica ll y confirn)ed left ve rsus right cervica l latera l fl ex ion passive end-range asymmetries, defined as lO° or greater, were used. The groups consisted of (1) individuals who had I to 8 years previously traumatized their neck, and (2) individuals with no histOry of neck trauma. They reported that both groups demonstrated a significant reduction in lateral flexion asymmetry up to 4 hours. By 24 hours, though, 100% of the group with no previous neck trauma maintained their lateral flexion symmetries, whereas only 56% of the previous trauma group maintained their symmetry. By 48 hours, 75% of the previous neck trauma group had regained their asymmetries to the poinr of no significant difference from their preadjustive values. However, 88% of the subjects with no histOry of neck trauma still continued to exhibit left versus right lateral fl exion symmetries of less than 10°. The most recent work of Nansel et al. demonstrated adjustment specificity on the restOrarion of cervica l spine range of morion
11 1IiIIIIoIogy: An EsIIllIlllIlppl'OlCll Toward 1II_ltlldng the ClIII'OIII'KIIc SlMlxatlon (127). Adjustments delivered to the upper cervical segments (C2-C3) induced significant restoration of cervical rotation symmetry. Likewise, adjustments delivered to the lower cervical segments (C6-C7) induced significant restoration of cervical lateral-flexion symmetry. Even subjects that exhibited both rotational and lateral flexion asymmetries still demonstrated these axis-specific findings . Thus, it appears evident that correction of biomechan ical aberrations of the subluxation requires adjusrive specificity, in terms of conracr, to derive specific mechanical outcomes. Unfortunately, in the above srudies, even though live patients wefe used, globa l range of motion was used as the outcome measure instead of interseg-
21 7
any, doubt that spinal manipulation has a significant effect on the reduction of mechanica l lowback pain over other forms of "accepted" physica l therapies (J29) . It is probably on ly a matter of time before this degree of conclusive evidence is shown to exist for mechanical thoracic and neck pain. However, Cassidy in two separate studies
demonstrated a significant reduction in pain levels after a single cervical rotary adjustment directed to the same side of pain (130,131). Conversely, spinal motion aberrations are not
always directly related to presenting symptomatology (70) . Studies investigating the relationship berween pain and segmental spinal movement have not demonstrated any significa nt differences
menta l motion.
between
Yeomans performed an observational study, using 58 case studies, to examine the potential effects of the adj ustment on intersegmental cervical mobility (128). Yeomans used radiographid template ana lysis. Both the Henderson and Dorman (14) and Panjabi and White (46) approaches were used to determine segmental cervical spinal mobility. Spinal manipulative therapy was applied ro the restricted motion segments, as determined by static and motion palpation, cervical Stress radiographs, and ranges of cervical motion. The treatment regime averaged three rreatmentS per week, ranging from 2 to 6 weeks. At this point, if the condition had not been resolved, the frequency of treatments decreased until the symptoms plateaued. The Henderson and Dorman method showed a statistically significant increase in mobility at every level except C I. The Panjabi and White method demonstrated premanipula-
groups (60,61) . Vernon used static and dynamic roentgenography to conclude that there is a higher prevalence of abnormal motion patterns and pathologic changes in symptomatic subjects (132). Phillips failed to demonstrate a relationsh ip between abno rmal clinical findings and abnormal spinal motion in patients suffering from low-back pain (20) . Haas and Nyiendo stated that lumbar motion cannot be used with
tion average instability scores to be statisticall y
significantly greater than postmanipulation averages. This has important clinical implications. The author observed hypomobile segments rypically adjacent to unstable segments and theorized that by directing the adjustive force to the hypomobile segments this reintroduced proper motion, thus decreasing the biomechanical load placed on the unstable segment aiding to stabilize the unstable segments. From a clinical standpoint, do mechanical changes mean pain reduction? There is little, if
symptomatic
and
nonsymptomatic
any accuracy to diagnose or prognosticate a
patient'S low-back pain status, and conversely, that low-back pain cannot be used to characterize a patient'S lumbar segmenta l motion in lateral bending (6 1). Therefore, as chiropractic clinicians, we must be cautious in deducing abnormal segmental motion as the sale cause for the presenting pain. Nanse! et al. demonstrated that asymmetry magnitudes in cervical passive cndrange motion did not distinguish between subjects w ho had previous neck trauma and those who did nOt (126).
The Klnesiopalhology of Spinal Joint Degeneration The relationship between spinal motion and pathologic changes in the three-joint complex is a major concern to chi ropractors. Whether from the aging process, unhea lthy lifestyle, or microtrauma and macrorrauma, degenerative changes
218
The SUbluxation COmplex
produce changes in spinal movement patterns. Spinal degeneration with associated manipulable subluxations produces both increased motion (hypermobi liry) and decreased motion (hypomobility). Both may occut simu ltaneously in the same individual and result from a pattern of degeneration described by Hall in the cervical spine in 1965 (133). In the early stage, he noted cavities at the lateral margin of the anu lar fibers of the intervertebral disc that spread from one side to the other with accompanying loss of disc height. In the final stage the intervertebral distance is greatly reduced and the bone structure becomes distorted by osteophyte formation. In the next decade three stages of degenerative changes in the lumbar spine were outlined by Kirkaldy-Willis that provided a working model for the management of low back pain (134). Like the stages of cervical spine degeneration described by Hall, each phase of lumbar spine degeneration blends into the other. The earliest stage is 'characterized mainly by abnormal function with only slight anatomical and kinesiopathology changes. At the end of this phase, the changes in the threejoint complex may progress ro the unstable phase or proceed directly to those changes described in the stabilization phase. The unstable phase follows with increased abnormal motion recognized radiographically as an increase in translation, most commonly seen as retrolistheses. This is best viewed in lateral radiographs in flexion and extension (see Chapter 5). Spondylolisthesis and abnormal opening of the disc can be seen in flexion. Retrospondylolisthesis, narrowing of the intervertebral foramen and abnormal discal wedging, can be seen in extension. As the segment becomes more degenerated the degree of movement increases. The third phase is one of resrabilization, when motion in the apophyseal joints and disc becomes restricted from degeneration of carti lage, loss of disc substance, fibrosis, and the formation of osteophytes around the posterior joints and disc. This process then leads to stabilization of the
hypermobile motion segment that furthers the degenerative process and hypermobility in adjacent segments as the spine attempts to maintain an optimal global range of motion. Building on the work of Kirkaldy-Willis, Sandoz introduces a fourth phase of episodic fixa tions that correspond to manipulable subluxations (135). He describes these episodic fixations as acute, reversible, and usually occurring at the extremes of movement. In contrast, he notes, that chronic fixarions (non manipulable subluxations) that are encounteted in the final stage of stabilization, as a rule occur at or near the neutral position and are not reversible. [n light of the above work, Good and Mikkelsen have studied the correlation between discogenic spondylosis and the type of motion found in the sagittal plane of the intervertebral motion segments of the lower cervical spine (65). In global cervical flexion when there was little or no degenerative change, most cases of abnormal motion were hypermobile in character, not hypomobile. This contradicts the hypothesis in the Kirkaldy-Willis model, which suggests that in the face of this type of degenerative change, hypomobiJity is usually present. In a similar contradiction, when there were moderate degenerative changes, normal motion Or hypomobility was often present, not hypermobilit)'. Finally, hypermobility was as common as hypomobility when severe degenerative changes existed. [n global cetvical extension, the great incidence of hypo mobility occurring with absent or mild discogenic spondylosis agrees with the Kirkaldy-Willis model. However, hypermobiliry was still somewhat comlllOIl. With increasing discogenic spondylosis into the moderate and severe stages, hypomobility was the ru le and hypermobiJity was very uncommon. These findings, however, do not describe the degenerative condition of the posterior column (facet joints) in conjunction with the discogenic or anterior spondylosis, which would most likely influence the movements associated with flexion. McNab suggested that in rhe first stage of cervi-
cal disc degeneration, the involved segment became unstable and the movement of the related verrebra became excessive and irregular, thus another contradiction to the Kirkaldy-Willis model (136). Gertzbein et al. has studied centrode characteristics of the lumbar spine to identify spines with degenerative disease (137). Spines with minor, mild, and moderate degeneration have demonstrated abnormal translation motion, which is reflected in increased lengths of their centrodes. The differences between normal spines and spines with all categories of degenerative disc disease are statistically significant. These loci, or cenrrodes, are longest in the earliest stages of degeneration, but maintain their length through moderate degenerative disc disease. Furthermore, radiographic changes consistent with moderate disc disease are associated with inferior migration of the centrode. These findings suggest that the major abnormality of motion is erratic or translational motion rather than excessive motion.
Pathologic changes that upset the intrinsic equilibrium of the spinal motion segment are thought to contribute to the production of a manipulable subluxation.
Pathologic EHects of Joint Immobilization Poor vascularity of both the intervertebral disc and the articular cartilage of the posterior zygapophyseal )Olnts has deleterious consequences on the three-joint complex. Both structures are dependent on joint motion for exchange
of nutrients and removal of waste products. Compressive loading and unloading of the intervertebral disc and articular cartilage of the posterior synovial joints is dependent on segmental spinal motion and is necessary for a healthy three-joint complex. Grieve has documented that, without mobility, lack of nutrition leads to joint and tissue breakdown, producing inflammation
and the earliest stages of degenerative joint disease (138). Based on studies of rabbit knees immobilized for a 3-week period, Salter has demonstrated that irreparable lesions occur in the articular cartilage when normal movement is restricted (139). In addition to the restriction of synovial fluid flow, the mechanical stress led to damage and death of
chondrocytes from continuous compression of the articular cartilage. The irreversibility of the degenerative changes observed has led Salter to conclude that prolonged immobilization of joints prevents healing and increases disability. In addition to the deleterious effect on the joint, the adjacent bone and surrounding muscles also deteriorate (140). Woo et al. found, on gross inspection of the synovial joints after immobilization, that excessive tissue depositions were observed (141). This excessive fatty fibrous connective tissue formed mature scar [issue and created inrraarcicular adhesions. Immobilization resulted in a loss of water and glycoaminoglycans along with collagen changes. It is now recognized that the degeneration that occurs on immobilization differs significantly from that seen in osteoarthritis (142). Initiation of osteoarthritis is characterized by focal changes in articular cartilage rather than more generalized tissue involvement. A closer look at the effects of immobilization on the three-joint complex is covered in Cha pter 9.
Conclusion This chapter has focused on defining and analyzing "normal" morion for each region of the spine. This will provide a basis for understanding abnormal marion or alreration of normal joinr function that characterizes the kinesiopathologic component of the subluxation complex. Examining the kinesiopathologic component of the chiropractic subluxation in isolation, however, may be misleading because any movement modification may very well be the result of both
220 biomechanical and neurogenic reflexes working in concert. Whether movement restoration with its concomitant therapeutic effects transpires as a direcr consequence of rhe forces exerred onto rhe joints rhemselves, or rhrough neuromuscular reflexogenic mechanisms, is srill debarable. This chaprer may have lefr some srudents questioning wherher any cerrainty exists wirh regard to the mechanical properties of the manipulable subluxarion or the mechanisms involved in rhe therapeutic effects after a course of chiropractic manipulation. However, one who seeks understanding musr never forget thar as wirh all academic quests to gain knowledge and certainty, more questions will remain unanswered.
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Inrercxamincr conco rdance in detecting joim-pla)' asymmetries in the cervical spines of otherwise asymptomaric subjccts. J Manipulative Physiol Ther 1989; 12:429-33. Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophyseal joilll pain syndromes. Medj Aust 1988; 148:233-6. Bylield D. Preliminary studies with a mechanical model for the evaluation of spinal mOfion palpation in the lumbar spine. Proceedings of the 1990 International Conference on Spinal Manipulation, Washington, DC, May 11-12,1990,215-19. Herzog W, Read Ij, Conway PjW, Shaw LD, McEwen Me. Reliability of motion palpation procedures ro detect sacroiliac joint fixations. j Manipulative Physiol Ther 1989; 12;86-92. Dishman RW. Static and dynamic components of the chi ropractic subluxation complex: A literature review. j Manipulative Physiol Ther 1988; I 1:98- 107. Fischer AA. Pressure tolera nce over muscles and bones in normal subjects. Arch Phys Med Rehabil 1986; 67; 406-9. Fischer AA. Pressure threshold mete r: Its use for quantifica tion of tender spors. Arch Phys Mcd Rehabil 1986; 67;836-8. Vernon H, Core P, Beauchemin D, Bo nn oyer B. A correlative study of myofa scial tender points and join t fixations in the lumbar-pelvic spi ne in low back pain. I>roccedings of the 1990 Imemational Conference on Spinal M anipula tion, Washingron, DC, May 11-12, 1990, 236-40. Vernon HT, Aker P, Burns S, Viljakaanen S, Short l. Pressure pain threshold eva luation of the effect of spinal manipu lation in the treatmenr of chronic neck pain: A pilot study. j Manipulative Physiol Ther 1990; 13;13-16. DeBoer K"~ Harmon RO, Savoie S, et at. !mer- and inrra-examiner reliability of leg length differentia l measurement: a preliminary study. J Manipulative Physio! Ther 1983; 6(2);61-6. Fuhr AW, Osterbauer PJ.lmerexaminer reliability of relative leg-length evaluation in prone, extended position. J Chiro Tech 1989; 1(1);\3-18. Rhudy TR, Burk JM. Imer-exa miner reliability of functionalleg-length assessment. Am j Chiro Med 1990; 3(2);95. KeatingjC, Bergmann T"~Jacobs GE, Finer BA, Larson
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K. Interexaminer reliability of eight evaluative dimensions of lumbar segmental abnormaliry. J Manipulative Ph ysio1 n"r 1990; \3(8);463-70. Vernon H. An assessment of the intra- and inter-reliability of rhe posnlromcrer. J Manipulative Physiol Ther 1983; 62(2);57-60. Jo hnson WL, Vorro J. Biomcchanical measurements of changes in cervical muscle function following osteopathic manipubtive treatment. J Am Osteopath Assoc 1983; 83; 131. Vorro J , Johnston WL, Hubbard R. Biomechanical analysis of s)'mmerric a nd asymmet ric cervical function. J Am Osteopath Assoc 1982; 82: 140- 1. Triano jJ. The subluxation com plex: Outcome measure o f chiropractic diagnosis and trcatment. Chiro Tech 1990; 2(3); 11 4-20. Gal j , Herzog W, Kawchuk G, Conway», Zhang Y. Biomechanical studies of spinal mampulative therapy (SMT): Quantifying the movemenrs of vertebral bodies during SMT. JCCA 1994; 38( 1); 11-24. Herzog W, Nigg BM, Robinson RO, Read LJ . Quantifying the effects of spinal manipulation on gait using patients wi th low hack pain: A pilot study. J Manipula tive Physiol Ther 1987; 10:295-9. Herzog W, Nigg BM, Read LJ. Quantifying the effects of spina l manipulations on gait using patients with low back pain. J Manipulative Physiol Ther 1988; 11 (3); 151-7. Nansel DO, Cremata E, Carlson J , Szbzk M. Effect of unilateral spimll adjusrmenrs on goniomerricallyassessed cervica ll areral-flexion end-range asymmetries in otherwise asymptomatic subjects. J Manipulative Physio1 Ther 1989; 12(6) ;4 19-27. Nanscl 0, Pencff A, Cremata E, Carlson J. Time cou rse considerations for the effects of unibtera l lowe r cervica l adjustments with respect to the amelioration of cervical latera l-flexion passive end-range asymmetry. j Manipulative Physiol Ther 1990; 13:297-304. Nansel DO , Pend A, QuitOriano j. Effectiveness of upper versus lower cervical adj ustments with respect to the amelio ration of passive rotational ve rsus lateral-flex ion end- range asymmetries in otherwise asymptomatic subjects. J Manipulative Physiol Ther 1992; 15(2);99- 105. Yeomans SG. The assessment of cervical intersegmenta l mobility before and after spinal manipulative therapy. J Manipulative Physiol Ther 1992j 15(2):106-14. Manga R, Angus D, Pa padopoulos C, Swan W. The effectiveness and cost-effectiveness of chiropractic management of low-back pain. Richmond Hill, Ontario: Kenilworth Publishings, 1993. Cassidy jD, QUOIl JA, Lafrance LJ , Yong-Hing K. The cffect of manipulation on pain and range of motion in the cervical spine: A pilot study. j Manipulative Physiol Ther 1992; 15;495-500.
224 131. Cassidy JD, Lopes AA, Yang-Hing K. The immediate effect of manipulation versus mobilization on pain and range of motion in the cervical spine: A randomized controlled trial. J Manipulative Physiol Thcr 1992; 15(9),570-5. 132. Vernon H. Static and dynamic roentgenography in the diagnosis of degenerative disc disease: A review and comparative assessment. J M'JOipukttive Physiol Thcr 1982; 5,163-9. 133. Hall Me. Luschka's joint. Springfield, Illinois: Charles C Thomas, 1965:44. 134. Kirkaldy-Willis W, ed. The three phases of the spectrum of degenerative disease. In: Managing low back pain. 2nd ed. New York: Churchi ll LivingstOne, 1988: 117-32. 135. Sandoz R. The naruml history of a spinal degenerative lesion. Ann Swiss Chiro Assoc 1989; 9: 149-92. 136. McNab I. Cervical spondylosis. Clin Orthop 1975; 109,69-77.
137. Gernbein SD, Seligman J, Holtby R, et al. Centrode characteristics of the lumbar spine as a function of segmental instability. Clin Orthop 1986; 208:48-5 I. 138. Grieve GP. Common vertebral joint problems. ew York: Churchill Livingstone, 1981 :5-38. 139. Salter RB. Textbook of disorders and injuries of the musculoskeletal system. Baltimore: Williams & \'(filkins, 1970. 140. Levin S. Early mobilization speeds recovery. Physicians ports Med 1993; 7(1),70-4. 141. Woo S, Mathews JV, Akeson WH, et 411. Connective tissue response to immobiliry: correlative study. Biomechanica I measurcments of normal in immobilized rabbI! knees. Arthritis Rheum 1975; 18:257-64. 142. LanrL CA. Immobilization dcgeneration & the fixation hypothesis of chiropractic subluxation. Chiropractic Research Journal 1988; 1(t ):21-46.
........ Three Neurophysiologic Theories on the Chiropractic Subluxation Charles N. R. Henderson Key words
Chiropractic theory, subluxation, intervertebral foramen encroachment, joint receptors, proprioception, spinal cord traction, dentate ligaments
After reading this chapter you sholiid be able to answer the following questions:
Quesdon #1
Are the neural contents of the intervertebral foramen (nerve roots and dorsal root ganglion) equally sensitive to compression?
Quesdon #2
By what neurologic mechanism may nonvertebral joints such as the sacroiliac, ankle, or temporomandibular joint produce longterm influences on the central nervous system?
QU8sdon #3
What are two ways in which traction, through the dentate ligaments, may influence neural impulses within the spinal cord?
226 foramen, either spinal or interverrebral, which does produce pressures upon nerves, thereby inrerfering
T
his chapter reviews three theories that are
and inrerrupting the normal quantity now of men-
incorporated
tal impulse supply between brain and body and
into
OUf
neurophysiologic
model of the chiropractic subluxation. The name of each of these theories tells something of the mechanism by which we think the subluxation affects the nervous system: 1. lntervertebral encroachment 2. Altered somatic afferent input 3. Dentate ligament, cord distortion
Before reviewing these three theories, it is helpful to establish our perspective by stating a few fundamental points concerning theories and models, especia ll y those related to the subluxation. Theories should be plausible and scientifically acceptable. They are often described (and examined in scientific studies) by using models that help us visua lize the abstract principles involved. Our models allow us to operate in a world in which the very complexity at size of reality makes it unmanageable in its full essence. The utility of a model, then, is in its manageable size and complexity. We simpli fy the complex, shrink the enormous, and magnify the minute until we feel comfortable. However, the very ease or comfort we feel toward our models may lead LIS to forget that they are only models, not the full essence of reality. This is an important point. Our failure to appreciate the limits of ou r models leads to untold problems in our life and our science. Most simply put: We think with models bitt we live with reality. The reader shou ld keep this caution in mind while reading this and other chapters of this text. Defining the term subluxation is necessary, even if a bit difficult. Chapter 1 on terminology introduced us to the scope of the problem. Chiropractic educators, legislators, philosophers, scientists, and practitioners hold tenaciously to a wide range of definitions. Here is a small but influential sample: A vertebral subluxation is any vertebra out of normal alignment,
Out
of apposition to its co-respon-
denrs above and below, wherein it does occlude a
thus becomes THE CAUSE of all disease. A vertebral subluxation IS a verrebral subluxation whenever ir IS what is stared abovc, ALL elemenrs being prescnt. Ir is NOT a sub lu xation unless the inrerfercnce to transmission is present. There can be no pressure upon nerves unless the size, shape, diameter, or circumference of rhe foramen is changed. There can be no change in the normal size, shape, diamcter, or circumference of the fora · mcn unless one vertebra is subluxated between its
co-respondents above and below iemphasis BJPI. B. J. Palmer ( I I Subluxation is an aberrant relationship between twO adjacent articular structures that may have functional or pathologica l sequelae, causing an alteration in the biomechanical and/or neurophysiological reflections of these articular structures, their proximal structures, and/or body systems that may be directly or indirectly affected by them. ACA (21
.. . interference with ncrve transmission and expression, due to pressure, strain or tension upon the spinal cord, spinal nerves, or peripheral nerves as a result of a displacement of the spinal segments or orher skeletal struc[Ures. ICA (31
knervertebral Encroachment Theory A common theme in all of these definitions is that a chiropractic subluxation exerts a significant influence on the nervous system. In the chiroprac· tic profession, the most popular explanation for the su bluxation's impact on the nervous system is clearly the intervertebral encroachment theory. A number of other explanations have been offered, but these other explanations lack the simple appea l of the intervertebra l encroachment theory. Both doctor and patient can readily understand that pressure on the neural contents of the intervertebral foramen may disrupt the normal ingress and egress of nerve impulses.
227 It is now well established in the clinical literature that encroachment of neural
structures
within the intervertebral foramen (IVF) may produce pain and paresthesias as well as changes in
afferent barrage is being affected by manipulation of the dorsal rOOt ganglia." These small anima l studies are consistent with
muscle tone and autonomic activity. The working assumptions are that pressure on the contents of
clinical experience (6,7). Slowly applied compression to a normal peripheral nerve (for exa mple, peroneal n.-crossing legs) produces no pain but
the IVF eithet increases Ot decreases neural activ-
does produce numbness, paresthesias, and muscle
ity. increased neural activity produces paresthesias,
weakness. By contrast, rapidly applied compres-
pain, hypertonic muscles, vasoconstriction, and
sion to an inflamed nerve produces pain and
sweating.
Decreased neural activiry produces
paresthesias (Tinel's sign). At surgery, mechanical
numbness, muscle weakness/paralysis, vasodila-
compression of normal spinal nerve roots produces sensory and motor impairment without pain. However, even minimal mechanical deformation of inflamed nerve rOOts produces radiat-
tion, and dry skin. It is reasonable to ask, "Just how sensitive afe the contents of the IVF? " We have learned that normal dorsal root ganglia (DRG), but not the spi nal roots, may be stimulated by encroachment of the IVF. In small animal studies, compressive forces rapidly applied ro normal dorsal roOtS (10 mg) produced only brief (1 ro 2 seconds ) bursts of activity (4,5). Moreover, slowly increased pressure eventually produced a conduction block but did not evoke an active response within the root fibers. By contrast, DRG responded to small, slowly applied, compressive forces (100 mg) with prolonged repetitive firing. Most ganglia neurons fired for at least 4 ro 7 minutes; a few fired for 25 minutes. Chronica lly injured dorsal nerve roots behave very differently (5) . Injured roots may respond vigorously to mechanical pressure. Rapidly applied forces produce long bursts of activiry (15 ro 30 sec), and even very slowly applied 10-mg pressures fire nerve root fibers. In addition, chronic peripheral nerve injury produces spontaneous discharges within DRG. Wall and Devor (5) suggest that radiating limb pain reported during a Lasegue straight leg test could be caused by shifting the DRG ro a position of increased mechanical stress. These investigators suggest that DRG discharges associated with peripheral nerve injury may ex plain phantom limb sensation
and pain. They also comment: " .. . there are a number of therapeutic schools which claim that pain is increased or decreased by minor shifts in position of vertebrae and structures close to the vertebral column. It appears conceivable that the
ing limb pain. Recent studies demonstrate that sma ll-cali ber afferent nerve fibers do more than simply conduct impulses to the central nervous system. Stimu la-
tion of these primary afferents promotes the release of histologically potent neuropeptides, such as substance P (SP) and vasoactive intestinal peptide (VIP), at their peripheral terminals (8,9). This observation has sttiking implications. It suggests that the peripheral origins of sensory fibers are important sites for neurologically mediated effects. We will consider the possible consequence of such a mechanism on back pain. As shown in Figure 12-1, the posterior anular fibers of the intervertebral disc are innervated by the recurrent
meningeal (sinuvertebral ) branch of the spinal nerve (10,11 ). Figure 12-2 demonstrates that the zygapophyseal joints are richly innervated by the medial branch of the posterior primary ramus of the spinal nerve (12). Thetefore, irtitation of the DRG caused by intervertebral encroachment may cause release of neuropeptides within the intervertebral disc and the zygapophysea l joints. Earlier studies showed that SP and VIP stimulated breakdown of structural proteins (13,14). Over time, these neuropeptides may produce pathologic changes in the intervertebral disc and zygapophyseal joints. The plausibiliry of IVF encroachment as a contributor ro discogenic low-back pain is under investigation by scient.ists at the University of Iowa (14 ). These researchers have developed an
228
AllIn 12-1
Schematic diagram of amerior spinal column and spinal canal in nervation. 1, Nucleus puJpOSUSj 2, anu lus fibrosus; 3, amerior longirudinalliga mem/periosreum; 4, posterior longirudinal ligamem/periosteurn; 5, leptomeninges; 6, epidural vasculature; 7. filum terminalej 8, intrathecallumbos3cral nerve rOOfj 9, venera l root; 10, dorsal roO[; II , dorsal roor ganglion; 12, dorsal ramus of spinal nerve; 13, ventral camus of spinal nerve; 14, recurrent meningea l nerve (s inuvertebral nerve of Luschka)j 15, sympathetic branch to the recurrent meningeal nerve; 16, somatic branch to the recurrent meningeal nerve; 17. white ramus communicans; 18, gray ramus
commun icans; 19. lateral sympathetic efferent branches projecting from gray ramus communicans; 20, paraspina l sympathetic ganglion; 21. paraspinal sympathetic chain; 22, anrerior paraspinal afferenr sympathetic ramus; 2]. anrerior paras pinal efferent sympathetic branches; 24, lateral paraspinal afferenr sympathetic ramus. Note: Afferenr and efferenr parasp inal sympathetic rami may be combined. (Reprinted with permission from Jinkins JR, Whittem ore AR, Bradley WG. The anatomic basis of vertebrogenic pain and the autonomic syndrome associated with I"mbar disc extmsioll. AJR 1989; (152:1277-89.)
animal model of disc degeneration caused by IVF encroachment (Figure 12-3). In this model, structural disc proteins are broken down when substance P and VIP are released by senso ry nerves in the posterior an ular fibers of the disc. These investigators applied low-frequency vibration (approximately 4 Hz) to rabbits with experimentally reduced IVFs as well as to control animals with normal IVFs. They o bserved that mechanica l stimuli are more effectivel y transmitted to the ORG when the IVF dimension is experimentally
decreased . Chronic mechanical stimulation of ORG caused small-caliber afferents in the superficia l anu lar regions of the segmental disc to release substance P and VIP. These proteolytic neuro peptides caused degeneration of the disc. A ptogressive degenerative cycle developed wherein disc degeneration produced further IVF encroachment that increased the ORG stimulation. This resulted in further release of substance P and VIP and, subsequently, further degeneration of the intervertebral disc.
229 tio ns" of vertebral joints are somerimes effec-
tive in resolving the neurologic dysfunctio n of a subluxa tion. In addition, it has been suggested by numerous clinical investigarors rhat altered afferenr input from spinal structures such as the
zygapophyseal jo ints could produce signs and symptoms previously attributed to intervertebral encroachment (15-20) . These investigators repo rted sign ifica nt somatic sensory and motor
responses to altered articular affe rent input. Responses consisted of changes in nociceptive and kinesthetic sensibilities, muscle to ne, deep
tendon reflexes, jo int mobility, and sympathetic activity. T herefore, clinical and basic research investigations suggest an impo rtan t alternative
mechanism for the effects of a chiropractic ..... 12-2 Part of the lower spinal innervation (lateral view). I, Ante ri or primary ramus of the spin al nerve; 2, anterior primary ramus branch to the interven eb ral disc; 3. posterior primary ramus of the spinal nerve; 4. media l branch of the posterior primary ramus with an adjace nt zygapophyseal joint capsule (a nicular) branch, and a descending branch to the zygapophyseal joi nt ca psul e (a rticul at branch ) one joint lower; 5, lateral branch of the posterior primary ramus; GRC, gray ramus com municans; TVp, transverse process; Z}C, zygapophysea l joint capsule; arrow, mam il oaccessory ligament. (Reprinted with pennission from Giles LGF. Anatomical basis of low-back pain. Baltimore: Williams & Wi/kilts, 1989.)
Altered Somatic Anerent Input Theory Chiropractors find rhe IVF encroachment theory to be very useful, and it is well supported by clinica l and research literature. Bur, what about upper cervical adjustments? The fVF encroachment theory can nOt apply to joints lacki ng intervertebral foramens such as Occ-C1 or C1-C2. 00 sacroiliac or extremi ty joints subluxate? If so, how is the nervous system affected? Clinica l experience suggests that chiropractic adjustments often bring clinica l improvement in the absence of demonstrable encroachment within the intervertebra l fo ramen. Directionally nonspecific "mobi liza-
adjustment. A chiropractic adjustment may "normali ze" articu lar afferent input ro the central nervous system. It is proposed that normalized a rticular sensory input reestablishes notmal nocicep-
tive and kinesthetic reflex thresholds, with subsequent recovery of muscle rone, jo int mobility, and
sympathetic activity. In a stud y of 20 subjects, Mooney and Ro bertson (17) injected hypertonic sa line into the L4-L5 or L5-S1 facet joints. They used a rthroscopic guidance to ensure proper needle placement. These injections produced low-bac k pain a nd radiaring leg pain. The entire ipsilateral lower limb and the foot were involved in some patients. W hen la rger volumes of hypertonic saline were injected, or when subjects had preexistent lumbar facet disease, the pain radiated further down the limb. These investigators noted marked myoelectric activity in the ipsilateral hamstring muscles with diminished straight leg raisi ng (by 70%) . A subsequent intracapsular injection of the local anesthetic Xylocaine abolished all of these responses. Several subjects with preexistent facet disease had decreased straight leg raise (below 70 0 ) or depressed deep tendon reflexes before saline injection. It was particularl y interesting that each of these subjects demonstrated a no rmal straight leg raise and normal deep tendon reflexes within 5 minutes after an intracapsular injection of Xylocaine. The authors commented, " Based on this
230
Rgln12-a Proposed working model of dorsal rOOt ganglia-neuropeptides-mediared degeneration of the spinal motion segmenr. 1, Environmental or structural factors (for example, vibration/spinal instabiliry ) srimulare the synthesis or transport of neuropeprides of dorsal root ganglia (2), which in turn promote the synthesis of degradative enzymes and inflammatory agents (3). causing progressive degradation of the spinal morion segment (4). The resulting abnormal spinal morion segment renders the dorsal root ganglia more susceptible to mechanical stimuli, thereby creating a self-perpetuating, progressive, chronic condition. (Reprinted with permission (rom Pedrini-Mille et af. Stimulation of dorsal root ganglia and degradation of rabbit anll{II5 {ibro5115. Spine 1990;
15{l2}:1252-6.}
preliminary experience, we no longer consider diminished straight leg raising or reflex changes to necessarily implicate nerve root pressure by disk protrusion." Thabe (18) examined the segmentally related muscles of 20 upper cervical and 20 sacroiliac joints with restricted motion. Using needle probe electromyography (EMG), he observed marked spontaneous myoelectric activity in these muscles. Normal muscle does nOt demonstrate spontaneous EMG activity at rest. Within 2 minutes after injection of Xylocaine into the involved joints, there was marked reduction in spontaneous EMG activity. Spontaneous EMG activity was also reduced after gentle mobilization (nonthrust, "muscle energy" technique) applied to the involved joints. It was an interesting contrast that
manipulation (high-velocity thrust techniques) of the involved joints produced immediate and complete abatement of spontaneous myoelectric activity. Thabe concluded that manipulation of the fixated joints produced a potent normalizing influence on the central nervous system, putatively caused by modified afferent input from joint receptors. In a series of related studies, Korr et al. (16) investigated decreased electrical skin resistance (ESR) as an indicatOr of increased sympathetic motOr activity after a variety of biomechanical stresses. In one study, they observed referred pain accompanied by segmental patterns of decreased ESR after injections of hypertOnic saline into deep paraspinal tissues, deep interspinous ligaments, or paravertebral muscles. More superficial injections
231 (skin, superficial interspinous ligaments, perios-
teum of spinous processes) produced on ly local pain and locally decreased ESR, or no pain and no changes in ESR . These investigators also reported ESR changes in response to acute postural stresses. In this study, the pelvises of nine seated subjects were laterally tilted 15° and the ESR was evaluated over a 2-hour period. Orher subjects received a heel lift (V. to ~-inch hard rubber wedges) in one shoe. Heel lift subjects performed their normal daily activities and were
evaluated for ESR over 1 or more days. All subjects experienced reversible decreases in ESR after
coordination of joint motion. [n addition, these investigators reported that reflex changes in muscle tone or coordination were temporarily abol-
ished by intraarticular injection of a local anesthetic. Elecrrocoagulation of the joint capsule permanently abolished reflex responses to noxious stimuli applied to the joint. The studies discussed to this point demonStrate the influence of relatively short-term, noxious afferent input on central nervous system function. Few investigations have examined the impact of chronic noxiolls sensory input. However, patients seen in chiropractic and medical
Biguer er al. (19) demonstrated that a vibratory stimulus (100 Hz) applied to the left suboccipital triangle region of normal subjects modifies
offices have frequently experienced chronic pain, lasting months or years. The recent development of an animal model for chronic pain and rheumatoid arthritis has permirred rhe study of chronic,
the visual location and movement of a target in
noxious articular influences on the central ner-
body-centered visual space. This stimulus apparently acts through the muscle spindles, which are especially dense in rhe cervical region (21-23). In
vous sysrem (25-271. In this model, a mineral oil suspension of Mycobacterium butyriC/im (Freund's adjuvant) is injected into the base of the
a review of causes and treatments for the "dizzy
rat's tail. The ensuing reversible arthritis has
patient," Brown (20) noted:
pathologic and biochemical fearures thar resemble human rheumatic disease and appears to produce chronic pain. Mantyh et al. (28) examined changes within the superficial region of the dorsal horn of the spinal cord. They observed a reduction of specific neuropeptide receptors in adjuvant
these acute postural stresses.
Intervertebral joint receptors from the upper cervical spine also play an important role in providing balance information and possibly in control of eye movements .... Some patients with cervical arthritis, whiplash. or other neck injury comp lain of persistent symptoms of light-headedness or imbalance for months to years after their incident . . .. Treatment modalities include vestibular suppressants, deafferentation, neck manipulation, and visual correction.
Our understanding of the basic neural processes that underlie clinical observations such as those just related has evolved from a number of animal studies. Freeman and Wyke (24) demonstrated that low-threshold mechanorecep-
arthritic rats. These receptors respond to input
from primary afferent nociceprors. This study demonstrated an anatomic change within the central nervous system in response to chronic altered
sensory information from joints. Clinical chiropractic experience indicates that a simi lar effect
may be produced by joint subluxation. Patients frequently experience chronic pain and neuro-
logic dysfuncrion long after the site of peripheral injury achieves an apparent full recovery.
tors in the articular capsu le of the car's ankle joint
facilitate and reciprocally inhibit muscles that move the joint. In their experiments, stimulation of articular nociceptors simultaneous ly increased
the activiry of both flexor and extensor muscle groups in the ipsilateral limb as well as affecting motor activity in the contralateral limb. Joint lesions can, therefore, produce morbid changes in the tone of muscles that cross the joint or disrupt
Dentate Ugament, Cord Distortion Theory We now turn our attention to the rhird and final theory for our consideration. The "dentate ligament, cord distortion" theory is especially inter-
esting to those chiropractors who limit their
232 adjustments to the upper cervical region. With the publication of his book, The Subluxation Specific: The Ad!ilstmmt Specific, B. j. Palmer (1) firmly stated: No vertebral subluxation CAN exist below axis; therefore no adjustment with any DIRECT INTENTION OR DESIGN could be given below
an axis,
to
ge, sick people well. iemphasis by BJPI
B. J. Palmer ascribed the influence of subluxation to compression of the spinal cord. For approximately 20 years he adamantly denied the need to adjust below the axis. In later years he relented, admitting some value to adjustments below the axis, but asserting that these were "minor" sub-
luxations. He maintained that only occiput! atlas/axis subluxations constituted "major" subluxations.
Little has been published on the dentate ligament, cord distortion theory. A paper by Grostic (29) relates two mechanisms by which the dentate liga ments may adve rsely influence the 'conduction of neural impulses within the spinal cord: direct mechanical irriration through dentate ligament traction; and venous occlusion and
resultant local blood stasis and ischemia of the upper cervica l cord, also produced by dentate ligament traction. Grostic observes that the strength
of the dentate ligaments in the upper cervical region and the dynamics of cervical spine lengthening on flexion contribure ro rhe possibiliry of spinal co rd distress with upper cervica l misalignments. Referring to the work of Breig (30), he notes that there is an approximately 30-mm change in cervical spinal canal length from full extension to full flexion. Dural attachments to the foramen magnum a nd possibly to the axis and atlas are also noted. He estimates that an average
lateral misalignment between the skull and atlas of 3° produces an approximately 3 mm lateral displacement of the atlas. This 3-mm lateral displacement is approximately 23% of the total width of the spinal cord in the upper cervica l region (approximately 13 mm). A recent study corroborates the argument that cord distraction could produce a conduction block. Jarzem et al.
(3 1) reported decreased spinal cord blood flow and concurrent interruption of somatosensory
evoked potentials afrer experimental cord distraction. A srudy by Emery (32) underscores the mechanical strength and immobilizing character of the upper cervical dentate ligaments. Emery relates numerous cases of perinatal necropsy that
demonstrated fatal kinking of the medulla-spinal cord junction in hydrocephalic children because of the interaction of a freely movable brainstem and a fixed upper cervical cord (fixed through strong dentate ligament attachments). We have reviewed three theories that are incorporated into our current neurophysiologic
model of the chiropractic subluxation . It is probable that elements of a ll three theories are active during a subluxation, in addition to numerous other mechanisms nOt covered in this presenta-
tion. We trust that further scientific research, and development of our working models, will enable the training of more effective chiropractic researchers, educators, and clinical practitioners.
Relerences I. Palmer BJ. The subluxa tion specific: The adjustment specific. Davenport: Palmer School of Chiropractic, 1934. 2. American Chi ropractic Association. Indexed synopsis of ACA policies on public health and related maners. Arlington: American Chiropracric Association, 1992. 3. International Chiropractors Association. Policy handbook and code of eth ics. 2nd ed. Arlington: International Chiropractors Association, 1991. 4. Howe lF, Loeser 10, Calvin WH. Mechanosensitiviry of dorsal rOOt ganglia and chronically injured axons: A physiological basis for the radicular pain of nerve rOOf compression. Pain 1977; 3:25-4 t . 5. Wall PO, Devor M. Sensory afferent impulses originate from dorsal root ganglia as well as from the periphery in normal and nerve injured rats. Pain 1983; 17:321-39. 6. Macnab I. The mechanism of spondylogenic pain. In: Hirsch C, Zotlerman Y, cds. Cervical pain. New York: Pergamon Press, 1972:89-95. 7. Greenbarg PE. Brown MD. Pallares V5, Tompkins lS. Mann NH. Epidural anesthesia for lumbar spine surgery. Spinal Dis 1988; 1,139-43. 8. Levine JO, Clark R, Devor M. Helms C, Moskowitz MA, Sasbaum AI. Intraneurona l substance P conrributes to the severity of experimental arthritis. Science 1984; 226,547-9. 9. Kidd SL. Mapp PI, Gibson 5J. et al. A neurogenic mechanism for symmetrical arthritis. Lanc("[ 1989; 11 :11 28-30.
233 10. Edgar MA, Ghadially JA. Innerv,lUon of Ihe lumbar spine. Clin Orthop 1976; 115:35-41. II. Jinkins JR, Whittemore AR, Bradley We. The anatomic basis of vertebrogenic pain and Ihe autonomic syndrome associated with lumbar disc extrusion. AJR 1989; 152:1277-89. 12. Bogduk N. The innervation of the lumbar spine. Spine 1983; 8(3 ):286-93. 13. Lon M, Carson DA, Vaughan JH. Substance P activation of rheumatoid synoviocytes: Neural pathway in pathogenesis of arthritis. Science 1987; 235:893-5. 14. Pedrini-Mille A, Weinstein IN, Found EM, Chung CS, Coel VK, Srimularion of dorsal root ganglia and degradation of rabbit annulus fib rosus, Spine 1990; 15(12):1252-6. 15. Korr 1M, Wright HM, Chace JA. Cutaneous pan'erns of sympathetic activity in clinical abnormalities of the musculoskeletal system. J Neur Transm 1964; 25:589-606, 16, Korr 1M, Wright HM, Thomas PE. Effects of experimC'ntai myofascial insules on cutaneous patterns of sympathetic activity in man. J Neur Trans 1962; 23:330-55. 17. Mooney V, RobertSon J, The facet syndrome. Clin Orthop 1976; 115:149-56. 18, Thabe H. Electromyography as a [001 to document diagnostic findings and therapeutic resuhs associated with somatic dysfunctions in the upper cervical spinal joints and sacroiliac joines. Manual Med 1986; 2:53-8. 19, Bigucr B, Donaldson IML. Hein A,jeannerod M. Neck muscle vibration modifies the representation of visual morion and direction in man. Brain 1988; 111 :1405-24. 20. Brown Jj. A systematic approach to the dizzy patient, Di'gn Neurorology 1990; 8(2):209-24. 21. Cooper S, Daniel PM. Muscles spindles in man, their morphology in (he lumbricals and the deep muscles of the neck. Bra;n 1963; 86:563-94.
22. Abrahams Vc. The physiology of neck muscles: Their role in head movement and mainrenance of posrure. Can J Physiol Pharmacol 1977; 55:332-8. 23. Abrahams Vc. Sensory and motOr specia lization in some muscles of the neck, Trends Neu rosci 198 1; 4:24-7. 24. Freeman MAR, Wyke B. Articular reflexes al the ankle joint: an electromyographic study of normal and abnormal influences of ankle-joint mechanoreceptOrs upon reflex activity in the leg muscles. Sr J Surg 1967; 54:990-100l. 25. De CaStro Costa M, De Surter P, Cybels J, Van Hees J. Adjuvant-induced arthritis In rats: A possible animal model of chronic pain, Pain 1981; 10: 173-85. 26. Col paert FC. Evidence that adjuvant arthritis in the rat is associated with chronic pain. Pain 1987; 28:20 1-22. 27. Besson J-M, Gui lbaud G, cds. The arthritic rat as a model of clinical pain? New York: Elsevier Science Publishers (Biomedical Division), 1988. 28. Mantyh CR, Gates T, Zimmerman RP, et al. Alterations in the density of receptor binding sites for sensory neuropeptides in the spinal cord of anhritic rats. In: Besson J-M, Guilbaud G, eds. The arthritic rat as a model of clin· ical pain? New York: Elsevier Science Publ ishers (Biomedica l Division), 1988. 29. Grostic JO. Dentate ligament-cord distOrtion hypothesis. Chiro Res) 1988; 1:47-55. 30, Breig A. Adverse mechanical tension in the central ncr· vous system. Stockholm: Almqvist and Wiksell International, 1978. 31. Jarzem' PF, Quance DR, Doyle OJ, Begin LR, KostuikJP. Spina l cord tissue pressure during spina l cord distraction in dogs. Spine 1992; 17(85):5227-34. 32. Emery JL. Kinking of the medu lla in children with acure cerebral oedema and hydrocephalus and its relationship to the dentate ligaments. J Neurol Neurosurg Psychiatry 1967; 30:267-75.
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Vertebral Subluxation and the Anatomic Relationships of the Autonomic Nervous System Peter Cauwenbergs KeyWDrda
Autonomic, preganglionic, postganglionic, splanchnic, somatic, visceral efferent, visceral afferent, sympathetic, parasympathetic, enteric, somatovisceral reflex, viscerosomatic reflex.
After reading this chapter you should be able 10 answer the following questions:
QuestIon #1
How are the three components of the autonomic nervous system differentia ted?
Question #2
How does the location of preganglionic axons differ between the sympathetic and parasympathetic nervous systems?
Question #3
How do the functions of the sympathetic and parasympathetic nervous systems differ?
QUBSdon#4
On what basis can the treatment of visceral disorders be included in the scope of chiropractic practice?
13
V8I'tIIbrIl SUllluxIl1lon and IhII Anatomic Relallollallipa 0I1h11 AutoIIOIIIIc Nervoos System
T
235
tory, vascular, gastrointestinal, etc.), and glandu-
lar (exocrine and endocrine) tissues. The ANS
he structure of the nervous system is com-
functions to a large extent in response to environ-
monly divided into the central nervous system (eNS), which consists of the brain, brainstem, and spinal cord, and the peripheral nervous sysrem (PNS), which includes all neuronal processes outside of the eNS, such as cranial nerves and spinal nerves as well as ganglia associated with these nerves. Beyond pure anatomic
mental stimuli that may originate either outside the body or from within a specific organ or tissue. These sensory signals are carried to the eNS by afferent neuronal con nections, where they are
description, however, such subdivisions are incon-
sequential because functional components of the nervous system extend beyond these artificial structural limits. Numerous examples can be
identified in which single neurons extend axonal processes either centrally or peripherally into or out of the eNS, thus crossing the anatomic barrier between the eNS and PNS to form an integrated, functional system. The student of neuroanatomy shou ld strive to understand both structural and functional relationships within the nervous system because this integrated knowledge
integrated with other somatic or visceral sensa-
tions. An appropriate regulatory efferent response is then transmitted through the ANS to affect an alteration of viscera l function, if necessary. Therefore, external or internal sensations such as pain, temperature, proprioception, touch, pressure, vibration, and stretch may act reflexive to elicit an autonomic response that functions to achieve and maintain homeostasis. Num~rous examp les of the effects of somatic or visceral sensations on vis-
ceral functions mediated and regulated through the ANS can be cited and will become apparent in this chapter as the various functional systems are described. However, in many instances the neurophysiologic mechanisms involved remain
of neuroscience is not on ly much more interesting
poorly understOod, primarily because the inter-
and meaningful but also abundantly more useful in the clinical setting. At the same time, students shou ld realize that we are now only beginning to understand the mechanisms whereby the nervous
neuronal connections that constitute the rele-
system monitors and modulates functional activi-
ties throughout body systems and, conversely, how stimuli remote from the eNS may be integrated into neuronal functions within the brain and spinal cord. The autonomic nervous system (ANS), is defined traditionally as the self-regulating, visceral motor (efferent) portion of the nervous system, al though it is now recognized that the ANS has a major visceral afferent component. The ANS is a n excellent example of structural and functio nal integra tion, encompassing the eNS, PNS, and numerous other body systems. The term self-regulating refers to the fact that in many ways the ANS functions independently of conscious control. Visceral m otor (efferent) identifies the ANS as that part of the nervous system that functions largely to activate or regulate organ systems. includine the heart. smooth muscle (resoira-
vant neuronal pathways have not been described adequately. It now appears that a more comprehensive definition of the ANS shou ld include conscious conttol of external factors, such as somatic sensa-
tions, which influence the regulatOry activity of the ANS. The ANS, although predominantly selfregulatory, is not limited to self-regulation. This is of particu lar clinical significance because therapeutic intervention that alters somatic or viscera l
function may have effects in body systems apparently remote from the site of applied therapy. A growing body of evidence suggests that there exists a close correlation between somatic (sen-
sory and motOr) functions and visceral (sensory and motor) functions . It appears that somatic and visceral functions are coordinated closely through somatoviscera l and viscerosomatic reflex mecha-
nisms involving the ANS, PNS, and eNS. Therefore, therapeutic interventions such as vertebral manipulation, ingestion of analgesic or anti inflammatory agents, and even surgery, to name a
236
The SUbluXation CGmpIex
few, can alter somatic sensations (proprioception, for example) in such a way that viscera l functions may become altered. However, as srated previously, the underlying neuronal mechanisms require further elucidarion through scientific investigation ro understand the complexity of factors that interact to regulate organ function (1). T he purpose of this chaprer is ro provide a clear, up-to-date description of the structural and funct ional anatomy of the ANS. The relevant neuroanatomy is discussed in some detail, focusing on neu ronal centers involved with autonomic
function within the PNS and eNS as they are currently understood. Throughout this chapter an integrared functional approac h is employed in an effort to clarify the sometimes complex functiona l interactions that occur. Ir is hoped that a sound understanding of the ANS will stimulate students and field practitioners to pursue scientific research into this basic and as yet poorly understood area of neuroscience, and that this chapter will provide a firm foundation for furure research in chiropractic.
OVerview of the Autonomic Nervous System The autonomic nervous system (ANS) can be subdivided into three components: the sympathetic, parasympathetic, and enteric (intestinal) nervous systems. Each division of the ANS is composed of distinct neuronal populations, interconnected
by
axonal processes that form an integrated functional unit. Neuron pools that make up the sympathetic and parasympathetic divisions are localized either within well-defined nuclei of the brainstem and spina l cord or within ganglia located in the periphery, whereas neurons of the enteric division are isolared in rhe wall of the gasttointestina l tracr. Also, higher neuronal centers locared in the hypothalamus, thalamus, hippocampus, and other areas of the cerebrum funcrion to integrare ascendi ng afferent stimul i from all regions of the body and are the source of descending efferent impulses, which function to control and modulare
autonomic activIty. Like the nerve parhways of somatic portions of the nervous system, the ANS consists of visceral sensory axons that enter the eNS, ascending viscera l sensory tracts within the brainstem and spinal cord, visceral reflex arcs, and descending visceral motor tracts that influ-
ence neural activity of the sympathetic, parasympathetic, and enteric divisions of the ANS. The sympathetic and parasympathetic di visions are similar structurally, whereas the enteric
division, which is modulated by other autonomic centers, is distinct structurally and functionally from other components of the nervous system. Sympathetic and parasympathetic divisions both originate from
preganglionic neurons located
within the eNS, which extend thinly myelinated axonal processes that synapse with dendrites of postganglionic neurons located mostl y in peripheral gangl ia. All preganglionic neurons are similar functionally because, regardless of their locarion or which autonomic division they are part of, these neurons are cho linergic (Figure 13-1). In contrast, postganglionic neurons extend unmyelinated axonal processes that innervate specific viscera directly. In addition, unlike preganglionic neurons, which secrete the neurotransm itter acetylc holine, posrganglionit: neurons vary in the transmirrer rhey synthesize and secrete. Sympathetic postganglionic neurons are largely catecholaminergic (those rhar innervate swear glands are cholinergic), and parasympathetic postgangl ionic neurons are entirely cholinergic. Sympathetic postganglionic neurons are further subdivided funcriona ll y into et- and P- catecholaminergic neurons, which exert different influences on target tissues. Genera ll y et-catecholaminergic innervation is excitatory to smooth muscle, and p-carecholaminergic stimulation is inhibitory. The two-neuron chain (pre-postganglionic) pattern of innervation is unique to the ANS and is fundamentally different from the single-neuron innervation pattern characteristic of somatic neuronal systems. An anatomic feature that ma y assist in disringuishing conceptually between the sympathetic and parasympathetic divisions is the characteristic location of rhe ganglia, which con-
13
vertebral S8xatlon and IIIe AIIat8mIc Relallollshlps 0I1IIe Autonomic NllrVIIIII System
237
5
1. 2. 3. 4. 5. 6. 7.
Parasympathetic ganglion Parasympathetic pastganglionic neuron Parasympathetic preganglionic neuron Artery Sympathetic pastgongl ionic neuron Sympathetic trunk Sympathetic pregonglionic neuron
6
7 10
9
8 . Splonchntic nerve 9 . Sympathetic preverterbal ganglion 10. Viscus
A111'113-1 Schematic diagram illustrating the general structural pa ttern o f peripheral components of the autonomic nervous system. Note that th e sa mara of preganglionic neurons are loca ted within the eNS (brain a nd spinal cord). whereas postganglionic neuronal soma ta are in the peripheral ga nglia . Generall y, sympathetic postga ngli onic 3xons are long and course along arteries to reach ta rget viscera (e.g., the eye), and pa rasym pathetic postga ngli on ic axons are sho rr. Also note that a ll preganglionic neurons a re cholinergic (red ) as 3 f C parasy mpath etic postganglion ic neurons, whi le symparheric posrga nglionic neu ro ns a re ca rechola mineri gic (b lue).
238
The WIIuxlltlon Complex
tain postganglionic neurons. Sympathetic ganglia are localized near the eNS, indicating that sympathetic preganglionic axons are mostly short, and axons of parasympathetic preganglionic neurons are long, because parasympathetic ganglia are located some distance away from the eNS, near to the viscus they innervate (Figure 13-1). The sympa thetic and parasympathetic divisions of the ANS function to regu late and mainrain the internal body environment. At times of emergency, when there is a sudden change in external or internal body conditions, such as during an argument, an examination, an athletic competition, or a drastic temperature change, the sympathetic division allows the body to cope with these stresses. The sympathetic response to external or internal stress has been referred to as the fight or flight reactiol1. This reaction, which is initiated by autonomic neuronal centers in the hypothalamus, results in increased cardiac Output (rate and stroke volume), increased blood supply to appendicular muscles, increased blood· glucose levels and activation of sweat glands, erector pili muscles, and dilator pupillae. In this way, sympathetic activity is protective because it allows for a rapid response to potentially dangerous external factors.
In contrast, the parasympathetic division of the ANS serves a major role to store, conserve, and replenish body energy and can be said to be [he vegcmrive component of the nervous system, functioning primarily at times of rest and digestion. Activation of parasympathetic neuronal centers causes increased secretion of sa li va, mucus, and digestive enzymes into the gastrointestinal tract and functions to maintain basal cardiac, respiratOry, and metabolic rates. Gut motility is initiated primarily through mechanical reflex activation of the enteric division of the ANS and is modulated by parasympathetic and sympathetic neuronal influences. Although the functions of the ANS are extremely important for the maintenance of homeostasis and at times for the surviva l of the individual, hyperactive or hypoactive autOnomies
caused by pathology, trauma, aberrant physiology, or altered biomechanics can be detrimental and may give rise to characteristic symptomarology. To understand and to accurately diagnose clinical presentations of abnormal autOnomic function, a sound knowledge of the peripheral and central components of the ANS is necessary.
Peripheral Components of Ute Autonomic Nervous System Sympathetic DIvision The peripheral components of the sympathetic division, as described by Warwick and Williams (2), include gray and white communicating rami, two bilaterally symmetric and ganglionated sympathetic trunks that house postganglionic neurons; clusters of prevertebral ganglia, which also house postganglionic neurons; splanchnic nerves, which innervate prevertebral ganglia; and vascular nerve plexuses, which conduct postganglionic axons to target viscera . In fact, most sympathetic postganglionic axons course along arterial vessels to reach viscera that they innervate. Many sympathetic axons within these vascular nerve plexuses penetrate the arterial or arteriolar wall along which they pass to supply smooth muscle in that wall and serve to regulate blood flow and blood pressure. Also in these vascular nerve plexuses are large numbers of parasympathetic axons that innervate viscera and numerous visceral afferent nerve fibers, which are sensory to the viscera and pass back to the eNS by autonomic nerves. In addition, vast numbers of sympathetic postganglionic axons course together with somatic nerve fibers within spinal nerves and their branches to reach target structures in the body wall and limbs. Still other postganglionic axons innervate viscera such as the heart and lungs as direct branches from the sympathetic trunks. The sympathetic division, which is the largest division of the ANS, therefore innervates all regions of the body by three different routes:
13 vertebral SlMIxatlon and 1IIa AnatumIc RelallolishIps of 1IIa AUllllIOIIdc NarvtMIS System (1) bv arterial nerve plexuses; (2) as a component of somatic nerves; and (3) by direct nerve branches from the sympathetic trunks.
239
nic nerves that end in prevertebral ganglia, where
additional postganglionic neuronal cell bodies are located (Figure 13-1). In summary, preganglionic axons terminate
Spinal Origin and Peripheral Distribution of Sympathetic Preganglionic Axons The sympathetic division is commonly referred to as the thoracolumbar portion of the ANS because all sympathetic preganglionic neurons are localized in the thoracic and upper lumbar (TI-L3) spinal cord segments. Within these cord segments preganglionic neurons form a well-defined column of cells that is called the intermediolateral cell column because of its intermediate and lateral posirion between the posterior and anterior
horns of gray matter. Axons of sympathetic preganglionic neurons, which are thinly myelinated, exit the spinal cord along with axons of somatic moroneurons t.hrough anterior roots of spinal
by synapsing with dendrites of postganglionic neurons located in one of two ganglionated strucmres, either ganglia of the sympathetic trunk or prevertebral ganglia. (Note: One exception to this general scheme that is described later is the medulla of suprarenal glands.) It is also important to realize that each preganglionic neUfon
normally innervates up to 20 postganglionic cel ls either within a single ganglion or distributed among a number of paravertebral or prevertebral ganglia. In one early study it was found that the ratio of preganglionic to postganglionic neurons in the superi or cervica l ganglion (described further) may be as high as 1 to 196 (3) . Functionally this innervation pattern allows for divergence of
nerves at the same spinal level as their soma of
sympathetic activation and coordination of post-
origin. On exiting the intervertebral foramen,
ganglion ic response at several spi nal levels (4). For this and other reasons that will become
preganglionic axons branch from the spinal nerve as a white communicating ramus (whi te because
these axons are myelinated), which joins the paravertebral sympathetic trunk. Large numbers of preganglionic axons end by synapsing with dendritic branches of postganglionic neurons, the cell bodies of which are located in these ganglia . Many preganglionic axons innervate postgan-
glionic cells in trunk ganglia located at the same vertebral level as the intervertebral foramen through whic h they emerge. Alternatively, numerous preganglionic axons or their collateral branches course along the length of the sympathetic trunk to innervate postganglionic neurons
in trunk ganglia located more crania ll y or caudally than their spina l level of preganglionic origin (Figure 13-1). Although all sympathetic axons enter the sympathetic trunk through white communicating rami, indicating that white rami are evident only at spina l nerve levels Tl through L3, nOt all of these axons terminate in sympathetic trunk ganglia as juSt described. Many preganglionic axons branch from the sympathetic trunk without having synapsed and course as splanch-
apparent, sympathetic activation results in a mass response, such as generalized constriction of cutaneous arteries, as compared with the more local-
ized parasympathetic response. Peripberal Distribution of Sympathetic PostgangIjonic Axons The peripheral distribution of sympathetic postganglionic axons can be divided into two groups on the basis of the location of postganglionic somata. The first group consists of postganglionic neurons located in ganglia of the paravertebral sympathetic trunk. Postganglionic cells in these gangl ia are concerned generally with innervation of viscera in the head, neck, and thorax, includ-
ing lacrima l and salivary glands, pupillary dilatOr, heart, and lungs. These neurons also supply superficial structures in the head, neck, body wall, and limbs, including sweat glands, erector pili muscles, and smooth muscle in the walls of arte ries and arterioles. The second group consists
of postganglionic neurons located in abdominal and pelvic prevertebral ganglia . These postgan-
240
The Subluxation Complex
glionic cells innervate organs associa ted with the
gastrointestinal and urogenital systems, including the stomach, small an d large intestine, pancreas, liver, ga llbladde r, kidn eys, urina ry bladder, and external genitalia. The following is a detailed description of the origin, cou rse, and anatOmic
relationships of sympathetic postganglionic axons. The discussion focuses first on branches of the sympathetic trunk and subsequentl y on the distribution from prevertebral ga nglia. A sound knowledge of the postga ngli onic diStribution pattern is crucial to the understanding of autonomic functio n and clinical conditio ns that occu r w hen this function is disturbed.
Relationships of the Sympathetic Tnmk The paired sym pathetic trunks and their ga nglia extend the length of the ve rtebra l column (pa ravertebral) and are closely related to the a nterolatera l aspect of ve rtebral bodies and intervertebral discs throughout their cou rse . For this reason, conditio ns such as abno rmal biomechanics, subluxations, bony spurs, and other pat ho logies at intervertebral and costoverteb ral joints, wh ich 3 fC commonl y seen in chiropractic offices, as well as more severe conditions such as ank ylosing
spondyl itis and severe osteoporosis, may have a profo und influence on sympathetic functions (5). The trunk cou rses th rough the cervica l region posteri or to the ca rotid sheath, where it is related closely to prevertebral muscles and fascia (Fig ure 13-2). In the thoracic region the tru nk passes along the necks of upper ri bs and is related directly to the fibrous ca psu les of costovertebra l joints in the lower thoracic regio n (Figure 13-3). The sympathetic trunk continues into the abdo m-
inal cav ity by coursing between the medial arcuate ligament of the diaphragm (a nteriorly) and the psoas major muscle (poste ri o rl y). As the trunk descends through the abdomen, it lies adjacent to lumba r ve rtebral bodies and in tervertebra l discs anterio r to the psoas major muscle and posrerio r to the inferio r vena cava (on the ri ght) or postero la teral to the abdominal ao rta (on the left) (Figure 13-4). Near its ca udal termination the trunk courses posterior to the common iliac vein, descends anterio r to the .ala of the sacrum just
medial to [he anterior sacral foramena, where it lies related directly to the origin of piriformis and termi nates finally by joining the trunk of the opposite side anterior to the coccyx a nd coccygeus muscle as the single gangli on impa r (Figure 13-5).
The Cervical Sympathetic Tnmk atld Its Brallches In the neck extensive fusion of sympathetic trunk ga nglia ta kes place dur ing em bryon ic development (2), resu lting in three (superior, middle, and inferior) cervica l ga nglia that a re joined by the cervical continuation of the sympathetic trunk (Figu re 13-2). The largest is the superior cervical ga ngli on, which is believed to have developed from the coalescence of the up per four cervical ga nglia (2). This ganglion lies at the level of C I-C3 verteb rae interposed between the ca rotid sheath anterio rl y and the longus capitis posteriorly and, li ke the lower cervical sympathetic trunk, is enveloped by prevertebral fascia. Pregangl ionic innervation of the superior cervical ga nglion, as in the middle and inferior cervical ga ngl ia, is derived from neurons in the upper three thoracic spina l cord segments. Postganglionic axons of neurons in the superior cervical ganglion are distribured to target structures either a long bra nches of the internal carotid a rtery or through a number of direct nerve branches from the ganglion . In addition, the first four cervica l spina l ne rves, like a ll spinal nerves, receive gray com mun icating rami composed of unmyelinated axons of postganglionic neurons from the superior ganglion and its caudal connection with the middle ganglion. These POStganglionic axons are distributed to blood vessels, erector pili muscles, and sweat glands in rhe territory of each of these spina l nerves. Extending from the superio r limit of the superior cervica l ganglion, the internal ca rotid nerve conducts postganglionic axons to the internal carotid artery, which lies immediately anterior to the ganglion with in the catOtid sheath. The internal ca rotid nerve in this way forms the internal carotid plexus, which supplies the artery and its branches to regu late cerebral blood flow,
13
Vertebral Subluxation and 1IIe AnatoDie Relationships 011lle Autonomic Nervous System 8
3
241
2
I. Superior cervical
ganglion 2. Right vagus nerve 3. Cervical sympathetic trunk
7 6
4. Scalenus anterior
5
5. Middle cervical ganglion 6. Inferior thyroid artery 7. Phrenic nerve 8. Longus capitis
9.
Longus cervicis
10. Subdovian artery Inote abnormal pasition) II. Trachea 12. Esophagus 13. Recurrent laryngeal
4
10
nerve 14. Common carotid artery Agll'lla~2
Cervica l sympathetic trunk within the rcrropharyngcal space. The preverrebral fascia has been removed and rhe COlllmon carotid artery and vagus nerve are shown reflected to the left with the trachea and pharynx.
although this is now thought to be onl y a minor role of the sympathetic division. The internal carotid plexus enrers the cranial cavity along [he surface of the internal carotid artery as it passes through the carotid cana l and provides the clinically importanr sympathetic innervation ro arteries that supply the cerebrum, meninges of the anterior and middle cranial fossae, hypophysis, orbita l contents, and the upper parts of the face and sca lp. It is this portion of the sympathetic division that ma y be involved in the cause of migraine headache. As the internal carotid artery passes through the cavernous sinus, the nerve plexus on its surface extends branches that join the oculomotor, trochlear, abducens, and ophthalmic nerves through which sympathetic postganglionic axons are di tribured. Thrombosis of the cavernous sinus, as may occur with infections of the orbit, nasal cavity, paranasal sin uses, and tympanic cavity, may therefore impinge on these cranial nerves, leadi ng to characteristic crania l nerve signs and symptoms, including those associated with sympathetic blockage, as observed in a classic Horner's syndrome. The signs associated
with sympathetic nerve blockage at this ite include ptosis caused by the loss of sympathetic innervation to the levator palpebrae superious through the ocu lomotor nerve and miosis caused by unopposed parasympathetic activatio n of the sphincter pupillae. Sympathetic postganglionic axons reach the eye to supply the dilator pupillae and arteria l vessels of the eyeball a long two routes. Some axons branch from the oculomotor nerve, pass through the ciliary ganglion without synapsing, and enter the eye with parasympathetic fibers in short ci liary nerves . Other POStganglionic fibers continue a long the nasociliary branch of the ophtha lmic nerve ICNVI ) to enter the eyeball as long cilia ry branches. The internal ca rotid plexus also supplies sympathetic innervation to arteries and mucous glands in the tympanic cavity through the caroticotympanic nerve, which joins the tympanic branch of the glossopharyngeal nerve (CN IX ) to enter the tympanic plexus. In addition, arteries and mucous glands in the nasal cavity, and nasopharynx, hard palate, and soft palate receive sympathetic innervation by way of the deep pe-
242
The Slauxatlon Complex
trosal branch of the internal carotid plexus, which jo ins the greater petrosal nerve in the foramen lace rum.
The greater petrosal nerve traverses the pterygoid cana l to reach the pterygopalatine ganglion through which sympathetic axons pass without synapsing a nd enter the infraorbital and nasopa latine branches of the maxillary nerve (CNV,). These sympathetic postganglionic axons supply the lacrimal gland and mucosa of the nasal cavity, paranasa l sinuses, nasopharynx,
hard palate, and soft pa late. In addition to the interna l carotid plexus, other nerve branches of the superior cervical ganglion innervate structures within the posterior
cranial fossa, oral cavity, neck, and thorax. Small branches from the lateral aspect of the ganglion join the vagus (CNX) and hypoglossal (CNXII) nerves in the carotid sheath and are distributed with these rwo cranial nerves to blood vessels and mucus glands in the mucosa of the oral cavity, o ropharynx, pharynx, larynx, trachea, and esophagus, as well as the submandibu lar, sublingual, and intralingular salivary glands. The jugular nerve branches from the superior cervica l ganglion to connect with the glossopharyngeal (CNIX ) and vagus (CNX) nerves ro a lso innervate the oral cavity and orophatynx. In addition, the meninges in the posterio r cranial
fossa receive sympathetic innervation through a plexus of postganglio nic axons that originate in the superior cervical ganglion and join the internal jugular vein to enter the cranial cavity by way of the jugular foramen. The cervica l sympathetic trunk also contributes to the cardiac plexus through ca rdiac branches that arise bilaterally from a ll three cervica l ga nglia. The cardiac branch of the superior cervical ganglion courses inferiorly along the anterior aspect of the longus cervicis muscle (Figure 13-2) partly enveloped by preverrebral fa scia, where it ma y be influenced by da mage or increased tonicity of this muscle. On the right the cardiac branch passes most commonly posterior to the subclavian arrery, where it is related directly to the cupula of parietal pleura and ma y
be affected by pathology in the apical region of the lung. The nerve continues into the thorax on the posterolateral aspect of the brachiocephalic trunk to enter the cardiac plexus posrerior to rhe arch of the ao rra, alr hough some axons may contribute to the anterior ca rdiac plexus. In contrast,
the left cardiac branch of the superior cervica l ganglion enters the thorax most commonly along the anterior aspect of the common ca rotid artery
to reach the ante rior portion of the cardiac plexus anterolatera l to the a rch of the ao rta. Like the right ca rdiac branch, the left nerve may contribute to the posterio r ca rdiac plexus as well. En route, both the right a nd left cardiac branches of the superior cervica l ganglia commonly receive communications from
the extern al laryngeal,
recurrent laryngeal, and cardiac branches of the vagus (CNX) nerve, indicating that, on reaching the ca rdiac plexus, the ca rdiac nerves are mixed,
ha ving both sympathetic and parasympathetic compo nents . In addition, cardiac nerve branches
of the middle a nd inferior cervica l ganglia commonly have communicating branches with that of th e superior ce rvical ganglion.
The cardiac plexus, which also receives direct cardiac branches from the upper four or five rhoracic symparhetic trunk ganglia (described further), is divided into anterior (supe rficial) and posterior (deep) plexuses. The anterio r ca rdiac plexus is dispersed alo ng the a nterior aspect of the right pulmonary artery inferior to the arch of the ao rta. The posterior cardiac plexus, which receives input from the ante rior plexus, is located
near the bifurcation of the pulmonary trunk posterior to the arch of the aorta. Also, scattered
amongst the nerve fibers of the card iac plexus a re small ganglia that comain para ympatheric postganglionic neurons thar innervate the heart (see following discussion). Sympathetic posrganglionic axons course through the cardiac plexus along the right and left corona ry a rteries and thei r branches, which they innervate, a nd then penetrare the atrial and venrricular walls to supply cardiac muscle directl y. Whereas the ante rior ca rdiac plexus suppl ies some input to the right coronary and left pulmona ry plexuses, most ca rdiac
13 Vertebral Subluxation and IIIe AnatomIc IIeIatIoIlllipI 0I1IIe AutIJnonjc NervOUl Syltem innervarion reaches the heart by way of the posterior (deep) cardiac plexus, which can be divided into right and left halves. The right half of the posterior cardiac plexus supplies the right coronary plexus, right atrium and venrricle, and right pulmonary plexus and helps to form the left coronary plexus. The left half of the posterior cardiac plexus receives some input from the anterior
(s uperficial) cardiac plexus and innervates the left atrium and ventricle, the left coronary plexus, and the left pulmonary plexus. Most sympathetic postganglionic neurons are
catecholaminergic, and their activation, including those that innervate the heart and coronary ves-
sels, causes the release of norepinephrine (p-catecholaminergic). Interestingly, this neurotransmitter performs a dual role to control and regulate cardiac function. Cardiac myofibers are stimulated by norepinephrine to COntract mote forcefully and more rapidly. Concomitantly, smooth muscle in the walls of coronary arteries is inhibited, causing dilation of these vessels and increased blood flow to the heart, although Berne and Levy (6) suggest that the coronary circulation responds primarily to the metabolic needs of the myocardium and is predominantly under nonneuronal control. In fact, the sympathetic division may serve its greatest regulatory role of cardiac function indirectly by affecting the release of norepinephrine and epinephrine into the bloodstteam from medullary cells of the supratenal glands. In addition to sympathetic postganglionic axons, visceral sensory (afferent) axons are also
present in all cardiac branches of the sympathetic trunk, except those arising from the superior
cervical ganglia. Cardiac pain is transmitted through these sympathetic cardiac nerves to upper thoracic spinal cord segments and for this reason may be referred to the medial aspect of the arm and adjacent thoracic wal l. These neuronal pathways also may provide a viscerosomatic reflex mechanism whereby cardiac pain
243
From the superior cervical ganglion the sympathetic trunk courses inferiorly along the anterior aspect of the longus capitis and longus cervicis muscles to connect with the middle cervical ganglion at the level of the sixth cervical vertebra (Figure 13-2). Occasionally this ganglion is poorly defined or absent, in which case the postganglionic neurons normally present in the middle ga nglion are dispersed along the length of the cervical sympathetic trunk. The middle cervical ganglion is formed most common ly by the coalescence of the fifth and sixth cetvical ganglia and is related to the inferior thyroid artery, which is innervated by a sympathetic plexus derived from this ganglion. Sympathetic postganglionic axons are distributed to branches of this artery that supply deep posterior neck muscles, prevertebral muscles, and the external venebral arterial plexus
as well as the thyroid and parathyroid glands. Also, postganglionic axons derived from neurons
predominantly in the middle a nd inferior cervica l ganglia form a nerve plexus on the externa l carotid artery. This external carotid nerve plexus
supplies the artery and follows its branches to innervate Structures supplied by the artery in the neck and face. Postganglionic axons from the middle ganglion commonly enter the fifth and sixth (occasiona ll y the fourth and seventh as well) cervical spina l nerves by gray communicating rami to be
distributed to the periphery through these nerves and their branches to innervate sweat glands, and erector pili muscles as well as cutaneous and mus-
cular arteries in the shoulder and upper limb regions. Because of the cervical origin of postganglionic axons that control and regulate blood flow to the upper limb, any condition that interferes with this autonomic function, including trauma, pathology, spastic neck musculature, and abnormal somatoviscera l reflexes, may compro-
mise this blood supply and may lead to numbness, tingling, and pain the upper limb, a condi-
provokes increased tonus and even spasm of mus-
tion common ly associated with thoracic outlet
cles innervated by upper thoracic spinal cord seg-
syndrome. The cardiac plexus also receives a large cardiac branch from the middle cervical ganglion,
ments, as is observed in angina pectoris and cardiac arrest.
244
The Subluxation Complex
which courses along the lateral border of the longus cetvicis muscle. On the right this cardiac nerve passes posterior to the common carotid
artery and is related directly to the trachea and enters the right half of the posterior cardiac plexus. The catdiac branch of the left middle cervica l ganglion follows a similar course into rhe
thorax but passes between the left common cararid and subclavian arteries to enter the left half of the posterior ca rdiac plexus. A number of nerve cords that form the inferior continuation of the sympathetic trunk join
the middle cervical ganglion to the infetior cervical (cervicothoracic) ganglion . Some nerve fibers of the cervica l sympathetic trunk pass posterior and anterior to the vertebral artery to reach the inferior ganglion and may contribute to rhe nerve
plexus around rhis vessel. A large nerve cord, called the ansa subclavia, passes inferiorly and anteriorly to the origin of the subclavian artery, loops arou nd this vessel just medial to the internal thoracic artery and joins the inferior cervica l ganglion posterior to the subclavian artery. The ansa subclavia common ly contributes to the nerve plexuses surround ing both the subclavian and internal thoracic arteries (Figure 13-2). The inferior cervical ganglion is considerably larger than the middle ganglion and is formed by the coa lescence of the C7,C8 and Tl ganglia. Other names given to the inferior ganglion are the cervicothoracie ganglion, because of its embryonic origin, and the stellate gangl ion, because of its shape. The inferior cervica l ganglion is positioned anterior to the C7 transverse process and extends inferiorly to the neck of the first rib just posterolateral [0 the origin of the vertebra l artery (Figure 13-2). The ganglion is also reiated directly to the cupula of parietal pleura and the lower vertebral attachment of the scalenus medius muscle. In some individuals the latera l border of the longus cervicis muscle is also related to the medial aspect of the inferior ganglion. Postganglionic axons from neurons in the
inferior cervica l ganglion join the C7,C8 and Tl spinal nerves through gray communicating rami
and are distributed by these nerves
[0
the peri ph-
ery, including cucaneous and muscular arteries of the forearm and hand. Other nerve branches of the inferior cervica l ganglion are a cardiac branch, which joins the posterior cardiac plexus along with the cardiac branch from the middle cervical ganglion, and vascular branches, which form plexuses on the subclavian and vertebral arteries as well as on the thyrocervical and cos tocervical trunks. The subclavian plexus extends into the axilla along the first parr of the axillary artery and its superior thoracic branch, but rarely reaches arteries in the upper limb because these appendicular vessels receive direct sympathetic innervation from nerves of the brachial plexus. The large vertebral branch of the inferior cervical ganglion courses along the vertebral artery through foramina rransversarii to form a verrebral ne rve plexus, which supplies arteries to the cervical spina l cord, externa l and internal vertebral arterial plexuses, and deep muscles of the neck. The vertebra l nerve plexus enters the crania l cavity with the vertebral arteries through the foramen magnum and courses along the length of the basilar artery and its branches, as far as the posterior cerebral arteries . In this way postganglion ic axons derived from the inferior cervical ganglion primarily supply sympathetic innervation that functions to regulate blood Aow to occipital and temporal lobes of the cerebrum and cerebellum as well as vital neuronal centers in the brainstem and cervical spina l cord. It has been suggested recently, however, that neural control of cerebral blood Aow may not be as important as once thought. Rather, it may be that the Aow rate of blood in cerebra l arterioles is regulated primarily by regional metabolic needs (6). Near the posterior portion of the circulus arteriosus, the vertebral sympathetic plexus meets that of the internal carotid plexus. If sympathetic function in the inferior cervical ganglion is compromised, as may happen in a variety of clinical conditions (for example, cervical rib; abnorma l biomechanics of the lower cervical and upper thoracic spine), a number of signs a nd symptoms associated with the syndrome referred to as vertebrobasilar insufficiency are observed . Also, upper limb symptoms
13 Vllrtellral SlMlxI1lon and 1118 AnatIImIc 1111111IoI1II11pa of 1118 AutonomIc Nervoua Syltllm may be present, resulting in a classic thoracic outlet syndrome. Hyperactive sympathetics may give rise to tinnitus, hearing loss, dizziness, facial nerve (CNVII) palsy, blurred vision, nausea, and vomiting, as well as cardiac and respiratory arrhythmia (7), which result from insufficient blood now to the brainstem and cerebellum. Migraine-type headache a lso has been reported ro occur after whiplash injury to the cervica l spine (8) a nd may be the result of trauma or pressure on the cervical sympathetic trunks.
The Thoracic Sympathetic Tnmk alld Its Brallches The thoracic sympathetic trunk consists of a series of small ganglia that vary somewhat in number. Generally there is one ganglion for each thoracic spinal nerve, a lthough the first thoracic ga nglion is most commonly fu sed with the inferior cervical gangl ion. As the sympathetic trunk descends through the thorax, the ganglia come to lie in direct COntact with the fibrous capsules of costovertebra l joi nts, except in the lower thorax, where they lie more medially adjacent to TIO-ll and Tl'-12 intervertebral discs (Figure 13-3 ). Numerous nerve branches ar ise from the tho-
racic sympathetic trunk, some of which are composed o f postganglionic axons of neurons in thoracic trunk ganglia, and other branches that consist of preganglionic axons of neurons located in the thoracic spinal cord. The nerves composed of preganglionic axons that innervate postganglionic cells in prevertebral ganglia are referred to as splanchnic (visceral) nerves and are described after the following description of the distribution of postganglionic nerve branches of the thoracic trunk. Each thoracic spinal nerve receives both white and gray communicating rami from the sympathetic trunk and its ganglia, with the white ramus joining the spina l nerve slightly more distal than the gray ramus (Figure 13-3 ). Occasionally, the white communicating rami are fu sed and only one mixed white and gray ramus is present. Each spinal nerve conducts these postganglionic axons to sweat glands and erector pili muscles, as well
245
as cutaneous and muscular arteries within the
thoracic and abdominal wall . Of particular clinical importance is the sympathetic nerve plexus formed by postganglionic branches of the thoracic sympathetic trunk on the aorta and its intercostal, esophageal, and bronchial branches. Segmental arteries that originate from intercostal arteries carry sympathetic innervation ro the external a nd internal vertebra l arterial plexuses and its radicular branches. By this rOute the autonomic nervous system can function to regu late blood flow to bones, joints, and ligaments of the thoracic vertebral column and structures within the spina l canal, including the spina l cord, spinal nerve roots, and meninges. The pulmonary plexus receives direct input of sympathetic postganglionic axons from branches of upper thoracic (T2-TS) sympathetic trunk ganglia as well as indirect input from the anterior and posterior cardiac plexuses. Also, as mentioned previously, the posterior cardiac plexus i formed in part by sympathetic postganglionic axons that enter the plexus directly from upper thoracic (T2-TS) trunk ganglia . From the pulmonary and cardiac plexuses, a sma ll network of sympathetic postganglionic axons branch away to supply the mucosa of the trachea and esophagus. Within the root of the lung bilaterally, sympathetic axons from the pulmonary plexus form a delicate nerve plexus along the surfaces of pulmonary and bronchial arteries as well as on the bronchial tree to supply smooth muscle in the walls of these Structures. Activation of the sympathetic division causes release of norepinephrine, which is inhibitory to bronchial smooth muscle, resulting in bronchodilation, and excitatory to arteria l smooth muscle, ca using constriction of pulmonary and bronchial arteries. However, neuronal control of bronchial smooth muscle has been shown to be relatively insignificant when compared with the bronchiolar response to loca l tissue factors (8) . For example, circulating levels of norepinephrine and epineph rine secreted into the bloodstream by supra renal glands during sympathetic acti vitation act as potent ~-ca te cholamillergic recepror stimulants that elicit rapid
246
I . Inferior cervicol gonglion 2. Thoracic sympathetic trunk 3. Trocheo
4. Right vagus nerve 5. Esophagus 6. Azygos vein 7. Intercostal vein
8. Intercostol ortery 9. Intercostal nerve
10. Communicating ramus II. Greoter splonchnic nerve
12. lesser splonchnic nerve
13. Costovertebrol joint 14. Diaphrogm
~ 18--3 Thoracic sympathetic trunk related to thoracic vertebral bodies, inrervertebral discs, and costovertebra l joints.
dilatation of the bronchial tree (9, 10). In contrast, other local factors sllch as histamine and the slow reactive substance of anaphylaxis that are released from mast cells into lung tissues after exposure to a llergens act as bronchoconstrictors ('11 ). It appears that local physiologic needs of the tissues serve as the primary regulatory control of pulmonary function, whereas direct ANS influences are limited.
Similarly, the ANS is believed to have little control over the pulmonary circulation during normal daily activity. Pulmonary vascular resis-
tance, which is a measure of the freedom with which arterial blood flows through the pulmonary circulation, is known to be inversely pro-
portional to cardiac output ( 12,13). That is, pulmonary and bronchiolar arteries expand or col-
lap e passively in response to an increase or
13 vertebral SubluXation and the Anatomic llelallollllllp. 01 the Autonomic NerVOUl SYI1em decrease, respectively, in blood pressure. However, a clinically significant role of the sympathetic division in the regularion of pulmonary circulation has been suggested by Fishman (15), who indicated that pulmonary obstruction ma y reflexly stimulate sympathetic vasomotor activiry to cause generalized constriction of pulmonary vessels and increased arterial pressure in the lung. It is also thought that constriction of larger pulmonary veins in response to sympathetic stimula-
tion may be the primary mechanism whereby blood is shunted from the pulmonary to the systemic circulation when needed . Lo summary, the principal mechanism whereby the sympathetic division regulates pulmonary function is humeral because, as in the contro l of cardiac function, it has its greatest influence through activation of the suprarenal glands. As mentioned previously, there are three pai rs
of bilaterally symmetric splanchnic (visceral) nerves that arise from the thoracic sympathetic trunks, ca lled the greater, lesser, and least (lowest) splanchnic nerves. The splanchnic nerves are
composed of preganglionic axons of neurons located in the intermediolateral cell column of the thoracolumbar spina l cord and do not synapse within sympathetic trunk ga ngl ia. Instead, these axons pass through the sympathetic trunk, bra nch medially away as splanc hnic nerves, and terminate finally by synapsing with dendrites of postganglion ic neurons in preverrebral sympa-
thetic ganglia (Figures 13-1 and 13-3). The prevertebral ga nglia are located anterior [Q the lumba r spine and sacrum in association with major bra nches of the abdom inal aorta. The largest splanchnic nerve branch of the thoracic sympathetic trunk is the greater splanchnic nerve, which is formed by five roots arisi ng from the fifth through ninth (sometimes 10th) thoracic trunk ganglia (Figure 13-3). Most preganglionic axons within the roots of the grea ter splanchnic nerve origina te in [he thoracic spinal cord segments
adj ace nt to these ga nglia. However, a small proportion of preganglionic neurons in upper thoracic spinal segments also may contribute to this
247
nerve. The lesser splanchnic nerve is somewhat
smallet, ha ving only twO rootS of origin, normally from the ninth and 10th (sometimes 10th and 11 th ) thoracic trunk ganglia, and the least (lowest ) splanchnic nerve is the smallest, a rising singly from the last thoracic trunk ganglion. All three splanchnic nerves course anteromediall y and inferiorl y along vertebral bodies and intervertebral discs to reach the diaphragm . The greater and lesser splanchnic nerves normally ga in access to the abdominal cavity by piercing the crus of the diaphragm, and the least splanchnic nerve enters the a bdo men with the sympathetic trunk by passing between the medial arcuate liga ment o f the diaphragm and the psoas major muscle. Often an enlargement of the greater splanchnic nerve, called the splanchnic ganglion, is ptesent just before the nerve pierces the diaphragm. Although the innervation of prevertebral ga nglia by splanchnic nerves is somewhat variable, a general pattern can be described. The greater splanchnic nerve terminates primarily by innervating postganglionic neurons in the celiac gan-
glion . This large prevertebral ganglion is located anterio~ to the crus of the diaphragm just lateral to the origin of the celiac trunk , a large branc h of the abdominal aorta at the level of the 12th thoracic vertebra l body. To a lesser degree the greater splanchnic nerve also innervates the aorricorenal
ganglion, a relativel y la rge cluster of postga nglion ic neurons that is dispersed along the abdominal aorta near the origins of [he superior mesenteric and renal arteries. The greater splanchnic nerve also innervates the suprarenal
gland (described later). The lesser splanchnic nerve, which courses with the greater splanchnic
nerve, supplies the celiac ganglion minimally and sends most of its axons to innerva te the aorticore-
nol and renal ganglia. The innerva tion pattern of the least (lowest ) spla nchnic nerve is to sma ll clusters of postganglionic neurons scattered along the renal artery and in the hilum of the kidney. For this reason the least (lowest) splanchnic nerve is often referred to as the renal nerve. The distribution of postganglionic axons of neurons in the
248 prevertebral ga nglia is described after consideration of the suprarena l glands. The suprarena l glands are discussed in some detai l because of the important functional role these glands play in the sympathetic division of the ANS. These glands are supplied by the greater splanchn ic nerve, an innervation pattern that may appear unusual in that preganglionic axons innervate med ullary cells of the gla nd directly. However, when one considers the embryonic origin of the gland, this innervation pattern can be better understood. H istologically the gla nd is composed of a layered cortex, which develops from mesodermal cells near the developing dorsa l mesentery of the embryo, and a central medulla, which is derived from neuroepithelial cells of the neural crest (17). The medulla ry cells of the gla nd in this way develop from the same primordium as all sympathetic postganglionic neurons and may be considered to be homologous to postganglionic neurons. Also, li ke most sympathetic postganglionic neurons, medulla ry cells syllthesize and secrete the hormones (neurotransmitters) epinephri ne and norepinephrine, wh ich whe n released into the bloodstream evoke a genera lized sympathetic (fight or flight) response. The suprarena l nerve plexus is composed of axons of the greater splanch nic nerve, wh ich reach the plexus on the anterior aspect of the crus of the diaphragm by passi ng through the celiac ga nglion and plexus without synapsing. The suprarena l glands, which are located just lateral to the crus of the diap hragm adjacent to the superomedia l pole of each kidney, a re said to have the largest sympathetic innervation relative to their size when compared with other organs. This is understandable, consider ing the important role this gland serves during sym pathetic activation. Preganglionic axons enter the gland and terminate on two types of medullary cells, called chromaf{ill and gallgliol1 cells. (Note: Cortica l laye rs of the gland that function to synthes ize a nd secrete glucocorticoid, mineralocorticoid, and corticosteroid hormones afC not innervated.) The chromaffin cells, whic h are innervated by synapselike junctions, syn thesize the catecholami nes
epinephrine a nd no repinephrine. These prod ucts then are stored in separate cytoplasmic granules recognized at the electron microscopic level to be distinct for one specific hormone. On stimulation of chromaffin cells by preganglionic axons, the granules bind with the plasmalemma and release their contents into adjacent blood vessels. The second medu llary cell type innervated by pregan glionic axons are multipolar neuron like cells, referred to as gal1glioll cells. However, the axons of ganglion cells and their terminations have not been studied definitively. It is possible that ganglion cells may serve to magnify incoming excitatory sympathetic stimuli and disseminate the signals to chromaffin cells. After release of these hormones into the bloodstream, they are circulated throughour the body and act to elicit the characteristic sympathetic response to stressful cond itions that the individual may be facing. The distribution of postganglionic axons frol11 ne urons in prevertehral ganglia follows a characteristic pattern in that they course through delicate nerve plexuses formed on the external surfaces of large branches of the abdominal aorta near the ganglion in which the axons originate. Each arterial nerve plexus supplies smoorh muscle in the wa ll of the vessels a long which it pa ses and terminates by innervating viscera supplied by the vessel. Axons of neurons in the celiac ganglion are distributed along branches of the celiac trunk, which come off the aOrta at the level of the '12th thoracic vertebra near the aortic hiatus of the diaphragm. The righr and left celiac ganglia are interconnected by a massive nerve plexus ca lled the celiac plexus, extending inferiorly to the level of the fi rst lumbar vertebra and surro unding the celiac trunk and origin of the superior mesenteric artery (Figure ) 3-4 ). Entering the plexus from each side are the greater and lesser splanchnic nerves and parasympathetic axons from the vagus (CNX) nerve (discussed further ). Exiting the celiac plexus are sympathetic preganglionic axons, which supply the suprarenal glands, parasympathetic (vagal ) axons, and sympathetic postganglionic axons, which enter subsidiary plexuses to be distributed to abdominal
13 Vertebral SUbluxation Md the Anatomic Reladonshlps of the Autonomic Nervous System
1. 2. 3. 4. 5.
249
Diaphragm Hepatic artery Splenic artery Celiac trunk Celiac ganglion plexus
6. Superior mesenteric artery
7. Superior mesenteric
ganglion and plexus Vagal trunk Esophagus Renal artery Aorticorenal ganglion and plexus 12. Abdomi na l aorta
B. 9. 10. 11 .
13. Inferior mesenteric
artery 14. Inferior mesenteric ganglion
15. Lumbar splanchnic nerves
16. Common iliac arteries
17. Superior hypogastric plexus a nd ganglion lB . Psoas major muscle 19. Lumbar sympathetic trunk
FigIre 13-4
Lumbar sympathetic trunk related to psoas major muscle and lu mbar ve rtebra l co lumn . Also shown are sympathe tic preverrebral ganglia dispersed along majo r branches of the abdo mina l ao rta.
viscera. These secondary nerve plexuses include the phrenic plexus, the left gas tric, splenic, and heparic plexuses, which cOllrse along branches of the celiac trunk, and the renal, gonadal, superio r mesenteric, and inferior mesenteric plexuses, whic h follow lower branches of the abdominal aorta. T he phrenic plexus is small and sends nerve axons alo ng the inferior phrenic arteries to the diaphragm a nd suprare na l gla nds. This sparse plexus contain s some preganglionic axons that have traversed the celiac plexus without synaps-
ing to aid in the innervation of the suprarena l glands. Also contained in the phrenic plexus are some postganglionic axons, which innervate smoo th muscle in the infer ior vena cava and then join the much larger hepatic nerve plexus. Axons that are sensory to the gallbladder also enter the heparic plexus as branches from the phrenic nerve (a mi xed somatic and viscera l nerve). Sympathetic postganglion ic axons in the heparic plexus reach the liver along branches of the hepatic artery and portal vein. The innervation that reaches the liver by this ro ute is believed
250 to function only to regulate blood flow to that organ, because the characteristic glycogenolytic response of the liver to sympathetic activation is a result of increased circulating levels of epinephrine and norepinephrine derived from suprarenal glands. A sma ll cystic plexus originating from the hepatic plexus contains sympathetic postganglionic axons that are inhibitory to smooth muscle in the wall of the gallbladder but excitatory ro the sphincter of the common bile duct. The hepatic plexus also contributes to the nerve plexus surrounding the gastroduodenal branch of the hepatic artery to innervare the right side of the stomach, duodenum, head of the pancreas, and the most distal ponion of the common bile duct. (Note: Sympathetic innervation of the gastrointestinal tract functions to inhibit neuronal
activiry in the enteric division of the ANS, as is described subsequently.) Also extending from the celiac plexus are the left gastric and splenic plexuses, which follow the arteries of the same name and terminate
by inner-
vating the left side of the sromach, tail of the pancreas, and the spleen. The sympathetic innervation of the spleen is excitatory to smooth muscle in the capsule of this organ and causes expulsion of the relatively large reservoir of blood into the genera l circu lation at times of need, such as dur-
ing exercise or serious blood loss caused by injury. More importantly, sympathetic influences on the spleen and other lymphoid organs function to regulate the immune system (50) . The immunoregulatory role of the sympathetic nervous system is elaborated in the final section of this cha pter. The renal plexus is derived from the more inferior portion of the celiac plexus as well as the aorticorenal and rena l ganglia, thus receiving input from the lesser and least (lowest) splanchnic nerves. Ganglia within the renal plexus give rise to posrganglionic axons, which follow (and supply) branches of the renal artery and innervare glomeruli and convolured tubules in the renal cortex. Both afferent and efferent arterioles of the
[ration rate is on ly minor because neuronal con-
trol is superseded by renal auroregulatory mechanisms (16,18). From the renal plexus the upper part of the ureter and gonadal (testicular/ovarian ) arteries also receive sympathetic innervation, which is excitatory to smooth muscle in their
walls. Finally, the superior and inferior mesenteric plexuses are located on the anterior aspect of the abdomjnal aorta surrounding the origin of the corresponding artery. The two plexuses contain postganglionic neurons in small ganglia dispersed along the first part of each vessel. Although some postganglionic axons from the celiac and aorticorena l ganglia enter the superior mesenteric
plexus, its principle input is from the lesser splanc hnic nerve, which terminates in ganglia within the plexus. Postganglionic axons from superior mesenteric ganglia follow all the branches of the superior mesenteric artery to supply inhibitory input to the enteric division of the ANS within the jejunum, ileum, vermiform appendix, cecum, ascending colon, and most of the transverse colon. However, sympathetic inner-
vation of the ileocecal sphincter, which reaches this site by the same route, is excitatory. The inferior mesenteric ganglia, which receives only a minor innervation from the celiac plexus, as well
as lesser and least splanchnic nerves are supplied primarily by lumbar splanchnic nerves and are described with these nerves in the next section of this chapter.
The Lumbosacral Sympathetic Trunk and Its Branches The lumbar portion of the sympathetic trunk, a continuation of the thoracic trunk, courses along
the anterolateral aspect of the lumbar vertebral co lumn
within the connecti ve tissue of the
glomeruli 3re innervated; however, the influence
extra peritoneal space (Figures 13-4 and 13-5). The lumbar trunk and its four ganglia lie in contact with medial fibers of the psoas major muscle and pass posterior to the common iliac vessels to gain access to the pelvis. Throughout their course in the abdomen the right trunk is related to the
of sympathetic innervation on the glomerular fil-
posterior aspect of the inferior vena cava, and the
13
vertebral SUbluxation ... the Analomlc IIeIatIonIhIpI of the AUlonomlc Nervous Syltllm
left trunk passes posterolaterally to the abdominal aorta. Both right and left trunks are surrounded by abdominal lymphatics, lumbar arteries, and veins, as well as connective tissues of the region. On entering the pelvis, the trunks lie anterior to the upper fibers of the anterior sacroiliac ligament and medial fibers of the iliacus muscle (Figure 13-5) . At this point the sacral sympathetic trunks course inferomedially just posterior to the imernal iliac vessels and anrerior to fibers of the piriformis muscle. The right and left trunks end anterior to the coccygeal anachment of coccygeus muscle by forming a small, unpaired ganglion IInpar.
Only the first twO or three lumbar spinal nerves emit white communicating rami [0 connect with the lumbar sympathetic trunks. It should be recalled that the reason for this is that the intermediolateral cell column is present in the spinal cord down to segments L2 or L3 only. Gray communicating rami, however, are present through out the lumbosacral region. These gray rami consist of 3xons of postganglionic neurons within lumbosacral trunk ganglia, which join somatic nerves of the lumbosacral plexus to supply sympathetic innervation to cutaneous and muscular arreries, erector pili Illuscles, and swear glands in the lower abdominal wall, buttock, perineum, and lower limb. The gray rami in the lumbar region are relatively long when compared with those in [he cervical, thoracic, and sacral regions, because to reach the lumbosacral plexus they course with lumbar arteries (which are innervated) around lumbar vertebral bodies and pass medial to the fibrous arrachments of the psoas major muscle. As in the thoracic: region, many preganglionic axons that enter the lumbar sympathetic trunk do not synapse in ganglia of the trunk; instead they branch from the trunk as four lumbar splanchnic nerves ro terminate in prevertebral ganglia. Of these, the first and second lumbar splanch nic nerves, which originate from the superior two or three lumbar ganglia, course posterior to the inferior vena cava and onco the anterior surface of the abdominal aorta, where they end primarily in
251
inferior mesenteric ganglia. In most individuals the first lumbar splanchnic nerve also contributes in a minor way to the innervation of the celiac, aorticorcnal, and renal ganglia. Postganglionic neurons scattered a long the origin of the inferior mesenteric artery within the inferior mesenteric plexus give rise to axons that follow the artery and its branches to supply sympathetic input to the enteric nervous system in the left half of the transverse colon, descending colon, sigmoid colon, and superior part o f the rectum. The third and fourth lumbar splanc hnic nerves are branches of the third and fourth lumbar trunk ganglia, which terminate by synapsing in small ganglia within the superior hypogastric (prelumbar) plexus. The third lumbar splanchnic nerve courses anteriorly to the abdominal aorta and common iliac artery, and the fourth lumbar splanchnic nerve passes posteriorly to the com· mon iliac vessels medial to the sympathetic trunk to reach the superior hypogastric plexus. The superior hypogastric plexus is located somewhat to the left of the median plane anterior to the bifurcation of the abdomina l aorta at the level of the fourth lumbar vertebra l body (Figure 13-5). It extends inferiorly anterior to the left common iliac artery, median sacral artery, fifth lumbar vertebral body, and sacra l promontory. In this position the plexus is related to the medial end of the sigmoid mesocolon and superior rectal vessels, which may receive nerve fibers from this plexus. The superior hypogastric plexus is continuous inferiorly with the right and left inferior hypogastric plexuses through the right and left hypogastric nerves (Figure 13-5). Preganglionic axons of the third and fourth lumbar splanchnic nerves terminate by synapsing with postganglionic neurons scattered amongst the nerve fibers of the superior hypogastric plexus, mostly, and to a much lesser degree, the inferior hypogastric plexus. Axons of these postganglionic cells innervate the inferior ha lf of the ureter and contribute to nerve plexuses o n gonada l (testicular/ovaria n) arteries. Many axons from postganglionic neurons in the superior hypogastric plexus exit the plexus inferiorly as the right and left hypogastric
252
4
5
6
Ftgare 13--5
7. Psoas major muscle 8. Lumbar sympothetic trunk
Pelvic sympathetic trunk and hypogastric plexuses.
nerves. These sympathetic axons pass through the inferior hypogastric plexus without synapsing for the most parr to innervate pelvic viscera either as direct nerve branches to the specific organ or indirectly by passing a long branches of the internal iliac artery. In males, the inferior hypogastric plexus lies in contact with the lateral aspect of the rectum and posterior aspect of the urinary bladder, seminal vesicle, and prostate gland. In females, this plexus is similarly related to the rectum and urinary bladder and lies adjacent to the cervix of the uterus, fornix of the vagina, and the inferior por-
tion of the uterine broad ligament. The inferior hypogastric plexus also contains sma ll clusters of postganglionic neurons, but these are predominantly parasympathetic (described later) . In summary, the sympathetic preganglionic supply for pelvic viscera originates in lower thoracic and upper lumbar (TIO-L2 or L3) spinal cord segments, branches from the lumbar sympathetic
trunk as lumbar splanchnic nerves, and terminates in small prevertebral ganglia, mostly in the superior hypogastric plexus. A small number of sympathetic preganglionic axons pass through both superior and inferior hypogastric plexuses to innervate postganglionic neurons in the wall of
the urinary bladder.
1. Common iliac ortery
2. Internal iliac artery 3. Superior hypogastric plexus 4. Pelvic sympothetic trunk 5. Median sacral artery 6. Inferior hypogastric plexus
Sympathetic postganglionic axons, mainly from cells in the superior hypogastric plex us, innervate pelvic viscera as componems of three delicate nerve plexuses, namely the middle rectal, vesical, and prostatic (male) or uterovaginal (female) plexuses. The lower rectum and anal cana l receive sympathetic innervation through
direct colic branches of the inferior hypogastric plexus and through the middle rectal plexus, which courses along the artery of the same name. Functionally thi innervation is inhibitory to the enteric nervous system of the rectum and anal cana l and is excitatory [Q the internal anal sphincter. Activation of this portion of the sympathetic division therefore causes relaxation of expulsory musculature and contraction of the internal anal sphincter. (Note: The inferior rectal nerve, a branch of the pudendal nerve, supplies the external ana l sphincter and inferior ana l cana l, which are under voluntary somatic sensory and mOtor controL) Sympathetic innervation of the urinary bladder, seminal vesicles, and ductus deferens reaches these structures through the vesical plexus. This plexus consists of delicate branches from the anterior portion of the inferior hypogastric plexus, which contain both postganglionic axons from cells in the hypogastric plexuses and syl11pa-
13 Vllrl8bl'lI Subluxltlon and 1118 AnItomIc RellldoIlII,.. of 1118 Aul....1Ic NllrvOUl Syl1em
253
in
ejaculatory ducts, and erectile tissue of the penis,
T11-L2 or L3 spina l cord segments, which synapse with postganglionic neurons in the muscular wall of the urinary bladder. The role of the sympathetic division in the control of bladder function is somewhat controversia l. Whereas some authors contend that sympathetic stimulation acts only to regulate blood flow to the urinary bladder (9), others indicate that micturition is controlled by
as well as the prostati c, membranous, and penile
cherie
preganglionic axons
from
neurons
complex spinal reflex interactions between sympathetic, parasympathetic, and somatic compo-
nents of the nervous system (3,6). Visceral sensations from stretch and pain receptOrs in the wall of the bladder reach the spinal cord by passing back along both sympathetic and parasympathetic nerves that innervate the organ and act to reflexively stimulate both spinal autOnomic centers. Low-threshold receptOrs, stimulared during filling of the bladder, are thought to elicit sympathetic activity in the upper lumbar spina l cord. This activiry stimu lates concomitantl y ~-cate cholaminergic receptors on fibers of the detrusor muscle, causing it to relax, and a-catecholaminergic receptors on the internal urethral sphincter, causing it to contract, together with parasym-
pathetic inhibition. Conversely, high-threshold receptors in the wall of the bladder, stimulated when the bladder is full, activate reflexly the parasympathetic division, causing the release of acetylcholine, which binds to muscarinic recep-
tor on fibers of the detrusor muscle and elicits contraction of this muscle to empry the bladdet. In addition, somatic motoneurons located in the
anterior horn of the sacral spinal cord reach the external urethral sphincter through the pudendal nerve. These somatic moroneurons are also stim-
ulated reflexly by low-threshold receptOrs during bladder filling, causing comraction of the externa l sphincter. At times of greater distension, supra -
spinal neuronal centers inhibit both sympathetic preganglionic and somatic mOtor neurons, pro-
portions of the urethra. Activation of the sympathetic division causes simultaneous contraction of seminal vesicles, internal urethral sphincter, and
ejaculatory ducts during ejacu lation, as well as subsequent constriction of arteries supplying erectile tissue of the cotpora cavernosa and corpus spongiosum. In the female, the uterovaginal plexus is formed by nerve branches from the inferior portion of the inferior hypogastric plexus, which course into the base of the btoad ligament of the uterus. Sympathetic preganglionic axo ns pass through the uterovaginal plexus ro e ither innervare the uterine
cervix directly or course along vaginal and uterine arteries to supply the vagina, body of the uterus, uterine tubes, and ovaries. Because of extensive hormonal control of uterine function,
the role of sympathetic and parasympathetic innervation is obscured. It is believed, however,
that sympathetic activity produces generalized vasoconstriction in the female urogenital system,
and parasympathetics cause vasodilation.
ParasympalheUc Division Peripheral components of the parasympathetic division of the ANS include long, myelinated axons of preganglionic neurons located in the brainstem and sacral spinal cord segments 52,53, and 54, peripheral ga nglia, which contai n postgangli o nic neurons located nea r the viscus they inner-
vate, and short, unm yelinated axons of postganglion ic neurons, which reach specific target viscera. The term craniosacral is often applied to the parasympathetic division becallse of the location of parasympathetic preganglionic nuclei in cranial (brainstem) and sacral regions of the CNS. In contrast ro the sympathetic division, most parasympathetic axo ns reach target organs as components of cranial nerves or sacral spinal
ducing relaxation of both the internal and exter-
nerves, a lthough some parts of the gastroi ntesti-
nal urethral sphincters, conrraction of the detrusor muscle, and urine flow.
nal tract receive parasympathetic inne rvation by
In the male, the prostatic plexus provides an
sympathetic inne rvation. Cranial nerves with
extensive autonomic innervation to the prostate
parasympathetic components a re the ocu lo motor (CNUI ), facial (CNVU), glossopharyngeal (CNIX )
gland, seminal vesicles, bulbourethral glands,
way of vascular nerve plexuses simi lar to the
254 and vagus (CNX) nerves. The parasympathetic division therefore innervates target viscera by three principal routes; as a component of specific cranial nerves, as a component of sacral
(CNllI) nerve and course anteriorly through the red nucleus and tegmentum of the midbrain. These parasymparhetic nerve fibers continue as a component of the third cranial nerve as it
spina l nerves, and by arterial nerve plexuses. A general structural panern that may assist the reader to understand the ANS more clearly is related to the fact that the parasympathetic divi-
emerges from
sion functions to regulate viscera l activity in the
rior cerebellar arteries near their origin from the
head, neck, thorax, abdomen, and pelvis on ly. For this reason, unlike the sympathetic division, parasympathetic nerves do not extend into the body wall Ot limbs. Also it should be recalled that, functionally, all parasympathetic neurons (preganglionic and postganglionic) are cholinergic, and stimulation of these cells generally acts to counterbalance sympathetic activity. Whereas
basilar artery. This is a clinically important relationship because pathology of these vessels, such
sympathetic activation elicits, for example, accelerated heart ratc, increased blood pressure, and
decreased gut motility to mobilize body energy reserves, parasympathetic activity decreases the
heart rate and blood pressure and increases gastroinresrinal peristalsis so as to conserve and
replenish energy stores. Parasympathetic Cranial Nuclei and Their Peripheral Distribution The crania l origin of the parasympathetic division is localized in bilaterally symmerric brainstem nuclei composed of preganglionic neurons. These parasymparhetic nuclei (also referred to as general visceral efferent nuclei) are centered near other nuclei of specific cranial nerves. The cranial nerves distribute these autonomic preganglionic nerve fibers to peripheral ganglia and postganlionic axons from the ganglia to target viscera. The mOSt superior of these is the EdingerWestphal (accessory oculomotor) nucleus, which is located in the periaqueductal gray of the midbrain at the level of the superior collicu lus. The Edinger-Westphal nucleus is therefore positioned adjacent, posterior, and superior
[Q
the main
oculomotor (somatic motor) nuclear complex. Parasympathetic preganglionic axons originating fro m neurons in the Edinger-Westphal nucleus join somatic mOtOr axons of the oculomotor
the cerebral peduncle in the
interpeduncular fossa. The oculomotor nerve
coutses through the subarachnoid space and passes between the posterior cerebral and supe-
as a berry aneurism, may impinge the oculomotor
(CNIlI) nerve at this site, producing a classic progressive ophthalmoplegia with loss of the pupillary light reflex. The oculomotor (CNIII ) nerve pierces the dura mater just lateral to the
posterior clinoid process at the apex of the petrous ridge of the temporal bone to enrer the cavernous sinus. The nerve passes through
this venous sinus, where it may be affected by infective thrombosis of the sinus, together with the trochlear (CN IV), abducens (CNVI ), ophthalmic (CNV,), and maxillary (CNV, ) nerves, as well as the terminal part of the internal carotid artery. Before exiting the middle cranial fossa through the superior orbital fissure, the oculomotor nerve may receive some sympathetic pregan-
glionic axons from the internal carotid nerve plexus and conduct these into the orbit. Parasympathetic preganglionic axons course in the oculomOtor (CN III ) nerve as it passes through the common tendinous ring of extraocular muscles and finally branch away from the inferior division of the oculomotor (CNlII) nerve to terminate in the ciliary ganglion. This small ganglion , which is located posteriorly in the orbit between the proximal attachment of the lateral rectus muscle (laterally) and the optic nerve (medially), contains parasympathetic
axons.
Postganglionic
axons
emerge from the ciliary ganglion as shorr ciliary nerves and enter the posterior aspect of the eyeball by piercing the sclera, run anteriorly through the perichoroidal space, and innervate the pupillary sphincter (constrictor) and ciliary muscle. This parasympathetic pathway balances the sympathetic system, which, as described above, sup-
13 Vllrtllllrll SWduxIIlon and tile Anatomic Relalloalllpa 01 tile AutonomIc NllrVOUI System plies the pupillary dilatOr muscle. Thus, the sympathetic and parasympathetic divisions are complementary functionally to regulate the amount of light entering the eye rhrough the pupi l by the pupillary light reflex. A bright light entering the eye stimu lates reflexly rhe Edinger-Westpha l
255
nerve. These parasympathetic axons continue with this crania l nerve as it emerges from the
brainstem at the border between rhe pons and medulla, courses through rhe subarachnoid space and exits the posterior cranial fossa , together
smooth muscle in the sphincter pupillae, in this way narrowing the pupillary aperture and reducing the amOunt of lighr entering the eye. Conversely, in reduced light levels the parasympa-
with the vestibulococh lear (CNVllJ) nerve, thtough the internal acoustic meatus. The facia l nerve courses larerally to reach the floor of the rympanic cavity, where it diverts posteriorly and inferiorly to enter the facial canal and emerge on the external surface of the skull through the stylo-
thetic division is quiescent, and sympathetic activ-
mastoid foramen . At the point in the nerve where
ity causes contraction of the dilator pupillae. Parasympathetic innervation of the ciliary muscle in the eye is activated reflexly during near
it bends posteriorly, called the genicII lum, the nerve is slightly enlarged into the geniculate ga nglion. This ganglion is the site where sensory neutOns, predominantly of the facial (CNVll) nerve, are locared. Parasympathetic preganglionic axons traverse this ganglion without synapsing, and many branch away from the seventh crania l nerve at this point to enter the tympanic plexus of nerves on the floor of the tympanic cavity. Other parasympathetic axons continue further along the facia l nerve to form the chorda tympani nerve, which branches more dista ll y (see following discussion) . Most axons that entered the tympanic plexus from the facia l (CNVll) nerve and some from the glossopharyngeal (CNlX) nerve (discussed later) coa lesce anteriorly in the tympanic cavity to form the greater perrosal nerve. This
nucleus, which causes contraction of circular
vision in the accommodation reflex. Contraction
of the ciliary muscle slackens the suspensory ligaments of the lens. This gives the lens a thicker shape and a llows the individual to focus better on near objects in the visual field. The facial (CNVI1) nerve a lso conducts parasympathetic axons to supply visceral mOtOr innervarion to lac rima l and salivaty glands. Parasympathetic preganglionic axons are conducred by rhe facial (CNVlI ) nerve to rwo periphera l ganglia, called the pterygopalatine and sllbmandibular ganglia. These preganglionic axons originate in the caudal pons region of rhe brainstem from rhe salivatory nucleus. This nucleus is locared adjacent cauda ll y ro rhe branchial motOr nucleus of the facial (CNVll) nerve, immediately superior to the dorsal motOr nucleus of the vagus (CNX) nerve. The superior portion of the salivatory nucleus (often referred ro as rhe sllperior saliva tory nllclells) contains preganglionic neurons, which are components of the facia l (CNVll ) nerve, whereas the mOre inferior part of the nucleus (inferior saliva tOry nucleus) conrribures to the glossopharyngea l (CNlX) nerve. Parasympathetic preganglionic axons in rhe glossopharyngea l (CNTX) nerve terminate by synapsing on preganglionic neurons in the otic ganglion. Preganglionic axons from neurons in the
superior salivarory nucieus course inferolaterally through the tegmentum of the pons along wirh branchial motOr axons of the facial (CNVU)
nerve emerges from the tympanic cav ity onto the
anterolateral aspect of rhe perrous temporal bone through a sma ll unnamed fissure and courses anteromedially to reach the foramen lacerum on the lateral aspect of rhe internal carorid artery as rhis vessel enters the middle cranial fossa from the carotid canal. At this point symparhetic axons of the deep petrosa l nerve join the greater petrosal nerve to form rhe nerve of rhe pterygoid canal. This last nerve conducts the parasympatheric preganglionic axons along wirh sympathetic and taste fibers to the prerygopalatine ganglion, which is located deep in the pterygopala tine fossa against rhe sphenoid bone, where it lies between the openings of the prerygoid canal (media lly) and rhe foramen rotundum (laterally). Only parasympathetic axons terminare in rhe
256 pterygopalatine ganglion by synapsing with dendrites of parasympathetic postganglionic neurons. Axons of these postganglionic neurons branch away from the ganglion and course in rwo directions. One group of parasympathetic nerve fibers joins the maxillary (CNV,) nerve, which enters the pterygopalatine fossa through the foramen rorundum, and
cou rses
through
the
inferior
orbital fissure and anteriorly along the Aoor of the orbit with the infraorbital branch of the maxillary nerve. The parasympathetic fibers then join the zygomatic nerve, which travels laterally and superiorly along the zygomatic bone to finally reach the lacrimal gland . It is also thought that some parasympathetic axons reach the lacrimal gla nd more ditectly from the pterygopalarine ganglion by coursing separately into the orbit through the inferior orbital fissure, a long the posterolateral wall of the orbit in the retroorbital plexus and into the lacrima l gland. Activation of
and crosses the medial surface of the tympanic membrane and handle of the malleus near its superior end to reach the anterior canaliculus of
the chorda rympani, through which it passes to exit the tympanic cavity. The chorda tympani emerges on the external aspect of the skull through the petrorympanic fis su re, grooves the medial aspect of the spine of the sphenoid bone, and comes to lie on the medial aspect of the latera l pterygoid muscle as it traverses the infratemporal fossa. Near the inferior border of the lateral pterygoid muscle, the chorda tympani joins the lingual branch of the mandibular (CNV J) nerve. The lingual nerve conducts these parasympathetic preganglionic axons into the Aoor of the mouth, where they branch from this nerve to terminate in the submandibular gan -
glion located on the superolateral aspect of the hyoglossus muscle. Postganglionic axons from neurons in the submandibu lar ganglion either
this pathway produces secreti on of scrOllS fluid
branch directly inro the submandibular salivary
from the gland, which is important for the main-
gland, whic h lies adjacent to the ganglion, or rejoin the lingual nerve to supply the sublingua l and intralingular sa livary glands. Release of acerylc ho line at postganglionic axonal terminals within these glands initiates rapid dilation of arterioles within the glands and secretion of saliva into the Aoor of the oral cavity. The glossopharyngeal (CN IX) nerve a lso conducts parasympathetic preganglionic axons from the salivatory nucleus. Axons of neurons in the more inferior portion of the nucleus join bra nchial motor axons from neurons in [he nucleus ambiguus to enter the ninth cranial nerve. This nerve stems from the medulla oblongata through several tiny rootlets at the superior limit of the groove between the o li ve and the pyramid. The glossopharyngea l (C IX) nerve has a short anterolatera l course through the subarachnoid space and exits the posterior cranial fossa, a long with the vagus (CNX) and accessory (CNXI ) nerves and first part of the internal jugular vein, through the jugular foramen . As the ninth cranial nerve passes through the jugular foramen, it has two enlargements, called the superior and inferior glossopharyngeal ganglia, which house sensory
tenance of the ocular conjunctiva. For (his reason
the physician must be concerned with possible desiccation and ulceration of the conjunctiva in a
patient wirh a facial (CNVU) nerve palsy. The second group of parasympathetic preganglionic axons emerge from the prerygopalatine ganglion and join nasal and palatine branches of the maxillary (CNV,) nerve to innervare mucus glands in the nasal caviry, nasopharynx, hard palare, and soft palate. Parasympathetic activity in this pathway causes mucus secretion in these regions. In addition to the parasymparheric contribution of the facia l (CNV U) nerve to the tympanic plexus, many preganglionic axons from the supe-
rior sa livatory nucleus continue paSt the geniculum of the facia l (CNVII ) nerve. These axons, a long wi th taste fibers, branch away from the nerve as the chorda rympani withi n the facial ca nal and course in the reverse direction back
into the tympanic cavity through a small bony channel ca lled the posterior canaliculus for the cho rda tympani. The chorda rympani enters the tympanic caviry at the posterior edge of rhe rympanic membrane nea r the handle of the malleus
13
vertebral SUbluxation and the Anatomic RelatIonshIps 01 the Autonomic Nervous System
257
This tympanic nerve conducts rhe parasympathetic axons through the tympanic ca nalicu lus, a
component is low. In fan, most axons in the vagus (CNX) nerve are sen ory (viscera l afferent), which conduct sensacions from the viscera to the brainstem. It may be that, as suggested by Gershon (J 9), excitatOry stimuli that reach the gut are magnifi ed gteatl y in the enteric division of the ANS (desc ribed under Enteric Division) .
small runnel near rhe anterior margin of rhe jugular foramen, into rhe morc anterior part of the
ciated with the vagus (CNX) nerve are localized
tympanic plexus on the floor of the middle ear
in the dorsal motor nucleus of this nerve located
cavity. Within rhe plexus some autonom ic fibers
from the glossopharyngeal (CN IX ) nerve may join the greater petrosal branch of the facial (C NVII ) nerve, but mOSt axons from the in fer ior sa livatory nucleus, together with a sma ll number from the superior sal ivatory nucleus (facial nerve ), form the lesser petrosal nerve. The lesser petrosal nerve exits the tympanic cavity through the same opening as the greater petrosal nerve and has a short anteromedial cou rse in the middle crania l fossa to reach the foramen ova Ie, through
in floor of the fourth ventricle near the midline of the medulla oblongata . Axons of these neurons traverse the tegmentum of the medulla ob longata anterolatera ll y and emerge from the brain tem as a series of rootlets in the groove between the olive and the pyramid just inferior to the rootlets of the ninth cran ial nerve. The vagus (CNX) nerve exits the posterior cranial fo sa through the jugular foramen, where, like the glossopharyngeal (CN IX ) nerve, the 10th cran ial nerve has two enlargements, called slIperior a/ld inferior vagal
which it exits the cran ial cavity most commonly.
ganglia, which contain sensory neurons. The
The lesser petrosal nerve conducts the parasympathetic preganglionic axons to the otic ganglion, which is attached to the medial aspect of the mandibular (CN VJ ) nerve near the roof of the infratemporal fossa. Within the otic ganglion,
vag us (CNX) nerve cou rses inferiorly through the neck, where it lies within the carotid sheath in the
neurons. Parasympathetic preganglionic axons of
the glossopharyngea l (CNIX) nerve pass through the superior glossopharyngeal gangl ion and branch away from the nerve at the level of the inferior ganglion to form the tympanic nerve.
rhe preganglionic axons relay to parasympathetic postganglionic neurons, rhe axons of which
branch from the ganglion and join the auriculotemporal nerve, and a small branch from rhe ganglion a lso joins the cho rda tympani inferiorl y. As a component of the auriculotemporal nerve,
postga nglionic axons reach the parotid gland, which is stimulated to synthesize and secrete
Parasympathetic preganglionic neurons asso-
posterior groove between the internal jugular vein
(laterally) and the interna l carotid artery (medially). In ferior to the superior border of the thyroid cartilage, the nerve maintains a simi lar relarionship wirh rhe common carorid arrery into the roor of the neck . Because of srructura l asymmerry
between the right and left sides in the superior mediasrinum,
rhe
cou rse of rhe
righr
vagus
(CNX) nerve in the thorax differs from that of the left side. The right vagus (CNX) nerve enters the tho-
saliva into the vestibule of the mouth when this porrion of the parasympathetic division is acti-
rax posrerior ro rhe rerminal porrion of rhe inrer-
vated. The fourth and final cranial nerve that has a parasympathetic (general visceral efferent) component is the vagus (CNX) nerve. Although this nerve has an extensive distribution to the gastrointestinal system, respiratory system, and heart, the density of parasympathetic pregan-
subclavian arrery anreriorly to reach rhe posrero-
glion ic axons within the nerve relacive ro that of
orher cranial nerves having a parasympathetic
nal jugular vein and crosses the first part of the medial aspect of the brachiocephalic vein, where ir gai ns access to rhe lateral aspecr of the rrachea .
The nerve passes medial to the azygos vein and posterior ro rhe righr primary bronchus, where
vagal axons are joined by sympathetic postganglionic axons from the second, third, and fourth thoracic sympathetic trunk ganglia to form the right posterior pulmonary plexus. Several vagal
258 branches from the posterior pulmonary plexus descend further and, together with a contribution from the left vagus (CNX) nerve, form the posterior esophageal plexus. Near the inferior end of the esophagus the posterior esophageal plexus coalesces into a single posterior vagal trunk,
which enters the abdomen through the esophageal aperture of the diaphragm. On the left side, the vagus (CNX) nerve enters the superior mediastinum posterior to the left brachiocephalic vein in the groove between the common carotid and subclavian arteries. The nerve reaches the posterior aspect of the left primary bronchus by coursing late ra! to the arch of the aorta, where it is crossed by the left superior intercostal vein and left phrenic nerve. In the left posterior pulmonary plexus the left vagus (CNX) nerve, like the right nerve, is joined by sympathetic postganglionic axons from T2-T4 sympathetic trunk ganglia . Two or three vagal branches descend from the left posterior pulmonary plexus and are joined by a small number ofaxons from the right posterior pulmonary plexus to continue down the esophagus as the anterior esophageal plexus. As is the case with the posterior esophagea l plexus, an anteriot vagal trunk is formed inferiorl y from axons of the anterior esophagea l plexus, and this trunk is transmitted into the abdomen with the esophagus. Within the abdomen the anterior and posterior vagal trunks are distributed to abdominal viscera by two principal routes . The posterior vaga l trunk, which originated primarily in the right dorsal mOtor nucleus, gives a small gastric branch to the posterior aspect of the stomach and a large celiac branch, which distributes parasympathetic preganglionic axons through the celiac, splenic, hepatic, suprarena l, renal, and superior mesenteric plexuses. These axons terminate by
synapsing with postganglionic neurons located in or near the viscera they supply. By traversing the celiac and superior mesenteric plexuses, these
vagal axons innervate the myenteric and submucosa l plexuses in the walls of the duodenum, jejunum, ileum, vermiform appendix, ascending colon, and transverse colon to a point near the
left colic flexure. The second route from the anterior vagal trunk supplies most of the stomach and by branches that traverse the lesser omentum innervates the pylorus, liver, superior and descending segments of the duodenum, and the head of the pancreas and sphincter of the common bile and pancreatic ducts. By acrivarion of the parasympathetic innervation, abdominal viscera are mobilized to replenish nutrient and energy stores of the body. Through pharyngeal, superior laryngea l, and recurrent laryngeal branches of both right and left vagus (CNX) nerves, mucus glands in the pharynx, larynx, and trachea receive excitatory parasympathetic stimulation. In addition, two or three ca rdiac branches arising from the vagus nerves as
they course through the neck and superior mediastinum terminate by synapsing with postganglionic neurons dispersed primaril y in the posterior cardiac plexus. Axons of these parasympathetic postganglionic neurons innervate cardiac muscle in the walls of the right and left atria by passing through the subepicardial tissue. Numerous parasympathetic axons also course through the atrioventricular bundle to innervate ventricular muscle fibers. In addition, smaller arteriolar branches of coronary arteries receive parasympathetic postganglionic innervation. Excitation of this portion of the parasympathetic division at times of reSt elicits slowing of the hea rt and constriction of coronary arterioles in response to the release of acetylcholine. At the same time rhe respiratory rate is also slowed by activation of postganglionic neurons in the pulmonary plexuses, which innervate circular smooth muscle in the bronchial tree to cause bronchoconstriction. Clinically, the function of the vagus (CNX) nerve can be affected either by direct effects on its neurons of origin in the cranial end of the medulla oblongata and along their peripheral course or by reflex mechanisms that may modulate the activity of vagal preganglionic neurons. For example, if the arterial blood supply to the brainstem is compromised, as in verrebrobasilar insufficiency, symptoms such as nausea, vomiting, cardiac arrhythmia, slowing of respiration , and a
13
Vertebral Subluxallon II1d the Anat.ic Relallollshlps 01 the AutoIMMIIIc Narv_ System
sense of suffocation may be observed . Also somatic and visceral afferent stimuli entering the CN5 through the vagus (CNX) nerve or other cranial and spinal nerves can affect the function of vagal preganglionic neurons and produce similar symptoms. A good example is how a persistent feeling of nausea and vomiting may be caused by excessive ear wax in the external
acoustic meatus, which stimulates the arricular (somatic sensory) branch of the vagus nerve. In addition, it has been suggested (7) that aberrant vagal activity may be caused by abnormal somatic sensacions entering rhe cervical spinal cord as a result of a cervical vertebral subluxation (see following discussion ).
259
Out the plexus (Figure 13-5 ). A large number of parasympathetic preganglionic axons pass through the inferior hypogastric plexus and continue as pelvic splanchnic nerves to supply postganglionic neurons within the specific viscus they innervate.
Pelvic splanchnic nerves can be traced superiorly to the left of the superior hypogastric plexus (some pass through this plexus without synapsing) to enter the sigmoid mesocolon and the mesentery of the descending colon . By this route parasympathetic preganglionic axons cross branches of the inferior mesenteric artery, which
Parasympathetic Sacral Nuclei and T heir Peripheral Distributions Clusters of parasympathetic preganglionic neu-
may conduct some parasympathetic axons to the colon. Most of these pelvic splanchnic nerve branches continue directly to the colon and end by supplying postganglionic neurons in the myenteric and submucosa l plexuses of the transverse colon (near the splenic flexure), descending colon,
rons are also present in sacral spinal cord seg-
sigmoid colon, and rectum. The rectum is also
ments (52,53, and 54) . Like sympathetic preganglionic neurons in the thoracolumbar spinal cord, these parasympathetic neurons are in the intermediate, lateral area of spinal gray matter. However, unlike sympathetic preganglionics, these neurons do not form a continuous column of cells; instead they are organized inro intermittent nuclei that cannOt be called a true intermediolateral cell column. Although the axonal course from neurons in sacral preganglionic spi nal nuclei is strikingly simi lar to that of sympathetic preganglionic
innervated by parasympathetic preganglionic axons, which join the nerve plexus on the midd le rectal artery, as well as by the inferior rectal nerves, ·which are branches of the pudendal nerve (52,53, and 54) . Parasympathetic preganglionic axons within the pudendal nerve, which is predominantly a somatic moror and sensory nerve,
are axons that did not branch into the inferior hypogastric plexus. The pudendal nerve also may conduct parasympathetic preganglionic axons to
the external genitalia, although the presence of
axons, axons of parasympathetic neurons exit the
postganglionic neurons in these tissues has nOt
sacral spinal cord as components of anterior rOOtS of 52,53, and 54 spinal nerves and have a long course through the subarachnoid space within the cauda equina. On exiting through anterior sacra l foramena within the anterior primary
been demonstrated. Finally, pelvic splanchnic nerves also conduct preganglionic axons from the inferior hypogastric plexus to parasympathetic postganglionic neurons in the wall of the urinary bladder.
rami of these sacral spinal nerves, parasympathetic axons branch away to form pelvic splanchnic
Other pelvic viscera are innervated by parasympathetic postganglionic axons that emanate from
nerves. These nerves therefore can be compared
the inferior hypogastric plexus together with sympathetic axons passing through the plexus. For
with thoracic and abdominal sympathetic splanchnic nerves, which also are composed of preganglionic axons. The pelvic splanchnic nerves enter
example, the testicular or ovarian plexuses, which
the inferior hypogastric plexus, where many parasympathetic preganglionic axons end by synapsing with postganglionic neurons dispersed through-
aorricorenai, renal, and superior hypogastric
originate predominantly from the sympathetic plexuses (see the Thoracic Sympathetic Trunk and Its Branches), receive parasympathetic postgan-
260
The SiaUXation Complex
glionic axons that are vasodilatory to the epididymis and ductus deferens (male) or ovary and uterine tube (fema le). Axons of postganglionic neurons in the inferior hypogastric plexus also enter the prostatic (ma le) or uterovaginal (fema le)
other autho rs have now adopted this view (3,6) . The human myenteric and submucosal plexuses
plexus to provide parasympathetic innervation to
w hereas the vagus nerves are known to conduct
arterioles, which supply erectile tissues in the corpora cavernosa and corpus spongiosum of the
axons to innervate the gast rointesti nal system.
within the wall of the g ut are estimated to con-
tain 10' neurons, which is comparable to the number of neurons in the spinal cord (21 ), fewer than 2000 parasympathetic preganglionic
penis or clitoris. Activation of this portion of the parasympathetic division during erotic stimula-
This huge dispariry of neuron numbers suggests
tion elicits vasodilation of these vessels a nd
innervated directly by the CNS. Furthermore, the
engorgement of erecti le tissues.
enteric nervous system ca n function in vitro, inde-
Sexual function or dysfunction is a good example of how centra l processing in supraspinal
uli to produce peristaltic contractions. This evi-
and spinal neuronal centers can influence peripheral autonomic activity. Integration of neuronal activity in various cerebral and spina l systems, including olfac[ory, limbic, sammie, and viscera l sensory, as well as visual and auditory systems, can govern autonom ic regulation of sexua l func-
tion. The fact that impotence is determined primarily by psychological factOrs points to the strong role of cerebral neuronal centers in the control of autonom ic function. Of parricular interest to the chiropractor and other primary
health care practitioners is the profound influence that somatic and visceral sensations ha ve on
autonomic
regulation
of
both
viscera l and
somatic functioning (see discussion in Central Pro-
cessing in the Control of Autonomic Function) .
Enteric Division
that many, if not most, neurons in the gut are not
pendent of CNS influences, and responds to stimde nce suggests that the myenteric and submucosal plexuses contai n sensory receptOrs, intr insic primary afferent neurons, imerneurons, and mOtor
neurons (19). From examination of congenitally aga nglionic sections of the gastrointestina l tract, such as occu rs in Hirschspru ng's disease, whic h are known to have preganglionic innervation
(22), it appears that in the absence of intrinsic enteric neurons, loca l coordi nat ion and integra-
tion of smooth muscle activity are lost (23). These researchers concluded that the enteric division of the ANS can function independent of CNS influences and is essen rial for the control of mOtor activi ry in the gastrointestinal system . It appears therefore that sympathetic and parasympathetic innervation of the gut serves to regulate neuronal activity within the enteric division but is not necessary for initiation of motOr activity in the gut.
Unti l recently the ANS has been described as having on ly rwo divisions: sympathetic and parasympathetic. As ea rl y as 1889, however, it was recog-
The enteric d ivision of the ANS therefore consists of sensory (viscera l afferent) neurons in the
nized that en teric function appeared to be con-
to mechanical stretch ing and chemica l changes
trolled autonomously by reflex mechanical stimulation of neurona l elements within the wall of the gastrointestina l system (20). Gershon (19), a
also con tain s moroneurons that innervate longitu-
renowned authority on the enteric nervous system , sta ted that the enteric nervous system was
wall of the gastroin testinal tract that are sensiti ve
that occu r in the wall. The enteric nervous system dinal a nd ci rcu lar smooth muscle fibers, arteriolar nerworks, and secretory cells within the gut wall. These motoneurons have connections with vis-
classified as a distinct division of the ANS in the ea rl y 1920s, but this notion was not accepted generally until the last decade. In his review paper, Gershon (19) presents convincing evidence
cera l afferent neurons within the wall, either thro ugh direct collate ra l axonal branches from
favoring an enter ic division of the ANS, and
moroneurons. Visceral afferem neurons are also
the sensory neurons or through interneurons
interposed between viscera l afferent and enteric
13 known
[0
vertebr81 SUbluXallon IIId IIIe Anatomic Relallonshlps GIllie Autonomic Nervoua System
have axonal processes that course back
261
for the maintenance of homeostasis through its
along arterial nerve plexuses like those of primary
regulation of a limentary blood supply, intestinal
sensory neurons within posterior
ganglia of
motility, gastric and intestinal secretions, and
spinal nerves. However, the axons of enteric vis-
fluid transport. [n times of stress, sympathicoto-
ceral afferent neurons (in the gut wall) innervate sympathetic postganglionic neurons in prevertebral ganglia and are believed to be able to influ-
shut down normal gastrointestinal functions.
TOOt
nia will override the enteric nervous system and
ence reflexly neuronal activity in the enteric ner-
vous system.
The neurons of the enteric division and their interconnecting axons are localized between the
layers of the gut wall within [he myenteric and submucosal plexuses (21). The myenteric plexus is located between the external longitudinal and circular smooth muscle layers and is distinct structurally from all other parts of the peripheral nervous system. In many ways the myenteric
plexus resembles structurally the CNS (24-26) and is described as having a blood barrier similar to the blood-brain barrier present in the brain and spinal cord (27). The submucosal plexus is located between the circular smooth muscle layers and the intestinal mucosa and contains
Central Processing in the Control 01 AutonomiC Function HypothalamIC Control 01 Autonomic function The principa l central control of autonomic function originates in the hypothalamus, which regulates autonomic activity either through descending neuronal pathways to nuclei in the brainstem reticular formation and spinal cord or through the pituitary gland to influence autonomic function hormonally. Primary hypothalamic nuclei concerned with autonomic regulation are the posterior, latera), preoptic, and mamillary nuclei,
although it is now thought that the mamillary
numerous pseudo-unipolar or bipolar neurons,
nucleus may be more concerned with the process
which resemble primary sensory neurons in posterior rOOt ganglia of spinal nerves and sensory ganglia of cranial nerves (28). It is believed that only a relatively small number of moroneurons within the myenteric and
of memory storage (29,50,51). Axons of neurons in these nuclei project primarily to the brainstem reticular formation, dorsal mawr nucleus of the vagus (CNX) nerve, and autonomic preganglionic
submucosal plexuses are in direct synaptjc contact with incoming parasympathetic pregan-
glionic axons of either the vagus (CNX) nerve or pelvic splanchnic (52,53, and 54) nerves (19). For this reason, and because of the structure of the myenteric plexus, which, like the CNS, appears to be isolated from other tissues, the enteric nervous system can function auwnomously. Reflex activa-
tion of parasympathetic and sympathetic preganglionic centers in the CNS by afferent (sensory) stimuli, however, plays a strong role in the regulation of activity in the enteric division. This becomes obvious at times of emergency or stress
when parasympathetic or sympathetic activiry within the CNS may supersede intrinsic control of the enteric nervous system . The normal function of the enteric nervous system is important
neurons in the spina l cord. There are four main tracts that conduct descending autonomic infor-
mation from the hypothalamus (Figure 13-6). First, the dorsal longitudinal fasciculus, which originates predominandy in the posterior nucleus
and to a lesser degree in the preoptic nucleus, courses into the tegmentum of the midbrain to innervate
midbrain
reticular
formation
and,
through the central tegmental tract, the dorsal motor nucleus of the vagus (CNX) nerve and spinal cord nuclei. Second, the medial forebrain bundle contains large numbers of descending axons from neurons in the lateral and preoptic nuclei and forms a major descending pathway to innervate the reticular formation, dorsal maWr
nucleus of the vagus (CNX) nerve, nucleus solitarius, and spinal cord nuclei. In addition, the medial forebrain bundle is a major route whereby
9 12 13
14
18 19
rn-----
20
10
21
1. 2. 3. 4. 5.
Anterior commissure
Dorsomedial nudeus Posterior nucleus Lateral nuclear area
Dorsal longitudinal fasciculus 6. Mammillategmental tract 7. Medial forebrain bundle 8. Fasciculus retroAexus 9. Habenular nudeus 10. Dorsal motor nucleus 11.
23 12. Paraventriculor
20. Central tegmental
nucleus
of the vagus nerve
13. Preopitic nudeus 14. Anterior nucleus 15. Supraoptic nucleus 16. Ventromedial nudeus 18. Midbrain retiduor nuclei 19. Cranial pontine
Nucleus solitarius
reticular nuclei
trad
21. Caudal pontine reticular nudei
22. Medullary reticular nuclei 23 . Reticulaspinal tracts
FIgIre 13-8 Schematic diagram illustrating hypochalamic nuclei and the principal descending neuronal parhways from the hypothalamus, which regulate autonomic activiry in the brainsrem and spinal cord.
ascending sensory information reaches the hypothalamus and deep cortica l centers in the cerebrum. Finally, the mamillotegmental tract and the fascicu lus retroflex us are descending pathways rhar originate in the mamillary and habenular nuclei, respectively, and innervate the brainstem reticular formation .
Afferent (sensory ) stimu li entering the CNS rhrough spinal and cranial nerves reach rhe hypothalamus by relaying in the nucleus solitarius and reticular formation of the brainstem. The nucleus solitarius, located in the superior part of rhe medulla oblongata, receives visceral afferent stimuli from most organs of the body and integrates this information ro modulate auronomic activity
in
ways. First, neurons in the nucleus project lower brainstem nuclei in the reticular forma tion, which in tUfn send reticulospinal axons to 3monomic preganglionic neurons in the spinal cord. By this pathway, sympathetic and parasympathetic preganglionic neurons are regulated reflexly. Second, neurons in the nucleus solitarius project to higher brain nuclei, such as the paraventicular nucleus of the hypothalamus, which further integrate information from still higher cortical centers and relay back to the nucleus solitwO
to
rarius
(0
regulate more complex autonomic activ-
ity. By this sophisticated interneuronal network the nucleus solitarius receives information from the highest cortical levels as well as from afferent sensory pathways and can coordinate gastrointestinal functions through direct and indirect projections to the dorsal mOtor nucleus of the vagus (CNX) nerve and spinal autonomic preganglionic neurons.
In summary, the hypothalamus is the major CNS center that coordinates and regulates autonomic neuronal activity. Various hypothalamic nuclei function ro integrate sensory stimuli ascending from the spinal cord and brainstem with info rmation derived from cortical and subcortical nuclei of the cerebrum and diencephalon. Outflow from the hypothalamus relays in the brainsrem reticular farmarion and nucleus solitarius and reaches autonomic preganglionic neurons in rhe brainsrem and spinal cord to modulate
neuronal activity in peripheral components of the
ANS.
Ranax RagutaUon of Autonomic Acllvtty The importance of sensory informarion in rhe control of autonomic function cannot be overstated. In fact, the primary CNS mechanism whereby auto nom ic neuronal activity is regulated originates in visceral and somatic sensations and is reflexogenic. Today the term autonomic nerVOllS system incorporates both visceral efferent and visceral afferent (also referred to as autonomic afferent) components, even though the original definition of the ANS was restricted to visceral efferent components exclusively. Under normal cond itio ns impulses of visceral sensation reach the CNS along peripheral processes of primary sensory neurons like those of somatic sensation and provoke reflex responses in the o rgans. When an organ functions abnormall y because of a parhologic condirion or injury, viscera l afferent neurons may conduct pain sensations to the spinal cord segments rhat supply rhe involved organ . Often these painful sensations are referred to a region of the body wall or limbs innervated by the same spina l cord segments as those that supply the painful viscus. Because visceral sensory neurons are localized in sensory gangl ia of cranial nerves and posterior root ganglia of spina l nerves and their peripheral processes are distributed wirh autonomic preganglionic and postganglionic axons to reach the viscera, it becomes important to have a good understanding of the spina l segmental pattern of autonomic innervation to the viscera (described in Peripheral Components of the Autonomic Nervous System) to differentiate somatic pain from referred pain of visceral o rigin . Autonomic afferents are divided into twO types, both of which exert profound influences on autonomic activity. These are the special visceral affe rent (olfacrary, gusrarary) and general visceral afferent (stretch, pain) sensations. These visceral sensations function at an unconscious level, for the most part, to provoke reflex responses in the viscera. However, visceral sensations also lead to conscious awareness of a feeling of fullness in
264
The Slmluxallon Complex
hollow organs such as the stomach, intestine, or urinary bladder and also contribute to the feeling of well-being or malaise (30). Generally, the somata of autonomic afferent
neurons are localized in sensory ganglia of the vagus (CNX) and glossopharyngeal (CN 1X) nerves, as well as in posterior root ganglia of tho-
racic and upper lumbar (Tl-T2 or T3) or midsacral (52,53 and 54) spinal nerves. Peripheral processes of general visceral afferent neurons are distrihuted to thoracic and abdominal viscera through white communicating rami of thoracic
and upper lumbar (Tl-T2 or T3) spinal nerves and follow sympathetic preganglionic and postganglionic axons without synapsing in peripheral autonomic ganglia to terminate in rhe wall of the
viscus. For sensations from pelvic viscera, the visceral afferent nerve fibers course with pelvic splanchnic nerves to reach rhe lower gastrointestinal tract and other pelvic organs. It is important to realize that, although general visceral afferent stimuli play a significant reflexogenic regulatory role at an unconsciolls
level in the ANS, somatic sensations also control autonomic activity
by reflex pathways. In fact, at
times when sympathetic activation is required, somatic sensations involving special senses (visual, auditory, olfactory, vestibular) or general sensations (touch, vibration, pain, temperature, pressure) most often initiate the auronomic response. Elevation of blood pressure and pupillary dilatation are well-known somatovisceral reflex sympathetic responses to painful sensations. Al,o, for example, relaxation of skeletal muscle with soft tisslle therapy sllch as massage, although largely caused by proprioceptive mechanisms, may be caused in part by renex activation of parasympathetics or inactivation of sympathetics. Viscerosomatic rcnexes are also recognized. For example, visceral pain is known ro cause increased ronus and even spasm of skeletal muscle. Although these reflex responses have been recognized for some time, little research has been undertaken to elucidate the mechanisms of somatovisceral or viscerosomatic interactions.
Autonomies In Chiropractic During the initial history of chiropractic, autonomics were held JI1 high regJrd and treatment of visceral disorders by manipulative therapy in chiropractic offices was common. The reason for this is simple: early chiropractic practitioners observed that spinal manipulative therapy ameliorates specific visceral disorders. Indeed, chiropractors today continue to reporr such observations (31). However, the chiropractic profession has received much criticism, primarily from allopathic medical practitioners, throughout most of this century, because of the lack of scientific evidence supporting this contention. For this reason spinal manipulative treatment of visceral problems reached the point where few if any chiropractors performed such therapy or would admit to doing so. It now appears that visceral disorders may once again be included in the scope of chiropractic practice, and again the frequency of reported successful treatments is increasing exponentially. The reason for this trend, once again, is obvious. It appears that reporrs from early chiropractors, although based on empirical observation alone, are now beginning ro find some foundation in basic science (32). Muller (33) in his synopsis of the role of autonomies in chiropractic recognized the need for a more scientific approach, but failed in his efforr because of paucity of valid research at the time. Since then, scienrific evidence supporting the role of chiropractic manipulative therapy is mounting. Sato and his co-workers (34,35) demonstrated a visceral response (decreased gastric motility) to somatic stimulation (skin pinch), a necessary first step roward elucid:lting the mechanism whereby spinal manipulative therapy may affect visceral function. More recent studies from Sato's laboratory (36,37) and others (38,39) support this early evidence and suggest that the mechanism of this somatovisceral response may involve renex activation of the autonomic nervous system. Smce these initial studies there has been ,\11 explosion of reports that describe relief of symptoms in vari-
13 V8r1eIIrai SlMixIIion IIId 1118 AnltomIc IIIIIItIoIlIIIIpI 011118 AuloIIOIIic NllrvlXII Syltem ous visceral disorders after spinal manipulative therapy at specific vertebral motion segments. Varying degrees of benefit have been reported after chiropractic manipulation of the vertebral column in such diverse visceral problems as headache (40,41), cardiovascular dysfunction (42,43), asthma (44), and dysmenorrhea (45). However, nearly all studies to date focus on the therapeutic benefits of spinal manipulative therapy and fail to investigate the cellular mechaI1Isms that underlie the observed effects of manipulation (46). One exception are rhe reports from Brennan's laboratory, which indicate an increased respiratory burst of immunologically competent cells (neutrophils and monocytes) after chiropractic manipulation of the thoracic spine (46,47). Effects of spinal maI1lpulative therapy that enhance the immune response have far-reaching implications for the chiropractic profession. A large body of evidence is accumu lating rapidly in the scientific literature (48) that indicates that the nervous system exerts a profound regu latory influence on immune activity and that this effect may be manifest through activation of the autonomic nervous system (48). The challenge for investigators in the field of chiropractic is to establish the links between spinal manipulative therapy, autonomic function, and rhe positive therapeutic effecTs of manipulation in patiencs with visceral disorders.
20.
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the gumea pig. II. Non-neuronal dements. 1976; 5,195-206. 27. Gershon MD, Burszrajn S. Properties of the enteric nervous system: limitation of access of mtravascular macromolecules to the myenteric plexus and muscularis externa. J Comp Neurol 1978; 180,467-88. 28. Schofield Cc. Anatomy of muscular and neural tissues in the alimemary canal. In: Code CF, ed. Handbook of physiology. Section 6, AJimemary Canal. Vol. 4: Washington, DC: American Physiological Society, 1968: 1903-1960. 29. Kupfermann I. Hypothalamus and limbic system: PCP'" tidergic neurons, homeostasis, and emotional behaviour. In: Kandel ER, Schwartz jH, Jessel TM, cds. Principles of neural science. 3ed ed. East Norwalk, Connecticut: In
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Appleton and Lange, 1991:735-49. 30. Barr ML, Kiernan jA. Visceral innervation. In: The human nervous system: An anatomical viewpoint. 6th ed. Philadelphia: JB Lippincort, t 988:364-76. 31. Wiles MR. Visceral disorders related to the spine. In : Gatterman MI, ed. Chiropractic management of spine related disorders. Baltimore: Williams and Wilkins, 1990,379-96. 32. Moon RD. Chiropractic models: Current understanding of vertebral subluxation and manipulable spinal lesions. In: Sweere, JJ ed. Chiropractic family practice: A clinical manual. Gaithersburg, Maryland: Aspen, 1992. 33. Muller RD. Autonomies in chiropractic: The control of autonomic imbal:mce. Toronto: The Chiro Publishing Co., 1954. 34. Sara A, Schmidt RF. Somata-sympathetic reflexes: Afferent fibers, central pathways, discharge characteristics. Physiol Rev 1973; 53,916-47. 35. Sato A, Sato V, Shimada I-~ Torigata Y. Change in gastric motlliry produced by nociceptive snmulation of the skin m rats. Bram Res 1975; 87:151-9. 36. Sato A, Swenson R. SympathetiC nervous system response to mechanical stress of spi nal columns In rats. J MaOlpulative Physiol Ther 1984; 7: 141-8. 37. Sato A. PhYSiological studies of the somato-autonomic reflexes. In: Haldeman S, ed. Modern developments in the pnnciples and pracrice of chiropractic. New York: Appleton-Century-Crofts, 1980; 93-106. 38. Leach RA. The chiropractic theories: A synopsis of scientific research. Baltimore: Williams and Wilkins, 1980; 133-42. 39. Coote JH. Central organi7.3tion of somarosympathetic reflexes. In: Haldeman 5, ed. Modern developments in the
44. 45.
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principles and practice of chiropractic. New York: Appleton·Century-Crofts, 1980: 107-16. Vernon HT. Spmal maOlpulallon and headaches of cervical origin: reviews of [he literature. J MaOlpulallve Phys,01 Thcr 1989; 12(6) ,455-68. Vernon H. Spinal manipulation and headaches of cervical origin: A review of literature and presentation of cases. M,nu,l Med 1991; 6,]3-9. TIlley RM. The role of palpatory diagnosis and mampula fion therapy In heart disease. Osteopathic Ann 1976; 4,272-7. Crawford J. Hickson G, Wiles MR. The management of hypenensive disease: A review of spinal mampulation and the efficacy of conservative therapeusis. J Manipulative Phy,;ol Ther 1986; 9,27-31. Monti RL. Mechanisms and chiropractic management of bronchial asthma. Dig Chiro Econ 1981; 26:48-51. Kokjohn K, Schmid OM, Triano JJ. Brennan Pc. The effect of spinal manipulation on pain and prostoglandin levels in women with primary dysmenorrhea. J Manipulative I'hYSlol Ther 1992; 15(5),279-85. Brennan pc, Kokjohn K, Kaltinger CJ. et al. Enhanced phagocytic cell respiratory burst induced by spIRal manipulation: potential role of substance P. J Manipulative Phy,;ol Ther 1991; 14,399-408. Brennan PC, Triano JJ , McGregor M, Kokjohn K, Hondras MA, Brennan DC. Enhanced neutrophil respiratory burst as a biological marker for mampulation forces: Duration of the effect and association with substance P and rumor necrosis factor. J Manipulative Physiol Ther 1992; 15(2),83-9. Fabris N, Jankovic BD, Markovic BM, Spector NH, eds. Ontogenetic and phylogenetic mechanisms of neuroimmunomodulation: From molecular biology to psychosocial sciences. Ann N Y Acad Sci 1992; 650. Pantic VS, Pamic SM. Opposite actions of alphaandregenic vs beta-a ndrogenic influences on humeral immune response in guinea pigs. In : Fabris, Jankovic, Markovic, and Spector, eds. Omogemic and phylogenetic mechanisms of neuroimmunomodulation: From molecular biology to psychosocial sciences. Ann N Y Acad Sci 1992; 650,165-169. Loewy AD, Spyer KM. Cemral regulation of autonomIC functions. New York: Oxford Universiry Press. J 990. Ciriel10 J. Calaaaresu FR, Renaud LP, Polosa C, eds. Organization of the autonomic nervous system: Central and peripheral mechanisms. New York: Llss, 1987.
Review 01 the Systemic Ellects 01 Spinal Manipulation Patricia C. Brennan Key WOrds
Viscerosomatic effects, polymorphonuclear neutrophils (PMN), natural killer (NK) cells, respiratory burst, heat shock proteins (HSP), tumor necrosis factor (TNF), substance P (SP)
After reading this chapter you should be able to answer the fo llowing questions:
Question #1
Is there a response in vitro to polymorphonuclear neutrophils challenge after spinal manipulation?
Question #2
Has a change in tumor necrosis factor (TNF) been demonstrated after manjpulation?
268
1be SUbluxation Complex
C
urrently it is not possible to determine whether there are identifiable systemic consequences, including immunologic consequences, of vertebral subluxation, as it is defined in this text. The demonstration of such cause and effect relationships requires that stringent criteria are
satisfied (1). These criteria include the relative strength of the study designs used to determine causality, the consistency of the association, the temporal sequence of exposure (subluxation) and outcome (systemic effect), and freedom from bias of the diagnosis of a subluxation and the appearance of the presumed outcome. We have no convincing evidence that a vertebra l subluxation cat/ses a systemic effect. What we do know is that spinal manipulation, which is used by chiropractors ro tfear subluxation, elicits some very specific effects, quantifiable by well-defined techniques, on both cells and the concentrations of some soluble factors found in the body. These cells and soluble factors are involved in immune responses, but they play other physiologic roles as well. That spinal manipulation elicits viscerosomatic effects is a concept common to both chiropractic and osteopathy (2-7). Convincing evidence for such effects comes from anima l model systems, notably the work of Sato and Swenson (8), who showed that experimenta l mechanical stimu lation of rat spina l cord afferents decreased blood pressure and both adrenal and renal nerve activity. More recently, DeBoer et al. (9) demonstrated an inhibition of gastrointestinal myoelectric activity (EMG) in conscious rabbits by experimental manipu lation of the thoracic spine, and Deloof et al. (10) showed that stimulation of afferents in the central end of the cut vagus nerve inhibited gastric EMG for up to 6 minutes. In contrast, efforts to demonstrate viscerosomatic effects in humans after spinal manipulation have produced conflicting results. Vernon et a l. (11) reported a slight, but significant, increase in ~ endorphin levels after spinal manipulation; how-
ever, Christian er al. (12) were unable to demonstrate differences in the plasma levels of adrenocorticotropic hormone (ACTH ), ~-endorphlO, or cortisol between sham-treated or manipulated subjects before or after treatment. Although it has also been hypothesized that spinal manipulation affects cells of the immune system (4,13,14 ), until recently little experimental or clinical evidence supported this hypothesis. Vora and Bates' preliminary report (15 ) that spinal manipulation twice a week for 4 weeks increased the absolute numbers of B lymphocytes in five of eight patients with documented neuromusculoskeletal disorders has never been repeated. We have approached the question of systemic responses to spinal manipulation in a number of
ways. First, we studied rhe ability of polymorphonuclear neutrophils (PMN) from both healthy subjects and patients with low-back pain to respond in vitto to a particulate challenge after spinal manipulation (16-18). Further, in the healthy patients we explored the plasma concen[ration of the neuroimmunomodularor substance
P (SP), and we investigated the in vitro production of tumor necrosis factor (TN F) by mononuclear cells, primari ly lymphocytes (16, 17) . Second, we applied forces similar to those associated with manipulation to PMN in vitro and measured the production of stress proteins. Stre s proteins, also known as heat shock proteins (HSP), are believed to be protective against a variety of stressors. They a re highly conserved genetically and are produced by every eukaryotic and prokaryotic organism studied (19). Third, in a small pilot study, we explored the hypothesis that spinal manipulation reduced both pain and plasma levels of prostaglandins, specifically, prostaglandin PGF2a , in women suffering from primary dysmenorrhea (20). PGF2• is believed to be the putative cause of primary dysmenorrhea. To study cells responsible for the adaptive immune response, we determined the number and function of natural killer (NK) cells and other lymphocyte subpopulations in asymptomatic subjects with a variety of complaintS presenting ro the ational College
14 Review 01 the Systenc: EIIectJ 01 BI*III MnUaUon Chiropractic Center, our mam clinic (21,22). Finally, we examined, as a secondary outcome,
lymphocyte subpopulations in patients enrolled in a randomized clinical trial of manipulative therapy for low-back pain of mechanical origin (23).
269
that patient; (2) a low-force, high-velocity, lowamplitude procedure (LFP ["sham"] ) delivered to a single level of the lumbar spine; or (3) a series of educational lectures regarding lower back pain, with no physical contact between physician and patient or exercise recommendations pro-
vided.
Methods
MeasII'tIII18II of MlDpulation Forcea
Settilg All treatment interventions were administered at rhe National College Chiropracric Clinic, a private outpatient chiropractic teaching clinic in the
suburban Chicago, Illinois, area.
spina l manipulation, using intended force magni -
interventions Treatment
The procedures used to measure the forces delivered to the thoracic spine have been described in detail elsewhere (16,24). Briefly, subjects were positioned on a specially constructed force table and were then treated up to six times each with
interventions
were
performed
by
licensed chiropractic physicians. For the studies involving the thoracic spine, manipulation was
delivered to the clinically relevant segment between Tl and T6 and consisted of a high-velocity, short-lever, low-amplitude thrust sufficient to produce an auditory release or palpable joint
tudes ranging from 0% to 100% in increments of 20%. Each manipulation was performed on separate days, with the magnitude delivered on any particular day assigned randomly.
OUtcome MeasIl'8S
low-velocity, light-force thrust to the selected segment. In the primary dysmenorrhea study, the
In those studies involving the collection of blood, the blood samples were collected by venipuncture in ethylendediaminetetra-acetic acid (EDTA) Vacutainer tubes Becton Dickinson, Rutherford, NJ . The blood was colleCted 15 minutes before
interventions were delivered with the subject
treatment and 15 minutes after treatment in the
placed in a side-lying position with the bottom leg straight and the top leg flexed at the knee and hip. Subjects who received manipulation received a high-velocity, short-lever, low-amplitude thrust to all clinically relevant vertebral levels within TIO and LS-Sl and the sacroiliac joints. Subjects who received a sham manipulation in this study were placed in a side· lying position with both hips and knees flexed. The manipulation consisted of a thrusr ro rhe midline base of the sacru m. In the randomized clinical trial of manipularive therapy for chronic low-back pain of
PMN, SP, and TNF studies. In the primaty dysmenorrhea srudy, the postintervention blood sample was collected 60 minutes after treatment because it takes that long for preexisting PGF'a to clear the circulation. Isolation of cells was performed within 30 minutes of collection over a modified Ficoll-Hypaque gradient as previously described (16). Plasma was separated by centrifugation and stored frozen at either -20°C or -70°C until assayed for the analyte of interest. Both SP and PGF'a are stable for at least a year when stOred frozen. We analyzed all samples within a month of collection. In the randomized clinical tria l, blood was collected at the initia l visit, ar the twelfth visit, and again after a 2-week, no-treatment follow-up period. Lymphocyte profi les were determined within 1 hour of collection of the blood sample.
movement. Sham manipulation consisted of a
mechanical
ongln,
patients
were
randomly
assigned to one of three intervention groups: (1) a high-force, high-velocity, low-amplitude manipulation procedure delivered to all levels of the spine between Tl2 and SI and including the sacroiliac joints that were clinically relevant for
270 Perceived abdominal and back pain were measured in the women with primary dysmenorrhea with a visual analogue scale, and the effect of menstrual distress on the activities of daily living was measured with the menstrual distress questionnaire (20). The respiratory burst (RB) of PMN was measured using the chemiluminescent (Cl) response to an in vitro challenge with a standardized suspension of opsonized zymosan. Endotoxin-stimulated TNF production by cultured mononuclear cells was determined in the culture supernatant solutions by a standard cytotoxicity assay using actinomycin D-treated 1929 mouse fibroblasts (6). Enumeration of lymphocyte subpopulations was performed using cell surface-specific mono· clonal antibodies labeled with fluorescent dyes and either conventional fluorescence microscopy or flow cytometry (22,25). Functional assessment
of NK cell activity was made with a standard slCr release cytotoxicity assay (25). The soluble factors measured in the plasma of subjects in these studies were the neuroim-
munomodulator SP and the prostaglandin PGF,. metabolite, 1S-keto-13,14-dihydro-prostaglandin F,. (KDPGF,.) . Substance P was determined by radioimmunoassay (RlA) using commercially available reagents after a petroleum ether extraction (16,30). KDPGF,. was determined in rhe women enrolled in the dysmenorrhea study by RlA as previously described (20). The in virro production of HSP by PMN in
Results and Discussion Polymorphonuclear cells isolated from apparently healthy subjects or from patients with diagnosed low-back pain of mechanical origin who receive a single spinal manipulation to the thoracic or the lumbar region of rhe spine are primed to respond to a particulate zymosan challenge with an enhanced RB as measured by CL. Results from a typical series of patients are shown in Figure 14· 1. The mean before versus aftcr treatment peak count~second/cell difference in response for cells from subjects receiving a thoracic spine manipu-
lation ranged from 2.2 to 2.9, depending on the srudy (16- J 8,26). The magnitude of rhe after versus before treatment enhancement of the RB was similar in PMN isolated from subjects who received a manipulation to the lumbar spine, ranging from 2.15 to 3.2 peak counts/second/cell (25,26). The P values for these data, based on paired students' t-tests, were consistently less
than .001. The force threshold for this response was found to lie somewhere between 450 and 500 N for the thoracic spine (24). Representative
Before treatment After treatment
response to manipulation forces was determined
by western blot analysis after exposure of the cells to a static pressure of approximately 200 pounds/square inch, which is equivalent to 1379 KiloPascals. For the western blot procedure, 10 III previously frozen PMN samples were loaded onto an 8% polyacrylamide mini-gel and subjected to electrophoresis. The proteins were then transferred to O.4S-llm nitrocellulose paper and incubated with a primary antibody specific for 70-kD HSP. This incubation was followed with a secondary biotinylated antibody. Bound antibody was detected using an avidin-horseradish-peroxiclase srain.
A1t1'114-1 Peak CL response of PMN isolared from peripheral blood obrained 15 minutes before and 15 minutes after each rrearmenr. Shown is the mean peak
response of all subjects % 2 standard error of the mean (SEM). (From Brennan PC, e/ al. Enhanced phagocytic cell respiratory burst mdllced by spinal manipulation: Potential role of substance P. J Mampulative Physlol Ther 1991; 14:399.)
14 Review of the Systemic Effects of SpkIaI ManIpulatIon
ftgIre 14-2 Representative manipulation force magnitudes of the manipulation procedure (upper curve) and sham procedure (lower curoe) are shown. For comparison, the rime has been shifted so both the
sham and the manipulation procedure are aligned. (From Brennan PC. et al. Enhanced phagocytic cell respIratory burst mduced by spmal mampuJatton: POlenttol role of substallce P. ) Mampulative Physiol Ther 1991; 14:399.)
manipulation force magnitudes for the manipula-
271
received a thoracic spine manipulation (Table 141), we found that there was approximately twice as much endotOxin-stimulated TNF produced by cells isolated afrer manipulation compared with the production by cells isolated before manipulation (17). Similarly, manipulation of the thoracic spine resulted in approximately a twofold increase in rhe concentration of plasma SP (Table 14-1). These results strongly suggest that spinal manipulation results in at least short-term priming of PMN for an enhanced RB and also a shortterm priming of mononuclear cells for enhanced production of the cytokine TNF. The fact that these priming effects are accompanied by modest but significantly increased plasma levels of the undecapeptide SP suggests that SP is functioning as a regulatory molecule in our subjects as opposed ro a mediaror of pain. Whether SP or TNF is the proximate priming agent for the enhanced RB of PMN is unclear. However, we suggest that there is a positive feedback loop between TNF, SP, and probably other cytokines as well.
tive versus the sham procedure are shown in Fig-
In a preliminary nonrandom trial to examine
ure J 4-2. The force threshold for this biologic response delivered to the lumbar spine is estimated at approximately 400 N (Triano, unpublished). When we examined the in vitro endotoxin-stimulated production of TNF by mononuclear cells isolated from subjects who had
the number and percentage of T cells, B cells, and NK cells using conventional fluorescence microscopy, there was no statistically significant difference between patients and asymptomatic control subjects in percentage of lymphocytes, or in percentage of T and B cells (22). Neither was
SP, TNF, and CL 15 Minutes Before and 15 Minutes After Spinal Manipulation
TIm.
Before
SP(n _ 21) (pmoln plasm.)
29.8
±
TNF (n = 26) (pg/mI/1O' cells)
Cl (n- 26) (countlSec/cell)
15.3
810.6
±
595.5
2.8
±
1.2
42.0'
1309.4
±
766.81
5.0
±
1.8t
treatment
After
52.0
±
treatment Values arc (he mean :I: SO. · Paired srudem's t before versus afrer = 2.913; P = .009 tl)aircd srudems t hefore versus afrer = 3.615; P = .001 :t:Palrcd students (before versus lifter =5.715; P =.000 From Brennan PC et al. Enhanced phag<x:yric cell resplrarory hurst induced by spinal manipulation: POtential role of substance P. J Manipulative Physiol Ther 1991; 14:399.
272
Flow Cytometric Analysis of Lymphocyte Subpopulations in a Nonrandom Sample of Patients and Asymptomatic Control Subjects
Pe .. ent Lymphocyte Subpopulatlon
Asymptoma tic controls
Patients Shown
IS
Total T
TH
Ts
NK
Tot,l B
85.7±1 .8 83.9 ± 4.1
47.2 ± 3.3 46.9 ± 4.1
25.3 ± 2.5 29.2 ± 4.8
14.9 ± 2.3 8.6 ± 1.6
12.8 ± 3.1 13.9 ± 2.4
(he mean:!: 2 standard error of the mean (SEM) .
there a difference in the absolute numbers of these cells. However, the mean percentage of NK cells in patients was significantly less than the percentage of NK cells in controls (unpaired t = 4.35; P = .000). The absolute number of NK cells was also significantly lower in patients than in asymptomatic subjects (unpaired t = 2.62; P = 0.011). Using sensitive flow cytometric techniques, we verified these findings (21). Table 14-2 shows flow cytometric results from this study. Although both the percentage and absolute numbers of NK cells were lower in patients presencing to our main clinic, the functional ability of NK cells as determined in a cytotoxicity assay did not differ between the twO groups in this study (Table 14-3). In a recently completed trial of manipulation for the treatment of chronic lowback pain of mechanical origin in 209 patients, the mean percentage of NK cells before any treatment was administered was 9.1 ± 0.84 (23). This compares favorably with the data presented in Table 14-2 and is less than the published minimum critical values for this lymphocyte subset in healthy adults (27). The results of this study are the first that examine lymphocyte profiles in patients with diagnosed low-back pain using flow cytometric analytic methods to quantitate cells. Table 14-4 shows the mean percentage of each lymphocyte subpopulation for each intervention at the three sample times, and Table 14-5 displays the mean absolute number of each cell type. The appropriate method for determining whether there were treatment differences over time is the test of significant treatment-rime inreractions in
the context of a repeated measures analysis of variance. As shown in Table 14-6, the cell rypes for which the interaction tests were at or near sta-
tistical significance are: TH counts: P = .0208; total T cell percentage: P = .0928; and total T cell counts: P = .0908. Interaction tests for differences in either percent or absolute counts of B cells, TS cells, NK cells, or cells bearing both the NK and TS marker were not statistically significant (Table J 4-6). Thus, we failed to demonstrate dramatic effects of spinal manipulation on several immune cell subsets. However, these negative results must be interpreted in the light of some methodologic issues. Lymphocyte profiles were not the primary outcomes in this trial, and medication usage was restricted only if it was intended to relieve the symptoms associated with low-back pain. Detailed histories of the use of medications, such
Functional ability of NK cells in a Nonrandom Sample of Patients and Asymptomatic Control Subjects Pe ..ent NK Cell Cytotoxicity lor K5li2 Target Cells' Effector. Target Ratio EHector: Target Ralio
6.25:1
25:1
Asym ptomatic controls Patients ·Shown is (ht mean
7.4
43.1 ± 7.6
63 .8 ± 10.4
48 .8 ± 9.4
66.0
%
±
2 standard error of Ihe mean (SEM).
14 Review of Ibe SyltenK EIIIICtJ
0' SpiIaI ManIpulatIon
273
Mean (Standard Deviation) Percent of Lymphocyte Subpopulations in the Total Lymphocyte Pool at the lnitial Visit, Fin al Treatment Session (12th Visit), and After a Two-Week No Treatment lnterval (Follow-Up) Treatment
Cell Type
M,nlpul,lIon
lFp·
lecture Series
Toral T cells
54 81.4 (5.2) 82.5 (4.9) 82.0 (4.8) 53 50.6 (7.4) 51.0 (8.8) 51.3 (7.5) 53 23.4 (5.9) 23.2 (6.4) 23.5 (6.2) 53 9.3 (5.7) 9.4 (5.6) 8.8 (4.6) 53 3.5 (2.7) 3.6 (2.6) 3.3 (2.4) 54 15.5 (4.7) 15.4 (5 .1) 15.1 (4.5)
46 82.1 (4.6) 82.9 (4.0) 83 .2 (4.2) 45 50.6 (7.7) 51.1 (7.0) 50.9 (8.0) 45 23.5 (6.3) 23 .6 (5.0) 23 .7 (5.4) 45 8.4 (3.5) 8.9 (4.7) 9.0 (5.2) 44 3.0 (1.4) 3.2 (1.8) 3.2 (2.0) 46 15.1 (5.0) 13.9 (4.3) 14.0 (4.5)
48 83.0 (5.6) 83.0 (5.5) 83.0 (6.0) 48 47.8 (5.6) 48.6 (6.0) 48.4 (6.0) 48 25.4 (5.2) 25. 1 (5.2) 25.5 (5.5) 48 9.2 (5.1) 8.6 (5.8) 8.9 (5.2) 41 3.5 (2.0) 3.4 (2.4) 3.3 (2.2) 48 16.1 (8.4) 14.9 (6.2) 14.5 (5 .6)
n Initial 12th visit Follow-up TH cells n Initial 12th visit Follow-up Ts cells n Initial 12th visit Follow-up NK cells n Initial 12th visit Follow-up TsNK cells n Initial 12th visit Follow-up B cells n Initial 12th visit Follow-Up
• Low-fon.:c. high-velocity, low-amplitude procedure. From Brennan PC, et 31.: Lymphocyte profiles In pariems with chromc low back pain enrolled
In
a clmical trial. J Mampula-
rivePhysiolThcr 1994; 17:219-227.
as drugs for depression (psychoactive drugs) or drugs with cyclooxygenase-inhibiting activity (such as over-the-counter cold medications), were not obtained from these patients. Both classes of drugs can influence levels of leukotrienes and prostaglandins, and these, in turn, can either upregulate or downregulate the immune system,
depending on their concentration (28). Thus, potential confounding by medications cannOt be
assessed in this study. A second limitation may be the time frame over which the interventions were administered. All treatments were given over a 2-
week period, with the follow-up evaluation 2 weeks later. In the immune system, there is continuous renewal and selection of immunocompe-
tent cells, and the total number of cells is under strict control. Each newly produced lymphocyte can establish itself only on loss of other cells, and
274
The Subluxadon Complex
Mean (Standard Deviation) Absolute Numbers of Each Lymphocyte SubpopulationfJlL in the Total Lymphocyte Pool at the Initial Visit, Final Treatment Session (12th Visit) and after a Two-Week No-Treatment Interval (Follow-Up) -
,.' ~~
-
'.
'.. -.'
.-J..I;......~
.~!....~. III
'2
~
.•
=-11
Treatment Cen Type
Total T cells
n Initial 12th visit Follow-up TH cells n Initial 12th visit Follow-up Ts cells n Initial 12th visit Follow-up NK cells n Initial 12th visit Follow-up TsNK cells n Initial 12th visit Follow-up B cells n Initial 12th visit Follow-up
Manipulation
54 2068 (685) 1969 (724) 2078 (1016) 53 1247 (379) 1184 (442) 1289 (670) 53 585 (237) 549(266) 588 (379) 53 223 (142) 211 (132) 213 (126) 53 85 (70) 83 (70) 82 (66) 54 413 (232) 385 (243) 413 (339)
LFP" 46 2197 (919) 2173 (861) 1930 (554) 45 1351 (613) 1336 (598) 1174 (406) 45 620 (313) 610 (281) 545 (204) 45 211 (108) 224 (133) 205 (119) 44 78 (48) 85 (57) 77 (54) 46 409 (224) 365 (169) 335 (161)
lecture Series 48 2051 (640) 1936 (636) 1890 (540) 48 1192 (429) 1151 (442) 1113 (374) 48 629 (246) 584 (224) 579 (208) 48 223 (137) 198 (133) 202 (123) 41 84 (53) 77 (56) 77 (55) 48 390(242) 371 (248) 351 (223)
• Low-force, high-velocity, low-amplitude procedure. From Brennan PC, er al. Lymphocyte profiles in patienrs with chronic low back pain enrolled in a clinical rrial.
J Manipula-
tive Physiol Thcr 1994; 17:219-227.
that new cell then has to compete with other newly produced or resident cells for survival. In such a dynamic system, it takes time to establish sufficient numbers of new cells to be detected as differences in either percentages or absolute numbers. In short, we simply may nOt have treated these patients over a long enough time frame or followed them long enough to derect changes in
lymphocyte profiles. A third limitation of this study is that we were not able to couple our determination of lymphocyte profiles with a functional assessment of either NK cells or any other lymphocyte subset. The design of the trial allowed for sporadic entry of patients inro the trial. FUllc-
tional assays for NK cells require target cells labeled with SICr, and it was not economically
14 Review 01l1li SyUllle BIIctJ 01 SpInal MInIIUItIOn
Repeated Measures Analysis of Variance Tests for Treatment-Time Interaction Cell Type
Val.e
Total T cells Counts Percent
TH cells Counts Percent
0.0908 0.0928 0.0208 0.9468
Ts cells CountS Percent
NK cells Counts Percent Ts/NK cells Counts Percent B cells Counts Percent
0.2075 0.9723 0.5473 0.3196 0.7231 0.3547 0.1459 0.4394
From Brennan PC. et al. Lymphocyte profiles in patients with chronic low back pain enrolled in a clinical trial. JManipulative Physiol Ther 1994; 17:219·227.
nor rechnically feasible to prepare such cells daily when we did not know if a new parient would be entering the trial. Similarly, assays for T or B cell function require considerable preplanning. Therefore, the assessment of functional ability of T cells, B cells, and NK cells in patients with chronic low-back pain awairs further srudies. In our published pilot study of women with primary dysmenorrhea treated with spinal manipulation (20), we found that the perception of pain and the level of menstrual distress were significantly reduced by spinal manipulative therapy 60 minutes after administration of the intervention (Table 14-7). For perceived abdominal pain, there was a statistically significant difference berween the preimervention and postintervention scores of
rhe rwo groups, with the sham trearment group
275
having higher postintervention scores (F = 5.92; P = .019). Similarly, there was a significant differ-
ence berween groups for the menstrual distress scores. The group receiving sham treatment had higher postintervention scores (F = 9.97; P = .003). Interestingly, regardless of treatment, the plasma KDPGF,. levels significantly declined after intervention, and overall, the differences berween plasma levels of KDPGF,. were statistically significant (I = 3.276; P = .002). However, the sham treatment group and the manipulation group were not significantly different from one another (Table 14-8). The data reported in this small pilot study suggest that spinal manipulative rherapy is effective in relieving the perception of pain and menstrual distress in women with primary dysmenorrhea, at least for a short time after treatment. The data further demonstrate that this reduction in pain is accompanied by a reduction
in PGF,•. The reduction in PGF,. in the group that received sham treatment was not altogether
unexpected. A similar placebo effect on prostaglandin levels has been reported in trials of pharmacologic agents for primary dysmenorrhea (29). Ir is also possible that manipulation effects other mediators of the pain associated with primary dysmenorrhea such as circulating vasopressin or leukotrienes. Nevertheless, whatever the mechanisms at work in this study, it is clear that spinal manipulation and possibly the spinal mobilization used for the sham procedure affect plasma prostaglandin levels 60 minutes after treatment. A trial conducted over several menstrual cycles is in progress and is expected to resolve some of the questions raised by the pilot study. Finally, Kokjohn previously reported that PMN subjected to an in vitro pressure force similar to forces achieved during a spinal manipulation did nOt manifest rhe Stress response with the production of HSP (19). Slight modificatio~s resulting in improvement in the western blot technique used in our laboratory have clearly demonstrated that PMN do produce a 70-kD HSP when subjected to a force of 680 N pressure. Heat shock (45°C water bath for 60 minutes) produces
276
>
Pretreatment and Posttreatment Means and Mean Differences in Pain and Menstrual Distress Scores .'
Outcome Measure
and Inte .. enllon Abdomina l pain' SM (n; 23) Sham (n; 21)
" . ... t..
..':"'~.~ t9.,~
'.
#_-
,
~ _~~
.
••~
_
Pretreatment
Posttreatment
Mean
Means
Means
Dlneron.lS
SO
5.87 6.00
3.78 5.19
2.09 0.81
2.30 1.50
4.83 5.21
2.96 4.43
1.87 0.78
1.94 1.57
44.22 47.86
25.17 37.57
19.05 10.29
15.36 11.27
,
Back pain·
SM Sham Menstrual distress t SM Sham
SD, sta ndard deviation; SM, spinal manipulation · '0 en VAS; 0 = no pain t MDQ; 0 = no distress Modified (rom Kokjohn K, et al. The eHeer of 5 31 manipulation on pain and prostaglandin levels in women with primary dysmenorrhea. J Manipulative Physiol Ther 195 . 15,279.
a simi lar 70-kD HSP. Control cells incubated at 37°C do not produce a band corresponding to the 70-kD marker protein. The extent to whi: h HSP are produced in response to the more dynamic thrust of a spinal manipulation is unknow '. We believe that the resulrs summari I here and reported in detai l in the publicatit cited support the hypothesis that spinal mam ,Iation evokes short-term system ic effects. They are a beginning, but they are only a beginning. As in
most resea rch, the questions raised by the results are rn o re numerous than the answers the research
provides. To name but a few of these questions, we know that there is a shorr-term reduction in perceived pain in women with primary dysmenor-
rhea afte r manipulative therapy; we do not yet know if this persists through successive menstrual cycles. We do not know if the placebo effect of sham manipulation on plasma KDPGF'a disappears in succeeding menstrual cycles, as it does
>
Pretreatment and Posttreatment Means and Mean Differences in Plasma VT\o.~r Pretreatment Means
Posttreatment Me.ns
Spinal manipulation (n; 20)
133.86
Sham manipulation
142.82
Treatment
Mean
116.18
Dlneronco. 17.68
SO 32.253
126.27
16.55
33.948
(n; 19) SD, srandard deviation. From Kokjohn K, et al. The effect of spinal manipulation on pain and prostaglandin levels in women with primary dysmenorrhea. J Manipulative Physiol Thcr 1992; 15:279.
277 with pharmacologic placebos. We do not know if women who receive spinal manipulation experience a diminution of their pain as treatment progresses. We do not know if the function of NK cells changes with manipulative therapy. We do not know the biologic significance of HSP or if they are actually produced by circulating PMN in vivo. We have no idea about the relationship of a variety of cytokines such as TNF, or neuroimmunomodulators such as SP and the RB of PMN, in patients with musculoskeletal conditions. It is hoped that studies planned or in progress will address these issues.
Acknowledgments The work summarized in this chapter was supported by The National College of Chiropractic, by grants from the Foundation for Chiropractic Research and by a restricted grant to the Foundation for Chiropractic Education and Research made possible by the Foundation for the Advancement of Chiropracric Education. I am indebted to all of my colleagues in the Research Department of The National College of Chiropractic who have been involved in the studies summarized in this chapter. Most of their names appear in the Reference section of this paper. lowe a special thanks, however, to Drs. Hondras and Kokjohn, and Ms. Graham, without whom this work would not have been possible.
References t. Sackett OL, Haynes RB, Guyatt GH, Tugwell P. In: Clini-
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5.
ca l epidemiology: A basIc science for clinical medicine. 2nd ed. Toronto, Omario: Lietle, Brown, and Company, 1991. Seal Me. Viscerosomaric reflexes: A review. J Am Osteopath Assoc 1985; 85:786-801. Johnston RJ. Vertebrogenic autonomic dysfuncrionsubjective symptoms: A prospective study. J Can Chiro Assoc 1981; 25,51-7. Kerr 1M. Somatic dysfunction, osteopathic manipulative treatment, and the nervous system: A few facts, some theories, many questions. J Am Osteopath Assoc 1986; 86,109-14.1986. Korr 1M. The spinal cord as organizer of disease processes. II. The peripheral autonomic nervous system. J Am Osteopath Assoc 1979; 79,82-90.
6. Korr 1M . The spinal cord as organizer of disease processes. Ill. Hyperactivity of sympathetic innervation as a common factor in disease. J Am Osteopath Assoc 1979; 79,232-9. 7. Korr 1M. The spinal cord as organizer of disease processes: Some preliminary perspectives. J Am Osteopath Assoc 1976; 76,35-45. 8. Sara A, Swenson RS. Sympathetic nervous system response to mechanicalsrress of the spinal column in rats. J Manipulative Physiol Ther 1984; 7: 141-7. 9. DeBoer KF, Schutz M, McKnight ME. Acute effects of spinal manipuladon on gastrointestinal myoelectric activIty in conscious rabbits. Manual Med 1988; 3:85-94. 10. Deloof S, Bennis M , Rousseau JP. Inhibition of amral and pyloric electrical activity by vagal afferent stimulation in the rabbit. J Auton Nerv Sys 1987; 19:13-20. II. Vernon HT, et al. Spinal manipulation and betaendorphin: A controlled study of the effect of spinal manipulation on plasma beta-endorphin levels in normal males. J Manipulative Physiol Ther 1986; 9: 11 5-23. 12. Christian GF, et al. Immunoreactive AcrH, p-endorphin and cortisol levels in plasma following spinal manipubrive therapy. Spine 1988; 13:1411-7. 13. Leach RA. The chiropractic theories. 2nd cd. Baltimore: Williams & Wilkins, 1986. 14. Spector NH. Anatomic and physiologic connections between the central nervous and the immune systems. In: Research Forum. Davenport, Iowa: Palmer College of Chiropractic, 1987. 15. Vora GS, Bates HA. The effects of spinal manipulation on the immune sysrem (a preliminary report). 1980; ACA J Chiro 1405103-5. 16. Brennan PC, et al. Enhanced phagocytic cell respiratory burst induced by spinal manipulation: Potential role of substance P. J Manipulative Physiol Ther 1991; 14,399-408. 17. Brennan PC, et al. Enhanced neutrophil respIratory burst as a biological marker for manipulation forces: Duration of the effect and association with substance P and rumor necrosis factor. J Manipulative Physiol Ther 1992; 15:83-9. 18. Brennan PC, Hondras MA. Priming of neutrophils for enhanced respiratory burst by manipulation of the thoracic spine. In: Wolk S, ed. Proceedings of the 1989 International Conference on Spinal Manipulation. Washington, D.C., March 31-Aprill, 1989. Foundation for Chiropractic Education and Research, Arlmgton, Virginia, 160-3. 19. Kokjohn K, er al. In vitro stress response of PMN to manipulation forces. In : Callahan 0, ed. Proceedings of the 19921nternarional Conference on Spinal Manipulation, May 15-1 7, 1992, Chicago, Illinois. Foundation for Chiropractic Education and Research, Arlington, Virginia, 123-4. 20. Kokiohn K, et al. The effect of spmal manipulation on pain and prostaglandin levels in women with primary
278
2 J.
22.
23.
24.
dysmenorrhea. J Manipulative Physiol Ther 1992; 15,279-85. Graham MA, Brennan PC. functional ability of natural killer cells as an outcome measure for chiropractic treat· Olem efficacy. In: Walk Sj ed. Proceedings of the 1991 Lnrernariona l Conference on Spinal Manipulation, Arlington, Virginia, April 12-13, 1991. Foundation for C hiropractic Education and Research. 84-6. Lohr GE, et al. Natural killer cells as an outcome measure o f chiropractic treatment efficacy. In; Walk 5, ed. Proceedings of the 1990 International Conference on Spinal Manipulation, May t 1-12, 1990, Washington, D.C. Foundation for Chi ropractic Education and Research; 17,2 19-227, 109- 12. Brennan PC, et al. lymphocyte profiles in patients with chronic low back pain enrolled in a clinical trial. J Manipulative Physiol Ther 1994. Triano Jj, Brennan PC, McGregor M. A study of threshold response lO thoracic manipulation. In: Wolk S. ed. Proceedings of the 1991 International Conference on Spinal Manipulation, Arlington, Virginia, April 12-13, 1991 . Foundation for Chi ropractic Education and Research, Arlingron, Virginia, 150-2.
25. McGregor M, Brennan PC, Triano JJ. Immunologic response to manipu lation of the lumbar spine. 1n: Wolk S. ed. Proceedings of the 199 1 Interna tiona l Conference on Spinal Manipulation. Arlington, Virginia, April 12-13, t 991 . Foundation for Chiropractic Education and Research, Arlington, Virginia, 153-5. 26. Brennan PC, et al. Qualiry control in a randomized clinical trial using cellular chemiluminescence. In: Ca llahan D, ed. Proceedings of the 1992 International Conference on Spinal Manipulation, May 15-1 7, 1992, Chicago, Illinois. Foundation for Chiropractic Education and Research, Arlington, Virginia, 125. 27. Reichert T, et al. Lymphocyte subset reference ranges in adult Caucasians. Clin lmmunol lmmunopathol 199 1; 60,190-208. 28. Phipps RP, Stein SH, Roper RL. A new view of prostaglandin E regulation of the immune response. lmmunol Today 1991 ; 12,349-5 1. 29. Fedele L, et al. Dynamics and signifi cance of placebo response in primary dysmenorrhea. Pain 1989; 36:43-47. 30. Arimura A, et al. Radioimmunoassay of somalOsta tin. Metabolism Suppl 1978; 27:1139-42.
Spinal Cord Mechanisms 01 Relerred Pain and Related Neuroplasticity RIchard G. Gillette KeyWords
Convergence-projection, supersegmental, convergence, neuroplasticity, central sensitization, facilitated state, long-term potentiation, phasic inhibitory control, tonic inhibitory control
After reading this chapter yo" should be able to answer the following questions:
Question #1
What is the contribution of central neuronal plasticity and referred pain?
QuesUon #2
What mechanism may account for on-going back pain independent of proprioceptive afferent input from the periphery?
QuesUon #3
By what mechanism can spinal manipulation inhibit low-back pain?
280
The Uluxatlon Complex
I. Referred pain and hyperalgesia from deep tissue damage
A. Skin versus deep tissue pam B. Axial versus extremity deep tissue pain
II. Clinical phenomenology of referred low back pain A. Clinical presentation B. Where is the pain coming from? Ill. Neurobiologic explanations of referred pam
A. Peripheral axon-reflex explanation B. Convergence-projection explanation C. Suprasegmenral convergence explanation IV. Neurophysiologic evidence for central convergence
A. Single-neuron recording evidence B. Clinical implications V. The contribution of central neuroplasticity to referred back pain and hyperalgesia A. Pain referral and spinal plasticity B. Nociception-triggered "central sensitization" C. Clinical implications VI. Sympathetic nervous system and low back pain A. Single-neuron recording evidence B. Clinical implications VII. Neurophysiology of paraspinal antinociceptive mechanisms A. " Phasic" inhibitory controls B. "Tonic" inhibitory controls
C. Clinical implications VIII. Recapitulation and conclusions
Pain Referral from Deep Tissue Injury Most clinically significant pains are rriggered by damage to deep somatic and visceral tissues. For
many years clinicians have observed thar when tissues lying deep to the skin are injured,
spinal cord segment as that innervating the damaged srructure (isosegmental convergence); however, the painful region often expands or spreads (radiation of pain) ro tissue areas served by other adjacent spinal segments (1-4,7). This dynamic change in the perceived area of pain is usually triggered by continued or recurrent
injury of the original site of deep tissue damage ( 1-4). The patient with deep tissue referred pain also has difficulty locating the source(s) of his or her pain, which cOntrasts with a skin injury, in which the patient seldom if ever mislocates the source of the pain (1,3,4). As a general rule, the deeper and the more proximal the damaged structure, the greater the degree of pain mislocation by the patient (2-4). Referred pain also arises rapidly and becomes maximal in only a few minutes after deep somatic or visceral tissue injury and may
last from hours to days in normal individuals (1,2) or for much longer periods (weeks, months, years) in symptomatic patients (1-4). Besides being difficult to localize, pains of deep somatic or visceral origin have a dull aching quality and are often associated with tissue tenderness that results in exaggerated painful sensation on palpatory stimulation (called referred tellderness or hyperalgesia) (1-3). This referred tenderness, felt locally in the area of injury, can be provoked also in the area of referral where the tissues are normal. Interestingly, local anesthetic injections into the referral area blocks the referred hyperalgesia but not the local tenderness, whereas injections into the area of deep injury block both the local and the referred tenderness (2-4). These findings suggest that painful input from the damaged deep tissues is crucial for the producrion and elaboration of both the local and the referred hyperalgesia. Because deep referred pains are poorly localized by the patient, it is difficulr for the anending
inflamed, or diseased, the patient reports that nor
physician to diagnose the exact source and cause
only is the local area of damage painful but sur-
of the patient'S problem. This is especially so when there is deep tissue damage of axial structures like the back (or head), but it is seldom a problem in the case of an extremity injury like a sprained ankle (l,2).
rounding and sometimes distant uninjured areas
are also painful; this phenomenon is called pain referral (1-6). Referred pains are ofren felt in, or referred to, structures innervated
by the same
281 Because of the importance of the symptom of referred back pain and its alleviation in clinical chiropractic practice, and because of the recent appearance of uniquely new findings on the lumbar spine pain-signaling system (8-13), this chapter focuses on the neurophysiologic correlates of lumbar spinal pain and referral.
Clinical Phenomenology of Pain Originating from the Lumbar Spine Commonly, chiropractic physicians are asked to help patients whose primary complaint is back pain and, more specifically, low-back pain (Figure 15-1) (14). The crucial initial clinical question for determining diagnosis and subsequent treatment is, "Where is the pain coming from?" Traditionally, the back pain is assumed in most instances to arise from previous or ongoing injury or disease of lumbar "motion-segment structures" such as facet (zygapophysial) joints, muscles,
ligaments, intervertebral discs, bone or periosteum, meninges (dura), and associated vascular elements (2,4,1-23) (also see Chapter 2).
Indeed, numerous clinical investigations have shown that all of these spinal tissues, when appropriately stimulated, can give rise to generalized low-back and referred leg pain (called referred or l/ol/radlCular pain) in normal or symptomatic individuals, and local anesthetic blockage of these same Structures or their neural innervations can eliminate such pain (2,4,15,1720,22,24,25). Typically, the pain arising from these structures is poorly localized to the lowback and hip region bilaterally and is reported as having an aching quality felt deep to the skin surface (Figure 15-1 A). In addition, associated abnormal skin sensations are sometimes reported, including hyperalgesia to mechanical and thermal stimuli (2,25,26). In addition to these features, the low-back pain patient frequently reports that the pain spreads (radiates) from the back into the hip and leg as the condition continues to worsen (Figure 15-18) (2,15,17,19,21-24). The radiating leg pain is often called sciatica (2,19,22,23) and
should be clinically distinguished from the superficially localized "electric shock-like" leg and foot pain arising from segmental nerve rOOt compression (ca lled true radicular pail/) (19,23). Radicular and nonradicular (referred) leg pain are currently believed to arise from quite different pathophysiologic processes (1,2,19,23).
Explanatory Hypotheses Neurobiologic explanations of referred pain have historically rested on either some anatomic feature of the peripheral innervation, on some organizational feature of the spinal cord, or on some process occurring in the brain (Figure 15-2). The clearest formulation of a peripheral explanatory hypothesis of pain referral was that of Sinclair and colleagues published some decades ago (Figure 15-2A) (6) . They speculated that: .. . the factor in the production of referred pain is the existence of branching among the sensory pathways conveying the sensation of pain. This branching is of such a rype that one limb of a branched axon passes to the site of origin of the disturbance and the other passes to the sites to which the palO is referred (axon reflex). This mechanism works in twO ways: first by leading to a misinterpretation by the central nervous system of the true origin of the pain impulses and secondly by the liberation of metabolites at the terminals in the region where the referred pain is experienced, thus giving rise to secondary pain impulses actually having origin at the
periphery (6) . Evidence suggests that this explanation is inadequate for pain referral in general and referred lumbar pain in particular for at least three reasons. First, the patient'S report of the location of the back pain usually involves widespread areas of the back, hip, and legs that are served by completely separate and nonoverlapping peripheral neural innervations (16,18,19,23). Second, the peripheral branching of somatosensory pain afferents with one branch in back tissues and the other branch innervating the hip or leg is yet to be confirmed experimentally (1,27). Third, and mOSt importantly, this rype of "stacic" anatomic explanation cannot account for the consistent
282
The SubluxaUon Complex
J
A
~
B
figure 15-1 Referred (nonradicular) pain panern for the lumbar spine. A, Diagram illustrating area (stippled region) of perceived low back pain resulting from low back "'motion-segment" tissue (for example, facet joint or disc) damage. B, Same patient some days later, showing enlargemem of pain area and "radiation" of pain into the hip and proximal thigh caused by rein jury of the back. BOth depictions are derived from numerous clinical studies in humans.
283 Brain
Dorsal harn
Ascending
systems
Periphery
Theory
_____-----10P-
"Referred" _ LBP «
.
Leg
"Referred" LBP
_Oy----BaCk
+ « --
.
~Leg ).----'9___
Back
"Referred" LBP
Sinclair et 01.
B Convergence
projection
Ruch
C
Psychologic Theobald
) A111'115-2
A Axon reRex
9
Leg
Summary diagram il1ustraring three "classic" neurophysiologic explanations of referred pain. See text
for details. clinical observation that these pains are "dynamic," that the painful area grows in size
and later Kellgren (19) suggested that there must be an underlying popu lation of pain-signaling
and spreads into uninjured tissue regions (for example, hip and leg) served by other spinal segmeocs as the condition worsens or is exacerbated by reinjury (Figure 15-1B) (2,7,15,17,22,23) . All of these considerations argue against the periph-
the clinically relevant deep spinal sources. Moreover, they argued that when these neurons are driven to activity by painful (nociceptive) injury
era l axon reflex mechanism as an exp lanarion for
referred deep tissue pains in general and low-back pain in particular. If peripheral innervation is unable to explain the clinical symptomology, then where do we go to find a more satisfactory explanation? An obvious place to look is within the central nervous system itself. Because of the uniformity of the pain pattern produced by provocative stimulation of lumbar paraspina l structures, Livi ngston (4),
neurons that receive convergent input from all of
messages coming from any injured spinal tissue,
the brain interprets the projected impulse activity of these cells to mean that pain is originating from all of the tissue areas having potentia l connections with these neurons, and so the pain is "referred" to a much larger region than the actual area of injury. This idea, ca lled the convergence-projection theory of pain referral (Figure 15-2B), had originally been suggested by Ruch (5) to explain pain referra l of viscera l disease to somatic tissues of the body. Even though ample
284 neurophysiologic evidence supporting somatovisceral convergence-projection at the spinal cord level has appeared in recent years (1,7,28), a
that is, within the "receptive field" of the cell. Recall that a neuron's receptive field is that area of tissue within which peripheral stimulation
search for somatosomaric convergence in pain-
causes the neuron to generate an action potential, that is, the neuron receives information from that
signaling neurons serving the vertebral column has never been attempted until recently. A consideration of these issues prompted experiments in
animals (rats and cats) to see if spinal cord neurons could be found that show convergence of nociceptive input from the low-back, hip, and leg region, as originally suggested by Kellgren (19) and others (2,4,18,22). This evidence is discussed in detail in the next sections of this chapter. Finally, Theobald (29) many years ago postulated that deep tissue pain and referral might result from the processing of neuronal impulse traffic from the damaged and referral territories only at psychological (that is, suprasegmental) levels (Figure 15-2C). This possibility has received only limited experimental analysis, yet there is no question now that single nerve cells in
the somatosensory thalamus and neocortex show the requisite evidence of interaction of peripheral inputs. However, the available evidence relates only to somatic tissues of the extremities (30). Because nothing is known about how suprasegmental regions of the somatosensory pathway process pain input from the vertebral column, our
appraisal of the neurobiologic evidence related to referred low-back pain is restricted to that obtained at the spinal cord level.
Neurophysiologic Evidence lor Central Convergence-ProjecUon Lo
OUf
initial experiments, we have recorded from
individual somatosensory neurons within the
spinal cord that respond to tissue damage in the low-back region, neurons likely to mediate lowback pain (8,10,11). We found that most of these "low-back," pain-signaling neurons, located exclusively in the lateral dorsal horn of the lumbar cord (Figure 15-3), were responsive to noxious, damaging stimuli applied to many different tissues of the low-back, hip, and proximal leg;
tissue (1,7). Because of the remarkable input convergence to these cells from multiple back and hindlimb tissues, we now refer to these neurons as "hyperconvergenr" low-back pain neurons
(hereafter, "low-back neurons"). Individual low-back neurons were found to be either responsive to noxious and non noxious stimulation (mulrireceprive or wide-dynamic-
range [WDR) neurons, 77%) or noxious stimulation only (high-threshold or nociceptive-specific [NS) neurons, 23%) of paraspinal muscles, ligaments, discs, periosteum, facet joints, dura, and
skin as well as tissues of the hip and leg (Figures 15-3 and 15-4). Evidence strongly suggests that WDR neurons are responsible for the generation of subjective pain in humans and NS units appear not to contribute to this sensation (7). In addition, all of the WDR and NS neurons that we examined were found to be more powerfully activated by nociceptive input from deep tissues than from skin, which we believe may explain why back pain is felt to originate from deep rather than superficial tissues. We have also established that some of the recorded neurons (for example, units shown in Figures 15-3, 15-4, 15-8, 15-10) project axons into well-recognized ascending pain
pathways (for example, the spinothalamic, spinoreticular, and spinocervical tracts) (8). The low-back neurons we examined also had very large, hyperconvergent receptive fields in the low-back and proximal leg that included both skin and deep somatic tissues innervated through both the dorsal (back/hip) and ventral (leg/ventral spine) primary rami (Figure 15-3). The finding that low-back neurons respond to damage of many paraspinal structures implies that damage to any deep lumbar tissue probably produces the same or similar pain and may partially explain why it is often difficult to identify a specific cause of low-back pain (15,19,20,21,23,25). It had been shown in earlier studies that analogous
285 Convergent Neuron 50~---,~----------------------------.
Unitary recording
Time (sec)
t
500
L4 •
Brush-press-pinch
o Skin pinch only [J Deep pinch 50.-----------~--------r-------------__.
O~~~~~~~~~~
o
• • •
300 Time (sec) Press Pinch Rgere Hi-3 Recordings from a representa tive "hyperconvergenr" (WDR ) low back neuron located in laminae II of the lateral dorsa l horn of the L4 spinal cord {spinal cross-section at left}. Response hisrograms reflect number of action potentials/unit of time. Stippled areas show locations of deep receptive fields; the shaded area denotes the cutaneous receptive field. Note that the unit was modestly responsive (lower hisrogram ) to innocuous (brush, press ) mechanical stimulation but morc responsive to nox ious (pinch) stimulation of skin receptive field-the "classic WDR response .... Neuron was maximally responsive (upper histogram ) ro noxious mechanical (dry needling) and chemica l (hyperronic-6% NaCI) stimulation within the deep paraspinal receptive field. (From Gillette, Kramis, and Roberts, unpublished data.)
Brush
spinal neurons serving the limbs are responsive to sensory inputs from fewer individual tissues over very small areas, often JUSt from skin (1,7,11,31), making diagnosis of an origin of pain in a limb much easier than for the low-back. Finally, these neuronal response properties, especially the "hyperconvergence" from multiple
back and leg tissues (Figure 15-5), march rhe requisite features of the convergence-projection explanation of pain referral originally proposed by Ruch (5) and Kellgren (19). We discuss in the following section whether central convergence is sufficient ro account for referred low-back pain and hyperalgesia.
286
1118 SUbUlIIlon Complex WDR neuron: effect of hypertonic saline Preolgogen
40
Brush
Press
Pinch
Algogen
-N11e "'--- Inject 6% soline
n.re 16-4
•
----P-os-tO-19-og-en----~'A
50 sec/div
Neuropiasric changes in a low-back neuron after noxious stimu lus-induced ce ntral sensitization. Top (prea lgogen) histogram illustrates baseline response to innocuous brush, press, and noxious pinch stimulation app li ed at dot location in the unit's receptive field shown at right. Middle hiscogram shows neuron's response to injeccion of noxious, hypertonic (6%) saline into a lumbar facet joint (a rrow) that produces long-lasting ongoing discharge in the unit, and sensi ti zation of the cell to subsequent mechanical stimulation (lower, posralgogen histogram) while enlarging the receptive field (co mpare upper and lower RFs). (From eillette, Kram;s, and Roberts, unpublished data.)
Central sensitization • Ca2+ PKC
.IEG:c-fos
• Dynorphin • NO, PGs • EAA,NMDA • SP, CGRP
LTM
NOC
"Hyperconvergence"
----"
Disc
.,/Y Ugaments
t
Muscle
t
Periosteum
~
Joint
~
Dura
Mation - Segment - Tissues
Agure 15-5 Schematic diagram illustrating some of the cellular mechanisms thought to be involved in centra l sensitization of low-back neurons. Paravertebral morion-segment-tissue damage causes re lease of excitatory amino acid (EAA; for example, gluramate) and neuropeptide transmitters (SP, CGRP) from converging nociceptive (NOG) affercms that "sensitize" spinal low-back neurons through changes in second-messenger (Ca2., PKC) cascades and postsynaptic (for example, giurarninergic\NMDA) receprors. As central sensitization progresses (open arrowheads), genes are induced co transcribe through lEGs (for example, c-f05) new pronocicepr,ive proteins (for example, dynorphin) ro further enhance neuronal excitability and effectiveness of nociceptive (NO e) and nonnociceptive (LTM) input (opell arrowheads). "+" denotes excitatory synaprjc ac tions.
288
The SubluXation COtnpIex
The Contribution of Central Neuronal Plasticity to Referred Pain On several occasions since the publication of Theobald's original hypothesis (29), investigators have been drawn again to a centraVpsychogenic
explanation to account for some of the more perplexing characteristics of referred back pain that cannot be explained by convergence-projection alone (32,33). Four features of low-back pain in particular appear to be troublesome: ( I ) its dynamic spread or radiation to involve tissues
served by multiple spinal segments; (2) its occurrence in response to normally nonnoxious stimu-
lation like minor movements, deep pressure, and
touch; (3) its occurrence and persistence in many patients in the absence of identifiable peripheral tissue pathology, and sometimes, (4) its relief by treatment with a placebo. However, an appea l to suprasegmcnta l processes to explain these issues is not needed because changes in the response properties of spina l low-back neurons now appear to be sufficient (11) . Based on the neurophysiologic evidence discussed later, features 1, 2, and 3 may be interpreted as being caused by
expansion of their superficial and deep receptive fields after noxious stimulation of paravertebral tissues (Figure 15-4) and often showed ongoing or background discharge independent of any further peripheral stimulation (8,10,11). These dynamic neurophysiologic changes, ca ll ed activity-dependent "central sensitization"
(11,12,28,35-37), may explain why tenderness develops over a wide area after a localized back injury and why the pain seems to expand and radiate to the hip and out into the proxima l leg (features 1 and 2) . Similar dynamic neuronal processes were described some years ago by Korr (38) (the "facilitated state") and more recently by Patterson and Steinmetz (39) ("spina l fixation") to explain spinally mediated autonomic and motor pathophysiology. Although these concepts were not proposed as explanations for clinical
pain symptomology, it still appears quite likely that what Korr and Patterson and Steinmetz have
described is very much like what we call central sensitization.
With regard to the modern view of the cellular mechanisms underlying neuroplastic changes, our findings (8,10-13) and those of others (28,35-
enduring excitability changes in these spina l neu-
37,40) indicate that centra l sensitization is caused
rons, changes that render these units excessively responsive to a variety of inputs after painful paraspina l damage (8,10-12,34). Evidence is also presented to show that these same neurons are under the influence of powerful inhibitory controls that may operate in a variety of clinica l settings to alleviate pain (feature 4). To examine these issues more closely, we
at least in part by changes in the intrinsic characteristics of the spinal neurons involved rather than by changes in the damaged peripheral tissues (Figure 15-5). This process, however, is impor-
review the results of our recent animal experi-
ments designed to explore neuroplastic processes in relation to the neurophysiology of the low back (8,11-13). We have found, for example, that not only are low-back neurons activated by noxious mechanical and chemical (algesic) stimulation of the lumbar region, they are also "sensitized" by this input (68% of 37 units exam ined), meaning that they become hypetresponsive to all subsequent stimuli delivered to their receptive fields (Figure 15-4; compare top and bottom histograms). These neurons also showed dramatic
tantly dependent on an initial activation of lwci·
ceptive (NOC) afferents and the subsequent corelease of excitatory amino acids (EAAs, for example, glutamate and aspartate) and neuropeptides (for example, substance P [SP] and calcironin gene-related peptide [CGRP]) from their central axon terminals (28,35-37,40). These substances in turn bind to postsynaptic glutamate (37,40) (for example, the N-methyl-D-aspartate or NMDA) and neuropeptide receptors (35,36,40,41) on spina l nociceptive neurons, where they trigger a cascade of cell ular changes, including increases in ion channel-mediated electrical activity as well as alterations in intracellular enzyme cascades (Figure 15-5). The biochemical cascades use various second-messenger systems (for example Ca" and
15 Spinal Cord Mechanisms of Referred Pain and Related NeuroplasUclty
289
Skin/deep paraspinal tissues
+
I \
\
Lumbar ~ \ sympathe~c
~ ~
trunk
,
\
1-\.. •. ...._, \
..J' __ f
\
,,
, ' , I' \
, ,,
,'-''
I
I
,,
\
ALL
I
/
/
/
,,
,, \ I
I I I
DISC
,
I
I
,, \ I I I I I I
vise
,I
I
,
-'
,/
/
I
I I
I I \
, \
,
flgUra 15--8 Diagram of neuronal pathway proposed ro mediate responses of low-back neurons CO sympathetic trunk stimulation-the "direct sensory afferenr loop." Electrical stimulation of sympathetic trunk (S) activates somatic (D lSC) andlor visceral (VISe) nociceptive afferems which act directly or via imerneurons co excite and sensitize hyperconvergent (WDR) low hack neurons. U+" denotes excitatory synaptic actions; Ei. excitatory interneuron; Ii, inhibirory interneuron.
290
TIle SUblUXallon COIIIpIex
o
Phentolamine
blocks
, ,,, : " -Lumbar
,, ,
FIgIre 1.7 Diagram of neuronal pathway proposed
::r
(Q mediate responses of low-back neurons to sympathetic trunk stimulation-the "i ndirect sympathetic efferent/sensory afferent loop. " Electrical srimularion of sym pathetic chain (S) activates preganglionic axons, which excite sympathetic postganglionic neurons. These neurons in [urn excite primary (LTM and NOe) affeceors through a sympathetic-sensory coupling co indirectly excite and sensi tize hyperconvergent (WDR) low-back neurons. Sympathetic efferent-to-afferent coupling appears to be noradrenergically (NE) mediated because it can be blocked by phenrolaminc; however, other unknown mediarors ("?") such as prostaglandins and cyrokines may also conrribure. "+" denotes excitatory synapric actions.
7-B
l3-M6um Skin-deep unit
• • Paw
~
pinch
'~
l6-7 Joint brad
•
l6-7 Multifidus 6% NoCI
~
~
.0.
VI
60 50 40 30 20 10 0
•
Quod. brad
•
Hamstring
brad
• • Dura
Duro
pinch
brad
BOsec
RIaI'I1H Brief, "phasic" suppression of impulse discharge (top record, and middle histogram at "1") in a lowback neuron by innocuous "brush" stimulation of the superficial receptive field (black area in top figure). This unit was vigorously excited and sensitized by skin pinch (stippled area) and by noxious mechanical and algesic stimulation of deep paraspinal (records 3, 4, 7, 8) and hindlimb (records 2, 5, 6) structures. Brad, bradykinin; 6%
NaCI, hyperronic saline; Dura, spinal dura mater. Unit isolated in the lateral dorsal horn of spinal segment L3. (From Gillette, Kramis. and Roberts, unpublished data.)
292 protein kinase C or PKC) to trigger phosphorylation of membrane receptors (for example, glutamate and neuropeptide rypes) and ion channels (both ligand- and voltage-gated) that ultimately leads to enduring increases in neuronal excitabiliry (11,28,35-37,40,41). The excitabi liry change is reflected in a dramatic increased responsiveness to both nociceptive
(NOC) and nonnociceptive, low-threshold mechanoteceptive (LTM) affetent input (Figures 15-4 and 15-5) from the neuron's teceptive field and a tendency fat the cell to genetate ongoing discharges on its own (Figures 15-3 and 15-4) (8,10-12). Interestingly, this persistent increase in neuronal
tesponsiveness shows many of the featutes of a fotm of synaptic learning or plasticiry, called "Iongterm potentiation," or LTP, wherein temporally
tions along the rostrocaudal axis of the spinal cotd (9,11) . Increased activiry in these afferents is
believed
to
"unmask"
latent
excitatory
synapses (34,44) that contact low-back neurons so that progtessively more nerve cells are tectuited into the active (impu lse-genetating) population as nociceprion continues. Furthermore, there is some limited evidence to suggest
that this spread of excitability is in part mediated by the local telease and diffusion of neuroactive pep tides like SP and CGRP ftom these afferents (27) as well as the local release of pro nociceptive substances like dynorphin and NO from targeted spinal neurons (Figute 15-5) (35,41). All of these mechanisms appear to be able to opetate in concert
to
produce
increases
In
neurona l
excitabi lity actoss populations of spinal nocicep-
coincident synaptic inputs are strengthened, a pro-
rive neurons, including those serving the low
cess that appears to be widesptead in many parts of the brain (28,34-36) and spina l cord (42,43) . Fina lly, nociceptor afferent input to spina l neurons, (28,35,40,41) including low-back neurons (11,13), also leads to alterations in gene transctiption (through immediate eatly genes [IEGs] like c-fos and c-j un ) and the associated production and release of pain-promoting neuroactive peptides like dynorphin and diffusible messengets like nItriC oxide (NO) and prostaglandins (Figure 15-5) (28,35,40,41). One might speculate that, through these mechanisms, a positive feedback cycle of pronociceptive excitabi liry is triggeted, tefreshed, and maintained fat va tying lengths of time within individual pain-signaling neurons of the low-back sensory system by periodic nociceptive and nonnociceptive paraspinal inputs (Figure 15-5) (11,34). It is also important to consider how the spread of excitabiliry across populations of painsignaling neurons in adjacent spinal segments might OCCUt duting the elabotation a nd tadiation of low-back pain (featute 1) (2,7,19,20,22). Recent evidence suggests that there are a number of processes involved, including activation of
back (11-13) . One cou ld furthet speculate that if sensitization of these spinal neurons continues for a long time because of petsistent or tefteshed nociceptOr activation, the back pain may become selfsustaining (that is, chtonic) and independent of nociceptive affetent input from the petiphety (11,34). This may explain why patients suffering from chronic low-back pain seldom show evidence of petiphetal tissue pathology (32) (feature 3); that is, the peripheral tissues have healed but the centtal netvous system is still abnormal (8,41). Finally, some tecent experimental findings suggest that the development of central sensitization and petsistent pain may be promoted and maintained by the progressive loss of inhibitoty controls that normally play on spinal nociceptive neutons to ptevent hypetexcitabiliry (28,35). It is believed that the small inhibitory neurons operating within the pain system are particularly vulnerable to "excitotoxic effects" of excessive and prolonged NMDA teceptot activation by the nociceptive EAA transmitter, glutamate (28,35,41 ). This also might OCCUt in the low-back pain-
increasing numbers of paraspinal nociceptive
available to assist in the verification of this suggestion .
afferents with widely divergent central tetmina-
signaling system; however, there is no evidence
15 Splnal Cord MechanIsms 01 Referred Pain and Related NeuropIasIlclty
293
Law-level (nannaxiau,) mechanical input
Injured/inAamed malian-segment tissues
t
NOC
figlr816-9 Schematic illustrating proposed neural circuitry involved in producing "phasic" anrinociception or response suppression shown in Figure 15-8, In the depiction, a low-back (WDR) neuron has been sensitized by nociceptive (NOe) afferent bombardment reaching the cell from damaged paravertebral structures. The diagram illustrates how activation of low-threshold mechanoreceptive afferems (LTM) by innocuous mechanical (for example, couch, press, brush) stimulation could acrivate small) spinal inhibitory neurons that subsequently inhibit the hyperexcitable low-back neuron-resulting in a decrease in pain transmission (.1. LBP). 1<+" denotes excitatory synaptic actions; "-" denotes inhibitory synaptic actions.
294
T1nI SUbluxation Complex
~ 60
j.1i V>
o
_ 200, Pinch __ Skin 3.2 N
l6
•
1.2 N
o
- 3.2 N
3.2 N
FIgIre 16-10 Single-unit recordings showing that high-level mechanical stimu lation of paravertebral tissues can effecti ve ly supp ress impulse activity in low-back neurons. This neuron was initially inactive, but afte r pinching the skin receptive field (upper hisrogram) and injecting algogens (for examp le, Brad, 6% NaCI) inro deep paraspinai tissues (responses noc shown ), the ce ll developed an ongoing discharge that was effectively inhibited during and after forceful mechanical stimu lation over the LS-6 facer joinr (3.2 N stimulus, black boxes ). Although noxious (3 .2 N) mechanical input very effectively anenuated unit discharge, less forceful probing had no affect (1.2 N stim ulu s, open box). Exci[atory "breakthrough" (" Brush skin" region of hisrogram) during 3.2 N stimulus-induced inhibition demonstrates that the discharge suppression is neurally mediated. Uni t isolated in lateral lamina II of L5 dorsal horn. (From Gillette, Kramis, and Roberts, unpublished data.)
295
Sympathetic Nervous System Involvement in Low-8ack Pain Because persistent low-back pain is often found to exist in the absence of any detectable, ongoing injury or disease (32), and because other types of chronic pain have been found to be dependent on activity in the sympathetic division of the autOnomic nervous system (31), we have also tested to determine whether low-back neurons respond to electrical stimulation of rhe lumbar sympathetic trunk, located juSt outside the spinal column (10). We found that most (70%) spinal neurons serving the low-back region were indeed acrivated by applying electrical pulses to visceral and somatic afferent and sympathetic efferent axons within the sympathetic trunk, suggesting that activity in these nerve fibers may contribute to
low-back pain (10,11) . This finding in animals is consistent with reports from clinical studies by others indicating that some chronic low-back pain patients benefit from local anesthetic or ablative blocks of the sympathetic trunk ( 10,31,45). This procedure of blocking the sympathetic trunk is not commonly used to diagnose or treat low-back pain, partly because there has been no clear physiologic evidence to suggest that the sympathetic division of the autonomic nervous system has a direct influence on pain from this region.
Our data indicate that at least two types of nerve fibers in the lumbar sympathetic trunk contribute to the activation of these spina l neurons (1O). One type is sensory, being the parent axons
of nociceptor (NOC) and mechanoreceptor (LTM) sensory afferents originating in muscles, ligaments, and other retroperitoneal (visceral) tissues near the spinal co lumn and running in the
sympathetic trunk to finally enter the spinal cord over the dorsal rOOts to directly affect low-back neurons (Figure 15-6) (10,11,16). The convergent input to low-back neurons from visceral nociceptive afferents projecting through the sympathetic chain (Figure 15-6, VISC) cou ld help to explain how pain from pelvic visceral disease is referred
to the low-back region (9,10), a classic example of viscerosomatic convergence (5). The sccond type of activated nerve fiber appears to be sympathetic motor efferent fibers that project out to all tissues, where they act to control blood flow and other processes (10,31). Activity in these sympathetic efferent fibers indirectly trigger activity in other sensoty mechanoreceptive (LTM) and nociceptive (NOC) afferent fibers (10,11,31) that in turn project back into the spinal cord to affect low-back neurons (Figure 15-7). We have also shown that this sympathetic process can be blocked by the alpha-adrenergic antagonist drug phentolamine (Figure 15-7), which mOSt commonly is used to control hypertension or for other diagnostic tests unrelated to pain (10,11). We are investigating whether this drug may provide a safe and harmless means for testing whether the sympathetic nervous system contributes to low-back pain in patients with chronic discomfort (26). The importance of these sympathetically mediated effects is in their capacity to greatly increase the excitatory synaptic drive onto already sensitized low-back neurons to maintain
them in a hyperexcitable state (Figures 15-6 and 15-7). Conceivably, a sympathetically triggered, non nociceptive (LTM) afferent drive could eventually be sufficient to maintain the spinal lowback neuron (Figure 15-7) in a sensitized state, even aftcr peripheral tissues have healed and related nociceptor afferent input has decreased (feature 3) (10,11) .
Neurophysiology of Paraspinal Antinociceptive Systems While studying the response properties of the low-back pain-signaling neurons, we have also examined, to a limited extent, inhibitory phenomena that may be imporram in pain suppression as
opposed to pain production. For example, a subset of the dorsal horn, low-back neutons, from which we have recorded (approximately 20%),
Decending analgesic systems
High-Ievellnoxious) mechanical input
+
+
-::::::::::==:::::=:"':All
t
Injured/inRamed motion·segment
tissues
DISC
t
NOC
figure 15·11 Diagram of the postulated neural circuitry believed to underlie the inhibitory phenomena shown in Figure 15-10. Brief bur noxious mechanical input to paravertebral tissues activates paraspinai nociceptive afferenrs (NOC) that activate spinal inhibito ry inrerneurons both directly (segmentally) and indirectly through a suprasegmemai analgesic loop. The spinally and sup raspinally activated inhibitory imerneuron decreases the electrical excitability and impulse discharging of "already sensitized" low-back (WDR) neurons, leading ro a decrease in perceived low-back pain (.1. LBP). The descending analgesic system can also be independently activated by higher-order brain regions (tOP, open arrow) to produce "context-dependent" antinociception (for example, with placebos). "+" denotes excitatory synapric acrions, and "-" deno tes inhibitory synapric actions.
Decending analgesic sys
t
LTM
t Injured/inflamed motion-segment fi.$U8$
t
NOC
Haurelli-lZ Composire diagram iliusrraring how borh "phasic" (Figure 15-9) and "ronic" (Figure 15-11 ) anrinociceptivc circuits might be coactivated by mechanically forcefu l, chiropractic manipulation (eM) and how these mechanisms could work together to reduce the hyperexcitability of "sensitized" low-back pain transmission neurons. A subsequent decrease in excitability and impulsing across the majority of low-back (WDR) neurons would lead to a subjective decrease in referred low-back pain, that is, an analgesia (J., LBP). "+" denotes excitatory synaptic actions, and "-" denotes inhibitory synaptic actions.
298
The SUl*lxalion COIIIpIex
show complex forms of response suppression to mechanical stimulation o f paravertebral srrucru res (8,10,11). T hese inhibirory res ponses fell into rwo groups, based on the modality of triggeri ng a fferenf input and the duratio n of the inhibito ry
effects produ ced. In some insta nces, brief inh ibition of cellula r discha rge (both ongoing and stimulus-evoked ) could be obta ined by a pplying innocuous mechan ica l stimul ati on ro the sk in
recepti ve field of these cells (Figure 15-8). Interesti ngly, the suppression of neuronal responding
>
Neuro physio logic C orrela tes o f R eferred Low-Back Pain
".... .''.'~\I'.~""""~'.!I"i~'" " , '
.~
Clinical Feature Poorly localized back, hip, and leg pain.
Pollulated Heurel Correlate
Referred pain to arise from deep tissues
Nociceptive input to low-back neurons from
,..1
Spinal neuron "hyperconvergence" and large
unit receptive fields
Spontaneous, ongoing low-back pain
Referred hyperalgesia (stimulus-provoked tenderness)
Radiation of pain
Persistent, referred low-back pain
Pain relief (analgesia) by treatment interventions (for example, CM) and placebos
deep tissues more powerful than skin input Ongoing discharge in many spina l low-back neurons after central sensitizationfLTP Increased responsiveness to mechanical (LTM and NOC) input in the receptive field after centralsensitizationlLTP Unit receptive field expansion over time because of central sensitizationlLTP Recruitment of additional low-back neurons into the active population by: • Release and spread of pro-nociceptive neuroactive substances from afferents • "Unmasking" of latent excitatoty synapses by NOC inputs and sensitizationlLTP • Recruitment of additional low-back neurons by sensitizationILTP and release of diffusible substances SensitizationILTP produces: • Sympathetically mediated increases in LTM and NOC input-refreshes and maintains neuron hyperexcitability • Increased nonnociceptive (LTM) afferent drive maintains neuron hyperexcitability • Loss of inhibitory controls promotes hyperexcitability Recruitment of "tonic" and "phasic" antinociception by: • Coactivation of paraspinal NOC and LTM afferents • CentraUpsychogenic triggers
LTM, mechanoreceptor; NOC, nociceptor; LTP, long-ferm potentiatio n; CM, chiropractic man i pui <: ~ i o n.
15 81*'11 Cord Mer;ballilma 01 RelIII'I'III Pain and Rllated Nelroplatlclty
299
in these cases immediately ceased on the removal
of deep somatic tissue inflammation, and more-
of the innocuous stimulation (Figure 15-8). This short-lived (" phasic" ) response suppression is reminiscent of the spinally mediated pain-gating postulated some years ago by Melzack and Wall (Figure 15-9) (1,46). It was also found that noxious mechanical pressure applied to deep tissues of the back and hip (Figure 15-10) produced a more marked and longer-lasting ("tonic" ) inhibition of neuronal discharge that showed striking similarities to the segmental (47,57) and suprasegmentalldescending modulatory inhibition (Figure 15-11 ) described originally by Le Bars and co-workers (48,49) and more recently by others (1,7,11,50,51). Evidence suggests that these inhibitory mechanisms use both GABA-ergic and opioid-ergic transmitter
over, that this system can be activated by further transient noxious stimulation. These speculations
a nd neurophysiologic findings are consistent with recent clinical trial results showing the antinociceptive effectiveness of forceful, chiropractic manipulation (CM ) in low-back pain patients (54-56). It appears then that the low-back nocireceprive neurons that we have investigated are subject
to powerful inhibitory controls that may be activated by various location-specific mechanical interventions (for example, spinal manipu lation) and location nonspecific interventions (for example, placebos [11,26,49,54,55]) currently applied for the amelioration of lumbar spine pain (feature 4 ).
pharmacologies to suppress nocireceptive neUfon
excirability (1 ,7,34,49,52 ). These ex perimental findings are consistent with a speculative hypothesis published several years ago that argued that the mechanical forces produced by various forms of chiropractic manipulation (CM ) were of sufficient magnitude to coactivate both low-threshold mechanoreceptive (LTM) and high-threshold nociceptive (NOC) afferents in paraspinal tissues (47,53) . It was further argued that this type of sensory input could simultaneously activate both "phasic" and "tonic" antinociceprive systems, which wou ld
act to suppress the hyperexcitability of spinal cord neurons set up by noxious input from damaged paravertebral structures (Figure 15-12) (47,53) . Perhaps both of these inhibitory processes could act to decrease neuronal excitability by clamping membrane voltages at levels that favor rhe promotion of " long-term depression " (o r LTD ) of neuronal excitability rather than LTP (34,42). Finally, these central anrinociceptive systems may operate in conjunc-
tion with peripheral antinociceptive mechanisms, particularly when there is inflammation in damaged peripheral tissues (34). Indeed, Stein and associates (52) have recently shown that a powerful, peripheral opioid-ergic antinociceptive system is upregulated in peripheral tissues in the presence
RecapitUlation and Conclusions Table 15-1 summarizes our current understanding of the neurophysiologic processes that underlie the sensory/symptom dimensions of referred lowback pain and hyperalgesia (8- 11,34,47,53 ). This summary includes a number of working and speculative hypotheses concerning the neurobiologic correlates of lumbar spine pain phenomenology and should help explain some of the unique clinical features of this problem in humans, including its persistence, poor localization, deep referra l,
tendency to radiate, and its attenuation by placebos and other interventions.
The futu re holds much promise for those researchers prepared for a protracted campaign of attack on this refractory and expensive health care problem.
Acknowledgments The experimental work described in this chapter was supported by the National Institutes of Hea lth; R.S. Dow Neurological Sciences Center of Good Samaritan Hospital and Medical Center, Portland, Oregon; the Tarter Trust of the Medica l Research Foundation of Oregon; and Western States Chiropractic College, Portland, Oregon. The author would also like to thank Professors
300 Robert Boal, PhD, and David Peterson, DC, for critically reviewing an earlier version of this chapter.
Ref8l'tll1C8S I. Fields HL. Pain. New York: McGraw-Hili, 1987. 2. Hockaday jM, Whlfry CWM. Parterns of referred pain 10
the normal subject. Bram 1967; 90:481-96. 3. Lewis T. Pam. London: Macmillan, 1942. 4. Livingston WK. Pain mechanisms. London: Macmillan,
1943. 5. Ruch TC. Visceral sensation and referred pain. In: FulfOn JF, ed. Howell's textbook of physiology, Vol 15. Philadelphia: Saunders, 1946. 6. Sinclair DC, Weddell G, Feindel WH. Referred pain and 7.
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15. 16. 17.
18. 19.
associated phenomena. Brain 1948; 71:184-21 t. Price DO. Psychological and neural mechanisms of pam. New York: Raven Press, 1988. Gillette RG, Kramis Re, Roberts WJ. Characterization of spma l somalOsensory neurons having receptive fields in lumbar tissues of cats. Pain 1993; 54:85-98. Gillette RG, Kro.mis RC, Roberts Wj. Spinal projections of cat primary afferent fibers innervating lumbar facet joints and multifidus muscle. Neurosci Len 1993; 157,67-71. Gillette RG, Kramis RC, Roberts Wj. Sympathetic acrivacion of cat spmal neurons responsive to noxious stimulation of deep tissues in (he low back. Pain 1994; 56,31-42. Kramjs Re, Gillene RG, Roberts Wj. Neurophysiology of chromc back pain. In: White A, ed. Spinal mediCine :lnd surgery: a multidisciplinary approach. St. LoUIs: Mosby, 1995. Roberts WJ, Gillette RC, Kramis RC. Dorsal horn plasticity relating to low back pain. Journal of the CCA 1992; 36(2),108-9. Roberts WJ, Gillette RG, Kramis RC, Byers MR. Bilateral c-(os expression in dorsal horn after unilateral low back capsaicin injections: enhancement by prior conditioning stimulation (Abstract). IASP World Congress of Pain 1993; 7,747. Shekelle PG, Brook RH. A community-based study of the use of chiropractic services. Am J Public Health 1991; 81,439-442. Bogduk N. Lumbar dorsal ramus syndrome. Med J AUSI 1980; 2,537-41. Bogduk N. The innervation of the lumbar spine. Spine 1984; 8,286-93. Fernstrom U. A discographic study of ruptured lumbar intervertebral discs. Acta Chir Scand Suppl 1960; 258,1-60. Hirsch C, Ingelmark BE, Miller M. The anatomical basis for low back pain. Acta Orthop Scand 1963; 33:1-17. Kellgren JH. The an:nomical source of back pain. Rheumatol Rehabil 1977; 16:3-12.
20. Kuslich SO, Ulsnom CL, Michael EJ. The tissue origin of low back pam and SCiatica: A report of pain response to tissue stimulation dUring operations on the lumbar spine using local anesthesia. Orthop Clin North Am 1991;
22,181-7. 21. Mooney V. Where is the pain conllng from? Spme 1987; 12,754-9. 22. Mooney V. Robert'ion J. The facet syndrome. Clm Orthop 1976; 115,149-56. 23. O'Brien JP. Mechanisms of spinal pam. In: Wall PO, Melz3ck R, eds. Textbook of pain. London: Churchill* Livingsmne, 1984. 24. EI Mahdi MA, Latif VA, Janko M. The spinal nerve root innervations and a new concept of the clinicopathological interrelations in back pain and sciatica. Neurochirurgia
1981; 24,137-41. 25. Hansson P, Lindblom U. Quantitative evaluation of sensory disturbances accompanying focal or referred nociceptive pain. In: Vecchiet L, Albe-Fessard 0, Lindblom U, cds. New trends in referred p3in and hyperalgesia. London: Elsevier, 1993. 26. Fine PG, Roberts WJ. Gillene RG, Child TR. Slowly developing placebo responses confound rests of Intravenous phentolamine to determine mechamsms underlying idiopathic chronir: low back pain. Pain J 994;
56,235-42. 27. Mense S. Referral of muscle pain: New aspects. APS Journal 1994; 3:1-9. 28. Coderre TJ, Kan J, Vaccarino AL, Melzack R. Contribution of central neuroplasticiry to pathological pain: ReView of clinical and experimental evidence. Pain 1993;
52,259-85. 29. Theobald CW. Referred pain: A new hypothesis. Colombo: limes of Ceylon, 1941. 30. Guilbaud G. Cenna! neurophysiologIcal processing of jOint pain on the basis of studies performed In normal animals and 10 models of experimental arthritiS. Can J Physiol Pharmacol 1991; 69:637~6. 31. Roberts WJ, Kranus RC. Sympathetic nervous syStem inJ1uence on acute and chronic pain. In: Fields HL, ed. Pain syndromes in neurology. London: But[erworth,
1990. 32. Haldeman S. Failure of the pathology model to predict back pain. Spine 1990; 15:718-24. 33. Waddell G. A new clinical model for the treatment of low back pain. Spine 1987; 12:632~4. 34. Gillene RG, Boal R. Molecular neurobiological mechanisms underlYing the anrinociceptive action of spinal manipulative therapy: Recent research and some new hypotheses (submitted for publication). 35. Dubner R, Ruda MA. Activity-depcndem neuronal plasticity following IIssue injury and in(Jammalion. Trends Neurosci J 992; 15:96- 103. 36. McMahon 58, Lewin GR, Wall PD. Central hyperex* citability triggered by noxious Inputs. Curr Opm Neuro-
b;oI1993; 3,602-10.
301 37. Woolf CJ, Thompson WN. The induction and mainte· nance of central sensitization is dependent on N·met.hyl· D·aspartic acid recepwr activation: implications for rreat· ment of posr· injury hypersensitivity states. Pain 1991; 44,293-9. 38. Korr 1M. The neural basis of the osteopathic lesion. J Am Osteopat.h Assoc 1947; 47: 191-8. 39. Patterson MM, SteinmetzJE. Long-lasting alterations of spinal reflexes: A potent.ial basis for somatic dysfunction. Manual Med 1986; 2,38-42. 40. Coderre TJ. The role of excitatory amino acid receptors and intracellular mcsstngers in persistent noc,icepcion after tissue injury. Mol Neurobiol 1994; 7:229-46. 41 . Zimmermann M, Herdegen T. Control of gene transcription by Jun and Fos proteins in the nervous system: beneficial or harmful molecular mechanisms of neuronal response to noxious stimulation? APS J 1994; 3:33--48. 42. Randic M. Jiang MC, Cerne R. Long-term potentiation and long·term depression of primary afferent neurorrans· mission in the rat spinal cord. J Neurosci 1993; 13,5228-41. 43. Wall PD. Neurophysiological mechanisms of referred pain and hyperalgesia. 111: Vecchiet L, AJbe· Fessard OJ Lind· blom U. eds. New trends in referred pain and hyper3lgesia. London, Elsevier, 1993. 44. Wall PD. The presence of ineffective synapsts and circum· stances which unmask them. Phil Trans R Soc Lond Bioi 1977; 278,361-72. 45. Sluijter ME. The use of radiofrequency lesions for pain relief in failed back patients. Internationa l Disability Studies 1988; 10:37-43. 46. Melzack R, Wall PD. Pain mechanisms: A new theory. Science 1965; 150:971-79.
47. Gillette RG. Potential antinociceptive effects of nigh -level somatic stimulation: Chiropractic manipulative therapy may coacrivate both tonic and phasic ana lgesic systems. Trans Pac Consort Chirop Res 1986; 1:AI-9. 48. le Bars 0, Dickenson AH, Besson JM . Diffuse noxious inhibitory controls (DNIC): Effects on dorsal horn con vergent neurons in the rat. Pain 1979; 6:283-304. 49. Lc Bars 0, Villanueva L, Bouhassira D, Willer Jc. Diffust noxious inhibiwry controls (DNIC) in animals and in man. Path Physiol Exp Ther 1992; 4:55-65. 50. Basbaum AI, Fields HL. Endogenous brain control sys· tern: brainstem spinal pathways and endorphin circuitry. Annu Rev Ncurosci 1984; 7:309-38. 51. Fields HL, Heinricher MM. Anatomy and physiology of a nociceptive modulation system. Phil Trans R Soc Lond 8io11985; 308,361-74. 52. Stein C. Peripheral mechanisms of opioid analgesia. Anesth Analg 1993; 76,182-91. 53. Gillette RG. A specu lative argument for the coactivation of diverst somatic receptor popu lations by forceful chiro· practic adjustments. Manual Med 1987; 3: 1-14. 54. Postacchini F, Facchini M, Palien P. Efficacy of various forms of conservative treatment in low back pain. NeuroOrthopedics 1988; 6,28-35. 55. Waagen G, Haldeman S, Cook G, Lopez OJ DeBoer KF. Shon term trial of chiropractic adjustments for (he relief of chronic low back pain. Manual Med 2:63-67, 1986. 56. Herzog W. Biomechanical studies of spinal manipulative thmpy. J CCA 1991; 35,156-64. 57. Chung JM, Fang ZR, Hoci Y, lee KH, Willis WO. Pro· longed inhibition of primate spinothalamic [(act cells by peripheral nerve stimulation. Pain 1984; 11 :259-65.
The Subluxation Syndromes
T
he subluxation syndromes are the aggregate of signs and symptoms produced by subluxation of the various spinal and pelvic motion segments. Case studies, along with a limited number of larger studies, link the subluxation of articulations with patterns of signs and symptoms characteristic of each region of the spine and pelvis. Each subluxation syndrome presents pathophysiology and dysfunction typical of that region of the spine along with appropriate diagnostic and therapeutic measures employed by the chiropractic ptofession. In each syndrome articular subluxation is amenable to manual therapy, including manipulative and adjustive procedures. Although the focus of this section of the text is the identification and management of subluxation syndromes, it must be emphasized that the focus of chiropractic care is the patient. Patient-centered care has been identified with the long-standing satisfaction experienced by chiropractic patients. This satisfaction has been related to chiropractors' egalitarian manner in dealing with patients, understandable explanations of the patient'S condition, and holistic approaches to the care of each individual. This care includes use of the patient's belief that they will recover, touching the patient both diagnostically and thera-
304
Tbe SUIIIuxatIon !yUIll'Ol11ll
peutically, and counseling aimed toward healthier Iife-sryle changes. Paramount in the chiropractor
Chapter 19
patient encounter is actively involving the patient
spine is referred to rhe thoracic region of the spine. As in any pain pattern referred from a sub-
in the recovery process and in health promorion. This focus on the patienr as an individual and nOt just on subluxarions or pain patterns prevents
separation of the patient from the disease and is the ingredient soughr by patients when seeking health care.
Chapter 18
Cervicogenic Headache describes the mechanisms whereby headaches result from cervical subluxations. Cervicogenic headaches are frequently classified as muscle tension headaches involving referred pain; however, through autonomic modulation, some migrainous presenta-
tions are benefited by manipulation. Chapter 16 presents the evidence supporting the rreatment of cervicognic headaches with manipulation.
Chapter 17
luxation in another area of the spine, manipula-
tion of the subluxation produces dramatic relief from the referred pain .
Chapter 20
Thoracic outlet syndromes can be produced by cerVIcal and first rib subluxations that respond dramatically to manipulation. The hand and arm symptoms produce by these subluxations are often misraken for other causes of thoracic ourler syndrome. The anaromic relation -
ships thar lead to compromise of the structures passing through the thoracic outlet are discussed in Chapter 20 in addition to management of thoracic ourlet syndromes.
Chapter 21 Cervicogenic Sympatheric
Syn-
dromes relates subluxation of the cervical spine
to sympathetic syndromes that show a favorable response to manipulation. Cervicogenic vertigo, Horner's syndrome, and Barre Lieou syndrome are among the sympathetic conditions thar may be produced by the dysfunction caused by subluxation of the cervical spine. Subluxation of cervical motion segments from "whiplash" injuries is commonly treated by chiropractors, with supporting evidence that early manipulation of rhe neck after this rype of injury proves beneficial to the patient.
Chapter 18
Cervicogenic Dorsalgia is a syn-
drome in which pain originating in the cervical
The Cerebral Dysfunction Theory
presents a theory that explains the various mani-
festations of cerebral dysfuncrion purporredly relieved by manipulation. The proposal that decreased blood flow that inhibits normal cerebral functioning can be reversed through manipulation is supported by ophthalmologic measurement. The widespread effects of improvement in cerebral function through spinal manipularion of upper cervical vertebrae has been demonstrated.
Thoracic and costovertebral subluxation syndromes cause needless suffering when the sharp chest pain produced by these subluxa-
tions goes unrecognized. The mechanism, diagnosis, and management of thoracic and cosroverte-
bral subluxations is presented. Early recognition and appropriate treatment of these syndromes can prevent much needless anxiety and suffering.
Chapter 22
Patients with facet subluxation syndrome has been shown to benefit greatly from chiropractic manipulation. Subluxation of the lumbar facet joints, which produces low-back pain, has been the focus of numerous srudies that have demonstrated the effecriveness of manipularion in rhe trearmenr of pain-producing subluxa-
tions in the low back.
Chapter 23
The intervertebral disc syndrome has been demonstrated in some cases to respond to chiropractic manipulation. Both flexion dis-
tracrion therapy and procedures using rorarion
have proven beneficia l. The mechanism, diagnosis, and management of intervertebral disc syndromes using manipularion are discussed.
18 Cervlcoll8lllc Headache
Chapter 24
Sacroiliac subluxation syndrome has a favorable response rate of 97% to manipulation of the sacroiliac joints. Long considered the
most
controversial
subluxation
syndrome,
sacroiliac subluxation as a cause of buttock and referred leg pain is recognized as responsive to manipulation. Chapter 24 discusses the mechanism, diagnosis, and treatment of sacroiliac subluxation syndrome.
Chapter 25
Coccygeal subluxation syndrome produces coccydynia, one of the most painful conditions [0 respond [0 manipulation. Mechanisms of injury, diagnostic procedures, and therapy directed to the coccygeal subluxation syndrome are presented in the final chapter.
305
Cervicogenic Headache Howard Vernon KeyWOrds
Cervicogenic headache, tension headache, vertebrogenic migraine, convergence projection, central sensitization, central facilitation, aura
After reading this chapter you should be able to answer the following questions:
Question #1
What is the most common level of motion segment blockage (subluxation) found in subjects suffering "cervical headache"?
Question #2
What is the proposed neuroanatomic basis of headache referred from the neck?
Question #3
What cervical subluxogenic signs have been noted in headache sufferers?
18 Cervlc8llll1c IIndlClIe
T
he role of the cervical spine in headache
continues to be an unresolved controversy.
In 1988, a spectrum of headache subtypes that might have some kind of cervicogenic involvement was defined (1), (Figure 16-1). At that time the spectrum ranged from "tension headache with neck muscle pain" through "cervicogenic
headache," defined in chiropractic terms as symptomatic head pain and cephalic dysfunction caused by subluxation of a spinal joint, to a proposed "vertebrogenic migraine." Coincidentally, in 1988, the [nternational Headache Society (IHS) classification of headaches (2) published its report and, for the first time, recognized a headache subtype known as cervicogenic headache (CH). The definition of CH according to the LHS classification is shown in the box on p. 305. This headache owes much of its definition to the work of Ottar Sjaastad and his colleagues (3-6), which first appeared in print in 1983. In a subsequent publication (7), this very narrow definition of CH was challenged, and contrasted with the characteristic headache subtypes that chiropractic, manual medicine, osteopathic,
and physiotherapeutic experts had addressed in the literature spanning the greater part of this century. The IHS version of CH was also contrasted with the headache subtypes that had been included in the clinical studies of the outcome of spinal manipulation, again, by the same array of practitioners. In these studies of both tension-type and migraine-type headaches (definitely different from the narrow IHS features of the CH category), the results of manipulation to (presumably) some cervical spine dysfunction range from fair to excellent. This leaves us with a quandary, asking the following questions: is there a putative cervical com-
ponent in tension-type and migraine-type headaches?; is it similar to or different from the dysfunction in CHI; and, do the results of manipulation studies automatically imply the existence of a causative cervical component to these forms of
benign headaches?
307
Alternatively, is there one kind of cervical component that might contribute to, or manifest
as, different forms of headache experiences, and thus may be diagnostically labeled as different headache categories? This chapter explores this quandary with a clear bias toward accepting this alternate hypothesis. This is done by first briefly reviewing the results of clinical studies of spinal manipulation for headaches. Then, current research on pain mechanisms in CH is reviewed.
Also, literature on findings of cervicogenic dysfunction in headache groups that are clearly not LHS-CH is reviewed. Finally, the argument is made for the alternative hypothesis: that subluxation/dysfunction of the spine makes a significant contribution to the cause of a number of benign forms of headache.
Headache and Spinal Manipulation In 1991, a review article of all studies of manipulation for the treatment of headaches (7) summarized the work extent to 1988. This work is summarized in Table 16-1. Since that time, only two treatment studies employing manipulation have appeared in the scientific literature; only one of them in a peer-reviewed publication. In 1989, Stodolny and Chmielewski (8) reported on 31 subjects (24 women, 7 men; average age, 48 years) with "cervical migraine." They employed tests for intersegmental blockage and found that 100% of subjects demonstrated spinal motion segment blockage at CO-Cl; 75% at C7-Tl, and 25 % between CI-C2 and C3 (see Cervicogenic Dysfunction). The treatments consisted of two to three manual therapy sessions, largely employing manipulative techniques. They reported results at the end of 7 days that included: • Complete relief of headache in 75% of subjects • Average increases of cervical range of motion
of 9° (statistically significant) • Fixations reduced in 28 of 31 subjects • Reports of dizziness in subjects gready reduced There was no further follow-up reported. Obviously, no control comparison or blinding of
308
MU5CU CONIUCIION H!ADACHI
- Neck
muscle
bialeedback
MYOFASCW. _AND NICK PAIN
ClIMCAL
SPONDYlOSIS
- Travell and Simons
- Edmead.
-GrallRadford et 01.
- peatfiekj
OCCIPITAl. MlURALOIA. VAIIIANIS
ClRVlCOGINIC
HUDACHI
- Sjaa.tad
ClIMCAL HIADACHI
VU1IIROOIII MlGllAlNi
- Bogduk -Boalte
- Figar
;~m - Bialeedbac:k in postural pasifians - TENS and acupuncture
MEDICAL/
MUSCUlAR
-Vernon -Wight
POSTTRAUMI T1CHEADACH
VIORAl.
NEUROLOGIC NEURAL
CHIROPRACT JOINT DYSFUNCTIO
AND U:FLEXOGEN FIgIre 1.1 Types of headache with involvement of the cervical spine. (From Vemon HT. Vertebrogenic headache. In: Vernon HT, ed., Upper Cervical Sy"drome. Chiropractic Diagnosis and Management, 1988.)
the assessors was included in their protocol, so their results must be interpreted cautiously, all the more so because of the short treatment period. In 1992, Boline and Nelson (9) reported at a scientific meeting on the progress of their randomized comparative trial of chiropractic manipulation and the antidepressant drug amitryptiline in the treatment of "muscle contraction headache." This trial included 150 subjects (87 women, 63 men) with an average headache duration of 6 years. After the 6-week treatment phase, sub-
jects in both treatment groups demonstrated clinically and statistically significant reductions of headache activity. Neither group had statistically greater reductions rhan rhe other. However, ar the end of a furrher 6-week no-rrearment follow-up phase, subjecrs treared with chiropracric manipularion had significantly less headache activity than rhose receiving drug therapy, possibly indicating rhat the benefir obrained by chiropracric manipularion was more durable and may have correcred some of rhe underlying causative (bur srill poorly
18 C8rvtcapnlc IIBIdIcbe
>
Imernational Headache Society Classification of Cervicogenic Headache D iagnostic C rite ri a
A. Pain localized to neck and suboccipital region. May project to forehead, orbital region, temples, vertex, or ears. B. Pain is precipitated or aggravated by special neck movements or sustained neck postures. C. At least one of the following: 1. Resistance or limitation of passive neck movements
2. Changes in neck muscle contour, texture, tonc, or response to passive stretching or conuaction
3. Abnormal tenderness of neck muscles D. Radiologic examination shows at least one of the following: 1. Movement abnormalities in flexionextension 2. Abnormal posture 3. Fractures, congenital abnormalities, bone tumors, rheumatoid anhritis, or other distinct pathology (not spondylosis or osteochondrosis) From IntematiODOl Headache Society. Classificatioo and eliagnostic crircria for headache elisorden, ctaIIial DCUraJpas and facial poiD. CcpbaJaio 1988; 8(Suppl):7.
understood) mecha nisms fo r the kind of headaches suffered by these subjects. When one combines these data wi th those of the previous stud ies, it can still be concluded that spina l ma nip ulation a ppears to provide clinicall y significa nt levels of relief for benign headache types in patients w ho receive the treatment.
Unfortuna tely, the lack of contro lled studies prohibits any fir m concl usions regardi ng the efficacy of the treatme nt. Additionall y, it is virtua ll y impossi ble to assert the concl usion tha t rel ief of headache by ma nipulation proves the hypothesis tha t spina l dysfunction (presuma bly rhe target of
309
agent is one acceptable hypothesis to ex plai n these results, other equall y plausible expla nations exist, including the strong place bo effect that is typica lly ge nerated in headache pa tients, the natural history effect, and the selection bias. Once agai n, contro lled studies are required for theoretical and pathophysiologic conclusions, as well as conclusions regarding clinical efficacy, to be drawn.
Mechanisms of Pain in Cervicogenic Headache In 1988, a vertebrogenic model o f headache was presented, (1) which conta ined four categories: (1) extrasegmenta l, referrin g ro rhe long regiona l myofascial StruCtures such as the tra pezius and lo ng extensor muscles, the ligamentum nuchae,
and the interface berween the occipitofronta lis muscle and these regio nal cervicoth o racic struc-
tures; (2) intersegmenta l, referring to the threejoint complexes of C2-C3- C4 and the a rticulations of CO-Cl-C2, with their ligaments and deep intersegmental muscles; (3) infrasegmenta l, referring to the nerve structures in and aro und th e intervertebral fo ramina, and, in the cervical
spine, lying near the latera l portions of the vertebrae (in other words, the sympathetic trunk, the ve rtebral nerve, the C2 dorsa l roar ga nglion, rhe greater, lesser, and third occipita l nerves, and the sensory roots of C1); a nd, fina lly, (4 ) intrasegmenta l, referrin g to the spinal cord and medulla ry do rsa l horn wi th the nucleus subcauda lis of the trigeminal nerve. Much has been learned a bout these mechanisms since 1988, cenrering on the pa in pathways of the upper cervical cord and their conve rge nce o n ce lls in the nucleus subcaudalis, a mechanism
ca lled by Bogduk (10) the trigemino-cervical nucleus (Fig ure 16-2) . Upper cervica l cord and trigemina l nucleus su bcaudalis ne uro ns are partic ularl y res po nsive to
the manipu lati ve treatment) causes or is assoc i-
deep nociceptive inputs tha t, as Hu has said :
ated with rhese fo rms of headache. This is because, a lthough correction of the causarive
neurona l relays of convergent afferent inputs that
"unmask o r strengthen . .. cen tral somatosensory
310 Summary of Clinical Studies of Spinal Manipulation for Tension Headache and Migraine Autho .. Lewit (1971)
A
No. 01 Sublects 41
Lewit (1971)
A
93
T-t
Vernon (1982) Jirout (1985) Droz and Crot (1985) Turk and Ratkolb (1987) Boline et a!. (1993) Wight (1978) Parker et a!. (1978, 1982)
B A B
33 200 332
T-t T-t Occipital
A
100
T-t
75% success
B
150
T-t
B A and B
57 85
Mig Mig
Manipulation> drug at follow-up 75% success Manipulation = 28%
Stodolny and Chmielewski (1989)
Trelto ..
He.dl.he T-t
Rllulll
Manipulation most effective Manipulation most effective 85%-90% success 80% success 80% success
success initially
A
31
Mig
47% at 2-yr follow-up 75% success
A, Medical Doctor; B, Doctor of Chiropractic; T~(, tension-rypej Mig, migraine Adapted from Vernon HT. Spinal Manipulation and headaches of cervical origin: A review of luerature and presentarion of cases. Manual Medicine 1991; 6:73-9.
normally are relatively "ineffective" ("silent" [11]) in exciting (these) neurons" ([12] p. 72). As such, deep nociceptive inputs are particularly effective in creating ,he mos, significant increase of cutaneous hypersensitivity and an increase in the receptive fields of dorsal medullary horn neurons. In clinical terms, this underlies several important features of deep tissue pain, including its poor localization (explained by multiconvergence on numerous central neurons), hyperalgesia (so-called secondary hyperalgesia), spread of hyperalgesia, and its referral to distant cutaneous regions. All of these phenomena are well-known attributes of myofascial and, in particular, spinal pain syndromes. These are also all important components of myofascial dys-
function and pain referral likely to be operative in headache of cervical origin. Deep pain inputs activate local and, in some cases, distant muscles, presumably in some kind of early protective response. However, it can be presumed that this muscular reactivity contributes to the pain and dysfunction of clinical syndromes involving the neck and jaw articulations. There is a complex neurochemical control of rhese mechanisms that balances inhibitory and excitatory influences within the entire sensorimotor system involved with cephalic and facial pain. All of these mechanisms are consistent with ,he phenomenon of ce1ttral se1tsitizatio1t, which has been demonstrated previously in spinal sys-
18 cervicollllilic IIeadachII
311
Scar/soft 6ssue injury
Substantia gelatinosa &
trigem·inal
Cervical sensory ----1<2~ """'" root
nucleus
overlap
To shoulder lreferred poin'
A111'118-2: The rrigeminocervica l nucleus (From Hooshmand H. Chronic pain. London: eRe Press, 1993:52.)
312
TIle SWIIuxalloo Sylldrolnes
terns (13). This phenomenon is consistent with the model of neuroplasticity proposed by Dubner and Ruda (14), in that changes in central processing of nociceptive transmission contribute ro the
development and prolonged maintenance of the pathophysiology associated with pain arising from deep somatic tissues.
Implications for Headache of Cervical Origin Central sensitization provides a mechanism CO explain the clinical phenomena seen so regularly in headache sufferers of ( I ) persistent somatic pain; (2) pain referred from the cervical spine or posterior occipital region into the frontoorbiral regions being perceived as "headache," bur, in fact, being referred neck pain; (3) tender hyperalgesic muscle zones ("[rigger points"), wh ich often expand as the headache pain increases; (4) muscular tension in the deep suboccipital, superficial occipita l, and cran iofacia l muscles, which has, for many years, been thought ro be the sole basis of muscle contraction or tension-type headache ( 15) . Conversely, the mechanism of "convergencesensitizatio n-projection" also serves to explain how pain arising from intracranial Structures such as posterior cerebellar tumors or the intrace rebral blood vessels (as proposed by Moskowitz [161 in the case of migraine) may be referred to the posterior occipital and suboccipital regions, masquerading as cervica l pain. In summary, the rrigeminocervical nucleus and the extensive afferent convergence from numerous craniocervica l peripheral tissues onto
these second-order neurons (a phenomenon called cOl1vergence-pro;ection (1 71) serves ro explain the neuroanaromic basis of headache referred from the neck. The neurophysiologic basis of such pain referral, particularly from inflammarory pain arising from the posterior suboccipita l muscles and joints, is explained by the phenomenon of "central sensitization" and the neuroplastic changes that these second-order neurons undergo in response to prolonged peripheral deep somatic
pain. These are the mechanisms thought for many years by chiropractors ro arise from the subluxation or dysfunction state of the vertebral motion segment. Certainly this is consistent with the older model of "central facilitation" proposed by Korr and his colleagues (18) and adhered to by several generations of chiropractors.
Cervicogenic Dysfunction in Headache In the final section of this chapter, evidence for the spina l subluxation phenomenon in groups of headache sufferers is explored. A 1992 report ( 19) on cervicogenic dysfunction in muscle-contraction (that is, "'tension-type" ITTH I) and common migraine (that is, "migraine without aura" IMWAI) defined the components of cervicogenic dysfunction, and the literature up ro 1988 was reviewed in defence of the notion of a broad, highly prevalent basis of cervicogenic dysfunction in headache. A 1991 report (7) also addressed how this high prevalence of cervicogenic dysfunction in these types of headaches argued against the position adopted by the IHS (based principally on the work of Sjaastad and his colleagues (3-6) that "cervicogenic headache" was a narrowly defined, infrequently encountered form of headache. In the 1992 report, the components of cervicogenic dysfunction were outlined as follows:
J. Hypomobility-variously
termed subluxation, joint blockage, segmelltal dysfullction, {ixatioll 2. Tender points in the soft tissues-variously ca lled tender muscle points, trigger points,
/,yperalgesic zones 3. Reduced regiona l ranges of cervical motion 4. Radiographic findings of: a. Static misalignment b. Dynamic intersegmental abnormality Two other features should be added to this list now:
5. Static segmenta l misalignment on palpation (most often, C I or C2 is cited)
1B Cervlcogenlc Headache 6. Static malposition of the head and neck (specificall y, anterior carriage of the head a nd low rounded shoulders) The reader is directed to the 1992 report for a review of the literature supportive of each of these components before 1988 . The recent literature (with a few notable exceptions) is now reviewed.
Hypomobility In 1985 and 1986, Jull (20,2 1) had reported on both the relia bility of upper cerv ical joint motion palpation and its use in headache subjects to determine the lesioncd segment. The comparison between headache and nonheadache subjects (21) showed dysfunction at CO-C1, Cl -2, and C2-3 in 60%, 40%, a nd 55% of headache subjects, as compa red with 5%, 120/0, and 220/0, respectively, in control. These palpatory findings were confirmed by Jull , Bogduk, a nd Marsland (22) and Dwyer et al. (23) using diagnostic anesthetic blocks as the go ld standa rd. In rhe 1992 report by Vernon et a I., three motion palpation procedures (as described by Fligg [241) were used: A-l' glide, rotation, and la tera l flexion. A ma jor blockage in either of these three procedu re on either side at CO-C3 was indicative of segmental fixation. It was reported that no su bject in either the tension-type o r migraine group had fixations at none of the upper cervica l segments, whereas on ly 16% in each group had a fixation at only one level. In rhe tension-ry pe grou p, 54% had fixations at two levels and 30 0/0 at all three, whereas fo r migraine subjects these figures were 42 % and 42 %, respectively. In both grou ps 84% had a fixarion at at least two of three upper cervical segments.
In 1993, Warson a nd Trort (25) used multiple outComes (others are discussed later) ro assess cervica l headac he subj ects. They reported on the reliabili ry of posterior-to-anterior gl ide palpation in 12 of their subjects exa mined o n two occasions by the same exa miner, with Kappa values ranging from 0.67 to 1.0, depending on the segment. They a lso included as positive signs of joint dys-
313
function the presence of tenderness and muscle stiffness (see later discussion). When a ll three sig ns-fi xa tion , tenderness, and palparory stiffness-were included, far mo re positive findings were found in headache subjects (N = 30) than in controls (N = 30) . The most preva lent level was
CO-Cl.
Cranlovertebral Tender Points Tenderness to palpation of the sk in (26) and deep tiss ues o f the craniovertebral and paraspinal region is the most commonl y repo rted sign o f headache o f cervica l origin. Virtuall y every relevant au tho r has repo rted o n the subject, from Lewit (27), who reported on " pa in over the posteri or arch of arias," to Sachse et a l. (28), who reported simila r suboccipita l a nd sca pular tenderness, to Graff-Radford et al. (29) and Jaege r (30), who have reported on the numero us cervical tender po ints that serve to perpetuate myofascial head pain, to sjaastad et a l. (3,4 ), who report o n the high preva lence of tendern ess at C2-3 . Bouquet et al. (31) reported on 24 cervicogenic headache sufferets, 21 of whom had an ipsilateral trigger point at C2-3 . They a lso commented on a frequenrly rota red and enlarged C2 spinous process, evidence of some static misa lignment that typica ll y accompanies the spinal subluxa tion . In j aeger's report o n 1 J cervicogenic headache sufferers, tenderness and misa lignment aro und the transverse process (TVP) of arias were rh e most frequent palpatOry findings. In the 1992 report, the pressure a lgometer (32) was used to verify true tenderness in cervica l tender points in tension-ty pe and migraine-w ith out-a ura sufferers. This type of assessment has been used with great success by fibromyalgia (33) and headache (34) researchers. In fact, the IHs classifi ca tion (2) includes the presence (or absence) o f pericrania l tender points as part of the subcl assi fi cario n of tension-type headaches. The 1992 stud y reported on the preva lence of six standard craniocervical tender points in these headache groups, na mel y: • Medial occipital brim • Lateral occipital brim (near the TVP of arias)
314 Tender Points: Prevalence of Cervicoscapular Tender Points in Tension-type and Migraine Patients: Distribution by the Number of Points
.21 H•• dache groups NO. oITPs
eM
MeH
Totat
6 5 4 3 2 1 0
8 16 4 28 20 16 8
% 10 5 10 25 25 10 15
9 11 7 27 22 13 11
Spearman r = .98, P!; .05. From Vernon er al. Cervicogenic dysfunction. J Manipulative Physiol Ther 1992; 15:425.
• • • •
Suboccipital (Cl-2) Midcervical (C2-3) Trapezius Levator scapulae
Table 16-2 shows the distribution of numbers of tender points (bilateral points counted as 1; therefore, the maximal count was 6) in the two headache groups. Eighty-five percent (85%) of TTH had at least one; 75%, at least two; and 50% had four or more. In rhe migraine group, these figures were 92%, 76%, and 44%, respectively, indicating a high prevalence of tender points in both groups. Table 16-3 shows the most prevalent locations, showing a strong (predictable) prevalence for the upper cervical region. The findings of Watson and Trott (25), in which detection of joint dysfunction in headache (HA) subjects and non-HA subjects included pressure palpation for tenderness, were described above. Again, this procedure was found to have good intraexaminer reliability, and was found ro distinguish HA subjects from non-HA subjects with higher prevalence of findings in the HA subjecrs.
Finally, tenderness ro palpation has been used as one of the cardinal signs by Bogduk and his colleagues (20-23) to locate the level of zygapophyseal Jomt dysfunction potentially responsible for neck pain and headache. These tenderness findings correlate very well with the signs of joint hypomobility previously discussed. This combination of tenderness and hypomobility (as with Watson and Trott) correlate very highly with joint blockades used as a gold standard for diagnosis, and are used with greater frequency (35,36) as a successful therapy in headaches. A finding associated with muscle tenderness is increased muscle stiffness. In 1992, Vernon and Gitelman (37) reported on a single case of bilateral TTH with cervical dysfunction. Pressure algometry showed clinically significant tenderness bilaterally in the suboccipital region. Muscle stiffness of the midcervical paraspinal and trapezius muscles was measured using Fischer's tissue compliance meter (38). Higher than expected values were found in both muscle sites.
Tender Points: Distribution of Cervicoscapular Tender Points in Tension-type and Migraine Patients: Distribution by the Location of Points
Headache groups location olTP
eM
MeH
Tot.t
Midcervical Lateral-occipital Suboccipital Trapezius Levato r scapula Medial-occipital
91 68 64 55 32 23
% 78 56 56 39 33 17
85 63 60 47 32 20
Spearman r = 1.00, P S .05.
From Vernon et a!. Cervicogenic dysfunction. J Manipulative Physiol Ther 1992; 15:425.
18
CervIcogeIIIc: II
tM he
315
Sakai et al (39) used a computerized compliance meter in a comparison of 37 lTH subjects and 63 normals. In 65% of HA subjects there was significantly increased trapezius stiffness, whereas the overall mean values (756 + 121 versus 538 + 89) significantly distinguished headache from control subjects. An orally admi nistered muscle relaxant greatly reduced this increased stiffness in headache subjects, implying that
flexion and 70% for extension. These results agree with those of Pfaffenrath et al. For the rest for the cervical spine, a pattern emerged of greater hyper mobility at C1-C2, and hypomobility at C4-5-6 . Finally, regarding the neutral cervical curve, it was found that 77% of all subjects had a substantia l reduction (quasia lo rdotic or fully alordotic) or abnorma l reversal of rhe cervical lordo-
active tension contributed to the stiffness.
SIS.
It is evident that the more recent studies of myofascial dysfunction (pain/tenderness and stiffness) employ more sophisticated methodologies
Nagasawa et al.'s (43) recent report adds furrher to our knowledge of cha nges in cervical function in headache sufferers as determined by x-ray analysis. They compared 372 lTH subjects with 225 normal controls. They found a statistically significant reduction of the neutral curve as
and instrumentation and are being conducted in
case-control design formats. The findings of these studies even more strongly substantiate the clinical and empirical experience of a high prevalence of craniocervical tenderness in headache sufferers,
which is strongly associated with other signs (including misalignment and joint hypomobility) of spinal segmental subluxation . Studies rhar also employ manipulation or joint blockade have, by the relief of symptoms obtained, further implicated cervicogenic joint dysfunction in the cause
of headache.
Radologlc findings 01 CervJcogenlC Dyslln:tIoo Pfaffenrath et al. (40) used a computer-aided method of analyzing segmental cervical motion on flexion-extension radiographs. They found a statistically higher incidence of restrictions at CO-CI in cervicogenic headache subjects as compared with normal controls. In a 1992 report on lTH and MWA subjects, a similar method that rated segmental movement against the normative data from Dvorak et al. was used (41). In addition, Penning's method (42) was used for CO-Cl (with Fielding's norms for flexion and extension at CO-CI). The mean ± 1 SO (standard deviation) for occipital flexion in both headache groups was 3.17° ± 2.24°; whereas for extension it was 10.6 ± 7.7°. The percentage of subjects showing reductions in motion below a lower cutoff for normal (-1 SO) was 90% for
measured by a "cervical spine curvature index"
(14.6 + 11.9% versus 19.4 + 11.1%, P < .001). They also found that segmenta l instability was less frequent in lTH than in controls. Finally, they found a higher frequency of low-set (in other words, rounded) shou lders in lTH (57.5%) versus controls (41.8%, P < .01, X2 = 16.6). These findings confirm that lTH sufferers have significant cervical posrural and segmental motion abnormalities, typical of subjects whose headaches would be labeled as "cervicogenic."
Cervical PoatIn, MuscIUr Weaknen, and
Range 01 MotIon
Watson and Trott (25) studied 60 subjects, 30 with recurrent cervical headache (a combination of lTH, MWA, and "cervicogenic" HA) and 30 controls. They studied : (1) the degree of anterior head carriage, which they measured photographically, (2) the isometric strength and endurance of the upper cervical flexor muscles, measured by strain gauge dynamometry, and (3) the presence of "joint dysfunction," by combining manual palpatory findings of restricted joint play, tenderness, and stiffness (as described above). They found a smaller mean angle of forward head position (FHP) in headache sufferers (thar is, a straightened cervical spine). As well, headache sufferers had smaller strength values
316 and smaller endurance values of upper cervical flexors. These findings correlated well with the degree of FHP. They concluded that FHP increases the load on the posterior muscles that rotate the head (occiput) backward to maintain the orthostatic horizontal position of the eyes. This, in turn, weakens the antagonist muscles (upper cervical flexors) and contributes to upper cervical joint and myofascial dysfunction, ultimately leading to upper cervical pain. This nociception reinforces the local muscle spasm (as found experimentally by Hu et al [12]) and creates a vicious cycle of pain, spasm, altered mechanics, pain, etc., all leading to the potential for referred cranial pain. Further evidence for the development of regional muscular stiffness and reduced range of cervical motion comes from Kidd and Nelson's report (44), using a very simplistic observer's evaluation of neck ROM in 64 subjects, 37 with and 37 without benign headache. The headache sufferers more frequently had a reduction of two or more ranges of motion.
All of these findings combine to create a composite of cervicogenic dysfunction, much of which has been observed in noncervicogenic-type headache sufferers (for example, TTH and MWA). This profile includes regional alterations in anterior head posture, straightened cervical curve and low-set shoulders, regional muscular stiffness and reduced ROM, upper cervical subluxogenic signs including misalignment, joint hypomobility, and frequent segmental myofascial tenderness. The high potential for upper cervical pain to occur, not only unilaterally, but bilaterally, creates potent opportunities for cranial pain referral.
Summary The literature on headaches of cervical origin has been reviewed, focusing on three areas: (1) the results of studies employing manipulation and facet or neural anesthetic blockade, (2) recent advances in the understanding of craniocervical pain mechanisms, and finally (3) recent studies of
cervicogenic dysfunction in several caregories of headache, including TTH, MWA, and "cervicogenic." This chapter author believes the current LHS approach to "cervicogenic headache" is too narrow and will create many false misattribu[ions, typically in the direction of underdiagnosing the cervicogenic component of a great man y more benign headache conditions. In conclusion, rhis chapter aurhor would reiterate the 1988 (1) model of vertebrogenic headache, modifying it slightly, as follows: ... there are likely three categories of benign headache:
1. Those in whom the cervicogenic component is etiological. This group, ideally, will derive primary benefit from spinal manipulative rherapy (SMT) or other treatmentS aimed at cervical dysfunction; 2. Those in whom the cervicogenic component is secondary but synergistic. This group ideally could derive significant benefit from SMT in conjunction with other therapeutic measures; and, 3. Those in whom the cervicogenic component is negligible, reactive or fully absent. This group would derive little if any benefit from SMT. As in 1988, it is still the case today that only careful yet comprehensive research, taking full account of cervicogenic dysfunction, will ultimately determine the validity of this model.
References 1. Vernon HT. Venebrogenic headache. In: Vernon I-IT, ed. Upper cervical syndrome: Chiropracuc diagnosis and management. Baltimore: Williams & Wilkins, t 988.
2. Internationa l Headache Society. Classification and diag· nostic criteria for headache disorders, cranial neuralgias and facial pain. Cepha lalgia 1988; 8(Suppl),7. 3. Sjaastad 0, Saunre C, Hovdahl H, Breivek H, Gronback E. Cervicogenic headache: An hypothesis. Cepha lalgia 1983; 3,249-56. 4. Sjaastad 0, Fredrickson TA, Stolr-Neilsen A. Cervicogenic headache, C2 rhizopathy and occipital neuralgia: A connection. Cephalalgia 1986; 6: 189-95. 5. Fredrickson TA, Hovdahl H, Sjaastad O. Ccrvicogcnic headache: Clinical manifestations. Cephalalgia 1987; 7, 147-60.
1B CervIcoganIc 'leadache 6. Fredrickson TA. Cervicogenic headache: The forehead sweating pattern. Cepha lalgia 1988; 8:203-9, 7. Vernon HT. Spinal manipulation and headaches o f cervical origin: A review of literature and presemation o f cases Manual Med 1991; 6:73-9. 8. Srodolny J. Chmielewski H. Manu31 therapy in the [reatmem of patients with cerv ical migraine. Manual Med 1989; 4,49-5 1. 9. Boline P, Nelson C. Chiropractic and pharmaceutical therapy: a r:mdomized clinical trial for the treatment of chronic muscle conrracrion headache. Proceedings o f the FCER International Conference on Spinal Manipulation, Washington D. C., 1991: 177-80. 10. Bogduk N. A neurological approach to neck pain. In:
Glasgow EF, Twomey IV, Scali ER, Kleynhans AM,
11.
12.
13.
14.
15. 16. 17.
18. 19.
20. 21.
22.
23.
Edczak RM, eds. Aspects of manipulative therapy. 2nd ed. New York: Churchill-Livingscone, 1985: 136-46. Mense S. Considerations concerning the neurological basis of muscle pain. Can J Physiol Pharmacol 1991 j 6%1()"16. Hu JW, Yu X-M, Vernon HT, Sessle BJ. Excitacory effects on neck a nd jaw muscle activity of inflammatory irritant applied co cervical paras pinal rissues. Pain 1993; 55,243-50. Woolf CJ, Thompso n SWN. The induction and maintenance o f centra l sensitization is dependent on N-methylD-aspartic acid receptor activation: implicarions for the treatment of post-injury pain hypersensitivity stares. Pain 1991; 44,293-9. Dubner R, Ruda MA . Activity-dependenr neuronal plasticity following tissue injury and inflammation. Trends Neurosci 1992; 15:96- 102. Pozniak-Parewicz E. "Cephalgic " spasm of the head and neck musculature. Headache 1976; 15:261-5. Moskowitz M. The neurobiology of vascular head pain. Ann Neuro11984; 16:157-68. Ruch TH. In : Fulton JF, ed. Howell's textbook o f physiology. 15th ed. Philadel phia: WB Saunders, 1947,385-401. Korr 1M. The neural basis of the osteopathic lesion. Am Osteoph Assoc 1947; 19 1-5. Vernon HT, Steiman I, Hagino C. Cervicogenic dysfunction in muscle contraction headache and migraine: A descriptive srudy. J Manipulative Physio l Ther 1992; lHI8-29. Jull G. Manual diagnosis of C2-3 headache. Cephalalgia 1985; 5(SuppI5),308-9. Jull GA. Headaches associated with the cervical spine: A clinical review. In: Grieve GP, ed. Modern manual therapy of the vertebral column. New York: Churchill livingstone, 1986. Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophyseaJ joint pain syndmmes. Med J Aust 1988; 14U33-<>. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal
317
joint pain parrerns I: A study in normal volunteers. Spine
1990; 15A53-7. 24. Fligg B. Motion palpatio n of the upper cervical spine. in: Vernon HT, ed. Upper cervical syndrome: Chiropractic diagnosis and management. Baltimore: Williams & Wilkins, t 988. 25. Watson DH, Trort PH. Cervical headache: An investigation of natural head posture and upper cervical fl exor muscle performance. Cepha lalgia 1993; 13:272-82. 26. The Quebec Headache Study Group. Painful intervertebral dysfunction: Robert Maigne's original contribufion to headache of cen·ical origin. Headache 1993; 33,328-34. 27. Lewit K. Manipulative therapy in the rehabilitati on of the loco motOr system. London: Butterworth, 1991. 28. Sachse J, Eckhardt E, Lieb A. A pheno menological investigation in migraine patients. Manual Med 1982; 20,59-<>4. 29. Graff-Radford S8, Reeves JL, Jaeger B. Ma nagement of chronic head and neck pain: Effectiveness of altering factOrs perpetuating myofascial pain. Headache 1987; 27,186-90. 30. Jaeger B. Cervicogenic headache: A relationship fO cervical spine d ysfunction and myofascial trigger points. Proceedings of the 3rd Congress of the International H eadache Society, Florence, Italy. Cepha lalgia 1987; 7(suppl 7),398-9. 31. Bouquet J, Boismare F, Payenneville G, Leclerc D, Monnier j.C, Moore N. Lateralization of headache: Possible role of an upper cervica l [rigger point. Cephalalgia 1989; 9,15-24. 32. Fischer AA. Pressure algometry over normal muscles: Standards values, validiry and reproducibility of pressure threshold. Pain 1986; 30,115-26. 33. Tunks E. Crook J , Norman G, Kalahen S. Tender points in fibromyalgia. Pain 1988; 34:ll-l9. 34. Bovim G. Cervicogenic headache, migraine and tensiontype headache: Pressure-pain threshold measurements. Pain 1992; 51:169-73. 35. Gawel MJ. Rothbart PJ. Occipital nerve block in the managemem of headache and cervica l pain. Cephalalgia 1992; 12,9- 13. 36. Rorhbart PJ. Uni lateral headache with featu res of hemicrania continua and cervicogenic headache: A case report. H ea dache 1992; 32:459-60. 37. Vernon HT, Gitelman R. Pressure algometry and tissue compliance measures in the trea tment of chronic headache by spinal manipulation: A single case/single treatmenr report. J Ca n Chiro Assoc 1990; 34, 14 1-4. 38. Fischer AA. Clinical use of the tissue compliance meter for documentation of soft tissue pathology. Clin J Pain 1987; 3,23-30. 39. Sakai F, Ebihiara S, Horikawa M. Akiyama M. Quantitative measurement of muscle stiffness in tension-type
318 headache: Development of a new method. Cephalalgia 1991; 11(suppllll:115-16. 40. Pfa(fenrath V, Oandekaf R, Mayer E, Hermann G, Pollman W. Cervicogenic headache: Results of computerbased measurements of cervical spine mobility in fifteen patients. Cephalalgia 1988; 8:45-8. 41. Dvorak j. Froelich 0, Penning L, Baumgartner IT, Panjabi MM. Functional radiographic diagnosis of rhe cervi· cal spine: Flexion/extension. Spine 1988; 13:748-55.
42. Penning l. Functional ronrgenderzock. Bij degenerative en
tramatische afwijkingen def laag-cervicale bewegingssegmenten. University of Gronikge, Netherlands, 1960. 43. Nagasawa A, Sakakibara T, Takahashi A. Roentgenographic findings of the cervical spine in rcnsiolHYpe headache. Headache 1993; 33:90-5. 44. Kidd RF, Nelson R. Musculoskeletal dysfunction of the neck in migraine and tension headache. Ileadache 1993;
33:566-9.
Cervicogenic Sympathetic Syndromes: Etiology, Treatment, and Rehabilitation Donald AU·Rltson
Key WIIrds
Cervical sympathetic ganglia, Horner's syndrome, Barre-Lieou syndrome, Meniere's disease, cervicogenic vertigo
After reading this chapter you should be able to answer the fo llowing questions;
Question #1
How does the position of the upper cervical ganglion make it vulnerable to an upper cervical subluxation?
QuesUon #2
How can a subluxation produce cervicogenic vertigo?
Question #3
What is the role of manipulation and other forms of chiropractic adjustment in the treatment of cervicogenic sympathetic syndromes?
320
Tb8 8u1*1xatlon 8YIIIII'8l11111
T
he extremely flexible cervical spine-the body's most complicared and mobile articular system-is located strategically between the head and body. Ir is designed for mobility, which significantly influences irs Stability. Subluxation syndromes affect both the mobility and stability of the cervical spine. The cervical spine is an anatomic complex of many crucial and sensitive tissues crowded into a
sma ll area. It is the "Times Square" of the human frame, with enormous volumes of traffic going in borh direcrions. Many delicate and vital structures pass through this 7-inch portion of the spine, which is made up of seven of rhe mosr fragile vertebrae. These are held together by 17 articu lar joints, 12 joints of Luschka (for a total of 29 joints), six
periods of stress. The cervical sympat hetic trunk (CST) consists of asce nding preganglionic axons, which traverse the white rami communicantes.
Peripherally,
postganglionic fibers accompany
sensory fibers to specific cutaneous areas that closely correspond ro sensory dermaromes.
There are generall y three cervical sympathetic ga nglia that arc formed fro m the fusion of the eighr primordial cranial nerves. The cervicothomcic or stellate ganglion is the lowermost and is considered to be a fusion of the first thoracic and inferior cervica l ganglia. The usua l position of the cervicothoracic ganglion is anterior to the base of the transverse process of the seventh cervical ver·
tebra. This ganglion supplies gray rami communicantes to the cervical spinal nerves 6, 7, and 8 and also ro the first thoracic nerve. An inferior cervi· ca l card iac nerve also arises from this ganglion.
The middle cervical ganglion is the smallest
intervertebral discs, and a musculoligamenrous
and most variable in form and position . It is com·
network that invo lves approximately 50 pairs of muscles. The musculoligamenrous system, along with the architectura l shapes of the vertebrae and
mon ly located in close proximity to the inferior thyroid artery and the cricoid carti lage. In addition to supplying the gray rami communicantes to
joints, allows enormous maneuverability and
cervica l nerves 5 and 6, it also gives rise
range of motion, but also supports the head, which weighs approximarely 8 to 10 pounds. At leasr 70 clinically separate and disrinct syn-
middle cervica l cardiac nerve (I). The superior cervica l ganglia is the largest of
dromes arise from abnorma lities of the tissues of the cervical spin e. Even morc syndromes arise from distant Structures bur are associated with
signs and symptoms referable to the cervical spine, head, shoulders, and upper extremities.
These disorders are related to the subluxation syndrome and constitute a sizable portion of any chiropractor's practice.
Anatomy
[Q
the
the three, sometimes extending 3 to 4 cm, and lies
opposite the transverse process of C2. This ganglion has many branches, including the internal carotid nerve, which distributes nerve fibers [Q intracranial vascular smooth muscles. Communi-
cations also exisr berween the superior ganglion and the inferior ga nglion of the glossopharyngeal nerve, the inferior and superior ga nglia of the
vagus, and the hypoglossal nerve. Pharyngeal branches join the pharyngeal plexus as well as the eXlernal carotid and superior cervica l cardiac
This brief overview add resses anatomy relevant
plexus. In general, these fibers accompany the named blood vessels and perform vasoconstrictor,
to injury of the cervica l spine.
secretory, and pilomotor functions. The external
the auto nomic nervous system has major functions in vasoconstriction of the sk in and shifting
carotid nerves supply all of the major and minor glands of the head and neck (2). The cervical sympathetic trunk lies deep to the deep layer of the cervica l fascia and reStS on the longus col i and longus capitis muscles. The
of blood supply to more essential organs during
nerve is posterior and medial to the carotid artery
Sympathetic NerVOIIS System The sympathetic, or thoracolumbar, division of
17
Cervlcogenlc Sympathetic Syndromes: Etiology, 1reatmen1, and RehabIlitation
and the vagus nerve and usuall y ascends from its origin in the root of the neck superomedia ll y (1). The anatomic intimacy between the sympathetic di vision of the autonomic nervous system
and the somatic nervous system is most appropriate, because it is one o f the ma in fun ctions o f the sympathetic nervous systems to continuall y tune visceral, metabolic, and circulatory acti vity ro the rap idly cha nging requirements of the skeleta l muscu lature. Every motor activity, orga nized th ro ugh the somati c innerva ti on origi nating in the spinal
cord, also involves the simultaneous coordinated acti vity of the sympathetic nervous system and the tissues and processes regulated by it. For the sympa thetic nervous system (0 meet its suppOrtive responsibilities to the musculoskeletal system, it must be continuall y apprised of the acti vities and requ irements o f th at system. Hence, integration is pos ible onl y with sim ultaneous afferent input both to the mOtOneuron a nd to the sympathe ric prega nglionic neurons in the cord, from the higher centers thro ugh descending pathways, a nd fro m countless musculoskeletal reporting stations, th ro ugh the do rsa l rOOts (3). If there is a su bl uxa tion syndrome present at a particular level o f the ve rtebra l column, this a ffects the a bility of the spina l cord to effectively integrate incoming and outgoi ng info rmati on. The rapid mo ment-to-moment adjustments in acco rdance wi th levels of exertion and postureor antici pation, conscious or unconscious, of exertion-a re o rchestrated largel y by the sy mpathetic nervo us system (4 ). Sympathetic Effects in Health y Tissue If we acce pt that in several pa tho physiologic states sympathetic efferents can produce pain a nd hyperalgesia, an obvious question is, to what exten t ca n similar effects occur in normal healthy tissue (5). We know that man y peripheral targets, in addition to blood vessel , receive sympathetic suppl y. For in ta nce, there is good evidence fo r an innerva tion of muscle spindles, Pacinian corpuscles, and other specia lized end o rga ns in skin (6) .
321
We also might ex pect a modification of sensory inflow to occur seconda ry to cha nges in blood flow or piloerection. It is therefore not surprising tha t ph ysiologic experiments have identified some actio ns of sympathetic efferent in norma l skin. Cold therm orece ptors can be excited by low-freq uency stimulation of the sympathetic trunk (7). Simila rl y, some sensiti ve mechanorecepto rs with unmyel inated axo ns are also tra nsiently excited (8), a n effect that is pro ba bly ca used by small cha nges in the tension in the tissues secondary to vasomoror changes (9). A most importa nt question is w hether nociceptOrs a re excited by sympathetic stimulation. Here a ll work ers agree that, for normal nociceprors, with A, d, o r C axons, no direct excitation occurs (10-12.) . Together, these studies sugges t tha t in no rma l tissue, sympathetic activity has onl y modest sensory effects (5) . Wo uld the presence o f a subluxation complex change this modest sensory effect ? Sympath eticall y Mediated Pain The moSt important conditions are those o f causalgia and refl ex sympathetic dystroph y. Causalgia is a conditio n that occasiona ll y follows trauma ro a major nerve. The term was coined by Mitchell in the middle of the last century to indicate the presence of persistent burning pain in such cases. The more general term ref/ex sympathetic dystrophy is used to categori ze pa tients with some o r all of the fo llowing symptoms: spontaneo us burning pa in; hyperalgesia (indicates both pain to norma ll y innocuo us events a nd increased sensitivity to noxi ous events); hyperpathia (dela yed and exaggerated painful res ponse ro stimuli ); disturbances o f vasomoto r and sudomOtOr contro l; and dystrophic changes in the peripheral tissues, such as abno rmalities of hair and nail growth a nd osteo porosis. Although there is still much confusion in the use o f these terms, refl ex sympa thetic dystroph y is genera ll y used when the condition is not associated with obvious periphera l nerve trauma . Swelling is the most co nstant physica l finding, which if not treated ea rl y is often foll owed by the rapid onset of stiff-
322
The SUl*lxItlon ByI"'...I. .
ness (13). Precipitating events include minor tissue trauma and fractures, non trauma ric nerve lesions slich as those seen in diabetes, and even lesions ro rhe central nervous system. Cou ld a subluxation syndrome be a factor in this condition? There are twO main reasons for believing that the sympathetic nervous system may be important in the genesis of pain in these conditions. First, sympathetic function is frequent ly abnormal. The skin of the affected region is often initially warm and red, larer pale and cold. Anhydrosis or hyperhydrosis may be present. The dystrophic changes thar occur are likely secondary to changes in blood flow to the area. A second and more compelling reason for implicating the symparheric nervous system is [hat maneuvers that alter sympathetic activity frequently alter the patient'S pain. For instance, visual and auditory stimuli, emotional disturbance, or thermal stress all provoke sympathetic arousal and a ll can exacerbare the pain in these patients (5). A final important clinical finding is rhar pain often radiates exrensively beyond the area of damaged tissue or the innervation territory of the damaged nerve. The spread usually ignores traditiona l boundaries such as nerve territories or dermatornes. In extreme cases, it can spread to encompass large areas of the body surface. Central Changes The abi lity of peripheral nerve lesions or peripheral tissue injury to alter spinal somarosensory processes is becoming well recognized. The ascending spinal pathways that transmit information rostrally begin to respond more vigorously to peripheral inputs and indeed can become responsive to totally new inputs that normally do not drive them. These cells also relay aberrant activity generated from the periphery. This process can develop quite rapidly with peripheral tissue injury, and it is possible that once establ ished it may become largely independent of the precipitating event (14). The subluxation syndrome, if at the level of the injured peripheral nerve or tissue, affects the spinal somatosensory processing.
A second type of disturbance is seen in the response properties and patterns of reflex organization in the sympathetic nervous system. Within the dorsal horn, the representation of the body surface is very compressed, especially in the medioleteral plane. Expansion of receptive fields over quite substantial areas of the body surface are therefore possible and provide an explanation for the radiation of pain (5). Neck Proprioceptors Proprioceptors provide information to the central nervous system (CNS). The receptors that send the information are specialized and located in extraspinal and spinal structures. Muscles, by their share of volume in the body, contain the most. The receptors are somewhat different and more numerous in the spinal musculature, especiall y in the cervical muscles. A review of the receptors, spinal muscles, and their spinal a nd CNS correlates has already been published (15) . The essential points plus new information are covered jn this section as jt relates to the development of symptoms after trauma to the cervical area. Muscle Receptors Most muscle contains at least four types of receptors, namely: 1. 2. 3. 4.
Muscle spindles Golgi tendon organs Paciniform corpuscles Free nerve endings
Of these, muscle spi ndles and Golgi tendon organs have been thought to signal changes in muscle length or force development. However, paciniform corpuscles and free nerve endings also playa role in proprioception.
Muscle Spindles In the cervica l musculature, the spindles are arranged in elaborate configurations such as paired, parallel, and tandem (Figure 17-1). These spindles, because of their volume per gram of tissue and their configurations, signal enormous volumes of information ro the spinal
fIIIure 17-2 Diagram of spindle complex located in the intertransverse muscle group of the C2-C3 joint
c ~
17·1
Diagrams of musc le spindles in various
configurations. A, Four paired spindles. Note that no
inrrafusal fibers are shared. B, Parallel spindles. Note
region. Tendons 3rc shown as stippled regions. Goigi tendon organs at the ends of spindles are shown as
encapsulated regions containing broken lines. (Adapted (rom Bakker D, Richmond F. Muscle spindle complexes in muscles around upper cervical vertebrae in the cat.] Neurophysio/1982; 48:62-74.)
the capsule discontinuity at the equatorial regions of
spindles. C, Spindle array in which five spindles exist in raodem sharing onc common nuclear bag fiber.
(Adapted from RIChmolld F, Abrahams V. Morphology and enzyme h,stochemistry of dorsal musdes of the cat neck. j Neurophysiol 1975; 38:1312-2 1.)
contracting fibers, they may be signaling changes in muscle length.
Free Nerve Endings cord and CNS when tiny changes occur in muscle. With a subluxation syndrome in the cervical spine, the information entering the spinal cord and CNS therefore is affected.
Free nerve endings are distributed widely throughout all types of muscle and connective tissue. They respond to mechanical stimuli and muscle contraction (16). Mechanoreceptors (lS) also provide information to the spina l cord and CNS.
Golgi Tendon Organ The Golgi tendon organ (GTO) is an encapsulated receptor that lies in series with extrafusal fibers at the musculotendinous junction (Figure 17-2). Most GTOs are located in the rostral half of the large muscles. In neck muscles, spindles and GTOs are often clustered together in complicated receptor arrays. Stretching of muscle, whether tonic or dynamic, causes the GTOs to inhibit the muscles.
Paciniform Corpuscles Paciniform corpuscles are small cylindrical encapsulations that ensheathe the end of a sensory nerve. [n muscle, because they are located near
Biomechanics The essential biomechanics of the cervical spine, both upper and lower, are expertly reviewed by Moroney (17). Other pertinent information is presented here. There are five intervertebral discs (lVD) from C2 through C7. The discs adhe re above and below to hyaline articular cartilage, which covers the articular surfaces of the vertebral bodies. These five [VDs account for 25% of the total length of the cervical spine (18). Compared with the foraminal diameter at the neutral position, there are statistically significa nt reductions in foramen diameter, 10% and 13% at
324 20° and 30° of extension, respectively. Conversely, in flexion, there 3re statistically significant increases of 8% and 10% at 20° and 30° of flexion, respectively. A subluxation syndrome affects the spinal mechanics, causing the verrebrae above or below the affected area to move more excessively. It has been stated that the foraminal encroachment by an uncovertebral osteophyte with narrowing of the foramen results in direct compression of the nerve rOOt and is thought to be a major source of pain in cervical degenerative disc disease. Anatomically, the nerve roots have less protective epineurium as compared with the peripheral nerves, and this has been implicated in their susceptibility to compression. Therefore, the understanding of the alteration in the size of the foramen with cervical motion becomes an important factor in understanding the mechanism of trauma and its management. Also reported were greater absolute and relative changes in the foraminal size at C6 and C7 foramens compared with the C5 foramen. This may be related to the relative flexibility of these levels. The srudy by Yoo and co-workers (19) shows that the percent change of C5 foramen size was only 55% to 60% of C6 and C7 foramen size change, possibly reflecting a two-thirds decrease in flexibility. This relatively decreased motion may prevent greater excursion of the facets at the C4-5 interspace, accounting for the decrease in the alteration in the foramen size of C5 (19) .
Age In sagittal motion, there is an inverse relationship between age and range of motion; that is, as age increases, mobility decreases (18). Hayashi et al. (20) compared three groups of healthy volunteers aged 20 to 40, 40 to 60, and 60 to 82 years. They found a 25% reduction in the maximum flexionextension achieved when the group aged 60 to 82 was compared with that aged 20 to 40 years. Seventy-one percent of the decrease occurred at the
C5-C7 motion segments. If there is a subluxation syndrome at these levels, it will further decrease the flexion-extension excursions. Dvorak et al. (21) showed that significantly decreased motion differences were found between age-groups within gender, and between gender groups, in corresponding decades. Results of rotation out of maximum flexion suggest and support earlier conclusions that rotation of the CI-C2 segment does not decrease with age, but rather increases slightly to perhaps compensate for the overall decreased motion in the lower segments. A subluxation syndrome at CI-C2 therefore affects the overall motion of the cervical spme. ~8I'vert8brallllscs Pertinent information regarding the disc is thoroughly covered (22), and new information is provided here. The major biochemical changes observed in the disc matrix with aging are similar to those described in other connective tissues. The most noticeable in the disc, however, is dehydration of nucleus pulposus (NP) and the loss of sulphated glycosaminoglycans (GAGs), accompanied by a large increase in noncollagenous proteins. The water content of the NP of the human disc decreases from 88 % of dry weight at birth to 69% at 77 years. [n the anu lus fibrosis, water content declines from 78 % at birth to 70% at 30 years, thereafter remaining relatively constant. The absolute amount of collagen also may increase with aging, but only slightly as a fraction of dry weight. Numerous histopathologic studies of human discs at autopsy have confirmed that a high incidence of primary degenerative changes are present in individuals older than age 30, and this increases with age. However, retrospective investigations of the medical records of these individuals do not show a history of back complaints in all cases. This indicates that disc degeneration does not invariably lead to clinical symptoms of back pain . From these findings we may conclude that, with aging, biochemical changes take place
its ability to achieve efficient dissipation of the mechanical stresses imposed on the spine during everyday activities (23). A subluxation syndrome
syndrome that restricts movement affects this monitoring by the CNS. Both Pacinian corpuscles and Golgi tendon organs are mechanoreceptors and are reportedly active in response to changes
limits movement at a particular motion segment;
in tension.
this also affects the blood supply to the disc. The nucleus pulposus of the human, like that of the dog, startS losing notochordal cells and depositing a hyalinelike matrix within a few years of birth. Because there is evidence in dogs that the rate at which this process takes place is genetically determined, it is nOt illogical to hypothesize that the disc cells of humans are similarly programmed. If this is so, then the response of discs
Recent studies have shown that the IVD has a complex structure and mechanical properties that vary from tegion to region and change with age. There is evidence that the disc is capable of some regeneration. These findings plus evidence the disc is innervated suggest that the IVD may be more than a pad that absorbs shock and maintains the spaces between the vertebral bodies. The concentration of nerves in the middle third of the disc may be sensing superoinferior compression or deformation. The circumferential arrangement of the nerve bundles about the disc and the superficial-to-deep location of the mechanoreceptors may enable the IVD to sense peripheral compression of deformation as well as alignment (25). However, a subluxation syndrome limits normal movement and function of the disc, affecting its
within the matrix of the disc, which can reduce
within the human spine to restricted movement may, in part, be heritable. In animal experiments
surgical methods were used to restrict spina l movement; such procedures induced profound changes in disc metabolism within 6 months of application. In the case of the human spine, disc changes arising from inadequate nutrition may occur for several reasons, for example, the subluxation syndrome, caused by insidious or traumatic circumstances, maintenance of bad posture
such as sitting, driving, flying for long periods, lack of appropriate exercise, and smoking. These extrinsic influences, coupled with an aging disc cell population and the sttesses of everyday activities, can lead to failure, which itself contributes to degenerative discs (24). In
human
cervical
discs,
nerve
fibers
appeared to enter the disc in the posterolatera l direction and course both parallel and perpendicular to the bundles of the anulus fibrosus. Netves were seen throughout the anulus but were mOSt numerous in the middle third of the disc. The presence of nellral elements within the IVD indicates that the mechanical status of the disc is monitored by the CNS. If the nonencapsulated nerve endings in the anulus fibrosus are pain receptors, their presence may explain the occur-
rence of neck or shoulder pain when there is dislocation or trauma to the disc. If the nonencapsulated nerve endings in the anu lus fibrosus monitor the mechanical status of the disc, a subluxation
inherent properties.
hIIna to tile Cervical SI*I8 Nearly 4500 years ago, an Egyptian physician described a patient with a cervical spine injury as "one having a dislocation in a vertebra of his neck while he is unconscious of his two legs and his two arms, and his urine dribbles, an ailment
not to be treated" (26). Although the current outlook is nOt so bleak, cervical spine injuty continues to be a catastrophic event. There are approximately 280 spine injuries per million population each year in the United States, and approximately 10% to 30% result in spina l cord injury (27,28). The most common cause by far is motor vehicle accidents, with falls and sports-related injuries also being important traumatic events (29,30). T he mortality after traumatic spina l cord injury is 47.7% , compared with 6.7% for all trauma victims. Forry percent of patients die
before reaching a hospital, and a further 10% die in the hospital (31). Injuries to the upper cervical
326 spi ne account for one third of cervical spine injuries, but they are responsible for 80% of the deaths of acute cervical trauma. Of those that survive, up to 70% suffer from significant neurologic deficits (32). Mechanism of Injury: General Spinal injuries may be classified according to the mechanism of injury (33,34 ). Classification of Spinal Injuries
and disc space are also distupted, and bilatera l facet joint dislocation results. These injuries are unstable and are associated with a high incidence of cord damage. Flexion-rotation injuries disrupt the posterior ligamentous complex and produce unilateral facet joint dislocation. These injuries tend to be stable and are not usually associated with spinal cord injury, although cervical rOOt injury is common. The most severe of the fl exion injuries is the teardrop fracture. Both columns are disrupted, and there is bilateral facet joint subluxarion . The spine is unstable, and severe cord
Hyperflexion
injury is seen.
Anterior subluxation syndrome Bilateral interfacetal dislocation Wedge compression fracture Flexion teardrop fracture
result from a blow to the anterior part of the head or from an acceleration (whiplash) injury.
Hyperflexion and Rotation Uni latera l interfacetal dislocation
Hyperextension Hyperextension fracture-dislocation Fracture of posterior arch of atlas Traumatic spondylolisthesis (hangman's fracrure) Laminar fracture Subluxation syndrome
Vertical Compression Compression fracture Burst fracture
Jefferson burst fracture (C l )
Mixed Mechallism Atlantooccipital dislocation Odontoid fractures Total ligamentous disruption Flexion injuries usually result from blows to the back of the head or forcefu l decelerations as might be experienced in motor vehicle accidents. Pure flexion trauma may result in wedge fracture of the vertebral body, without ligamentous injuries (33). These injuries are stable and are rarely associated with neurologic injuries. With mo re extreme trauma, the posterior column is disrupted. In severe injuries, the anterior ligament
Hyperextension injuries to the cervical spine
Extension injuries 3fC twice as common as flexion injuries, and approximately one third involve the
atlantoaxial joint. These injuries are more often than not associated with cord damage. Hyperextension appears to be the most common mechanism of injury, accounting for approximately one third of all cases of cervica l spine fracture (32) . Hyperextension combined with compressive forces (for example, in diving) may result in fracruredislocations. The lateral vertebra l masses, pedic1es, and laminas are often fractured in this injury (34). Because both anterior and posterior columns a re disrupted, this injury is both unstable and associated with high incidence of cord dysfunction. Violent hyperextension, with fracture of the pedicles of C2 and forwa rd movement of C2 on C3 , produces the "hangman's fracture." The fracture is unstable, but the degree of neurologic compromise is highly variable because the bilateral pedicular fractures serve to decompress the spinal cord at the site of injury (35). Burst fractures are caused by compressive loading of the vertex of the skull in the neutral position. This type of injury is converted into a flexion or extension type with only minimal angu lation of the injury fo rce, and this is relatively rare as a pure entity. Compressive forces in
the lower cervical spine resu lt in the explosion of compressed disc material into the vertebral body. Depending on the magnitude of the compression
loading and associated angulating forces, the resu lting injury ranges from loss of vertebral body height with relatively intact margins to complete disruption of the vertebral body. Posterior displacement of comminuted fragments may result, producing cord injury. Despite the cord injury, the spine is usually stable (34). A considerable number of fractures are misread on initial evaluation in the emergency room
(36-38). The incidence of missed fractures ranges from 1% to 33%, with mOSt series reporting 100/0 or more. The most common reasons for missed diagnosis are failure to take radiographs or misinterpretation of the radiograph (39). Missed injuries are often unstable, and secondary neurologic lesions are 7.5 times more common in patients who are not diagnosed at initial evaluation (37) . The major factor in the development of a secondary injury is failure to immobilize the neck (40). Mechanism of lnjury: Specific
Occupational Lifestyle Trauma to the Ceroicai Spine The existing literature on back and neck pam suppOrtS two major conclusions:
1. That the prevalence of spinal pain in the United States and elsewhere is so great that it constitutes a major health problem . 2. That spinal pain is associated with identifiable activities. A style of living or a line of work can contribute to the onset or exacerbation of
back and neck disease (4 1). For society at large, prevalence rates for back and neck disorders vary from one study to another. However, they are characteristically high across investigations. Put another way, the proportion of any population that is afflicted by a back or neck problem at some point in life is exceedingly large (42). Musculoskeletal disorders of the neck and shou lders are receiving an increasing amount of anention. Earlier reports from Japan suggest that the problem was growing, and Swedish statistics
on occupational injuries show an increase in the number of reported neck and shoulder disorders during the yea rs 1982 to 1985. Factory workers as well as office workers have been mentioned as risk groups, and women workers in Sweden
report relatively more injuries in the neck, shoulders, and arms than do men. A variety of risk factors has been suggested for neck and shoulder disorders. One example is the introduction of modern technology resulting in specialized monotonous tasks that impose sra[ic or repetitive loads. These monoronous tasks affect the muscles, which in turn contribute to the development of subluxation syndromes. Consequently, a relationship has been shown bet.Ween [ime spent working with office machines, including visual display units, and the occurrence of musculoskeletal symptoms. Other studies have indicated that the problem is multifactorial, with mental strain, lack of control, and low job satisfaction being important elements in the development of the disorder. A recent study of 420 medical secretaries found that 63% had experienced neck pain some time during the previous year. Shoulder pain during the previous year had been experienced by 62 %. Age and length of employment were significantly related to neck and shoulder pain. Furthermore, working with office machines 5 hours or more per day was associated with a significantly increased risk of neck pain, shoulder pain, and headache. Finally, a poorly experienced psychosocial work environment was significantly related to headache, neck, shoulder, and low-back pain (43). Workplace design, posture, joint mechanical problems, subluxation syndrome, and monotonous work have been identified as important factors in the development of occupational neck and shoulder disorders. To reduce the static muscular state caused by monOtonous work, the introduction of spontaneous as well as scheduled pauses are advocated. Pain may result in the development of Stress symptoms such as sleep problems, anxiery, or feeling depressed (44). Musculoskeletal disorders of the neck and upper limbs, including the
328 sub luxation syndrome, ha ve frequentl y been repo rted in workers engaged in jo bs involving awkwa rd postures and high-fo rce, high-repetiti ve mo vements. Some investiga tors have pointed o ut that, a fter controlling fo r potential co-factors such as age, constitutio n, and disease, the length
The lifestyle habits of indi vidua ls ca rrying purses o r briefcases continuall y o n one side
slowl y d istorts the neck-shoulder muscles on that side, contributing to altered cervica l mechanics
a nd pa in . Likewise, slee ping on the stomac h pre-
disorders in workers performing manual tasks.
disposes rhe cervica l spine to micro rrauma of rhe deep muscles, and liga mento us and caps ular structures. This not o nl y ca uses subluxatio n syndro mes to deve lo p, bur th erapeutic interventio n
So me epidemio logic data suggest tha t vibra tion may contribute to upper limb disorders as a result
by a chi ro practo r is difficult or im possible unless the ha bit is cha nged .
of exposure and va ri ous ergonomic factors are
the maj o r contributo rs to the o nset o f soft tissue
o f repea ted mic ro rrauma on the tissues and jo ints
of the hand-arm system. The term ClIlnlllative trallma disorders has recently been suggested to refer to musculoskeleta l a ffli ct ions a rising fro m chronic exposure to microtrauma . A recent stud y
ind ica ted that musculoskeleta l impa irment to the upper limbs was mo rc severe in chainsaw o perato rs tha n in the controls who did solely manua l work. This suggests that vibration stress is a n importa nt contributor to the development of musculoskeleta l disorders in workers using handheld vibrating tools (45 ). The in crease in musculoskele tal disord ers,
a long with the recognition of a multi facto ria l ca use, has created a shift in interest from the trea tment of these disorders toward their prevention. O ne commo nl y used preventive measure is the back/neck school. Although initially directed
Athletic Trauma to the CeMJical Spil1e Athl etic injuries to the cervica l spin e can be seri-
ous or fatal. O ne reason is the vulnera bil ity and location of the cervica l spine. Another is the mechanica l disadva ntage the head-neck coupling has to impact trau mas. Injur ies have been ca used
by football, soccer, skiing, wa ter sports includ ing di ving, boxi ng, hockey, a nd the use of the tra mpo line (4 7-49). The number of persons participating at all levels of athletic competiti on has increased tremendously in the past twO decades. Concomitantly, rhere has been a pro po rtiona te increase in
athletic injuries and related problems. If yo u beco me in vo lved in the trea tment of SPOrtS injuries, and are responsi ble fo r the ca re of ath -
back/neck
letes, at some time you undoubtedl y may be required to manage a n injury that could be crip-
schools ha ve become po pu lar too ls for secondary
pling o r even fa tal. In such a crisis, ca re is a m3t-
preventi o n. Secondary preventio n refers to interventio ns des igned to eliminate, reduce, o r prevent
ter of sound judgment and basic know ledge of emergency techniques (50) . Athletic injuries to the neck and cervica l spine
mainl y
toward
chro nic
disord ers,
further develo pment of pain . A back/neck school may be described as an educationa l package fo r increasing the pa rticipants' kn owledge of their bac k pro blem and its relationship to environmental and individua l facto rs. With increased knowledge, it is ho ped that the patient will modify persona l behavio r a nd surroundings (for exa mple,
can in volve rhe bo ny clements, IVDs, li gamento us and muscular suppo rting structures, elements of
the brac hia l plexus, nerve roors, and the spinal cord itself. Spina l cord in juries related to sports and recrea ti o n appear to be in creasin g in Ca nada.
wo rkplace) to conrro l, limit, o r prevent th e pain .
Sports a nd recreation moved from the third to the
A recent stud y showed th at neck schools, despite good compliance, a ppea r to be of lim ited clinica l va lue fo r prevention of neck and shoulder disorders (46).
second leading cause o f spinal injuries trea ted at
two To ronto Hospitals between 1948 and 1983. Shallow-water di ving was by far the leading contributing activ ity. Most o f th e in juries we re cervi-
17 carvlcogellic Sympathetic SylD'omel: EtIoIagy, 1reatment, and IlehabllIlIion cal and mOSt caused complete paralysis below the level of the injury. Of the 47 injuries caused by diving, 33 were injury to the cord, 8 to the root, and only 13 constituted a spinal injury without neurologic deficit. The mechanism was the head striking the pool or lake bottom, with fracturedis location the most frequent type of spinal IIllury. Hockey injuries were also assessed. Most of rhe injuries were in rhe middle to lower cervical
region, with fracture-dislocation rhe mOSt COIllman type of bony injury. Of the 42 injuries, 28 were spinal cord injury, 12 of which were
COI11-
plete injuries. The leading mechanism was a push or check into the boards, with the helmeted head striking the boards with neck slightl y flexed (51) . Another factor that contributes to the extent of spinal cord injury is either preexisting, or
development of, spinal stenosis (52,53). In soccer players, the simple effect of heading rhe ball over rime caused degenerative changes in rhe cervica l spine and injuries to the brain. Repetitive sma ll traumas over an extended period have a detrimental effect on the cervical spine and eNS (54).
Motor Vehicle Fiexiol/-Extellsiol/ II/juries The mechanism of motor vehicular injuries to the individual is addressed in detail because it is so common and of immense interest
[0
chiroprac-
rors.
II/troductiol/. The important concept that all who deal with motor vehicle accident (MVA) injuries shou ld understand is that our anatomy dictates a great deal of why the injuries occur. Think, for a moment, abour your head, which weighs approximately 8 to 12 pounds and sits on top of the mOSt flexible area of your body, your neck. The flexible neck has approximately 29 joints, 50 pairs of muscles, and a ligamentous capsular nerwork that is very complex. The neck sits on a stable base, the upper back, or thoracic spine. So we have a ball-the head, a flexible chain-the neck, on a rigid base-the upper back.
329
Any sudden motion of the body causes the head to wobble or to be whipped around on the neck, a flexible chain of 29 joints, developing great forces and the potentia l for man y subluxation syndromes. This is the essence of most MVA problems.
Mechallism of II/jury. Eighty petcent of MVAs occur at speeds of less than 25 mph. Most "whiplash accidents" occur as a result of rear-end coll isions (55) . Data from the Research Accident Investigation Center, University of Rochester, shows rhar, even at low speeds, the occupa nts of the ve hicle that was struck will sustain serious injuries (56). Panjabi and White have shown that a 10.8 mph rear~end collision wirh an impacr durarion of 0.1 seconds produces an acceleration of the lead vehicle of five times the force of gravity. The significance of this is that collisions occurring at relatively low speeds resu lt in large forces being app lied to the lead vehicle. If this causes easy acceleration of the lead vehicle (for example, on a wet/slippery surface), this will cause extensive damage to its occupants. According to the National Highway Traffic Safety Administration (NHTSA), "a ten-mile an hour collision is equ ivalent to catch ing a 200 pound bag of cement dropped from a second stOry window. People don't understand the dynamics of cras hes." (57) McKenzie has shown that the inertia of the occupant's head and neck are in unstable equilibrium. The struck veh icle reaches its peak acceleration before the occupant's head-neck and upper back have acce lerated to any significant amount. As the head, neck, and upper back try to catch up to the peak acceleration of the vehicle, they have to attain speeds of 2 to 2.5 times the maximum vehicle acceleration. The head relies on ly on the neck, through which the force of acceleration is transmitted. As a result, the force loads at the headneck can be quire extreme, which has been shown to exceed 100 pounds for collisions not exceed ing 15 mph (58). This shows that even a minor acci-
330
TIle SlMlXIIIon By........
dent causes significant damage to the neck of the occupant of the sttuck vehicle.
Who Is Injured More? Passengers in rhe right front seat are injured more because they are less prepared than the driver for a collision (59). Women sustain injuries rwice as often as men.
Men have greater neck muscle strength, which seems to dampen the effects of the " whipping" cervical spine (59,60) .
surface may cause more damage to the car. The physical health of the individual is significant. Any previous body mJury or degenerative changes, especially to the vertebral column, is reinjured, causing longer treatment and rehabilitation time. A young, fit, healthy person without previous injury will rehabilitate in less time than an older, unfit person (66).
The Extension Acceleration Injury: Rear End. Macnab (60) found that patients who sustained
Other Factors That Affect the Mechanism of [njury. The age of the person is very important
an extension-acceleration injury suffered more
because preexisting traumas, the presence of degenerative joint and disc disease, sma ller stature, Jess muscle tone, and decreased ligamentous function, in addition to decreased reaction times, all can contribute to the severity of soft tissue injury (61). The high proportion of osteoporosis predisposes seniors to fractures of the vertebral bodies (62) . The motion of the head at impact, such as rotation, causes damage to the C2 dorsal root ganglion (63). Data from the University of Rochester Accident Investigation Center show rhat even though all cars have head rests, they are usually not properly positioned, and they reduce the frequency of neck injuries by on ly 14%. Most car seats are designed for the average person and are weak . Because they do not fit the contours of the back properly, excessive movement occu rs or the seat breaks, both contributing to injuries of the entire vertebra l co lumn. The size of the vehicle srriking rhe lead ve hicle is very important. Seat belts, even though they are necessary in preventing the more serious head,
spine, which includes a variety of sensitive tissues in the anterior compartment of the neck, this is
facial, chest, and spina l injuries, contribute ro more spinal and paraspinal tissue injury. Injuries
problems. Because of the anatomy of the cervical
understandable. The extension injury can cause some or all of the following ro occur: • Tearing of the fibers of the sternocleidomasroid muscle
• Tearing of the fibers of the scalenus anterior muscle • Marginal fracture of the vertebral body • Anterior protrusion of disc
• Retropharyngeal or prevertebral hematoma • Compression of the vertebral artery at C1 • Compression of the C2 dorsal root ganglion • Fracture of the spinous process
• • • • • • • • •
Compression of the spinal nerves C5-6-7 Posterior subluxation syndrome of C4 on C5 Compression of the spina l cord Dislocation of C3, with tearing of the Sharpey's fibers Tearing of the longus colli muscle Damage to the sympathetic chain that lies anterior to the longus muscle Fracture of the posterior arch of C1 Tearing of the anterior longitudinal ligament Temporomandibular joint pathomechanics
to the spine occur one to three times more fre-
quently in belted drivers (64,65).
Road Conditions. A wet slippery surface causes more damage to the occupants of the vehicle struck, because of the magnification of acceleration (57) . In comparison, a dry or loose grave l
The Flexioll Deceleratioll [lljury: Head-Oil . The injuries are not as severe because of the fol· lowing: 1. The victim usually anticipates the accident and tenses for it.
17 Cervlcog'lIlc By_bile By ..........: Etiology, TreaIiii8iiI, ... Rellalillbidoii 2. The chin stops the head by resting on the sternum (60).
331
>
Symptoms of Cervical Trauma
The flexion injury can cause: • Tearing of the fibers of the splenius and semispinalis muscles • Posterior separation and protrusion of the disc • Tearing of the interspinous ligament • Tearing of the posterior longitudinal ligament • Anterior subluxation syndrome of C5 or C6 • Flexion rotatory injuries of the cervical and
upper thoracic muscles caused by seat belt use (64,65). The lateral flexion injury will cause, on the flexion side: • Pathomechanics of the intervertebral jointsjoints of Luschka • Facer jamming caused by the anatomy of the upper thoracic and lower cervical spines On the contralateral side: • Tearing of the fibers of the following muscles: • Sternocleidomastoid, scalenus group, superior trapezius and intertransversaii • Capsules of the intervertebral joints • Traction of the nerve
rOOtS
• Superior subluxation of the first rib
Symptoms. From the analysis of some of the tissues injured, one can understand why cervical injuries are so difficult to assess and at times take so long to resolve. Some of the major symptoms that are the result of cervical trauma are listed in the box at right. A few of the symptoms listed reviewed in the following text.
JIl
the box are
Horner's SyndrOme Horner's syndrome is the most common complication associated with the cervica l sympathetic trunk (CST). The complex of findings includes ptosis, anhydrosis, miosis, and enophthalmos. Other effects associated with CST injury can include alterations in cerebrovascu lar blood flow,
• Pain • Radiculitis • Thoracic outlet syndrome • Muscle spasms/srrain/sprain • Limited range of movement • Cervical dorsalgia • Altered cervical mechanics • Hematoma • Sympathetic dysfunction • Headaches/sleep disorders • Vertebral artery syndrome • Vertebral subluxation syndrome CIoinI. • Headaches • Changes in brainstem function • Disequilibrium • Lightheadedness • Depression • Syncope • DeCreased concenrration • Vertigo • Blurring of vision • Meniere's disease • Nystagmus • Homer's syndrome • Barre-Lieou syndrome • Neck-tongue syndrome increased salivary viscosity, and lability of blood pressure (I). Blurring of vision is another sign of injury to the CST. With injury, the CST can cause flattening of the lens. This causes lack of normal accommodative power of the lens (67). Concomitant spasm of the vertebral arteries could explain in some cases the causes of tinnitus, deafness, and mild confusion. The injury to the CST may also explain voice changes, difficulty swa llowing, a nd dryness of the mouth (68). Anatomic observa tions show [he cervical sy m~ pathetic (CS) nerves are relatively immobile as
332 compared with the vagi. The CS trunks lie embedded in the fascia of the prevertebral muscle, longus colli, anterior to the transverse processes a nd posteriot to the carotid sheaths. The gray rami communicantes pierce the cervica l muscles in their course to the cervica l spinal nerves (69). Other symptoms of injury to the cervical sympathetic trunk include throbbing headaches, tenderness of the anter io r neck, and persistent supraorbital anhyd rosis (70) .
Meniere's DIsease Meniere's disease is characterized by patients having recurrent attacks of vertigo with a fluctuating hearing loss, tinnitus, and fu llness in one ea r. Acute attacks can last up to severa l hours, and residual symptoms can remain for days or even longer (71). Meniere's disease has a lso been given the name endolymphatic hydrops (72) a nd is characterized specifica lly by paroxysma l vertigo, tinnitus, and sensorineura l heating loss (73) . The cause is unknown (72); conditions ranging from polyarteritis nodosa, syphi lis (73), and trauma to the cervica l spine have been implicated (74). Davis (75) showed thar vertigo tesulted from cervical nerve root irritation, which he thought
was caused by hypertrophic arthritis of the cervica l spine, a nd whic h responded to cervica l traction. Jackson, as mentioned by Braaf and Rosner (74), stated, "Meniere's syndrome may be part of the cervical syndrome and as much as the symptoms of equi li bratory disturbances are very much the same in both instances and are due to teflex stimulation of the sympathetic nerve supply to the inner ear and [Q the eye." Trauma to the cervical spine causes the development of subluxation syndrome. Th is produces mechanical damage and irritation of [he cervica l nerves or intermittent compression of the vertebral artery_ With damage or irritation [0 the cervical nerves, reflex mechanisms are set up through the sympathetic nervous system, affecting any or all crania l nerves, producing mainly sensory and vasomotor symptoms.
Treatment involves cervical traction (74), but one must be careful regarding fotces on the mandibular, because this will affect the temporomandibular joints. Chiroptactic therapy to testore biomechanical integriry by eliminating the subluxations is necessary and provides relief if not a cure (70,76).
BarrHJeoo Syndrome The Barre-Lieou syndrome was first described by M. Barre in 1926. He described the headache as mainly suboccipital, ve rtigo as mainly precipitated by turning the head and not accompanied by any other vestibular dysfunction, and tinnitus along with visual symptoms. He noted that the patients were unable to read for long periods and usually had consulted a specialist in eye disease, but there were no objective findings. Other secondary symptOms and signs include hoarseness that appears and disappears suddenly, severe fatigue, and radiographic findings localized to C4-5-6 levels. There was also an aching on one side of the face or the eye (77). Similar symptoms have been observed in patients injured in traffic accidents. and attention has been focused on this relationship (78) . One difficulty in assessing the syndrome is that the crania l symptoms are related to excessive movement of the neck. Research has led to a variety of opinions as to the cause of Barre-Lieou syndrome. Some of the more pteva lent a re occlusion of the vertebral arrery (79,80), involvement of the cervica l sympathetic systems (77), and interference with neck reflexes. (8 1) Stewart (77), in his review of the neurologic aspects of the cervical spine, outlined the following: the fifth cervica l root conta ins sympathetic fibers that join the carotid plexus, furnishing sympathetic fibers to the neck and head. The sixth cervical root contains sympathetic fibers that proceed to the subclavian and the brachial plexus. The seventh cervical root supplies sympathetic fibers to the cardioaortic and phrenic plexuses. There are also preganglionic sympathetic centers that arise from the medial latera l gray of the cervica l cord at the C5 a nd C8 levels and produce
fibers ro form the white rami communicantes.
This tangled web of sympathetic fibers and small ganglionic masses from the cord follows the vertebral artery in its course in the transverse fora-
mens of C4 to C7. Changes in the position of the vertebra can precipitate a variety of symptoms. Tamura (78) found a lateral soft disc in patients with Barn,-Lieou syndrome at the C3-4 level, which exerted pressure on the C4 and especially its ventral root. Twenty of the 40 patients had surgery to remove the disc and, except for tinnitus, all symptoms had settled, compared with the group that did not have surgety. C4 nerve rOOt communicates with the superior cervical
ganglion of the sympathetic chain through a communicating branch of postganglionic fibers. Irritation by a soft disc could give sympathetic nervous symptoms, and that can be explained as follows: • Headaches may result from spasm of the internal and external carotid vessels. • Vertigo may be caused by ischemia of the brain produced by sympathetic vasoconstriction of the internal carotid artery and its intracerebral branches. • Tinnitus may be produced by sympathetic stimulation of the corticotympanic nerve, which derives from the internal carotid plexus. • Ocular symptoms could be explained either by the influence of the internal carotid plexus on the ciliary muscles, causing interference with
their normal regulation, or by reduced blood flow in the ophthalmic artery. • Facial pain may be related to the fact that the superior carotid ganglion has communicating branches with the facial nerve and trigeminal ganglion. • The bilateral nature of the symptoms could be explained by the transverse branches, which connect the sympathetic trunk on one side to the other. Clinically, a subluxation causes some or all of these signs and symptoms. Chiropractic correction of the subluxation syndrome will relieve these signs and symptoms.
Elridge and Li (82) described a case of disc herniation of C4-5, in which the corneal sensitivity and corneal reflexes were absent, along with anesthesia of the cheek and tongue. Laminectomy gave relief of all symptoms on the second postoperative day.
Cervicogelilc VeI·tIgo It is important to stress that a cervical subluxation may be present in all forms of vertigo and dizziness. In no field is manipu lation more effective than in the treatment of disturbances of equilibrium (83). Vertigo, the sensation that you or the world around you is spinning, is a common form of disequilibrium and is one of the three most common complaints after "whiplash" injury (84). The other two are neck muscle tenderness! pain and headache. The body's main communication center for balance or equilibrium is found in the brainstem (medulla) . The brainstem contains the vestibular nuclei, which gather and process information on position and movement through the semicircular canals-;:entral-and the spinal cord-peripheral.
Mech anisms
1. Cervical sympathetic irritation: Injury to the cervical spine may also damage the sympathetic chain. This will affect the muscles and the blood vessels directly to the eyes (77). These factOrs either cause increased input to the vestibular nuclei or affect how the vestibular nuclei respond, both causing altered function of the vestibular nuclei. 2. Abnormal neck reflex: Because the cervical musculature and joints are richly supplied with proprioceptors (15), when injury occurs, high volumes of information enter the spinal cord/brainstem. This affects the homeostatic equilibrium of the brainstem nuclei, resulring in vertigo/disequilibrium (85). A subluxation in the upper cervical spine also affects the homeostatic equi"librium of the brainstem nuclei. Hinoki (84) has shown that patients with cervical soft tissue injury after whiplash show abnormal e1ectromyelographic dis-
334 charges from the neck musculature, and rhat rhe level of these discharges are closely related to the patient's symptoms of vertigo during a course of treatment. Suzuki (86) showed that electrical stimu lation of normal cervical muscles does not cause vertigo, and when injured muscles are stimulated, they cause vertigo. 3. Mechanical compression or stenosing of the vertebral artery (79,80): Because trauma to the cervical spine can cause (1) tissue damage, (2) subluxation, (3) muscular spasm or splinting, (4) pain, any of these causes further muscular spasms or splinting, contributing ro stenosing of the vulnerable vertebral artery as it passes between the occiput and Cl. We therefore must consider multiple mechanisms in the causes of cervical vertigo (87). Richmond (88) has shown that cat spinal muscles contain a high density of proprioceptors, and she believes that humans have the same high density. When there is damage to the muscles, they provide a great deal of proprioceptive information to the spinal cord and brainstem nuclei, namely, the vestibular nuclei . These twO factors: (1) overexcitement of the cervical musculature and (2) disturbance of the homeostasis of the brainstem nuclei, contribute to vertigo (84). The factors induce disequilibrium in a trigger-andtarget relationship, in which the cervical proprioceptors act as triggers and the brain stem/central nervous system is their target, causing vertigo and uncoordinated movement patterns of the eye (89,90) (Figure 17-3 ). Vidal et al. (91) have shown that stimulation of the rostral portion (innervated by C1-C2) of the splenius capitis muscle in a cat caused nystagmus, but stimulation of the cauda l portion (C3-C5) did not. Hildingsson et al. (92) stated "it seems that patients with chronic symptoms after soft-tissue injury have a localized lesion of the brain stem or an afferent proprioceptive dysfunction of the cervical spine contributing to oculomotor disturbances-one being nystagmus." Cervicogenic vertigo is easily assessed in [he clinic, and patients who have their symptoms
along with upper cervical muscle a nd joint trauma had significant results with chiropractic therapy (85) . Treatment After any period of inactivity, the muscles of the neck lose tone, strength, and endurance. The joints become stiff, the liga ments become tight, and any usual activity precipitates loca l muscle spasm, which itself is painful (93). Any protocol that is developed must take these factots into consideration to ensure that all injured tissues are treated effectively and that the patient does not ex perience increased pain (94). A number of researchers (95-10\ ) have shown the beneficial effects of manipulation/mobilization of the cervical spine. The results include increased range of motion and decreased pain . Other researchers (102- \ 05) have shown that manual therapy, including manipulation, transcutaneous electrical nerve stimulation, and traction, was not significant. The general consensus is that mani pulative therapy (96,97,101 ) and manual therapy (95,97,99,100) have a dramatic and positive effect by decreasing cervical pain and increasing range of motion. These studies show a treatment effect. When one considers the importance of the cervical spine regarding its tissues, its position, and the fact it affects all partS of the body, one immediately rea lizes that the next level of care-rehabilitationmust be comprehensive, dealing with all the tissues in the traumatized area and with the rotal patient. With trauma to the cervica l spine, Bogdan et al. (105 ) have shown that two different syndromes occur:
1. The "cervicoencephalic syndrome," characterized by headache, fatigue, dizziness, poor concentration, disturbed accommodation, and impaired adaptation to light intensity. 2. The "lower cervical spine syndrome, characterized by cervical and cervicobrachial pain . The cervicoencephalic syndrome parients had more trouble dealing with divided attention. II
17 Cervlcogenlc Sympalllelic Syndromes: Ellology, Treatment, and Rehabilitalion
335
Trauma also contributes to injury of the inter-
vertebral disc (106) and affects inner ear function (107), leading to inefficient muscular control of balance and erect posture, cervical hypolordosis
(108), abnormal muscle tension (109), postural effects through inhibition of the soleus muscle (/10), and injuries to the head, cervical muscles, and disc in the lumbar region (III) . Because cervical muscles are so important regarding control of movement and providing en or mOllS vol urnes of
proprioceptive information to the spinal cordJ
Joints
CNS (15), it is of absolute importance to understand their response ro injury and methods to effectively rehabilitare them. Arthrogenous muscle weakness is weakness of muscles accing ahom an injured or inflamed
Agore 17·3 Relationship of propriocepcors co the cemralnervous system.
joint (112). Laboratory studies show that partial and complete muscle injuries exhibit disruption of muscle fibers near the muscle-tendon junction.
Healing of partial injuries is characterized by an initial inAammatory response followed by a healing phase marked by fibrosis. Biomechanical studies show that muscle failure occurs at forces much larger than maximal isometric force, and
stretch is necessary to create injury (113). There may be up to a 20% loss of muscle strength after 1 week of muscle immobilization and another
20% decline in residual strength every subsequent week of immobilization. Atrophy may occur even faster if the muscle is immobilized in a shortened position (l 14). The side effects from immobiliza-
tion extend beyond the muscles. If an associated joint is kept from moving, producing a subluxadon syndrome, significant joint capsule, cartilage,
subchondral bone, and bone-ligament changes occur (I 15). Early mobilization helps to avoid these unwanted local side effects and also promotes proper tissue healing. Collagen fiber growth and realignment can be stimulated by early tensile loading of muscle, tendon, and ligaments. The formation of adhesions between repairing tissue
and adjacent structures can be limited by early motion. Proprioception is better maintained and recovers faster as well with early motion (114).
The cervical injuries for which therapeutic
exercises arc appropriate include acute cervical strain/sprain syndromes, brachial plexus neurapraxia, brachial plexus axonommesis, vertebral
body end plate fractures, wedge compression, and other stable fractures, along with peripheral nerve injuries (11 6). The goal is to reduce muscle tension in abnormal, sensitized tissue and m develop the ability to
relax such muscles when they are being maximally employed for movement and weight displacement. This may seem paradoxical, but all students of muscle physiology appreciate that Auid, efficient movement can only be achieved with a relaxed, steady, properly programmed sequence of muscle action, or muscles will fatigue,
cramp, and be painful (1 I 7). It has been shown that progressive resistance exercises can markedly increase neck muscles'
strength and decrease lateral force imbalance (118). Using the protocol outlined (94), it was found, in a preliminary study of 200 patients, that the group that received chiropractic treatment and progressive, resisted exercises remained
longer in therapy and had less pain and increased range of motion. Interestingly a 6-month followup found that the exercise group requested fewer chiropractic treatmentS and more patients main-
tained their overall improvement (119).
336 Because the cervical muscles play a crucial role in normal cervical function, the mechanism of the injury and its tehabilitation and methods to enhance the efficiency of these tissues are continually being exploted. Using a low-energy laser that stimulates collagen synthesis and promotes more rapid healing, the following was shown: when the laser was combined with exercises in acute MVA victims, it produced very pronounced increases in extensor muscle strength (120). Also found effective in rehabilitating cervical injured patients is a new system-the "phasic'" component-which seems to be related to the vestibular ocular reflex. In a study addressing this component, chronic cervical injured patients responded significantly to new types of exercises that were " phasic," involving eye-head-neck-arm and body movements (121).
Conclusion The cervical spine is truly the most complex and interesting 7 inches of the human frame. One can easily understand how its injury and subluxation syndromes cause a constellation of signs and symptoms, not just localized, but referred cephalad to the head, and caudal to the rest of the body. The next frontier is irs accurate diagnosis, effective treatment, and total rehabilitation.
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The Cerebral Dysfunction Theory Allan G. J. Terrett
KeyWords
Cerebral dysfunction, hibernation, diaschisis
After reading this chapter you should be able to answer the following questions:
Question #1
Is decreased circulation to the brain leading to loss of cell function reversible?
QuestIon #2
Is decreased cerebral blood flow a rational explanation for previously observed effects of spinal manipulation?
341
A
Brain HIbernation
ing ability, memory, or general feeling of well-
Ischemic penumbra was a term coined in 1981 (3) to describe a condition in which CBF was berween normal blood flow (allowing normal functioning) and blood flow low enough to result in irreversible tissue damage (causing cell death), much like a solar eclipse, in which the penumbra is an area berween normal light and darkness. In this penumbra state, neurons may be paralyzed (elecrrocerebra l silet;lce) yet viable (ionic pump
being; and decreases in tiredness, clumsiness, irri-
function is maintained).
tability, depression, or anxiety. Some patients return again when they feel problems with these functions. These effects cannOt be explained by theories common ly put forward to explain the effects of manipulation, such as:
CBF is normally approximately 0.5 mVglmin in human beings with a cerebral oxygen consumption of approximately 0.035 mVglmin . A decrease in CBF is compensated for by an increase in oxygen extraction from the bloodstream (that is, the brain has a perfusion reserve) . Such compensation (to a llow normal neuronal functioning) can be made down to a level of approximately 0.23 mVglmin (4,5). Neurophysiologic research (4-18) demonstrates that if circulation to the brain is further decreased, cells may remain al ive, but their func-
fter spinal manipulation, patients often comment on the relief of some other health complaint, which is apparently nOt related to the problem for which treatment was given.· Over time, observant practitioners are able to recount instances in which patients mentioned improvement in vision, concentration span, learn-
Nerve compressioniirrirarion Spinal cord compression/irritation Somatovisceral (autonomic) reflexes Viscerosomatic reflexes Sympathetic nerve irritation Joint fixation (intrinsic and extrinsic) Vertebrobasilar ischemia lntraarticular meniscoid locking Neurodystrophic hypothesis The cerebral dysfunction theory (1,2) was developed to explain some of the reported and observed effects of manipulation . It is proposed that manipulation can result in increased cerebral blood flow (CBF), which restores normal cerebral functioning. Therefore manipulation can have hibernocerebrosomatic,
hibernocerebrocognitive, and hibernocerebropsychologic effects. "Nore: This chapter has given onl y an overview of the
cion ceases. If adequate circulation is restoted, neuronal function is reactivated. Therefore areas
of the brain can functionally hibernate (Figure 18-1 ). The relationship berween cerebral electrical activity and blood flow has been amply proven in experimental studies. Differences in actual figures are related to the experimental animals being studied. Neurologic deficits begin to appear in awake monkeys when regional CBF decreases to below 0.23 mVglmin (6) and a gradual silencing of neurons sets in; some cells continue to fire at
levels at which others have become silent (5), wi th some cells still active at 0 .06 mVglmin (7). Local CBF of apprOlomately 0.15 mVglmin abol-
concepts mentioned. The development of reversible
ishes somatosensory potenrial recordings in the
penumbra and irreversible infarction zo nes appear to depend on time, as well as intensity of ischemia. Some regions of (he brain are more vulnerable to ischemia than
baboon cortex (8). Evoked potentials may be altered, yet recover, when flows of 0.16 mVglmin are maintained for 14 to 60 minutes (8). Cerebral conduction time (a function of evoked response) is affected when CBF decreases to below 0.15 mVglmin (9). CBF below 0.18 mVglmin in cats causes cessation of sponta neous neuronal spike
others: white matter is more resisram than gray maner; and there are differences in effects of different degrees of ischemia between humans, subhuman primates (even between monkeys and baboons), and other animals (for example, cars and rats).
342 CBF
ml/g/min about 0.23 about 0.10
Normal Cellular Functioning
, - - - - Electrical failure threshold
Hibernation
tI___~~~~~~~~::~::~~' Lethal threohold Cell Death
0.00 - ' - - - - - - - - - - - - - - ' Rgure 1B-1 The effect of changes in cerebral blood flow on brain function. Regional CBF above
approximately 0.23 mUg/min allows normal cell functioning. Neurologic deficits begin to appear when
CBF decreases to below 0.23 mUg/min. Regional CBF below approximately 0.1 mUg/min results in irreversible cell death.
activity in the cerebral cortex (10) . In humans, flattening of the electroencephalogram (EEG) occurs immediately if hemispheric flow decreases to below 0.16 to 0.17 mllg/min, as evidenced by measurementS of CBF and EEG during clamping of One carotid artery in endarterectomy (11,12). This flow level (approximately 0.23 mllg/min) can be regarded as "critical" because electrical function in the cortex is disturbed below, but is normal above, this "critical" level (Figure 18-1). The brain uses glucose as its sole substrate. Glucose is oxidized to CO, and H,O . Cell energy metabolism relies On the production of adenosine triphosphate (ATP) from adenosine diphosphate (ADP). To maintain neuronal integrity, a constant supply of ATP is required to exclude sodium ions (Na·) from the cell and to maintain potassium ions (K·) within the cel l. Cerebral blood flow of less than 0.10 mllg/min results in deterio ration of the energy state, and ion pump failure, as in the absence of oxygen to produce ATP, anaerobic glycolysis is used. Glucose can be converted without oxygen to lactate and ATP, but the amount of energy yielded is small . This eventually leads to the accumulation of lactic acid with resultant inttacellular and extracellular acidosis. When energy requirements are inadequate to maintain the normal dis-
tribution of K· (intracellular) and Na· (extracellular), membrane depolarization and ion pump failure occur, with a massive efflux of K· from the cells. This occurs at approximately 0.08 to 0.1 mllg/min in lightly anesthetized baboons and is most likely applicable to the human brain (Note: the threshold of membrane and metabolic failure is higher in smaller anima ls) (4,5) . If such chaos persists for 5 to 10 minutes, irreversible cell damage and death occur (Figure 18-2). Recovery of neurOnS suffering decreased blood supply is related to the duration of ischemia. Evoked potential in the baboon cortex could not recover after flow levels of 0.11 mllg/min for 15 to 65 minutes (13); most neurons recover from long ischemia (2 to 3 hours) only if flow levels remain above approximately 0.12 mllg/min (6) (Figure 18-3) . Hibernation occurs between these two flow thresholds (0.12 to 0.23 mllg/min, a difference of only approximately 0.11 mllg/min) and is characterized by electrical silence with normal or only slightly elevated extracellular potassium concentration. The residual perfusion (in the hibernation range) supplies sufficient oxygen to maintain a close to normal tissue concentration of ATP. Although changes in the concentrations of phosphocreatine (reduced), lactate (increased), ADP (i ncreased), and adenosine monophosphate (AMP; increased) occur, resu lting in some degree of energy failure, research suggests that this does not lead to neuronal damage (3,4,14-16).
CBF
ml/g/ min about 0.23
Normal Cellular Functioning
- - - Electrical failure threshold
Hibernation
about 0.10 t - - -"""- - - leIhal threohold
Death
0.00 Rgure 1B-Z
Ischemia and cell death. Further decrease in CBF below rhe lethal threshold (approximately O. I
mUg/min ) results in brain cell death.
1B The Cerebral Dysfunction Theory
Normal Cellular Functioning ml/g/min CBF
about 0.23
Electrical"- - - Failure threshold -
about r----~ 0.10 -r--------l.ethal threshold
Cell Death 0.00 Agure 18--3 Recovery from hibernation. Most neurons recover from long ischemia only
if flow levels remain
above about 0.12 ml/glmin. Increase in CBF (from the hibernation range) to above the electrical failure threshold results in restoration of normal brain
function.
Although electrical aCtlvlry may have been lost, recovery without irreversible damage (histologic signs of structural infarction) may occur (even if the increase in blood flow is very small) only as long as the residual blood flow has been on the safe side of the threshold for energy failure and ion pump failure. There is some evidence that clinical and electrical function may turn on and off in rhe ischemic area of rhe brain (17,18) .
Diaschisis Ir is proposed that diaschisis possibly occurs after hypofunctioning of one part of the brain. Diaschisis was a term proposed by Von Monakow in 1914 (19) to describe functional depression of brain function at structurally intact sites remote from the brain lesion. Human and animal srudies have confirmed that localized damage to one area of the brain does cause teduction of excitatory impulses to another part of the brain, resulting in depression of rhe distanr region (20) (Figure 18-4). Neurophysiologic research into diaschisis has been done in animals and stroke victims (21-32). These represent the most severe and dramatic manifestations of diaschisis. Research has demonstrated that lesions in one hemisphere can affect functioning in:
343
Contralateral cerebral hemisphere (33-36) Ipsilateral thalamus (34,37-39) Ipsilateral basal ganglia (34,37) Ipsilateral visual cortex; both primary and associated visual conex (34,37,40-43) Contralateral cerebellar hemisphere (33,44-47) Research has also indicated that reduction of regional CBF or metabolism in the ipsilateral frontoparietal cortex can occur in patients with lesions of the thalamus (42) and with small infarctions of the internal capsule (34,42). Crossed cerebellar diaschisis has been reponed (48,49) after hypertensive hemorrhages. Although diaschisis is proposed as part of the cerebral dysfunction rheory, further research is needed to determine whether decreased brain functioning in the hibernation range has this effect; and to detetmine the necessary severity, size, and location of the hibernating region needed to produce alterations in functioning of distant regions of the brain .
Examples of Brain Hibernation Clinical recovery of patients with embolic transient ischemic attacks is evidence of a state of ischemic hibernation, with complete reversibility. Similarly good recovery in minor stroke patients occurring over days or weeks suggests a cortical hibernation state of longer duration (5). Hibernation of cortical functions can occur for months, or even years, and then when blood flow is increased, lost function returns. Cases reported in the literature tend [0 be the uncommon and the most severe and dramatic manifestations of this syndrome, but they are presented here to demonstrate that even in severe cases, with return of adequate CBF, cerebral function can return to normal. This theory proposes that more subtle disabilities commonly occur in the brain, but that they have nOt been considered and investigated .
1. Roski et al. (50) reported a 50-year-old patient with a documented 7-year loss of vision (right superior homonymous hemianopia and part of
344
Tb8 SUbluxIItIon Byndl'OlI"
?'
Excilatory impulses
V
345
1B The C8I'eIII'aI Oylflllctlon Theory the right inferior quadrants). He had an expressive dysphasia (his speech was slow and deliberate), difficulty with reading, writing, and spelling, and weakness of his right hand and a right arm drift. A computed tomograp hy (Cf) scan demonstrated a lesion in the left occipital lobe. A dynamic flow study demonstrated decreased flow in the distribution of the left middle cerebral artery. Selective arteriography demonstrated occlusion of the left internal carotid and right vertebral arteries. After an anastomosis fro m the left superficial temporal artery to the angular branch of the left middle cerebral artery, the vis ual defect immediately completely resolved. In addition, his speech was noticeably improved and his right hand grasp was normal, with no arm drift. 2. Brain dysfunction associated with decreased regional CBF has been reported in cases of depression (51-53), anx iety (51,54), persona lity disorders (55,56), a nd attention, concentration, and memory defects (51). Examinations of CBF in depressed patients (aga inst control groups matched for age, sex, and handedness) showed highly reduced values for gray matter blood flow, as compared with controls, in both hemispheres (51,53). The degree of depression was significantly inversely correlated with regional CBF (most manifest in the frontal regions ). The authors believed that beca use depression is not associated with cerebral atrophy; functional hypoactivity of the neurons seems the most probable explanation for the
In a normal physiological stare, locus B is facilitated by stimulating impul ses from neurons in locus A. If neuronal activiry in locus A is decreased so that excitatory impulses from locus A are decreased, then function in locus B will be decreased. (A dapted from Meyer jS, Halo T, Imoj A. Clinical and
figII'e 18-4
experimental studies of diaschisis. I,,: Wood JH (ed).
Cerebral blood flow: Physiologic alld clinical aspects. New York: McGraw-Hili, 1987: 481-502.)
cogn itive dysfunctions (arrention, concentration, and memory defects) seen in depression .
Another point relating depression to reduced CBF is that electroconvu lsive thera py (ECf), which has antidepressa nt effects, causes cerebral blood vessel vasodilation. Gorman (1) states: It is not surprising that chirop ractic manipulation lifts depression . ... lr is possible that ch iropractic manoeuvres wi ll become an importanr rool in psychiatric treatment.
3. Aphasias/dysphasias (associated with lesions of the posterior para-Sy lvian association cor-
tex) have been reversed after arteria l anastomosis (50,57,58) . Jacques and Garner (57) described two patients with aphasia (one was global, the other expressive) and mOtor weakness (hemiparesis) that markedly regressed after superficial temporal to middle cerebral artery anastomosis (ST-MCAA). 4. Hand weakness has been reported to decrease after arterial anastomosis (increase in CBF) (50,57,58). Lee et al. (59) mention several improvements in neurologic status after an
increase in CBF after ST-MCAA in patients at least 3 months after ischemic infarcts, so that all neurologic improvement would have occurred .
They found that, after ST-MCAA: • One
patient
with
subjective
weakness
improved • 52 % (11 of 21 patients) with mild sensory
346
The SUbluXallon Syndromes
and/or mOtOr weakness, or mild speech and! or visual impairment improved • 40% (twO of five patienrs) with moderate
two who did not eventually recover (remained hemiplegic). Patienr I also recovered from a non fluent dysphasia.
sensory and/or motor weakness, moderate
speech and/or visual impairment, or moder· ate functional impairment improved
• 7 t % (five of seven patients) with severe sensory and/or motor weakness, severe speech and/or visual impairment, or gross funcrional disturbance (but able to ambulate) improved (59) . 5. Macou and Rice (60) described the reversal of a fixed hemiplegia afrer ST-MCAA bypass graft. 6. Skyhoj-Olsen et al. (61), in a study of eight patienrs with completed stroke, have described a clinical enriry of patients with middle cerebral artery (MCA) occlusion, delayed collateral filling of the occluded vascular bed, and a deep infarct on CT, but normal overlying cortex. Patienrs had good recovery from the initially severe deficits, including cortical deficits like aphasia and neglect, in a matter of weeks or monrhs, suggesting hibernation of long
Brain Hibernation and Spinal Manipulation Orthodox medicine operates best when a pathologic condition is clearly definable (radiographs, blood tests, cu ltures, biopsies, etc). Chiropractic usually relates to illnesses without concrete dimensions (for example, pain, aching, numbness, dizziness, etc.), but that are still disabling. Neurologists understand the effects of vascular occlusion and the resulrant ischemic and stroke
syndromes. The signs, symptoms, and syndromes
that this theory addresses are not listed in standard neurology texts because the signs and symp[oms are not so devastating as strokes, bur they
that six of these demonstrated immediate
sti ll cause severe health problems to the patient. Most observant practitioners of manipulation would be able to remember patients who have described feel ing berrer and having clearer thinking and clearer vision after neck adjustments. Some patienrs whose jobs involve complex calculations return for spinal manipulation because they believe they need it when they have difficulties with complex computations. These and other effects are commonly reported to chiropractors. It is surprising they have received very little atten-
improvement in neurologic examination the
tion in the current chiropractic literature.
day after surgery (that is, after an increase in brain blood flow). Changes included Improvement in hemiparesis, speech, handwriting, or
The theory of brain hibernation as an explanation for many of the effect; of spinal manipulation was originally proposed by two medical practitioners (I): Eric Milne, a general medical practitioner who had an interest in spinal manipulation, and Frank Gorman, an ophthalmologist who had an inrerest in migmine. With different educationa l backgrounds, and a patient group complaining of a much larger range of complaints, they saw additional applications for, and developed a differenr theory for, the mode of action of spinal manipulation. They noted that, after spinal manipulation for headache, patients
duration in the overlying cortex.
7. Spetzler et al. (62), in a study of 76 patienrs who underwent extracranial-inrracranial arter-
ial bypass to increase cerebral vascularization, found that 32 presented with chronic fixed neurologic deficit (greater than 3 months), and
combinations of these.
8. Powers et al. (63), using positron emission tOmography (PET), studied four patients with subarachnoid hemorrhage and hemiparesis caused by cerebra l vasospasm. PET measurements of regional blood flows obtained early in the course of the vasospasm showed that, in the two patients who recovered, regional
blood flows were 0.1 5 and 0 .1 62 mllg/min, compared with 0.12 and 0 .11 7 mllg/min in the
347 often commented that some other health complaint was relieved as well (for example, tiredness, glare distress, dizziness). After spinal manipulation in cases of interim disability, such as dizziness, wirhout rhe headache, rhe patient often mentioned the disappearance of some other health complaint. With time the list of conditions for which spinal manipulation was indicated enlarged. The mechanism proposed to expla in these postmanipulation effects was that increased CBF resulted in hibernating areas of the brain becoming functional again (Figure 18-5). This theory proposes that arteria l insufficiency to the brain resulting in decreased cerebral
>
Signs and Symptoms That Are Theorized to Be Caused by Decreased Cerebral Performance
• • • • • • • • • • • • • • • • • • • • • • •
functioning:
I. Is caused by constriction of the artery lumen, possibly because of 3. Stress on the arteries in the neck caused by misaligned or malfunctioning vertebrae b. A sympathetic response c. Some mechanism still unknown 2. Normally causes no loss of core brain functions (those that are involved in the business of existing, such as eating, walking, talking, etc.), but that it has a wide range of possible manifestations affecting sophisticated brain functions (those not essential to our existence, such as higher mathematics,
• Loss of interest in sex
concemrarion, "the mind," peripheral vision, mood, emotion. The box at right lists signs and symptoms that are theorized to be caused CBF ml/g/min
Normol M Cellulor ~ • • • • • • •~ about Functioning t 0.23 I-- Electrical - ~ - - Failure threshold L A about .J----- T 0.10 t
Hibernation - - Lethal threshold
3. 4.
5.
o
0.00
.L-_ _ _
Cell_Death N_ _ _ __ ---'
~
f11111'118-5 Theoretical increase of CBF above the electrical failure thresho ld following manipulation, resulting in resroration of normal brain function.
Giddiness/dizziness Lethargy/excessive tiredness Difficulty sleeping/insornnia Depression Nervousness Restlessness/anxiety Miserablelirritable Disoriented Personality change Hyperkinesia in children Whining child syndrome Tantrums Headache Problems with memoty Learning disability Poor concentration Difficulty thinking Clumsiness Changes in visual acuity Visual disorders Auditoty difficulty Mixing up words Losing track of conversation while talking
6.
by decreased cerebra l functioning attributable to decreased CBF Is common and can occur without any major trauma, or after seemingly trivial trauma Causes symptoms in people who are considered "normal," and their symptoms are dismissed Has degrees of severity. As the degree of ischemia increases, the number of functioning cerebra l cells decreases, and the disability becomes more severe (Table 18-1) Causes people to be disabled by a mental illness of which they a re unaware, which has a simple physical cause
348
>
Disorders T hat Are Proposed to Be Produced by Progressive Decrease in Cerebral Blood Flow (CBF) ~.....
r~:~'(J'
. . . . ~, ... ·.~u~,,.Normal CBF (Oxygen Normal) All Cerobral Units Operational
No giddiness
Decrealod CBF (Leu Oxygen Than Normal) Not All Cerabral Units Operational
Giddy with use of the arms, or
Normal visual
field Able to read fine print Happy Able to cope with calculations
Well rested Well coordinated
Never or rarely
suffers headaches
postural changes Some loss of peripheral vision Some visual difficulty Irritable under stress Difficulty with calculations . Easily tired Problems with manual tasks under stress Headaches under stress
Further Decrease In CBF (Poor Oxygon Supply) Few Cerobral Units Operational
Giddy all or most of the time
Tunnel vision Only able to read large print Irritable all the time
Unable to cope with calculations Feels continually tired Clumsy
Commonly suffers headaches
7. Can be relieved by spinal manipulation (by increasing CBF)
Many people suffering from these complaints may be:
This theory proposes that it requires more "brain power" (active brain function) to be happy (not irritable), to ha ve a good memory (not be forgetfu l), to perform complicated physical tasks (not be uncoordinated), to be bright and alive (not tired), to be articulate when speaking (not mixing words, stuttering, or losing track), to perform complicated mental tasks, to have full visual fields, and to be headache free. A child may be criticized and ridiculed as to intelligence or ability when in fact he or she has the potential but the cerebral dysfunction does not allow the child to use his or her assets.
• Given a psychologic label (a nd often medication) • Told they are growing old • Called a hypochondriac • Labeled hysterical and so their disability is largely ignored because: • They do nOt show any measurable parameters • They do not respond to usual methods of treatment • The absent functions are highly sophisticated and are not important to the basic business of existing (which is a poor substitute for
18
the possibilities operational)
when
the
TIll CIrebrII OyIhllc1lon n..y
brain
IS
fully
So the patient can still go about his or her day-to-day activities, but everything may be an effort, or the application of more willpower may be necessary even for quite moderate achievements, or he or she suffers excessive tiredness or irritability. An observer would not necessarily be aware of these handicaps, and because a doctor cannot detect the disabilities on radiographs, cr scans, blood or laboratory tests, etc., the disabilities are usually dismissed by the examiner. These disabilities are important to the patient, however who may begin to assume they are normal conditions. Gorman (64) reported on patients who underwent spinal manipulation for visual disorders. He used four ophthalmologists, independent of the author and of each other, who were asked to examine patients before and after treatment, using standard ophthalmologic assessment methods. In all cases the vision improved (either the visual field andlor visual acuity). Comments by the ophthalmologists in their reports on the nonvisual field or acuity disabilities that improved after spinal manipulation included : Decreased depression Decreased anxiety Feels more positive Feels happier Feels more outgoing Does not wake up every morning feeling tired Loss of dizziness Loss of slurred speech Loss of headaches Improved arm movement
Feels the light is brighter in her eyes Loss of sore eyes, and loss of appearance that the writing moved when reading Loss of a SCOtoma in the visual field
Testil9 tile Theory The value of any theory is in developing methods of testing it.
349
If spinal manipulation is a method of reactiv3ring hibernating cerebral neurons, the implications are enormous to both patients and the future of chiropractic. If furure studies indicate this possibility, then many of the remarkable anecdotes of chiropractors will be well worth the trouble of serious investigation.
One method of investigating this theory is to: I. Develop methods of quantifying the signs and symptoms listed in the box on p. 347 where no quantification system exists. Where quantification systems do exist, use them (visual acuity, visual fields, anxiety scales, depression scales, etc.) 2. Measure CBF in subjects before and after spinal manipulation, and determine if there is any difference. Methods of measuring CBF are available (52,56,65-75). 3. Remeasure parameters listed in step 1 after spinal manipulation and determine if there are any differences and whether these correlate with changes in CBF listed in step 2. The author has found only one report in which researchers claim to have demonstrated that spinal manipulation increases CBF. Zhang et al. (76), in a srudy of "cervical visual disturbance" in 114 people (where vISion also improved after spina l manipulation), state that: Determination of blood flow by x-ray in 18 cases of our series shows that blood flow of the cerebral
hemisphere grearly improves after manipulative treatment. The same is true in similar animal tesrs.
The method they used to determine this is not described. Zhang et al. (76) believe that this effect of manipulation is caused by irritation of sympathetic nerves in the neck, resu lting in constriction of the vertebral artery. Although this is an attractive and commonly used theory (77-80) to explain symptoms and subsequent symptomatic relief, it is not supported by recent research (81), which found that vertebral artery blood flow was profoundly unresponsive to stimulation of any component of the cervical sympathetic system and concluded that the theory that irritation of
350
TIle SUbIuXI1Ion By........
cervical sympathetic nerves can alter vertebra l artery blood flow is untenable. However, the vascular resistance in the carotid arrery did increase with stimulation of the cervical sympathetic trunk. It is not known by what mechanism cervical manipulation may increase CBF, but before people starr postulating theories as to how blood flow is increased, further resea rch inco this possibi lity is needed to determine if spinal manipulation does in fact have this action.
Conclusion Cerebral dysfunction has been proposed to explain some of the observed effects of spinal manipulation. Basic science resea rch indicates that cerebral dysfunction (hibernation) does occur. Clinical observations suggest that this ma y be a mode of action to explain some of the effects of spinal manipulation. Future research is needed. If this theory is correct, there are possi ble implications for: Education/learning Psychology/psychiatry Performance enhancement (physica l and mental) Bri dg ing gaps between professions Increasing sco pe of chiropractic practice Widening referral sources from Industry Educators General practioners Psycho logists Psychiatrists Speech therapists Rehabilitation therapists Occupational therapists Providing an explanation for some of the previously unexplainable effects of chiropractic therapy
Rel8l'811C8S I . Gorman RF. Chiropractic medicine for rejuvenation of the mind. Academy of Chiropractic Medicine, 1983. Published privately; Available (S30) from: R. F. Gorman, 7-324 Marrickville Road, Marrickville. Australia 2204.
2. Terren AGJ. Cerebr31 dysfunction: A theory to explain some of the effects of chiropracnc mantpul:mon. J Chlro Tcrhnique 1993; 5(4I1Dec): 168-73. 3. Astrup J. Siesjo BK, Symon L. Thresholds," cerebral ischemia: The ischemic penumbra. Stroke 1981; 12(6)(Nov-Dec):723-5. 4. Jafar JJ, Cromwell RM. Focal Ischemic thre~holds. Chapter 28. In: Wood JH. Cerebral blood now: PhYSiologic and clinical aspects. New York: McGraw-lilli, 1987:449-57. 5. Lassen NA, Asrrup J. Ischem ic penumbra. Chaprer 29. In: Wood JII. Cerebral blood flow: Physiologic and clinical aspects. New York: McGraw-Hill, 1987:458-66. 6. Jones T I t, Morawetz RB, Crowell RM, et al. Thresholds of focal cerebral ischemia in awake monkeys. J Neurosurg 1981; 54:773-82. 7. Heiss WO, Rosner G. Functional recovery of corucal neurons as relared to degree and duration of ischemia. Ann Neurol 1983; 14:294-30 I. 8. Bransron NM, Symon L, Crockard HAt et al. Relallonship between the conical evoked potenrial and local COrtical blood flow following acute middle cerebral artery occlusion in the baboon. Exp Neurol 1974; 45: 195-208. 9. H argadine JR, Brannon NM, Symon L. Cenrral conducrion rime in primate brain ischemia: A srudy in baboons. Stroke 1980; 11(6):637-42. 10. Ileiss WO, H ayakawa T, Waltz AG. Cortical neuronal function durmg ischaemia. Arch Neurol 1976; 33:813-20. II. Troiaborg W, Boysen G. Relationship belween EEG, regional cerebral blood flow :lOd internal carotid artery pressure during carotid endarterectomy. Electroencephal· ogy Clm Ncurophysiol 1973; 34:61-9. 12. Sundt TM, Sharbrough PW, Anderson RE, et 31. Cerehral blood flow measurements and electroencephalograms during carotid endarterectomy. J Neurosurg 1974; 41:310-20. 13. Bransron NM, Symon L, Crockard HA . Recovery of the cortical evoked response following temporary middle cerebral artery occlusion 111 baboons: Relation to local blood flow and pOl.' Stroke 1976; 7: 151-7. 14. Sa lfo rd LG, Plum F, SieslO BK. G raded hypoXia-oligemia in rat brain. I. Biochemical aiterations and their implications. Arch Neurol 1973; 29:227-33. I S. Sa lfo rd LG, Plum F, Brierley JB. Graded hypoxia -oligemia In rat brain. II . Neuropathological aheratlons and their Implications. Arch Neurol 1973; 29:234-8. 16. Morawerz RB, OeGlrolanu V, Olemann RG, et al. Cerebral blood flow determined by hydrogen clearance durmg middle cerebra l artery occlusion in unanesthetized monkeys. Stroke. 1978; 9:143-9. 17. Symon L. The relationship between CBF, evoked potentials and the clin ical features in cerebral ischaemia. Proceedings of the 2Jrd Scandinavian Neurology Congress. Acta Neurol Scand 1980; 62(Suppl 78): 175-90. 18. Symon L, Hargadine J, Zawirski M, et al. Central (on-
18
TIle CIII'8brII Dyllll1c1lon n->y
duc.:tlon f1mc as an Indc'<: of ...c.:hacOlm In subarachnoid h.lcmorrh.lge. J Neurol S4.:, 1979; 44:95-103. 19. Von Monakow C. Die Lokalisation imgrossbirn und cler anbau der funkrion durc.:.h koruble herde. Wicsnadcn: J~ Bergnun. 1914:26-34.
(Quoted III Rcfercm:c 20) 20. Meyer JS. Hata T, Im31 A. Clinical and expenmental studIes of diaschisis. Chapter 31. In: Wood JH. Cerebral hlood flow: Ph)'siologu.: and clinical aspects. New York: ~kGr;'lw-llili. 1987:48 1-502. 21. Ackerman RII, Correia JA, Alperl NM, er al. Positron
22.
2J.
14.
H.
26.
17.
28.
29.
30.
3 1.
.n. 33.
.34.
35.
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351
cr CBF measurements m prevalent cerebrovascular disorders (stroke). Stroke 1984; 15:80-90. 36. Ilata T, Gotoh F, Ebihara S, et al. Three dllnensionallocal cerebrovascular CO 2 responsiveness by cold xenon method. In: Meyer JS, Reivich M. Lechner H. et 31., cds. Cerebral vascular disease 5. Amsterdam: Excerpta Medica, 1985. 37. Kuhl DE, Phelps t-.1E. Kowell AP, el 31. Effects of stroke on local cerebral metabolism and perfUSion: mapping by emission computed tomography of I8FDG :md IINHl' Ann Neurol 1980; 8:47-60. 38. Metter EJ, Wasterlain CG, Kuhl, et al. ''- FOG positron emission compU[ed mrnography: A study of arhasia. Ann Neurol 1981; 10,173-83. 39. Wise RJS, Bernardi S, Ftackowi.1k RSJ, et al. Serial observations on the pathophYSiology of acute stroke (the transinon from Ischemia to infarction as reflected in regional oxygen e,,(racnon). Bram 1983; 106: 197-222. 40. Bosley TM, Rosenquist AC, Kushner M, et al. Ischemic lesions of OCCipital cortex and optic radiations: Positron emission tomography. Neurology 1985; 35:470-84. 41. Heiss WD, Vyska K, Kloster G. et al. Demonstration of decreased functional actiVit)· of visual cortex by IIC methygluc'ose and positron emission tomography. Neuroradiology 1982; 23:45-7. 42. Lassen NA, Henriksen L.. Paulson DB. Regional cerehral blood flow In stroke by IHXC Inhalation and emi'ision tomography. Stroke 1981; 12:284-7. 43. Phelps ME, Mazziotta JC, Kuhl OF, et al. Tomographic mapping of human cerebral metabohsm: Visual sumulanon and deprivation. Neurology 1981; 31:517-29. 44. Baron JC, Bousser MG, Comar D, et al. Crossed cerebellar diaschisis m human supratentorial brain infarction. Trans Am Neurol Assoc 1980; 105:459-61. 45. Martin WR\'(1, Raichle ME. Cerebellar blood now and metabolism in cerebral hemispheric infarCtion. Ann Neuro11983; 14,168-76. 46. Meneghetti G. Vorstrup S, Mickey B. er al. Crossed cerebellar diaschisis in ischemic stroke: a study of regional cerebral blood flow by I uXe inhalation and smgle photon emiSMon computerized tomography. J Cercb Blood How Metab 1984; 4,235-40. 47. Kushner M, Alavi A, Reivich M, et al. Comralateral cerebellar hypomer:tbollsm follo\vil1g ccrebr:tlln4)uhs. AM Neurol 1984; 15,425-34. 48. K.maya II, Endo H, Sugiyama T, et al. Crossed cerebelbr diaschisis m patients with putamlnal hemorrhage. J Cereh Blood Flow Mcrab 1983; 3\suppl 1),527-8. 49. Kell)' RE, Ackerman RH. Davis SM, et al. Positron emission tomograph)' 111 cerebrovascular disease, with special emphasis on the verrebrobasilar territOry. In: Bergucr R. Bauer RB, cds. Venebrobasllar arterial occlusive disease . New York: Raven Press, 1984: 19-i-213. 50. Rosk. R, Spenler RF, Owen M, et al. Reversal of seven year old visual field defect with extracranial-mtracramal anastomosis. Surg Neurol 1978; 10:267-8.
352 5 1. Mathew Rj. M eyer J5, Semchuk KM, et al. Cerebral blood flow in depression. Lancet 1980; l{SIS l ): 1308. 52. Mathew Rj. Meyer jS, Semchuk KM, et al. Regiona l cercbral blood flow in depression: A preliminary report. J Clin Psychiarry 1980; 41(12 PI2pl-2. 53. Mathew RJ, Meyer J5, Francis DJ, et aJ. Cerebral blood flow in depression. Am J Psychiatry 1980; 137( 11), 1449-50. 54. Mathew Rj. Wilson WHo Anxiety and cerebra l blood flow. Am] ) sychiatry. 1990; 147(7):838-49. 55. Mathew Rj, Weinmann ML. Barr DL. Personality and regional cerebral blood fl ow. Bf J Psych iatry 1984; 144,529-32. 56. Mathew Rj . Wilson WHo Chroniciry and a low a ntero· posterior gradicnr of cerebra l blood flow in schizoph renia. Am J Psychia try 1990; 147(2):21 1-3. 57. Jacques S, Ga rner JT. Reversa l of aphasia with supe rficial temporal artery to middle ce rebral artery anastomosis. Surg Neurol 1976; 5: 143-5. 58. Ausman JI , Lee MC, Geiger JO, et al. Clinica l results of middle cerebral artery-superficial temporal artery anastomosis in ischemic stroke patients in internal carotid artery distribution. Presented at The American Association of Neurological Surgeons, March 1978, New Orleans, Louisiana (Quoted by Reference 13). 59. Lee M, Ausman JI , Geiger jD, et al. Superficial temporal to middle cerebral artery anastomosis: Clinical outcome in patients with ischemia of infa rction in internal carotid artery distribution. Arch Neurol 1979; 36: 1-4. 60. Macou jB, Rice jE Reversal of a fixed hemiplegia due to middle cerebral artery occlusion by delayed STA-MCA artery bypass graft. In: Spenler RF, Ca rker LIl, Selman WR, Martin NA, eds. Cerebral revascularization for stroke. New York: Thieme-Stranon, 1985:470-4. 6 1. Skyhoj-Olsen T, La rsen B, Herning M, Skriver EB, Lassen NA. Blood flow and vascular reactivity in colla terally perfused brain tissue: Evidence of an ischemic pen um bra. S"oke 1983; 14,332-4l. 62 . Sperzler RF, Roski RA, Zabramski J. Middle cerebral artery perfusion pressure in cerebrovascular occlusive disease. Stroke 1983; 14:552-5. 63. Powers Wj, Grubb RL, Baker RP, et 011. Regional cerebral blood flow and metabolism in reversible ischemia due to vasospasm. J Ncurosurg 1985; 62,539-46 . 64. Gorman RF. An observer's view of the treatment of visual perception deficit by spina l manipulation: A survey of 16 patients. Sydney, Australia: 1991 (published privately). 65. Mathew Rj, Wilson WH, Tant SR. Determinants of resring regional cerebral blood fl ow in normal subjects. Bioi Psychiarry 1986; 2 1(10),907- 14. 66. Obrist WD, Thompson HK, Wang HS, er 011. Regional cerebral blood fl ow estimated by IJJXenon inhalation. S"oke 1975; 6,245-56.
67. jagsi jL, Obrist WOo Regional cerebral blood flow determined by IJJxenon clearance. Chapter II. In: Wood JI-I, cd. Cerebral blood flow: Physiologic and clmical aspects. New York: McGraw-Hili, 1987:189-201. 68. EwingjR, Robertson WM, Brown GG, et al. Ill Xenon inhalation: Accuracy in derection of ischemic cerebral regions and angiographic lesions. Chapter 12. In : Wood jH, ed. Cerebral blood flow: Physiologic and clinical aspects. New York: McGraw-Hill, 1987:202-19. 69 . Yonas H, Gur 0, Latchaw RE, et a!. Xenon computed tomographic blood flow mapping. Chapter 13. In; Wood jH. cd. Cerebral blood flow: Ph ysiologic and clinical aspects. New York: McGraw-Hill, 1987:220-42. 70. Gobbel GT, Cann eE, Iwamoto HS, et al. Measurement of regional cerebral blood flow in the dog using ultrafast computed tomography: Experimental validation. Stroke 199 1; 22,772-9. 7 1. Holman BL, Hill TC. Perfusion imaging with single photon emission computed tomography. Chapter 14. In: Wood jH, ed. Cerebral blood flow: Physiologic and clini cal aspects. New York: McGraw· Hill, 1987:243-56. 72 . Herscovitch P, Powers WJ. Measurement of regional cerebral blood flow by positron emission tomography. Chapter 15. In: Wood jH, ed. Cerebral blood flow: Physiologic and clinical aspects. New York: McGraw-Hili , 1987,257-7l. 73. Farrar JK. Hydrogen clearance technique. hapter 16. In: Wood jH, ed. Cerebral blood flow: Physiologic and climcal aspects. New York: McGraw-Hili, 1987:275-87. 74. Warner OS, Kassell NF, Soarini OJ. Microsphere cerebral blood flow determination. Chapter 17. In: Wood jH, ed. Cerebra l blood flow: Physiologic and clinical aspects. New York: McGraw-Hill, 1987:288-98. 75 . Ginsberg MD. Autoradiographic measurement of local cerebra l blood flow. Chapter 18. In: Wood jH. ed. Cerebral blood flow: Physiologic and clinical aspects. New York, McGraw·Hill, 1987,299-308. 76. Zhang C, Wang Y, Lu W, et al. Study on cervical visual disturbance and its manipulative treatment. j Tradu Chin Mod 1984; 4(3),205-10. 77. Neuwinh E. The vertebral nerve in the posterior cervic.ll syndrome. YStareJ Med 1955;55:1380. 78. Stewart DY. Current concepts of "B.ure syndrome" or the posterior cervical sympathetic syndrome. Clin Orthop Rei Res 1962; 24040-8. 79. Maigne R. Orthopedic medicine: A new approach to vertebra l manipulations. Springfield, Illinois: Thomas, 1972,155, 169. 80. j ackson R. The cervica l syndrome. 4th ed. Springfield, Ill inois: T homas, 1977:245-6. 8 1. Bogduk N, Lambert G, Duckworth j W. The anatomy and physiology of the vertebral nerve in relation to cervica l migraine. Cepha lgia 1981; 1:1-14.
Cervicogenic Dorsalgia Glenn R. Engel
KeyWords
Cervicogenic dorsalgia, herpes zoster, anterior cervical doorbell sIgn
After reading this chapter you should be able to answer the following questions:
Question #1
What are the two cervical spine structures most commonly linked to production of cervicogenic dorsalgia?
QuestlIII#2
What neurologic mechanism has been proposed to account for cervicogenic dorsalgia?
354
History and Examination
C
As in any malady, the consu lting chiropractic
ervicogenic dorsalgia is pain expressed in
practitioner must explore a thorough hisrory
the dorsal region and having its genesis in a disordered cervical spine. Although this descrip-
gem ly question the patient in the direction of vis-
tive phrase locates the anatomic region whence the patient's symproms emit, th e term cervico·
genic dorsalgia is seldom an adequate diagnosis for the doctor of chiropractic. The diagnosis of
when investigating thoracic pain. One should dilicerogenesis, being mindful of systemic signs of disease and visceral referral patterns in somatic pain syndromes. The clinician must be ever alert
to the possibility of cardiac or lung pathology
cervicogenic dorsalgia serves as a rough anawrnic
giving rise to symptoms of a suspected cervi co-
locator and is best accompanied by an indicator of the level of focal segmental dysfunction and, if possible, the suggested pathologic nature of the lesion giving rise to the dorsa lgia, for example, subluxation of the C5-6 right posterior facet joint with right cervicogenic dorsalgia . An all-
genic dorsalgia, especially when resu lts of testing of the relevant musculoskeletal structures are normal. Lack of reproducible symptoms on stress
encompassing diagnosis such as this conjures lip necessary treatment interventions instantly in the
tender point in a soft tissue structure.
mind of the practicing clinician. Dorsal pain of cervica l origin is frequently observed in clinical practice (1,2). The cervical spine is a freely movable and rather delicate
testing all relevant musculoskeletal structu res is a definite worry ro an astute clinician, as is any
diagnosis that relies solely on the palpation of a Beware the empty orthopedic examination. Radiographs of the cervicodorsal region showing degenerative change and or structural malpositions may prove misleading, especially when stress-testing th e relevant structures proves nega-
structure sacrificing much in terms of stability for
tive. It has been ob erved that a lesioned gut, for
the considerable mobility it enjoys. When one
example, a duodenal ulce r, is o ne of the most frequent progenitors of viscerogenic thoracic pain, with cholecystic disease a more disram second.
compares the cervical spine, possessed of its great
mobility, with the dorsal spine and its relatively fixed nature, it is easy to comprehend the focal action of static and dynamic stressors on such
freely movable segmental Structures. One must recognize the commonality of cervical dorsalgia before embarking on an examination for dorsal (thoracic ) pain of structural origin, since chronic and low-grade cases of cervicogenic dorsalgia may prove extremely difficu lt to elicit. It is not unusual to encounter dorsal pain of cer-
vica l origin with the patient steadfastly denying any neck pain . These cases are rarely overtly trau-
Clinically herpes zostet has often arisen as a nonmusculoskeletal cause of dorsalgia. Grouped vesicular lesions on an injected base o r a nest of small ruptured vesicles often bears witness to the
herpetic origin of the dorsal pain. The greatest diagnostic difficulty arises when there is no apparent development of a herpetic dermatologie lesion, or the lesions rose and passed undetected by the patient or his or her doctor. Occasionally in herpes zoster, pain precedes the vesicular eruption by a number of months even in th e relative ly
by residual
yo ung adult. The vesicular lesion when it does
static effort and postural stresses imparted to the mid to lowet cervical spinal joints and their sup-
arise ma y be so insignifica nt as to be dismissed as
portive soft tissue structures. The clinician mUSt
From a historical perspective there is occasionally an obvious clue as to the cervical origi n
matic and are more common ly caused
function as the ever-determined and doggedly persistent sleuth in cases of dorsalgia. One must gather all essential evidence and clues, both large and small, to determine the condition involved and take appropriate action.
nothing more than a small pimple.
of the patient'S dorsal complaint ("Doctor, when I turn my head to the left I get a stabbing pain in my left shoulder blade," or "Doctor, I have a heavy pain in my mid back and my neck is stiff
355
18 and hurts to move in all directions. "). This type of historical comment is most often encountered
when dorsal pain is of recent origin. Much less obvious is the chronic cervicogenic dorsalgia of 4 to 5 years' or more duration or the low-grade subacute case of several months' durarion, where neck symptoms are entirely denied or
passed off as insignificant. A methodical search of the patient's history, looking for incidents of neck trauma, such as motor vehicle accidents or sports injuries or ancillary symptoms such as recurrent
headaches, upper extremity pain, or paresthesia or chest pain of unknown origin, may often prove rewarding!
If no overt trauma is encountered in
the history, frequently a clue may be obtained on exploring the nature of the patient's employment. Often, especially in the more chronic cases of cervicogenic dorsalgia, the patient is engaged in a desk-computer type occuparion or some other vocation of static effort, with the cervical spine flexed, shoulders sloped, elbows unsupported, and the suspensory apparatus of the neck and upper back unduly taxed. Often the patient seeks relief of the painful dorsalgia by abandoning the irritating posture in favor of walking about or lying down. Genera lly most cervicogenic dorsalgia is eased by rest, although the occasional case is exacerbated by eccentric postures of the neck while sleeping. Causative mechanisms of cervicogenic dorsal-
gia involve a look at the most commonly involved Structures seen co underlie most cervical pain syndromes, both local and referred.
agent through rhe discogram needle. The logical conclusion is that pain referred from the cervical disc caused by herniation wirhin rhe disc or internal disc disruption is located in the interscapular-scapula r area of referral. It has vague loca lizarion in that the superior discs refer to a superior dorsal level and lower discs refer more caudally. Dorsal pain thus expressed is often of a more diffuse nature and less spot specific. Scapular pain on irritation of the ventral (motor) nerve roots intradurally has been found by Frykholm (3). Dorsal pain of cervical origin was also recognized by Cyriax (4). Cyriax's description of this cervicogenic dorsal pain phenomenon is one of discal-dural irritation. Cyriax perceived that when pressure is exerted on the dura mater, usu-
ally by a small, displaced fragment of disc bulging out the posterior longitudinal ligament, a localized tender spot forms within the dorsal region. Cyriax notes that this lesion is ve ry much a secondary phenomenon attributable to cervica l dural irritation, although it is often mistakenly considered a primary lesion of "dorsal fibrositis," " ttigger point," or "mya lgic SPOt."
Cyriax states that usually when a full and painless range of movement has been restored to the offending cervical segments the dorsal pain and tenderness also eased. Cyriax also nOtes the amount of misdirected massage,
injection,
and
manipulation
aimed
genic dorsalgia that must be ruled out is cervica l
locally at this painful expression of cervical segmental pain referral. In the chiropractic realm, cervicogenic dorsalgia is most common ly misdiagnosed as a "sublux-
disc involvement. Discogenic nonneurogenic pain,
ated rib" or a "trigger point" in local muscula-
dorsal pain emanating from disc disruption with-
ture. If a trigger point were truly to exist in local dorsal musculature, it is likely also true that this myoneural trigger point usually would lie on the
Certainly one causative mechanism of cervico-
oU[ actual nerve root compression or irritation, is
often encountered clinically and frequently is not recognized. Cailliet (2) reports thar, in the performance of cervical discography, merely touching the anterior surface of rhe cervical disc with the needle caused pain in the "shoulder blade" or "interscapular region." This dorsal pain could be abolished by the injection of a small amount of local anesthetic
course of an irritated sensory nerve from a
lesioned spina l segment. "Trigger areas" according to Golding (5), are tender spots usually on the course of a sensory nerve root from the involved
spinal segment. Subluxation of the posterior facet joints is an important causative agent in the production of
356
11111 SlMlxatlan Syndl'Olll8l
dorsal pain. It is also possible to have dorsal pain emanating from both a discal source and posterior cervical facer subluxation in the same patient. Lower cervical subluxation may lead [Q irritation of the medial branches of the dorsal primary ramus (sensory facets) or the recurrent meningeal nerve (the disc). Maigne (1) describes anastamoses between posterior branches of the lower cervica l and upper dorsal nerves, especia lly T2. The T2 dermatome is quite extensive in the middorsal region. The T2 nerve is seen to run paravertebrally in a groove exiting close to the surface at TS level, then running laterally toward the scapula. This is thought to be the o rigin of the painful dorsal spot. Thoracic pain of cervica l origin may be quite simple to evoke on examination of the cervical spine, especially in the acute phase. Such is certainly not always the case for the subacute or chronic pain syndrome. Diagnosis may be as simple as having the patient actively rotate his or her head roward the acute restriction, w ith subjective pain noted in the dorsal region. rn the case of acute cervical disc herniation, especially when overt trauma is involved, a deep, constant dorsal ache is often encountered with cervical spine ranges acutely limited in a global fashion . Radiation to one or both arms, or pares-
thesias of the fingers of one or both hands should certain ly create suspicion and concern in the mind of the clinician. Along with routine sensotimOtor testing, a search for pathologic reflexes indicating upper motor neuron involvement should also be done. Many times the latter is entered into when the deep tendon reflexes (DTRs) are seen to be pathologically hyperactive. A Valsalva maneuver, either reinfotced by having the patient'S neck in the position of greatest aggrev3rion of symptoms or maintained in neutral, may evoke dorsal pain and may force one to consider a space-occupying lesion in the cervical spine such as disc prolapse or herniation . Painfully restricted forward flexion in the cervical spine, especially when other movements are
largely pain free, is certainly indicative of disc involvement but is by no means exclusive. Adding bilateral nerve stretch testing (maintaining bilatera l simu ltaneous tension on the brachial plexus furthe r restricts an already limited flexion by causing increased tension on the spinal dura already compressed by posterior migration of disca l elements. As related eariier, the subacute or chronic dorsalgia (in some cases many years) may be harder to track from the cervical spine and hence requires some diligent searching on the part of the examiner. In add ition to carefu l motion pa lpation of cervica l spine segments, all passive ranges must be examined, being certain to overforce gently in all directions, looking for dorsal referral and slight limitations of end range movement. Be sure to include forced flexion with associated left and right rotation in addition to the other routine ranges of motion. The head then is supported in slight flexion while the supraspinous ligament is rubbed vigorously with the index finger of the palpating hand. The ligament is fr ictioned as it courses between the spinous processes of the cervical vertebrae. Occasionally painful radiations or paresthesia to the dorsal region or upper extremity is reported, not to mention focal selective tenderness. Symptoms thus expressed are thought to arise from irritation created by hypermobility/instability or a segmenta l reflex mechanism. Posteroanterior thumb pressure then is directed over the spinous processes and should be quite forceful. The patient should be instructed to relax the neck while the fo rehead is supported by one of the examiner's hands in a slight altitude of flexion, allowing the posterior supportive tissues to remain slack. The patient shou ld be assured that the procedure is necessary and painful but not in any way dangerous. An attempt is thus made to literally "rock the vertebral segment," looking for dorsal or upper extremity radiations from facilitated joint structures. Selectively deeply rubbing the facet joints with a palpating finger also may occasion the production of sought-after
19 radiating symptoms. If necessary, forcefully deviating the spinous processes with the thumb toward and then away from the involved side also might prove revealing. The "anterior cervical doorbell sign" is seen
approximately 60% of the time in cervicogenic dorsalgia (1) . Moderate pressure with the index finger directed horizontally over the anterolateral portion of the lower cervical spine (the ventral emergence of the nerve root) and held for a few seconds, exploring segmental level after segmental level, may trigger the patient's dorsal pain . This phenomenon has often been dismissed as emanating from "scalene trigger points", when in fact radicular irritation is often paramount.
Skin roll is a useful procedure in which the skin and subcutaneous tissue of the dorsa l region and posterior cervical spine is "pinch ro lled"
approximately one and one-half finger's breadth from the spine. Hyperalgesia is often seen focally in the region of TS-T6 and T2 as well as CS-C6 and C6-7, corresponding to the irritated cervical segment and the entrance and emergence of the second dorsal nerve. It shou ld be noted that this maneuver serves as a useful test in cases of
fibromyalgia where the patient exhibits hypersensitivity to this procedure in addition to that experienced on palpation of the consistent pattern of tender points. If test results are thus far equivocal for cervical dorsalgia, it is useful to traction the brachial plexus in various positions. Tractioning the plexus through various maneuvers may serve
to disclose the dorsa l complaint when other more direct measures aimed at the cervical region have
failed. Direct tractioning (stretching) of CS and C6, C7 and C8, and Tl nerves are thus employed. It is also useful to add lateral cervical spine deviation away from the tractioned root to elicit dorsal or extremity symptoms. Occassionally it is necessaty to rotate the cervical spine globally while the rOOtS are tractioned to produce a catch of dorsal pain . In the case of radiating upper extremity symptoms it is frequently useful ro maintain the involved arm in the position that most intensifies
symptoms and then move the cervical spine
357 through extreme ranges of motion, looking for symptom escalation or amelioration.
Certainly local palpation of the region of dorsal tenderness is necessary to assure the patient
that you have found " the spot." Nowhere is the example of misleading tenderness clearer than in the case of cervicogenic dorsalgia with a clearly defined "dorsa l spOt." Frequently dorsal segments in the region of the dorsal spot a re " fixed" and tender to palpation. Local musculature is frequently hypertonic, as evidenced by loca l taut and tender fibers. The upper extremities should be examined neurologically, noting strength, deep tendon reflexes (DTRs), and sensory changes if present. Strength testing shou ld be done in a repetitive challenge, comparing right with left. Frequently triceps strength (C7) is somewhat diminished on the side of dorsal pain even when no upper extremity symptoms are present and when DTRs are symmetric.
Radiographic examination is of course always required when the history unearths a traumatic origin to the dorsalgia, the possibility of metastatic disease, or the presence of a rheumatologic disorder such as seronegative spondyloarthropathy or rheumatoid arthritis. Such instances as these may require radiographic stud y of both cervica l and dorsal regions. In less obvious or chronic cases, an inexperienced or hurried examiner may not exact a refer-
ral pattern from the cervical spine and may ca ll for imaging of the dorsal region on ly. It is not uncommon for these dorsal radiographs to prove misleading, the cause of the patient's malady thought to be due to scoliosis, or dorsal degenerative changes. It is also not uncommon for radi-
ographs of the patient's cervica l spine to appear negative in a case of cervicogen ic dorsalgia. This is especially true when dealing with the younger patient, frequently a young college student. Degenerative change, reversal of curve, or seg-
mental levels of disturbed kinematic functioning may be present on the cervical radiographic stud y and may hint at the cervical origin of the patient'S
358
TIle SlMlXIIIIan By•••••
dorsal pain. It is absolutely imperative to remember that local radiographic evidence of degenerative change or structural change takes on its greatest importance only when it is consistent with the findings of a thorough examination. The obvious exception to this would be evidence of lyric disease, fracture, or rheumatic disorder of the more exotic variety.
Once the diagnosis of cervicogenic dorsalgia has been established, it remains necessary to iden-
tify the pathomechanical mechanism as precisely as possible; it is on this precise diagnosis that treatment is based.
traction often can be successfully employed. In the chronic or subacute case of cervicogenic dorsalgia, it is ohen necessary to influence the zone of referred pain to bring about a more immediate response co treatment. Manipulation
of subluxated thoracic segments along with treatment directed to the painful focus in the surrounding soft tissues complements manipulation of the subluxated cervical segments. The clinician may elect to employ manual compression, ultrasound, transcutaneous electri-
cal nerve stimulation (TENS), or needle or electrical acupuncture in the treatment of painful thoracic and cervical foci.
Treabnent The treatments of cervicogenic dorsalgia are varied and rely on the evocative mechanism and its severity. For example, the patient giving a history of going headlong into the boards during a hockey game and presenting with neck stiffness, globally restricted cervical movements, an inescapable deep central dorsal ache, parasthetic hands, and equivocal long tract signs will be managed much differently than the acutely fixed neck locked while taking a shower and experiencing only dorsal referred pain. In the first case, imaging with an eye to referral to a neurosurgeon would be urgently appropriate, whereas in the latter case stabilization in a soft collar, ice therapy, soft tissue, and later light intermittent traction therapy and ultimately specific spinal adjustment may be indicated. Fortunately, most cases encountered present with either acute, subacute, or chronic unilateral subluxation with periscapu-
lar pain encountered on the homolateral side of restricted cervical motion.
Manipulation of the painfully restricted cervical segment in the direction of free movement often is met with a reduction in dorsal pain and a free range of cervical movement. Intermittent
It is often necessary to alter habitual work postures with ergometric training to reduce the stress of static postural effort on posterior cervi-
cal joints. Additional strengthening of cervical spine supportive tissues is often necessary, espe-
cially in cases of cervical discogenic segmental hypermobiliry. Rarely, a cervical support collar may be recommended for a period of 3 weeks to abolish cervicogenic dorsalgia. This may be recommended on an intermittent basis and used when the
patient mUSt assume a habitually irritating posture. Although rarely necessary, if this merhod is chosen it should be combined with a program of nonirritaring neck-strengthening exercises.
References I. Maigne R. Orthopaedic medicine: a new approach ro vertebral manipulations. Springfield,lllmois: 1972:261 . 2. Caillier NO. Neck and arm pam. 2nd ed. Philadelphia: F.A. Davis, 1984. 3. Frykholm R. Deformities of dural pouches and structures of dural sheaths m cervical region producing nerve rOOt compression: conmbucion [Q etiology and operanve treatmeR{ of brachial neuralgia. J Neuro Surg 1947; 4:403-13. 4. Cyriax J. Textbook of orthopaedic medicine. Vol l. Diagnosis of soft tissue lesions. 8th ed. Bailliere Tindall, 1982. 5. Golding ON. A synopsis of rheumatic diseases. 4th cd. Wdgh,· PSG, 1982.
The Thoracic Outlet Syndrome: First Rib Subluxation Syndrome lohan T. Szaraz
KayWorda
Thoracic outlet syndrome, cervical ribs, interscalene triangle, trigger points, ischemic compression
After reading this chapter YOII should be able to answer the following questions:
Quaatloo #1
What are the anatomic boundaries of the thoracic outlet?
Quaslloo #2
What are the contents of the thoracic outlet?
Quaslloo #3
In which direction does the first rib commonly subluxate?
QuasIloo#4
Which muscle group is frequently implicated in thoracic outlet syndrome?
360
TIle SWlUXltlon Syndl'lllll8l
S
Anatomic Features
ignificant confusion and controversy sur-
The "thoracic outlet" presents an opening bor-
round the tho racic outlet syndrome (1).
dered laterally by the first rib, medially by the verteb ral col um n, and anteriorly by the c1aviculo-
Historically, anatomists refer to th e superior aper-
ture of the thorax as the thoracic inlet and to the diap hragm-covered inferior aperture as the thoracic olltlet (2,3) . Sir As hley Cooper, in 1821, fi rst described the symptOm complex of the thoracic outlet syndrome (4). Forty years later Coote (5) excised a cervica l ri b with successful obliteration of symp-
manubrial comp lex. Contents of this thoracic
outlet include the lower trun ks of the brachial plexus and the subclavian artery (Figure 20-1 ). Anoma lies in this region, including cervical
ribs and fibrous bands, have been popularly linked to causation. The mere presence of an anatomic anomaly does not establish its causal
toms. Other ea rlier authors considered anacornic
relationship. Instead, the occurrence of neurovas-
abnormalities of the cervical spine to be the primary cause of the vascular compression and
Further comroversy and confusion stems from
cu lar dysfunction at the thoracic outlet depends on the interplay of three conditions (18 ). The mOst basic factor is the anatomic fact that the neurovascular bundle, comprising the subclavian artery and the lower trunk of the brachial plexus, normall y passes through several narrow spaces. Secondarily, a variety of physiologic and anth ropomorphic factors cou ld accen-
the fact that there are several subsets .of syndromes. Adson and Coffey (9) described the
tuate content-container incompatibi lity and lead to intermittent compression and repeated minor
sca lenus anticus syndrome and their diagnostic
gnomon ic of thoracic outlet syndrome (10). He
trauma to the bundle. And finally, space availabiliry may be further compromised by osseous, fibromuscular, a nd vascu lar anomalies of this region that would be innocuous without the twO
surm ised that arterial compression meant that the
preceding twO conditions.
resulting neurologic symproms as thoracic ou tl er
syndrome (TOS) (6,7) . By 1916, the presence of cervica l ribs in 1% of the population had been establ ished; however, on ly 10% of those we re symptOmatic (8).
maneuver (Adson's test) in 1927. Adson believed that intermittent vascu lar obstruction was patho-
brachial plexus was also irritated . However, pu lse obliteration can be found in 1 % to 94% of completely normal subjects (11-13) . The costoclavicu lar syndrome was described by Falconer and Weddell in 1943 (14 ). Two years later, Wright (13 ) identified the hyperabduction syndrome. It was Peet et al. (15 ) who coined the broader term thoracic outlet compression syndromes (TOCS) . Recently, Lee et al. (16) and others (17) proposed rhat subluxarion of the first ri b may irritate neurovascular structures at the cervicorhoracic area and cause rad icu lar symptoms in the arm,
hand, and neck, commonl y described as thoracic outlet syndrome.
Narrow Passages hversed by the Neurovascular BInIle T he subclavian vessels and brachial plexus traverse three narrow straits within the cervicoaxil-
lary cana l before reaching the arm . Interscalene Triangle T he interscalene triangular space is bordered anteriorl y by the sca lene anticus muscle, posteri-
o rl y by the scalene medius muscle, and inferio rl y by the medial border of the first rib (Figure 20-1, A). This interscalene triangle transmits all trunks of the brachial plexus, but only the subclavian artery traverses this triangle, not the su bcla-
361
(A) Interscalene triangle Scalene
Scalene anticus Scalene posticus
(8) Costoclavicular triangle
C8 spinal nerve
I Subclavian artery
(C) Subcoracoid space
Median nerve
Pectoralis
minor
Radial nerve
Rt11r120--1 Diagram of the neurovascular bundle traveling through the three potenrial narrow passages. A, Interscalene triangle. B, Cosroclavicular triangle. C, Subcoracoid space. Note that the lower branch of the brachial plexus is directly under the subclavia n artery, resting on the first rib. (Modified fro m Trot/ell l G. Simons DC. Myofascial pain and dysfunction: The trigger point manual. Baltimore: Williams & \Vilki"s. 1983.)
362
The Subklxatlon SyndrOO188
vian vein . The distance bcnveen the two sca lenes
Arrhropomorphic Factors
at the base varies significantly (19). There are therefore occasions when both the artery and the nerve trunk are cla mped within this tight fibrofascia I triangle (20) . Another anatomic va riation is the slope of the first rib. If the slope is unusua ll y steep, the artery wou ld be fi rml y wedged between the rib a nd the tendo n. Th is obliquiry seems to be mote marked in women (2 1) and possibly in advancing age.
Acromioclavicular descent is also prominent in
individuals with an asthenic physique, because the poorly developed shou lder muscles allow the scapula 10 rotate anteriorly and laterall y. This is further aggrevated by a long slender neck, where the cervical rOOts are even farther away from the costoclavicu lar passage, subjecting them mo re to
exaggerated tension and angulation (27-29). Postural and Dynamic factors
Costoclavicular Triangle The neurovascular bundle immediately enters a second tr iangular space bounded anteriorly by the middle third of the clavicle, posteromedially by the anterior border of the first rib, and posterolaterally by the upper border of the scapula a nd the subscapularis muscle (Figure 20-1, B). Both the upper and lower borders of this triangle are mobile; hence they are subject to physiologic narrowing, depending on the position of the arm
and activities of the shoulder musculature. Subcoracoid Space The last narrow strait is provided by rhe insertion of the pectoralis minor tendon into the coracoid process (Fig ure 20-1, C) . During shoulder abduction, contraction of rhe pectoralis minor tendon may significantly narrow the subcoracoid space
over the neurovascu lar structures (22-24 ).
Physiologic Factors Compromising the Narrow Passages Developmental FaclOrs In the upright positio n the space created between the clavicle and the first rib is chiefly determined by the inclination of the clavicle at the acrom ioclavicular joint. Aging leads to progressive
Certain body postures and arm positions may
consistently produce sym proms. The most nOtable is hyperabduction and external rotation of the a rm, such as sleeping with the arm behind the pillow. Occupations such as painting and automobile repair, require the arm to be overhead for
prolonged period. The anarom ic mechan ism responsible for the symproms in hyperabduction are costoclavicu lar
compression and bowing of the axillary artery at the subcoracoid space (13,30,3 1). Abduction of the arm beyond 90 0 requires external rotation of the scapula, which brings the clavicle upward and backward at the sternoclavicu lar joint, closing the
cosroclavicu lar space ( 13,23 ). Hyperabduction ro 180 0 is always accompanied by externa l rotation of the humerus, which ten ses the costocoracoid
ligament and the pecroralis min or, which accentuates compression of the subclavian vein (23,32) . Other symptom-producing factors may include wearing a heavy bag with a shoulder strap or carrying a heavy briefcase consistently with the sa me arm. In both situations the clavicle is brought directly o r indirectly against the neurovascu lar bundle (33). Water skiers, whose arms are strenuously pulled forward and downward with the body ti lted backward, compress their costoclavicu lar space as the neurovascular bundle
son why women are fOllf times more prone ro
is dragged aga inst the first rib and the sca lene anticus tendon. Hikers carrying bulky backpacks with cross-shou lder belts suffer lower plexopathy (back palsy) (34) by the same mechanism as do
develop TOS than ate men (22,23,26).
soldiers standing at arrenrion for a prolonged
acrom ioclavicu lar descent, w hich is more marked
in women (20,24,25 ). This may explain the rea-
363 period, shoulders drawn backward and chest thrust forward. These positions nOt only depress the clavicle but also elevate the first rib, thereby closing the costoclavicular passage (23).
vical rib articulating with the first rib on the symptomatic side. He believes that a cervical rib more than 5.5 em long tends to lift up and kink the subclavian artery and stretch the seventh cer-
Another insidious compressive mechanism is
vical nerve root. However, it is generally consid-
during deep inspiration, especially when forced or labored, as in patients with emphysema. The first rib moves upward and forward during deep inspiration by as much as 34 and 22 mm, respectively, in men and by as much as 28 and 14 mm in women (35). More importantly, this is repeated approximately 33,000 times each day. In patients with emphysema, the increased functional residual lung capacity keeps the first rib in an elevated position. Added to this are the repeated strained cervical movements during forced breathing, mediated to the first rib by the scalenes. The scalenes therefore hypertrophy and can potentially narrow the interscalene passage. In emphysema patients the neurovascular bundle is repeatedly subject to stretch, compression, and friction (20,36).
ered that abnormal fibrous bands extending from the tip on an incomplete cervical rib to the first rib are the most common causes of true TOS (1,11,20,22). Furthermore, these fibrous bands are clinically treacherous because they are invisible on x-ray films and may exist without con-
Strucbl'aI AnomaIIea ComPl'O/lllUlll the Narrow Panages fIItther Anomalous Ribs The association of cervical rib with TOS is well
comitant rib anomalies.
Anomalous Muscle Insertions Excessive and sustained scaleni muscle contrac-
tion has been thought to cause neurovascular symptoms (11,42,43), presumably by strangling the subclavian artery and neurovascular bundle. It is now believed that such muscular actions alone are unable to produce the symptoms without some form of anomalous muscle insertions
(24,44) . These anomalous muscle insertions may be as a fused scalenus anticus and medius inser-
tion, occupying an extended area over the middle third of the first rib (24), or a split tendinous insertion of the scalenus medius muscle (33), or even a hypertrophied scalenus minimus muscle (20).
documented. Irs incidence in routine, nonsympto-
matic patients is between 0.002% to 0.5% (9,37,38). Only approximately 10% of those with cervical ribs experience symptoms. Familial occurrences with other congenital anomalies have been reported (20,39). It is more common on the left side, although bilateral cervical ribs were found in 50% of surgical candidates (24). It is believed that cervical ribs develop in intrauterine life more often with prefixed than with postfixed brachial plexus (20), because of the lesser resistance encountered by the small first thoracic nerve root in a prefixed plexus (40). Rayan (41) reports numbness and tingling in the forearms of a 14-year-old girl and a 12-year-old boy brought on by athletic activities at school, caused by a cer-
Other Anomalies A number of unusual causes have been reported in [he literature as contributing to neurovascular compression in the costoclavicular compartment:
fracture of the clavicle with subsequent pseudarthrosis (45), malunion of a clavicular fracture (46), unreduced dislocation of the clavicle (47), and other rare causative factors such as osteo-
chondroma of the clavicle and first rib (26).
BiomechMical Considerations fIIICtIonaI caun Because chiropractors are intimately interested in
functional disturbances of various kinds causing
364 symptoms, rather than anatomic or pathologic causes, it is nOt unusual therefore that we see and recognize patients with symptoms of neurovascu-
lar compression syndtomes related to functional disturbances at the cervicothoracic junction. One of the major anatomic Structures that may be in -
motor system involves associated structures, like a chain reaction . Patients who complain of neck,
shoulder, arm, and hand pain, and manifest poor postural habitus, invaribly demonstrate lower cervical, upper thoracic, and upper rib dysfunc-
volved in patients presenting with brachialgia,
tions. The typical restriction of movement involved with a first rib dysfunction is restriction
paresthesias, and pain along the ulnar nerve
of cervica l rotation and lateral nexion.
distribution is the first rib. Lindgren and Leino (48) report on 22 cases of thoracic outlet syndrome-diagnosed patients who presented with a hypomobile first rib on the symptomatic side. They further report on five additional TOS patients, a year later (49) in whom the hypomobile or subluxated first rib was confirmed by cineradiographic study. These same authors also believe that normal mobility of the first rib is necessary for normal function at the cervicothoracic area and normal function at the thoracic outlet (50). Lewit (51) believed that there are different types of impingement syndromes. When the canal is a solid bone or a single groove covered by soft tissues, surgical decompression is often necessary.
However, when a canal is formed by bones linked by joints capable of movement, for example, the thoracic outlet, impairment of joint mobility must be taken into consideration in pathogenesis of an
entrapment syndrome. Under such conditions impaired function is the first change. If this functional loss lasts for a period, the increased strain on corresponding soft tissues, muscles, and ligaments may cause thickening of the ligament and in the end damage the nerve. This pathophysiologic mechanism is commonly shared in manual medicine (Figure 20-2) (52-56). If the offending Structure is found to be a cause of functional disability, as in joint dysfunction, treatment must be
directed toward restoring that lost function. Lewit calls chis "dynamic nerve compression" or
nerve compression due to impaired function (51). Successful trearment can be achieved by manipulation. Impairment of function anywhere in the loco-
li'lIIIUItic and Occupational causes Hargberg and Wegman (57) and others (58,59) evaluated the association and impact of occupational exposure and d;sorders of the shoulder and neck area. They found that certain tasks, repetitive in nature or involving a sustained task of handling materials in one direction primarily,
such as is typical of assembly line workers, requiring sustained, static contractions of the cer-
vicothoracic muscles, especially when these tasks are performed at shoulder level, are clearly associated with shoulder-neck disorders. Other commonly missed causative factors of TOS are adhesions and scarring associated with posttraumatic thoracic outlet syndrome. Dellon (60) and others (61) believe that rear-end collisions cause a stretch type of injury to the brachial plexus with subsequent scarring that causes
entrapment of the brachial plexus proximal to the first rib and hence are often missed in commonly used transaxillary first rib resections.
Clinical Features From our discussion thus far, it is obvious that
the clinical presentation is dependent on the underlying anatomic or functional disturbances with which patients present. In our experience,
patients present with moderate symptOms with progressive deterioration, especially when symptoms are dominantly vascular. The opposite is true with neurologic dominance of symptoms. Presentations are commonly significant, especially to the patient, because they include numbness and weakness but improve gradually with conservative care (See the box on p. 366).
365
Retained metabolites (lactic acid,
potassium, hydrogen ion)
~
ZG-! The pathophysiologic mechanism of functio nal disabil ity. (Modified (rom Bland j H . Cervical spine syndromes. j Muskuloskel Med 1986; 3(11):23-41.)
366
>
Symptoms of Thoracic Outlet Syndrome
_III pll. . lrrlllllan
• Numbness • Tingling (mostly ulnar side of hand, occasionally entire hand) • Coldness • Paresis (late manifestation) Early fatiguability Progressive weakness Dyscoordination
V_.,..,..... • • • • •
Swelling Heaviness Fatigue Cyanosis Engorgement of superficial veins in supraclavicular area
AMrlll "",pI_
• • • • •
Pallor Coolness Farigue Muscle cramps from reperitive use Ischemic pain
1iIyoIIIc111 "",,.....
• Catchy pain on movement of neck and shoulder(s) • Fatigue on exertion • Restricted and guarded cervical movements on rotarion and lateral aexion • Shoulder, arm, and hand deep, achy, constant pain Modified from Lebenson CS. Thoracic ourler syndrome: Diagnosis and conservative managemcnr.
J Manipula-
tive Physiol Ther 1988; 11:493-499.
The literature appears to selectively differentiate symptoms into (l) primarily vascular cause, and hence vascular symptoms, such as swelling, cyanosis, pallor, coolness, and ischemia; and (2) primarily neurologic such as numbness, tingling, and paresthesia. This may have prompted a number of authors to give subclassification to various causative factors involved. Each of these syndromes had obvious pathognomonic diagnostic
tests. Adson's maneuver was specific for the scalenus anticus syndrome in which neurovasculat compression occurred exclusively in the interscalene triangle. Naturally, treatment followed consequentially, a scalenectomy. Falconer and Weddell coined the term costoclavictllar syndrome for those patients with positive exaggerated military maneuver, which is thought to narrow the costoclavicular space, specifically (14). Later Wright advocated the diagnostic category of hyperabduction syndrome for patients who became symptomatic with hyperabduction of the symptomatic arm. In practice it is more practical CO associate patients with the dominant symptom either neurogenic or vascular, depending on the degree of compression and perhaps to a lesser extent on the lesion. This initial clinical impression often changes with treatment; dynamic, anthropomorphic factors may undergo change with life-style, general health, and aging.
Sensory Signa IDI Symptoms The most common presenting symptom of TOS is numbness and tingling. Sanders and Pearce (62) found that 90% of TOS patients had paresthesia in the hand, 80% had arm pain, 86% neck pain, and 69% occipital headache. Pang and Wessel (18), in their review of the TOS literature, elaborate that (1) neurologic disturbances are caused by involvement of the C8 and TI fibers of the lower trunk of the brachial plexus and that (2) sensory disturbances usually appear in advance of motor signs. The pain is usually described as a dull, constant, heavy ache, and its distribution does not respect the C8-T I dermatomal pattern. It is often diffuse in the supraclavicular and shoulder area and spreads down the arm. Paresthesia, however, is frequently segmental and mostly felt in the inner aspect of the arm and forearm, in the ulnar half of the hand, and in the fourth and fifth digits, including the hypothenar eminence of the hand. Constant numbness and tingling in the ulnar digits are almost pathognomonic and cer-
367 tainly disturbing to the patient, but occasiona lly a burning sensation and sharp localized pain may be experienced (1). [n some patients the pain is atypical, loca lized to the anterior chest wall, and may simulate angina pectoris (pseudoangina) (36) . Sensory symptoms are often precipitated by trauma to the shoulder gird le, a bout of heavy lifting or simply carrying heavy objects, or the habitual use of a heavy shoulder bag over the same shoulder. The pa in is often aggravated by the use of the arm or arms, because these symptoms are often bilatera l (63). The pain is worse by the end of the day, particularly in occupations involving the use of the arms overhead. Many patients are awakened during the night by arm pain and paresthesia, especially if the affected arm is raised above the pillow. Ribbe et al. (64) found that the mOst reliable symptoms were: (1) history of aggravation of symptoms with arm elevation, (2) history of C8-T1 paresthesia, (3) tenderness over the brachial plexus supraclavicularly, and (4) positive abduction and external rotation (AER) of the arm test. They found that three of these four tests were positive in 94% of thoracic outlet syndrome patients. This is considered the "TOS index." Arm positions that remove traction on the
brachial plexus bring relief of symptoms. Patients often find relief in sitting with elevation of the shoulder by resting the affected elbow on the arm of the chair or supporting the elbow with the opposite hand. This maneuver is effective for any brachial plexus compression syndrome, not only for TOS. With time, objective signs of sensory denervation appear as diminished sensation to pinprick and light rouch sensation over the C8-T1 dermatome. [nitially this hypesthesia is patchy over the ulnar digits, but with time it becomes even ly distributed over the entire ulnar side of the hand (65). When this is correlated with digital tenderness over the scalene anticus and supraclavicular
portion of the brachia l plexus, three of the four items of the "TOS index" of Ribbe are satisfied and the diagnosis of TOS is certain.
Motor SIgns and Symptoms Subjective mOtor symptoms often accompany the onset of severe pain and paresthesia. The hands feel weak and fine motor skills may be disturbed. Travell and Simons (66) discuss that the patient may report dropping things. Patients may complain of difficulty with burtoning their shirt or blouse in the morning. When this is accompanied by aching pain in the hand and forearm, especially in (he morning, arthritic process is often
suggested . Testing the individual muscles, however, shows weakness of flexors of the hand and digits, but the greatest weakness is invariably found in the intrinsic hand muscles (20). In longstanding cases, the most characteristic partern is
severe thenar atrophy with preservation of the interossei and hypothenar muscles (67) . Within the thenar group, there is also a selective wasting of the abducror pollicus brevis and opponens pollicis with preservation of the flexor pollicis brevis, producing the characteristic guttering along the lateral aspect of the thenar pad (18). This typical partern of lateral thenar muscle wasting and ulnar 'sensory changes clinically distinguishes TOS from carpal tunnel syndrome, with its typical median nerve neuropathy (18). It is not unusual, however, that carpa l runnel syndrome, especially when the patient presents with shoulder pain, is commonly confused with TOS. In fact, when a comparison of the symptom complex of the two conditions is made (Table 20-1), it is quite possible to confuse the two on symptom presentation alone. The simultaneous presentation of carpal tunnel and thoracic ouriet, however, is extremely rare (68) . Forced wrist flexion reproducing the paresthesia (Phalen'S sign) and the less reliable Tinnel's sign, tingling on percussion over the carpal tunnel, are good diagnostic tests (69).
vasomotor 0IstJI'bances and 1I'opIK Changes Vasomoror symproms, from exposure to cold, oration of the hand and in a dependent position
blanching of the hand and purplish red discolforearm when the arm is are usually preceded by
sensory and motor complaint. These are most dis -
The SWIIuxatlon Syndl'Ol1l8l
368
>
Comparison of Positive Clinical Findings in Thoracic Outlet (TOS) and Carpal Tunnel Syndromes (CTS)
'. " . . '. . . . .'.'".,. •
~
~
... .
'#C'., ... ,li
.
Symptoms Paresthesia Pain Hypesthesia Weakness Use numbness
Rest numbness Shoulder-arm pain Signs Hypertrophic scalene Hypesthesia Weakness Atrophy AER test positive Pulse obliteration Hyperabduction test Tinel's sign Phalen's sign Weak pinch Modified from Ca rroll RE, Hurst
'i'P_
~
.. I
TOS
CTS
44% 75% 70% 41% 0% 18% 8%
79% 52% 0% 43% 18% 18% 8%
3% 33% 37% 1%
5% 37% 37% 0% 0% 1%
0%
56% 20% 42% 0% 0% 0% 63% 42% 20%
I.e. The relationship of
VaSCUlar Disturbances Vascular symptoms are commonly divided into arterial and venous disturbances. According to Riddel and Smith (71), venous symptoms are more common and a re termed as effort thrombosis. Signs of venous congestion and distension are usually preceded by heavy ac he in the pectoral and supraclavicu lar region during continual exertion of the arm . Lord and Rosati (23) believe that subclavian vein compression and subsequent thrombosis occurs between the costocoracoid ligament and the first rib. Others (11,24) believe that the anterior scalene band ma y compress the subclavian vein against the clavicle during or after srrenous muscle contraction . In venous compression the discomfort graduall y increases over severa l hours after exertion, and the entire arm may become swollen and cyanotic. Arterial compression, however, produces "ischemic" -like cramping in the hand or forearm that may lead to paresthesia during sustained exertion of the elevated arm. This is usually
>
Differential Diagnosis of the Thoracic Outlet Syndrome
tho racic aurlcr syndrome and carpal runnel syndrome.
Clin Orthop 1982; 164,149-53.
turbing to the patient and, because they are often aggravated by emotional stress, usually result in diagnostic labels such as "neurotic." These vasomotor symptoms, unlike sensory symptoms, commonly occur at rest, independent of arm position,
and can become very severe without concomitant pain. Su nderland (20) believes that these vasomotor disturbances always occur alongside sensory and motor changes because mOSt of the sympathetic fibers to the upper limb course along the C8 and T1 nerve roots, converging on them as postganglionic fibers from the upper three sympathetic ganglia (20). This may have prompted the recent advances for alternative surgical correction using dorsal sympathectomy instead of rib resection (70).
• • • • • • • • • • • • •
Carpal runnel syndrome Ulnar nerve entrapment at the elbow Cervical disc syndrome Cervical spondylosis Lower cervical facet syndrome Superior subluxation of the first rib Impingement syndrome at rhe shoulder Subacromial bursitis Myofascial pain syndromes of shoulder girdle muscles Myofascial pain syndrome of scalene muscles Raynaud's disease Pancoast tumor Cardiac pathology
Modified from Liebtnson CS. Thoracic outlet syndrome: Diagnosis and conservahve management. J Manipula tive Physiol Ther 1988; 11,493-499.
369 relieved by rest and elbow elevation (claudication). Such intermittenr and position-dependent
>
The Followi ng Symptoms Should Be Asked For and Tests Performed
claudication may become worse in the winter
months and improve in warm weather (20). T his diagnostic feature is one of the differentiating components of vascular from neurogenic TOS, because neurogenic TOS is usually unaffected by climatic conditions.
Diagnosis There are no tests or signs that are pathognomonic of TOS. The diagnosis is by elimination of other syndromes such as carpal tunnel synd rome, cervical spondylosis, cervical disc syndrome, glenohumeral dysfunction syndromes, ulnar nerve entrapment syndromes, Raynaud's disease, space-
occupying diseses of the thoracic outlet such as Pancoast tumor, and cardiac pathologies (see the box on p. 368). Thorough and detailed case history and examination are cardinal feacores of diagnosis (see the box at right). Diagnosis should include the pathomechanics of the lesion such as TOS caused by subluxation of the first rib or TOS caused by myofascia l pain syndrome of the scalene muscles or as neurogenic TOS implicating cervical nerve rOot involvement or vascular TOS implicating involvement of the subclavian vessels.
Provocative Tests The most rehable test, according to Roos (72) and others (6 1,63), is the 3-minute elevated arm stress resr also known in the literature as abducrion and external roration test (AER). In this test the patient's arm is abducted ro 90° with elbow flexed to 90°. The patient then is asked to slowly but steadily open and clinch his or her fist for a full 3 minutes. Thoracic outler patients grad ua ll y develop symptoms of heaviness and fatigue in the involved arm and shou lders, wirh gradual onset of numbness 111 the hand and have to rest the arm for relief of progressive, crescendo distress that becomes intolerable. This test is positive in both neurogenic and vascu lar types of TOS and, when comhined with other objective signs, provides the
• • • • •
Distribution of pain Distribution of paresthesia Weakness or numbness in the arm and hand Aggravation of symptoms with arm elevated Aggravation of symptoms with head and neck movement
• Nocturnal symptoms Pllplal EllIlItIIIiaI
• Vertebral palpation • Ranges of active and passive mobility of the cervical spine • Evaluation of 1st and 2nd rib mobility • Brachial plexus compression supraclavicularly • Shoulder range of movement • Scapular movements • Postural assessment Head position Upper thoracic curve Lateral spinal curves • Elbow range of movement • Ulnar nerve compression at the elbow • Median nerve compression at the wrist • Hand grip strength • Radial and ulnar pulse tests • "Hands-up' test (abduction-external rotation--elevation rest) • Scalene palpation • Scalene relief test Modified from Ribb< EB, Lindgren Sill, Norgren LEH. Clinical diagnosis of thoracic outlet syndrome: Evaluation of patients with cervicobrachial symptoms. Manual Med 1986; 2,82-5.
most reliable tests for diagnosing neurogenic thoracic outlet syndrome (see the box on p. 370). Adson's test is nor cons idered a reliable test,
because pulse obliteration has been found in a large percentage of asymptomatic patients ( I 113); however, an increase in the symptoms with
The 8IMIXItIIIn By.......
370
> ........ ,..
Most Reliable Diagnostic Tests for Neurogenic TOS
• Ipsilateral side of neck • Supraclavicular, over brachial plexus • Infraclavicular
'IIIIIIII..-............
• ImmCdlate pain over braChial plexus • Gradual onset of usual symptoms in neck and arm WI£'., • Triceps (C7)
• Interosseous band muscles (C8, Tt) • Hand grip (C8) Itwll'II'. • Inner fOrearm (C8, Tt) • Ring and smaU fingers, medial side of band • Occasional radial distribution in forearm and thumb EIIIIIIII . . . . . l1li (J H)
• Premarure fatigue and heaviness in involved arm
• Gradual onset of paresthesia in the fingers, spreading through band and forearm • Grimacing and vocal complaints • Crescendo of distress throughout upper extremity
• Sudden, premature dropping of band into lap • Involved band quite slow to recover • Performed with arm abducted to 90° elbow flexed to 90" Adapted &om Uebemoo after ROOI DB. New concepti of thoracic: oudet oyndrome tha. explain etio'osy, symptoms, diapIosis and ....tmen•. Vase Sous 1979; 13:313-21.
var ious positions of the arm is a significant component (73).
Beclrodlagnostlcl Nerve conduction tests are given poor reliability in the literature for definitive diagnosis (1 J ,63,74,75) . According to euetter and Bar-
toszek (I), nerve conduction velocities and latency values are a ll normal unless there is concomitant peripheral neuropathy.
Radography Static radiographs of the cervicothoracic region must be taken to rule out congenital anomalies, although, according to Urschel and Razzuk (36), only 30% of thoracic outlet patients have associated congen ital abnorma lity. Recently, Panegyres et a l. (76) reported that their magnetic resonance imaging (MRI) study showed 70% sensitivity, with 87.5% specificity for deviations and distortions of nerves and blood vessels, and demonstrated the presence of radiographically invisible soft tissue bands in 20 TOS-suggested patients.
FtI1cUonal Evaluation Functional evaluation of biomechanical cervi· cotho racic lesions involves axia l rotation and simultaneous latera l flexion of the cervical spine as first described by Lewit (51) . There is a typ ical tender spot just beneath the clavicle at the manubrium stern i (55) rel ated to torsional stress from the subluxated first rib at the costosternal junction. Lindgren and Leino (48) describe the expiration-inspiration (E-I) test for first rib mobility (Figure 20-3) and report their study of 22 cases of TOS with 100% incidence of hypomobile first rib on the painful side. They further report a 17% recurence of TOS as a result of subluxation of the stump of the resected first rib (78). When the first rib subluxates, usually in an inspiratory position, it moves cranially at the costotransverse joint. When the patient turns the head to the left, the first thoracic vertebra rotates to the left and the transverse process (TP) moves anteriorly. Restriction of cervical rotation away from the side of lesion is most likely caused by the TP of the first th oracic vertebra bumping aga inst the first rib (50). Latera l flexion of the head toward the side of involvement is restricted because the superior position of the offending first rib; hence, restriction and fullness are sensed under the palpating hand (Figu re 20-4).
371 When superior subluxation of the first rib is suggested, all ranges of movement of the first rib should be evaluated. This includes bucket handle and ca liper motion, simi lar to all other rib functions (77). Individually and collectively, the ribs
undergo these two types of motion during respiration (79). The bucket handle motion is tested while latera lly flexing the head toward the contact position over the nonarticulating tubercle of the first rib (Figure 20-3). Normally the first rib depresses at the end point of its passive range of motion and a small accessory passive joint range (joint play) motion can be elicited. Abnormal inspiratory subluxation may be attributable to sca lene hypertonicity. Ca liper motion is tested by using the head as a lever to magnify this small movement (Figure 20-5). The thumb is placed on the nonarticulating tubercle of the rib, and the head is rotated away from the side. The normal movement is a slight anterior springing of the transverse process and the rib (end joint feel), giving no resistance to the palpating thumb.
Management fIIII't 20-3 The expiration and inspiration (£-1) movement of the first rib is palpated in relation to the clavicle. The right and lefr sides are compared.
The initial management of patients with thoracic outlet syndrome should always be conservative. Early operations should only be considered if vascular ischemia, serious embolic complication, or rapidly advancing denervarions and muscle wasting are the prominent features .
...... 20-4 Rotarion and lateral flexion of the cervical
RIIrt m-t; Evaluation of caliper rype of motion of
spine is restricted if the first rib is suhluxated superiorly. There will be fullness and loss of inferior end joinr spring of the first rib, as noted by (he
the first rib. When normally functioning, there wi ll he a small range of end movement at the extreme range of cervical rotation. The head is used as a lever to magnify this small accessory joint play.
palpating hand.
372 Surgical management has been severely criticized in the literature, especially when large studies show that only 24% of patients with thoracic outlet syndrome actually requite surgery (63,71,73,80,81). A well-informed patient is always a more compliant patient; hence, explanation of the pathomechanical state should always be given. This alleviates the patient's often ill-defined symptom picture and provides a more receptive patient to carry out instructions. These should include postural advice and reeducation, and avoidance
of carrying a heavy shoulder bag or handbag. Sleeping postures also must be evaluated, and the use of COntour pillow to support the cervical curve should be considered. Postural reeducation and correction of poor body mechanics are essential in the management of TOS. Round-shouldered or slouched postures often aggravate TOS and are the typical patient presentations. These postures not only place undue stress on the scalene and pectoralis muscles but also compromise the neural foramina and posterior zygapophyseal joints at the cervicothocacie junction. Prime concerns 3re correction of all associated
biomechanical dysfuncrions: the cervical spine, the first rib, both at the costovertebral and manubriocostal junction, the sternoclavicular and acromioclavicular joints, and the shoulder complex, with special attention paid to the scapulothoracic function. When the scalene muscles are involved, the stretching techniques advocated by Travell (66) are very effective in relieving acute spasms as well as relieving chronic, painful myofascial pain syndromes. Because the sternocleidomastoid (SCM) muscle is also an important part of the myotatic unit for accessory inspiration, it likely will be involved along with the scalene. If the SCM is involved, it may be the cause of temporal and occipital headache, a TOS patient's frequent complaint. Satellite trigger points (TPs) may develop in muscles along the radiating pain pattern of the scalene. Both pectorals are often involved in radiating chest pain (pseudoangina). Satellite TPs in
the long head of the triceps correspond with posterior arm pain and shoulder pain. Secondary TPs commonly develop in the brachioradialis, extensor carpi radialis, and extensor digitorum mus-
cles, resulting in pain associated with thumb and wrist movements. The scalene-relief test identifies scalene involvement with relief of the symptoms as compared with true neurogenic TOS, where various arm positions aggravate the symptoms
(Figure 20-6). Daily passive streching on the scalene muscles at home is critical to recovery (Figure 20-7). Chiropractors frequently use direct pressure over trigger points (ischemic compression), first discussed by Nimmo (82), writing in the }ollmal of the National Chiropractic Association in 1957. He believed that pressure applied to the belly of a contracted muscle interrupts the pain-spasm-pain cycle, and relaxation of the spastic muscle follows. Ischemic compression is widely used by chiropractors as well as stretching in the treatment
of trigger points (83). Chiropractic adjusrive techniques for the cervicorhoracic area, including corrections for first rib subluxations, clavicular subluxations, scapu-
lothoracic, and glenohumeral dysfunctions, have been well described by Szaraz (84); Kirk, Lawrence, and Valvo (85); Gatterman and Panzer (86), and mOSt recently by Peterson and Bergmann (79). Once the inferior component of the lesion is corrected, particular attention should also be paid to the cervical component of the lesion, especially because the scalene muscles intimately influence cervical dynamics, as has been classically described by Grice (87).
Conclusion The thoracic outlet syndrome is a challenging clinical entity. Careful history taking and thorough physical examination, including in-depth biomechanical evaluation of the cervicothoracic area, provides the practitioner with important
diagnostic clues to arrive at a solid clinical impression to undertake conservative therapeutic interventions.
20
The TIIoracIc Outlet ~: Iftt RIll SUbluxation . . . . .
373
A
B
~ 2IHI The scalene-relief teSt helps to identify the source of referred pain from active trigger points in the scalene muscles. A, This is the starring position and can be combined with Roos's test. B, Raising the shoulder elevates the clavicle, relieving pressure on the neurovascular bundle and shortening the scalene muscles. CJ As the shoulder is swung forward, the scapula is pcoccacred and the clavicle moves forward and upward to fully relieve clavicular pressure on the thoracic outler structures.
c
374
B
c A ~ 20-7
Side-bending stretching exe rcises are perfo rmed bilaterall y and dail y. A. Th e hand on the
side to be stretched is anchored under the buttock. B, To stretch th e scalenus posterior, the face is turned toward the direction of pull. C, The face looks forward to stretch the scalenus medius. D, The face is turn ed away from the directi on of the pu ll to stretch th e scalenus anterior.
D
375
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TIle SUl*Ixatlon Syndl'IIIMI
41. Rayan GM. Lower trunk brachial plexus compression neuropathy due to cervica l rib in young athletes. Am J Spons Med 1988; 16( 1),77-9.
42. Naffziger He. The scalen us syndrome. Surg Crnccol Obsrcr 1937; 64:119-26. 43. Oschsner A, Gage M, DcBakcy M. Scalenus amicus (Naffziger) syndrome. Am J Surg 1935; 28:669-95. 44. Clagen OT. Research and prosearch. J Thora c Cardiovasc Surg 1962; 44,153-66. 45. Barg:u WL, Marcus RE, Inleman FP. Late thoracic outlet syndrome secondary fa pseudoarthrosis of the clavicle. J Trauma 1984; 24,857-9. 46. Connolly J F, Dehne R. Delayed thoracic ourler syndrome from clavicular nonunion: Management by morseling. Ncbr Med J 1986; 71,303-6. 47. Ganga har DM , Flogaires T. Rerrosternal dislocation of the clavicle producing thoracic outlet syndrome. J Trauma 1978; 18,369-72. 48. Lindgren K·A, Leino E. Subluxarion of the firsr rib: A possible thoracic ourtCt syndrome mechanism. Arch Ph ys Med Rehabil 1988; 6%92-5. 49. Lindgren K·A , Leino E, Manninen H. Ci neradiography of the hypomo bile firsr rib. Arch Phys Med Rehabil 1989; 70,408-9 . SO. Lindgren K·A, Leino E, Hakala M, Hamberg]. Cervica l spine rorarion and lateral fl ex ion combincd morion in thc examination of the thoracic ourtct. Arch Phys M~d Reha· bil 1990; 7 1,343-4. 5 t. Lewit K. Impaircd joint function and entrapment syn· drome. Manuctlc Medizin 1978; 16:45-8. 52. Bland JH. Cervical spine syndromes. J Mu sc uloskcl Med 1986; 3( 11),23-41. 53. Kirkaldy· Willis \'(rH. Pathology and pathogenesis of low back pain. Chaprer 5. In: Kirkaldy-Willis WH, Burron C V, eds. Managing low back pain. 3rd ed. New York: Churchill Livingstone, 1983:49-79. 54. Philips H , G rieve GP: The thoracic outlet syndrome. Chapter 35. In: Grieve GP, cd. Modern manual therap), of the vertebral col umn. Edinburgh: Churchill Livingstone 1986,359-69. 55. Lewir K. Clinical aspects of disturbed fun crion of rhe locomotor system. Chapter 7. In: Lewir K. Manipulative therapy in rehabilitation of the locomotor system. 2nd cd. Oxford: Burterworrh· Heinemann, 199 1:231-67. 56. Rashbaum RF. Multidisciplinary spinal rehabilitati o n: management by o bjectives. C hapter 35. In: Hochschuler ST, COt ler HB, Guyer RD, cds. Rehabilitation of the spine, science and practice. St. Louis: Mosby, 1993,425-33. 57. Hargberg M, Wegman DH. Prevelence rates and odds ratios of shoulder·neck diseases in different occu pational groups. Br J Ind Med 1987;44 (9),602- 10. 58. Satow A, Taniguchi S. The development of a moror performance method for the measurement of pain. Ergonomics 1989; 32(3),307- 16.
59. Amano M , Umeda G, Nakajima H , Yarsuki K. Characteristics of work actions of shoe manufacfUring assembly line workers and a cross-sectional factor*Conrrol stud)' on occupational cervicobrachial disorders. Sangro 19aku 1988; 30,3- 12. 60. Dellon AL. The results of supraclavicular brachial plexus neurolysis (without rib resection ) in management of pOSt· traumatic "thoracic outlet syndrome." J Recon srr MicroSUIS 1993; 9( 1), 11-1 7. 6 1. Razi OM, Wassel HD. Traffic accident induced thomcic ourler syndrome; decompression without rib resection, correcrion of associated recurrent thoracic aneurysm. 1m Surs 1993; 78(1),25-7. 62. Sanders RJ, Pearce WHo The treatment of thoracic outlet syndrome: A comparison of different operarions. J Vasc Surg 1989; 10(6),626-34. 63. Sallstrom j, Schmidt H. Cervicobrachial disorders in cerrain occupations, with special reference [0 compression in the thoracic outler. Am J Ind Med 1984;
6045-52. 64. Ribbe EB, Lindgren SHS, Norgren LEH. Clinical diagnosis of thoracic oudet syndrome: Evaluation of patients with cervicobrachial sym ptoms. Manual Medicine 1986; 2,82-5. 65. Conn j. Thoracic o ueler synd rome. Surg Clin North Am 1974; 54,155-60. 66. Travell JG , Simons DG. M yofascial pain and dysfunction: the trigger point manual. Baltimore: Williams & Wilkins, 1983. 67. Gilliatt RW, LeQuesne PN, Logue V, Sumner AJ. Wasting of hand associat'ed with a cervica l rib or band. J Neural Neurosurg I'sychiatr)' 1970; 33:615-26. 68. Carrott RE, Hurst LC. The rel:ttionship of thoracic outlet syndrome and carpal runnel syndrome. Clin Orr hop 1982; 164,149-53. 69. Asbury AK, Dyck pJ , Johnson AC, et al. Coping with carpal runnel syndrome. Patient Ca re 1985; 19:76-90. 70. Urchcl H C Jr. Dorsa l sy mpathectom)' a nd management of thoracic outlet syndrome with video-assisted thoracic surgelY (VATS ). Ann Thomc Surg 1993,56 (3),7 17-20. 71. Riddel DH, Smith BM. Thoracic and vascular aspects of thoracic outlet syndromc. Clin Onhop 1986; 207:31-6. 72. Roos D8. New concepts of thoracic ourler syndrome thar explain etiology, symptoms, diagnosis :md treatment. Vasc Surg 1979; 13:3 13-21. 73. Stallworth JM, Horne JB. Diagnosis and management of thoracic ourlet syndrome. Arch Surg 1984; I J 9: 1149-5 1. 74. Daube JR. Nerve conducrion studies in the thoracic ourler syndrome. Neurology 1975; 25:347. 75. Ryding E, Ribbe E, Rosen I, Norgren L. A neurophysiological investigarion in thoracic oudet syndrome. Acta ChirScand 1985; 151:327-31. 76. Paneg),res ilK, Moore N, Gibson R, et at. Thoracic outlet syndrome and magnetic resonance imaging. Brain 1993; 1 16(P, 4 ),823-4 1.
377 77. Fligg B. Spmal biomechanics. CMCC, 1989. Personal communication. 78. Lindgren K-A, Lemo E, Lepantaio M. et al. Recurrent thoracic outlet syndrome after first rib resection. Arch Phys Me
83. Ganerman MI, Gae DR. Muscle and myofascial pam syndromes. In: Ganerman MI, ed. Chiropractic management of spine related disorders. Baltimore: Williams & Wilkins, 1990. 84. Szaraz Z. Compendium of chiropractic technique. CMCC 1984. 85. Kirk CR, Lawrence OJ. Valvo NL, eds. States manual of spinal, pelvic and extravertebral technic. 2nd ed. NCC 1985. 86. Ganerman MI, Panzer OM. Disorders of the thoracic spine. In: Ganerman MI, ed. Chiropractic management of spme related disorders. Baltimore: Williams & Wilkins, 1990. 87. Grice AS. Scalenus amicus syndrome: DiagnOSis and chiropractic adlustive procedure. JCCA 1977; 5:35-7. 88. Liebcnson CS. Thoracic outlet syndrome: Diagnosis and conservative man3gement. J Manipul3tive Physiol Ther 1988; II: 493-499.
• Thoracic and Costovertebral es n Adrian Grice
Costovertebral subluxation syndromes, scoliosis, coupled motion After reading this chapter you should be able to answer the following questions:
11111II1II #1:
Why do the traditional movement descriptions of flexion, extension, lateral flexion, and rotation need to be modified to describe segmental spinal motion?
QUIIIIIII #2:
How does altered motion in thoracic motion segments accompanying aging lead to degenerative changes in the thoracic spine?
Q 1II1II13:
What is the clinical significance of the transition area of spinous process rotation that accompanies lateral flexion?
379
C
omparatively little is known about the neurologic, biomechanical, and physiologic relationships of this region of the spine. This is peculiar when one realizes that the thoracic spine houses the sympathetic nervous system and spinal dysfunction has been implicated in the development of somatovisceral reflex dysfunction, vis-
ceral dysfunction, and pain. What is known about thoracic physiology and biomechanics has been largely extrapolated from known functions of the cervical and lumbar spines. It would appear that our knowledge of spinal function has been driven largely by the need to understand the causes and treatment of spinal pain, and therefore, the lumbar spine, and secondarily the cervical spine, has captured mOSt of OUf attention.
Much of the literature relating to the thoracic spine is devoted to pathologic conditions and conditions that, with a few exceptions, have little
to do with the clinical problems that are seen on a daily basis by the chiropractic clinician. Clinical experience, however, demonstrates
non physiologic, responses of viscera, including cardiovascular and respiratory systems and the locomotor system as a whole. The relationship may be through neurologic reflex changes or through direct biomechanical muscular function such as, for example, diaphragm contraction in respiratory change producing direct biomechanical effects on the rib cage and spine. Diagnostic evaluation of any segment or region of the thoracic spinal or rib cage therefore should consider:
1. The
locomotor
system
as
a
whole,
as
expressed in movemenc dynamics
2. Static body posture and our adaptation to graviry 3. The vertebral column and its function as an organ system 4. The cardiovascular and respiratory systems 5 . The visceral elements and reflex responses 6. The cervical spine and its postural reflex regulation and direct muscle attachments 7. The lumbar spine, its postural regulation, and direct muscle attachments
that pain syndromes and disorders of the thoracic spine and rib cage that do manifest themselves are quite frightening to the patient and produce
8. The functional interaction of the thoracic spine and rib cage
anxiety about internal diseases that mayor may
Clinically Relevant Anatomy
not be relevant. Pain, pathology, and degenerative changes in this region of the spine have been shown to relate to postural changes, including scoliosis and kyphosis, autonomic and visceral dysfunction or pathologic condition, aberrant spinal static or dynamic function, or aberrant costovertebral function (1-3). Aberrant static and dynamic function is related to dysfunction of the soft tissues, that is, the ligaments, muscles, and
discs. Joint function is regulated by sensorimotor reflex feedback loops. The sensory proprioceptive system gets its main input from skin, muscles, lig-
aments, blood vessels, and fascia and has been estimated to form 65% to 75% of the input; the special senses and viscera form the rest of the input. Thoracic spinal dysfunction therefore can be related to the overall neurologic regulation of the body's static and dynamic, physiologic and
The dorsal vertebrae are intermediate
In
size
between the cervical and lumbar vertebrae, and they increase in size from above downward, a
structural accommodation thought to relate to the increased demands of weight bearing (4). The rypical thoracic vertebra is so named because of the nature of rib attachments. The second to the eighth thoracics are considered rypical and contain two pairs of demifacets, one on the superior
posterolateral aspect of the body and one on the inferior aspect directly below, which form the articulation with the head of the ribs on each side. Viewed from the superior aspect, the typical vertebra shows a heart-shaped body with relative equal anterior-to-posterior dimensions, and the
spinal canal is round (Figure 21-1). The left side of the vertebral body sometimes has an impres-
380
TIle SUIIIuxatIan Sy........
fIIUN 21-1
fIIIre 21-2 Lateral view of typical th oracic vertebra,
1987.)
wedge-shaped vertebral body. (From Clemente. Anatomy, A regional atlas of the human body. 3rd ed. Urban and Schwarzenberg, 1987.)
Superior view of typica l thoracic vertebra . (From Clemente. Anatomy: A regional atlas of the human body. 3rd ed. Urban and Schwarzenberg,
sion formed by the aorta, which lies along the vertebral bodies and discs. From the lateral perspective, the vertebral body is slightly thicker on the posterior than the anterior. This vertebral shape is functional in forming the primary normal thoracic kyphosis. The superior and inferior disc end plates should appear parallel on radiographs. The pedicles are directed backward from the body, and the inferior intevertebral notches are large in size and deeper than in other regions of the spine, resulting in small but adeq uate intervertebral foramins that are circular in form (Figure 21-2). The laminae are broad and thick, and they overlap one another like tiles on a roof. They give rise
to
the
inferior
and
superior
articu lar
processes. The superior articular processes each have an ova l hyaline cartilage-<:overed facet that is /lat and faces posteriorly, slightly superiorly, and laterally. The inferior articular processes have on the an terior surface an oval hyaline cartilage a rticular facet that is slightly concave transversely and faces anteriorly, inferiorly, and medially. The superior and inferior facets overlap like shingles and, when viewed laterally, the joints create an angle from horizontal reported to be from 60° in
the upper thoracics up to 80° to 90° in the lower thoracics (5) (Figure 21-2). The spinous processes are long, triangular, directed obliquely downward, and terminate in a bulbous extremiry. The spinous tip in the middorsal region is at the level of the facet of the vertebra below and produces an angle of 45° up to 60°, steeper in some cases. The bulbous tip of a typical thoracic vertebra is an excellent level for adjusting the intervertebral fixations/subluxations. The clinician, by using an appropriate contact on the spinous process, may develop an a ngle of force from right or left in ferior to superior similar to the plane of the facet joints. The transverse process arises from behind the articular facet at the junction between the pedicle and the lamina . They ate thick and strong, quite long, and directed obliquely backward and outward, with a clubbed extremity formed by the attachment of muscles. Clinically it is important to note that in the upper and midthoracics the TVPs (transverse processes) are sometimes angled posteriorly and superiorly so that the tip is superior to the articular facet of that vertebra, a facet important in the angle to adjustive thrust. The purpose of both the spinous and transverse process is for the attachment of muscles, and the shape of these structures is determined by the
381 forces that act on them. The usual direction of thrust should be opposite to this direction of force. Most often a crossed bilateral is selected to facilitate the motion and nOt jam the facets, and the thrust being a torque directed from the superior is helpful. On the anterior surface the typical thoracic transverse process contains a small, concave, articu lar facet that articulates with the
tubercle of the rib. The thorax, or chest cage, is an osseous, cartilaginous structure whose principal function is to
proteer the principal organs of respiration and circulation. The rib cage is an important functional component of respiration, and Wyke showed, by freezing the costovertebral joints, that the neurologic stimu lus for respiration was suspended and respiration ceased (6). This fact may explain the benefit perceived by patients with chronic lung problems and asthma after adjustive care.
Viewed from the lateral aspect, the ribs form an angle of apptoximately 45°, as they move anteriorly and inferiorly, with a sharp superior angulation of the costal cartilages as they curve superior to attach to the sternum. The sternal costal joints of the true ribs, the first seven, unite at the sternum by hyaline cartilage. The next three or four ribs are false ribs, and the hyaline cartilages connect, forming a more elastic attach-
ment. The last cwo ribs have free endings without cartilaginous attachments or, in some cases, the
11 th rib forms part of the false rib cartilaginous structure. The 12th rib with the constant free distal end is called by some the floating rib. These costa l cartilage attachments have a good deal of elasticity in the younger age groups, but as we age these cartilages become deeply yellow in color and tend to calcify and lose their elasticity. The female thorax differs from the male in the sense that it usually has a lesser capacity, the sternum is shorter, and the upper margin of the sternum is on the level of the lower body of the third dorsal vertebra, whereas in the male it is on the level of the lower part of the second dorsal vertebra. The upper ribs are more mobile in the female and allow a greater enlargement in movement of the
upper thorax than in the male. These facto rs are important in consideration of prone adjustments
in the female, particularly in the older osteoporotic or aging patient. All 12 thoracic vertebrae articulate with ribs; however, T2-T9 have a double-rib articulation, forming a facet joint on the tip of each transverse ptocess that articulates with the tubercle on the angle of ribs, and on the body on each side of the vertebrae as just described. The first thoracic vertebra differs somewhat and is referred to as atypical. Tl is somewhat cervicallike, with the spinous process being thicker and proceeding posteriorly on a more horizontal plane. The vertebral body is broad transversely, with a concave superior surface slightly lipped on each side, causing the articular surfaces to be somewhat oblique. The clinician should consider the angle of the facets and the shape of the vertebral body in formulating the direction of the more effective adjustment. The concave body suggests an adjustment that includes distraction or longitudinal traction, whereas a direction of thrust from superior to inferior is indicated to facilitate an adjustment with less discomfort to the patient, a factor very important in cervica l
adjusting as well. The spinous process of the first thoracic is thick and may be almost as long as the vertebra prominens (spinous of C7), and during fl exion of the neck it also can appear to be quite prominent. This structure makes it an excellent COntact for rotational and lateral flexion adj ustments for fixations/subluxations becween C7-Tl and TI-T2. A thumb contact, commonly called a TM (thumb move), which is described later in this chapter, shou ld concern itself with the thoracic vertebral shape, different patient head alignment, and thrust direction during positioning, to specificall y affect C7-Tl o r Tl-T2. The head position and direction of thrust also change when we consider the holding elements involved, such as the direction of the muscle force. Again these factors are important for success and comfort in adjusting this region. As in all areas of the spine, the anatomy and the ho lding elements should be con-
382
TIll ......1tIan By......
sidered when applying an adjustment. In this review I do not deal with all the adjustments in the area; rather, special attention is drawn to
areas that have been shown to produce parricular difficulty for clinicians developing efficiency, specificity, and ease of adjusting. This first thoracic vertebra is such an area. It has a complete
facet for the first rib and a demifacet on the inferior of the body for the articu lation of the second rib. The presence of a cervica l rib may complicate pain syndromes involving the upper ribs and thoracics but provides no particular problem for treatment and in many cases is present for years
without symptoms . Thoracic outlet problems are common and clinically are often caused by irritation coming from the multiple pain-sensitive structures related to not only the vertebral facet joints but the rib attachments and the increased number of ligaments and muscles of this region. Muscle forces that act on these joints take their attachment from the cervical spine and occiput as well as from the thoracic spine and ribs. Correction should consider the related fixations in these regions of the spine and the interaction of the muscles. Further discussion of the cervical thoracic junction is presented in another chapter of
this text on thoracic outlet syndromes, by Dr. Szaraz. The inferior thoracic vertebrae, T9-T12, are also considered atypical, particularly Tll and T12, which display cha racteristics of lumbar vertebrae. The 9th thoracic mayor may not have an inferior demifacet, whereas the 10th usually has only one demifacet, often more laterally placed on the pedicle. The 11th vertebra is more similar in size to a lumbar, and the articular facets for the ribs are large r and are located on the pedicle, which are also larger and stronger. The spinous process is short and nearly horizontal. The rransverse processes of Tll-T12 are short and have no arriculation with the rib. The 12th thoracic differs from the other thoracics in that the superior facets have a cotonal facing, that of a tho-
are unique and often necessitate special attention
so that symptoms may be controlled. The thoracolumbar region exhibits the highest torsional stiffness and the highest frequency of fracture (4). The transverse process is shorrer, containing
tubercles similar to mammillary or accessory processes formed by the attachments of muscles. These anatomic and biomechanical factors make this vertebra an important transitional vertebra
for spinal curves and suggest that the optimal function of the spine is when the curves statically and dynamically do in fact make their transition at this level. Treatment should endeavor to restore or maintain this ideal function.
The presence of the anteroposterior (AP) curves in the spine gives it more resistance to
weight-bearing forces, providing a springlike effect and reducing vibration. The thoracic kyphosis, unlike the lumbar spinal lordosis, ensures that, in the neutral posture, the facets ca rry little if any weight. Posture is such that when standing we are inclined slightly forward . The result is that mild activity of posterior muscles, the erector spinae, maintains our posture.
During unsupported sitting, there is slightly more activity of the posterior muscles (7,8). This muscle also extends up the rib cage and helps posturally stabilize the spine and rib cage as a unit. During extension the facets impact, forming a closed pack system limiting motion. The anterior compartment of the thoracic motion segment is formed by the vertebral bodies, the intervertebral disc, and longitudinal ligaments. The anterior ligament is a strong band made up of several layers, stretching from occipit to sacrum, narrower but thicker in the thoracic
region, and serves to limit extension (Figure 21-3 ). The posterior longitudinal ligament up the posterior vertebra bodies is also thick and widens at the discal region and narrows at the vertebral body. The axis of motion of the thoracic segment being anterior to this ligament allows it to limit flexion and translation .
racic vertebra, w hereas the inferior facets have
The posterior compartment is formed by the
saggital facing, that of a lumbar verteb ra. The biomechanical demands placed on this vertebra
vertebral arch, the transverse processes, and the
zygapophyseal joints. The articular capsules are
383
~
Rgare 21-8 Anterior view of typical thoracic vertebra, anterior ligaments. (From Clemente. Anatomy: A regional atlas of the human body. 3rd ed. Urban and Schwarzenberg, J 987.)
21-4 Posterior view of typical thoracic vertebra. (From Clemente. Anatomy: A regional atlas of the human body. 3rd ed. Urban and Schwarzenberg, 1987.)
imporram Structures in this posterior compartment because they are pain-sensitive structures
spine, Nachemson (9) showed that the nucleus exerts a hydrostatic pressure that acts like a coil spring, which separates the vertebrae and produces a preload stretch on the ligaments of the
and are called on to limit the movement of the thoracic motion segments in all ranges. They are attached to the lateral margins of the articular processes and are reinforced by the ligamenta flava, which connect the vertebral lamina (Figure 21-4). The latter ligaments limit flexion and, to some degree, lateral flexion and rotation, and are
composed largely of yellow elastic fibers. In degenerative change the ligament may bulge, causing irritation to the nerve root.
The intrinsic elements of the thoracic spine, the discs, ligaments, and vertebral structure pro-
vide the intrinsic stability that is significant up to a few kilograms (4). As in other areas of the
ante rior and posterior compartments. Removal of
the posterior ligaments, particularly the elastic ligamenta nuchae, demonstrates that the ligaments also exert a compressive force or prestress
to the disc, all of which provides for protection and enhancement of motion. As previously discussed, the rib cage also produces resistance to motion, adding to thoracic stiffness twofold and load-bearing capacity threefold (10) (Figure 21-5). All of these factors are probably why disc lesions and facet problems are less frequent in the thoracic spine. The interspinous and supraspinous
384
Ft111'121 -6
Cross-section of costovertebral
connecrion. (From Clemente. Anatomy: A regional
atlas of the human body. 3rd ed. Urban and
Schwarzenberg, 1987.) ligaments limit flexion and are well developed in the thoracic region. Tenderness of the supraspinous in the midrhorax, a common clini-
cal finding, would seem to demonstrate that this region of the spine is frequently under flexion strain. Degenerative change in the anterior aspect of the dorsal vertebrae is also common, which may relate to increased compressive forces or at least to excessive anterior mobility of the body.
Biomechanics of the Tboracic Spine StaDe Concepts In general, it is often considered that the normal AP view of the thoracic spine should be relatively straight and balanced, whereas the normal lateral view should have a posterior curve. The thoracic kyphosis, along with the sacral curve, are formed during the embryonic stage and are called the primary curves. The thoracic kyphosis, as stated previously, is attributable primarily to the wedge shape of the thotacic vertebrae, particularly characteristic in the midthorax. Growth changes as seen on radiograph in this norma l vertebral wedging should be evaluated when an alteration in this so-called normal kyphosis is seen. A flat thoracic spine may be a normal variant in young girls who otherwise have normal posture and
may result from loss of this normal vertebral wedging. The optimal thoracic curve should be an even curve, extending from Tl to T12, with C7-Tl and T12-Ll being the transition points for the primary kyphotic curve as the spinal curves become the secondary cervical or lumbar curve, respectively. The apex of the thoracic curve should be at the level of T6-T7. Common clinically, variations are seen : (J) flattening of middorsal kyphosis is more common in females than in males; (2) elongation of the thoracic ptimary curve intO the lumbar spine, producing a shortradius lumbar curve is also common. Clinical experience suggests that these variations may well lead to symptoms or biomechanical stress that manifests as degenerative changes. Some varia tion in opinion is seen in the literature on what constitutes normal or optimal statics and dynamics, and because of our lack of knowledge it is difficult to draw precise correlations between aberrant biomechanics and pathologic conditions and render a good theoretical basis for pathogenesis in this region of the spine. The anatomic shape of the vertebrae, as well as the muscular artachments and their postural functions, would in theory dictate concepts of optimal posture for the thoracic spine. Because few studies are available to establish normals and optima Is for this region, we must rely on structural and functional integration to develop clinical models of optimal. Gray's Anatomy (11) holds that the cervical curve starts at C2 and ends at T2, the thoracic curve starts at T2 and extends to T12, and the lumbar curve starts at T12 ends at LS. The normal apex of the thoracic curve is reported at T 7. The spine was norma ll y seen to have a very slight lateral curve convexity to the right, thought to be caused by muscular development related to dominant right-handedness. Schmorl and Junghanns (12) reported that it was normal for 80 % of spines to have a mild physiologic scoliosis, left in the cervical thoracic region and right in the thoracic and lumbar regions, whereas 20% of spines showed the reverse of this curve. These curves begin developing at 6 years of age and were thought to be related to greater strength of right
21
385
ThoracIc IIId Costot8i'1IIIo .. SlMlxIllon Syndl'Olll8l
thoracic mu cularure caused by dominant righthandedness. It is interesting to note, however,
that' Figure 5 1 of their text, depicting these curves
with only a mild deviation (scoliosis ) presenred on postural analysis. Dynamic motion shou ld be equal to each side, and the curve should be uni-
in a preparation by Virchow, is more representa-
form, that is, each motion segment should partici-
tive of the four opposed rotational scolioses seen
pate smoothly and somewhat equally, reaching the end point of the motion with unifotm rythmn.
as normal and presented in chiropractic literature
by Ca rver (13), Beatty (14 ), and Homewood (15). The Four Opposed Rotational Scolioses (Carver) I. Right lower lumbar curve extending to L3-3 transitional vertebra
2. Left lumbar thoracic curve, apex T 12, ending T7-8 transitional vertebra 3. Ri ght thoracic cervical curve, apex T4, transi-
tion at C7-TI 4. Left cervical scoliosis, apex C4, with a counteraction at C I-2, CI right, C2 left. Carver's opinion was that the apex of the thoracic
kyphosis wa at T7-8, with the normal curve extending from T2- Tl2. There appears to be some general agreement in the literature that the basic asymmetry of the body as well as dominant handedness produces mild rotational curves in the spine that develop in ea rl y childhood. A left cervical curve and a right thoracic curve may by all reports be a normal functional compensation for right-handed individuals and may account in part for the common
low right shoulder seen in right-handed individuals. It is surprising how often in clinical practice one encounters a spinally healthy individual with the mild curves Carver considered as optimal: the four opposed rotational scolioses. The key factor in a functional spine seems to be symmetry of
mobility and balanced compensation rather than strictly alignmenr. The most importanr clinical factors in assessing the statics of the spine wou ld be ( I) the curves should be smooth and even, and each individual vertebra should participate uniformly in the configuration; (2) rhe apex and transitions of the curves should be at the levels just stated; and (3) the spine should fall so that the center of gravity passes through the center of the body of C7 and the center of the body of T12
Dynamics of the Thoracic SpIne The thoracic spine is the longest region of the spine but the least mobile. This lack of mobility is caused primatily by the fact that the height of the disc is approximately 20% to 25% that of the height of the thoracic vertebral body, a ratio that is the lowest in the spine, and the fact that rhe rib cage, with the double posterior attachments and [he anterior cosrosrernal atrachments, limits rota -
tion and lateral flexion. When the sternum is removed, the stiffness of the thoracic spine affected by the rib cage is negated (4 ). These movements are slightly less limited in the lower thoracic region, where the elasticity of the costal cartilages allows for a slightly greater degree of mobility in certain ranges. The thoracic vertebral facer facings limit flexion and extension ro some
degree but do little to impede rotation and lateral flexion of the thoracic segment, which is mainly
limited by the ribs. During extension the facets are seen to impact; thus bony cOntact limits this movement along with the anterior longitudinal ligament. All motion in the thoracic spine is
accompanied by movement in the ribs, which at times amountS to only a few millimeters of translating motion. Thoracic biomechanical dysfunctions, vertebral or costoverrebral, are intimately related because of the osseous structural arrangement and rhe muscular anachmenrs. When correcting dysfuncrion concern for sta tic alignment, joint motion and the extrinsic forces that are blocking the movement are of importance. White and Panjabi (16) emphasized six degrees of freedom in the thoracic motion segment similar
to
the
findings
in
the
lumbar
spine: (1)
anterior/posterior motion or translation along the Z axis; (2) lateral to medial motion around the X axis; and (3) superior to inferior motion
386
Tb8 SIMIxa1Ion 8Ylldl _
around the Y axis. The traditional descriptors flexion, extension, lateral flexion, and rotation do not conform to the actual movements in the spine because all movements are combined or coupled movements. The primary coupled motion is easily detected on a motion srudy plain film radiograph, and it is well understood that lateral flexion is combined with rotation and vice versa. It is important to note that tertiary motions in translation, flexion or extension, or motion along the Y axis, also accompany these main motions. Clinicians often believe that when the tertiary motion is lost in a motion segment (joint blockage or subluxation), the neurologic reflex changes that take place are the most significant to the patient, and explain some of the dramatic results obtained by the dynamic adjustive thrust when evaluation demonstrates little static or dynamic change other than the restoration of the para physiologic or tertiary motion. Panjabi and co-workers (17) showed that the average intervertebral translation motion was 1 mm in the sagittal plain. In my opinion, this amount of motion can be felt only through the end feel challenge method and clinically can be appreciated as altered after a dynamic adjustive correction. At times the palpable restoration of motion may represent resrorarion of tertiary motion, para physiologic motion, or translatory motion that may prove sometimes
to be the same motions. The axis of motion for rotation and lateral flexion is locared in the center of the body of the vertebra and, under normal circumstances, very little shearing or trans latory motion of the disc takes place. The axis of motion for flexion -extension is located in the center of the disc of the vertebra below, again not allowing or requiring much shearing or translation . Clinically, anterior disc lipping and degeneration are common radiographic findings in middle age (18,19). One cause of these pathologic changes is probably a shift of the axis of motion posteriorly and laterally caused by alteration in muscular activity that resu lts in hypermobility of the anterior body during movement with resultant increased shearing force to the disc and stress and strain to all of the
intrinsic structures. The alteration of movement or function produces a change in structure, resulting in the degenerative changes commonly seen in the anterior body of the thoracic spine and the osteophytic changes at the costotransverse joints. The musculature of the thoracic spine is dealt with in detail in most anatomy texts. Their action is usually described on a kinesiologic basis, with such descriptions as extensors/rotators or lateral flexors of rhe spine. For the clinician involved in spinal correction, the specific attachment of these muscles and their individual actions and effects on the motion and biomechanics of the individual vertebra are important. Some of the discussion in this area must be theoretical at this stage because of limited experimental research and technology to validate our opinions; however, speculation, again based on structure, function, and observation , is an important first stage. The Quiring and Warfel series (20,21) on musculature is a very good reference source for the clinician to use for the details of origin, insertion, nerve supply, and motor points. The detailed drawings allow us to speculate on rhe biomechanical action these muscles exert on the individual motion segment. It is interesting to note that the trapezius , latissimus dorsi, and rhomboids, which always receive much attention from clinicians in clinical and legal reporrs on spinal dysfunction, are listed in these texts as extremity muscles, and in my opinion, rightly so. Under normal circumstances these muscles have little effect on spinal postural or movement biomechanics except when the upper limb is active or load-bearing. As such, these muscles are not very often causative of spinal subluxation, whereas the deeper layers of spinal muscles are much more important and should capture the attent.ion of clinicians. It would appear that the reason the trapezius gets so much of our attention is because of its broad origin: from the external occipital protruberance superior nucha l line, nuchal ligament, spinous processes, C7, and spinous process of all 12 thoracic vertebrae. The insertion is into the lateral third of clavicle, spine of scapula, and
387 acromion. Palpable tenderness and spasm in the back musculature is often mistakenly related to this muscle, therefore neglecting the more important deep muscles. The latissimus dorsi arises from the lower six thoracic spinouses, the lumbosacral fascia, the crest of the ilium, and the lower three or four ribs. The insertion is into the bicipital groove of the humerus. Rib fixations related to this muscle are common with SPOrtS or activities that require torsion and arm motion. Treatment is difficult
because of the ease of trauma on returning to the sports activity. Rehabilitation of the patient with lower back or lumbodorsal problems who must return to lifting tasks should strengthen this muscle to stabilize the back in its lifting tasks. The rhomboids arise from the ligamentum nuchae, the spinous process of C7, and the spinous process of T1-5. They insert into the medial border of the scapula. In the prone position, elevation of the scapula and palpation of these muscles as well as of the trapezius can help determine if hypertonicity is present in these more superficial muscles or the deep muscles of the back. The main muscles that control thoracic biomechanics are the trunk muscles, the erector
spinae, and the transversospinal group (Figure 21-6). The erector spinae group is made up of the (1) iliocostalis, (2) longissimus, and (3) spinalis. 1. Iliocostalis The lumborum inferior portion arises from the sacrum, crest of ilium, and spinous
processes ofT11-12 and a11lumbars. Insertion is into the angle of the lower six to seven ribs. Origin of the medial lumbar portion is the angle of the lower six ribs. Insertion is into the upper medial portion of the angles of ribs Tl-T6. Origin of the upper portion is the angles of T3-T6 ribs, with insertion into TVPs of C4-6 . 2. Longissimus Portioll a) Thoracic portion origin ofTVPs of lumbar spine and the lumbodorsal fascia. Insertion into the TVPs of the lower 9 or 10 ribs.
FigIre 21-8 Erector spinae and rransversospinal muscles. (From Seeley. Anatomy & Physiology. 2nd ed.
St. Lotlis, Mosby, 1992.)
b) Cervicis portion, origin of upper 4th to 5th thoracic TVPs with an insertion into the TVPs ofC2~.
c) Capitus portion origin TVl's of the upper four to five thoracics and articular processes of lower three co four cervicals. Insertion is
into the posterior margin of the mastoid of (he occiput. 3. Spinalis Portion a) Thoracic portion arises from spinous processes Tl1-12, Ll-2, and the insertion is into the spinous processes of the fourth through the eighth thoracic spinous. b) Cervicis portion arises from spinous process Tl-2, C7, and ligamentum nuchae. The insertion is into the spinous processes of C2-4.
388 c) Capitus portion origin TVP of the upper six to seven thoracics and articular pillars of C4-C7 cervical vertebrae. Insertion is berween inferior, superior nuchal lines on the occiput. It should be noted by the clinician at this point that much of the attachment of these muscles is devoted to artachments to the ribs. These attachments help to stabilize the head of the rib into the thoracic TVPs. The nerve supply for these is the posterior primary rami branching from each segment; therefore, this muscle tends to act as individual slips, and can thus produce dysfunctions/fixation that can relate individual motion segments in fixation. Examples are occiput to cervical or thoracic, cer-
vical to thoracic or rib, and thoracic to lumbar. Careful palpation of the statics and dynamics can assist in differentiating these specific fixations and determining the related regions of the spine, both of which may need correction. Transversospinal Muscles The mOSt important muscle in this group is the semispinalis, which has three portions. Semispinalis thoracics has its origin from the TVPs of the lower six thoracics and the insertion into the
spines ofTI-4 and C6-7. Semispinalis cervi cis has its origin from the TVPs of TI-T6 and the articular pillar of C4-C7 with the insertion into the spinous processes of C2-C5 cervicals. Semispinalis capirus has its origin from the TVPs of Tl-6 and C7 as well as articular pillar C4-C6 and the insertion into the occipital line between superior and inferior nuchal line. Multifidus is a segmental muscle not as well developed in the thoracic region as in the lumbar spine or the cervical spine. The origin is from the spinous process of the vertebra above and the
which lie deep ro the multifidus in pairs and are present only in the thoracic spine. The origin is from the TVP of one vertebra and [he insertion is into the lamina of the vertebra above. Segmental motion is further supported by the interspinales muscles and inrertransversarii muscles, which are very small or even nonexistent in
some thoracic spines. Clinically these latter muscles may have little significance. The serratus posterior superior is a broad thin muscle that arises from the ligamentum nuchae C7, Tl-T4 spinous process, and inserts lateral to the angle of T2-T5 ribs. The serratus posterior/inferior, also broad and thin, arises from spinous processes of TII-TI2, Ll-L2, and lumbar fascia and insertS into inferior borders of the lower four ribs. Nerve supply is anterior primary rami for these latter muscles; rherefore, the whole muscle tends to act as a unit.
Kinematics 01 the Thoracic Spine Kapandji (22) reportS movement of the spine as a whole. His diagrams demonstrate 45° of flexionextension, 20° of lateral flexion to each side (rotal, 40°), and 35° of rotation to each side (total, 70°). Gregerson's and Lucas's study (23) of normal medical students using Steinmann's surgical
pins inserted
into the spinous processes
showed an average segmental roration of 6°. They showed a slight difference between sitting and standing, with sitting showing less motion in the lower thoracics. They reported a rota I range of motion similar ro the figure, suggested by Kapanji, 37° ro one side, or a total of 74° of rOtarion. In this same study, rotation during gait was
observed. During normal walking, T7-S was seen to stay relatively stable and formed the transition point for total body rotation developed by the
inserts into the transverse processes of vertebra
pelvis, as opposed to the counter-rotation seen in
below and extending as far down as three to four segments. The rotational components of the thoracic segments are further supporred by rotarory muscles,
the shoulders with normal arm swing. With each step the gross rotation motion of the body at the sacrum is approximately go, which reduces to 0°
at T7-S. The arm swing and shoulder motion
389 produces an opposite rotation of 6° at T2. T7-8 therefore would show the most rotation segmentally during normal walking and amounts to approximately 2.5°. The segmental rotation during walking at Tll-l2 and Tl-2 amounts to about 0.5°. These biomechanical observations would lend a logical correlation to the concept that T7 should be the optimal apex of the thoracic kyphosis. The most definitive study of the biomechanics and the range of segmental motion in the thoracic region comes from White and Panjabi (24) (Table 21-1 ). Flexion-Extension Ra nge of Motion: Sagittal Plain Rotation Median figures are 4° of motion for the upper thoracic segments, 6° for the midthoracics, and 12° of motion each for the Til, Tl2, and Ll segments. White and Panjabi (25) suggested that the instamaneous axis of motion for flexion is located in the anterior one third of the superior aspect of the vertebral body of the vertebra
below, and for extension in the amerior one third of the inferior aspect of the vertebra of the superior motion segment (Figure 21-7). La teral Flexio n R a nge of Motio n: Fron tal Plane of Mo tion As in other areas of the spine, lateral flexion is accompanied by a coupled motion, the main coupled motion being rotation in the sagittal plane. Lateral motion totals approximately 52° to each side with intersegmental movement of app roximately 5° to 6° in the upper segments and 8° to 9° in the lower segments. During lateral flexion the instantaneous axis of motion is located in the body of the vertebra below. Lateral flexion on plain fi lm radiographs demonstrates thar the primary coupled motion, in general in the upper thoracic vertebrae, is similar to a cervical motion segment in that the spinous processes rotate to the convexity (type 2 motion) . In the lower thoracic vertebrae, the normal behavior is similar to that of a lumbar segment; the spinous processes rotate to the concavity (type 1 motion). My own
Segmental Motion in the Thoracic Spin e
Inlersp ... TI-T2 T2-T3 T3-T4 T4-T5 T5-T6 T6-T7 T7-T8 TS-T9 T9-TIO TIO-TII Tll-Tl2 Tl2-Ll
Flllloll/tl1en.lon limits of Representative Ranges Angle (deg"e.) (deg"esl 3-5 4 3-5 4 2-5 4 2-5 4 3-5 4 2-7 5 3-8 6 3-8 6 3-8 6 4-14 9 6-20 12 6-20 12
Lale ..1Bonding limits 01 Rep" .. n1atlyt Rang .. Angle (degr... ) (deg"es) 5 5-7 3-7 5-6 5-6 6 3-8 4-7 4-7 3-10 4-13 5-\0
6 6 6 6 6 6 6 6 6 7 9 8
•
Allal Rolltlon Rep .... nlatl.e limits of Rlngll Angle (deg"es) (deg"es) 14 9 4-12 8 5-11 8 4-11 8 5-11 8 4-11 8 4-11 8 6-7 7 3-5 4 2-3 2 2-3 2 2-3 2
Whitt AA ILl, Panjabi MM: The basic kinematics of the human spine: A review of past and current knowledge. Spine 1978; 3, 12.
390
The s.xatlon SylD'omes
~~ L F E
L
R
R
o
() ()
L
R
o
l.aIeraI IIexion f1111'121-7
Insranrancous axis of morion (flex ion -extension, roration, lateral flexion ),
clinical observations of coupling patterns suggest that the optima l or normal patterns for the upper thoracic is a type 2 pattern and for the lowet thoracies a type 1 pattern, the transition point being
T6-7. The typing of motion patterns was developed in the lumbar spine and reported by Grice (26,27), Cassidy (28), and Gitelman (29) . These observations can be clinically produced by a radiographic study that places the seated patient with the dorsal spine against the bucky and laterally flexioning the patient, keeping the spine in contact with the bucky. Deviations from this pattern are common and in my opinion are clinically sig-
nificant on a long-term biomechanical basis. White and !'anjabi (4) discuss the disagreement about coupling patterns in the thoracic region and suggest that the complexity of the motion along with variarion in techniques of study may be the reason. They go on to observe that ab nor-
mal coupling patterns are seen in scoliotic defor-
mities. Rotation Range of Motion: Motion in the Horizontal Plane Rotation in the thoracic spine also ptoduces coupled motions, the prime motion being that of latera l flexion. These patterns of coupled motion, as in the case of lateral flexion, can be altered voluntarily by postural change. Vertical axial rotation of the thoracic spine to the right results in lateral flexion to the left, particularly in the lower thoracics. Clinica ll y, it must be remembered that there is an additiona l coupled motion in the sagittal plane during rotation. In the lower thoracic region, this motion appears to be extension,
whereas in the upper thoracic region it appears to be flexion. The coupled pattern in the upper thoracics can be altered by slight fl exion, producing
391 lateral flexion on the same side. I have found that the transition point for these movements in the
transverse and sagittal plane is approximately T6-7. This transition point and T5-6 are often clinically found to demonstrate marked spinous tenderness and subluxation. A flattening, or saucer effect, also may occur in the region of the spine and is usually related to the extensor group of thoracic muscles being overactive.
The rotation range of motion for the whole thoracic spine is 41 °. Each vertebral segment in the upper half of the thoracic spine moves approximately 4° to 5° to each side with a total of 8° to 9°, whereas the lower three thoracic segments move only about 2° to each side (4).
Biomechanics of the RII C8ge Very little has been added to the literature about rib motion since the author discussed the bucket handle motion and the caliper motion of the ribs in Haldeman's 1980 text, Principles of Chiropractic (30). The vertebral sternal attachments of the typical true rib T2-7, and including TI, form the basis for the concept of the bucket handle type of motion. These ribs from their double vertebral attachments
extend
outward,
then
forward,
downward, and inward to medially attach to the sternum. Kapandji (22) states that the double vertebral body transverse process attachment acts as a swivel for the rib, the angle of which controls the movement of the distal sternal end of the rib. This concept alters the bucket handle concept by demonstrating that one handle of the bucket being more rigidly fixed becomes the axis of motion around which the more flexible chest cage moves, therefore controlling the nature of the motion of the opposite handle of the bucket at the distal attachment. The result is that on inspiration, the distal portion of the rib elevates, thus causing the chest to rise. Steindler (31) states that the double anchorage of the rib into the vertebra limits [he motion to 10 at the spine attachment.
The elasticity of the chondral cartilages forms the basis for the concept of the caliper motion
seen in the vertebral chondral ribs 8, 9, and 10, as well as the 11th rib, and floating 12th rib. The double vertebral attachment serves to intimately connect thoracic vertebral motion to rib motion. Any type of rib resection results in excessive rotation and lateral flexion of the involved vertebrae, resulting in instability and scoliosis of the spine. Clinically, to properly analyze any spinal dysfunction, palpation of the rib cage and the thoracic spine is necessary. Many of the muscles that produce subluxa[ions/fixations in the thoracic spine also ca use
costovertebral dysfunction or subluxation; that is to say, primary thoracic vertebral fixation may result in costovertebral or costal-costal fixations,
or primary costal fixations may produce costovertebral or vertebral-vertebral fixations. This is caused by their biomechanical interaction or the muscular forces that interlock these segments. As in other parts of the body, when somatic dysfunction arises and pain is produced, the body compensates, which may result in control of the pain oc, with decompensation, may increase the stress or strain. Further pain may arise and result in further compensations. In any case, a lesion may
result in a wide variety of responses that often cloud the primary cause or condition . Nowhere in the body can it be more difficult to distinguish the major or initial problem than in the thoracic spine, probably because of the number of structures and joints located in this region and the complex
interactive
functions
between
these
related Structures. In many cases, successful treatment may not revolve around determining a major or minor lesion, but rather an organized progressive correction of each distortion pattern
should be systematically addressed. One of the primary functions of the rib cage is respiration. The alteration of breathing mechanics can be an important cause of spinal or rib
cage dysfunction. As previously stated, Wyke (6) drew attention to the fact that the rhythmic sensory input from the cOstovertebral joints is necessary to stimulate normal respiration; when the rib articulation was anaesthetized, respiration ceased .
He stressed that this sensorimotor feedback loop
392
ThII saxallon Syndl1lillll
was an essential function to normal respiration.
This factor may explain why patients with sleep apnea respond to postural changes and corrective changes in the musculoskeletal holding elements of the thoracic spine and ribs. Angina patients with fixed or arthritic dorsal spines may trigger attacks by poor posture or sleeping on their backs, and often they must sleep in a semisining position. Kapandji (22) further explains mechanics of motion of the ribs during respiration by showing that the costovertebral, COSWtransverse angle causes the upper ribs to raise on the anterior
aspect during inspiration. In the upper ribs, as the bucket at the spine handle rolls over in inspirarion, the distal handle elevates and the sternum as a whole raises. This movement can be simulated on one side to some degree by laterally flexing the thoracic spine and neck. Eva luarion of the biomechanics explains why movement and deep breathing can produce [he same anterior chest pain
when biomechanical problems exist. The costovertebral, costotransverse angle in the lower ribs is about 45° in the sagittal plane. Coupled with the downward angulation of the ribs as the rib moves laterally and anreriorly, this causes the lower ribs also
CO
elevate on inspiration, exagger-
ating the bucket-handle concept in the mid dorsals. Steindler (31) suggests thar the horizontal angle of the ribs as they move forward laterally is 50° for the first rib, 43° for the fourrh rib, and 42° for the seventh rib. The elasticity of the chondral cartilages allows the caliper-type motion in the lower rib cage. This motion can be simulated by deep inspiration or by rotation . Rotation to the right increases the AP and lateral dimension of the rib cage on the right and causes a decrease or concaviry of the rib cage on the left side.
Gross thoracic motion such as rotation and lateral flexion, when combined with inspiration and expiration, can help to locatc costovertebral lesions and determine whether the problem muscles are primarily postural muscles or respiratory muscles. Segmental palpation of the thoracic spine and ribs should take into consideration not only
spinal motion but also respirarion. Basmajian (32) discussed the mechanisms in respiration, sraring that dUring quiet breathing thoracic mobiliry is minimal and the diaphragm is the main muscle of respiration. The diaphragm contracts as a unit during inspiration and causes the ribs to move upward and outward. Clinically, a patient presenring with anxiery and stress shows
a tendency toward this type of flaring of the lower ribs and has poor vital capacity. The diaphragm is a tripartite muscle with right and left costal portions and a central crural portion. The muscle develops from eight slips: one or two from the sternum, two to seven from the costals
and lumbars, and eight from the crus, and when active acts as a unit. Continuous overcontraction
of rhe diaphragm causes a rypical lower dorsaUlumbar fixation, which is often present in the anxious patient, and in general involves the
lower ribs and lower dorsallumbars. Basmajian (32) describes in detail the activity of muscles during breathing, suggesting that complex variations in the pattern are possible. For our purposes ir is sufficient to extract that the
diaphragm, as well as the upper intercosrals and scalenii muscles, are constantly active during quiet inspiration, producing an increase of the thorax cavity in a verrical direction as well as in
the AP and lateral dimension particularly. Quiet expiration is a passive, nonmuscular phase of
breathing.
Accessory Muscles 01 Respiration and the Biomechanlcal Enects The quadratus lumborum has been shown to acr with the diaphragm, particularly during deep breathing, and serves to stabilize the lower ribs. When a person is under stress, the scalenii and quadratus lumborum muscles become important
causes of fixation of the ribs and spine and should be addressed in all patients suffering from stress.
During quiet breathing the first intercostals are always active and the second occasionally.
21
TlIorIcIc and COItDv.'IIIIII'1i SUIIIuxJIIon SyIIlll.11eI
393
and with greatcr inspiration the intercostal activity progresses to successively lower intercostal levels. Forced expiration shows a slight carryover
Blomechanical Diagnosis of Thoracic Spine and Ribs
of intercostal contraction that seems co assist in
This discussion is limited to the evaluation of musculoskeletal dysfunction, recognizing that organic dysfunction can produce pain patterns that simulate musculoskeletal disorders and vice
expiration when the diaphram relaxes; the lower intercostals from the 11 th and 12th pair are more important in assisting expiration. The scalenij muscles are considered by Basmajian to be primary muscles of respiration and have been shown in quiet breathing to elevate and anchor the first and second ribs. [n forced inspiration they became far more active and with norma l neck
posture assist in elevating [he anterior chest.
Adjustment of this fixation pattern for the cervical spine has been described (33); however, special attention to the upper ribs is important when the scalenii are involved. The sternocleidomastoideus is active only during deep breathing. The suprahyoid muscles also are found to be active except during deep sleep and with excessive activity can be involved in that so-called "lump in the throat" experienced during times of stress. The internal and external
obliques, as well as the transverse abdominis, are accessory muscles of respiration that limit forced inspiration and help to produce forced expiration; when tight they are thought to produce that feeling of "butterflies in the stomach." The pectOral muscles were also shown to be accessory muscles of respiration. There are con-
flicting reports as to the function of the trapezius as an accessory muscle of respiration. Tenderness
and hypertonicity of the pectOrals seem to be more common in female patients and may cause
neurovascular outlet signs and symptOms when hypertonic. Clinically, these muscles become important in patients who show stress and anxiety and
3TC
commonly seen as problems in acceleration/deceleration in motOr vehicle accident (MVA) patients. Steindler (31) discusses the effect of calcification of the costal cartilages, showing that the presence of signs in ribs and sternal region limits respiratOry function.
versa, which are important and may require dif-
ferentia l diagnosis. A careful history, a physical examination, and the use of pain drawings can go
a long way toward making a differential diagnosis and should be routinely done, particularly when spinal dysfunction is limited or inconclusive.
Beal (34), in a summary article, reviewed visceral somatic reflexes and their effect on the spine. Beal (35) and Cox et al. (36) showed that somatic dysfunction patterns can relate to under-
lying cardiovascular and coronary artery disease. Beal and Morlock (37) showed that somatic dysfunction patterns can also have a relationship to pulmonary disease. Bea l and Kleiber (38) showed that somatic dysfunction can be an important predictOr of coronary arterial disease. Johnston et al. (39) showed a relationship between somatic dysfunction and hypertension. SatO (40) demonstrated somatoautonomic reflexes related cardiac function to gastrointestinal function and urinary
tract function . Haldeman (41) presents a concept of multicausal factors in the production of pain in the lumbar spine and emphasizes the interrelationships of many factors in the manifestation of pain syndromes. The concepts discussed would be attributable to thoracic pain as well and should alert the clinician to multicausal factors in thoracic pain processes or diseases. His presentation discusses factors related to hyperesthesia often
found related to spinal problems and pain, and explained why multiple approaches and a multidisciplinary approach may in fact be beneficial for a number of patients. To assess a patient completely, a mu ltiple model of approach may be necessary. If one attempts to marry the medical pathologic model
394 with the functional model to expand our understanding of the lesion, as has been attempted in the lower spine by Cassidy in the Kirkaldy-Willis text (42) and by Haldeman (43), it becomes apparent that an organized functional diagnostic analysis is a more important part of the diagnosis of the patient. This part of diagnosis has been largely neglected by the medical physician and possibly overused by the chiropractic physician (44).
Classification of Pain In the Thoracic Spine Love and Kiefer in 1949 (45) were two of the first to review and report protrusion of the thoracic disc and its production of a variety of symptoms. Pain, being a common symptom, was often diagnosed as pleurodynia, intercostal neuralgia, or intercostal neuritis and fibrositis rather than discal protrusion. They were among the earliest to suggest that thoracic pain and rib cage pain were probably more attributable to musculoskeletal origin rather than co organic visceral origin, a fact that organized medicine struggles with even today. They further suggested that the upper thoracics were more likely to produce these types of musculoskeletal neuralgic pain in the back, whereas the lower thoracics were more likely to produce radicular pain projected to the abdomen and groin. More often they emphasized that intraabdominal disease was suggested rather than what they considered important: discal protrusion. Recognition that thoracic lumbar dysfunction can produce lumbar and pelvic pain has been reviewed and the mechanism suggested (46). Costosternal dysfunction of T5-7 ribs also has been seen nOt only to produce local pain but pain and muscle spasm remote from the articulation, in the lower abdomen, the groin, and upper leg as well as the lumbosacral region (47) . A number of other authors reported chest pain caused by costovertebral joints, intercostal, and posterior spinal muscles (48-52).
Scheuermann's
disease
can
produce
an
increased thoracic kyphosis and has also been seen clinically as a source of thoracic spinal pain. Bradford et al. (53), who reported the use of spinal fusion with Harrington instrumentation, demonstrated some improvement in pain but
relatev that, because of the incidence of com plicadons, conservative measures should be used for
such patients, except for cases of unrelenting pain or spinal cord compression. Burke and Murray (54) reported that conservative management of rest and rehabilitation, in cases of severe spinal injury with neurologic involvement, produced comparable results to surgical procedures, and rhat the development of less postchronic pain seemed to be evident. In rhe text, The Ad"/t Spille. Skubic and Kostuik (1) present a typical medical classification of thoracic pain syndromes:
1.
Thoracic Pain Syndromes without Neurological Deficit II. Thoracic Pain with Neurologic Deficit flI. Postthoracotomy Pain Syndromes
(See Classificarion Tables 21-2 and 21-3)
Medical Model of Pain: Emphasis on Pathologic Factors 1. Intervertebral Disc: Herniarion Degeneration Inflammation
2. a. Vertebral body: Spondylosis Osteoporosis b. Rib: Pathology Exostosis
3. Posterior joint:
4. a. Soft tissue:
Instability Congeniral abnormality Osteoarthritis Rheumatoid arthritis Ligamentous instability Ligamentous, muscle contracture
395 Classification of Pain in the Thoracic Spine ~..,.......----,. ~
•
I. Thoracic pain syndromes without neurologic impairment A. Viscerogenic and misceHaneous B. COstospondylogenic 1. Costochondral 2. Costovertebral 3. Facetal 4. Discogenic C. Neoplastic D. Infectious E. Structural 1. Scoliosis 2. Kyphosis a. Scheuermann's
b. Posttraumatic c. Osteoporotic
F. Cervical spondylogenic II. Thoracic pain syndromes wirh neurologic impairment A. Neoplastic 1. Extradural a. Primary b. Metastatic 2. Intradural-extrameduHary 3. Intramedullary B. Infectious C. Thoracic disc herniation
Ill. Postthoracotomy syndrome
b. Costocartilage: Calcification Inflammation Inflammation S. Nerve tissue: Compression or stretch 6. Visceral pathology
Chiropractic Model of Pain fIn:tIOnaI Factors: MecllaNcalIIIIoI'CIera 1. Posterior
change
joint
dysfunction,
aXIs
motion
I. Intrathoracic A. Cardiovascular
1. Angina pectoris 2. Myocardial infarction 3. Mirral valve prolapse 4. Pericarditis 5. Aortic aneurysm B. Pulmonary 1. Pneumonia 2. Carcinoma 3. Pneumothorax
4. Pleurisy 5. Infarction, embolus e. Mediastinal 1. Esophagitis, tumor 2. Mediastinal tumors II. Intraabdominal A. Hepatobiliary 1. Hepatitis 2. Abscess 3. Cholecystitis, biliary colic B. Gasrrointestinal 1. Peptic ulcer disease 2. Hernia-hiatal, inguinal, other 3. Pancreatitis
III. Rerroperitoneal A. Pyelonephritis B. Ureteral colic e. Aneurysm D. Tumor N. Miscellaneous A. Herpes zoster B. Poly myalgia rheumatica e. Hyperventilation syndrome D. Rib fracture, neoplasm 2. Discal dysfunction, internal or external strain, disruption 3. CostOvertebral altered motion or respiratory dysfunction 4. Costochondral or sternal altered motion or respiratory dysfunction
396 5. Ligamencous strain 6. Muscular: Postural fatigue Hypertonicity Imbalance or inappropriate action 7. Visceral-somatic dysfunction 8. Commonly accepted psychosocial factors: Chronic pain syndrome Psychologic factors, depression, hysteria Malingering
Sources 01 Pain in the Thoracic Spine The sources of pain in the thoracic region are thought to be similar to the structures in the lumbar and cervical spine. These structures gain their nerve supply from the sinuvertebral nerve and thoracic dorsal ramus. Wyke (55,56) reviewed the pain-sensitive structures in the thoracic spine. He described pain-sensitive nerve endings occurring in plexuses as free-ending of unmyelinated nerve fibers, which he found present in:
1. Fibrous capsules of the apophyseal joints similar to fibrous capsules of all synovial joints 2. The interspinous ligaments and ligament flava, particularly more dense in the posterior ligaments 3. The periosteal coverings, fascias, and tendons 4. The dura, epidural fatty tissue 5. The blood vessels supplying the joints and cancellous bone of the vertebrae 6. The epidural and paravertebral veins
thetic ganglia near the nerve root. The thoracic dorsal rami supply the posterior thoracic muscles and the costotransverse joints. The proximal portion of the ribs is supplied by the sinuvertebral nerve, and the distal portion of the ribs is supplied by the intercostal nerve. The zygapophyseal joints are innervated by the medial branch of the thoracic dorsal rami. It is likely that the thoracic disc is innervated by the sinuvertebral nerve, and it has been demonstrated penetrating the disc along with blood vessels. Discs under repair have increased density of free nerve endings, as well as increased numbers of nerve fibers within the disc that are thought to arise as a result of increased vascularity stimulated by repair process. Bogduk and Valencia (57) describe these neurologic relationships but remind us that, although it is likely that thoracic pain is caused by disorders of the thoracic synovial joints and muscles, no actual experimental evidence exists in the tho-
racic spine to confirm this conclusion. Wyke is of the opinion, however, that because the mechanism is the same in the lumbar and cervical spine, it is likely that the mechanism is the same in the thoracic region, and therefore further experiments will find similar findings to the evidence found in these regions . In the foregoing we have outlined a medical classification of pain related to the thoracic spine, demonstrating the emphasis on pathology. By reviewing Wyke's and Bogduk's tissue sources of pain and the suggested neurologic basis for the fact that pain can arise from non physiologic function of the thoracic spine, the muscular system,
Branches of the sinuverrebral nerve innervate the thoracic vertebrae, the dura mater, the
and the rib cage, the clinician must recognize the importance of spinal functional diagnosis and
epidural blood vessels, and the posterior longitudinal ligaments. The sinuvertebral nerve is composed of an autonomic branch and a recurrent somatic branch that comes off rhe anterior superior surface of the thoracic root and passes back into the NF (intervertebral foramina). The autonomic branch arises from gray ramus communicans at each segmental level, or from the sympa-
correction for control of pain . The clinician must
also recognize the possibility that dysfunction of somatic structures has important reflex effects on
the visceral organs as well as the cardiovascular and respiratory system, which is reviewed elsewhere in this rext, in some of the references in this chapter, and by Bronfort (58). The examination and correction of spinal biomechanics should
397 include careful monitoring of the effects of that correction as well as eva luation of the related organ systems. The osteopathic profession has, over the years, been more diligent in researching the relationship between spinal function, the autonomic nervous system, and visceral function.
Homewood (15) in 1962, updated in 1977, outlined the theory of somatovisceral functional relationships, and texts, such as Haldeman's two
texts (59,60), gave some scientific basis for the theory of somatovisceral dysfunction. Clinical practice, however, demonstrates that the differential diagnosis of somatovisceral, viscerosomatic
relationships, as well as organ pathology, are difficult to assess. Many authors have attempted to bridge these models: Gatterman (2), Schafer (61,62), Dobrusin (63), Bergman et al. (64), Plaugher (65). The integration of the medical model is an attempt to be certain that chiropractors will not neglect this model in their functional diagnostic approach. Overemphasis on the medical model has resulted in some instances in the total lack of the graduate's ability to understand the functional chiropractic model or its significance.
Diagnosis of musculoskeletal complaints in the thoracic region should include postural analysis, gross motion analysis, and static and motion
palpation analysis assisted by other procedures when clinically indicated . Johnston (66-68), in a three-part series, stressed the importance and inrerexaminer agreemenc on the diagnostic proce-
dure to elicit somatic dysfunction and imbalance. Kobrossi and Steiman (69) reported on the use of thermography in dorsal and abdominal pain syndromes. Stillwagon et al. (70) suggest that thermography can be helpful as a diagnostic and assessment tool for the subluxation complex. Case studies on skin temperature have been
reported by others, showing relationships between temperature changes and funcrional pathologies (71,72). Plaugher et al. (73) studied interexaminer-intraexaminer reliability and paraspinal skin temperature in the thoracic spine and reported substantial agreement of intraexaminer reliability
and a significant association with skin tempera-
ture changes and palpation findings. Kent and Gentempo (74) report that initial investigations using surface electro myelography (EMG) have shown an indication that it may be a reliable tool for the quantitive assessment of paraspinal muscle activity, and therefore it is a recommended outcome assessment tool for chiro-
practic care. Sweat gland activity also has been associated with somatic dysfunction and reflex alteration (75). Skin sensitivity (76) using skinrolling technique (77) and pressure algometry (78,79) have also been shown to be helpful in diagnosing spinal dysfunction and response to treatment. Radiographic assessment can assist in
assessing posture and bony position, pathologic conditions, spinal dynamic alteration, and seg-
mental alteration of motion (80-82). Cox et al. (83) reported that osteophytic lipping of the thoracic spine was more prevalent in gallbladder disease, gastrointestinal disorders, and diabetes mellitus, and in a nonspecific study, coronary heart
disease. Macones et al. (84) demonstrated hyperostosis as a result of mechanical forces at the costovertebral junctions, which they related to the iliocostalis muscle. This was shown to relate to occupation, the male sex, and dominant handedness. Osteophytic outgrowths also have been reported to produce compression on the sympathetic trunk (85,86). As stated before, the thoracolumbar junction with its increased stress is an
important site for degenerative change (87,88). The main diagnostic approach to developing an understanding of mechanical disorders is palpation. Fligg (89) outlined a classification of palpation. Schafer and Faye (3) discussed the importance of static palpation to elicit information
about the tissues related to the manipulative lesion, such as tissue texture, bony alignment, skin temperature, (inflammation) vascular change,
and muscular tonicity. Sweat gland activity and skin hydration should be added to this list and have long been of interest to our profession. Observation both follows and accompanies a good history. Observation of thoracic motion
398 should be assessed during gait, evaluating arm swing, the rhythm and amplitude, as well as postural change and gross spinal motion.
later Fligg at the Canadian Chiropractic College and presented in class notes since 1980 and published in other sources (29,30,33,95-100).
Gross spinal motion in all its ranges, flexion-
extension, lateral flexion, and rotation should be assessed with the patient both standing and sitting. These postural dynamic tests start with observation of the static posture, the alignment of the head, shou lders, and pelvis, with observation of scapular position symmetry of muscle contraction for PA and AP as well as the lateral posture. The degree of kyphosis and the overall postural balance and alignment for efficiency are important (90,91). Johnston (92) showed a high level of agreement in interexamination testing in gross passive
range of motion. Sportelli and Tarala (90) present a brief overview of physical examination of the spine, showing an integrated postura l orthopedic neurologic approach . Lateral flexion before a double plumbline should show an even curve from Tl ro T12 and symmetry of motion to each side. Rotation should be assessed for symmetry; full trunk rotation is best used to assess the motion from T6 to T12, whe reas full neck rotation is best suited to analyze motion from Tl ro T6. Flexion-extension is limited in the thoracic spine and is best analyzed with the patient in a seated posture, where observations of the thoracic muscular function can be more easily assessed . Coupling of the general techniques of static palpation and springing vertebral challenge in the thoracic spine elicits more infotmation about individual segments and does not depend on symmetry of spinal structures, which may be a problem, rendering fa lse information, because bent spinouses are a com-
mon complication in the thoracic spine (93). Faye (3) developed and taughr the techniques initiated and presented by Gi llet, who also had lectured to the profession and had prepared a series of lectures notes called the Belgian Chiropractic Research Notes (94). Liekens, a colleague of Gillet'S, was credited with developing a more precise movement-oriented procedure for spinal
palpation that has been developed by Grice and
Dynamic PalpaUon 01 the Thoracic Spine General Principles Related to Palpation Patient's Concerns 1. Place your hands on a patient with respect and concern for his or her comfort. In the thoracic spine, cross the patient's hands across the chest, locking the upper body into a unit for ease, control, and precision of motion.
2. Educate the patient as to the purpose of your test and effect a trial run within the patient's tolerance and pain concerns.
3 . Control the movement to provide for a smooth motion that allows you to focus an end-feel challenge of each segment.
Examiner's Concerns 1. Protect your posture from strain and fatigue and attempr to keep your body still, moving only your arms and hands to produce the motion.
2. Control the patient's active/passive motion with the indifferent hand throughout the movement, producing a rythmic motion with
minimal muscular effort, using your latger muscles. 3 . Palpatory fingers should be able to be stable and comfortable throughout the motion and to exert a comfortable challenge at the end of the motion.
4. Visualization of the anatomic structures and
their motion throughout the test is helpful in appreciating the dynamics. Fligg (89) teviewed the various motion pa lpat ion techniques: (1 ) sratic joint challenge, (2) joint play, (3) end joint analysis, (4) dynamic motion
21
TIIoracIc and C8at0vertabral SUblUXallon SyID'omel
palpation with the view of explaining the origin and application of each procedure. Static joint challenge developed out of static palpation procedures and was so common to
many practitioners that its origin is difficult to trace. The procedure is commonly used in the thoracic spine in the prone position. Fligg discusses the limitations of this procedure but points our that for acute pain it is often the palpatory procedure of choice. Joint play was developed by Mennell (101) and was primarily used in peripheral joints for evaluating ranges of involuntary motion . This procedure was included into spinal examination and by some was known as end ioint challenge. which had been used as a development of static joint challenge techniques. Faye, in lectures and in a text (3), popu larized the generalized end joint, spinal ana lysis procedures developed by Gillet and Liekens (94). This procedure is very effective in the thoracic spine because our upright posture produces a thoracic spine in almost complete exrcn ion; therefore the extension challenge (see Figure 21-7) is easily performed. Reliabiliry srudies of motion palparion all have shown good intraexaminer reliabi lity, but in general nor significant inrerexaminer reliabi liry. Love et al. (102) srudied the joint challenge technique in the thoracic spine and showed good imrareliabiliry bur nor significant interexaminer reliability. They also reported a common finding that T9-10 was the most frequent level of fixa tion using thi general joint challenge procedure. This lower dorsal area is commonly found blocked using the prone movable table palpation challenge technique as well. Dynamic motion palpation was developed out of Liekens' procedures, reported by Gillet and Liekens (94). Our development of this technique attempted to correlate actual spinal dynamics and interpret what forces would limit the motions (27)(33 ). Gillet and Liekens (94) traditionally classified fixations as (I) muscular, (2) ligamentous, and (3 ) osseous. Schafer and Faye (3) discuss this classification in more detail, changing the third c1assificarion to an articular fixation that
399
they describe as a more complete fixation that has developed adhesive changes. It is clinica ll y important to note that fixations can be unilateral and, by fixing one facet, can cause hypermobiliry at the opposite facet joint. If we carry this principle further, the clinician must realize that a motion segment may be hypermobile in one range of motion of the facet. and the holding elements can create hypermobility in another direction of motion within the same segment or facet. If a segment is blocked in motion at both facets, hypermobiliry might be established above or below the joint, and these hypermobile joints should not be adjusted in the plane of that hypermobiliry. Dynamic palpation allows us ro assess a number of planes of motion of these segments and, along with motion stud y radiography, deal more specifically with adjusting the direction of fixation and avoiding the direction or the segment of hypermobiliry. Dynamic Motion Palpatio n of the Thorac.ic Spine Basic Complete Screening Procedure (Figure
21-8) Flexion-Extension: Contact is in the interspinous space with three fingers or the thumb and index finger. Patient is controlled by having arms
Rgure 21-8
GilletIFaye joint challenge palpation .
400
IIgIre 21-8
Flexion dynamic palparion.
crossed in front with examiner's second hand on
AaIn 21-10
Extension dynamic palparion.
range. Test is done bilaterally using the opposite hands (Figure 21-11 ).
the elbows. Motion: Patient is gently flexed and extended by force on the elbows and the palpating hand detects motion between the spinous process at each level. As each segment is brought into full extension, a slight challenge is given to detect end feel of each segment (Figures 21-9 and 21-10). Lateral Flexion/Spinous Challenge Because of the unusual change in the normal coupled motion at approximately T6-7, alteration of the technique for the upper thoracics and lower thoracics is suggested. Contact of lower thoracics: The spinous of vertebra below is hooked with the middle finger, the index finger contacts the spinous of vertebra above, and the noncontact hand across the shoulders of the patient, providing the leverage to laterally flex the patient from neutral then ro one side. Movement from T12 upward to TS-7 should show movement of the spinous toward the concave side. At the end of the motion, a slight cha llenge evaluates the motion, its character, and
Palpation of upper thoracic from T6-8 up to Tl or above: Hook spinous of inferior vertebra, push spinous of superior vertebra while the patient is flexed to the same side. In the upper thoracic region of the spine, the spinous processes should move to the convexity. The examiner's nonpalpar-
ing hand can be placed across the shou lders or on the head, using the head as a lever, resulting in movemenr
and
control
of cervical
thoracic
motion and thereby challenging cervical muscles that may be involved in cervicorhoracic fixations (Figu re 21-12). Rotation Students often experience difficulty in palpating this region because of the large muscles and tight spinous overlapping. The indifferent hand is placed on the elbow or arm of the patient's arms that are crossed so that rhe contralateral arm is
on top. This posture forms a good lever to control rhe roration motion. The contact hand uses
the thumb or the thumb and index finger on one or
twO
adjacent spin ous processes. Rotation to
one side with an end point challenge is done by
21
TbGraclc II1II COItuVII'l8IIrai SWIIuxIIlGn By.........
Rgure 21-11 Dynamic palpation lower thoracic. Normal spinous deviarion to concavity T6-Tt2.
the indifferent hand controlling the rotation and the palpating fingers exerting slight challenge as they walk up the spine, testing rotation at each level (Figure 21 -13).
Rib Palpation Rotation Contact: Costovertebral fixations are best analyzed in the seated posture as in thoracic
401
Rgure Z1-1Z Dynamic palpation upper thoracics. Normal spinous deviation ro the convex_icy Tl-T6 .
vertebral assessment, with the patient's arms folded across the body, a cOntact on the arm or elbow of the outside arm similar to thoracic palpation, and the palpating fingers or thumb making a contact on the nonarticulating tubercle of the rib joint just lateral to the TYP. At times, depending on the patient's musculature, the examiner must move more laterally to the angle of the ribs to gain the best springing rib palpation (Figure 21-14).
Analysis: Range of motion, resistance, and blockage of end feel is noted of this caliperlike motion.
Rgure Z1-18
Rotation dynamic palpation.
Rgure 21-14
Rotation rib palpation .
402
TIle SlMlxallon SyID'omea
fIgIre 21-18
fIgUre 21-15
same finger contact, the respiratory function of Rib palpation: bucket handle open .
Lateral Flexion Contact Test I: Place the fourth finger on rhe larera l aspecr of rhe lower rib, rhe rhird finger on the inrerspace, and index finger on the upper ri b. Patient is laterally flexed using shoulder conract. Inrerspace motion is compared (Figures 21-15, 21-16) . Test II : With slighr larera l flexion and the
Rgare 21 ·17 expiration.
Rib palpation: bucker handle closed.
Respiratory function: inspiration,
the ribs ca n be assessed by asking the patient to deeply inspire and expire (Figure 21 -17) . Analysis: Free bucket-handle motion of the ribs should be felt during full lateral flexion and during respiratory funcrions. The upper ribs are protected by the arm and scapu la; it is advisable to take an a nterior chest contact for the upper ribs for this procedure. Sternocostal fixations can be assessed by contacting the sternal costa l junction with the fingers and producing posterior rotation and latera l flexion of the shoulders. Respiratory function of the
fIgIre 21-18 Anre rior rib palpation: bucker handl e and caliper morion .
403
..... 21 ·20
Adjusting table in motion: spinous
challenge.
~
21-18 Upper ribs respirarary funcrion:
inspiration, expiration.
shoulder also should be assessed with this same contact (Figures 21-18, 21-19). It must be realized that many individual techniques have been developed in spinal palpation. These methods allow for systematic assessment of dynamic thoracic motion and respiratory function of both the thoracic spine and ribs. [nterpretation of the results gives the clinician some appreciation of the forces, particularly a clue to the muscles involved in producing the fixation patterns. Joinr challenge and end feel challenge techniques are also of some value in assessing joint function at the multiple synovia l joints of this region. The use of movable tables allows for motion procedures to assess spinal motion in a passive posture (Figure 21-20). [t should be stated ar this poinr that fixations may be found singly or as a group pattern. Scoliosis and rotation deficits seen on radiograph
often show a characteristic group of vertebrae involved in fixation along with the rib cage, particularly as these problems become more chronic or when patienrs become less physically fit. [n my opinion, the process of joint fixation begins with muscular toniciry alteration : either spasm, inability to relax, or inappropriate excitability when at rest or w hen stress or activity takes place. Physiologically, if a muscle is under contraction for any sustained period, contraction or shortening of the muscle fibers takes place; thereby the body economizes on irs energy expenditure. The result is, however, loss of motion in the opposite direction to the motion created by that muscle on contraction . Once a range of motion is lost, the ligaments shorten, making the fixation more permanent. This process is said to take place starting within a few hours if motion does nOt occur and can develop to some degree of measurable chroniciry with days and weeks. Clinicians are of the opinion that they can perceive the difference between muscular fixations and ligamentous fixation; no research has been undertaken to assess this position. Once there is a consistent loss of motion within a joint, articular and cartilaginous changes take place. This final change is consistent with degenerative arthritis changes and demonstrates the importance of maintenance of spina l function and
404
1be Subluxation Synclrom8l
the management of fixation subluxations. The dynamic adjustive thrust has been shown to be the most effective tool for control of pain (103). The reasons may be mulriple, such as biomechanical, biochemical, or neurologic (104). In the management of spinal dysfunction, one should recognize thar there are stages of pathogenesis of any lesion, and our responsibility is to institute a
total management program not only of adjustmentS but at some stage a rehabilitative exercise and educational program. I am also of the opinion that in using the dynamic adjustive thrust, a more effective man-
agement approach is not only to elicit the direction of the fixation but also to attempt to elicit the muscular forces involved in producing the dysfunction and determine the stage of the pathogenic process; that is, muscular contraction or contracture, ligamentous and osseous changes, and to deliver the adjustment so that it affects rhese tissues as posirively as possible. To make these decisions, one must integrate all of the physical examinarion procedures along with radiographic analysis, including motion radiographic studies, to develop a complete understanding of the lesion. Korr (105) suggesred rhat much of rhe
or appropriare for rhe muscle groups can be established.
Dynamic Motion PalpatIon FhIIngs and SUggested A"ustlve CoI,oection Serratus Posterior Superior I. Lower thoracic Finding: reversal of spinous in lateral flexion Adjustment: a. Spinous push (Figure 21-21). b. Sitting rib adjustment (Figure 21-22) 2. Upper thoracic Finding: Restricted anterior rotation upper ribs Restricted spinous rotation
Adjustment: Thumb on spinous of thoracic, rhenar COntact on angle of rib (Figure 21-23 ) 3. Quadratus lumborum Finding: Restricted anterior rotation lower ribs
Adjustment: Thenar contact on rib angle, sitting rotation adjustment
(Figure 21-22) 4. Splenius Cervicis and Capitus Fi nding: Because rhis muscle a llows normal mechanics in [he upper rhoracics,
sensory input that alters reflex neurologic activity
palparory findings are limited;
in somatic dysfunction may in fact come from
anterior rotation of cervica l spine and
within the muscular system rather rhan from rhe joint proprioceptors. With this in mind, attention and treatment should be direcred toward assuring that these muscular reflex patterns are altered in our treatment. Dynamic palparion allows for some appreciation of these muscular forces and an adjustive technique can be selected, not only to correct the fixation but also to introduce a dynamic stretch wirhin the muscle that is preloaded or stretched before the thrust, thereby increasing the neurologic effecriveness of rhe adjustment. Empirical use of these procedures
occiput and hypermobility of flexion
seems
[Q
improve results when this consideration
is given. When thought is given to the specific muscle groups thar are involved in the dysfunction or to the muscle groups that should be actively controlling rhe optimal morion for that spine, an exercise and treatment program specific
RgIre 21-21
Reverse lumbar roll.
21
Thoracic II1II Cml1overt8bral Sul*lxadOll Syndromes
,.... 21~22 Sitting thoracic or rib adjustment.
405
Rgan 21-28 Spinous, TVP, or rib contact. Head may be turned toward or away.
or excessive spinous deviation in latera l flexion of the thoracic spinouses may give an indicatio n Adjustment: Prone TM wi th cervical spine turned away from contact
(Figu re 21-24) Secondary cervical fixation: prone TVP contact same position Semispinalis T horacis This muscle is the major muscle in controlling norma l thoracic mechanics. Its attachment to the spinous processes of C6-7, Tl-4 in separate slips
R!111'121-24 TM adjustment, head away from con tact, traction by indifferent hand.
down to TVP of T6-T 12 controls the normal mechanics of the thoracic spine in lateral flexion along with other muscle groups. Because this muscle controls norma l mechanics, it is difficult to demonstrate palpation findings. The ad justment recommended is to rake a spino ll s process contact with one hand and the TVP, pisiform contact at the lower fixation involved . The spinous contact produces the traction, with the head turned slightl y toward the lesioned side and the pisiform on appropriate TVP applies the thrust. Thrust is short amplitude and comes from a preload fro m superior to inferior distraction (Figure 21-25) .
Rgare 21-25 Thoracic spinous: TVP or rib cOntacr.
406
n.n !l-m
TVP or rib ro occiput adjustment.
Semispinalis cervicis hypertonicity produces a superior pull on the TVPs TI-6 and related spinous inferior C2-S . The combination adjustment thumb to spine opposite pisiform to TVP, neck turned toward lesioned side, thrust from superior to inferior is again indicated. The adjustment for semispinalis capirus is similar with contact on the
occiput; headpiece is lowered (Figure 21-26). The iliocostalis lumborum muscle, when hypertonic, fixes the lower six ribs bucket-handle down, caliper open. The secondary fixation involves the lumbar spine, type II fixation (27). Two adjustive procedures are effective. First is the sitting rotation rib adjustment (Figure 21-22). Contact hand is on the angle of the rib. Patient is positioned in rotation, slight lateral flexion away from side of contact. Thrust is given from inferior to superior. Second is the reverse lumbar roll (Figure 21-21). Patient is placed on side posture, lesioned side up, shou lder forward, pelvis and leg backward. Contact with forearm on the lower rib angles, fingers on the lumbar spinous process, thrust on rib angle superiorly and spinous processes are preloaded with a constant pressure from the superior, laterally; this preload pressure is reinforced by the second contacr hand on rhe anterior ilium, which becomes the main preload force with a mild posterior thrust. The iliocostalis thoracis portion is a main pos-
tural stabilizer of the thoracic spine, running
Allre21-U Inferior rib bilateral or unilateral. from the upper six ribs to the lower six ribs at the angle of the ribs. Spasm or hypertonicity would produce, in the superior ribs, bucket handle down, and in the lower ribs, bucket handle up. Any adjustment should be concerned with the direction of fixation. The thrust for the superior ribs should be inferior to superior (Figure 21-27), and the thrust for the inferior ribs should be from superior to inferior (Figure 21-28). Prone rib contact adjustment: Superior rib correction subluxation is to the in ferior. The crossed bilareral wirh contact on the angle of rib, second hand on opposite TVP to stabilize the thoracic vertebra . Torquing thrust of shallow depth assists in the correction (Figure 21-28). Inferior rib correction: The rib is subluxated to the superior. Bilateral, noncrossed hands, contact
hand thrusrs from superior to inferior on angle of rib; support hand stabi lizes opposite TVP, same shallow torquing thrust. Upper porrion iliocostalis: Upper ribs elevated, bucket handle superior. Spinous processes of cervicals fixed roward side of lesion. Double rib spinous contact (Figures 21-25, 21-26): Thrust on angle of rib from superior ro inferior. The indifferent hand contacts the spinous process
21
TIIoracIc IIId Costovel'le"''' a.JIatIon Syndromes
~ 21·!8 lnferior or superior rib adjustment. Thrust on either hand, opposite hand (indifferent) produces stabilization.
in the cervicals; patient's head is turned toward the side of contact. Longissimus thoracic portion of sacrospinalis: This muscle is an imporcanr postural stabi lizer, connecting TYPs of lower 9 to 10 thoracics and lumbar TYPs. Fixation produces a posterior inferior fixation of thoracic vertebral TYPs.
Prone adjustment: Contact TYPs thrust from inferior to superior. In the lower rhoracics, having
FIgIn 21·80 superior.
407
Rgure 21-28 TVP or rib COntact. Thrust may be from inferior to superior or from superior to inferior.
the patient arch the back against the preload and slightly resist with just the back muscles assists in the comforr of this adjustmenr and helps protect the patient from painful extension and jamming of the facets. The thrust is of a lower ampli tude and high velocity. Experience has shown that the procedure often taught (deep breath then breathe out and thrust), although it helps in patient relaxation, often leaves the patient without defense. This may result in trauma; therefore, the procedure just described (Figures 21-29, 21-30) is suggested. Supine: «Anterior Thoracic Adjustmenr" (Figure 21-3 1), described later, is also effective.
Lower thoracic bridge contact inferior to
Rgure 21·81
Supine lower thoracic or rib.
408
TIle SUl*lxItlon Sy'*-
___ Zl-82 Supine upper thoracic or rib.
___ Zl-38 Crossed bilateral with torque. TVP or rib.
Longissimus, Cervical Porrion Prone TVI' adjustment from superior to inferior with patient's head turned away from lesioned side is used. Secondary hand produces traction on cervica l TVPs (Figure 21-26). Supine upper dorsal TVP contact with patient's hands clasped around the neck assists in stretch ing this muscle and releasing fixation (Figure 21-32). Longissimus Capitlls Portion Prone TVI' contact adjustment from superior to inferior, secondary hand on occiput, head turned
away from lesioned side; headpiece lowered sligh tl y (Figure 21-26).
Deep segmenta l muscles, such as rotatores and multifid ii, respond well to crossed bilateral pisiform contact with tOrque (Figure 21-33); or pisiform TVI' spinous thumb contacts, causing rotatory shearing between adjacent segments (Figure 21-34). The supine anterior thoracic adjustment can be made specific if the contact hand is placed at the bend of the thoracic spille. The thrust is delivered headwa rd whi le the arms' lock the body as a ullit. This creates a flexion sepa ration of the segments involved and is very effective for segmental muscles (Figures 21-31, 2 1-32) . Segmental fixa -
A
B Rgure 21 ~84
A, TVP/spinous segmenraJ fix-small musclesi S, TVP/spinou5 segment3l fix-larger muscles.
21
T1IoI'acIc and CoatOV8I'I8IIrai S.mtuxltlon Syndl'Olll8S
409
tions involving small muscles that produce extension of thoracic segments can be corrected by aspinous contact thrust from inferior CO superior
(Figures 21-31, 21-32). General Adjustments The longitudinal stretch for both cervica l and thoracic segmenta l muscles is often helpful to release deep fixations . When the traction is appl ied to the cervical spine with a short-amplitude thrust, patient may feel release or stretch in the thoracic or even the lumbar spine. The standing thoracic lift is often used when a table is not ava ilable, when the thoracics are rigidly fixed, or during pregnancy. The lift affords traction headward; the chest is the genera l contact. The key factor is that the thrust is directed longitudinally along the a ngle of the facets. A drop centerpiece is helpful for prone adj ustments when indicated, as in pregnancy (Figu re 21-35). The anterior thoracic adjustment has received much attention. Bergman, in lecture notes, asks
the question, «Arc anterior thoracics really anterior?" He explains the common appearance of a
flartened or saucered mid thoracic spine as being caused by flexion of a thoracic vertebra, or by excessive activity of (he spina l extensors causing an extension stacking of a group of segments
above; hence the flat appearance (106). The
figure 21-88
Knife-edge spinous adjustment.
authors describe one method of a supine a nterior thoracic, which is also described in detail by Fligg CI 07). Fracheboud et al. (108) report T5-6 as the most frequent site of involvement. Interscapu lar pain, respiratory problems, chest pain, and stomach comp lai ms, in that o rder, were reported to be
related. The paper also attempts to show the app roa~h of various system techniques. My own observation would suggest that a muscle gro up such as the semispina lis thoracic, the spinalis cer-
vicis, or possibly the multifidus, which attaches to the TVP below and ro the spinous processes of vertebae above, would cause the lower vertebra to flex, particularly if bilateral contraction took place and the vertebrae above would extend. Other types of correction also are suggested in this case, and many other adj ustive procedures are avai lable to us for varying needs of the patient (Figure 21-36). These suggestions onl y serve [0 portray the thinking process in selecting the most effective correctio n.
Concluding Remarks
~
21-86
Drop center piece prone adjustment for
use during pregnancy.
This chapter was produced with the thought in mind to present an understandi ng of thoracic biomechanics that would stimulate thoughtful management of pain syndromes, pathomechanica l states, and neurophysiologic effects related to subluxa tion/dysfunction of the thoracic spine and
410
TIle Subluxation Syndromes
ribs. I have introduced a concept of not only considering joint posirion and joint mobility but also the holding elements: the muscles, ligaments, and discs. The suggestion has been made that the dynamic adjustment is probably the most effective tool in controlling pain and altering these intrinsic and extrinsic factors involved in abber-
ant biomechanical processes. lnherant in the discussion is the understanding of the pathokinesis that would allow us to develop other methods of treatment to benefit these intrinsic and extrinsic
factors involved in the process and their reflexbased or non-reflex-based relationship to the nervous system. Emphasis has been placed on the role of what would appear to be the most responsive tissue to treatment other than the nervous system involved in producing spinal biomechanical problems: the spinal musculature. An attempt was made to emphasize that there is an optimal neurologic pattern and therefore an optimal harmony of muscular control of the statics and dynamics of the spine. If the control or the harmony of muscular function is lost, it results in alteration of joint dynamics, or changes in the
tion but also of reestablishing neurologic balance and integrity to the system as a whole.
Relerenees 1. Skubic JW, Kosruik JP. Thoracic pain syndromes and thoracic disk hern iation 1988. In: Frymoyer JW, ed. The adult spine: Principles and practice. New York: Ra\'cn Press, 1991. 2. Garrermal1 M. Chiropractic management of spine related disorders. Vol 9. Baltimore: Williams & Wilkins, 1990: 176-204. 3. Schafer Re, Faye LJ. Motion palparion and chiropractic technic: Principles of dynamic chiropractic. Vol 4. 1st ed. Hunring'tOn Beach, C.,lifornia: The Motion Palpation Institute, 1989: 143-94. 4. White AA, Pnnjabi MM. Clinical biomechanics of the spine. Toronto: JB Lippincott, 1978. 5. Valencia F. Biomechanics of rhe thoracic spine. Vol 4. In: Gram T, ed. Physical therapy of the cervical and thoracic spine. New York: Churchill livingstone, 1988. 6. Wyke BO. Morphological and funcrional features of the innervation of the cosrovenebral joints. Folia Morph Prague 1975; 2),296-305. 7. Andersson GB, Ortengren R, Herbertz P. Quantitative electromyographic studies of back muscle activity related to posture and bod),. Orthop Clin Nonh Am 1977; 8:85.
8. Andersson GB, Ortcngrcn R. Myoelecrric back muscle
axis of motion of the motion segment, which causes excess wear and tear and sometimes pain.
9.
It is advisable for a clinician to address the kinesioparhogenesis of th e spine in a systematic manner with an understanding of optimal function,
degrees of abnormal function that may be present, and the demands of structural change (pathogenesis) that may occur. With this understanding of the problem, a more effective management program may be established. Such a program should deal with the acute reactive painful phase of treatment, the rehabilitative stabilization phase of treatment that involves patient responsibility, and, if necessary, the su pportive maintenance phase of care. Total management of the patient not only addresses the intrinsic and extrinsic factors related to aberrant spinal biome-
chanics but also the illness behavior, and finally, the well ness awareness and behavior of the patient. In the chiropractic model of care, the patient is approached on a physica l basis with the view of not only relieving pain and dysfunc-
10.
II.
12 , 13.
14. 15. 16.
17.
activity during sirring. Scand J Rehabil Med Suppl 1974; 3,73. Nachemson A. Lumbar intradiscal pressure, experimental srudies on post monem material. Acra Onhop Scand Suppl 1960j 43. Andriacchi T, Schultz A, Belytschko T, er al. A model for studies of mechanical interactions between the lumbar spine and rib cage. J BlOmcch 1974; 7:497. Gray H. Gray's anatomy: The classic collector's edition. New York: Crown Publishers, 1977. Smorl G,Junghanns H. The human spine in healeh and disease. New York: Grune Stratton, 1971: 32-34. Carver W. Carver's chiropractic a,nalysis of chi,ropractic principles as applied to pal'hology, re1arology, symptomatology and diagnosis. Oklahoma City: Self-published, 1909. Bearry HG. Anatomical adjustive technic. 2nd cd. Denver: 1939. Homewood HG. The neurodynamics of the venebral subluxation. Toronto: Valkyrie Press, 1962. Whire AA, Panjabi MM. Analysis of the mechanics of the thoracic spine in mall, Acta Orthop Scand [Suppl] 1969; 127. Paniabi MM, Brand RA, White AA. Mechanical properties of lower thoracic spine: As shown by three-dimensionalload-displacemcnr curves. J Bone Joint Surg 1976; 58A,642.
411 18. Vasilev V, Ovcharov V, Malinor G. Age-related changes in the thoracic intervertebral disc of humans. Nauchni Tr Vissh Med Insr Sofia 1971; 50,15-24. 19. Bastin JM, Thomes JD. AcqUIred blocks and vertebral fusions in casts of degenerative discopathy and of joint aging. Rev Rheum Mal Osteoarric J 973; 40:443--6. 20. Quiring OP, Warfel JH. The head, neck and trunk. Philadelphia: Lea & Feblger, 1969. 21. Quiring OP, Warfel JH. The exrrcmlncs 2. Philadelphia: Lea & Feblger, 1967. 22. Kapandll lAo The physiology of the Joints. Vol HI. The trunk and vem:bral column. London: Churchill LivingSfOne, 1974. 23. Gregersen GG, Lucas DB. An 10 vivo study of the axial rotation of the human thoracolumbar spine. J Bone JOint surg 1967; 49A,247. 24. White AA, Panjabi MM. The basic kinematics of the human spine: A review of past and current knowledge. Spine 1978; 3: 12. 25. WhHe AA, Panjabl MM. Spinal kinematics: The research slarus of spmal manipulative therapy. NINCDS Monograph 15:93. Washington, DC: U.S. Department of lIealth, Educ.:aion and Welfare, 1975. 26. Grice AS. J I3rmony of joint and muscle function in the prevenrion of lower back syndromes. J Can Chiro Assoc 1976; 20,2. 27. Grice AS. Radiographic, biomechanical and clinical fac· tors In lumbar lateral flexion. Part I. J Manipulative PhYSIOI Ther 1979; 2( I ),26. 28. Cassidy JD. Roentgenological examinations of the functional mechanics of the lumbar spine in lateral flexion. J Can Choro Assoc 1976; 20,2-13. 29. Guelman R. A chiropractic approach to biomechanical disorders of the lumbar spine and pelvis. In: Haldeman S, ed. Modern developments in the principles and prac· rice of chiropractic. New York: Appleton-CenruryCrofts, 1980. 30. Grice AS. A blomechanical approach to cervical and dorsal adjusting. In: Haldeman S, ed. Modem developments in the principles and practice of chiropractic. New York: Appleton-Century-Crofl, 1980. 31. Steindler A. Kinesiology of the human body under normal and pathological conditions. Springfield, Illinois: Charles C. Thomas, 1955. 32. Basmajian JB. Muscles Alive: Their (unction revealed by electromyography. Baltimore: Williams & Wilkins, 1967. 33. Grice AS. Scalenus anticus syndrome: DiagnosiS and chiropractic adJustlve procedure. J Can Chlro Assoc, 1977; (Mar),3-IO. 34. Beal MC. Viscerosomatic reflexes: A review. JAOA 1985; 85(12),786-98. 35. Beal MC. Palpatory testing for somatic dysfunction in patients with cardiovascular disease. JAOA 1983; 82(11),73-82.
36. Cox JM, Gorbis S, Dick LM, Rogers JC, Rogers FJ. PaJpable musculoskeletal findings in coronary artery disease: Resuhs of a double-blind study. JAOA 1983; 82( II ),86-90. 37. Beal MC, Morlock JW. Somatic dysfunction associated w.th pulmonary d;sease. JAOA 1984; 84(2),57-61. 38. Beal Me, Kleiber GE. Somatic dysfunction as a predic(Or of coronary artery disease. JAOA 1985; 85(5),70-75. 39. Johnston WL, HHI JL, Sealey JW, Sucher SM. Palparory findings in the cervicorhoracic region: Variations in normotensive and hypertensive subjects: A preliminary report. JOAO 1980; 79(5),55-63. 40. Saro A. The importance of somaro-auronomic reflexes in the regulation of visceral organ function. J Can Assoc 1976; 20(4),32-8. 41. Haldeman S. Why one cause of back pain. In: Buerger AA, Tabls JS, eds. Approaches (0 the validation of manipulative therapy. Springfield, Illinois Charles C Thomas, 1977. 42. Kirkaldy-Willis WH. Managing low back pain. 2nd ed. New York: Churchill-Livingstone, 1988; 4. 43. J laldeman S. The neurophysiology of pain. 2nd ed. In: Haldeman S, ed. Principles and practice of chiropractic. East Norwalk, Connecticut: Appleton & Lange, 1992; 165-84. 44. Schafer RC: Clinical biomechanics: Musculoskeletal actions and reactions. Baltimore: Williams & Wilkins, 1983. 45. Love JG, Kiefer EJ: Root pain in paraplesia due to protrusions of thoracic imerverrebra l disks. J Bone Joint surg 1949 Uun). 46. Maigne R. Low back pain of thoracolumbar origin. Arch Phys Med Rehab;1 1980; (Sep),61. 47. Tichy J, Mojzisov3 L. The role of sternocostal articulations in low back pain. Manual Medicine 1986; 2,122-5. 48. Arroyo JF, Jollier P, Junod AF. Costovertebral joint dysfunction: Another misdiagnosed cause of atypica l chest pa;n. Posrgrad Med J 1992; 68:655-9. 49. Chiacchi MS. The association of the serratus anticus and rhomboid major musculature in anterolateral thoracic pain syndromes: A synopsis. Dig Chir Econ 1991; 34(2),50. 50. Fam AG. Musculoskeletal chest wall pain. Can Med Assoc J 1985; (5ep),379-89. 51. Raney FL. Costovertebral-costotransverse joint complex as the source of local or referred pain. J Bone Joint Surg 1966; 48(A),1451-2. 52. Maurer EL. The thoracic-costal facet syndrome with introduction of the margin line and the rib sign. ACA J Ch;ro 1976; 10·5,151-64. 53. Bradford OS, Moe )E, Montalvo FJ, Wimer RB. Scheuermann's kyphosis. J Bone Joint Surg June 1975; 57A,4.
412 54. Burke BC, Murray DO. The management of thoracic and thoracolumbar injuries of the spine with neurological involvement. J Bone Joint Sueg 1976; 18:58. 55. Wyke B. The neurological basis of thoracic spinal pain. Rh.um3lol Phy. M.d 1967; 1017P56-68. 56. Wyke BO. Articular neurology: A review. Physiotherapy 1972; 58,94-9. 57. Bogduk N. Valencia F. Innovanon and pain patterns of the thoracic spine. In: Rurh Grant ed. Physical therapy of the cervical and thoracic spine. New York: Churchill-livingston, 1988. 58. Bronfon G. Effectiveness of spinal manipulation and adjustments. In: Haldeman 5, ed. Principles and practice of chiropractIC, 2nd ed. Ean Norwalk, Connecticut: Appleton & Lange, 1992. 59. Haldeman S. Modern developments in the principles :md practice of chiropractic. New York: Appleton. Cenrury·Crofts, 1980. 60. Haldeman S. Principles and pracrice of chiropractic. 2nd ed. EaSt Norwalk, Connecticut: Appleton & Lange, 1992. 61. Schafer RC. Clinical chiropractic: The management of pain and disability: Upper body complaints. Huntington Beach, California: The Motion l)alp~l[ion Instirute, 1991. 62. Schafer RC. Chiropractic and physical spJOal diagnosis. Oklahoma City, Oklahoma, Assoc Chirop Acad Press, 1980. 63. Dobrusin R. An osteopathic approach to conservative management of thoracic outlet syndromes. JAOA 1989; 89(81, I 046-56. 64. Bergman TF, Peterson DH, Lawrence OJ. Chiropractic technique. New York: Churchill Livingstone, 1993. 65. Plaugher G. Textbook of clinical chiropractic: A specific biomechanical approach. Baltimore: Williams & Wilkins, 1993. 66. Johnston WL. Segmental definition: Part I. A focal point for diagnosis of somatic dysfunction. JAOA 1988; 88(11,99-105. 67. Johnston WL. Segmental defimtion. Part II. Application of an indirect method in osteopathic manipulative treat· ment. jAOA 1988; 8812),211-7. 68. Johnston WL. Segmental definition. Part Ill. Definitive basis for distinguishing somatic findings of visceral reflex ongm. jAOA 1988; 88(3),347-63. 69. Kobrossi T, Steiman I. Thermographic JOvesngation of viscerogenic pain: A case report. JCCA 1990; 34:3. 70. Stillwagon G, Stillwagon Kl, Stillwagon BS, Dalesio DL. Chiropractic thermography. ICA Review, 1992; Jan/Feb: 3-8. 71. BcnEliyahu OJ. Infra-red thermal imaging of the vertebral subluxation complex. ICA Review 1992; Jan/Feb: 14-17. 72. Diakow RP. ThermographiC assessment of sacroiliac syndrome: Report of a case. JCCA 1990; 34:3. 73. Plaugher G, Lopez A, Melch PE, Cremala fE. The interand IntraexamJOer reliability of paraspinal skin tempera·
74.
75.
76.
77. 78.
79.
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84. 85.
86.
87.
88.
89. 90.
91.
rure differential instrument. Manipulative Physiol Ther 1991; 14,6. Kent C, Gentempo P. Paraspinal surface EMG and out come assessment for subluxation-based chiropractic care. ICA Review, 1992; Uan/Feb): 19-23. Adams T, Steinmetz MA, Heisey SR, Holmes KR. Physiological basis for skin properties in palpatory physical diagnOSIs. JAOA 1982; 81 :6. Bryner P, Baxter Aj, Sherwood BF. Thoracic paraspinal tenderness in chronic pain surferers. j Aust Chiro Assoc 1989; 19,132-6. Taylor P, Tole G, Vernon H. Skm rolling techmques as an indicator of spmal dysfunction. jCCA 1990; 34:2. Vernon H. Pressure pain threshold: Evaluanon on the effect of spinal manipulation on chrOniC neck pam: A ,a'<Study.j Can Chi,o As.oc 1988; 3214),191-4. Vernon H, Aker P, Burns S, Valjakanen S, Short l. Pressure pain thresholds: Evaluation on the effect of spinal manipulation in the treatment of chronic cervical pam: A preliminary repon. j Manlpulanve Physio! Ther 1990. Hildebrandt RW. Chiropractic spinography and postural roentgenology. Pan 11: Clinical basis. J Mantpulatlve PhYSIolTher 1981;4,191-201. Howe JW. The role of x-ray findings 10 structural diagnosis. In: Goldstein M, cd. The research status of spinal manipulative therapy. NINCDS Monograph 1975; 15,239-47. Wimerstem jF, Leverone RA. Full spine radiography: Irs methods and value. Digest Chlro Econ 1974; 17:26-30. Cox jM, Gideon 0, Rogers FJ. Incidence of osteophytic lipping of the thoracic spine in coronary hean disease: Resul" of a pilot study. jAOA 1983; 82( II ),93-4. Macones Aj, Fisher MS, locke jL. Stress·related rib and vertebral changes. Radiology 1989; 170: 11 7-19. Hilel N. Osteophyres of the spme compressing the sympathetic trunk and splanchniC nerves In the thorax. Spine 1987; 12161,527-32. llpschin M, Bernslein·Lipschin l, Hlld N. Thoracic sympathetic trunk compression by osteophytes associated with anhritis of the costovertebral JOint: Anatomical and clinical considerations. Acta Anat 1988; 48-54. Singer KP et al.1nfluence of zygapophyseal jOint onenta· rion on hyaltne cartilage at the thoracolumbar lunctlon. J Manipulative Physiol Ther 1990; 13(4):207-14. Singer KP, Giles LGE Manual therapy considerations at the thoracolumbar junction: An anatomical and functional perspective. j Mantpulatlve Physiol Ther 1990; 1312),83-8. Fligg DB. The art of motion palpation. jCCA 1984; 2813),331-4. Sportdli G, Tarola GA. The history and phYSical examination. In: Haldeman S, ed. PrinCiples and pracrice of chiropractiC. 2nd cd. EaSt Norwalk, Connecticut: Appleton & lange, 1992. Grice AS. Posture and posture mechamcs. JCCA 1970;
413 Uul), 19-21.
92. Johnston WL, Elkiss ML, Marino RV, Blum GA. Passive gross motion testing. Parr 1I. A study of inrerexaminer agreement. jAOA 1982; 8 I (5),304-8. 93. Lewu K. Deviation of the spinous processes. Br J Radiol 1957; 30(351),162-4. 94. Gillet H, Liekens ME. Belgian Chiropractic Research
Notes, 10th cd. Brussels, Belgium, 1973. 95. Fligg DB. Sacroi liac cross fix adjustment. jCCA 1983; 27,4.
96. Fligg DB. Lumbar closure adlustment. JCCA 1983; 27:2. 97. Fligg DB. Lower cervica l spine motion palpation (C2-7). jCCA 1984; 28, I. 98. Fligg DB. Upper ce rvica l techmque. JCCA 1985; 29:2. 99. Fligg DB. The anterior thoracic adj ustment. JCCA 1986; 30,4. 100. F1Jgg DB. Latera l recumbent rib adjustment. JCCA 1984; 28,2. 101. Menncll SM. JOint pam, diagnosis In treatment using manlpulanon techniques. 1st ed. Boston: Lmie, Brown, and Co, 1964.
102. Love RM, Brodeur RR. Imer- and imra-exammer reliability of morion palpanon for the thoracolumbar spine. 1 Manipulative Physiol Ther 1987; 10(1): 1-4. 103. Manga P, Angus D. The effectiveness and cost-effectiveness of chiropractic managemem of low back pam. University of Onawa, Canada, Pran Manga and Associates, 1993. 104. Leach RA. The chiropractic theories: A synopsis of scientific resea rch. 2nd ed. Baltimore: Williams & Wilkins. 1986. 105. Korr 1M. Proprioceprors and somatic dysfuncrion. j AOA 1975; 74(7), 173-5. 106. Zachman Zl. Bolles S, Bergman TF, Triana AD. Understanding the amerior thoracic adjustment (a concept of a sectional subluxarion). Chiropractic Technique 1989; 1(1),30-3. 107. Fligg DB. The anterior thoracic adJustmenr. lCCA 1986; 30(4),21 1-13. 108. Fracheboud R, Kraus S, Choiniere 8. A survey of anterior thoracic ad;ustmems. Chiropractic 1988; 1(3),89-92.
...... Facet Subluxation Syndrome David M. Panzer
KeyWords
Facet subluxation syndrome, spinal zygapophyseal joints, men iscoids, tropism
After reading this chapter you should be able to answer the following questions:
QuestIOn #1
What is the primary function of the lumbar facet articulation?
Question #2
What is the pattern of referred pain from spinal facet joints?
QuestIon #3
What are the 10 specific proposed effects that manipulation may have on spinal facet articulations?
22 Facet Subluxation By''''OI.
V
415
weight bearing. Normally they carry approximately one sixth of the total axial load of the vertebral motion segment (1). Because of their relatively small surface area, this is roughly equivalent to 10 times the weight per square inch borne by the standing knee joint (4) . Axial weight bear-
ertebral zygapophyseal (facet) joints have long been recognized as a source of spinal pain and dysfunction (1-11). In 1933, Ghormley (12) introduced the term facet syndrome, but after the work of Mixter and Barr in 1934 (13), interest in intervertebral discs and irrirared nerve roots overshadowed facet joints as a source of low-back pain. In more recent years, the facet
cases of degenerative disc narrowing (1). Increased zygapophyseal weight bearing is often
arriculations have received much more attemion.
considered an important component of lumbar
Kirkaldy-Willis and Burton (14) consider lumbar
facet syndrome that can readily be measured radiographically (4, 10,16,1 7). The innervation of the facet joints is well known. The joint capsule and adjacent tissues are innervated by twigs from the medial branch of
facer syndrome a "common ly occurring condi-
tion," and Cox (4) considers "facet subluxation syndromes probably the most common condition encountered in low back pain patients." This chapter explores the role of facet joints in spinal pain and pathomechanics.
Facet Syndrome Defined Facet syndrome may be broadly defined as pain or dysfunction amlng primarily from the zygapophyseal joints and their immediately adjacent soft tissues. Earlier definitions include the following (10): I. The condition characterized by an overriding of the facets of adjacent vertebrae, whereby the intervertebral foramina are narrowed from
the superior to the inferior 2. A state of subluxation with tcnsion, pressure,
stretching, or irritation of the vertebral joint capsule, as a result of postural strain or trauma but without narrowing of the related foramina
Specific diagnostic critetia for facet syndrome ate discussed later in this chapter.
Facet Clinical Anatomy and FuncUon The lumbar spine has been the focus of most srudy relating to facet joint mechanics. A primaty function of lumbar facer articulations is resistance to rotational and shear forces, thereby protecting
the disc (1,15). Lumbar facets also have a role in
ing is increased during extension, and reaches up to 70% of the intervertebral compressive force in
the posterior primary rami, each facet receiving
innervation from twO spinal levels (5,8- 10, 18,J 9). As the medial branch of the posrerior primary ramus traverses inferior to the facet surfaces, it
travels through a bony tunnel covered by the mammilloaccessory ligament (8,9, 19). Direcr nerve entrapmenr is possible at this site as a result of overriding (imbricarion) of facets that ma y occur with disc thinning or facet degenerarion (19) (Figure 22-1).
Menlscolds Intraarticular joint inclusions (synovial folds) have been described in all spi nal zygapop hyseal joints (11,20 ), but mOSt of the inrerest has centered on rhe lumbar spine. Typically, rhese structures consist of three parts: (1) a fibroadipose or loose connective tissue base arising from the joinr capsule, (2) a highly vascularized synovial inclu-
FigIn 22-1 Facet innervaeion. A, Nerve supply to the lumbosacral spine from the side; B, pare of the lower spina l innervation showing the mammilloaccessory ligament (arrow); and, C, a cross-sectional view of ehe spine. (22-1 A Modified from Cramer, Darby. Basic alld Clintcal Anatomy of the Spllle, Spmal Cord and A NS. St. LOllis: Mosby, 1995; 22-1 B Modified from Giles
LGF. Anatomical Basis of Low Back Pain. Baltimore: Williams & Wilkills, 1989.)
Mixed spinal nerve
Posterior primary division
~~~~~~:~~r----
(dorsol romus) Anterior primary division
(ventral ramus) lateral branch of PPD
Medial branch of PPD
Ascend ing division
Descending division
A
Nerves to spinous process and ----1il?r'¥.\ interspinous ligament
Nerve to articulor capsule
Posterior primary ' / r,""",, / rami
Posterior longitudinal ligament nerve to ver1ebral body
B
c
Anterior longitudinal ligament and nerve
Nerve to
I
body
417
+-=""""":--- Articular calilage ----'~-
Inf.rior arIicuIar oI .........u --+----+- Fibrous cap 01 IIWIitcaid ......111%1- Articular capsule ~=--f- Fill l ~ iIiF _Iiuue cell bu.
'J:::"
ftgIre 22·2: Diagrammatic representation of [be Jibroadipose meniscoid of a facer joint according to Engel and Bogduk. (Modified from Bergmann T, Peterson D, Lawrence D. Chiropractic Technique. Philadelphia: Churchill LlVlIIgstone, /993.)
sion zone, and (3) a tip of dense connective tissue or cartilaginous tissue that projects between the articular surfaces (7,14,18,20-23) (Figure 22-2). The primary functions of meniscoids are (18,20,21): 1. A space filler at the periphery of the joint surface 2. To increase surface area contact and therefore transfer load 3. To cover exposed articular surfaces and protect joint margins during flexion and exten-
sion. Mechanically, meniscoids have been implicated as a cause of the acute "locked back" or torticollis by becoming entrapped berween the articular surfaces (5,7,11,14,20-22,24,25). The success of spinal manipulative therapy directed at the facet joints may be explained by this mechanism. Dis-
traction of [he articu lar surfaces may release the entrapped meniscoid and allow resolution of the consequent muscle spasm (5,7, II ,20,22,24,26) (Figure 22-3 to 22-5). Other proposed mechanisms of meniscoid-relared facet joint dysfunction include:
1. Entrapment of the meniscoid outside the joint surfaces in the capsular recess (18,27) (see Figure 22-2) 2. A free fragment of facet cartilage avulsed from the articular surface but still attached to the capsule (18) 3. Deformation of hyaline cartilage by presence of the meniscoid
ll'opIsm Normally the upper lumbar facets are essentially sagittal in orientation, and the lower lumbar
joints are more coronal (15,28) (Figure 22-6).
418
The SUIIIuxatIDn Sy.III ....1IS
* t
A B C An illustration of the meniscoid entrapment theory. At A meniscus with a firm fibrous apex but deformable fatty body projects into a zygapophysial joint from the rostra l capsule; atthe apex deforms the articular carti lages formi ng a recess in which the apex becomes entrapped. Traction exerted through the body of the meniscus strains the joint capsule and evokes painj C, a manipulation that separates the articular cartilages releases the trapped meniscus and relieves the capsu lar strain. (Modified from Bogduk N. full G. The theoretical pathology of acute locked back: A basis for manipulative therapy. 1,78-82. 1985; Manual Med.)
fIIIItI H:-3
Tropism refers to an anomalous condition in which the articu lar facings are asymmetric (4). Because the facets guide the motions of the lumbar spi ne (1), it appears logical that asymmetric joint angles could disrupt normal biomechanics. Cyron and Hutton (15 ) have demonstrated unequal articular forces produced in tropism, with consequent increase in pressure and arthrosis at the more oblique (that is, more sagittal) facet (Figures 22-7 and 22-8). This results from rOtational tOrsion occurring at the joint. Increased wear on the anulus of the disc is postulated to occur as a result of these same forces (15). Cox states that "patients with anomalous facet facings are at high risk for developing a disc lesion on rotation " (4 ). Noren et aJ. (29) demonstrated that tropism was assoc iated with an increased risk of disc degeneration. Other studies, however, have failed to find association between tropism and
A B C A111'122-4 Treatment of the meniscus entrapment syndrome by manipulation. A, The meniscoid lies impacted against the joint marginj 8, longitudinal distraction, or flexion , of the joint reduces the impaction. Separation of the joint surfaces by a rotary maneuver widens the joint space to encourage the meniscoid to re-enter it. Capsular strain, and therefore the painful stimulus, is relieved; C, the joint is allowed to passively extend to its neutral position. If the meniscoid re-enters the joint space, pain stays relieved and norma l posture is restored. (Modified from Bogduk N. full G. The theoretical pathology of a"ute locked back: A basis for mmlipulative therapy. 1:78-82. 1985: Mant/al Med.) disc degeneration (30), disc herniation (31), and symptom reproduction by discography (30) . It seems safe to conclude that tropism, in the clinical context of a facet syndrome, constitutes a potential complicating factor. Furthermore, the treating physician may wish to modify manipulative therapies to accommodate the alteration of facet joint planes.
Facet Versus Disc Degenerative Joint Disease Degenerative JOInt disease (0)0) may occur at different rates in the discs and facets of the same motion segment. Ziv et aJ. (32) found severe fibrillation in histOlogic specimens of facets after the age of 30 years. Degeneration was more pro-
419
Reduced: hard edge remaining remodel. . fime A
B
c=== Normal position FIgIn 22:-6 Encrapment of a meniscoid at [he edge of a joint space, according to the joint blockage theory of Wolf (1975). A, The meniscoid has moved between the joint facets and its hard edge has impinged; 8, it has returned to normal position after treatment, A groove remains for a shorr time but over rime, [he articular cartilage will remodel. (Modi~ed from BergmamJ T, Peterson D. Lawrence D. Chiropractic Technique. Philadelphia: Churchill Livings/o".1993.)
nounced in the superior than in the inferior articular process. It was noted that even "young adults" showed ulceration or severe fibrillation, and that facet degeneration preceded disc degeneration. It was concluded that these facet changes were a likely source of back pain. Beaman et al. (33) also demonstrated that facet DJD occurs with or without disc DJD. These findings suppOrt the presence of a clinical entity unique to the facet joints, which can occur
independent of concurrent discal pathology or pathomechanics. They also counter previous studies that concluded that facet degeneration occurs only as a result of disc DJD (34). It should be noted that disc and facet degeneration do often occur together, and either or both may be a . . primary pam source.
Facet JOint as a Source of Pain Considerable evidence exists in support of the facer anicularions as a source of pain, and inner-
vation of the joint capsule and synovium have previously been described (5,8,10,18-20,22,23) . In addition to small-diameter nociceptive free nerve endings, the facet capsule and synovium have specific substance P-positive nerves (22), as does the adjacent subchondral bone (33).
Direct experimenta l evidence of the distribution of facet joint pain has been obtained by injection of hypertonic saline into the joint and mapping the pain produced. Mooney and Robertson (9) found that diffuse referred leg pain resulted from lumbar facet injection. They noted that the distance the referred pain radiated down the leg was dependent on the amount of facet irritation, and the time involved. They described the pain referral pattern as matching the typical "lumbago and sciatica" distribution. McCall et al. (35) conducted similar experiments that also demonstrated diffuse (nondermatoma l) pam referral patterns. Facet pain patterns were found to be consistent enough in the cervical spine that examiners
could predict the level of facet involvement in nine of nine patients based on pain distribution alone (3) . Confi rmation was achieved with diagnostic medial branch nerve blocks. Facet pain was even found in patients who had undergone previous anterior cervical fusion. Bogduk and Marsland (3) conclude that cervical pain is frequently zygapophyseal in origin and because cervical zygapophyseal disorders are poorly understood, or not even considered in conventional practice, patients with this complaint are more likely to gravitate to a pain clinic, and
420
Ang!eAI .......) 25 (15-47]
L2-l3
')
28 (17-51)
37 (15-57]
Y
)(
(
L4-1.5
AS (13-70)
(
L5-S1
53(36-70)
fIIIn 22-8
The shape and indinarion of the facets of the lumbar spi ne in the transverse plane (X Z pJane ) are shown. The facet inclination w ith the sagittal plane increases toward the lower leve ls. (Modified from Whit e, Pan;abi MM. Bogduk N, Twomey LT. Clinical Anatomy of the Lumbar Spine. Edinburgh: Churchill Livingstone,
1987.)
thereby constitute an inord inate pro portion of patients presenting with idio pathic neck pain. (3)
Other studies have taken the approach of injecting a local anesthetic or cortisone derivative into a specific facet joint believed to be causing pain. Relief confirms the facet articulation as the
primary source of pai n, and is generall y considered diagnostic of facet syndrome (6,8,9, 14,36). Helbig a nd Lee (6) showed that facets manifesting radiographic changes, especially marked DJD, responded best to facet injection. Kirkaldy-Willis and Burton (14) consider specific manipulation of
421
F
A
B
n.n 22-7
Tropism. A, Measurement of facet orientation; S, forces (F) acting on symmetrically oriemed superior
.rricui.r facets. (Modified (rom Cyron 8M, Hilt/on We. Articlliartropism. Spine 1980; 5(2):1 71.)
a facet joint or precise facet injection to be the " most reliable way to make a specific diagnosis." This view is not shared by Jackson (37), who found that control injections of saline were as effective as a local anesthetic in relieving facet pain . He concluded a placebo effect was responsible. It is quite possible, however, that the saline control group actually received a therapeutic effect
by stimulation of various articular recep-
tors (proprioceptive, nociceptive, etc.). This effect may be simila r ro the pain-modulating mechanisms of manipulative therapy (38,39) . It is also possible that improved joint mobiliry and reduced intraarticular or periarticu lar adhesions resulted from the capsu lar distension caused by the sa line injection.
Clinical Features of the Facet Syndrome In addition to low-back pain, classic lumbar facet syndrome includes the following symptoms (8):
1. H ip and buttock pain 2. Crampi ng leg pain above the knee 3. Low-back stiffness, especially in morning or after decreased activiry Lippitt (8) also includes the following signs:
1. 2. 3. 4. 5.
Local paralumbar tenderness Pain on spine hyperextension Absence of neurologic deficit Absence of rOOt tension signs Hip, buttock, or back pain with straight leg raising
422 B
A
I
I
IF I I I IF
F
R111'122-8 Tropism. Forces (F) acting on asymmetrically oriented superior articular facets. A, The force (F) acts at the poine of concurrency and is distributed unevenly to the articular facets . B, The fo rce is offset from the point of concurrency, and additional torsion is applied ro the joint. (Modified (rom Cyron 8M, Hutton We. Articular trbpism. Spine 1980; 5(2):171 .)
Wood (25) describes the onset of "acute locked facet syndrome" as sudden, typically following a trivial inju_rious force, often twisting or bending. He further describes "vety marked immobility, out of proportion to the pain-both in range of movements and in the time taken to move-often feeling foolish, so marked is the immobility. " In an attempt to establish an objective and more accurate set of diagnostic criteria, Helbig and Lee (6) formulated a scorecard system in which clinical features are given points. Scoring is as follows: Back pain associated with groin or thigh pain:
+30 points
Well-localized paraspinal tenderness: Reproduction of pain with extension-rotation: Significant corresponding radiographic changes (for example, facet asymmetry or DJD): Pain below knee:
+20 points +30 points
+20 points -10 points
All patients scoring 60 points or more (100 possible points) showed a positive and prolonged response to facet injection. It was concluded that this scoring system improves diagnostic accuracy and predictability of successfu l response to facet
B
lumbor angle
Disc angle
-.--
Disca~
lumbosacral angle
c
RIIre 22-8
A, Lumbosacral, lumbar and disc angles; B, lumbosacral extension ma lposition (i .e., increased disc angle) increases facet loadingj C, lumbosacral facer orientarion excessively lordotic posture. (Modified from Banks SD. Lumbar (aGet syndrome: Spinographic. assessment of treatment by spinal manipulative therapy. J Maniplliative Physiol Ther J 983; 6(4): 175-80.)
54"
424 JOint Injection. These diagnostic parameters can readily be adopted by the chiropractic physician. Radiographic features also may be helpful in the diagnosis of facet syndrome. Banks (17) found a significant increase in the lumbosacral angle (sacral base angle) of patients with facet syndrome compared with patients with disc herniation or normal controls (Figure 22-9). Similar results have been reported by Peters (10) and Cox (4). These results are consistent with increased weight bearing forming an important component of facet syndrome. Cox (4) states that "any discal angle over 15 degrees is a sign of severe facet syndrome." As previously mentioned, degenerative arthrosis, subchondral sclerosis, and tropism also may be significant radiographic features if they correspond to clinical findings. Cervical pain of zygapophyseal origin has been described as having the following clinical features (18,40) :
1. Characteristic local and referred pain (occipital to interscapular, depending on vertebral level) 2. Abnormal end feel of facet joint capsule 3. Abnormal quality of resistance to motion 4. Pain on palpation of segmental accessory movements 5. Confirmation possible with facet or medial branch nerve block
Thoracolumbar facet syndrome (Maigne's syndrome) also has been described, with pain typically referred to the iliac crest area . This pain is thought to be mediated by the cluneal nerves (14).
Treatment 01 Facet Syndrome ManlpulllIIon Spinal manipulation directed to the facet articulations is generally considered the treatment of choice for facet syndrome (4,7,11,14,16,22,25, 41-45). Specific zygapophyseal manipulation is also used to confirm a diagnosis of facet syndrome (14,45). It has even been postulated that
the success seen in rotary manipulation for lumbar disc herniation is attributable to the relief of associated facet syndrome (46). Because facet syndrome generally involves pain and joint dysfunction (11,25,40), it seems logical to apply treatment that not only relieves pain but helps correct the underlying dysfunction. Posterior joint dysfunction appears to have a specific intraarticular origin and is not simply the product of segmental muscle spasm . This has been demonstrated by performing manipulation under anesthesia, when the muscles are relaxed yet the intrinsic joint dysfunction is still quite evident (47,48). In fact, it has been noted that the joint dysfunction is rendered more obvious in the anesthetized patient (47). It also has been observed that periarticular injection of a local anesthetic relieves the pain but not the immobility of acute locked facet syndrome (25). Below is a summary of specific proposed effects manipulation has on facer arriculations: 1. Release of entrapped meniscoid (5,7,11,20, 22,23,26,27) 2. Reduction in articular cartilage displacement by chronically entrapped meniscoid (26) 3. Pain relief by co-activation of various receptors (24,38) 4. Reduced weight bearing (4,10,16) 5. Reduction of intervertebral foramen stenosis caused by segmental hyperextension (4) 6. Reduced intracapsular or extracapsular adhesions (7,11,22) 7. Relief of abnormal tension on joint capsule (7) 8. Reduction of postimmobilization collagen cross-linking (11) 9. Reduction of local vascular stasis (22) 10. Release of osseous mechanical locking Many studies have investigated the effectiveness of manipulation for low-back pain, but few have focused on facet syndrome specifically (49). Banks (16) demonstrated a normalization (reduction) of disc angle values after manipulation for radiographically verified facet syndrome. Cox et al. (41) reported excellent results in 69%, and
22
fleet SUbIuXItIon Byndl_
425
good or very good results in 15% of facet syn-
Even though he considers facet injection diag-
drome patients treated with manipulation. Nonmanipulative treatment in acute incapaci-
nostic rather than therapeutic, because "any ther-
tating episodes may include brief periods of bed rest and medication. But overall, "the value of muscle relaxants and of anti-inflammatory drugs is doubtful" (14).
facet_lion Injection of facet joints or adjacent nerves with a local anesthetic or antiinflammarory agent has
been described in this chapter. In addition to confirming the facet joint as a primary pain source, these techniques have been used ro treat facet syndrome. If manipulation fails, Kirkaldy-Willis and Burton (14 ) recommend intraarricular injection of bupivacaine or xylocaine followed immediately by manipulation. Postinjection muscular relaxarion may enhance the benefits of manipulation. They note that "facet injections nearly always relieve the pain for several hours. In approximately 50% of cases the patient is free of pain for weeks or months."
Lippitt (8), in an uncontrolled retrospective study, reported the following results after 11 7 facet injections in 99 patients with low-back and possible referred pain: excellent, 17%; good, 25%; fair, 9%; mediocre, 4 %; and no change, 44%. It should be noted that these were primarily chronic patients: 20 had undergone previous dis· cectomy, and 4 had spinal stenosis, and they were not screened in advance for specific facet syndrome cmeria. When the previously mentioned facer syndrome "scorecard" was used to select
patients for injection, Helbig and Lee (6) reponed a 100% prolonged response in cases scoring high (60 points or more) for facet syndrome indicators. They also point out that rhe composite of multiple signs and symptoms is more predictive than a single indicator alone. The patients treated in their study had all been treated unsuccessfully with rest, antiinflammatory medications, and physical rherapy (heat, massage, transcutaneous electrical nerve stimulation [TENS], exercise) for 2 months before facet injection.
apeutic effect is strictly coincidental . . . and ultimarely transient," Murtagh (36) found a 94% shorr-term response (up to 3 months' duration), and a 54% long-term response (lasting more than 3 months). He also found computed tomographic (Cf) or fluoroscopic guidance helpful in placement of the needle. Jackson (37) reported 85% of 390 low-back patients injected experienced some relief. He observed that the greatest relief immediately after injection was in lumbar extension and rotation.
He did not find these painful ranges of motion predictive of who would respond, however, and concluded that response to facet injection cannot be reliably predicted. He further concluded that facet joints are not commonly the single or primary source of low-back pain, and he questions the existence of facet syndrome as a distinct clini-
cal entity. He notes that further prospective, controlled, and randomized clinical studies are needed. A related form of treatment, facet denervation, was reviewed by Jackson (37), who concluded that "facet de nervation procedures generally provide inconsistent and frequently poor results, especially with time."
Predisposing Factors and Therapeutic Exercise The occurrence of facet syndrome has been correlated to a postutal increase in facet weight bearing, increased lumbar lordosis, or anterior sacra l
tipping (4,10,16,17,42). It also has been observed rhat facet loading may cause the backache associated with prolonged standing, which is relieved by placing the foot on a step, or by sitting (1). In other words, flexion relieves the loading. With these factors in mind, the following measures are recommended to assist in the treatment of facer syndrome and irs predisposing postural factors (10,42):
426
1111 SUIIUcatIon Syndl'Olll8l
I . Knee-chest (Williams) exercises 2 . 90-90 positioning or traction (hips and knees 90°) 3 . Pelvic tilt exercises to decrease lumbar lordosis 4. Abdominal strengthen ing exercises 5. Weight reduction as appropriate 6. Avoidance of high heels
13.
14.
15.
Conclusion
16.
The facet joints are widely recognized as a source of spina l pain, and the facet subluxation syndrome is a relatively common clinical entity, with well -defined features . Careful attention to clinical and radiographic indicators can enhance the accuracy of diagnosing this syndrome. Facet subluxation syndrome is generally amenable to conservative management with chiropractic manipulation and attention to predisposing fac tors. Such treatment helps address the important component of the manipulable subluxation (50).
21.
Rerlll'tlllC8.
22.
1. Adams MA, HUffon We. The mechanical function of the lumbar apophyseal joints. Spine 1983; 8(3):327-30. 2. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns. U. A clinical evaluation. Spine 1990; 15(6),458-<; I. 3. Bogduk N, Marsland A. The cervicalzygapophysea1loims as a source of neck pam. Spine 1988; 13(6):610-17. 4. COX JM. Low back pain mechanism, diagnosis, and [teatment. Baltimore: Williams & Wilkins, 1990:148-56, 437-<;6. 5. Giles LeE Anatomical basis of low back pain. Baltimore: Williams & Wilkins, 1989:27--40,58-104. 6. Helbig T, l..tt C. The lumbar facer syndrome. Spine 1988; 13(1),61-4. 7. Jones TR, et al. Lumbar zygapophyseal joim meniscoids: Evidence of (heir role in chronic mtersegmemal hypomobiliry. J Manipulanve Physiol Ther 1989; 12(5):374-85. 8. Lippirr AB. The facer joim and irs role in spine pain. Spine 1984; 9(7),746-50. 9. Mooney V. Robertson j. The facet syndrome. Clin Orthop 1976; 115,149-56. 10. Peters RE. Facer syndrome. Eur J Chlro 1984; 32:85-102. 11. Rahlmann JF. Mechanisms of imervertebral joim fixation: A literature review. J Manipulative Physiol Ther 1987; 1O(4), I77-87. 12. Ghormley RK. Low back pain with special reference to
17.
18.
19.
20.
23.
24. 25.
26. 27.
28. 29. 30. 31. 32.
the articular facets with presentation of an operative procedure.JAMA 1933; 101,1 773-7. Mixter WJ. Barr JS. Rupture of the Intervertebral disc with Involvemenr of the spinal cord. N Engl J Med 1934; 2110210-15. Kirkaldy-Willis WH, Burton CV. Managing low back pain. 3rd cd. New York: Churchill Livingstone, 1992,5()"'{;3, 122, 126, 137,203,21 1,248. Cyron BM , Hutton WC. Articular tropism and stability ofthe lumbar spine. Spine 1980; 5(2): 168-72. Banks SO. Lumbar facet syndrome: Spinographic assessment of rreatment by spinal manipularive therapy. J Manipulative Physiol Ther 1983; 6(4): 175-80. Banks SO. The u~ of spmographic parameters in (he differential diagnosis of lumbar facet and diSC syndromes. J Manipulative Physiol Ther 1983; 6(3): 113-16. Bogduk N, Twomey LT. Clinical anatomy of the lumbar spine. New York: Churchillllvingsrone. 1987: 30-2, 97-9, 140. Sunderland S.ln: Haldeman S, ed. Modern developments In the principles and pracnce of chlropracric. New York : Appleton-Cemury-Crofrs, 1980: 62-4. Giles LGF. Lumbosacral and cervical zygapophyseal joint inclusions. Manual Med 1986; 2:89-92. Bogduk N, Engel R. The menisci of the lumbar zygapophyscal joints: A review of their anatomy and clinical significance. Spine 1984; 9(5):454--60. Giles LGF. Pathoanatomlcal studies and c1imcal slgl1lfi· cance of lumbar zygapophyscal (facet) joints. J Manipula · tive Physioi Ther 1992; 15( 1):36-40. Giles LGF, Taylor JR. Osteoarthrosis in human cadaveric lumbosacral zygapophyseal jomts. J Mampulatlve Physiol Ther 1985; 8(4),239-43. Bergman TF, Peterson DH, Lawrence OJ. Chiropractic technique. New York: Churchill Livingstone, 1993. Wood L. Acute locked facet syndrome and ItS treatment by manipulation under local periarticular anesthesia. J Manipulative Physiol Ther 1984; 7(4):211-17. Lewit K. Manipulallve therapy in rehabilitation of the locomotor system. BostOI1: Bunerworfh. 1985: 17-19. Bogduk N,Jull G. The theoretical pathology of acute locked back: A basis for manipulative therapy. Manual Med 1985; 1,78-82. White AA, Panjabi MM. Clmical biomechanics of the spine. 2nd ed. San Francisco: JB lippincott, 1990:32. Noren R, Ct al. The role of facer joint tropism and facet angle in disc degeneration. Spine 1991; 16(5):530-2. Vanharanta 1-1, et al. The relationship of facet tropism to degeneranve disc disease. Spine 1993; 18(8): 1000-5. Cassidy JO, ef al. Lumbar facet jOllu asymmetry. Spine 1992; 17(5),570-4. Ziv I, et al. Human facet carnlage: Swelling and some phYSiochemical charaCieristics as a function of age. Spine 1993; 18(1), 136-46.
427 33. Beaman, et al. Substance P innervation of lumbar spine facer jointS. Spine 1993; 18(8):1044-9. 34. Buder D, et al. Discs degenerate before facets. Spine 1990; 15(2),111-3. 35. McCall IW, Park WM, O'Brien JP. Induced pain referral from posterior lumbar clements in normal subjects. Spine 1979; 4(5)0441-6. 36. Murtagh FR. Computed tomography and fluoroscopic guided anesthesia and steroid injection in facet syndrome. Spine 1988; 13(6),686-9. 37. Jackson RP. The facet syndrome: Myth or reality? Clin Orthop 1992; 279,110-21. 38. Gillette RG. A speculative argument for the coactivation of diverse somatic receptor populations by forceful chiro· practic adjustmentS. Manual Med 1987; 3:1-14. 39. Gillette RG. Personal communication, October 1993. 40. Jull C, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical1.ygapophyseal joint pain syn· dromes. Med J AlIs{ 1988; 148:233-6. 41. COX JM, Fromelt KA, Shreiner S. Chiropractic statistical survey of 100 consecutive low back pain pacienrs. J Manipulative Physiol Ther 1983; 6(3):117-28. 42. Ganerman MI. Chiropractic management of spine related disorders. Baltimore: Williams & Wilki.ns, 1990:161-3, 398-9.
43. Hourigan Cl, Bassett JM. Facet syndrome: Clinical signs, symptoms, diagnosis and treatment. J Manipulative Phys· iol The, 1989; 12(4),293-7. 44. Kirkaidy-Willis WH, Cassidy JD. Spinal manipulation in the treatment of low back pain. Can Fam Physician 1985; 310535-40. 45. Kirkaldy·Willis WH, Hill RJ. A more precise diagnosis for low back pain. Spine 1979; 4(2): 102-9. 46. Quon JA, er aJ. Lumbar intervertebral disc herniation: Treatment by rotational manipulation. J Manipulative Physioi Ther 1989; 12(3),220-7. 47. Lewit K. The muscular and articular factor in movement restriction. Manual Med 1985; 1:83-5. 48. Mennell JM. The validation of the diagnosis "joint dysfunction" in the synovial joints of the cervical spine. J Manipulative Physiol Thee 1990; 13(1):7-12. 49. BronEort C. Effectiveness of spinal manipulation and adjustmenrs. In: Haldeman S, ed. Principles and practice of chiropractic. 2nd ed. San Mateo. California: Appleton & Lange, 1992,420-9. 50. Garrcrman Ml. Indications for spinal manipulation in the treatment of back pain. ACA J Chiro 1982; 19(10):51-66.
Chiropractic Management of Intervertebral Disc Syndrome MlchaelJ.Hubka Kaywordl
Intervertebral disc syndrome, discogenic back pain, cauda equina syndrome, sciatica
After reading this chapter you should be able to answer the following questions:
Question #1
What is the natural history of intervertebral disc syndrome?
Question #2
Why is one type of treatment for all cases of intervertebral disc syndrome not in the best interest of the patient?
QuastIon #3
What signs and symptoms associated with intervertebral disc syndrome suggest the need for presurgical evaluation by an orthopedic surgeon or neurosurgeon?
23
I
ChIropracUc MllIIg8II1IIIt of ~ertebral iliac Syndrome
429
terms herniation, bulge, protrusion, prolapse. nrerverrebral disc synd rome is a common
cause of mechanical back pain and sciatica. The pathogenesis of intervertebral disc pain, and other causes of mechanical back pain, are poorly understOod, which may be the reason recent symptOm-based classifications of mechanical back pain have replaced diagnostic categories based on pathology (I). In this chapter, a simila r classification is used and the clinical features of four categories of intervertebral disc syndrome are described. Most patients with intervertebra l disc syn-
drome do not have a life-rhrearening or limbthreatening disorder and can expect spontaneous
recovery if rhey can wait long enough. However, this condition often causes severe pain, commonly
occurs during the most productive years of life, and takes a long time for recovery. A1so, the recurrence
rate of mechanical back pain is high; 40% to 85% of patients ha ve a recurrence within I yea r (2). Treatment is recommended to reduce pain, speed recovery, and prevent development of chronic and recurrent pain. Thorough understanding of the natural history of recovery is essential when planning treatment and discussing prognosis with the patient. Several different types of ch iropractic manipulation, including side-postu re rotational manipu -
larion, flexion-distraction mobilization, and extension mobilization, have been reported successfu l for intervertebral disc syndrome. When carefully applied, manipulation may help reduce pain and neurologic deficit and shorten the recovery period. Combined with exercise and education on risk factors for developing low-back pain, chiropractic treatment offers the best combination of passive and active conservative care for intervertebral disc syndrome.
Terminology 01 Intervertebral Disc Syndrome There is little consensus within the orthopedic and chiropractic professions on the diagnostic terms of intervertebral disc synd rome (3) . The
rupture, extrusion, sequestration. disruption, derangement, contained, and llo11contailled, which describe changes in the disc's morphology, are commonly used, althoug h their meaning may be unclear (3). The clinical relevance of disc pathology detected with advanced imaging is questioned, because pathologic conditions are not always cor-
related with symptoms. For example, tudies have shown that 20% to 30% of individuals without back pain or sciatica have a disc herniation or
other disc abnormality detected on computed tomography scan (4) and myelogram (5) . There are four categories of intervertebral disc syndrome, recognized by the location of pain during lumbar spine and leg movements and the presence of sciatica and neurologic deficit (see box). Di cogenic back pain is defined as back pain arising from the intervertebral disc. The pain may stem from mechanical strain or chemical irri -
tation of the anular fibers and is provoked by lumbar spine flexion and prolonged sitting (6-9) . Discogenic back pain is also known as disc disruption or derangement, and may be a common
cause of mechanical back pain . Schwarzer and associates (10) performed discography and zygapophysial joint blocks on 92 patients with chronic low-back pain to identify how frequently these structures were a source of pain. They
found that 39% had discogenic pain, 9% had zygapophysial joint pain, and 3% had combined discogen ic pain and zygapop hysial joint pain. They concluded that pain a rising from the disc is more common than zygapophysial joint
>
C lassification of Intervertebral Disc Syndrome
• Discogenic back pain • Discogenic back and leg pain • Sciatica without neurologic deficit
• Sciatica with neurologic deficit
430 pain, a lthough most patients (49%) had other sources of pain (10). A painfu l intervertebral disc a lso can cause referred pain in the leg, which is also known as somatic referred pain, scleratomal leg pain, or pseudoradicular pain (6, II ). Although the pain is generated from the disc, it is perceived in the back and leg. The mechanism appea rs to be afferent impulses from the disc 3C[iv3ring neurons in the central nervous system (CNS) that also happen to receive afferents from the leg (6). Stimulation of these CNS neurons, by impulses from the disc, results in the perception of pain arising from all the tissues subserved by these neurons; thus, the patient feels pain in the leg, although there is no signal actuall y emanating from the leg. The first two categories of intervertebral disc syndrome, discogenic back pain and discogenic back and leg pain, are also known as intervertebral disc syndrome without radiculopathy, because there are no sciatica symptoms, nerve tension signs, or neurologic deficits. Sciatica is a common problem, with a point prevalence of 1.5 % of the population and lifetime prevalence of 40 % of the population (2,12, 13) . Sciatica is defi ned as pain in the distribution of a lumbar nerve root, often accompanied
by
neuro-
logic deficit. Sciatica without neurologic deficit, the third category of intervertebral disc syndrome, is also known as irritative radiculopathy, because it is thought that the sciatica symptoms and nerve tension signs are caused by nerve root irritation. The fourth category of intervertebral disc syndrome, sciatica with neurologic deficit, is also known as rhizoparhy or compressive radicu-
lopathy, because the weakness, diminished sensation, and diminished reflexes are attributed to nerve root compression .
Symptoms and Signs of Intervertebral Disc Syndrome Because intervertebral disc synd rome is classified as mechanical back pain, the pain is increased by activity and relieved by rest (14, 15). However, in
some patients with inflammation caused by mechanical strain or chemical irritation of the anular fibers, pain may be present at rest, although it is usually less severe than when the patient is upright and active (8). Most patients experience some pain relief when lying on one side or supine and find that coughing, sneezi ng, straining, and prolonged sitting aggravate the pain (6,9, 16). Palliative and provocative facrors are similar for each category of intervertebral disc syndrome; however, the site of pain, nature of pain, and associated signs distinguish between each category.
Discogenlc Back Pain and IIIscogenic Back and Leg Pain Discogenic lower back pain is usually moderate to severe and described as a deep dull ache or
burning pain (6,9,16) . Bending forward at the waist is ve ry painful, and returning upright often requires the use of the hands on the thighs (Minor's sign). Prolonged sitting also aggravates the pain, and it may take some time for the patient to limber up after standing (9). Getti ng in and our of a vehicle is often very difficult. Discogenic leg pain is usually mild to moderate, described as a diffuse, dull ache and difficult ro localize. It is also known as scleratomal, somatic referred, or pseudoradicular pain (6). A characteristic feature of discogenic leg pain is that it is less intense than discogenic lower back pain, and is difficult to localize. On examination of patients with discogenic pain, patients may prefer to stand or lean on the edge of the examining table. Lumbar spine flexion is limited because of back pain; however, if the patient moves slowly, full flexion may be reached. Returning upright is also painful, and Minor's sign may be observed. Lumbar spine flexion is more painful than extension, a lthough both movements may be painful (9). A list of the trunk may be observed while the patient is standing or during lumbar spine flexion. Palpation over the lower lumbar spine discloses tenderness, and the most tender spinal level is often over the painful
23 ClIi ......ecllc MlnI.Bnalt oIlntIrvertIIIraI IIIIc By ....... interverrebral disc. The straighr leg raise is usually 90· , but may cause lower back pain and possibly referred pain in the leg. If the straight leg raise is limited, it is because of righr hamstring muscles and not nerve root tension. The sensation, strength, and reflexes of the legs are symmetrical and normal. In discogenic pain, the anterior primary rami traversing the disc are not irri -
tated or compressed, so there is no radiculopathy, no nerve root tension signs, or signs of neurologic
deficit (6,11).
SCIatIca without NetI'OIogIc DeftcIt In! Sclallca willi NetI'OIogIc Deftcll Patients with sciatica also have back pain and leg pain; however, the leg pain is typically mo re severe than the back pain (9). Sometimes, the parient has leg pain only. Lumbar spine flexion
Rgure 23--1
431
and prolonged sitting provoke the leg pain, which is sharp and superficial, easily outlined by the patient's fingers, and usually no more than 110 inches wide down the back or side of the thigh and calf (6). Bearing weighr on the side of sciarica may be painful and cause the parient ro limp, and a list of the trunk may be observed . The patient also may feel tingling, cold, numb, or cramping sensations in the calf (16). On examination of patients with sciatica, lumbar spine flexion is severely limited because of leg pain, and the patient's knee may bend on the side of sciarica. Again, lumbar spine flexion is more painful rhan extension (9). The straight leg raise test is limited below 60· by sciatica (16). In a rrue positive straight leg raise test, rhe parient prevents movement beyond the onser of sciatica by raising the affected hip and pelvis off the table.
Palpation for lumbar spine tenderness with the patient seated.
432
The SUbml1lon Syndromes
A..... 23-Z Straight leg raise test. Parients with symptom amplihcarion or somatiza-
tion syndrome may resist the straight leg raising by pressing down against the examiner (1 7) . erve root tension can be confirmed
by
lowering
the straight leg 5° and dorsi flexing the ankle, or internally rotaring the hip. Patients with sciatica without neurologic deficit have normal strength, sensation, and
reflexes of the legs, whereas in sciatica with neurologic deficit there is ome combination of weakness, hyperesthesia, and diminished reflexes. One percent of patients with sciatica have cauda equina syndrome, recognized by the presence of severe sciatica, saddle anesthesia, bladder inconti -
nence, loss of anal sph incter tone, and diminished anal wink reflex (2,18). In summary, to diagnose intervertebral disc
synd rome it is important to identify that the back
pain and leg pain are mechanical and aggravated by lumbar spine flexion and prolonged sitting. To identify the specific category of intervertebral disc syndrome, it is important to find out which is more painful, back pain or the leg pain, whether there are sympwms of sciatica with nerve root tension signs, and whether there is neurologic
deficit.
Examination
d. 1nt8l'vartabrallllsc Syndrome
The examination should be organized according to patient position and comfort: first standing, then sitting, supine, and finally lying prone. With the patient standing, observe for will ingness to move, spinal deformity, a nd pelvic obliquity. Observe the range and pain response during lumbar spine flexion, extension, and lateral flexion, and identify the movement that causes the most
A
B
figIre 23-8
Sensa ti on resting
orrhe lower extremi ty. A, L4 dermato me. B, L5 dermatome. C, Sl derma to me.
434
The SUbluxaUon Sylldromlla
c IlgIre 23-8
For legend see p. 433.
pain . Measuring lumbar spine motion by visual inspection has poor reliability, and only large discrepancies can be estimated. The patient's pain response to each movement is probably more reliable and clinically meaningful. Next, have the patient repeated ly raise up on the toes, one foor at a time, and inspect for weakness and ask about calf muscle fatigue or cramping. Have the patient dorsiflex one ankle while keeping rhe heel on the floor. Press down on the forefoor and assess dorsiflexion strength and compare each side. Check for symprom amplification or somarizarion by simularing spine loading (gently press down on rhe rop of rhe head), and spine rorarion (rorare the patient's hips and pelvis in rhe same plane) (17). Neirher tesr should cause any lumbar spine nor leg discomfort, even in these patients who are
experiencing severe back pain . With the patient sitting, perform Kemp's rest, and then pal pare for renderness and stiffness over each posterior inrerverrebral joint of the rhoracolumbar spine (Figure 23-1). Anorher resr for symptom amplification or somatization is the disrracrion leg raising resr, which is performed by exrending rhe seared patienr's knee (17). Wirh rrue sciarica, rhe parient will arch backward wirh borh arms in extension (Tripod sign) . In symptom amplificarion, rhe resulrs of rhis test are inconsisrent wirh rhe supine srraighr leg raise rest (17). Wirh the patienr supine, record rhe angle and pain response during the straighr leg raise resr (Figure 23-2). If sciarica is produced before 60°, confirm nerve roor tension by lowering rhe leg 5° and dorsiAexing rhe ankle and internally roraring
A
B
fIIIn 28-4
Strength testing of the lower extremity. A, L4 myotome. B, LS myotome. C, S1 myorome.
TIle SlMlxatlon Sy,*_
436
c figIre 23-4
For legend sec p. 435.
the hip. Perform Faber, Patrick's, Gaenslen's, and hip range of motion and assess for coexistent
sacroiliac or hip joint pain . Check for femoral nerve root irritation by flexing the knee off the examining table with the hip extended. In upper lumbar nerve root irritation, pain is referred to
the anterior thigh (16). Check the sensation, strength, and reflexes of the L4, L5, and 51 nerve rOOtS (Figures 23-3, 23-4, 23-5) . If there is asymmetry, measure the circumference of the thighs and calves. With the patient prone, palpate for tenderness over the spina l joints, sacroi liac joints, and paraspinal muscles (Figure 23-6). Check for hip or sacroiliac joint pain by performing Yeoman's test. Observe the buttocks for gluteus maximus
muscle atrophy, and test this muscle for 51 mOtor deficit. Finally, palpate the length of the sciatic nerve for tenderness or masses.
Diagnostic Imaging Syndrome
0' Intervertebral Disc
Plain lumbar radiographs are indicated only if the patient meets specific criteria (19). For patients with mechanical lower back pain, the indications include age older than 50 years, sciatica with neurologic deficit, chronic and recurrent back pain, and pain not responding to conservative care.
These and other important criteria for radiography are discussed by Dr. John Taylor in Part I, Chapter 5. If the patient does not meet the criteria for radiographs, the clinician should wait 3
A
B
FIIIn 23·5 Reflex resri ng of the lowe r extrem ity. A, Patella r reflex (L4 ). B, Hamstring reflex (L S). C, Achilles reAex (5 I).
438
The ....atIon Syndromes
c Rgure 23-5
For legend see p. 437.
weeks before ordering films and on ly if there is no improvement (9). The diagnosis of intervertebral disc syndrome
tions and interpretation of advanced diagnostic imaging are described in detail elsewhere (19).
usually does not require advanced imaging. Most
OIHarendal Diagnosis or ~tervertebral Disc Syndrome
patients can be rreared conservati vely without confirmation of a disc abnorma lity on magnetic
The differential diagnosis of discogenic pain includes other sources of mechanical back pain
is based on the patient's clinical presentarion, and
resonance (MR) or computed tOmography (CT)
(poste rior
imaging. However, advanced imaging is necessary
myofascial pa in ), nonmecha nica l spine pathology
as part of a presurgical workup (9,20) . Patients with bladder or bowel incontinence, foot drop,
(spi ne metastasis, tumor, and infection), and
severe bilateral sciati ca, or severe progressive neu-
rologic deficit should have a consu ltation with an orthopedic surgeon or neurosurgeon specia li zing in treatment of the lumbar spine (18) . The indica-
joint
pain,
sacroi liac
joint
pain,
referred back pain caused by visce ral or vascu la r disease (14,15) . The differential diagnosis of sciatica includes spinal stenosis (ce ntra l or lateral), vascular claudication, and tumors of the cord,
nerve root, or nerve sheath ( 14,15).
439
fi111'123-8
Palpation for lum bar spine tenderness with [he patienr prone.
Natural History of Intervertebral Disc Syndrome
onl y 20% ever rerum ro work (2 1). Generally, after the first episode of acute back pain, the
Thorough understanding of the natural hisrory of recovery is essential for planning treatment and providing prognosis. Although the narural history of mechanical back pain, as measured by subject's self-reports of pain and by return ro work, is well established, it is uncertain whether discogenic back pain follows the same pattern of recovery as other types of mechanical pain. For acute mechanical back pain, 80% will return to work within 40 days of the onset of pain (2,2 1). The ourlook is not as favorable for chronic back pain causing disability. The probability of ever reru rning ro work 6 months after an episode of pain is only 50%, and after ·1 yea r,
pain from persisting longer than 3 months is critica l to prevent development of chronic disability syndrome (22) . The narural hisrory of sciarica also favors recovery. Weber and associates (23) prospectively followed 208 patients within 2 weeks o f the onset of sciatica. They found that after 4 weeks there was a 35-mm mean reduction of pain on the 100mm visual analogue scale, and that 60% of the patients were back ro work (23) . Bush et al. (24 ) prospectively followed the clinical and cr findings of 111 conservatively treated parients with sciatica . At 1 year, all patients had made satisfacrory clinical recovery; the average reduction of
patient recovers quickly. Preventing the patient's
440 pain was 94%, and 76% of disc herniations showed partial o r complete resolution (24).
Treabllent 01 Intervertebral Disc Syndrome Although the exact pathogenesis of intervertebral disc syndrome is unknown, it helps to show the patient what is causing his or her pain in simple terms and with spine models, diagrams, and radiographs (when taken). These educational tOols help the patient understand the condition and gain confidence in the diagnosis and treatment. It also helps to tell the patient that the soft tissues causing pain do not show up on radiographs, and that radiographs may initially be misleading. However, if the patient does not improve as expected within 3 weeks, radiographs should be taken. Manipulation often causes an increase in back pain during the first 2 weeks of treatment (20). This response is normal and shou ld not be confused with an adverse reaction. The patient shou ld be warned about this possibility and reassured if it occurs. An analogy may help the patient understand why treatment may hurt, but nor harm. For example, many pacienrs can relare
to the phenomenon of postexercise muscle soreness afrer a new or unaccustomed exercise. Like-
wise, transient increases in pain caused by manip· ulation may be seen as a beneficial effect of restOring mobility to stiff and painful spinal joints. Explaining that manipulation releases painful scar tissue, which relieves pain and restOres mobility, also may be helpful. Side-posture rotational manipulation (20,25) flexion-distraction mobilization (26-29), and extension mobilization (30) have been reported to be successful for the treatment of intervertebral disc syndrome. The choice of treatment often depends more on the clinical training of the individ ual practitioner than on the patient'S condition. Not surprisingly, there is a trend for practitioners to advocate one method of manipulation in preference to others. This approach, adVQC3r-
ing only one type of manipulation for all cases, may nOt always be in the patient'S best interest. Side-posture rotational manipulation that has undergone extensive study, including randomized controlled trials and prospective and retrospective case-control studies (31-34). Two controlled trials exami ned the use of Maitland manipulation for sciatica (31,32). and one study examined side-posture rotational manipulation (34). Nwuga (34) showed that side-posture rotational manipulation was more effective than exercises and heat. The manipulation group was treated three times a week for 4 weeks, and the comparison group received exercise and heat therapy at the same frequency and duration. At 6 weeks' follow-up. the manipulation group had significantly greater improvement in spinal mobility and straight leg raising. Kuo and Loh (33) studied 517 patients with lumbar disc herniation and reported that 77% had relief of pain, allowing them to return to their activities of daily living. Cassidy et al. (20) reviewed the evidence in suppOrt of side-posture rotational manipulation for intervertebral disc syndrome and discussed the reasons why rotational manipulation is safe and unlikely to damage a healthy or herniated disc. The most serious complication associated with lumbar spine manipulation is cauda equina syndrome; however, from 19 11 to 1989 there were on ly 10 reported cases (35) . Shekelle et a l. (36,37) calculated the rate of occurrence of cauda equina syndrome as a complication of lumbar spine manipulation to be less than one case per 100 million manipulations. Although manipulation is safe and can be effective, one mUSt use ca re during its application. Side-posture rotational manipulation requires ca reful positioning for optimal results (20) . The patient is positioned in the lateral decubitus position with the sciatica leg on tOp. In patients without sciatica, the side of greatest spinal joint tenderness is placed up, away from the table. In this position, the doctor contacts directly over the tender spinal joints and appl ies gentle mobilization (20). If mobilization aggravates the patient's
23
FIgIre 23-7
ChlrGpractic Management 01 ~ervlll't8bral DIsc Syndl'Olll8
441
Lumbar spine side-posture mobilization and manipu larion.
leg pain, it should be discontinued, and the patient should be repositioned by modifying the lumbar lordosis. If mobilization only provokes back pain, and can be tOlerated by the patient, then a high-velociry, low-amplitude manipulation is applied directly over the tender spinal joints (20). Figure 23-7 shows the positioning for sideposrure manipulation of a patient with left-sided discogenic back pain or left sciatica. Although the strongest evidence supportS the use of rotational manipulation, clinical observation suggests that flexion-distraction mobilization and extension mobilization also may be effecrive for lumbar intervertebral disc syndrome. Flexiondistracrion mobilization is performed with rhe patient prone on a specially designed flexion table
(26). The docror contacts over the spinous process directly above the symptOmatic joint and lowers the caudal end of the table to the point of resistance. The doctor then alternately lowers and raises the caudal end of the table through a range of motion of approximately 2 inches. This gentle mobilization is repeated up to 20 times, within patient tolerance (26,38). Lumbar spine extension mobilization is applied with the patient prone, resting on the elbows and slightly extending the lumbar spine (Figure 23-8,A) (30). If sciatica is provoked, the position is discontinued. If lower back pain is provoked and can be tolerated by the patient, the patient is instructed to relax the lower back muscles as much as possible and gently stretch the
442
A
B Rgure 28-8 Lumbar spine extension mobilization with the patient prone. A. Resting on the elbows and slightly extending the lumbar spine. B, Maximallumhar spine extension.
A
B
FiIII'I ~8 Deep pressure massage for relief of referred leg pain. A, Lumbar paraspinal muscles. B, Sciatic notch.
444
TIle S.luxatlon Syn"'_
c A..... 28-8
For legend see p. 443.
lumbar spine into extension. Further extension
mobilizarion can be produced by having rhe patient fully exrend rhe elbows w hile keeping rhe pelvis on rhe table (Figure 23-8, R). Any position, manipu lation, or mobilization that increases the patient's sciatica or neurologic deficir should be avoided, and rhe parient's symptoms and signs shou ld be closely monitored (20,38,39) . Remember, an increase in back pain during rhe firsr 2 weeks of rrearment is norma l and should nor be confused wirh an adverse reaction; however, an increase in sciatica or neurologic deficir is nor normal, and rhe rrearmenr should be modified or stopped. Orher modaliries may be beneficial for interverrebra l disc syndrome, including shorr-durarion resr (40), lumbosacral corset (41 ), rracrion (42),
ice, massage, and inrerferential e lectrical therapy.
Deep pressu re massage over rhe lumbar paraspinal muscles, sciatic notch, and calf muscles
may help relieve referred leg pain (Figure 23-9), and iliopsoas muscle srrerching may help relieve back pain (Figure 23-10). Tracrion also may provide pain relief and can be applied in various positions (42). Figure 23-11 shows lumbar spine gravirational traction applied with the lu mba r spine in flexion and extension (43). The effectiveness of different exercise programs for mechanical back pain has been studied, including stretching, strengthening, coordination,
and aerobic exercises (1,44-52). No one exercise is more effective than anorher for reducing back pain. Elnagga r et al. (45) found rhat flexion and extension exercises were equa ll y effective for
445
~
23-10
Iliopsoas muscle strerching.
reducing chronic low-back pain. Flexion exercises reduced the severity of pain by 37% and extension exercises reduced pain
by 330/0; however, the
difference was not statistically significant. The only significant difference between flexion and extension exercises was that flexion led to greater sagittal plane mobility within a short period (45) . Figure 23-12 shows lumbar spine flexion exercises, and Figure 23-13 shows strengthening exercises for the hip extensor and paraspinal muscles. Lumbar spine muscle strengthenmg, ba lance, and coordination exercises can be performed with the
gymnastic ball (Figure 23-14). Aerobic exercises and general fitness exercises a lso may be beneficial and a re reviewed elsewhere (50,5 1). Firefighters who had poor genera l fitness were 10 times
more likely to have back pain than those that were most fir. Back school education reduced the freq uency of reinjury and medical costs for ciry employees with lower back injuries (7). Brown et al. (7) found that 6 months after completion of a back school program, participants had half as many injuries and fewer medical
COSts
compared with
nonparticipants. Although they fou nd no statisticall y significant differences between the total cOSts for participants and nonparticipants, the actua l dollars saved by back school participation was of practical value to the city. Back schoo ls typically insrruct the patient in the anatomy and pathology of back pain, principles of body mechanics and lifting, and stress and
446
A
B FIg&re 28-11
Lumbar spine gravitarional rHlction. A, Air-cushioned weighdessness. B, Back bubble slides along the
spine for pinpoinr rraction.
symptom management, and show exercises for restoring trunk strength and flexibility. Several back school programs have been designed and are available for clinical use (53).
MedIcal and Surgical Consultations Patients with acute and severe pain may benefit from a short course of analgesic medication, which can relieve pain and enable them to remain act ive and participate in conservative treatment (53). Patients with bladder or bowel incontinence, foot drop, severe bilateral sciatica, or severe progressive neurologic deficit shou ld have a presurgical eva luation by an orthopedic surgeon
or neurosurgeon special izing in treatment of the
lumbar spine (9) . Acute cauda equina syndrome is an absolute surgical indication, and debilitating SCiatica with progressive motor deficit not responding to conservative care is a relative indi-
cation (14, 15,18) . Besides the rare acute cauda equina syndrome, which is a surgica l emergency, patienrs with intervertebral disc syndrome deserve consec-
vative treatment before being considered a candidate for surgery. Weber (54) followed patients with herniated discs for 10 years and compared those treated surgically with those treated with bed rest, back school, and exercise. At the end of
23
A
B
CI ....p..actic MIIIIgement 01 ~v8l'l8bralllllc Syndrome
447
448
TIle SWIIuxation SyndI_
c D
RgIre 28-1! Lumbar spine flex io n exe rcises. A, Single leg pull to the chest. B, Both legs to the chest. C, Pir iformis muscle stretch. 0, H amstring muscle stretch.
23 C,*,opl'lC1lc Management 01 ~artaIIraI iliac Sylllrome
~
n13 Strengthening exercise for the hip extensor muscles and lumba r paraspina l muscles.
RtIII't 23·14
Gymnastic ball exe rcise.
449
450 1 year, the surgical group was significanrly berrer than the conservative group; however, at 4- and 10-year follow-up intervals, there was no significant difference between the groups. Shvartzman et al. (55) also found no significant difference in outcome and 5-year treatment costs of surgically and conservatively treated patients. They concluded that patients not responding to an initial 3-month trial of conservative therapy should not be managed surgically if they have not deteriorated. The option to undergo surgical or conservative therapy should remain with rhe patient. Many other studies clinically and radiographically confirmed the benefit of conservative therapy for the treatment of intervertebral disc syndrome (56-60).
Conclusion Chiropractic manipularion is a well-established treatment for mechanical back pain and is gaining recognition as an effective treatment for lumbar spine intervertebral disc syndrome. When carefully applied, and with exercise and education, chiropractic manipulation can relieve' pain and neurologic deficit, shorten the recovery period, and prevent the development of chronic pain and disability syndrome.
RefIll'flllCllS 1. Spitzer WO, er al. Scientific approach to the assessment and management of activiry-relared spinal disorders: a monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine 1987; 12:51-559. 2. Andersson GBJ. The epidemiology of spinal disorders. In: Frymoyer JW, ed. The adult spine, principles and practice. Vol I. New York: Raven Press, 1991:107--46.
3. Fardon D. er al. Terms used for diagnosis by English speaking spine surgeons. Spine 1993; J 8(2):274-7. 4. Weisel SW, et al. A study of computer-assisted tomography. I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1984; 9(6):549-51. 5. Hitselberger WE, Winen RM. Abnormal myelograms in asymptomatic patients. J Neurosurg 1968; 28:204-6 . 6. Bogduk N, Twomey LT, eds. Clinical anatomy of the lumbar spine. 2nd ed. Melbourne: Churchill Livingstone, 1991,151-73. 7. Brown KC, et al. Cost-effectiveness of a back school intervention for municipal employees. Spine 1992; 17(10), 1224-8.
8. Brown MD. The source of low back pain and sciatica. Semin Arthritis Rheum Suppl2, 1989; 18(4):67-72. 9. Hall H. A simple approach to back pain management. Patient Care 1992; 15(Oec):77-92. 10. Schwarzer AC, et al. The relative contributions of the disc and zygapophyseal joint in chronic low back pain. Spine 1994; 19(7),80 1-6. 11. Bogduk N: Pathology of lumbar disc pam. Manual Med 1990; 5(2). 12. Mundt DJ, et al. An epidemiological study of nonoccupational1ifting as a risk factor for herniated lumbar intervertebral disc. Spine t 993; t 8(5):595-602. 13. Riihimaki H, et al. Incidence of sciatic pain among men in machine operating, dynamic physical work, and sedentary work. Spine 1994; 19(2),138-42. 14. Oeyo RA. Early diagnostic evaluation of low back pain. J Gen Intern Med 1986; I (SeptlOCl),328-38. 15. Deyo RA, Rainville J. Kent DL. What can the hislory and physical examination tell us about low back pain? JAm Me
451 29. Sanders M, Stein K. Conservauve management of herniated nucleus pulposes: treatment approaches. J ManIpulative PhYSLol Thcr 1988, 11(4);309-13. 30. McKenzie RA. The lumbar spine: mechanical diagnosis and therapy. Waikanae, New Zealand: Spmal Publications. 1981. 31. Coxhead CE, et 011. Multicentre trial of physiotherapy m the management of sciatic symptoms. Lancet 1981; 1;1065-8. 32. Edwards BC: Low back pain and pam resulting from lumbar spine conditions: a comparison of treatmenr results. Aust] Phys;o11969, 15;104-10. 33. Kuo PI>-F, Loh Z-c. Treatment of lumbar intervenebral diSC protrUSions by manipulation. Clin Orthop 1987; 215;47-55. 34. Nwuga VC. Relative therapeutic efficacy of venebral manipulation and conventional treatment in back pain management. Am J Phys Med 1982; 61 :273-8. 35. Haldeman S, Rubinstein SM. Cauda equma syndrome in patients undergoing manipulation o( the lumbar spine. Spine 1992; 17(12); 1469-73. 36. Shekelle PC: Spme update: Spmalmanipulation. Spine 1994, 19(7);858-61. 37. Shekelle PC, et al. Spinal manipulation (or low-back pam. Ann Intern Med 1992; 117(7);590-8. 38. Ilubka MJ, et al. Lumbar intervertebral disc herniation: chiropractic treatment usmg flexion. extension, and rotational manipulative therapy. J Chiropractic Technique 1991,3(1);5-12. 39. Donelson R, Silva G, Murphy K. Ccnrraliz..1tion phenomenon: Its use(ulness in evaluating and treating referred pain. SPin, 1990; 15(3);211-13. 40. Deyo RA, DLehl AK, Rosenthal M. How many days o( bed rest (or acute low back pam? A randomized clinical trial. N Engl] Med 1986,315(17);1064-70. 41. Nachemson AL. Orrhotic rreatmenr (or injuries and diseases o( the spmal column. Phys Med Rehabil: State o( the Art ReViews 1987; 1(1):11-24. 42. LJunggren AE. Weber H, Larsen S. Autotraction versus manual fraction in patients wuh prolapsed lumbar inrervertebral diSCS. Scand J Rehahll Mcd 1984; 16: 117-24. 43. Back bubble, manufactured by the Chananooga Corp. Back Bubble Inc., P.O. Box 1285, SohUla Beach, Califor",.92075,(800) 457-7246. 44. Cady lD, et al. Strength and fitness and subsequent back injuries In firefighters. J Occup Med 1979; 21 (4):269-72. 45. Flnaggar 1M, et al. EHecrs o( spmal flexion :md extension exercises on low-back pain and spmal mobiliry in chronic mechanical low-back pain pauents. Spine 1991; 16(8);967-72.
46. Faas A, et 31. A randomized, placebo-controlled trial o( exercise therapy in patients with acute low back pain. Spllle 1993; 18(11); 1388-95. 47. Hansen FR, et al. ln tensive, dynamic back-muscle exercises, conventional phYSiotherapy, or placebo-conrroI treatment o( low-back pain. Spine 1993; 18( 1):98-108. 48. Manniche C, et al. IntenSive dynamic back exercises (or chronic low back pain: a climcal trial. Pam 1991; 47;53-63. 49. McCune DA, Sprague RB. Exercise (or low back pam. In: Basmajian jV, Wol( SL, cds. Therapeutic exercise. 5th cd. Baltimore: Williams & Wilkins, 1990:299-321. 50. Nutter P. Aerobic exercise in the trcatmenr and prevention o( low back pam. Spine: State o( the Art Reviews 1987; 2(1);137-45. 51. Rodriquez AA, Bilkey Wj, Agre Jc. Therapeutic exercise in chronic neck and back pam. Arch Phys Mcd Rehabil 1992,73;870-5. 52. Spran KF, Ct al. F(ficacy of flexion and extension treatmentS incorporatmg braces (or low-back pain patient) with retro(itsplacemem, spondylolisthesis, or normal sagittal translation. Spine 1993; 18( 13): 1839-49. B. Injury prevention technologies: back school programs. 21343 Cold Springs lane, Suite #443, Diamond Bar, Califor",. 9 1765, (909)598-6344. 54. Weber H: Lumbar disc hermation: a conrrolled prospective study with ten years o( observation. Spine 1983; 8;131-40. 55. Shvartzman L, et al. Cost-effectiveness analysis of extended conservative therapy versus surgical inrervenrion m the management of herniated lumbar intervertebral d;sc. Spllle 1992; 17(2); 176-82. 56. Debuche-Cavallier M, et al. lumbar disc herniation. computed tomography scan changes after conservative treatment of nerve rOOt compression. Spme 1992; 17(8);927-33. 57. Ellenberg MR, ct al. Prospective evaluation o( the course o( disc herniations in patients with proven radiculopathy. Arch Phys Med Rehab;) 1993; 74;3-8. 58. Maige j, Rime H, Deligne B. Computed tomographic (ollow-up study of (orry-eight cases of nonoperauvely treated lumbar intervenebral disc herniation. Spine 1992; 17(9);1071-5. 59. Saal JA, Saal JS, Henog RJ. The natural history o( lumbar intervertebral disc extrusions treated nonoperatlvely. Spone 1990, 15(7);683-6. 60. Alaranta H, et al. A prospective study o( patients with sciatica. Spine 1990; 15(12):1345-9.
Sacroiliac Subluxation Syndrome David M. Panzer Meridell. Gatterman
Key WOrds
Sacroiliac subluxation syndrome, track-based motion, closed kinetic chain
After reading this chapter you should be able to Qflswer the following questiotls:
Question #1
What three joints make the pelvic ring an atypical spinal motion segment?
Question #2
How may the track-bound motion of the sacroiliac joints contribute to the sacroiliac subluxation?
Question #3
What single activity is most likely to aggravate the pain from sacroiliac subluxation syndrome?
453
M
anipulation of the sacroiliac joints for
(he treatmem of sacroiliac subluxation
has been described in chiropractic literature since the earliest textbooks (1-5). Ignored as a cause of back pain by traditional medicine after Mixter and Barr (6) focused attention on disc herniation and surgery in 1934, the sacroiliac joints until recently were not commonly considered to be mobile enough ro cause significant dysfunction from restricted motion. It is now recognized that the sacroiliac joints arc moving, weight-bearing,
synovial joints that exhibit the same characteristic subluxation and joint dysfunction that plagues other diarthrodial joints. They are subject ro reversible joint blockage (manipulable subluxations) that occur within their limited range of
motion, frequently at the extreme of possible range of movement. They become irritated and have a tendency ro hypermobility when motion at adjacent articulations is restricted. They are prone ro develop degenerative disease, as do
been described as track bound, with opposing joint surfaces moving along and directed by a convex ridge on the iliac surface that glides in a concave sacral depression (12) (Figure 24-1). The axis of this rotation has not been consistently described and may shift with minimal translatory movement. The slight translation observed has been described as giving the joint a shock absorption capability (13). The twO posterior joints and the anterior symphysis pubes have been likened to an atypical motion segment, with the sacroi liac
joints guiding motion, as do the posterior facet joints and the symphysis pubis, providing slight translation in a manner similar to the intervertebral discs ( 14 ). This three-joint complex is a c1osed-kinetic-chain, with each articulation having determinate relations with each of the other joints in the pelvic ring ( 15 ). Gillet and Liekans (16) described the sacrum as floating within the
other synovial joints.
Sacroiliac Joint Motion Although sacroiliac joint motion is commonly considered ro be very slight (3° ro 5°), it has been demonsrrated in both anatomic specimens and
living subjects (7-9). Several factors affect sacroiliac motion, including age, gender, and configura-
tion of the joint surfaces with complementary ridges and depressions. The degree of sacroiliac motion decreases with age more rapidly in men than in women. Female sacroiliac joints tcnd
[0
be flatte~ with a wider retroarricular space and longer interosseous ligaments, all promoting greater mobility (10). Reversible ligamentous laxity has been observed with pregnancy and to a lesser degree during the menstrual cycle, attributed ro the hormone relaxin (1 I). Both translation and rotation (Chapter 1) have been described as normal motion in the sacroiliac articulations. The primary movement pattern has
F81'124--1 Motion of the sacroiliac joinr primarily occurs in the oblique sagittal plane, with the axis of rotarion centered around rhe iliac tubercle. The joint surfaces appear ro move along the tram tfrail, the convex ridge of the iliac surface gliding in the sacral grooves. (From Mior S. Canadian Memorial
Chiropractic College).
454
The SUbluxation Syndi'Oll18l
pelvic ring, cushioning the slight amount of observed physiologic movement. They developed a method of monitoring this movement using palpation with the back of the hand to challenge end feel of the sacroiliac joints (Figure 24-2).
Jomt may be forced into a new pOSItion where ridge and depression are no longer complementary. They note that this abnormal joint position may be regarded as a blocked joint (manipulable subluxation) . It is thought that the resultant restriction of movement or aberrant motion
Sacroiliac Subluxation Sacroil iac subluxation may take the form of simple joint locking or this may be accompanied by compensatory hypermobility in adjacent joints, especially in menstruating and pregnant females . Vleem ing et aJ. (17) state that it is theoretically possible that with abnormal loading a sacroiliac
that occurs from a shift in the normal axis of rotation then produces a sacroiliac subluxation
syndrome. The characteristics of a sacroiliac subluxation have been described by Turek (18 ) as ligamentous stretching sufficient enough to permit the ilium to slip on the sacrum as an irregular prominence on one articular surface
becomes wedged on another prominence of the other articular surface. He states that this is consistent with surface irregularities that have been noted on examination of the sacroi liac joint su rfaces.
Clinical Considerations The clinical findings associated with sacroiliac subluxation syndrome are described by Turek as intense muscle spasm accompanied
by severe pain
(18). The cause of sacroiliac subluxation is often indicated by the patient'S history. Frequently they describe a fall on the buttocks or a lifting injury that involved torsional stress . Stepping off of a cu rb or twisting such as getting out of bed have been reported (14).
Pain Pattern The pain of sacroiliac syndrome is typically located over the ipsi lateral buttock, dull in character, and made worse on sitting. It occasionally
Ag1I'824-2 The screening method urilized by Giller used rhe dorsum of the hand ro challenge end feel.
may extend down the lateral and posterior calf, occasionally as far as the ankle, foot, and toes (Figure 24-3). Sensory changes rarely occur bur occasionally take the form of paresthesias in the ipsilateral lower extremity. Pain referred from the sacroiliac joints is experienced in the posterior dermatomal areas of LS, 51, and 52, radiating over the sacrum and into the buttocks. Pain referral from the anterior ligaments radiates into the anterior derm.tomal areas of L2 and L3, particularly into the thigh region immediately below the
455
• XX XX Xx
•••
F11P'124-8 Pain parrern of a patient with a right sacroiliac syndrome. (- , aching; x, burning; -, numbness.) (From Catterman MI. Chiropractic management of spine related disorders. Baltimore: Williams & Wilkins, 1990.)
groin (19,20) . Pain from a hypermobile sacroiliac joinr also may be experienced in the ipsilateral hip because of contraction of the ipsilateral piriformis muscle, which originates at the sacrum and ilium (Figure 24-4) . A hype rmobile joint generally stabilizes within 3 to 6 weeks when abnormal motion is restricted
by a trochanteric support
bandage (Figure 24-5). Localized tenderness is produced on palpation of the subluxated sacroil-
iac joint. The patient also may exhibit a li mping gait to minimize pain on weight bearing.
Although localized pain and tenderness have demonstrated higher interrater reliability than other palpatory indicarors such as motion pa lpation, misalignment palpation, and muscle tensio n
palpation (21), pain alone cannOt be considered the major criteria for diagnosis of subluxations. Nonmanipulable subluxations in which force-
456
xx xx xx x x x
Piriformis syndrome. Trigger poin(~ (.) located near the belly and insertion of the piriformis muscle refer pain (x) in a characterisric partern. (From Calterman M l. Chiropractic management 0/ spine related disorders. Baltimo re: Wiilliams & Wilkins, 1990.)
f1111'124-4
FIgIre 24-5 A hypermobile joint can be stabilIzed with a right elastic rrochanreric bandage. The sacroiliac joint is generally stabilized within 3 to 6 weeks with this form of continuous stabilization. (From Gatterman. Chiropractic management of spme related disorders. Baltimore: Willtams & Wt/kilts , 1990.)
Pelvic Compression Pain, especially in irritated or inflamed joints, can indicate sacroiliac involvement when compression
ful manipulation is contraindicated may exhibit pain and tenderness from hypermobility and, III extreme cases, instability (see Chapter 8).
Tests lor Sacroiliac Dysfunction Sacroiliac dysfunction can be detected by a number of orthopedic tests. As with other areas of the spine, however, the manipulable subluxation is best detected through motion palpation. Specific rests detect sacroiliac involvement, bur give no indication as to whether manipulation is indicated.
is applied to the pelvis. Pressure can be applied to the iliac crests with the patient lying on the side or supine (Figures 24-6). Pain provoked in the sacroiliac regions indicates a positive test in any of these positions, but does not differentiate the exact nature of the sacroi liac problem or give an indication of the appropriate treatment.
FigII'8 of FoIr (FABRE) Test The acronym FABRE stands for flexion, abduction, external roration, and extension, which forms a figure of four when the thigh is passively put through these movements (Figure 24·7). Pain can be localized to either the ipsilateral hip or sacroiliac joints by this rest.
24 Sacrollac SUI*Ixatlon Syndrome
457
B A
Flgll'824-8 Co mpression applied to the il iac cresr(s) with the patient side lying (A) or supine (8 ) may produce pain in irritated o r inflamed sacro ili ac joints. Sacroiliac involvement is also suspected jf pain is prod uced whe n sacroiliac joint fun ction is provoked by press ure a ppl ied to se para te th e ili ac crests (C).
c
458
A
B
Rgure 24-1 A, Joint play ar rhe hip can be resred by moving the knee through an arc beginning with the
knee and thigh flexed, adducred, and internally rotated, and B, ending with the thigh flexed, abducted, and externally rotated. C, Pain in the sacroiliac joinr can be differentiated from hip pain by the Patrick Fabere test. (Figure C From Catterman. Chiropractic management of spine related disorders. Baltimore: Williams & Wilkins, 1990.)
24
A!111'124-8
Sacroiliac Subluxation Syndrome
Normally the straight leg can be raised to Q
90° without discomfort. Pain at 45 Of, less particularly, of the electric shock type that radiates into the feet, the back, or the opposite side indicates nonspecific irri tation of the sciatic nerve or root. Pain produced from 70° [0 90° and localized to the sacroiliac joint is more indicative of a sac roi liac lesion. (From Gattenllon. Chiropractic management of spine related disorders. Baltimore: WilUams & \Vilkins, 1990.)
A!111'124-8
Hyperextension of the ipsilateral thigh
produces pain with lesions of the sacroiliac joint. (From Cotterman. Chiropractic management of spine related disorders. Baltimore: Williams &- Wilkins, /990.)
459
460 Straight Leg RaIse (SUI, Lasegues' SIgn) Raising the straight leg is used in detecting sciatic nerve irritation and also can indicate sacroiliac involvement when pain is localized to the ipsilat-
eral articulation. Sciatic involvement is generally pain producing when the straight leg is raised to less than 45°, whereas the rest becomes positive for sacroi liac dysfunction when raised between 70° and 90° (Figure 24-8).
ThIgh Hyperextension (Yeomam's Test) Pain localized to the sacroiliac joint on hyperextension of the ipsilateral thigh indicares a test positive for sacroiliac involvement bur nOt the nature of the problem. Performed with the patient in the prone position, extension of the thigh is often noticeably restricted in the sa me
side as the pain with a sacroi liac subluxation (Figure 24-9).
RadOlll'aphIc AndIngs The sacroiliac joints are difficult to visualize radiographically and are best viewed with the beam passing posterior to anterior. Plain fi lm radiographs cannor detect a manipulable subluxation, a lthough several marking systems have been used to detect pelvic misalignment. Pelvic instability can be demonstrated by radiokinetic tests that stress the sacroi liac joints and the symphysis pubis (Figure 24-11, A, B, C). The patient stands
fIgIre 24-10
E
Pelvic instability can be demonstrated by
radiok inetic reSts that stress the sacroiliac joints and
the symphysis pubis. In A, the patient is standing with the weight evenly distributed for the neutral PA view of [he symphysis pubis. In B, the patient is standing on [he lef[ leg while [he right leg hangs free. Note [he superior sheer of the left pubic bone. In C, the patient is standing on the right leg while the left leg hangs free. The pubic bones are now aligned. (From Catterman. Chiropractic management of spine related disorders. Baltimore: Williams & Wilkins, 1990.)
c
461
• ..--r; ) J
Sitting
B
- I Lying
Rg&re 24-11
Relative changes observed in functional
leg length durmg change from supine to sitting position
when a simple sacroiliac subluxation/fixation is present. Leg A rcprcsenrs the side of the PI ilium (flexion malposlfion) and leg B the AS ilium (extension malposition). Because of the relative anterior
displacement of the acterabululll resulting from the flexed ilium (and opposite for rhe extended ilium), the
leg that is functionally shorr reverses as rhe patient sirs and the hip Jomt is flexed ro 90°, (From Cotterman. Chiropractic management of spme related dIsorders. BaIt/more: \'(ItlJimm
& \,(/ilkms, 1990. )
on rwo blocks approximarely 6 inches from the Aoor. The blocks are alternately removed to allow one leg to hang free (22). A neutral view with
inclusion of the sacroiliac joints in all views is recommended. Instability of the sacroiliac joints is confirmed by separation of the symphysis pubis in the vertical plane (23).
Mechanics 01 Sacroiliac Subluxation and Dysfunction Because motion of the sacroiliac joint occurs largely in the sagittal plane (24) (Aexion and extension) (25), it is not surprising that rhe plane of blocked sacroiliac joint motion is generally nexion or extension with accompanying malposition in this plane. The ilium, fixed in a flexed position in relation to the sacrum, has been termed a PI (posteroinferior) ilium, wirh rhe pos-
462 terior superior iliac spine (PSIS) as the reference point (26). The AS (anterosuperior) ilium describes an ilium fixed in an extended position. When the ilium flexes, the following occurs (26): 1. PSIS moves posteriorly and interiorly 2. ASIS (anterior superior iliac spine) and ipsilateral pubis move superiorly 3. Acetabulum moves anteriorly, laterally, and slightly superiorly, causing functional shortening of the leg 4. Sacrum moves relatively anteriorly and interiM orly on the ipsilateral side (25) Opposite movements occur during iliac exten-
sion. Among the findings mentioned is the movement of the acetabulum. When the pelvis becomes locked in a torqued position with one ilium in extension and the other in flexion, the relative position of the acetabulae may be different enough to result in measurable difference in functional leg length (Figure 24-11). It is important to nOte that this phenomenon is quite distinct from anatomic leg length discrepancy (26) and is generally correctable with appropriate sacroiliac manipulation. Common postural features of funcrional and anatomic leg length discrepancies are unleveling of the greater rrochanters and/or iliac crests while standing. Alterations 10 the static alignment of anatomic landmarks may also assist in the diagnosis and classification of sacroiliac subluxation (25). Table 24-1 gives examples of common palpatory characteristics that differentiate a flexion malposition (PI ilium) from an extension malposition (AS ilium) (25,26).
Common palpatory characteristics which differentiate a flexion malposition (PI ilium) from an extension malposition AS ilium) ~
.
~
.
~.
"
;~
,.,-.
r....
.;."
..\-
PI
AS
1. Prominent and inferior PSIS 2. Superior positioned ASIS 3. Functionally shorter leg supine, prone and standing 4. Functionally longer leg sitting (see Figure 24-11)
1. Less prominent and superior PSIS 2. inferior positioned ASIS 3. Functionally longer leg supine, prone and standing 4. Functionally
5. Lower iliac
5. Higher iliac
crest (standing)
1
shorter leg sitting
(see Figure 24-11) crest (standing)
sacrum and ilium while the patient raises and
lowers each leg (Figure 24-12). Although these standing motion tests are widely used, intraexam-
palparory examination of comparative sacroiliac
iner reliability has been shown to exceed interexaminer reliability, and the validity of these procedures has yet to be fully demonstrated (28). Palpation of overall sacroiliac movement may be complicated by aberrant motion that may occur because of a shift of the axis of rotation caused by subluxation. Another teS! for sacroiliac pathomechanics is the "sacral push." The doctor sits behind the seated patient with thumbs spanning the space between the PSIS and the sacral base (across the sacroiliac joint). As the patient extends the torso, the sacral base glides anteriorly and can be followed by the doctor's thumbs (25). Motion in the oblique coronal plane can be monitored by having the patient flex and laterally bend to each side as if to tie their shoe. Restricted motion in this plane is moS! easily restored by using a sacral
motion by palpating the relative motion between
contact.
A survey of current texts used in chiropractic
education shows a variety of dynamic examination procedures that are used in addition to the aforementioned static tests (19,20,25,27,28). These dynamic procedures are directed at the assessment of sacroiliac function. Perhaps the most widely used of these tests is the standing
24 S8C1'OIIIIc Slauxallon SyID'ome
B
A
f1111'124-12 A, Relative morion of (he left sacroili ac joint is palpated with the rhumb placed over the second sacral tubercle and the other ove r the PSIS. B, With
normal motion, the PSIS moves downwa rd I to 2 em as the leg is raised. C, If the joint is fixed the PSIS does nor move downward.
c
463
464
~ 24-14
The patient with a sacra l rotational fixation is positioned in side postu re, with the side of fixation involvement placed down . The hand contacts the upper portion of the sacrum, and with a scooping
motion the thrust is delivered anteriorly, away from (he
locked joint. detect abnormal resistance to specific gliding movements or the presence of increased pain ro identify potential sacroiliac dysfunction (25).
figure 24-18 Relative motion in the oblique corona l plane can be monitored by having the patient flex and laterally bend (0 each side as if to tie their shoe .
The preceding tests are examples of tests that evaluate sacroiliac range and qua lity of motion. Another dynamic palpatory procedure used in evaluation of sacroi liac joint function is joint play
exam ination. Joint play motions are completely passive in nature, that is, they acc produced entirely by the doctor without active movement of the patient. These movements can be produced with the patient sitting, prone, or side-lying a nd are thoroughly described in current chiropractic procedural texts (25). Joint play tests seek to
Treatment 01 Sacroiliac Subluxation Syndrome The treatment of choice for sacroiliac subluxation syndrome is specific manipulative therapy (Figure 24-14) directed at the sacroi liac articulations (14,19,20,25) . Prospective clinical studies have shown a successfu l response in more than 90% of patients receiving daily manipulation over a 2- ro 3-week period for chronic disabling sacroiliac syndrome (19). Mobilizing and stretching techniques, as well as exercises, also can be helpful in the management of this condition (29).
References I. Smith OG, Langworthy SM, Paxson Me. Modernized
chiropractic. Vol 2. Ceda r Rapids, Iowa: L1wrcnce Press, 1906,217-73.
24 Sacrollac SUbluXallon Syndrome
" - " 24-16 The side pos[Ure technique for manipulation of a right superior sacroiliac joint fixation has the doctOr's stabil izing hand rracrioning the patient's supe rior shou lde r while the thrusting hand contactS the affected ilium. The manipulative thrust is directed through the ilium, down the thigh and the long axis of the patient's flexed leg. The patient's superior leg is tcactioned with the doctor's inferior thigh, and a body drop is simultaneously instituted as the thrust is delivered. 2. Palmer 8J. An exposition of old moves. 2nd ed. Davenport, Iowa: Palmer School of Chiropractic, t 91 1: 121-2. 3. Gregory AA. Spina l treatment: auxiliary methods of frear· ment. 2nd ed. Ok lahoma City: Palmer-Gregory College, 1912,545-9. 4. Carver W. Carver's chiropractic analysis of chiropractic principles as applied ro pathology, reiafOlogy, symptoma· (Ology, and diagnosis. Vol I. 3rd ed. Oklahoma Ciry: Paul Parr, 1921. S. Forester AL. Principles and practices of spinal adjustment. Chicago: National School of Chiropracric, 19I5:374-S. 6. Mixter WJ, Barr JS. Rupture of the intervertebral disk with involvement of the of spinal canal. N Engl J Mcd 1934; 211,220. 7. Weisl H. The movement of the sacro· iliac joinr. Acta Anat 1955; 2],80-89. 8. Colachis SC Jr., Warden SC, Bechral CO, Strohm BR. Movement of the sacroiliac joint in the adult ma le: a pre· liminary report. Arch Phys Med Rehabil 1963; 44:490-8. 9. Frigerio NA, Srowe RR, Howe JW. Movement of the sacro-iliac joint. Clin Orthop 1974; 100:370-7. 10. Bowen V, Cassidy JD. Macrocopic and microcopic anaromy of the sacro-iliac joint from embryonic life until the eight decade. Spine 198 I; 6:620-8.
o
465
II. Maclennan AH. The role of the hormone relaxin in human reproduction and pelvic girdle relaxation. Scand J RheumaroI 199 1;S88:7- 1S. 12. Kapandji IA. The physiology of the joints: the trunk and vertebral column. Vol 3. New York: Churchill Living· stone, 1974:S9. 13. Wilder DG, Pope MG, Frymoyer JW. The functiona l tOpography of the sacroi liac joint. Spine 1980; 5:S7S-9. 14. Ganerman M: Chiropractic management of spine related disorders. Baltimore: Williams & Wi lkins, 1990:111-12. 15. Brunstrum S. Clinica l kinesiology. 3rd ed. Philadelphia, FA Davis, 1979:11. 16. Gillet H, Liekans M. Belgium chiropractic research notes. 4th cd. Huntingron Beach, California: Motion Palpation Institute, 1981 :9. 17. Vleeming A, Volkers ACW, Snijders Cj. Stoeckerr R. Relation between form and function in the sacroi liac joint. Part II. Biomechanical aspects. Spine 1990: 15(2): 133-S. 18. Turek SL: Orthopedics principles and their application . 3rd ed. Philadelphia: JB Lippincott, 1977: 1469. 19. Cassidy JD, Mierau DR. In : Haldeman S, ed. Principles and practice of chiropractic. 2nd ed. San Mateo, California: Applewn and Lange, 1992:211-24. 20. Kirkaldy Willis WH , Burton CV. Managing low back pain. 3rd cd. New York: Churchi ll Livingstone, 1992,123-6. 2 1. Keating JC, Bergmann TF, Jacobs GE, Finer BA, Larson K. Interexaminer rel iability of eight evaluative dimensions of lumbar segmental abnorma lity. J Manipulative Physiol The< 1990; 13(8),463-70. 22. Ballinger PN. Merrill's atlas of radiographic positions and radiographic procedures. Vol I. 5th ed. St. Louis: Mosby,247. 23. Dihlman W. Diagnostic radiology of the sacroi li ac joints. Chicago: Year Book, 1980:12-16. 24. White AA, Paniabi MM. Clin ical biomechan ics of the spine. 2nd ed. San Francisco: JB Lippincott, 1990,1 12-15. 25. Bergmann TF, Peterson DH, Lawrence DJ. Chiropractic technique. New York: Churchill Livingstone,
1993A77-98. 26. Panzer DM. In: Gatterman MI. Chirop ractic management of spine related disorders. Baltimore: Williams & Wilkins, 1990,278-8 1. 27. Wa lters PJ. In: Plaugher G, ed. Textbook of clinical chiropractic. Ba ltimore: Wi lliams & Wilkins, 1993: 153-61. 28. Herzog W, Read LJ, Conway PJW, Shaw LD, McEwen Me. Reliability of motion palpation procedures w detect sacroiliac joint fixations. J Manipulative Physiol Ther 1989; 12(2),86-92. 29. Don Tigny RL. Mechanics & treatment of the sacroi liac joint. J Manual Manipulative Ther 1993; It 1):3- 12.3; 1(1),3- 12.
• Coccygeal Subluxation Syndrome John P. Mrozek
KeyWDrds
Coccydynia, pelvic diaphragm, anal verge
After reading this chapter you should be able to answer the following questions:
question #1
What is the correlation between coccygeal angulation and coccydynia?
Questloo #2
What is the procedure for reduction of a coccygeal subluxation?
25
COCCygeal SUbluXation Syndrome
P
ain in the coccygeal area is referred to as coccydynia in the relevant literature. Coccydynia was first described by Simpson in 1861 (1). He noted that when injury to the coccyx or surrounding tissue occurred, contraction of the muscles attached to the coccyx would elicit the characteristic pain of coccydynia (2) . The term, denoting a painful coccyx, indicates a symptom rather than a pathologic diagnosis. Hence one should determine the ca use of this condition when the taking the history. Coccydynia is described as occurring as a single clinical entity or in combination with other painful presentations such as low-back pain . The diagnosis in most instances relies a great deal on the elicitation of local pain and tenderness. The refractory nature of this complaint suggests a greater role for possible inclusion of psychogenic overlay in the differential diagnosis. The history and physical examination, however, show the local nature of this complaint. Local well-demarcated areas of pain are not generally associated with pain of psychogenic origin (3) .
Anatomic Considerations A number of structures are potentially implicated when coccydynia is encountered. The hard and soft tissues that make up the pelvis and lumbar spine constitute the clinical area of concern. Referred coccydynia can be the result of exrrasegmental reference from a lumbar disc lesion (3,4). Evaluation of the lumbar spine structures and appreciation of the relevant neuroanatomy arc necessary to ensure a proper
assessment. A diagnostic clue for the consideration of referred pain wou ld be found in the history. Although referred pain may persist in a number of body positions, local coccydyn ia mOSt often is present as the result of direct pressure as encountered by sirting (3) . The coccyx consists of usually four rudimentary vertebrae. Variations in segments of one less
467
or one morc also exist. The shape of the coccyx was seen as beaklike by early observers. The term coccyx is derived from the Greek word fo r cuckoo. The three inferior coccygeal segments often fuse in middle age. In old age the first coccygeal segment often fuses to the sacrum (5). The pelvic diaphragm and its immediate surround constitute the major muscular considerations when dea ling w ith the coccyx. For genera l purposes the pelvic diaphragm is formed by the levator ani and coccygeus muscles (Figures 25-1 and 25-2)
Levator AnI The levaror ani muscles form the posterior two thirds of the pelvic floor, and the anterior one third is formed by the perineal membrane, which bridges the pubic ram i inferior to the anterior fibers of the levator ani muscles. The levaror ani is penetrated by the ana l canal, and the perinea l membrane is penetrated by the urethra in the man and by the urethra and vagina in the woman . Origin: pelvic surface of the body of the pubis to the ischial spine Insertion : the central perineal tendon, the wall of the anal cana l, the anococcygeal ligament, the coccyx Action : raise the pelvic floor. This action assists the abdominal muscles in compressing the abdominal contents. This is important in coughing, vomiting, urinating, and trunk fixation during strong movements of the upper limbs such as lifting. Innervarion : third and fourth sacral nerves and the inferior rectal nerve
Coccygeus This muscle forms the posterior and smaller part of the pelvic diaphragm. Origin: the ischial spine Insertion: lateral aspect of the fifth sacral vertebra and coccyx
468
Sacrospinous ligament
Coccygeus muscle
Sacrococcygeal joint - - -....._-,-"" 1st intercoccygeal joint ----'~,,-';ili
r---:-;------
Levator ani muscle
Anterior socrococcygeal ligamen Anococcygeol raphe Anal opening Perineal body
FIgIre 21H
This illustration represenrs the relevant muscles and ligaments rhar pertain to the sacrococcygeal area
from the posterior view.
(From Duckworth, Friesen L.)
Action: supports the coccyx and pulls it forward after defecation and childbirth Innervation : fourth and fifth sacral nerves (5) The g luteus maximus a lso attaches to the coccyx. This anatomic reality must be taken into consideration when planning treatment of the coccygeal area. The gluteus maximus is the chief extensor of the thigh. The nerve supply is the inferior g luteal nerve. Both the innervation and
action must be assessed when formulating a treatment regimen. The relevant ligaments associated with the coccyx include the sacrotuberous, the sacrospinous, and the anococcygeal. In addition to their coccygeal attachment, the sacrotuberous and sacrospinous ligaments he lp resist sacra l nexion (between the innom inarcs) caused
by
gravita-
tional effects of erect posture. Sandoz refers to
lateral sacrococcygeal lig< ~~,G.~_-+
____
Coccygeus muscle Sacrospinous ligament
'-;-7T~--_ 4th sacral nerve Sacrotuberous ligament
5th sacral nerve Intercornual ligament
levator ani muscle Anococcygeal raphe
Perineal body
RIIN 25-2
External anal sphincter muscle
This illusrrarion represenrs rhe relevant muscles and ligamenrs rhat pertain ro rhe sacrococcygeal area
from rhc anrerior view. (From Duckworth, Friesen L.)
25
Coccygeal SUbluxation Syndrome
these structures as "check ligaments" of nuration (6). These two ligaments reinforce and add strength to the sacroiliac joint capsule (7) . The anococcygeal ligament is the median fibrous intersection of components of [he levator ani muscle. It is located between the anal canal and the coccyx (5) (Figures 25-1, 25-2). The actual configuration of the coccyx, particularly as seen on the lateral radiograph, shows an interesting pattern of variation. Observations vary from slight forward angu lation to partial dislocation that accompanies sharp forward angulation. These are radiographic interpretations and do not correlate necessarily with a
painful presentation. As indicated earlier, there is some variation in the fusion pattern of the coccygeal segments. Where coccygeal segmental movement is preserved, the first intercoccygeal joint represents the fulcrum of movements of the coccyx (1) . The greater the angulation, the greater the likelihood of developmental instability of the joint. Insult that stretches the articular and periarticular structures of intercoccygeal joint contributes largely to coccydynia .
Diagnosis Coccygeal area pain can present in a variety of ways. The general considerations include acute, chronic, loca l, and referred. As reported earlier, the low back has been cited as a locus of pain referral to the coccygeal area. Postacchini and Massobrio (1) noted a high incidence of back pain in patients with idiopathic coccydynia compared with the general population (1,8 ). Malbohan et al. (8) reported that the pelvic diaphragm was clinically involved in nearly a ll of the 1500 cases of low-back pain that they studied. Assessment of the pelvic diaphragm was recommended in cases of recurrent low-back pain. The symptoms and signs of acute and chronic coccydynia include pain with sitting, bowel movements, and intercourse. Point tenderness at the tip of the coccyx should be assessed.
469
Many aspects of coccygea l area pain can be evaluated on ly by internal rectal examination (9). The rectal approach allows for direct palpation of the coccyx and pelvic diaphragm . Tenderness of the levator ani and coccygeus ca n be ascertained with digital pressure applied to the areas latera l to the coccyx. Palpating the coccyx by contacting it with a lubricated gloved index finger internally and thumb pressure applied externa ll y a llows for assessment of relative mobility. This method allows the examiner to assess for coccygea l angulation. The coccyx should be moved anteriorly and posteriorly and side to side. Patient positio n for the rectal examination sho uld be prone with abdominal suppOrt or the lateral decubitus (Figure 25-3) . The histOry is integral to the formulation of a proper diagnosis. The historica l workup involves questions related to a number of conditions, including gastrointestinal, genitourinary, gynecologic, musculoskeletal, and psychologic ab normalities. The answers to inquiries regarding rhese a reas give clues to the understanding of the patient's complaint. For rhe chiropractor, the sacroi liac joint is high on the index of suspicion for referred pain. This joint mUSt be assessed and treated if indicated. A good general rule wou ld involve the reproduction of pain. That is, if the examiner can recreate the pain of the involved area, then the examiner can infer that the source of the complaint has been found. In this case, if joint challenge of the sacroi liac area reproduces the coccydynia, then the examiner can be reasonably sure that the source of the pain resides in the sacroi liac joint.
lreabllent Allowing that referred pain has been ruled Ollt, the treatment of choice for coccydynia is by direct means. Following the description outlined in the diagnosis section of this chapter, the gloved index or middle finger is inserted beyond the ana l verge
470
The SUbluXadoo 8YIIlll'Ol11l8
Pubic symphysis
r---'''''-..----+-+ - - - - - - 1 - + ;--------
~~~~'it~~~~:::=:~~~~==~~= :
Bladder Urethra
External anal sphincter Internal anal sphincter
Rectum External anal sphincter
Sacrococcygeal joint 1sf in,tercoccygeol joint
Infernal anal sphincter
FIgIre 25-3 The method of digital examination of the sacro·coccygeal area as seen from the latera l view.
(From
Duckworth. Friesen L.)
with the palmar aspect applied against the coccyx. The free hand is applied against rhe sacrum externally. Assuming an anterior or flexion subluxation
of the coccyx, pressure is app lied to rhe coccyx in a slowly increasing increments for approximately 40 seconds. If tOlerated, the practitioner can apply slowly increasing pressure to the sacrum to augment (he treatment.
The practitioner must always be mindful of [he patient'S reaction ro this pressure. This can best be monitOred by having the patient turn the head to the side if in the prone position. In this position the practitioner can view the facial response and observe for the customary reaction to pain. One must be careful not to proceed beyond the patient's tOlerance. While applying pressure, the practitioner can slowly sweep the contact finger from side to side of the coccyx, assessing the soft tissues in the area . This digital cOntact with the soft tissues can reduce tension in the pelvic diaphragm.
The application of digital pressure to the coccyx and the slow sweeping of the soft tissues should be repeated a second time while within the anal canal. The practitioner should then remove the gloved finger from the cana l and observe for blood, feca l, or other matter. The results of this procedure should be duly noted in the chart. In general, uncomplicated coccydynia should respond quickly to this type of treatment. Two or three treatments over a period of 7 to 10 days are usually sufficient to achieve alleviation of symptoms (10).
Acknowledgments The excellent drawings are provided by the skilled hand of J. W. A. Duckworth, MD . His contribution is greatly appreciated .
References I. Posracchini F, Massobrio M. Idiopathic coccygodynia: analysis of fifty-one cases and a radiographic study of the normal coccyx. J Bone Joint Surg 1983; 65A: 1 11 6-24.
25 COCCy..... SUI*IxItIon Syndrome 2. DiGiovanna EL, SchlOWltz S. An osteopathic approach to diagnosis and (tc-atment. New York: JB Lippincott, 1991,452-6. 3. Cyriax J. Textbook of onhopaedic medicine. Vol I. Diag· nasis of soft tissue lesions. 5th ed. London: Balliere, Tindall & Cass
471
7. Kirkaldy-Willis WHo Managing low back pain. 2nd ed. ew York: Churchill Livingstone, 1988:7 1. 8. Malbohan 1M, Mojzisova l, Tichy J. The role of coccygeal spasm in low back pain. Manual Med 1989i 4,140-1. 9. Zohn DA, Mennell JM. Musculoskeletal pain: Di3gnosis and physical treatment. Boston: linle, Brown, 1976,195-6. 10. M3igne R. Orthopedic medicine. Springfield: Charles C Thomas, 1972,315- 16.
Glossary AlII
atlanto-odontoid-inrerspace
• prIOrI from cause to effect, based on theory instead of experience ~
any chiropractic therapeutic procedure that utilizes controlled force, leverage, direction, amplitude, and velocity, and which is directed at specific joints or anatomical regions. Chiropractors commonly use such procedures to influence joint and neurophysiological function
ro put in a straight line; arrangement of position 111 a straight line _ _It
~
greatness of size, magnitude, breadth,
IIfIIIII'IIII
form of massage employing slow, rhythmic stroking executed with minimum force and light pressure
IIIIItIe de'''~llIdun any recoverable deformation IIIIIIIcIty property of a material or structure that returns it to its original form following the removal of the deforming load
_ 1liiy
(_,eel,
discrete, short-range movemenrs of a joint, independent of the action of voluntary muscles, determined by springing each vertebra at the limit of its passive range of motion
or range
enteric that portion of the autonomic
.1IICIIo1II prtICIIM'e includes categories and
nervous system that controls gastrointestina l activity
classifications of procedures, technologies, or equ ipment that have not received the benefit of the experimental method. Items included originate and depend upon experience and observation only
IIIIlInOaK the portion of the nervous system that is predominantly self-regulated and serves to control visceral function
CIIIIrII ..llll1zadun a state where neurons activated by noxious mechanical and chemical stimulation become sensitized by this input, making them hyper-responsive to all subsequent stimuli delivered to their receptive fields
IlIcIItIdun increase in afferent stimul i so that the synaptic threshold is more easily reached; thus, there is an increase in the efficacy of subsequent impulses in that pathway or synapse. The consequence of increased efficacy is that continued stimulation produces hyperactive responses
n.......
IrIc1Ian deep, circular massage to irritate or stimulate a muscle or increase its tonus and/or its arterial perfusion, or express swelling by moving the skin over the subcutaneous tissue
homIoItIIII maintenance of static or conStant
Cll'Vlc8lllI1c iIIIdIChII symptomatic head pain
conditions in the internal environment;
and cephalic dysfunction caused by subluxation of the spinal joint.
level of well-being of an individual maintained by interna l physiologic harmony
CGlllllllllldun changes in structura l relationships
hYPII~"""'IY excessive mobility of a motion segment that is not so severe as to be incapacitating, life-threatening, or require surgery
to accommodate foundation disturbances and maintain balance
473
474
instability excessive mobility of a motion segment to the extent that there is potential for development of incapacitating deformities or pain
as a result of strucrural changes in the articula r holding elements Intlll'llllll11ental motion relative motion taking place between two adjacent vertebral segments or within a vertebral motion segment; described as the upper vertebra on the lower
IICh8mIc compression application of progressively stronger painful pressure on a trigger point for the purpose of eliminating the point's tenderness; blanches the compressed tissue, which usually becomes hyperemic (flushed) on release of the pressure
joint play discrete, short-range movements of a joint, independent of the action of voluntary muscles, determined by springing each vertebra in the neutral position IItIng (dynamic) designation of the abnorma l movement characteristic of onc vertebra in relation to subadjacent segments. Dynamic listing nomenclature:
flexion restriction; extension restriction; latera l flexion restriction (right or left); rotational malposition (right or left) m~
lllllluxation subluxation in which altered alignment, movement, and/or function can be improved by manual thrust procedures
m-.latlon manual procedure that involves a directed thrust to move a joint past the physiological range of motion, without exceeding the anatomic limit
manual therapy procedures by which the hands directly contact the body to treat the articulations and/or soft tissues marie Iystem treatment of visceral conditions through adjustment of vertebrae at the levels of neuromcric innervation to the organs involved .
mobllzatlon movement app lied singularly or repetitively within or at the physiologic range of joint motion, without imparting a thrust or impulse, with the goa l or restoring joint mobility.
motion IlIIII118I1t a functiona l unit made up of the rwo adjacem arricularing surfaces and the connecting tissues binding them to each other. motor II1II functiona l unit of striated muscle comprised of the motOr neuron and all the muscle fibers supplied by the neuron.
myolllClal pain Iyndrome pain syndrome characterized by pain in regional muscles accompanied by trigger points that refer pain specifically to each muscle. myolasclalll'ltlllllr point hyperirritable spot, usua ll y within a taut band of skeletal muscle or in the muscle's fascia, that is painful on compression and that can give rise to characteristic referred pain, tenderness, and autonomic phenomena. palpation act of feeling with the hands; application of variable manual ptessure through the surface of the body for the purpose of determining the shape, size, consistency, position, inherent motility, and health of the tissues beneath. motion palpation: palpatory diagnosis of passive and active segmenta l joint range of motion . static palpation: palpatory diagnosis of somatic structures in a neutral static position. paIpatory IIIdIa sensory skills used in performing palpatoty diagnosis.
parasympathetic that portion of the autonomic nervous system that functions to store, conserve, and replenish body energy. pelrillage
same as kneading.
pIaatIc deformation
nontecoverable deformation.
plaatlClty property of a material to permanently deform when it is loaded beyond its elastic range.
475
GIoslII'y
poat hoc, .... propIIr hoc (latin) after this, therefore, because of this (a false reasoning)
structures
lIII*Ixatlan a motion segment, in which
11"'_" a population of autonomic neurons located in the central nervous system that have
alignment, movement integrity, and/or
axons innervating postganglionic neurons located
between joint surfaces remains intact
in the peripheral ganglia or viscera
(1011811.......
a population of autonomic neurons located either in peripheral ganglia or the wall of specific viscera, which have axons innervating viscera
putative
supposed, reputed
......x
result of transforming an ingoing sensory impulse into an outgoing efferent impulse without the act of will
renax lllerapy treatment thar is aimed ar stimulating afferent impulses and evoking a given response (i.e. neuromuscular) property of returning to the former shape or size after distortion
......1C8
IOI1IIIIc strucrures in the body wall and limbs are referred to as somatic structures
-1DtIfII"
physiologic funcrion are alrered although contact
lIII*Ixatlan complex a theoretic model of motion segmenr dysfunction (subluxation) that incorporates the complex interaction of pathologic changes in nerve, muscle, ligamenrous, vascular, and connective tissues
IIII*IxIIlon IYID'Om8 an aggregate of signs and symptoms that relate to pathophysiology or dysfunction of spinal and pelvic motion segments or ro peripheral joints IUbaIIIIC8 P a pepride present in nerve cells scartered throughour the body and in special endocrine cells in the gut
lylllll8lry similarity in corresponding patts or organs on opposite sides of the body
IY111PIIIIeIIc: that portion of the autonomic nervous system that function to regulate body functions in response to stress
produced by activity, reaction, and change originaring in rhe musculoskeletal system
tapotMII8IIt
IOIIIIIlI-vIIcIraI ......x reflex activation or
punctation
inhibition of visceral function in response to
somatic sensation
.... 1IIIIIon ......1 two adjacent vertebrae, and the connecting tissues binding them to each orher
_1Ch..
a descriptive term with reference to
viscera (e.g., splanchnic nerves 3fC autonomic nerves that innervate abdomina l viscera)
Idm...
measure of resistance offered to external loads by a specimen or structure as it
deforms Ib. ..._ palpable rissue rexture abnormality characterized by fine or stringlike myofascial
a ta pping or percussing movement in
massage; it includes clapping, beating, and I1InIIIr (IOiIII
local areas of hypersensitivity
found at consistent anatomic sites, which do nOt
refer pain pressure but produce a pain response to light palparion (see (ibromya/gia)
ther....,uc any treatment considered necessary to return the patient to a preclinical status or estab lis h a stationary status IhruaI sudden, manual application of a controlled direcrional force upon a suitable part of the patient, the delivery of which effects an adjustment
II'ICIIon
force acting on a longitudinal axis to
draw structures apart
476
GlOssary
vtIC8I'II anarent autonomic nerves that serve to
vllcerosomade reflex
increa se organ function are called visce ra l efferent nerves
inhibition or somatic function in response to visceral sensation
vl1C8l'8l8ll111't111t nerves that serve to conduct sensory information from the organs to the cenrral nervous system are called visceral afferent
sensitivity to the rate of loading or deformati on;
nerves
vIIC8I'OIOIIIIIIc convergence convergent input to somatic neurons form viscera l nociceptive
afferents that project through the sympathetic chain, producing somatic pain from visceral disease
v18C08111dc1ty
reflex activation or
property of a material showing
twO basic components are viscosity and elasticity vIacolity property of materials to resist loads that produce shear
Index A Aherranr monon, 7 Acces�ory ligJlncnrs. of mtcrvenebra: foramen, 27-28 Activaror methods, chiroprm:ric rene, techniques,118-119 Ac.:uprcs!)ure pomt stimulation, chIropractic reflex rc(hniqllc�, 117 Adhc!tlOn, fixation c.H1scd hy,1""9 Adju!.t11lcnr, 12 neurologu.: cffcas of, I S8 osseous manual thrust techniques, 91 spc(lfic,H2 Age,cervicogcnic sympathetic syndrome. 324 Altered !o.omarll; afferent mpur theory,subluxation, 229-2.11 Anatomic consideration,,>,468-470 Anaromy rcl:nionships Juronomlc nervOliS sy....rcrn. and vertebrJI subluxJtlon,2]4166 spmal 'iuhluxarion, 18 34 Ank)"losis. soft tissue, 9 Amino(1(cptlVC' sy....tem." paraspinal, ncurophY!.Iology of. 291. 291-294, 295·299, 296297 Anulus fihrosu..... suhluxation,1223
164 132, 1l1·1l1
Block
dcrangemcm,7
functional, 7
dyskinesia. 7 ncurology, vertebral subluxation
Intervertebral, 8 spmal jomt, 9
complex, 156
vertebrae, 140-141, 143
postcrior, 154 Athletic trauma,(0 ccrvical spine, cer\'icogenic sympathetic s)'ndrol1le, 328·329 AriamoaxiallolntS, kinesiology,
Blood flow, chiropractic reflex techniques, effects on, 109 Brain hibernation,341·343, H2143 examples, 343-346
198-199,200·20 I Arlanrooccipiral Jomts,kineSiology,
Brain hybernation. and spinal monipulorion, 346-349, 347.
196·198,196-199 Autonomic nervous s}'�tem,263
348r
overview of, 136-238,2.17 peripheral components 0(, 238· 261 C
symparhetlc division,238-253 Autonomies
Canal, transverse, 162
activity, reflex regulation of, 163264 In chiropractic, overview, 26426'>
C3psules, articular, 19,20 Central convergence-projection, 284-287, 28S·287, 294, 297 Central facilitation, SO
effecrs, 109-111 chlropracric reflex techniques, 109·111
CentT31 neuronal plastlclry, referred pain, 28S-287, 288· 294
function central processing
In
control of,
261-264
Centr31 sensitization, SO Cerebral dysfuncrion theory,340· 352
hypothalomlC conrrol, 261-263 Axoplasmic transport, aberrant, subluxation, 183
Cerebrospinal fluid flow, altered, subluxation,184 Cervical ll1jury, of spinc, �table, 9 Cervical jOlllt
B
subluxotlon, 132-134, Il I
Arthropathie�. mflamll1<1cory. 130·
subluxation, 178-J80
capsules, 19.20
Arrhmis degenerative. !lonm.tllipulahle vertehral suhluxJtion complex,
Biomechanical models,
Articulation
Barre-UeOl! syndrome, 332·333 Bennctt's vascular reflexes, chiropractic reflex techniques, 115-117
disfunction, 7 lock,acure? 7 Cervical posture,cervicogenic headache, 315-316 Cervical region, pam generators unique to� 29
477
478
Index
Cervical segments
neck proprioceptors,322
manual cranial therapy, 119
hypermobile,chiropractic
paciniform corpuscles,323
massage, I13
management of,134-135
pain, sympathetically mediatedj
metabolism,effects on,109
unstable,chiropractic management of,134-135 Cervical spine hypermobility causes of,126-134 clinical manifestations of, 124125
321-322 rehabilitation,319-339 road conditions, 330 sympathetic effects, in healthy tissue,321 sympathetic nervous system,320323
definitions of,124
sympcoms, 331
radiographic evaluation of,125,
trauma,to cervical spine,325-331
126-127 instability
treatment,319-339 and rehabilitation, 319-339
causes of, 126-134
Cervicogenic vertigo,333-336
clinical manifestations of, -124·
Cervicogenicity
125 definitions of,124 radiographic evaluation of, 125, 126-127 kinesiology,196-207 lower,kinesiology,199-203, 201t,202-203 radiography, 80-84, 82-83 Cervical sympathetic tfunk, and branches of,240-245, 249 Cervicogenic dorsalgia, 353-358 Cervicogenic sympathetic syndrome, 319-339
dysfunction,radiologic findings of,315 headache, 306-318,308 cervical posture, 3]5-316 dysfunction in,312-316 headache of cervical origin,312 hypomobility,313 mechanisms of pain in, 309312,311 muscular weakness,315-316 tender points,craniovenebral, 313-315,314t Chapman lymphatic reflexes,
age, 324
chiropractic reflex techniques,
anatOmy, 320-323
115
athletic trauma,ro cervical spine, 328-329 Barre-Lieou syndrome,332-333 biomechanics, 323-336
Chiropractic: An Illustrated History, 94 Chiropractic reflex techniques, 105-122
cervicogenic vertigo,333-336
activacor methods, 118-1 L 9
extension acceleration injury,rear
acupressure point stimulation,117
end,330 flexion deceleration injury,headon,330-331 free nerve endings, 323 Golgi tendon organ, 323, 323 Horner's syndrome, 331-332 intervertebral disc, 324-325
Bennert's (neuro) vascular reflexes, 115-117
activation of,111 reflex muscle spasm from spinal injury,110 from visceral disease,1 10 reflexive effects, 109-1 J I sacrooccipital technique (SOT), 119 somatoauronomic reflex manual therapy,113 theory of,110 specific technique procedures, I 13-120
spondylotherapy,118 temperature,effects on, 109 Chiropractic subluxation. See Subluxation Chiropractic terminology,13-14 Chiropractic treatment methods, defining,11-12 Chromaffin cells,248 Chronic segmental facilitation,1 J 0 Classification model,subluxation,177-178 pain in thoracic spine,395t Coccygeal subluxation syndrome, 467-472 Coccygeus, 468-470 Compensatory hypermobiliry,209210 Compression dorsal root ganglion, 180-181 nerve, 180-181
reflexes, 115 connective tissue massage, 113115 facilitation, segmental, chronic,
muscle spindles, 322-323,323
nociceptor, sympathetic neurons,
spinal cord,181-182
Meniere's disease,332 injuries,329
visceral disease,111-112 Nimmo technique, 113
Chapman (neuro) lymphatic
distraction techniques, 119-120
muscle recepcors,322-323
musculoskeletal dysfunction, and
blood flow, effects on, 109
mechanism of injury, 329-330 motor vehicle flexion-extension
muscle energy techniques,117
evidence of, 110-111 immobilization, effects of,108109 Logan basic, 117-118
Connective tissue component, vertebral subluxation complex,158-159 massage, chiropractic reflex techniques, 113-1 15 vertebral subluxation complex, 165 Contact points, osseous manual thrust technique, 102-103
479
Index
Convergence-projection,312 central,284-287,285-287, 294, 297
Discogenic back pain and discogenic back and leg pain,
Enteric division,vertebral
431-432
Corporotransverse ligament,27 Cranial nuclei,parasympathetic, peripheral distribution of,254-
Dislocation
subluxation,260-261
articular,incomplete, 8
Erratic movement,7
locked,less than, 8
Etiology, sympathetic syndromes,
Displacement,vertebral, 9
259 Cranial therapy,manual,
Disrelationship
cervicogenic,319-339 Examination of intervertebral disc
chiropractic reflex techniques,
intervertebral, 8
119
structural,9
Cumulative trauma disorders,328
chiropractic reflex techniques, 117
syndrome,433-437 Extension acceleration injury,rear
Distraction techniques, chiropractic reflex techniques,
end,cervicogenic sympathetic syndrome,330
119-120 D Deep tissue injury,pain referral from,280-281 Deformity,of disc,manipulable lesion,180 Degeneration arthritis,nonmanipulable subluxation,132-134, 133
Dorsal rOOt ganglia compression/traction,180-181 vertebral subluxation complex,
ligament,absence of,130 Drive,line of,osseous manual thrust technique,103 Dynamics of thoracic spine,386
immobilization,150, 154-155
Dysanhritic lesion,7
154-155 moror system,182-183 subluxa
Dysfacilitarion,neuromuscular,8
in headache,312-316 radiologic findings of,315
spinal, and functional radiograph, 73-84
180 disease,degenerative,137-139, 138
Fixation caused by adhesion,179 caused by nuclear fragments, 179-180 total,9 Flexion deceleration injury,head
E Economic issues, subluxation,16 Efferent activity,161 End feel,and joint play,98 osseous manual thrust technique, 98 End plate,vertebral,subluxation,24
deformity,as manipulable lesion,
1l0-111
partial,8
Dystropia,reflex, sympathetic, 321
syndrome,439
Disc
segmental,chronic,evidence of,
Fight or flight reaction,238
disease, Ill-112
imaging of intervertebral disc
Diminished venous return,162
synovial impingement, 7 Facilitation
musculoskeletal, and visceral
differential, of intervertebral disc
Diaschisis,343, 345
syndrome, 7
Fanning,interspinous space,7
Dystopia,7
complex,159-160
subluxation syndrome,415-428
metameric, 8
complex,motor unit, 8
tests, vertebral subluxation
dysfunction,7 locked,8
segment,7
cervicogenic
Dyskinesia,anicular,7
syndrome,437-439
joint,19
central,50
Dysfunction
articular,7 Diagnosis,470
Facet dysfunction,posterior,9
155-156 Down syndrome,transverse
disc disease,137-139, 138 vertebral subluxation complex,
F
radicular pain,29-30
Endocrinology,vertebral subluxation complex,166 Endolymphatic hydrops,332 Energy techniques,muscle,
on,cervicogenic sympathetic syndrome,330-331 Flexion-extension range of motion: sagittal plain rotation, 390 Foramen,intervertebral,26, 26-28 accessory ligaments, 27-28 Force manipulation,measurement of, 269 of thrust, 99-102 osseous manual thrust technique,99-102
480
Free nerve endings,cervicogenic sympathetic syndrome,323 Functional block, 7 Functional radiograph, and spinal dysfunction, 73-84
kinesiology, 207-208 segmental vertebral, 9 spinal,9 Hypothalamic control, autonomic funcrion,261-263
Intervertebral encroachment theory,subluxation,226-229, 228-230
Intervertebral foramen, 26, 26-28 accessory ligaments, 27-28 Intervertebral joint restriction,
G Gamma gain, 213 Ganglia
mechanism of,210-214 Imbibition,23 Immobilization degeneration, 150,154-155
cells,248 submandibular, 255 Geniculum,255 Golgi tendon organ,cervicogenic sympathetic syndrome,323, 323
effects of, 108-109 joint, pathological effects of, 219 pathological effects of, 219 Impingement,synovial, facet, 7
Ischemia compression, chiropractic reflex techniques, I J3 intraneural microcirculation, subluxation, t 83 macrocirculation,subluxation, 184
Inflammation arthroparhies,130-132,131-132
H Headache cervicogenic. See Cervicogenic headache vcrrebrogenic, model of, 316 Historical issues, subluxation,14
vertebral subluxation complex, 163-165,164-165,165-166 Instability cervical spine causes of,126-134 clinical manifestations of, 124125
Homunculus, sensory, 31
definitions of,124
Horner's syndrome, 331-332
radiographic evaluation of,125,
Hydrops,endolymphatic, 332
126-127
Hyperalgesia, 28, 280
intersegmental,8
Hyperemic subluxation,7
lumbar spine
Hypermobiliry,7, 124,135 cervical segments,chiropractic management of,134-135 cervical spine causes of,126-134 clinical manifestations of, 124125 definitions of, 124 radiographic evaluation of, 125, 126-127
causes of, 137-14'1 clinical manifestations of, 141143 intersegmental,chiropractic managemenr of,143-144 postSurgical,139-140,142 Interlaminar joints, 19 Intersegmental hypermobiliry,
J Joint aberration, 8 bind, 8 dysfunction, 8 fixation,Korr's theory of,212214 immobilization,pathologic effects of,219 lesion,manipulable,8 locking, mechanical, 180 motion abnormal, 7, 207-210 characteristics of,osseous manual thrust techniques, 91-93,92-93 play, and end feel,osseous manual thrust technique,98 restriction, intervertebral, mechanism of,210-214
lumbar, chiropractic
K
management of, 143-144
compensatory,209-210
Intersegmental instability, 8
Kinematics,of thoracic spine, 389t
kinesiology,208-209
Interspinous space, fanning of, 7
Kinesiology
lumbar intersegmental,
Intervertebral blocking, 8
chiropractic management of, 143-144
Intervertebral disc cervical, 24-26
lumbar spine, 135-144
cervicogenic sympathetic
causes of, 137-141
syndrome, 324-325
clinical manifestations of, 141143 as manipulable lesion,180 Hypomobility,7 cervicogenic headache,313
atlantoaxial joints, 198-199,200201
atlantooccipital joints, t 96- t 98, 196-199
cervical spine, 196-207
innervation of,24, 25
lower, 199-203, 201r,202-203
subluxation,22. 22-26
characteristics of normal motion,
syndrome,chiropractic management,429-452 Inrervertebral disrelationship,8
191-193,191-193 and chiropractic subluxation, 190-224
481
"'x
Kinesiology,com'd hypermobility,208-209 compensarory,209-210
vertebral, 9
Manual therapy,6, J 2
Logan chiropractic reflex
hypomobiliry,207-208
Long lever arm procedures,98-99
immobilization,of joint,
Low back pain,sympathetic
parhologic effeers of,219 intervertebral joint restriction, mechanism of, 210-214 Korr's theory, of joint fixation,
nervous system,289-290, 295 Lumbar intersegmental hypermobility,chiropractic managernem of,143-144 Lumbar intersegmemal instability,
212-214 lumbar spine, 204-207,205t, manipulable subluxation, biomechanical effects,215-
analysis of,193-196,194-195 regionaVintersegmenral,196-
clinical manifestations of,141-
StruCture of,210-211 thoracic spine,203-204,204t, Kinesioparhology
radiography,79-80, 79-81, 8081 t
Medical and surgical consultations, Meniere's disease, 332 Metabolism,chiropractic reflex Metameric dysfunction,8 ischemia, subluxation,183 Misalignment,8 Mobilization,6,12,92
Lumbosacral sympathetic trunk,
versus manipulation, 97-98 osseous manual thrust techniques,91
Lymphatic reflexes,Chapman,
spinal,9
chiropractic reflex techniques,
spinal joint degeneration, 217-
115
Model classification,subluxation, 177-178
219
Motion
Kinetic intersegmental subluxation,
M
8 Kinetic subluxation,8
Macrocirculation ischemia,184
Korr's theory,of joim fixation,
Malposition, vertebral,
212-214
subluxation,178-179
l
Laxity,as manipulable lesion,180 Lesion,manipulable, 8 Levator ani,468 Lifestyle modification,subluxation, 185 Ligatights,8 Line of drive,osseous manual thrust technique, 103 lock,8 back, acute, 7 cervical joint,acute,7 facet,8
Mechanical disorder,8
Microcirculation, intraneural,
and branches of,250-253
205
113
techniques,effects on,109
kinesiology,204-207, 205t, 206pain originating from,281,282
function of,211-212
chiropractic reflex techniques,
449-451
instabiliry,135-144
208
207 muscle spindle
Massage
reflex techniques,113-1 I S
hypermobiliry,135-144
143
range of,
See Osseous manual thrust technique
Lumbar spine
143
abnormal,207-210,214-215
113 Manual thrust technique, osseous.
connective tissue,chiropractic
clinical manifestations of, 141-
217 motion
techniques,119 and somatoautonomic reflexes,
chiropractic management of, 143-144
206-208
cranial,chiropractic reflex
techniques,117-118
aberrant,7 kinesiology,209 abnormal,assessment of, kinesiology,214-215 analysis of, 193-196, 194-195
Manipulable lesion,8
joint,abnormal,7
Manipulable subluxation,6, 10-11
normal, characteristics of, 191193,191-193
kinesiology aspect of, biomechanical effects,215-
palpation,61t,61-62
217
range of,regionaUinrersegmental, 196-207
Manipuladon,6,12,91,92,97 force,measurement of,269 versus mobilization procedures, 97-98 osseous manual thrust techniques, 91 palpatory indicators for, 58-59 spinal,headache,307-309,310r subluxation,11 Manipulative procedures,92
restriction,8 segment,6,11,91 Moror system degeneration, subluxation,182-183 Moror unit,derangement complex, 8 Moror vehicle flexion-extension injuries,cervicogenic sympathetic syndrome,329
482
Index
Movement, erratic, 7
Neurofunctinal subluxation, 8
Muscle
Neurologic dysfunction, 8
energy techniques, chiropractic reflex techniques, 117 receptors, cervicogenic sympathetic syndrome, 322-
Neuromechanical lesion, 8
spasm from, reflex, visceral disease, chiropractic reflex techniques, 110 spindle
chiropractic subluxation,225-
syndrome,322-323, 323 Structure of, 210-211 weakness, cervicogenic headache,
142 radiographic evaluation,135.
233
135-137,137 spondylolytic spondylolisthesis,
reflex techniques,113 Nociception
139,140-141 unstable cervical segments, 134-
spinal origin, 28-33 sympathetic neurons,activation
cervicogenic sympathetic
143 postsurgical instability, 139-140,
Neurophysiologic theories, on
Nimmo technique,chiropractic
323
clinical manifestations of,141-
of, 111 Nonmanipulable subluxation, lO11,123-145
135 Nuclear fragments,fixation caused by, 179-180 Nucleus pulposus, subluxation, 2324
acute trauma,126-127,128 o
blocked vertebrae, 128-130, 130,
315-316 Musculoskeletal dysfunction
140-141, 143 cervical spine,hypermobiliry,
mechanical, 8 and visceral disease, chiropractic reflex techniques, 111-112 Musculoskeletal manifestations, of visceral disease, chiropractic reflex techniques,112 Mycobacterium,butyricum, 231 Myologic component, vertebral subluxation complex, 160-162
causes of,126-134 degenerative arthritis, 132-134, 133 degenerative disc disease, 137139, 138 Down syndrome,transverse ligamenc, absence of,130 hypermobiLity cervical segments, 134-135
N Natural history of imervertebral disc syndrome,440-441 Neck proprioceprofs, cervicogenic sympathetic syndromes, 322 Neospinothaiamic tract, subluxation, 31, 31 Nerve associated with sympathetic nervous system, 29 inflammation, vertebral subluxation complex, 164 roots, inflammation, vertebral subluxation complex,164
clinical manifestations of,124125 radiographic evaluation of,125, 126-127
Neurodystrophic hypothesis,
components of, 97-98 contact points, 102-103 force, of thrust,99-102 historical perspective,88, 88-90 joint motion, characteristics of, 91-93,92-93 joint play, and end feel, 98 line of drive,103 manipulation, 91 versus mobilization procedures, 97-98 mobilization, 91
143-144
procedure, selection of, 94-98
lumbar spine, 135-144
short lever arm procedures,98-99
causes of,137-141
sofr tissue therapy, 103
clinical manifestations of, 141143 inflammatory arthropathies, 130132,131-132 instability clinical manifestations of, 124-
subluxation complex,158
classification, 94, 95-96 clinical application, 93-94
chiropractic management of,
Neuroarticular dysfunction, 8
Neurodysarthritic lesion, 8
87-104 adjustment, 91
lumbar intersegmental,
cervical spine
Neurodiagnosis, vertebral
Osseous manual thrust technique,
cervical spine
Nervous system, autonomic, 263 Neurobiomechanical lesion, 8
Orthospondylodysanhritics, 8
125
subluxation, 91-94 terminology,90-94 three-point tension, 98 thrusting, 98-103, 100 Osteologic lesion, 8 Osteopathic lesion,8, 176 articular,8 spinal, 8
definitions of, 124 p
lumbar intersegmental, chiropractic management of, 143-144
vertebtal subluxation complex,
lumbar spine
157
causes of, 137-141
Paciniform corpuscles,cervicogenic sympathetic syndrome,323 Pain central transmission of,30-31
483
Index
Pain,cont'dcervicogenic headache, 309·312, 311 deep tissue mjury, referral from, 280-281 generarors
peripheral distributions of, 259260
cervical spine,80·84, 82·83
Paravertebral subluxation, 8 Partial fixation,8 Pathological effects, of immobilization, 219
unique ro cervical region,29
Perception,of pain,28
unique ro thoracic region, 29
Pharmacologic considerations,
low back, sympathenc nervous sysrem,289-290, 295 lumbar spme,281,282 nonradicular,281 radicular,24, 28 t dorsal roor ganglia,29·30 referral, 280 referred, 28 t cemral neuronal plasticity, 285· 287, 288-294 somatic, 28 referred, 30
vertebral subluxation complex, 166
185
156-158 Paleospinorhalamic tract, subluxation,31-32, 32 Palpa(1on history of,in chiropractic, 57·58 motion,61t.6 t ·62 reliability of. improving. 62t,62· 65 sratic, 61-62t, 62 Palparory diagnosis,of
Referral, pain, 280 Referred pain
osseous manual thrust technique, 102-103 stimulation, acupressure,
tender, craniovertebral, 313-315,
61, 61t neurophysiology of,291, 293294, 295-299, 296-297 Parasympathetic cranial nuclei,
Political issue,subluxation,14-15 Posteriot articulations, 154 Posterior facet dysfunction, 9 Posterior ligament complex, instability,8
Parasympathetic division,vertebral subluxation, 253·260 Parasympathetic sacral nuclei,
mechanisms,279-301 dysfunction, 9 chiropractic reflex techniques, 110 somarosomatic, 18 t -182 somarovisceral, 182 sympathetic dystrophy, 321
Postganglionic axons, sympathetic, peripheral distribution of,239· 253
techniques. See Chiropractic reflex techniques theory, somatoauronomic, 110
Postsurgical instability, 139· t 40, 142
viscerosomatic, 182 Reflexive effects, chiropractic reflex
Posture,cervical, cervicogenic headache,315-316
spinal origin of, 239,241, 246 Primary chiropractic lesion,9 Proprioceprors, neck, cervicogenic sympathetic syndromes,322
techniques, 109-11 J Rehabilitation, cervicogenic sympathetic syndromes,319339 Reliability, of palpation, improving, 62t,62·65 Road conditions, cervicogenic sympathetic syndrome,330
Pseudosubluxation, 9 Psychoneuroimmunology,
S
subluxation, 183 Pterygopalatine, 255
peripheral distribution of,254259
287, 288-294 neuroplasticity, spinal cord
muscle spasm,from spinal injury,
314t
peripheral distribution,and
Parasplnal antinociceptive systems,
central neuronal plasticity, 285-
Reflex
Preganglionic axons,sympathetic,
chiropractic,reliability of, 60-
regionaUintersegmental,196-
contact, 102-103
subluxation, 56-67 manipulation, 58·59
subluxation evaluation, 68-86
acupressure, stimulation of, t 17
Palparory indicators,for Palpatory procedures, spinal.
135, 135-137, 137 static, and spinographic analysis,
207
117
syndromes, 321-322
81t nonmanipulable subluxation,
Receptor·tonus technique, J t3
Poim
chiropractic reflex techniques,
vertebral subluxanon complex.
dysfunction, 73-84 lumbar spine,79-80, 79-8/, 80-
Range of motion,
14 Placebo effeer, subluxation,184·
sympathetically mediated,32 t· 322
functional, and spinal
70-73, 71, 72t, 74-78
Philosophical issue,subluxation,
spinal origin,28-33
cervicogenic sympathetic
Radiography
Sacral nuclei, parasympathetic, peripheral distributions of,259·
R Radicular pain, 24, 281 dorsal rOot ganglia, 29-30
260 Sacroiliac joints,slipping, 9 subluxation syndrome, 453-466
484
Sacrooccipital technique (SOT), chiropractic reflex techniques. 119
degeneration,kinesiopathology, 217-219 stiffening, 9
complex,6,9, 11,36,147-148 myopathy, 9 verrebral, 9
Salivatory nucleus,superior,255
Spinal kinesiopathology, 9
defined,6-10, 10
Sciatica,281
Spinal lesion, functional, 7
dentate ligament, cord disrorrion
withourlwirh neurologic deficit, 432-433
Spinal manipulation,systemic effects of,267-278
Sectional subluxation,9
Spinal manipulative therapy,12
Segment, facilitated, 7
Spinal motion segment, 11
Segmental dysfunction, 9
Spinal palpatory procedures,
Segmental facilitation,chronic, evidence of, 110-11 I Segmemal vertebral hypomobility, Sensory homunculus, 31 Short lever arm procedures,
61,61t
fixation,caused by nuclear
Spinal subluxation,9 Spindle, muscle, structure of,210211 Spine, cervical injury,stable, 9
technique, 98-99
Spinographic analysis
Soft tissue
and static radiography,70-73, 7 J, 72t,74-78
ankylosis,9
Spino reticular tracts, 31-32,32
therapy, osseous manual thrust
Spondylodysarthritic lesions, 9
technique,103 Somatic afferent input theory, altered, 229-231 Somatic origin, pain of,28 Somatic referred pain,30 Somaroaumnomic reflex
180-18] economic issues, 16
osseous manual thrust Slip, sacroiliac joints, 9
lesion,180 dorsal root ganglion,traction,
chiropractic, reliability of,60-
anatomy related to,18-34
9
theory, 231-232 disc deformiry, manipulable
Spondylolisthesis, spondylolytic, 139, 140-141 Spondylolytic spondylolisthesis, 139, 140-141 Spondylorherapy,chiropractic reflex techniques, ]]8
fragments,179-180 historical issues, J4 hyperemic,7 hypermobility, as manipulable lesion, L80 intersegmental,kinetic,8 intervertebral disc, 22, 22-26 cervical,24-26 innervation of,24,25 intervertebral encroachment theo,)',226-229,228-230 intervertebral foramen,26, 26-28 ischemia, intraneural microcirculation,183 kinesiology and, 190-224
manual therapy, J '] 3
Sprain,9
kinetic,8
theory, chiropractic reflex
Static palpation, 61-62t,62
lifestyle modification,185
techniques, 110 Somaroauronomic relationships, vertebral subluxation complex, 157 Somatosomatic reflex, 109 subluxation,181-182 Somatovisceral reflex,182 subluxation, 182 Spinal cord compression/traction, 181-182 mechanisms, referred pain, neuroplasticity,279-301 Spinal dysfunction and functional radiograph, 73-84 Spinal hypomobilities, 9 Spinal injury,reflex muscle spasm from,chiropractic reflex techniques, 110 Spinal irritation, 9 Spinal joint complex, 9
Static radiography, and
macrocirculation ischemia, 184
spinographic analysis, 70-73,
manipulable, 6
71, 72t, 74-78
manipulation,10-11, I I ,123-
Stiffening, spinal joint,9 Stress reduction,subluxation,185 Subluxation, 6, 9,11,12, 14,15, 16,226, 234
145 kinesiology aspect of, biomechanical effects. 215217
adhesion,fixation caused by, 179
mechanical joint locking,180
altered somatic afferent input
model,178-185
theory,229-231 anulus fibrosus,22-23 apphyseal, 7
classification,177-178 moror system degeneration. 182183
articular capsules,19,20
neospinorhalamic tract,31,3 J
axoplasmic transport,aberrant,
neurofunctional,8
183 basic scientific evidence for, 1555,37-38 biomechanical models,178- J80 cerebrospinal fluid flow,altered, 184 clinical issues,15-16
neurologic models,180-183 neurophysiologic theories 225-233 nonmanipulable, 10-11, 123-145 nucleus pulposus, 23-24 origin of word,6-10
Oil,
485
Index
Subluxation,conr'dosseous manual thrust rechniques, 91-94 paleospinorhalamic tracr,3 1-32, 32
palpawry diagnosis,56-67 paraverrebral,8 philosophical issue,14 placebo effect,184-185 political issue, 14-15
Sympathetic trunk cervical,and branches of, 240lumbosacral,and branches of, relationships of,240,249, 252,
250,252,262 Symptoms/signs of intervertebral
psychosoci.1 models,184- J85
Synovial folds,zygapophyseal joint,19-21 Synovial impingement, facet, 7
sectional, 9
Systemic effects,of spinal
specific, adjustmenr,specific, 232 spinal, 9 spinal cord,compressionlrraction, 181-182 static. intersegmental. 9
manipulation,267-278 T Temperarure,chiropractic reflex techniques, effects on, 109 Tender points,craniovcrtebral, cervicogenic headache,313315,314t
stress reduction,185
Tenderness,referred,280
studies in, review of, 38-53
Tension,three-poim,98
supraspinal comrol, 32-33 syndrome,6,9,11,36 vertebral,9
osseous manual thrust technique, 98 Terminology
terminology,5-17,7t
chiropractic,13-14
theoretic. I models of,175-189
intervertebral disc syndrome,
trophic models,183-184 usage of term,14-16 vertebral. See Vertebral subluxation Submandibular ganglia,255 Sympathetic nervous system,238253 cervicogenic sympathetic
narrow passages,362-363 postural and dynamic factors, 362-363 provocative tests, 369-370 radiography, 370 sensory signs and sympwms,
roor,traction,180-181
reAexes,182
other anomalies,363 physiologic factors compromising
262
thoracic,and branches of,245-
somamvisccral,viscerosomatic
motor signs and symptOms,367, 368t
250-253
disc syndrome,431-440
somamsomaric reflex,181-182
361
management, 371-372, 373-374
245,249
psychoneuroimmunology,183 radiography evaluation,68-86
inrerscalene triangle, 360-363,
430-431 in subluxation,5-17,7t Testing theory,348t,349-350
Textbook of Clinical Chiropractic, 94
Thoracic ourlet syndrome, 359-377
366-367 structural anomalies compromising narrOw passages further,363 subcoracoid space, 361, 362 subluxation syndromenarrow passages traversed by neurovascular bundle,360362 traumatic and occupational causes,364 vascular disturbances,368-369 vasomotor disturbances and trophic changes,367-368 Thoracic region,pain generators unique to,29 Thoracic spine biomechanical diagnosis,394395 biomechanics of,385-389 biomechanics of rib cage,391392 dynamic palpation,399-410
anatomic features,360-363,361
dynamics of,386-389
anomalous muscle insertions,363
flexion-extension,range of
anomalous ribs,363
motion,sagittal plain rotation,
in low back pain, 289-290, 295
anrhropomorphic factors, 362
390
nerves associated with,29
biomechanical considerations,
syndromes,320-323
Sympathetic neurons, activation of, by nociceprors, I I 1
363-364 clinical features,364-369
kinematics of,389-392 kinesiology,203-204,204t,205 lateral Aexion, range of motion,
costoclavicular rriangle,361, 362
frontal plane of motion,390-
peripheral distribution of,239-
developmental factors,362
391
253
diagnosis,369-371
mechanical disorders,396-397
eiectrodiagnostics,370
pain
Sympathetic postganglionic axons,
Symparhetic preganglionic axons, peripheral distribution,and
first rib,359-377
spinal origin of,239,241, 246
functional cause, 363-364, 365
classification of,395
functional evaluation, 370-371,
medical model, pathologic
Sympathetic syndromes, cervicogenic,319-339
371
chiropractic model, 396-397
factors,395-396
486
-.ex
V
pain, cont'dsources of, 397-399 respiration, accessory muscles,
Vagal ganglia,superior/inferior, 257 Vascular abnormalities,162
393-394
Vascular component,vertebral
rib cage, examination/adjustments, biomechanics of,379-414 rotation range of motion,motion in horizomal plane,39 t -392 static concepts, 385-386 Thoracic sympathetic trunk, and branches of,245-250,252,262 Three-point tension, osseous
subluxation complex,162-163 Vascular reflexes, Bennert's, chiropractic reflex techniques, 115-117 Vertebrae adjacent,154 blocked, 140-141,14] nonmanipulable subluxation, 128-130, 130
manual thrust technique,98
evaluative procedures,161,163 hiStory, lSI, 151t,151-152 immobilization degeneration, 154-155 inflammation,163-165,164-165, 165-166 kinesiology component,153-155 lumbosacral sympathetic trunk, and branches of, 250-253 model, overview of, 151-153, 152 myologic component,160-162 neurodiagnosis,158 neurodysrrophic hypothesis,157
Vertebral dysfunction,9
neurologic component,155-158
force of,99-102
Vertebral dyskinesia, 9
pain, 156-158
osseous manual thrust technique,
Vertebral end plate,subluxation,
parasympathetic cranial nuclei,
Thrust
98-103, 100
peripheral distribution of,
Vertebral locking,9
Traction dorsal rOOt ganglion,180-181
Vertebral malposition,subluxation, 178-179
nerve,180-181 spinal cord,181-182 Transforaminal ligamenr,27 Transmission of pain, 30-31 Transverse canal,162 Transverse ligament, absence of, Down syndrome,130
Vertebral subluxation adjustive procedures, neurologic effects of,158 and anatomic relationships, of autonomic nervous system, 234-266 arthritis,164
Trauma acute,nonmanipulable subluxation,126-127, 128 ro
24
cervical spine,cervicogenic sympathetic syndrome, 325-
articular neurology,156 auronomic activity, reflex regulation of,263-264 autonomic function central processing in control of,
331 Treatment,470-471 of imervertebral disc syndrome,
261-264 hypothalamic control,261-263 autOnomic nervous system
441-451 methods, chiropractic,defining,
overview of,236-238,2]7 peripheral components of, 238-
11-12 and rehabiliration, cervicogenic sympathetic syndromes,319-
261 autonomics in chiropractic,264265
339 Trigger point. See Point Trophic influences,vertebral subluxation complex,157-158
u
cervical sympathetic trunk,and branches of,240-245,249
254-259 parasympathetic diviSion,253260 parasympathetic sacral nuclei, peripheral distributions of, 259-260 pharmacologic considerations, 166 postganglionic axons, sympathetic,peripheral distribution of,239-253 preganglionic axons,sympathetic, spinal origin/peripheral dIStribution of,239,241,246 somatoautonomic relationships, 157 spinal nerves, 155 sympathetic division, autonomic nervous system, 238-253 sympathetic trunk,relationships of, 240,249,252, 262 syndrome,9 therapeutic benefits,159-160, 161-162,163 thoracic sympathetic trunk,and
complex,9,149-174
branches of,245-250,252,
concept of,6
262
connective tissue,158-159,165
(rophic innuences,157-158
diagnostic tests,159-160
vascular component,162-163
dorsal root ganglia,155-156
vertebral end plate,24
chiropractic management of,
endocrinology,166
vertebral malposition,178-179
134-135
emeric division, 260-261
viscerosomaric relationships,157
Unstable cervical segments,
487
Vertebral subluxation,conr'd zygapophyseal joint,19-22 synovial folds,19-21 unique characteristics of, 21 Verrebrobasilar insufficiency,244 Vertigo,cervicogenic. 333-336 Visceral disease musculoskeletal dysfunction. 111-I12musculoskeletal manifestations of. ]'1 2
reflex muscle spasm from. 110 chiropractic reflex techniques, 110
Z Zygapophyseal joint,19-22 cervical
Visceral motor,235
synovial folds,2]
Viscerosomatic reflex,subluxation,
unique characteristics of, 2]
182 Viscerosomatic relationships, vertebral subluxation complex, 157 Viscoelasticity,108
innervation of,21,21-22 synovial folds,19-21
