Microneurosurgery, 4 Vols., Vol.4A, CNS Tumors: Clinical Considerations and Microsurgery of Intracranial Tumors: TEILBD IV, Tl A

3

Robert De/aunay Rhythm1938. @VGBild-Kunst,Bonn 1993

Neuroradiology

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3 Neuroradiology

Historical Review

I

Plain Radiographs Wilhelm Conrad Roentgen was Professor of Physics at the University of Würzburg when he made his discovery of X-rays in 1895. The first X-rays, or radiograph, (of Roentgen's wife's hand) was made in January, 1896. This heralded the era of diagnostic radiology, and Roentgen was awarded the Nobel Prize for Physics in 1901 for his discovery. Skull radiographs, supplemented by chest and, when appropriate, spinal radiography, quickly became part of the investigation of patients with neurological diseases. Not surprisingly, the diagnostic yield was limited. In 1912, Schuller published his detailed monograph on skull radiography, the first substantive work on radiographic changes created by CNS lesions. Plain radiographs still provide useful information in many cases of extrinsic tumors, and in some intrinsic as well (Diethelm and Strnad 1916).

Contrast Encephalography In 1918, the first neuroradiological contrast study was performed when Walter Dandy introduced air ventriculography, replacing ventricular cerebrospinal fluid with air injected directIy through a needle introduced through a burr hole (Dandy 1918). This was followed by his introduction of lumbar pneumoencephalography in 1919.The use of air in the ventric1es and CSF systems proved very useful in imaging the cisternal systems and surface contours of the CNS, and in hydrocephalus, sites of blockage could be accurately localized. With intracranial masses, the type of ventricular displacement and deformity acccurately predicted the side and location of the mass, whether it was tumor, hematoma, or abscess. Between 1920 and 1972, cerebral pneumography was a key investigation method, producing high diagnostic rewards in expert hands. As diagnoses were deduced from indirectIy visualized structural changes within the brain and cisternal systems, interpretation had to be of the highest order. However, tumors not causing such changes could remain undetected.

performing direct intracarotid punctures for other reasons for seven years). In 1948, Seldinger obviated the need for direct carotid puncture procedure, and made cerebral angiography safer and less painful, with the percutaneous transfemoral technique. AIl these technical advances resulted in the widespread use of arteriography in the diagnosis of brain tumors until the introduction of cr scanning in 1972. Not only did this technique permit accurate localization of tumors, their vascularization patterns, and displacement effects, it also provided a confident pathological diagnosis in many cases of meningiomas, gliomas, metastases and hemangioblastomas. At present, arteriography, in selected extrinsic and intrinsic tumors, continues to provide essential information in diagnosis, in surgical planning and in neurointerventional decision making. Considerable improvements in radiological equipment and in contrast less allogenic media have continued right up to the present day. Modern catheter technology has also made angiography much safer and has enabled superselective techniques to be used for both investigation and treatment. The specific indications for angiography, in the management of CNS tumors are comprehensively presented in well knownmonographs on cerebral and spinal arteriography (Newton and Potts 1974, Salamon and Huang 1976, Huber et al. 1979). Even though we have had full access to high-resolution MR scanning for the last five years, we have considered it useful to perform angiography for tumors intimately related to or involved with major arterial feeders or draining veins and sinuses. In these circumstances. arteriography provides detailed information on three aspectsof the vascular system that magnetic resonance angiography (MRA), despite promising advances in quality, cannot yet achieve: the condition of the arteries, veins, and their collaterals (particularIy their dilatation, hyperplasia, stenosis, and ocdusion); the amount of displacement of the arteries and veins.and the quality of flow (slow versus fast, shunts within a tumor). In addition, arteriography is crucial in the evaluation and preoperative embolization of, highly vascular tumors. Venous samplingin suspected ACTH-secreting pituitary adenomas is often usefulin confirming the diagnosis and localization.

Cerebral Angiography Neuroimaging: The next important advance was the introduction of cerebral arteriography by the Portuguese neurologist, Egas Moniz, working in Paris in 1927.Moniz was impressed by the many European misgivings about the safety of ventriculography expressed at a meeting of the Royal Society of Medicine in London in 1924. He set about to find another way of diagnosing cerebral tumors and, in 1926, with his co-worker, Almeida Lima, conducted initial trials on dogs and on a cadaver. Subsequent trials in four patients were failures, but they persevered and demonstrated the first brain tumor in a patient by angiography in 1927. Cerebral angiography, as performed by Moniz, involved bilateral open exploration of the carotid arteries and direct puncture of the common carotid artery, using sodium bromide and later, Thorotrast as contrast agents. Direct percutaneous common carotid puncture for visualization of the cerebral vessels was pioneered in 1936by Loman and Myerson (they had been already

Computed

Tomography

Neuroradiology effectively became neuroimaging on April 19.

1972when Ambrose, a neuroradiologist,showed for the firsttime how it was possible to directly image the brain. In his presentation to the British Institute of Radiology in London, he described"a scanning apparatus which uses crystal detectors and a computer to analyze the information content of a beam of X-rays,andconstruct a tomographic picture from the readings so obtained." The term computed transverse axial tomography (CAT scanning,later simply CT scanning) was given to the technique by Ambrose and Hounsfield (a physicist who produced the original concept andinitial design for the EMI scanner, for which he received the Nobel Prize for Medicine in 1979). Ambrose went on to show how this "new and fundamentally different X-ray method" was 100 times more sensitive than conventional radiographic procedures, and was able to distinguish

Historical Review verysmalldifferencesin tissue density.Apart from normal brain anatomy,it was also possible to appreciate very subtle density differencesbetween normal brain parenchyma, edematous brain, blood,and cerebrospinal fluid, as well as a striking contrast with thehigh-densitybone. Examples of cerebral tumors, intracerebral infarction,and hemorrhage, were immediately discernible. Until this drama tic breakthrough, a diagnosis of suspected pathologywithin the central nervous system had to be indirectly deducedfrom techniques that imaged bone, the ventricles and subarachnoidspaces and blood vessels. Yet even with extensive lesions,when using all the available techniques, it was still not alwayspossible to make a diagnosis, unless the lesion contained abnormalblood vessels, or was associated with edema causing a masseffect.Also, the occasional discrepancy between prominent symptomsand subtle neurological signs often led to an inappropriate neuroradiological search (for example, a posterior fossa lesionrather than a frontallobe tumor). Theintroduction of CT scanning resulted in a rapid decline in the use of isotope brain scanning, diagnostic pneumoencephalography(by 90%) and angiography (by 60%) in neurosurgical unitsin the year following the installation of such a scanner. By 1975,the superiority of CT over all previous studies in the detectionof intracranial tumors was clear (Ambrose 1975). There is no question that the advent of CT scanning marked the most remarkable advance in the investigation of intracranial diseaseso far produced in the twentieth century. At the same time,howevercritical research was being conducted into the applicationsof nuclear magnetic resonance (NMR) in imaging biologicaltissues.

Neuroimaging: MagneticResonanceImaging ThesuccessfulNMR experiments by Purcell and Bloch in 1945 led to the development of NMR spectroscopy in the 1950s and as an indispensableanalytical tool in numerous sciences, 1960s rangingfrom biology and chemistry to solid-state physics. CommercialNMR spectrometers were pioneered in both the Onited Statesand Switzerland by 1958. Odeblad, a Swedish physicist and gynecologist, was the first toapplyNMR spectroscopy in medicine (1955, 1960). He studied theprotons in human milk, saliva, cervical mucus, gingival tissue, andthe eye. The NMR experiments by Cope (1970), and Hazlewood(1971)provided a better understanding of the nature of cell water,and helped confirm the concept (1962) of the existence of intracellularwater as multiple polarized layers adsorbed onto cell proteins.These works formed the basis for current interpretations ofedema. The real breakthrough in NMR technology carne with the inventionof Fourier NMR spectroscopy in 1966 in California by DrW.A. Anderson and Professor Richard Ernst of the Swiss Federal Institute of Technology in Zurich. The use of pulse techniquesand Fourier transformation to boost sensitivity and to increase versatility revolutionized the field. Spectroscopy, especiallyof large organic molecules and of less sensitive nuclei suchascarbon-13,becamefeasible. Damadian (1971) drew attention to the in-vitro observation of differencesin the values of the proton nuclear spin-lattice relaxationTI time in some normal tissues (in the rat), benign

195

tumors (fibroadenomas), and malignant rat tumors. He suggested that spin-echo NMR might be used as a method of discriminating between malignant tumors and normal tissue. His patent application in 1972 "of apparatus and methods for detecting cancer in tissue" was the first proposal of an NMR tumor imaging concept. Weisman (1972) showed that in-vivo recognition of animal tumors was possible with NMR. The necessary concept for imaging with NMR required at least a two-dimensional representation of nuclear density, and Lauterbur (in 1973) was the first to solve the problem. His was a landmark paper, describing the technique for generating twodimensional and three-dimensional images of objects, inciuding living organisms, from NMR signals in magnetic field gradients. Essentially, by applying the linear magnetic field gradient along a number of different directions relative to the object, a number of different one-dimensional profiles are obtained. These could then be combined by computer to give a two-dimensional image of the object, using a method similar to the projection-reconstruction procedures used in CT by Hounsfield in 1972. Lauterbur correctly forecast the potential in vivo application of the technique in the study of tumors. In a later paper, in 1975, he suggested the combination of MRI with high-resolution pulsed Fourier transformation NMR spectroscopy to make possible noninvasive, nondestructive, spatially resolved. chemical analyses of the interiors of objects (magnetic resonance spectroscopy, MRS). Lauterbur's technique was quickly matched by related techniques from other pioneering research groups. At least eight different approaches to image formation were put forward by these groups. Mansfield and Grannell (1973) described NMR "diffraction." Hinshaw (1974), described two further techniques involving time-dependent magnetic field gradients. He advanced the term "spin mapping" in recognition that an NMR image is a map of nuclear spin density and related parameters. In 1976, Hinshaw put forward "the multiple sensitive point method" of image formation by NMR, which was then used in the first NMR ciinical trials in Nottingham. Kumar, Welti and Ernst (1975) carne forward with another approach, conceptually more sensitive, which resulted in the first practical demonstration of two-dimensional NMR spectroscopy. This technique remains one of the most informative in molecular biology, allowing a complete determination of the three-dimensional structure of proteins and nucleic acids in solution. The present-day rapid-sequencing, high-resolution MR images have been a consequence of the development of equipment such as the large magnet with an intense and homogeneous field, extensive radiofrequency equipment (transmitters and receivers), gradient coils, and advanced computer system for the two-dimensional Fourier transformation of extremely large data sets. Supporting control and display units and facilities for digital data storage are also indispensable. The first demonstration of intracranial pathology by nuclear magnetic resonance (NMR) tomography of the brain was produced by Hawkes, Holland, and Moore-physicists-and Worthington, a neuroradiologist, in Nottingham, England in 1980. In the 1990s, high-resolution magnetic resonance imaging (MRI) has become the imaging modality of choice for investigation of central nervous system neoplasms.

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Isotope Brain Scanning Radionucleotide imaging of brain tumors was first shown to be of localizing value in the late 1940s. The highest accuracy was achieved in intracranial masses with increased vascularity and edema, such as meningiomas, cerebral abscesses, and metastases (provided the latter were over 2 cm in diameter). Diagnostic accuracy rapidly declined in the case of gliomas and astrocytomas. Thus, the number of false negatives was comparatively high, depending on the type and location of the tumor. In the 1960s, the gamma camera was introduced by Anger, and with the ready availability of isotopes (such as technetium-99) with moderately short half-lives, isotope brain scanning became the least invasive investigation of initial choice for a suspected brain tumor. Di Chiro (1964, 1969) popularized the technique, which reached its zenith between 1970 and 1973. There were three major limitations to brain isotope scanning detecting a tumor. First, a positive result depended on disruption of the blood-brain barrier, or considerable alteration in lesion vascularity. Supratentorial low-grade gliomas were missed in up to 25% of cases (Baker 1976). Second, the lesion had to be greater than 1.5 cm in diameter. Third, the gamma carneras then in use were more sensitive to superficiallesions, and deeply placed central nuclear tumors and tumors in the posterior fossa were frequently missed. False-negative rates of 60% for brainstem tumors and 30% for cerebellar tumors were reported (Burrows 1976).Overall false-negative rates of up to 25% in proved cases of malignant brain tumors were reported by Baker in 1980 from the U. S. National Cancer Institute. In addition, the gross lack of specificity of a positive scan and the lack of information on the secondary effects of the lesion and its internal composition meant that the differential diagnosis often remained broad, including abscess and infarct. This necessitated the routine use of more discriminating, and more invasive, tests (cerebral angiography and pneumoencephalography) to confirm the diagnosis prior to surgery. Conventional radionucleotide studies do remain useful in two situations. Isotope bone scanning is a very sensitive detector of bone destruction, and still merits consideration in patients with suspected metastases, both cranial and extracranial. In cases of CSF rhinorrhea, the intrathecal injection of isotope may often prove the existence of a CSF fistula. When combined with the recovery of positively emitting, previously' placed intranasal pledgets, not only is the diagnosis confirmed, but also the site of origin of the fistula is proven.

Functional Neuroimaging Xenon CT Nonradioactive xenon is an inert gas with an atomic number close to that of iodine, which, when inhaled in sufficient quantity, crosses the blood-brain barrier and remains in the brain for a sufficient time to permit serial CT scans to be performed. Regional cerebral blood flow (rCBF) can be accurately and reproducibly measured, using calculations derived from CT numbers and end-tidal xenon concentrations. Decreased rCBF can be shown in cerebral infarction, transient ischemic attacks, gliomas,

and hypometabolic interictal seizure foci. The major advantages of the xenon CT technique are its high degree of anatomical specificity and its ability to measure the blood-brain partition coefficient in normal and pathological tissue. However, there are enough significant practical, theoretical and biologicallimitations to restrict its widespread use.

Emission Computed Tomography Emission computed tomography in its two forms, positroncomputed tomography (PET) and single photon emission computed tomography (SPECT) combines advances in radionucleotideisotopes with computer technology that permits the mathematical reconstruction of data obtained from multiple projections. Both provide true three-dimensional images of the brain with a maximum resolution of 5.0 mm, and measure concentration of radioactive tracer in nC/ml (Table 3.1). Table 3.1 Neuroimaging: tomographic techniques (alter Di Chiro, Encyclopedia of Neuroscience, Neuroimaging: vol. 2,1990, p. 795-799) Technique

CT

MRI

Property measured

Associated physical parameters

Units

Roentgen ray attenuation coefficient Net transverse nu-

Electron density, atomic number Proton density, T" T2' Ilow Glucose and oxygen utilization rates, blood flow, etc. (depending on radiotracer

HU

0.7mm

Beamhardening

Not relevant

0.3mm

Field inho-

nCi/ml

5.0mm

clear magnetization ECT Concentration 01 (PET, SPECT) radioactive tracer

Maximum resolution

Artilacts engendered

mogeneity

Scatter, attenuation

Positron Emission Tomography Positron emission tomography (PET) is based on the detectionof two high-energy roentgen ray photons that have been emittedas the result of the destruction of a positron. Positrons are produced in a cyclotron from certain radionucleotides with short half-lives. Availability has been limited to research centers, and it remains quite expensive. PET has proved useful in the evaluation of cerebral blood flow, cerebral volume, oxygen transport and metabolism, glucose utilization,amino acid transport and metabolism, and proteinsynthesis. Its role in tumor management has been in the study of functional changes within and around tumors, and the courseof

such changes after treatment. The recent discoveryof a drugthat blocks specific rate-determining steps in brain tumor mitosis (Aston University, ICRF, Plough-Schering) may expand the use of PET from pure research to more routine clinical use.

Current Neuroimaging with CT and MRI

197

SinglePhoton Emission Computed Tomography

Magnetic Resonance Angiography

Singlephoton emission computed tomography (SPECT) is a lowcosttechnique of imaging the three-dimensional distribution of radioisotopes.The technique uses the same kinds of gamma-emittingisotopesroutinelyemployed in most hospital nuclear medicinedepartments,and does not require the availability of an on-sitecycIotron (necessary for PET). SPECT scanning permits the creation of multiplanar tomograms that measure local cerebralbloodvolume,localcerebral blood flow,blood-brain barrier abnormalities,and other cerebral metabolic parameters.

Magnetic resonance angiography (MRA) exploits the fact that cerebral arteries are routinely visible on spin-echo images, due to the flow-void phenomenon. MRA techniques rely on special pulse sequences (sensitive to flow) and on sophisticated processing of the data to give images similar to standard contrast catheter angiograms. The major present applications for MRA are screening for atherosclerotic disease of the extracranial and major intracranial vessels around the circle of Willis. MRA can be used as a screening test for intracranial aneurysms in asymptomatic patients (e. g., family members of patients who have had aneurysms). Recent improvements in the sensitivity and resolution of MRA have been impressive enough for us to use it in the evaluation of certain intracerebral tumors to help decide which of these merit additional study by selective cerebral arteriography. Although intrinsic and extrinsic tumor vessels can be routinely visualized, MRA is of little value in precisely identifying the feeding vessels, and certainly provides no information about the quality (e. g., fragility) of these feeding arteries (see Fig. 3.14, 3.49, 3.48).

CurrentTrends Neuroimaginghas continued to evolve to become a comprehensivediscipline that investigates and displays both normal and abnormal, structural and functional anatomy in the central nervoussystem. Of future importance will be the integration of noninvasivetechniques that precisely demonstrate, to resolutions of 1-3 mm, both structural and functional areas of the brain together.

Echo-planar MRI Magnetic Encephalography Magneticencephalography (MEG) has shown how this precise localizationcan be achieved in the somatosensory and motor areasof the cortex. No doubt the same precision will be achieved withthethreemajorarea componentsof speech.Of more immediate usefulnessare techniques that allow the noninvasive assessmentof alterations in the vascular and CSF systems in and around cerebraltumors,such as magnetic resonance angiography (MRA) andechoplanar MRI.

Echo-planar MRI technology involves the production of ultrafast MRI images (1-2 seconds). It has been used to study real time CSF dynamics and blood flow in vessels and, in addition, may ultimately prove beneficial in the utilization of MRI for the evaluation of cerebral metabolic processes. Unfortunately, it is not inexpensive to adapt it to present MRI imaging capabilities. The need for a high-strength magnet (3.0 Tesla or more) and some uncertainties about the long-term safety may inhibit further clinical development. Future development of fast T2 imaging techniques (3-4 minutes) may prove to have more widespread applicability than echo-planar MRI.

CurrentNeuroimaging with CT and MRI Whilemanyof the problemsof tumor detect~on,localization,and pathologicalcharacterization were solved for extrinsic tumors by the advent of high-resolution CT and MR imaging, especially afterthe introduction of nonionic contrast agents, the pathophysiologicalsignificance of many of the changes seen on MR with intrinsictumors remains uncertain. For neurosurgeons, the sensitivityofcurrent CT and MR in localizing pathology is truly impressive.yet the lack of pathological specificity has been a disappointment.The cIinical history and examination are, and will remain, vital discriminatorsin narrowing the differential diagnosis. To makethe best use of current neuroimaging techniques, close discussionsbetween neuroradiologists, neurosurgeons, and neuropathologistsare more important than ever. Hopefully, parallel developmentsby these associated specialists willlead to a better understandingof tumor pathophysiology (Table 3.2). It is not the intention of this chapter to provide a compendiumof intracranial pathologies and their various radiocharacteristics,but rather to stimulate critical analysesof graphic

how current neuroimaging can be better utilized. Detailed information on these topics and specific lesion characteristics are well reviewed in the literature (Kazner et al. 1988, Bradley et al. 1990) and in current textbooks (Brant-Zawadzki and Norman 1987, Orrison 1989, Higer and Just 1989, Grossman 1990, Chakeres 1991, Dietemann 1993). A higher level of gray /white matter contrast is obtainable with MRI when compared with CT. The degree of anatomical detail shown on the three orthogonal planes is greater with MRI. MRI offers increased sensitivity with earlier detection of smaller lesions in areas previously difficult to image with CT. MRI provides higher-resolution detail of the posterior fossa and skull base. MRI does not have the problems of bone-volume averaging and beam-hardening artifacts that contribute to the false-negative results obtained with CT in these regions. This increased sensitivity of MRI over CT extends to the evaluation of head trauma (Han 1984).

1

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3 Neuroradiology

Table3.2 Current neuroimaging (CT and MRI)capabilities General aspects Morphologicalchanges Neoplasms: primary and metastatic vascular lesions: aneurysm, AVM,ischemia, hematomas Inlectious diseases White-matterdisease: MS, leukodystrophies, encephalopathies CSF system (hydrocephalus, secondary atrophy) Congenital anomalies Traumatic lesions Location01the lesion Extrinsic Intrinsic(neocerebral, neocerebE¡Jllar,limbic-paralimbic, central nuclei, and intraventricular) Postoperative morphological changes (local and remote) Hematoma Edema Inlarction CSF hygroma and hydrocephalus Completeness 01surgery Residual or recurrent pathological tissue Special aspects: secondary lunctional changes CSF dynamics Hemodynamics Biologicalbehaviour 01the lesi.on Progressive Regressive Inactive Parenchymal dynamics Atrophyand related degenerative changes Tissue intensity changes: perilesional changes ? Biochemical metabolic interactions ? Inliltration01tumor cells Posttreatment effects: surgery, chemotherapy, or radiatiotherapy

Table 3.3 Comparison 01 CT with MRI

Technique Sensitivity Specilicity Spatial resolution Soft-tissue contrast

Blood-brain barrier evaluation Functional capabilities Developed by Ho

CT

MR

First to directly image CNS Limited Fair High

Direct images 01CNS

1) Moderate High-resolution images 01bone Poor gray-white neuroanatomy

2) Limited pathological sensitivity Intravenous con-

trast uselul Poor

Éxcellent Moderate Very high, in three planes 1) Excellent High-resolution images 01bone marrow, CSF spaces, graywhite anatomy, and most gross neuropathology 2) Moderate pathological sensitivity Intravenous gadolinium very uselul Limited

Comparison of CT with MRI During its development, it was predicted that MRI wouldhave three advantages over CT, namely, that (a) MRI scanning usesno ionizing radiation, (b) it requires no moving parts to perform a scan, and (c) multiplanar (axial transverse, coronal, and sagittal) tomograms are easily obtained, since the scanning mechanismis entirely electronic (Holland et al. 1985). The ability of MRI tomography to directly produce coronal and sagittal, as well as axial transverse, images has shown itself today to be the best meansof precise lesion assessment (Table 3.3). In Chapter 2, the importance of identifying the subgyral, gyral, or lobar peduncular origin of the primary location of many intrinsic brain tumors is stressed. Tumors in these locations distort the normal morphology of the brain and make localization difficult. MRI has made this localization much easier. Neurosurgeons, in particular, are most grateful for the specific anatomicallocalization that current MRI, when properly used, is able to provide. Sagittal and axial MRI provides excellent extrinsic tumor imaging detail. Coronal MRI imaging is the most useful image plane inpreoperative localization and surgical planning for intrinsic tumors, as the white-matter peduncular architecture of most gyri can be

most favorably recognized in this planeoFor the frontal and temporal gyri, on the other hand, the horizon~al or sagittal viewsare more helpful. Careful analysis of pre-gadolinium and postgadolinium TI MRI scans in three planes will nearly alwaysprovide the precise anatomical information that is a prerequisite for preoperative surgical planning.

MR Image Selection Unlike CT, MR allows an almost infinite number of manipulations to obtain a diagnostic image and to vary the contrast on images. The choice of independent tissue variables that provide the best contrast on diagnostic evaluations include pro ton density, T ¡-weighted, Tz-weighted, and "flow" -weighted images.The selection of which pulse sequences to use in the evaluation of anysuspected pathology is important not only in eliminating false negatives and in maximizing sensitivity, but is also vital for subsequent correct interpretation. With an initial (diagnostic) study of a suspected tumor, all three types of main sequences (proton density, T,-weighted, and Tz-weighted images) need to be obtained before a study can be regarded as complete. In reality, it is useful to regard each set of images as totally different imaging methods (as different as MRI is from CT), each with its own advantages, disadvantages, and limitations. Therefore, at least three completely different sets of MRI images have to be interpreted using different criteria. In addition to being fully aware of technical variables and limitations, it is especially important for neurosurgeons to realize that artifacts and distortions of real anatomy, especiallyat interfaces, can be significant (Pusey et al. 1986, Kelly 1987). (Table 3.6). With MRI the differences between T,-weighted and Tz-weighted images in various normal and pathological tissues are greater than the variations in proton density. The selectionof various pulse sequences is used to "weight" the images toward TI or Tz data. This forms the basis for the increased sensitivityof MRI. The choice of image sequence parameters can still be critically important in lesion detection (Table 3.4). Some convexity

Current Neuroimaging meningiomas without secondary parenchymal changes can detectionunlessappropriate TI and T2sequences are perescape formed. MRI may underrepresent or overrepresent tissues at interface s betweenCSFand brain parenchyma.The width of sulci is commonly exaggerated, and adjacent gyral surfaces underrepresented. Anatomical resolution is best with TI images, and pathologicalsensitivity greatest with T2 sequences. Image interpretationfollows hnes similar to those used in CT interpretation. Detailedanalyses of geometric factors and 2 tissue contrast factorsare crucial.

MR appearance White 'Increased signal (short) T,W

ContrastMRI

Usefulnessof MRI in Distinguishing VascularMass Lesions from Tumors

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Table 3.4 Interpretation of T1-weighted and T2-weighted MR images (alter Orrison, Introduction to Neuroimaging, Boston: Little, Brown, 1989, p.87)

Increased signal (long) T2W

Doubts about the sensitivity of CT in identifying tumors promptedAmbrose to develop a contrast agent. The comparison of contrast with noncontrast scans enabled CT to demonstrate tumorneovascularization and alterations in the blood-brain barrier.MRI carne into clinical use before a suitable contrast agent hadbeen developed. The hope was that, with its increased sensitivity over CT and with suitably chosen T2 sequences, a contrast agentwould not be needed. This was not the case. Since 1986, MRI with paramagnetic contrast agents such as Gd-DTPA has increasedthe sensitivity for detection of CNS lesion to a higher leve\.Forexample,compared to a noncontrasted scan, MRI with Gd identifies 15% more metastatic tumors. Contrast MRI is of greathelp in differentiating tumor from perilesional changes. The useofcontrast studies is of major importance when one considers that over 50% of patients with intracranial neoplasms have few localizingsigns and normal neurological examinations.

with CT and MRI

Typical causes

Fat Normal white matter Paramagnetics Lymphoma Chronic hematoma H20 CSF Paramagnetics Edema Inflammation Infarcts Neoplasms Multiple sclerosis Normal gray matter Lymphoma Chronic hematoma

Black or gray Decreased signal (long) T1W

Decreased signal (short) T2W

Ca2+ Blood or CSF flow H20 CSF Edema Inflammation Neoplasms Normal gray matter Lymphoma Ca2+ Blood or CSF Fat White matter Lymphoma Acute hematoma

White: increased signal = short T1' long T2 Black: decreased signal = long T" short T2

this work focuses on brain tumors, vascular lesions can Although sometimespresent as mass lesions. The noninvasive differentiationbetween these two types of pathology is important. MRI is ableto provide far more useful information on the structural and temporal changes associated with hemorrhage and infarction thanCT is.Sometimes even the underlying pathological vascular lesioncan be determined (e. g., AVM or cavernomas). MRI can identify changes associated with subarachnoid hemorrhage, aneurysm,angioma, and occlusive vascular disease. Ischemia, infarction,hematoma (epidural, subdural, intraparenchymal, and interventricular)can also be evaluated.

Functional Studies MRI candefine functional relations between

normal and abnor-

mal tissues better than previous studies. By itself, though, its lack of specificity remains a limitation, especially when attempting to differentiate neoplasms from other disease processes. Current workis aimed at to increasing our functional knowledge of brain tumors. Sodium-gated MRI may provide more information regardingtumor grade and local extension. MRI is very sensitive in displayingperilesional changes, of uncertain significance and conflictinginterpretation. This problem will be further examined below.

Failure of MRI to Detail Surgical Pathophysiology Two other important considerations must be integrated in the synthesis of the final surgical strategy. First, the pathology of the tumor, and second, its functional effects (Iocally, globally and systemically). Unfortunately, these are the two areas where MRI, even with its exquisite sensitivity, has failed to live up to early expectations. This failure has been a particular disappointment and a frustration to surgical decision-making. For many tumors, the specific MR imaging parameters that precisely define pathology (consisten<;y, vascularity, adherence, and extension or infiltration) are yet to be determined. The maximum MRI resolution attainable at present is down to 0.3 mm.The benefits from this degree of detail need to be exploited with a more precise correlation with tumor morphology and histology, and with a better physiological undestanding of the peritumoral changes seen so well on T2 images. Closer cooperation between neurosurgeons, neuropathologists, and neuroradiologists in correlating pathological findings, radiological images, and surgical findings will help determine those specific additional MRI sequences that may best answer these questions of profound surgical interest.

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3 Neuroradiology

Future Correlation 01 MRI with Functionallmaging

demonstrated in white matter, depending on the direction in which pulsed gradients were applied. These effects enabled specific white-matter tracts to be identified, depending on the direction of their fibers. The technique may have application ina wide range of neurological diseases, and results in better localization of lesions and improved detection of disease (Doran et al. 1990,Fazekaset al. 1991,Marshall et al. 1988).

Curiously, the ability of MRI to detail brain morphology, and developments in the understanding of functional localization within the brain, come nearly 100 years after the same topics split the neuroscience community. Psychiatrists, behavioral psychologists, and neuropharmacologists are now increasingly interested in MRI correlations of morphology and higher cerebral functions. Certainly, neurologists and neurosurgeons continue to be interested in new neuroimaging techniques that can precisely correlate specific functional are as (e. g., speech areas) with tumor location on MRI. The precise assessment of epileptogenic foci around mass lesions, whether tumor or vascular, is of crucial concern in microsurgical decision-making, and for the prognosis of a seizure disorder. Very promising is the use of pulsed magnetic field gradient spin-echo technique, as changes in signal intensity can be

Recent MRllmprovements Three-dimensional MRI technology will soon be available. The most recent MRA quality and detail is impressive. Hopefully,visualization of the brain parenchyma and blood vessels in three dimensions will supply the surgeon with a more realistic viewof internal CNS pathology and its relationships to surrounding structu res.

The Application of Neuroimaging Capabilities to CNS Tumors Lesion Morphology

(Structural

associated mass effect. Interstitial edema is seen around the ven. tricJes in association with hydrocephalus, and is a result of the increased hydrostatic forces driving fluid into the periventricular space. Cytotoxic edema is demonstrated in conjunction with ischemia and infarction. In additio~ to an identification of edema, newer techniques. incJuding gradient echo technology, can identify flow voidssignifying peritumoral vessels. Intratumoral vessel identification usually supports the diagnosisof a malignant lesionoGradient echo techniques can identify tumor caJcification, a finding uncommon in high-grade lesions unless the tumor has been transformed froma low-grade one. Though MRI and CT can provide important structural information as to the nature of the lesion preoperatively. MRI is much better at identifying hemorrhage within a tumor. The tumors most commonly associated with intratumoral hemorrhage are high grade gliomas and metas tases from hypernephroma, melanoma, thyroid carcinoma, and choriocarcinoma.

Changes)

cr and MRI provide images reflecting changes in the morphology of the CNS parenchyma. These advanced neuroimages can identify changes in CNS structures resulting from vascular occlusive disease, hemorrhage, infection, degenerative disease, and neoplasm. The effects of these processes on the surrounding CNS can be seen as well, although their significance remains unclear (e. g., perilesional changes). MRI and CT provide instant information concerning the size, site, extension, shape, and number of lesions and secondary changes. CT was the first study to provide direct images of the brain, cisterns, and ventricles. The effects of tumor, incJuding edema, mass effect, midline shift, and cerebral herniation, conld be readily seen. The addition of iodinated contrast, which demonstrates disruption of the blood-brain barrier, allowed for increased tumor detection. Previous noncontrasted scans that showed a pool of edema were frequently seen to "light" up, demonstrating a previously unrecognized tumor. Combined with cJinical information (particularly the age of the patient and the length of the history), the current images quickly suggest whether a tumor is most likely to be primary or secondary. MRI is an even more sensitive method of determining structural abnormalities than CT. (CT has now become the second most sensitive test for identifying CNS neoplasms). The introduction of Gd-DTPA with MRI provides the most sensitive test yet for identifying CNS abnormalities. Tz-weighted sequences on

MRI are particularlygood at demonstrating edema. The common forms of brain edema are vasogenic, hydrostatic (interstitiai) and cytotoxic. Vasogenic edema is the most common type identified, and is that frequently associated with white matter edema. It is manifested as an increased T2 signal around areas of abnormal blood brain barrier. Typically, this is seen along white-matter tracts, as it tends to spare gray-matter structures. In higher-grade tumors, vasogenic edema can be spaceoccupying, and thus be responsible for a large amount of the

Lesion Location (Topography)

.

Not only do the structural images of lesions help to identify them on CT and MRI, but their location also plays an important role in determining the differential diagnosis. CT and MRI are usually able to determine if a tumor is extrinsic, intrinsic, transitional, or intraventricular. MRI is very effective in demonstating the morphology of tumor-associated herniation as related to the CNS compartments. The common CNS compartments visible on MRI. and involved in herniation syndromes, are listed in Table 3.5.The subarachnoid spaces (incJuding suJci, fissures, and cisterns) are the most common sites involved in brain-tumor herniation. and these areas are well delineated on MRI. As a result, it is possible to describe the topography of a herniation of brain tissue or tumor (or both) precisely from an expanding intracranial neoplasm. This subarachnoidal herniation may be related to direct compression by the tumor, or bordering

The Application of Neuroimaging Capabilities to CNS Tumors gyri(or folia), with compression of neighboring compartments. Extrinsicand intrinsic tumors commonly compress the surroundingsu1ci(and fissures) as an initial manifestation of herniation. Theinvolvedsu1ciare usually compressed and displaced by a dislocatedneighboring gyrus (or the tumor itself, or both). With a knowledgeof the topography of the gyrus involved, one can anticipatethe su1ciand gyri involved. It is important to note that precise structurallocalization of everybrain tumor and its associated herniation should be attemptedon the basis of neuroimaging. However, this informationshould no! be used to diagnose the patient's clinical condition.Many examples are provided at the end of this chapter, demonstrating the uncertain and confusing lack of correlation betweenthe topography of CNS tumors (and associated effects) andthe patient's clinical status. Certain tumors have a propensity for certain locations. PrimaryCNS B-celllymphoma is commonly found in close proxim¡tyto deep central nuclei. Metastases tend to be multiple and appearat the gray-white junction. Metastatic breast, lung, and occasionallyprostate tumors, have a propensity to deposit on the dura. Neuroimaging (MRI and CT) frequently demonstrates osseousherniation of tumor (or brain) that may occur through arachnoidal granulations, with partial or full-thickness bony destruction.In addition, bony erosion may be seen (primarily in meningiomas)in the parasellar region, middle fossa (into the pterygopalatinefossa), sphenoid bone, mastoid, clivus, and calvarium. Tumorsmay grow into the bone surrounding the dural sinuses (cavernous,superior sagittal, petrosal, transverse, sigmoid, and torcular),and the foramina and fissures (cribriform plate, optic' foramen,superior and inferior orbital fissures, foramen ovale and foramenrotundum Meckel's cave, acoustic foramen, jugular foramen,and occipital foramen. Finally, tumor expansion may be seen into the mucosal sinuses (frontal, sphenoethmoidal and maxillary)(Table3.5).

J..

Table3.5 Common compartments

Durall septal Tentorial(cerebral downwards, cerebellar upwards) Sublalcial Ventricular Lateral(Irontal, corpus, trigone, occipital, temporal) Thirdventricle (inleroanterior, middle, posterior) Aqueduct Fourthventricle Osseous Arachnoidalgranulations Calvarial Duralsinus Foramenand lissures (11,111, V, VII-VIII, IX-XI, and occipital foramen) Mucosalsinus (frontal, ethmoidal, sphenoidal) Intravascular

Precise localization of lesions with respect to extrinsic and intrinsic location enables the neurosurgeon to correlate the surface topographical anatomy in vivo to that represented on MRI and thus to precisely plan the opera tive approach.

Other Diseases CT and MRI are also helpful in the identification of lesions other than tumors and vascular abnormalities. Those lesions that frequently enter into the differential diagnosis are: infectious processes, the sequelae of AIDS, parasites, and granulomas. These can be suspected on the basis of their structural changes and location, and in correlation with the history. Certain pathogens have a predilection for certain areas. For example, toxoplasmosis has a predilection for the central nuclear areas in the adult and the periventricular region (with ca1cifications) in the neonate. Cysticercosis may appear as a ca1cified mass with surrounding low attenuation, and it may enhance with contrast (as a ring or in a homogeneous pattern). The presence of multiple ca1cifiedmasses, in the proper setting, in the cortical and subcortical regions should aro use suspicion of an infectious etiology. CT and MRI have been useful in identifying white-matter disease. The plaques of multiple sclerosis are often identified on MRI, as increased periventricular signal'in the deep white matter. Leukodystrophies have certain additional characteristics, including abnormal decreased signal intensity in the central nuclei and thalamus, correlating with an increase in trace metals or iron in these gray-matter structures.

Ventricular Abnormalities Morphological changes depicting abnormalities within the CSF system can be readily identified with CT and MRI. Interpretation of additional changes, seen better on MRI, can usually determine whether the cause of the hydrocephalus is obstructive in nature or due to a reabsorption problem.

involved in herniation syndromes

Subarachnoid Sulcal(cerebral, cerebellar) Cisternal(basal) Parachiasmatic, parasphenoidal, subtentorial, paramesencephalic, parapontine, parabulbar, cisterna magna Fissural Sylvian,interhemispheric, transverse, cerebello-mesencephalic, cerebellDpontine,cerebellomedullary

Duralsinus

201

Postoperative Morphological Changes One of the great advantages of the CT and MRI era is the possibility of noninvasive postoperative imaging. This capability has been of life-saving benefit to individual patients, and has had longterm consequences in reducing postoperative morbidity in following up pathological processes and in monitoring different therapies. As outlined in Chapter 4, our understanding of the way tumors alter neurophysiological mechanisms and upset the integration of the central nervous system is still incomplete. In patients with an unexpected postoperative course, CT provides quick and usually reassuring information. Life-threatening hematomas (either focal or remote) and hydrocephalus can be swiftly diagnosed and treated. Infarction and delayed subdural collections can be identified. CT in the first 1-5 postoperative days is clearly more pragmatic than MRI (less costly, and less disturbing for the patient). The adequacy of therapy, including completeness of tumor removal, is far better assessed by MRI 3-4 weeks after surgery, when many operative changes (edema, small hematomas) have subsided. At later intervals, serial MRI scans provide information regarding residual or recurrent pathological tissue, or the effects of additional treatments.

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FunctionalChanges In addition to the structural information provided, CT and MRI have proved useful in yielding information on secondary functional changes. The functional CNS dynamics of CSF and blood can be assessed with CT and MRI. In addition, the biological behavior of lesions (aneurysms, angiomas, neoplasms, hematomas, abscesses, infections) can be followed. Progressive, regressive, or inactive processes can be diagnosed by comparing serial scans over time. Combined with the clinical history, the nature of parenchymal dynamics (including atrophy and degenerative changes) can be interpreted. T)1e tissue-intensity changes seen with MRI have specific characteristics related to various constituents at different times (e. g., phases of blood breakdown within a lesion over time). Perilesional edema, metabolic biochemical interactions, and perilesional infiltration of tumor cells are other parenchymal dynamic changes that await more intense investigation by MRI and MRS.

Difficulties and Limitations of Neuroimaging Even with the optimal use of CT and MRI, neurosurgeons have come to recognize significant limitations and difficuIties with regard to differential diagnosis, topography, extent of lesion, perilesional changes, adherence, and cleavage planes (Table 3.6). In over 90% of cases, the CT and MRI images provide us with a clear differential diagnosis. However, it is important to remember that these images are merely electronic shadows (different gray-scale shades) presented on a macroscopic, inanimate, two-dimensional framework. This is far different from the complex, living, fourdimensional milieu that really exists; it should not be overlooked that the fourth dimension is time, and the pictures in front of us provide only a static image at a fixed point in time. It is sometimes difficuIt to differentiate between neoplasm, vascular lesion, infection, and degenerative disease. The ability to distinguish lesion type solely on the basis of image characteristics is inconsistent. Even the same type of lesion can appear completely different. It can be especially challenging to differentiate a neurinoma from a meningioma or, less commonly, a meningioma from a glioma. "Butterfly" lesions may reflect glioblastoma, lymphoma, progressive muItifocal leukoencephalopathy, or other uncommon processes. A single contrastenhancing lesion may represent a glioma, abscess, Iymphoma, metastatic or anoaItogether different process. Certain morphological characteristics seen on CT, such as calcification, may not be visible on MRI. Small meningiomas not producing edema can be missed on MRI, aIthough the use of gradient echo techniques and the use of contrast has helped overcome this problem. Still, the diagnosis is inaccurate in 10% of cases. Certain vascular lesions, including cavernomas, microangiomas, telangiectasias, and cryptic angiomas cannot be distinguished on MRI. In addition, these lesions can mimic tumors, and vice versa. This lack of neuroimaging spedficity is a problem that neurosurgeons are frequcntly confronted with. Other tests are of no help, but the patient expects a firm recommendation. Compounding this diagnostic uncertainty is the question of the pathological or behavioral activity of vascular mass lesions. If the lesion is active (enlarging, demonstrating a propensity to bleed) management is straightforward. However, the lesion may have been

Table 3.6

Difficulties and limitations of neuroimaging

Differential diagnostic difficulties Process: neoplasm, vascular, infectious, degenerative Between neoplasms: meningioma, glioma, metastasis, ete. Between vascular lesions: cavernoma, venous angioma, telangiectasia, microangioma, cryptic angioma, ete. Necrotie tumor parenchyma, cyst, old hematoma Topographic difficulties Extrinsic: epidural, intradural, subdural, or mixed Intrinsic: expanding lobar concepts to the subgyral, gyral,lobar, or hemispheric peduncle 1. Neocerebral, neocerebellar 2. Transitional: Limbic (septal areas, substantia innominata, amygdala, hippocampus) Paralimbic (temporal pole, fronto-orbital, anterior insula, eingulate, parahippocampal) 3. Central gray matter a) Basal ganglia (eaudate, putamen, pallidum) b) Central nuciei (thalamus, meta-, epi-, sub-, and hypothalamus) c) Brainstem (mesen-, meten-, myelencephalon) 4. Intraventricular (lateral ventricle, 111, aqueduet and IVventrieles) Paraxiallesions: parasellar, ehiasmal, tentorial,peduncular, pineal, pontine, bulbar Herniation-infiltration . Subfaleial, subtentorial, parachiasmal, parapineal Borderline Extension of Lesion - Expansion - Infiltration Perilesional changes (hYPodensity, hyperdensity, or hypo- or hyperintensity) Edema, isehemia, infaretion Metabolic ehanges Infiltrationby tumor Seattered tumor cells Cleavage-no cleavage Adherenee between tumor and Arteries, veins, sinuses Dura, araehnoidea, pia Parenchyma Ependyma { Plexus

peritumoral struetures Infiltration Invasion Adherenee Gliosis Membrane formation

Detailed lesion construction Neoplasms 1. Homogenous or heterogenous 2. Cyst: fluid or tumor tissue 3. Consisteney: soft or hard 4. Vaseularity - Ouantitative: - Oualitative:

active and bled, but destroyed itself in the process (autodestruction), or it may be inactive (dormant). Deciding these questions with any rational certitude on one set of MRI images is not possible. In the posterior fossa, CT images are often degraded by bonevolume averaging, whereas MRI permits better tumor localization, and may allow tumor consistency interpretation. The resolution detail with the soft tissues is also higher with MRI. Overall. the routine use of sagittal, coronal, and axial MRI images provides more precise localizing detail than CT. As we plan OUT opera-

The Application of Neuroimaging Capabilities to CNS Tumors

Tumors can be either circumscribed, semicircumscribed, or, less commonly, diffuse. MRI signal and CT intensity changes are often unable to define cIear tumor boundaries with any confidence. Often, "irregularly shaped" tumors appear diffuse and inoperable, yet, at surgery, an oddly shaped but well circumscribed lesion is found that can be removed with only a moderate degree of difficulty. In the early or intermediate phases of growth, gliomas tend to expand within one segment of one gyrus, or within one part of a central nucIeus, or within one section of the ventricular system. Based on normal anatomical knowledge, it is consistently rewarding to make a formulation of the anatomical origin of a lesion and then, during surgery, find its center in just that location. In the early phase of growth, only 1% of gliomas, are in our experience truly diffuse (and in less than 0.1% of them there is gliomatosis). Most commonly, a lesion that appears to be infiltrative due to its peculiar shape is, upon removal, expansive, compressing and distorting adjacent structures, but is not in fact infiltrative.

tiveapproaches, we wish we had a greater understanding of the topography and real nature of each individual lesion, but this informationremains incomplete.

Topographic Difficulties Extrinsic.In spite of advances in neuroimaging, it sometimes remainsdifficult to determine whether a lesion is extrinsic or intrinsic.If it is extrinsic, even with the use of contrast it is often unclearwhether the lesion is extradural, intradural, subdural, subarachnoid,or mixed, as cIear identification of the dura itself is frequentlyjust not possible (see Cases 3.5, 3.7, 3.11, 3.12, 3.28, 3.31,3.32). lotrinsic.The localization of intrinsic tumors can be just as problematic.This was especially true when using the traditional "lobar"view of the brain, which is far too broad and prevents a criticaland more detailed analysis of the likely site of tumor originoOur current concepts (see chapter 1) define the tumor locationbetter, and have important surgical implications. Intrinsiclesions should be thought of in gyral concepts, after subdivisioninto one of the neocerebral / cerebellar, limbic, central nuclearor intraventricular tumor categories. We have to be more precise inourevaluationof intrinsictumor location, realizingthat thefocalsurgicaland functional anatomy may be quite distinct. In planningsurgicalresection, it is very important not to consider all tumorsin one lobe as being of the same category. It is essential for thesurgeonto attempt to describe the location of a tumor as referableto a specificgyrus or subgyrus, as most glial tumors arise from a segmentof only one gyrus (see Cases 2.1-2.14). In addition, the assumptionthat the superimposition of a tumor on the underlying anatomymust reflect infiltration of the lesion may give a false impressionof the true topography of the lesiono Infiltration may be "overread" unless the real anatomy of a tumor is understood. Forexample,the anatomical distortions of three contiguous gyri bya tumor,which is in fact arising in only one should not be necessarilyregarded as tumor infiltration of all three. "Overcalling" the extentofmalignantinfiltrationand

"underreading" the tru~ ana-

tomicallocationof a tumor can seriously distort surgical planning, andlead to intraoperative surprises. Paraxial.Paraxiallesions can also pose a problem in location. In many instances, parase llar, parachiasmal, paratentorial, parapeduncular,parapineal, parapontine, and parabulbar lesions are notsharplyseen on CT and MRI. Again, superimposition of normal and abnonnal structures may cause a paraxial lesion to appearinfiltrating (see Cases 3.5, 3.32. 5.9-5.11). lo addition to a false appearance of infiltration, herniation of cerebraltissue is often so distorted that it may be misinterpreted. Thedegree of herniation, whether subfalcial, subtentorial, parachiasmal,parapineal, or latero-orbitofrontal, can easily be underestimatedor missed (see Case 5.17). Bouodaries.Extrinsic tumors are usually well circumscribed pathologicalentities and, with the vast majority of virgin (i. e. not previouslyoperated) tumors, the tumor boundaries can be seen adequatelyon CT or MRI. Deciding whether there is true dural or venoussinusinvolvement,or

both, can be a major problem in a

smallnumber of cases. Preoperative imaging of intrinsic tumors however, does not reliablyprovide the surgeon with precise tumor boundaries.

203

Peritumoral Changes In addition to our present limitations in defining tumor boundaries, the extension of the tumor is often difficult to determine. In a review of many preoperative images, the difference between tumor expansion that compresses normal structures and frank infiltration is obscure. Tumor infiltration 'is vicariously inferred from the T2 peritumoral changes on MRI associated with tumors (These changes, generally, are bright are as on TTweighted images that irregularly circumscribe mass lesions with finger-like projections extending into surrounding parenchyma) (Table 3.7 and Fig. ,

2.9, p. 148). Trittmacher et al. (1988) identified two types of peritumoral changes on MRI. Type I occurs characteristically around benign tumors such as meningiomas. It is localized on MRI to the region immediately around the tumor, and persists indefinitely (hyperintense area) on MRI. It is believed by many that this type of peritumoral change represents the permanent effects of severe edema, ischemia, and necrosis (with subsequent MRI changes) related to longstanding tumor compression of the surrounding brain. Type 11 occurs with both extrinsic and intrinsic tumors, and can be localized or diffuse on neuroimaging. It is distinguished by its tendency to spread throughout the ipsilateral hemisphere, and often it is quite irregular in outline. This type of peritumoral change tends to resolve on postoperative MRI over 8-12 weeks, but may persist (even diffusely) indefinitely in some situations following tumor removal. The etiology of this type of peritumoral change is not well understood. Some authors favor the proposal that glial tumors tend to spread along white-matter tracts, incIuding association, projection, and commissural fibers. It is suggested that tumor proteins disrupt the blood-brain barrier, and that the abnormal vessel walls allow tumor cells to escape and proliferate in the surrounding white matter. It is concIuded that this process is represented by these T2 changes. In theory, since gliomas have a higher water content than normal brain, proton imaging sensitivity should reflect this on the TI and T2images. Tumors in general have prolonged TI and T2relaxation times (TR) that produce less signal with a short TR (e. g., TI) and an increased signal intensity with a longer TR (e. g., T2). These changes are directly related to a change in the water content of both the tumor and the peritumoral area. Clearly, these

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3 Neuroradiology

Table 3.7 Perilesional changes (hypodensity, hyperdensity, or intensity) Severe changes

Minor changes

No changes

Tumors Tumors Tumors Acoustic neurinoma Metastasis Craniopharyngioma Glioblastoma Epidermoid, derLow-grade astrocymoid toma Glioma Chondroma, chorOligodendroglioma (High grade --+Iow doma Ependymoma grade) Pinealoma Pituitary adenoma Meningioma Pineoblastoma Optic glioma Neurocytoma Plexus papilloma Ganglioneurocytoma Ganglioglioma Lipoma Vascular lesions Infection Subependymoma Abscess Giant aneurysms (Tuberous sclerosis) Parasites Large cavernomas Colloid cyst Echinococcus Vascular lesions Toxoplasmosis AVM White-matter

diseases

Progressive multifocal leukoencephalopathia Multiple scierosis Ischemia Infection Radionecrosis

Other angiomas Hemangioblastoma

Infections, parasites (e. g., cysticercosis) Chronic subdural hematomas

Trauma

ocelusions in the distribution of the venous drainage of the deep white matter that are demonstrated as peritumoral changes on imaging. We have witnessed glioblastomas without peritumoral changes on preoperative MRI that intraoperatively proved to be encapsulated tumors without evidence of thrombosed veins. Meningiomas with Type 11 perilesional changes on MR almost inevitably have arachnoidal-pial reactions, with incorporation of leptomeningeal vessels (both arteries and veins), leading to marked adherence and adhesive lobar changes and making microsurgical removal difficult (see Cases 3.43, 3.45 on p.236). Meningiomas without such perilesional changes on MRI do not show such intense adherent and adhesive reactions (see Cases 3.42, 3.44, 3.46 in pp. 235-238). Other etiologies resulting in Type 11 peritumoral changes might inelude other types of edema, or the effects of treatment by surgery, chemotherapy, radiation, or a combination of these modalities. We have coneluded that the peritumoral increased signal intensity is a nonspedfic finding (see cases 3.52-3.57 in pp. 243-245). This is confirmed by a number of studies demonstrating that T2 changes do not correlate with malignancy in biopsy-proved specimens of correlative material. It remains for newer techniques to elarify this, in conjunction with pathological proof. Some help may come from new techniques, including PET and Na-MRI that show promise, especially in distinguishing radiation necrosis from recurrent tumor.

Cleavage characteristics are not specific for tumors, and the diagnosis of tumor infiltration may be incorrect. In the early and intermediate phases of glial tumor growth, our experience suggests that the Type 11changes are not representative of frank infiltration. Later stages of the same process may have even more striking T2 changes, which at this advanced stage do indeed reflect true tumor infiltration. It is fair to say that operability should never be based solely on this identification of perilesional T2changes. They can be very misleading. In fact, a comparison of noncontrast and contrast high-resolution CT scans has given a better idea of the true extent of certain large tumors with extensive perilesional changes than TI and T2 MRI views. In our experience, tumors (even high-grade gliomas) tend to remain local processes in their early and intermediate phases of growth. Moreover, the appearance of the many of the Type 11 perilesional changes remind us more of the patterns of deep venous drainage observed by Hassler (1966), Wolf and Huang 1964), and others. Although venous drainage has been studied extensively, there are not enough combined studies of white-matter deep venous drainage correlated to CT and MRI in the neuropathological state to draw firm conelusions (Fig. 1.96). We have identified venous thrombosis during glioblastoma resection, and note the positive correlation between this finding and the degree of marked T2perilesional changes on the preoperative films.In these cases, the distribution of these marked T2perilesional changes corresponded very well with the venous patterns detailed by Hassler, Wolf, and Huang. Even small superficial subpalliallesions may demonstrate these deep venous patterns, perhaps representing engorgement and obstruction of the centripetal and centrifugal valveless venous system secondary to thrombosis. The increased water content may be secondary to small venous

Extrinsic tumors. Some tumors have a elear line of demarcation around them that allows for easy surgical removal in a specified eleavage planeoPreoperative imagingcan often demonstratethis. Other tumors do not reflect this on imaging, but still can be readily shelled out. Others, with a seemingly elear interface between the parenchyma and tumor on preoperative imaging, may be densely adherent and extremely difficult to resect. This problem of immense practical importance is a biologicalone,for which CT and MRI provide the surgeon with no real usefulinformation. The distinct planes of the pia, arachnoid, and dura, and whether these planes have been compromisedby adherencereactions, cannot be gathered from even the best neuroimagingstudies (Figs. 3.1, 3.2). Many adherent tumors can be carefully peeled off normal structures. Others may be more difficult to remove ("adhesive" ones). These are tightly adherent to normal brain,as if tissue adhesive had been applied (like a stamp to an envelope). Even the most careful attempts to remove these tumors result in the removal of normal parenchyma. Unfortunately, only limited preoperative information regarding tumor adhesiveness can be obtained from present neuroimaging modalities. The biological activities of extrinsic tumors frequently lead to a reactive arachnoiditis, triggering a variably intense reaction between the pia and arachnoid layers (and often involving the dura). This "arachnoiditis" gives rise to pseudocapsule formation. prominent near dural contact areas of the tumor boundary, but petering out at parenchymalboundaries.Meningiomaswith significant peritumoral changes on T2 images tend to be extremely adherent at the interface between the brain parenchyma and local vasculature (Table 3.8). The plane around an extrinsic tumor, and its relationship to the dura, arachnoid, and pia, is often unclearon present imaging due to pseudocapsule formations. The tumor

The Application of Neuroimaging Capabilities to CNS Tumors

205

Dura mater Arachnoid

Interarachnoidal (subarachnoidal) space Subpial space

Trabeculae

Pia Limitans membrane

-5

Cortex

Perivascular space

a

Blood vessel

Fig,3,1 Note the position 01the subarachnoid (reallyan interarachnoidal)vessel within a pial sleeve(Irom Hutchings and R. O. Weller, J Neurosurg1986; 65: 323, Fig, 9, See also Krisch et al., CellTissue Res 1983; 228:597 -640) a The dura, arachnoid, and piallayers OrangeDura BlueArachnoid GreenPia YellowLimitans membrane b Subarachnoid hemorrhage e Leptomeningitis

interfacewith arteries,veins,and dural sinuses is frequently even lessclear.On present CT or MRI studies, we rarely see individual cranialnerves and their relationships with skull base tumms. They are only discovered during surgical exploration (which is frequentlydifficult). In the sellar region, MRI and CT can demonstrate displacementof the pituitary stalk, especially on coronal views and thinsectionreconstruction. In some cases, extrinsic tumors can be definedin relation to the pituitary stalk and gland. Intrinsictumors. A cleavage plane is even more difficult to identify whendealingwithan intrinsictumor. Tumor relationships to arteries,veins, and glial surfaces are often vague and ill defined. Gliosis,as distinct from tumor or perilesional edematous changes, isnot readily seen on MRI. Even when a cleavage plane is identified,the lesion may still be difficult to extirpate due to undetectedand unsuspected adherence or adhesiveness.

Table 3,8

Membranes of

tumor and pseudocapsule formation

around the tumor Dural Arachnoidal

Arachnoid pia Gliosis Ependymal changes

Pituitary adenoma, meningioma, chordoma, chondrama, glomus tumor Craniopharyngioma, pinealoma, germinoma, teratoma, neurinoma, dermoid epidermoid, optic glioma, cyst Meningioma, craniopharyngiomá, etc, Glioma, cavernoma, metastases, angioblastoma, medulloblastoma, meningioma Ependymoma, subependymoma, plexus papilloma, intravenous glioma

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3 Neuroradiology

.',

--J '

~,

..

~~~,flr

.

~

.,.,

a

o

@

Fig.3.2 The demarcation of CNS neoplasms:-the spectrum of possible effect on surrounding tissue planes. Vessels within the area are purposely excluded, in order to emphasize the pathological changes within the leptomeningeallayers Orange Tumor Yellow Dura Blue Arachnoid Green Pia Red Glia limitans Gold Cortex 1 No adherence to surrounding structures, excellent cleavage plane, total demarcation 2 Adherence to surrounding structures, fair to poor cleavage plane, poor demarcation

b

';

."

"

.

o

a 1 2 3 4

...,,

."

0) @ Epidurallesion (i. e., chordoma, chondroma) No adherence to the underlying dura Adherence to the dura Penetration through the dura, with adherence to the arachnoidlayer Infiltration into the arachnoid and piallayer with disruption of the limitans membrane

3 Penetration through surrounding structures, no cleavage plane 4 Infiltration into surrounding structures, severe adherence

0) @ 3 Penetration through the dura with adherence to the arachnoid layer 4 Infiltration into the dura, arachnoid, pia and limitans layers

b Intradurallesion (i. e., meningioma) 1 No adherence to the encasing dura 2 Adherence to the dura

e 0' e Subdurallesion (i. e., meningioma, adenoma) 1 No adherence to the underlying arachnoid 2 Adherence to the dura

0) @ 3 Penetration through the arachnoid with adherence to the piallayer 4 Infiltration into the dura, arachnoid, pia, and limitans layers

@

r---

d

o

@

d Intra-arachnoid lesion (i. e., craniopharyngioma, epidermoid, neurinoma) 1 No adherence to the surrounding arachnoid

optic

glioma,

0) @ 2 Adherence to the overlying arachnoid and dura 3 Penetration through the arachnoid with adherence to the piallayer 4 Infiltration into the arachnoid, pia, and limitans layers

Summary

207

.~ CD @ e Subpial-subcorticallesion (i. e., glioma) 1 No adherence to the surrounding white matter 2 Adherence to the overlying cortex, limitans, and pia layers

DetailedLesion Reconstruction Neoplasms may be homogeneous or heterogeneous on imaging, but tfUetumor consistency (soft or hard) and viscosity cannot be determined until surgery. Cysts associated with tumors may appear isodense and yet may contain hematoma, CSF, solid tumortissue,or tumor fluid (or a combination of all these) CT can identify the density of a specific area and can shed light on the presenceof calcium, blood, CSF, and other dense materials. MRI canprovide general information as to the true composition of cysticlesions.Usually, the contents of a cyst have a higher protein contentthan CSF, so an increased sign~l compared to CSF is seen on Tb while a decreasedsignal is seen on TI' However, neither MRI nor CT can accurately elucidate the true composition of a lesion preoperatively.This, of course, has considerable impact in deter-

o 3 4

@

Penetration through the ependymallayer into the underlying ventricle Infiltration into the surrounding white matter

mining whether a lesion should be aspirated stereotactically or attacked directly. Only limited information regarding the vascularity of a lesion can be obtained from present neuroimaging. Gradient echo techniques can usefully demonstrate flowing blood. Flow voids on MRI usually indica te vessel patency. CT, MRI, and angiography together may readily show whether a lesion is hypovascularized or hypervascularized, but no other inforrriation regarding its qualitative and quantitative vascular aspects can be ascertained from preoperative images. No information regarding tumor vessel fragility is obtainable. Thus, tumor vascularity is understood only in gross terms prior to surgery. However, MRA is now improving rapidly, and may provide answers to this crucial aspect of operative planning.

Summary Plainradiographs of the skull (in the initial assessment and sometimesin the follow-up of certain extrinsic tumors involving the skull),chestradiographs, and plain spine radiographs, where indicated,continue to be important in preoperative evaluation. Pneumoencephalography, myelography, and cerebral and spinal angiography were the mainstay of neuroimaging until twenty years ago. Although uncomfortable, invasive, and associatedwitli some morbidity, myelography and angiography are still excellent studies for the diagnosis of pathologicallesions. Angiographyis essential in selected patients with tumors close to, or involving,major arteries or routes of venous drainage. Present dayMRA can help in the evaluation of these patients. Cerebral aneurysms are a disease of the intra-arachnoidal spaces, while AVMS involve not just the intra-arachnoidal space, but alsothe cortex and white matter. The mainstay of neurodiagnosticevaluation of these conditions has been angiography. IntrinsicCNStumors, on the other hand, are almost exclusively a whitematterdisease.As a result, for gliomas white-matter imaging studies(suchasCT and MRI) are paramount. The precise localization 01intrinsic gliomas is critical for the best operative approach to thelesion(with a minimum of risk) and for the correlation of surgical findingswith neuropathological studies. We have found that

the neuroanatomical conceptsof tumor topography using a sectoral architectural arrangement, permit accurate interchanges between neurosurgeons, neuroradiologists, neuropathologists, neurophysiologists,and anyone else interested in CNS neoplasm patients. Noninvasive scanning methods with CT and MRI allow for the identification of small or occult lesions with great accuracy. Small avascular lesions lacking tumor blush and mass effect, which were often missedpreviously,are now readily detected.CT and MRI provide us with excellent images representing in-vivo CNS structures and related pathological changes. They deliver immediate, noninvasive images of the CNS parenchyma and craniospinal bony axis in triplanar views. The technologies of CT and MRI are quite distinct. CT uses ionizing radiation to produce an image based on the numerical differences in electron densities in the CNS and surrounding tissues. Thus, in describing CT changes attributed to lesions, one uses terms dealing with density as related to the brain parenchyma (hyperdense, isodense, hypodense). MRI, on the other hand, is more complex, based on mobile hydrogen protons which, when exposed to radiofrequency waves in a strong magnetic field, generate signal differences during their

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relaxation phase. Therefore, the images generated are described in terms of image intensity, i. e., bright, hyperintense, hypointense, etc. MRI is more sensitive than CT, and is the current gold standard for detecting CNS lesions. Present-day neuroimaging has reduced those lesions in which the nature of the lesion remains largely speculative down to between 5 and 10% of cases. The nature of the majority of CNS lesions is diagnosed correctiy as being of a vascular, inflammatory, autoimmune, degenerative, or neoplastic nature. In general, the differential diagnosis is excellent, but in individual cases uncertainty remains. Commonly, a glioma cannot be ruled out in favor of an unusual presentation of a.more benign tumor (neurinoma, meningioma, epidermoid, etc.), or an infrequentiy encountered lesion (chronic granulomatous processes, such as tuberculosis or sarcoid, hamartoma, abscess, or infarct). This lack of specificity provided by preoperative MRI scans is of ongoing concern to neurosurgeons. Triplanar MRI is superb in its anatomical resolution. It is probably only in less than 5% of patients that a precise topographical diagnosis cannot be made. Certainly, extrinsic and intrinsic tumors can be readily distinguished. Despite the high quality of neuroanatomical detail brought about by modern neuroimaging, new mapping techniques arestill necessary to better formulate precise surgical approaches. For example there is still no reliable way to identify the sulci (so clear on neuroimaging) at surgery. Current neuroimaging, despite its 1.0 mm resolution capacity and exquisite sensitivity, has been unable to provide answers to many areas of critical surgical and pathological interest. The layer of origin of extrinsic tumors is often very difficult to determine. MRI is poor at demonstrating the dura as a separate stucture in cases of tumors occupying the epidural, subdural, or subarachnoid spaces. As a result, it is clear that MRI can rarely provide information on cleavage planes, the degree of any arachnoiditis, or the degree of adherence or adhesiveness, or both (except for meningiomas with perifocal hyperintensity, in which MRI predicts severe adherence between the tumor surface, arachnoid, and pia) (Table 3.9). Table 3.9 Interpretrative cautions in the neuroimaging of tumórs (CT,MRI) Oislocation effect of the mass Magnification effect Superimposition effect (parachiasmal, ínsula, Sylvian fissure, transverse fissure) Hypodensity, hyperdensity or -intensity Edema Scattered tumor cells True tumor infiltration Metabolic changes Radionecrosis Hematoma Infarction Boundaries Bone, dura, sinuses Arteries, veins and sinuses Dura, arachnoid and pia Parenchyma Ependyma Choroíd plexus

{

Infiltration Invasion Adherence Adhesiveness Gliosis Membrane formation

The significance of peritumoral changes with different tumors is uncertain. Clearly, peritumoral changes do not represent tumor penetration into cerebral adjacent tissues by gliomas. The occurrence and significance of tumor infiltration as related to peritumoral changes remain uncertain. Neuroimaging has resolved many of the problems in tissue differentiation, but the excellent resolution of MRI raises new questions about pathophysiological interpretation, especially with regard to peritumoral changes. In addition, it is important to avoid clinicalinterpretations of neuroimaging studies, especially with regards to herniation syndromes. The interpretation of cystic changes seen well on MRI can be difficult (i. e., a real tumor cyst, hemorrhagic fluid, a hematoma, or solid tumor tissue?). The qua lity of vascularization of a tumor is unpredictable with MRI. MRA shows some promise in this respect, but at present only helps us decide which tumors merit further study by arteriography. The concept of sectoral white-matter structure brings together the disciplines of neuroanatomy, neuroradiology, neurophysiology, and neuropathology in relation to intrinsic brain tumors. The network of connections in the cerebral cortex, basal ganglia, and spinal cord have been areas of intense research effort. However, the white-matter subsystem of the cerebrum (and cerebellum) is much less studied. Perhaps this conceptual architectural plan will encourage future generations of specialists in these disciplines to "map" this largely unexplored continent.

MRI has provided the basic framework of the white matter,to which we now need to add the fine detail. It is important to constantiy keep in mind the fact that current high-resolution pictures only complement the clinician's skill, in formulating an accurate differential diagnosis, based on a complete history and physical examination. The belief of some that the history and physical examination are rendered superfluous by present neuroimaging sophistication is dangerous, and undermines the benefits these images provide. Decisions on treatment must remain clinical judgments, considerably aided by carefui evaluation of the detail provided by modern imaging. The major disadvantages of MRI include extended scan times and confinement in a claustrophobic space. It remains problematic to scan critically ill ventilator-dependent patients.Other limitations include: remote scanner locations, minimal support staff, and lack of nonferromagnetic monitoring equipment and ventilators. Future MRI advances will no doubt shorten scan times, making the use of MRI in critically ill (and immediately postoperative) patients worthwhile. Routine three-dimensional imageswill be come readily available. MRA will improve to the point where the detail is sufficient for preoperative tumor planning eventually obviating the need for arteriography in most patients. Echoplanar MR with perfusion and diffusion imaging will eventually help our understanding of the dynamic consequences of tumors and their effects on the CSF system. MRS will advance sufficientiy to provide preoperative pathological information as well as standardized monitoring of treatment effects. MEG appears very promising for functional localization. Other further advances in neuroimaging technology will provide neurosurgeons with increasingly precise and dynamic information relating to tumor topography and pathophysiologic characteristics.

Conclusions . Cases

209

Conclusions Greatadvances have been made in the neuroradiographic visualizationof CNS tumors, but we must be carefu!! The precise localizationof intrinsic tumors on neuroimaging must not be described iniobarterms (what lobe?), but in terms of what part of a gyrus (anterior,middle, or posterior) and which sector (or, in the case of a centralganglion and central nudei, which section). Neuroimaging studies cannot reliably provide information as to which tumorsare diffuse and which are circumscribed. We must be carefuinot to make judgments on the basis of neuroimaging regarding: localization, construction, extension, peritumoral changes, andherniation. Neuroimaging provides an exact diagnosis in 90% or more instances (retrospectively), but prospectively, in a given individualpatient, be careful. The combination of information fromMRI, PET, and SPECT (and other new technologies) will be helpfulin these respects.

Cases

The following 59 cases are presented to illustrate and further elucidate the discussed difficulties of differential diagnosis. Case 3.1-3.9 3.10-3.13 3.14 3.15-3.21 3.22-3.33 3.34-3.41 3.42-3.57 3.58-3.59

Diagnostic difficulties between intrinsic and extrinsic tumors in parachiasmatic area. Differential diagnostic difficulties between meningioma and other tumors. Difficulties concerning the origin of intraventricular tumors. Difficulties with tumors in parapineal areas, their precise location and tumor type. Difficulties concerning tumor localization and type in the posterior fossa. Radiological difficulties between neoplastic, infective, degenerative and traumatic disease processes. Problems associated with perilesional changes. White matter changes.

Diagnostic DifficultiesbetweenIntrinsicand Extrinsic Tumorsin the ParachiasmaticArea

Case3.1 A 52 year-old a lemalewith a one-year hislory01pelil mal seizures, progressing lo diminished memoryand mental sluggishness. MRI views (T1): a coronal, b sagittal. There is a well-delineated lesion in the superior anteriorpart of the right septal region.Origin? Postoperativeviews(2 weeks postoperalively):e coronal, d sagittal. The tumor (oligodendroglioma,

grade11) arasefromthe righlside ofthe paraterminal gyrus. Following transcallosalremoval, the palient remains neurologicallynormal.

b

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3 Neuroradiology

a

e

e

Case 3.2 A 3-year-old female who complained of headaches following a fall from her bed. MRI views: a horizontal (spin-echo), b coronal (spin-echo), e sagittal (T,). There is a large, well-circumscribed lesion, with erosion of the sella and calcifications extending from the infrasellar into the suprasellar region. Not the displacement of the ventricular system but little ventriculomegaly (though the mass extends to the foramen of Momo). Postoperative views (3 weeks postoperatively): d sagittal (T,), e coronal (T1).The tumor (craniopharyngioma) was entirely epidural, pushing the dura upwards to the foramen of Momo (Iike an adenoma). This illustrates the point that the dura is not visible on neuroimaging. The child remains neurologically normal following pterional removal.

Cases

211

II

,\ b

e Case3.3 A 48-year-old man, with progressive headaches over severalmonths, recent weight gain (25 pounds), impotence, and an unsteadygait. MRIimages (T1): a sagittal, b corona!. There is a wellcircumscribed lesion in the area of the third ventricle, with obstructive hydrocephalus. Postoperative views: e sagittal, d corona!. This tumor (craniopharyngioma) was treated elsewhere by a ventricular

d peritoneal shunt. Two large pathological vessels terminated in the tumor, and a meningioma was assumed (a, b). The tumor was removed using a combined approach. The patient remains neurologically normal, with intact visual fields. He needs substitution therapy.

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3 Neuroradiology

a

b

d

e

Case 3.4 A 29-year-old male with 6 months of diminishing visual acuity (and color scotoma) and a right homonymous hemianopsia. MRI views (T1): a horizontal, b coronal, e sagitta!. There is a lesion in the parase llar, parachiasmal area (Ieft greater than right). Preoperative diagnosis: glioma of left parolfactorial area. Postoperative views: d sagittal, e corona!. The well-circumscribed tumor (pilocytic astrocytoma) originated from the left optic chiasm and optic tract. Following transsylvian removal, the patient remains neurologically normal, except for a right homonymous hemianopsia (with no endocrine abnormalities).

Cases

a

b

e

d

Case 3.5 An 18-year-old female with 2 years of progressively diminishing visual acuity and then rather acute vomiting, dizziness, somnolence, visualloss (to finger counting) and a right third nerve palsy. MR views (T1): a horizontal, b coronal, e sagittal. There is a multilobulated, but well circumscribed, lesion in the left medial frontal-basal area, with extension superiorly to the foramen of Momo, and inferiorly into the basal cisterns. Preoperative diagnosis: craniopharyngioma. Postoperative views (T1): d sagittal, e coronal. A wellcircumscribed intrinsic tumor (pilocytic astrocytoma) was removed, using a left transsylvian approach, from its origin along the olfactory tracts. The patient continues to do well 4 years postoperatively, with minor weakness on the right side and a right homonymous hemianopsia. In addition, visual acuity (in the residual field) remains severely diminished.

213

214

3 Neuroradiology Case 3.6 A 16-year-old male, with progressive . difficulty using the right hand and foot (1 year), right-sided sensorimotor dysfunction (6 months), right upper quadrantanopsia. and speech dilficulty. Neuroimaging: a horizontal (T2), b coronal (T1), e sagittal (T1). A well-encapsulated multilobulated lesion in the lelt substantia innominata, septal, and parahypothalamic area. Note the cystic and solid portions. It was unclear whether the lesion was extrinsic or

a

b

intrinsic. Postoperative views: d sagittal (T1), e horizontal (T1), f coronal (T1). The tumor (pilocytic astrocytoma combined with a dermoid cyst) arose lrom the optic tract, with compression of the chiasm and extension into the basal cisterns. The M1 and A 1 segments (and perforators) 01 the circle of Willis were adherent to the tumor. The dysphasia and right hemiparesis improved markedly, and the right upper quandrantanopsia remained unchanged 101lowing left transsylvian complete removal 01the tumor.

e

_..1

...

*-

f

..

Cases

a

b

e

d

e

Case 3.7 A 16-year-old mal e with generalized seizures (for 3 years), progressive right-sided se nsorimotor weakness, and right homonymous hemianopsia. MRI views: a coronal (spin-echo), b horizontal (T1), e sagittal (T1). An encapsulated lesion, with a cystic portion, in the subfrontal, suborbital region and extension into the lentiform and subinsular areas. Note the compression of the left mesencephalon from lateral to media!. Preoperatively, it was not clear, whether the lesion was extrinsic or intrinsic. Postoperative views: d sagittal (T,), e coronal (T1).The tumor (pilocytic astrocytoma, Grade 1)arose from the left optic tract and extended back to the lateral geniculate body. Following transsylvian removal, the right hemiparesis improved markedly, but the right homonymous hemianopsia persisted.

215

216

3 Neuroradiology

e

b

a

Case 3.8 An 11-year-old female with progressive left-handed weakness over 2 years (but no visual field abnormalities). Contrast CT views (1983): a horizontal and sagittal. b corona!. There is á lesion in the right parahippocampus area. The lesion was observed over 2 years, with no change in size. Note the degree of ventricular compression. The location of the lesion could not be diagnosed preoperatively. e Postoperative view: This compact, well-circumscribed tumor (hamartomaastrocytoma. Grade /) arase in the area of the mamillary body and filled the subchiasmal area. The tumor was explored by a right-sided transsylvian approach, with an incision in substantia innominata just over the right carotid bifurcation and piecemeal complete removal of the tumor. The patient recovered fully, and has no visual field deficits.

~

~"':iiIIB Fig. 3.9c-f

Do

b

Cases Case3.9 A 45-year-old man,sufferingIrom generalizedseizures. MRIviews(T1):a horizontal,b coronal, e sagittal.Thereis a lesion in thefrontal,temporal, insulararea,with midline shiftanddistortion 01the mesencephalon.Note thattheexact location andextension01the tumoris difficult to pinpointThepatient underwentradiotherapyand chemotherapyin anotherhospital, but developedprogressive receptivedysphasia, rightupperquadrantanopsia,and discrete motorfunction loss in therighthand. Postoperativeviews (2 weeks post-operatively): d sagittal,e horizontal, f coronal.The tumor (anaplasticastrocytoma, Grade111) was explored andcompletelyremoved througha transsylvian approach.It arose Irom theamygdalaand hippocampalarea, and extendedup into the Sylvlanlissurewithout inliltratingthe insula. The patient'srecovery was veryimpressive,and he remainedin good conditionfor 3 years.

e

e

Differential DiagnosticDifficulties between Meningioma and Other Tumors

Case3.10 A 55-yearoldlemalewith apathy andmentalslowing. ContrastCT view: a Horizontal.A well-encapsulatedcystic lesion in the leftfrontalarea (suspi" ciouslor a glioblastoma).Postoperative view:b horizontal.At surgery,this tumor turnedout to be a benignmeningioma, andthe patient made an uneventfulrecovery.

a

217

d

218

3 Neuroradiology

a

e

e

Case 3.11 A 47-year-old female, who had suffered one generallized convulsion and 2 months of progressive dysphasia. MRI views: a horizontal (spin-echo), b sagittal (T,), e coronal (T1). A well-circumscribed lesion in the left middle parietallobulus (supramarginal gyrus). Postoperative views (1'/2 years post-operatively): d coronal, e sagittal (T1).The tumor extended from the gyrus in a mushroom-like fashion (with a sharp border at the surface). Initially diagnosed as a meningioma, it later turned out to be an anaplastie astroeytoma. The patient's neurological status remains intact, despite the location.

Cases Case3.12 A 37-yearoldman,with generalizedseizures.MRI views.(T1): a horizontal, b coronal.A large lesion arisingIrom the middle temporallossa and extendingalong the tentorialedge (with subtentorialherniation),displacingthe brainstem. Not theextremedisplacement01the mesencephalonand upper pontinearea.Preoperatively, itwasnot clear whether thelesionwas extrinsic orintrinsic.Postoperaa tiveview(15 months postoperatively):e horizontal.The tumor (pleomorphicastrocytoma,

219

b

Grade 111) originated

Iromtheleftparahippocampalgyrus, extruded intothe middle lossa, andinliltratedthe dura. Thisenormousadherent andvascularizedtumor wasremoved completelytwice within 2years.Radiationtherapywasapplied. The patientwas capable 01 workinglor 4 years, but thensufferedanother localtumor recurrence anddied.

e

Case3.13 A 32-yearoldmale with progressiveheadachesand diplopia(4 weeks). MRI views:a horizontal(spinecho),b coronal (T1), e sagittal(T1).A well-circumscribedle~ion in the anteriorpart 01the right cingulategyrus and adja- a centmedialpart 01the superiorIrontal gyrus (F1),withextension underthe lalx to the oppositeside. Postoperativeview(31/2 yearspost-operatively): d sagittal(T1).The exact position01the tumor (an anaplasticoligodendroglioma,Grade 111) is well seenlollowing interhemisphericremoval. Thepatientmade a lull recovery. e

b

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3 Neuroradiology

Difficulties concerning the Origin 01 Intraventricular Tumors

a

d

,

. <,

e

Case 3.14 A 26-year-old female with progressive headaches, papilledema (diminished visual acuity), diplopia, and slight weakness of the right armo MRI views: a horizontal (T2),b coronal (T,), e sagittal (MRA),d horizontal (MRA).A large intraventricular lesion of uncertain originoPostoperative view (2 weeks postoperatively): e sagittal (spin-echo). The tumor (giant-cell astrocytoma), originating in the septum pellucidum, was removed via an anterior interhemispheric, transcallosal approach. The patient made a fullrecovery.

Cases Difficultieswith Tumors in Parapineal Areas, theirPrecise Location, and Tumor Type

a

d

e

Case 3.15 A 53-year-old female with 4 months of headache and dizziness. MRI views (T1):a horizontal, b sagittal, e coronal (posteroanterior view). A large, well-circumscribed lesion arising within the trigone of the right lateral ventricle and extending into the paramesencephalic cistern. Note the compression of the upper brainstem (despite the patient's normal neurological status). Post-operative views (3 weeks post-operatively): d coronal (posteroanterior view), e horizontal. The tumor (meningioma) arose from the trigone, and was covered by a thin layerof ependyma as itentered the paramesencephalic cisterns. Following posterior interhemispheric subsplenial removal, the patient remains neurologically normal (with no visual field deficits).

221

r 222

3 Neuroradiology

Case 3.16 A 44-year-old female with progressive headaches, dizziness, and diminished coordination on the right side. Neuroimaging views: a contrast CT (1978) horizontal, b venous-phase carotid angiogram. A large lesion filling the posterior lateral ventricles bilaterally. The lesion had been thought to represent a sarcoma,and bilateral ventriculoperitoneal shunts were performed elsewhere. Despite radiotherapy, her symptoms intensified. Postoperative(10 years postoperatively): e, d CT. A large incisural meningioma was removed, and the patient remains completely symptom-free alter 14 years.

Case 3.17 A 3-year-old female with progressive left-sided weakness. Contrast CT view: a horizontal. A giant well-circumscribed lesion arising from the tentorium and expanding into the right parietal and occipital lobes (with obliteration of the ventricular system). Postoperative view(1 week postoperatively): b horizontal.The tumor (a fibroblastic meningioma) was removed using a posterior interhemispheric, supratentorial approach. The child made a fuI! b recovery.

Cases

223

Case3.18 A 29-yearold female with progressive headaches, vomiting, diplopia, and right sixth nerve palsy. MRI view(T1):a sagittal, b horizontal. A well-circumscribed parapineal lesion of unclear origino Preoperatively, it was thought to originate in the corpus callosum and extend into the third ventricle. Postoperative contrast CT(4 months postoperatively): e horizontal.The tumor (anaplastic plexus papilloma, Grade 111) extended from the trigone, with a large cystic portion compressing the splenium and posterior portion of the corpus callosum. Following interhemispheric (parietal-occipital) removal, the patient remained symptom-free for 2 years. Radiation therapy was applied. Shedied 2 years later from a recurrent tumor

b

with dissemination along the CSF pathways.

Case 3.19 A 64-yearold female with progressive headaches, disorientation, papilledema, and loss of convergence. MRI views (T1): a horizontal, b sagittal. A large, well-circumscribed, multilobulated parapineallesion. Preoperative diagnosis: teratoma. Postoperative views(3 weeks postoperatively):

-

a

--

224

3 Neuroradiology Case 3.19c horizontal. The tumor (glioblastoma, Grade IV)was removed via the interhemispheric, supratentorial approach. Note the residual tumor in the left pulvinar and left parapineal regions.

e

b

a

Case 3.20 A 23-year-old male with progressive headaches (papilledema), dizziness, diplopia, and diminished concentration. MRI views (T1):a sagittal, b coronal. A large, well-delineated, but expanding lesion in the parapineal, supratentorial, and infratentorial area, with extension into the dorsal mesencephalon. Preoperative diagnosis: pinealoblastoma. Postoperative view (8 months postoperatively): e sagittal. The tumor (primitive neuroectodermal tumor, Grade IV)was removed via the combined paramedian, supratentorial, and infratentorial approach.with postoperative radiotherapy, the patient has remained neurologically normal (for 2 years).

,Cases

225

Case 3.21 A 42-year-old man with subacute dizziness, balance difficulty, vomiting, and dysmetria. MRI views (T1): a sagittal, b coronal. A well-delineated lesion in the upper vermis, extending into the incisure. Note the cystic components of the tumor. Postoperative views (9 months postoperatively): e sagittal paramedian. A medulloblastoma was removed via the suboccipital supratentorial approach.

b

Difficultiesconcerning Tumor Localization andType in the Posterior Fossa

b

Case 3.22 A 31-year-old female with left hypoacusis and facial dysaesthesia.MRI view (T1):a horizontal. A well-circumscribed lesionin the left cerebellopontine angle. with partial entrance into theporusacusticus.The preoperative diagnosis was acoustic neuri-

noma. a Postoperative view (2 weeks postoperatively). The tumor (meningioma) was removed, with full return of cranial nerve (VII and VIII) function.

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3 Neuroradiology

Case 3.23 A 56-year-old female with right-sided facial dysesthesia. MRI view(T1): a horizontal. A well-circumscribed lesion extending well into the porus acusticus. b Postoperative view (6 weeks postoperatively). The tumor (meningioma) was completely

removed using the lateral suboccipital approach, with complete return of all cranial nerve function. (The right fifth nerve dysfunction may have been due to contralateral distortion by the tumor).

a Case 3.24 A 51-year-old male with progressive headaches, tinnitus, hypoacusis, and gait instability. MRI view (T1): a horizontal. A large, circumscribed lesion with dilatation of the porus acusticus. Note the unusually extensive amount of perilesional change and the severe fourth ventricular displacement. Postoperative CT view (1

month postoperatively): b horizontal. This acoustic neurinomawas extremely adherent to the ventral cerebellar surface. The facial nerve was well preserved, but the patient had a temporary post. operative facial palsy.

Cases

227

b

a Case3.25 A 24-year-old female with progressive right facial dysesthesiaand weakness, hypoacusis, sixth-nerve palsy, ataxia, anddysmetria.CT view: a horizontal. A large, circumscribed lesion extendinginto Meckel's cave, with enlargement of the foramen ovaleand destruction of the surrounding petrous bone. The preoperativediagnosis was fifth-nerve neuroma. b Postoperative view

(1 week postoperatively): complete removal of the tumor (melanoma) see Fig. 115 a-b, p. 135, which show an almost identical lesion with a giant basilar aneurysm (Valavanis et al. 1985, Springer) and Fig. 137 e, p. 278, Ya$argil, Microneurosurgery Vol. 11, Stuttgart 1984.

Case3.26 A 59-year-old male with progressive left. facial hypesthesiaand weakness, hypoacusis, and miId cerebellar symptoms. MRI view (T1): a horizontal. A small, circumscribed lesion extendinginto the porus acusticus, with a broad attachment. The

preoperative diagnosis was meningioma. b Postoperative contrast CT(6 weeks postoperatively): total removal of the tumor (metastatic carcinoma).

Case3.27 A 12-year-old lemalewith progressive cerebellar symptoms. MRIview(T1): a horizontal. A large, well-encapsulated lesion, expanding the porus acusticus and displacing the surrounding brainstem and cerebellum. Postoperative view (1 month postoperatively): b horizontal. Total removal 01the tumor (ependymama),which has extended through the loramina of Luschka into the lateral pontobulbar cisterns.

a

b

228

3 Neuroradiology Case 3.28 A 40-yearold female with right.sided facial dysesthesia, right hypoacusis, and vertigo. MRI views: a horizontal (T2), b sagittal (T1). A well-circumscribed lesion, extending into the pontobulbar region and including the cerebellopontine and prepontine cisterns. Note the extensive pontine lateral and dorsal displacement. The preoperative diagnosis was dermoid. Postoperative views (21/2 months postoperatively): e horizontal (T1), d sagittal (T1).The tumor (chordoma) has been totally removed, with restoration of the pontine position. Note the preoperative erosion of the clivus, which was not well recognized.

a

Case 3.29 A 17-year-

.

a

old male with progressive headaches and papilledema. MRI view (T1): a sagittal. A large, circumscribed fourth ventricular lesion, extending through the foramen of Magendie. The patient's father had been operated on for a supratentorial meningioma. b Postoperative view (3 years postoperatively). Total removal of the tumor (plexus papil-

b loma).

Cases

229

a Case 3.30 An 18-year-old male with 2 months of progressive headaches, vomiting, dizziness, nystagmus, ataxia (positive Romberg), and dysmetria. Neuroimaging view: a contrast CT (1983), horizontal and sagittal views. A large, encapsulated lesion, filling and enlarging the lourth ventricle and with extension through the foramina of

Magendie into the foramen magnum. Note the extreme amount of medullary compression (which was not symptomatic). b Postoperative MRI (T1) (5 years postoperatively). The tumor (dermoid) extended down to the C 1-level with severe compression of the medulla anteriorly. The patient made an uneventful recovery.

b

a Case3.31 An 8-year-old girl with headaches, ataxia, and diplopia.MRIview(T1):a sagittal.A poorly delineatedlesion at the isthmus01the fourth ventricle on the left. b Postoperative views (31/2 monthspostoperatively). The tumor was attached to the left upper

floor of the fourth ventricle, just superior to the stria medullaris. The nature of the lesion remains unclear, even after surgery. Histology revealed a lipoma. The patient has a permanent palsy of the left sixth and seventh cranial nerves.

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3 Neuroradiology

a b Case 3.32 A 48-year-old male who had experienced trouble in turning his head for 6 months, with vertigo and gait ataxia. Physiotherapy was ineffective. Due to tinnitus he went to se e an ENT specialist, who made an CT scan revealing an infratentorial tumor. a MRI,coronal (posteroanterior view), b MRI, horizontal: extrinsic

e tumor, probably a meningioma. e Postoperative. Exploration revealed, surprisingly, an intrinsic tumor originating from the left biventerlobuleand tonsil,expanding intothe cerebellopontinecisterno Histology: pilocytic astrocytoma, Grade 11.Postoperative fuI! recovery.

a

e Case 3.33 A 24-year-old female with headaches that had developed over a few weeks, followed by attacks of vomiting. MRI views: a, b Tumor with hematoma in the left anterior lobulus quadrangularis and mesencephalon. Exploration disclosed a tumor

extending in a mushroom-like fashion from the superior vermisinto the mesencephalic cisterns. e, d Postoperative views. Histology: pilocytic astrocytoma,

Grade 11.Postoperative

full recovery.

Cases

231

RadiologicalDiagnostic Difficulties betweenNeoplastic, Infective, Degenerative, andTraumatic Disease Processes

a b Case3.34 A 65-year-old female with progressive disorientation andlefthemiparesis.MRIviews (T1):a coronal. b sagittal. A well-circumscribedlesion in the inferior right temporo-occipital area, involvIngthe posterioraspect of the inferior temporo-occipital gyrus. The

e preoperative diagnosis was glioblastoma. Postop view (4 months postoperatively: e horizontal. The patient made a full recovery following removal of the tumor (purulent absce!$s). It is noted that the patient had a prior history of purulent sinusitis.

:"'."

..

a b Case3.35 A 67-year-old male with headache. but no parietallobe symptoms. MRI views:a horizontal (T2).b sagittal (T1).A well-encapsulatedlesion in the left parietal lobe, very suspicious for an abscessbecause of a tooth abscess. Despite antibiotic treatment,

L--"

e the patient's symptoms progressed. Postoperative view: e horizontal (T1). Residual tumor (glioblastoma) remains following subtotal removal. It is interesting that the patient had no visual field deficits.

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3 Neuroradiology

a

b

e

d

Case 3.36 A 54-year-old man with progressive apathy, confusion, and right leg weakness (previously treated with antibiotics for an elevated temprature). MRI views: a horizontal (T2), b coronal (T1). An irregular, but circumscribed lesion in the right parasplenial area,

with perilesional changes. Preoperative diagnósis: glioblastoma. Postoperative views (10 months postoperatively): e horizontal(T2), d coronal (T1).Complete resolution of the tumor (abscess)following transcallosal removal.

Cases

233

b

{ Case3.37 A 9-year-old female with sleep attacks, petit mal seizures,and diplopia. MRI views (T,): a sagittal, b corona!. A wellcircumscribed les ion in the superior portion of the fourth ventricle, with surrounding perilesional changes. e Postoperative view (2 years postoperatively). The tumor (tuberculoma) was removed via an infratentorial supracerebellar approach. The tuberculoma extended along the superior pontine peduncle, and consisted of a single hard pebble.

-

b Case3.38 A 50-year-old woman suffering generalized seizures. MRIviews(T,): a horizontal T1 b sagittal T2. A bilateral, perifalcine . lesionwithextensive perilesional changes. Preoperative diagnosis: falxmeningioma.e Postoperative view(10 months postoperatively).

e The tumor (tuberculoma)was extremely adherent and vascular (permitting only partial removal). The patient made a full recovery with antituberculosis drugs..

234

3 Neuroradiology Case 3.39 A 23-year-old female presenting with vertigo, right homonymous hemianopsia, and Gerstmann's syndrome. MRI view: a horizontal (T2). A large lesion in the parieto-occipital area, suspicious for glioma withperilesional change. b Postoperative view (2 years postoperatively). Through a left posterior interhemispheric approach, the cuneus and precuneus were notably soft, and biopsy revealed cerebral infarction. The patient recovered fuI! neurological function, except for a persistent right homonymous hemianopsia. (Interestingly, the patient 2 years later developed further symptoms, and was diagnosed with multiple sclerosis.)

a

a

b

b

Case 3.40 A 66-yearold female with rightsided hemiparesis, more in the arm than the leg. MRI views: a horizontal (T1), b coronal (T2) (anteroposterior view), e sagittal (T1). A welldelineated les ion in the superior part of the precentral gyrus. Note that there is not shifting of the lateral ventricle b. reoperative diagnosis: glioma. d Postoperative view (2 weeks postoperatively). Exploration showed no tumor, but cerebral infarction. Par-

e

-

tial improvement.

Cases

Case3.41 A 63-year-old man,with4 years of temporallobeseizures and progressivevertigo, dizziness,headaches, and syncope.MRI view: a horizontal(T,), b coronal (T2). Apoorlydelineated lesion inthe right anterior portion 01the middle frontal gyrus (F2),extending to the frontalorbitalarea. Preoperativediagnosis:glioma. Biopsyof this lesion revealedchronic encephalomalacia (relatedto a head trauma someyears previously).

a

235

b

ProblemsAssociated with Perilesional Changes

Case3.42 A 55-yearoldlemalewith progressivementaldeterioration,memoryloss, dysphasia,right arm a paresis,and generalized seizures.MRIviews: a horizontal(T2), b coronal(T,). A l8.rge, well-encapsulatedlesion inthe rightSylvianfissure.Notethe severe displacementof the deep structuresbut the absence01perilesional changes.Postoperative vlews(3 weekspostoperatively).e horizontal (T1),d coronal(T,). The tumor(meningioma)was vascular,but not at all adherentto the surroundingstructures.The patientmadean uneventlul recovery.

D b

,

236

3 Neuroradiology

a Case 3.43 A 45-year-old female with progressive papilledema and left-sided field cut. MRI view: a sagittal (T2). A small, circumscribed lesion, with severe perilesional change. Postoperative view (3 years postoperatively): b sagittal (T1). The tumor (meningo-

a Case 3.44 A 65-year-old woman, with anosmia and progressive mental deterioration. MRI view: a coronal (T1). A large, well-encapsulated lesion arising from the planum sphenoidale with severe compression of the fronto-orbital area. Note the absence of perilésional changes. Postoperative views (5 years postoperatively): b coronal

endotheliomatous meningioma) was completely removed, despite extreme adherence to surrounding tissues. The patient is neurologically intact.

b (T1). The tumor (meningioma) was found to have only minor adherences to surrounding structures. Interestingly, the patient had no preoperative chiasmal syndrome, and suffers only an anosmiaasa permanent neurological deficit.

Cases

a

---

~-

237

.b

d Case3.45 A 71-year-old female with olfactory aura and progressivevertigo and ataxia. MRI views: a horizontal (T2), b sagital (T1). A well-circumscribed lesion arising from the planum spenoidale, withsevereperilesional changes in both frontal lobes. Postoperativeviews(2 years postoperatively): e horizontal (T1),d sagittal (T1).

The tumor (meningioma) was removed using the right pterional approach. It was very adherent to the fronto-orbital structures, as evidenced by the residual encephalomalacia. The patient made an uneventful recovery, however.

238

3 Neuroradiology

a

b

e Case 3.46 A 54-year-old female with 2 years of progressive headache, ataxia, and language difficulties. MRI views: a horizontal (T2)' b sagittal (T1).A large, well-encapsulated lesion occupying the parapineal region, with severe displacement of the mesencephalon. Note the absence of significant perilesional changes. Despite the placement of a shunt (elsewhere), the patient deteriorated, with the

development of a right homonymous hemianopsia and enlargement of the left funduscopic blind spot. Postoperative views(5 months postoperatively): e horizontal (T1), d sagittal (T1).The large tentorial tumor (meningioma) was removed via a left occipital, parasagittal approach. No adherence to surrrounding structures was seen. The patient made an uneventful recovery.

Cases

239

a

e Case3.47 A 5-year-old male with progressive right homonymous hemianopsia,headaches, and papilledema (over 1 year). MRI views(T1):a horizontal, b coronal, e sagittal. A large, well-circumscribedlesion in the left parachiasmal area, with extension into the ambientcistern and hypothalamus. Note the complete absence of perilesionalchanges. Postoperative view (2 weeks postopera-

tively): d sagittal. The tumor (craniopharyngioma) was extremely adherent to A 1, M 1, and the anterior choroidal arteries (and branches). Postoperatively, the patient suffered a mild right hemiparesis that improved within 3 months. (This degree of adherence is unique in the senior author's experience of 174 craniopharyngiomas).

240

3 Neuroradiology

a

b

e

d

Case 3.48 A 33-year-old male who had suffered hypacusis for 18 years (increasing over the previous 3 years) and diminished corneal sensation on the right. Neuroimaging views a MRI (T1) horizontal, b MRI (T1)coronal, e MRA, horizontal. A large, well-circumscribed lesion in the right cerebellopontine angle with severe.brain-

stem displacement (but no clinical sequelae). d Postoperativeview (2 months postoperatively). The tumor (acoustic neurinoma) was not adherent to any of the surrounding cranial nerves. The facial nerve was preserved, and the patient had no postoperative paresis.

Cases

a

b

e

d

Case3.49 A 40-year-old female with right-sided tinnitus, hypoacusis, facial paraesthesia, ataxia, and horizontal nystagmus. Neuroimagingviews:a MRI(T1)horizontal, b MRI (T1),coronal, e MRA, horizontal.A well-encapsulated lesion in the right cerebellopontine angle,with enlargement of the porus acusticus. Not the absence of perilesionalchanges and severe compression of the fourth ven-

241

tricle and brainstem (with no clinical sequelae). Postoperative view (6 months postoperatively): d MRI (T1)horizontal. The tumor (aeoustic neurinoma) was extremely adherent to the surrounding cranial nerves and brainstem. Despite preservation of anatomic integrity, the patient developed a postoperative facial palsy for 2 years.

242

3 Neuroradiology

a Case 3.50 A 38-year-old male with minor vertigo and normal cochlear nerve function. MRI view(T1): a horizontal. A well-encapsulated lesion in the left cerebellopontine angle, without invasion of the porus acusticus. Note the absence of perilesional changes. Postoperative view (2 weeks postoperatively):

b Horizontal. The tumor (acoustic neurinoma) demonstrated no adherence to the surrounding cranial nerves. Cochlear funclion was preserved.

~ 't' ".

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,"

...

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Case 3.51 A 53-yearold with mild left facial dysestheasia and neck pain. MRI views (T1): a horizontal, b coronal (posteroanterior view), e sagittal. A well-circumscribed lesion, ventral and lateral to the pontomedullary junction. Note the absence of perilesional changes. Postoperative view (3 weeks postoperatively: d sagittal. The tumor (endotheliomatous meningioma) arose from the base of the clivus, close to the jugular foramen. No adherence lo the surrounding neuroelements was demon-

e

d

strated. The patient made a full recovery.

-..:. ..

Cases

243

Edema

Case 3.52 A 48-year-old mal e with progressive headaches. MRI view: Horizontal (T2). Two discrete lesions (internal capsule and superior Irontal gyrus) with extensive perilesional change. Note that the distribution 01these perilesional changes corresponds to the distribution 01the deep medullary venous system (see Chapter 1). The tumor (metastatic hypernephroma) was operated on twice.

a Case3.54 A 72-year-old male with progressive headaches. MRI views:a horizontal (T1), b horizontal (T2). A well-delineated right

Case 3.53 A 56-year-old male with epileptic seizures and a moderate left-sided hemiparesis. MRI view: Horizontal (T2). A well-circumscribed lesion in the right precentral gyrus, with marked perilesional change. This tumor (bronchialcarcinoma metastasis) was operated on.

b anterior temporal pole lesion, with marked perilesional change (seen best on T2). Histology: adenocarcinoma.

244

3 Neuroradiology Case 3.55 A 32-yearold male with progressi ve left hemiparesis. Neuroimaging views: a MRI (T2) horizontal. An illdefined les ion in the left pulvinar -thalamic region, with surrounding perilesional change (obscuring the definition of the tumor). Postoperative contrast CT (2 weeks postoperatively): b horizontal. Nearcomplete removal of the tumor (g/iob/astoma).

a

b

Case 3.56 A 56-yearold male with progressive headache. Neuro-

imaging view:a MRI(T2) horizontal.

A lesion in

the right precuneus, with marked bilateral perilesional changes. The patient underwent radiotherapy before surgery. Note the similarity of these changes to the deep medullary venous architecture as described by Hassler (see Chapter 1, Figs. 1.84, 1.86). b Postoperative views: contras! CT

a

b

(1 year postoperatively). The tumor (g/iob/astoma) has been totally removed.

Case 3.57 A 56-yearold female suffering headache. A4R/0ews (T2): a horizontal (basal), b horizontal (lateral ventricle system). A small meningioma at the right lateral temporal pole associated with marked

a

b

perilesional

change.

Cases

245

WhiteMatter Changes

Case3.58a Adenoleukodystrophy(from Dietemann,IRMen Pathologiede L'Encéphale,1993, b Metachromatic leukodystrophy(from DietemannIRMen Pathologiede L'Encéphale, 1993).

a

b

Case3.59 A 48-yearoldfemalesuffering headaches.Neuroimagingview:a contrast CT, horizontal.A large, wellcircumscribedfalx lesion.Thetumor (meningioma)was removedin 1981. PostoperativeMRI(T2) (10yearspostoperatively):b horizontal. Perilesional change.

a

b

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4

Neurophysiology

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248

4 Neurophysiology

Introduction So dramatic has be en the explosion of knowledge in the basic neurosciences over the last twenty years that Sherrington's concept of the integrative action of the nervous system tends to be too easily forgotten. In 1906, in a lecture at Yale University, he stated, "the central nervous system, though divisible into separate mechanisms, is yet one single harmoniously acting whole". Clinicians and investigators, building upon and refining past neurophysiological observations, are beginning to appreciate the actual complexity of CNS physiology. Similar realization of the physiological dynamism of neoplasms has also begun, suggesting that previous ideas about clinicopathological correlations are too simplistic to account for the variability and range of patient symptomatology. A greater appreciation of the principIes and variables that govern and maintain neurological function is critical if the abnormal physiological responses consequent upon CNS tumors are to be better understood. To avoid the present volume reaching encyclopedic proportions, the reader is assumed to have a working knowledge of general and applied neurophysiology. What fo11ows is a brief review of the important aspects of six of the major physiological components of the central nervous system (including aspects of their integration and variability). These are deemed those most relevant to the altered neurological dynamics brought about when tumors develop within the CNS. Other systems will be better defined in the future, and may be added to the six presently being discussed. In addition, we must in the future consider the biophysical and biochemical properties of neoplasms, which may be responsible for the production of toxic or irritative sub-

stances effecting the other subsystems (paraneoplastic effects). Similarly, the degree of influence of neurotransmitter systemson other brain systems is one of major importance, which will dominate research endeavors into the twenty-first century. Rather than describing physiological principIes in strictlyconventional terms, we will regard the CNS as a complex structure composed of interrelated subsystems, as shown in Table 4.1. In this framework, the CNS is viewed as an integrated network ofheterogeneous organs, each with its own structure and dynamic function.

Table 4.1

Functional subsystems of the CNS

Structural aspects

Functional aspects

Neural/ glial parenchyma

Neuronal and neuronal system (polysynaptic reflexes lo higher brain funclions and behavior) and glial physiology Hemodynamics, endothelial physiology CSF dynamics and neurochemical physiology Neuroendocrine physiology

Vascular syslem slructure and ultraslruclure CSF-producing tissue Hypothalamus, pituitary, and pineal Circumventricular organs CNS immunological system

Neurohumoral physiology CNS immunological physiology and capacity

Physiological Subsystems Each subsystem has inbuilt homeostatic mechanisms with internallimits that define its capacity to accommodate the influences of pathological entities such as tumors. These capabilities vary with age, sex, and general health, and with the site and extent of a tumor. Each subsystem is intimately related to, and influenced by, the other subsystems (Fig.4.1). An understanding of the significance of changes within each subsystem, and of the sequence of interactions triggered in others, is a major inte11ectual cha11engeto the clinician and researcher alike. In addition, the tumor must also be considered as a dynamic subsystem in its own right (Table 4.2). Any change in one system may affect a11of the other systems, or it may cause change in only some and not in others. If a11systems are affected, the potential changes are the summation of multiple possible probability functions. For example, the development of a tumor may initia11yaffect one subsystem alone (e. g., the parenchymal system, by nonmechanical changes). Subtle cognitive changes in such a patient may go unrecognized. Later, the size and site of the tumor may bring about mechanical changes directly acting on the CSF and vascular systems, exponentially increasing the potential combinations of possible changes. As a specific example, a falcine meningioma may initially affect leg function (heaviness or clumsiness while walking), later cause headaches (in the mornings, with a rise in intracranial pressure during sleep), and thereafter produce leg weakness (progressive

Table 4.2 Tumor mechanical possible CNS effects

and non-mechanical

aspects and their

Mechanical aspects

Effects

Structures and functions affected

Mass

Compression, obstruction, occlusion, irritation, displacement, strangulation False transmitter, inappropriate hormones, metabolic, vascular "steal" tissue adherence and destruction by chemical other reactions Mount own immune attack; elicit immune reaction

CNS neural/glial parenchyma, vascular structures, CSF paths, neuroendocrine anomalies Metabolic neurall glial disruption, dysfunction, destruclionfocally and globally

Non mechanical aspects (biochemical, melabolic, and secrelory)

Immunologic, antigenic

Immune attack; effects on CNS capacity to mounl immune response

edema, cortical venous drainage impairment), finally resulting in leg paralysis (direct pressure effect on motor fibers, obstruction of venous drainage). End-stage downward blockage of the foramen

Physoliogical SUbsystems of Momo may even lead to obstructive hydrocephalus, transtentorial herniation, midbrain compression, coma, and death. The end result is thus the product of multiple system changes. Of course,the functional reserve capacities of the brain are considerable,and variations in the limits of these capacities account for the spectrum of different symptomatologies that afflict patients. A keen appreciation of these limits is crucial for optimum operativestrategies with low morbidity.

Fig.4.1a The interaction 01CNS physiological subsystems CVOCircumventricularorgans (neurohumoral) 10 Immunologicalorgan (neuroimmunological) LO Liquidorgan (CSF) NE Pituitary-hypothalamic axis and neurotransmitters (neurohormonal) PO Parenchymal organ (neural / glial) VO Vascular organ (neurovascular)

b Fig.4.1b The interaction 01 tumors with CNS physiological subsystems. Note that there are both mechanical and nonmechanical (biophysicaland biochemical) effects 01tumors on the CNS subsystems

249

250

4 Neurophysiology

The various subsystems are now considered in further detail, concentrating on those areas of structure and function most relevant to tumor pathophysiology. As will be repeatedly emphasized, none should be thought of entirely in isolation from the others (Fig. 4.2).

a

Neural and Glial Parenchymal Systems The central nervous system is formed from two essential and distinctive classes of cells, which can be regarded as separate but indissoluble symbiotic parenchymal systems. Neurons constitute the highly specialized gene tic, anatomical, trophic, and functional units of the nervous system, but which have lost their capacityfor cell division. Neuroglial cells constitute the nonneuronal supporting cells of the CNS and peripheral nervous system (PNS), and are capable of dividing throughout adult life, especially in response to disease processes or injury. Both classes of cellsare derived from neuroectoderm. Some developmental, structural, and functional features of each are worth emphasis in order first, to better understand the clinical effects (or lack of them) of CNS pathological processes, and second, to analyze the macrophysiological consequences of the tumors most familiar to neurosurgeons-i. e., brain displacements, herniations, peritumoral edema, and hydrocephalus. A detailed review of the neurobiology (including biophysical and biochemical aspects) of these two classes of cells is beyond the scope of this section. Excellent presentations of the structural and functional bases advanced to explain the relationships between nerve cells and behavior are found in Jacobson (1991), Asbury et al. (1992), Crockard et al. (1992), Kandel et al. (1991), Paxinos (1989), Niewenhuis (1985), Niewenhuis et al. (1988),and Jones and Peters (1985).

Cerebral Cortex

b Fig.4.2a Lateralb medial view01the leltcerebral hemisphere, showing proved lunctional cortical areas (Irom Zilles, and Rehkamper, FunktionelleNeuroanatomieBerlin,Springer 1993, p. 112, Fig.A.3a, b) AA Corticalareas, predominantlyacoustic AS Corticalareas, predominantlysensomotoric AV Corticalareas, predominantlyvisual A1 Primaryauditorycortex (area 41) A2 Secondary auditory cortex (parts 01area 42) B Motoricspeech center 01 Broca (area 45 and possibly parts 01 area 44) L Limbiccortex M1 Primarymotoriccortex (area 4) O Ollactorycortex PF Prelrontalcortex PM Premotorcortex (parts 01area 6) SMASupplementarymotoricareas (parts 01area 6) S1 Primarysomatosensoric cortex (area 3,1,2) S2 Secondary somatosensoric cortex V1 Primaryvisual cortex (area 17) V2 Secondary visual cortex (area 18) W Sensory speech center 01Wernicke(parts 01areas 42 and 43)

Since the acceptance of the neuron as the basic functional unitof the nervous system in the late 1880s,immense effort has been made to understand how the brain works. Two schools of neuroscientific thought have relentlessly pursued the central tenetsof their hypotheses for nearly a century. One group (the localizationists) has focused on the unique properties of individual regions (Dax 1836, Broca 1865, Fritschard-Hitzig 1970, Ferrier 1873-1876, Jackson 1864, Wernicke 1874, Munk 1878, Henschen 1890, Wildbrand 1890, Horsley 1886, Sherington and Grünbaum 1906, Cushing 1990, Krause and Vogt 1911, Kleist 1934, Foerster 1937, Penfield, Boldrey, and Rasmussen 1937-1965). The other group (antilocalizationists) believed that function is more diffusely structured (Flourens 1824, Goltz 1881, Freud 1891,Pierre Marie 1906, von Monakow 1914, Goldstein 1927, Lashley and Clark 1929). Lashley and Clark followed the global concept of cerebral function based on the theory of cerebral equipotentiality. Chapman and Wolff (1961) have tried to reconcile these two theories, which they regard as "not antagonistic, but indeed, complementary" (Clarke and Dewhurst 1972). Von Monakow introduced the term "diaschisis" emphasizing the fact that the cerebral cortex functions through an interplayof many parts, each producing transient effects upon the other in chronological sequence. A discussion on the subject of localization of function occurred at a meeting of the International Medical Congress in London in 1881, and this marked a milestone in the development of knowledge on the suject. Goltz of Strasbourg confronted Ferrier of London, arguing against specific cortical localization beca use precise ablations of the cerebral cortex in one of Goltz's animal models showed restitution of function, and because general, rather than specific, deficits occurred after cerebrallesions in another. Ferrier argued in favor of the precise cere-

Physiological Subsystems bral localizationof specific brain functions, as his monkeys showedthat localized lesions could produce loss of specific functions.A council appointed by the congress ruled in favor of Ferrier (Green1990). Ongoing work over the last 100 years has led the way to the understanding that cortical localization and brain function is much broader and more complex than previously recognized. Ourcurrent views have focused on the functional patterns formed by regions sharing common characteristics (Mesulam 1985, see p.127).It has been our experience that corticallocalization is multidimensional,with topographical, physiological, and chronologicalaspects.We believe that cortical function is rooted in complex, chronologicallydependent interactions between localized are as offunctionallysimilar neurons.

Symptomsand Signs of Cerebral Tumors Despitethe tremendous neuroradiological advances of CT and MRIover the last twenty years, which readily allow confirmation or exclusionof a brain tumor, the diagnosis of such a tumor still occursby general practioners only rarely. The vast majority of tumorsdo not cause symptoms or signs in the early and intermediateperiods of growth. Both extrinsic and intrinsic tumors can reachenormousproportions and yet result in only minor symptoms (that are often ignored both by the patient and by the family),and minimal signs (not sought for, or easily overlooked, byskepticalprimary physicians). In 1920, Walter Dandy wrote "It seemsincredible that a brain tumor as large as one's fist can exist in either cerebral hemisphere and still escape localization by expertneurologists and neurologic surgeons. Yet nearly al! cerebraltumorseventuallyattain this size,and a very high percentage ofthem can neither be accurately localized before operation nor be found by an exploration of the brain." Clearly, despite major advancesin our neurodiagnostic capabilities over the last 70 years,these observations by Dandy are as true today as they were in histime.

Localization

Abasiccharacteristic of space-occupying lesions in the CNS is the mechanicalseparation of white-matter fibers with growth. Hematomas,cysts, abscesses, and tumors spread and displace the surroundingaxonal bundles, rather than transecting them. The classicalnotionthat mass lesions produce symptoms by the destruction ofadjacentneurons, axons, glial cells, and vascular structures (or evenimmunological system components) is simply not correct. Damageto the neuroparenchymal structures can indeed occur, but it is generally a late phenomenon related to overwhelming acuteor sustained compression, or aggressive end-stage mitotic infiltration. From the onset, the white matter around a mass lesion (regardlessof etiology) rages a "biological battle" with the lesiono Duringthis battle, the presence or absence of neurological symptomsdependsto a great degree on the abilityof the local glialcel!s (biophysical and biochemical activities) to counteract the mechanicaland nonmechanical (biophysical and biochemical) effectsofthe mass. Such factors as the degree, duration, and rapidityofcompression,the histological nature of the mass, the age and generalmedicalcondition of the host, and even the topographical

251

location of the mass within the CNS, can tip the balance in one direction or the other. The application of this concept to tumor-astroglial interactions allows one to understand how very large tumors may be asymptomatic, or very small ones quite troublesome, how clinical symptoms and even signs may come and go, how different individuals with exactly the same lesions may respond in vastly different ways, or how different mass lesions in the same location may produce the same symptoms. For example, it has been classical!y taught that the clinical presentation of an abscess and glioma are often indistinguishable. The reasons for this are now clear. Both produce symptoms by the separation of white-matter fibers and not by the destruction of neurons (Cases 4.25-4.30). This also supports the notion that the precise localization of intrinsic cerebral neoplasms should be related more to white-matter topography than cortical gyral maps (see Chapter 1). Based on this concept, we believe that discrete intrinsic tumors can be approached in al! areas of the CNS. Gliomas in eloquent are as (posterior left inferior frontal gyrus, upper brainstem, cervical spinal cord, etc.) can be safely removed, even in asymptomatic (or mildly symptomatic) patients. The present tendency to consider a mass "inoperable" simply based on its location in a highly functional zone should be reexamined and abandoned. Many clinical examples of these are advanced in the case presentations (Cases 2.11-2.17, 2.20-2.32, 3.1-3.9 4.1-4.3, 4.18-4.24, 4.32-4.39, 5.17-5.19, 5.27-5.32).

Herniations In the early stages of tumor expansion, a steady-state condition between al! the physiological systems is maintained, so that slow tumor growth is compensated for by CNS subsystem responses. As the tumor expands, it distorts the adjacent brain. As a consequence of the viscoelastic properties of the brain, on the one hand, and the incompressible nature of its three main constituents, on the other, the brain is slowly pushed away from the distorting tumor mass, provided the expansion occurs slowly (over many weeks, months, or even years). This results in a slight axial movement of the brain away from the tumor mass and into the neighboring subarachnoid space. The major factor allowing for spatial compensation for the tumor mass is the gradual expulsion of CSF from the surrounding CSF spaces. This eventually results in compression of the subarachnoid space over the hemispheres (with effacement of the sulci), and perhaps obliteration of the basal subarachnoid cisterns. This compensatory mechanism, however, is limited, and when it has been exhausted, further tumor expansion may produce progressive displacement of a vulnerable part of the brain (uncus, cingulum, tonsil, etc.) from its normal intracranial position, across the free border of a dural sheath (tentorial edge, falx), or through the foramen magnum. This results in the commonly recognized classical herniation syndromes (Tables 4.3a, b). Herniation occurs not only along the dural incisures (tentorium, falx) or in the occipital foramina, but also in much more local intraparenchymal, intrasulcal, fissural and intraventricular locations (Fig.4.3a-d). The classical herniation syndromes are based on the compartmentalization of the CNS into only five spaces: two supratentorial (divided by the falx cerebri), two posterior fossa (divided by the falx cerebelli) and spinal. It is clear that this concept is far too simple, as the compartmentalization of the CNS is

252

4 Neurophysiology

Table 4.3a Cerebral tissue herniations in the supratentorial structures (adapted with permission lrom Okazaki, Fundamentals of Neuropathology, New York, Igaku-Shoin 1989, p. 90) Structure

Displacement

Primary eftect

Secondary eftect

Uncal and mesial temporallobe herniation

1. Lateral displacement 01midbrain 2. Anteroposterior stretching 01 midbrain with caudal displacement

Aqueductal obstruction Kernohan's notch Stretching 01perforating arteries

Acute hydrocephalus

Caudal bilateral central displacement 01midbrain

1. Stretching 01perlorating arteries 2. Compression 01PCA 3. Third nerve injury 4. Sixth nerve injury 5. Tonsillar herniation

Descending transtentorial herniation

{

Compression

}

Lateral displacement 01basal structures

Cingulate gyrus herniation

Under Iree edge 01lalx

1. Local compressive necrosis 2. Compression 01ACA (distal)

Extrinsic masses

Local delormity 01adjacent gyral cortex and white matter, with later centripetal displacement 01lobe

1. Eftacement 01subarachnoid space, and sulci (and cisterns later) 2. Ischemic necrosis 01underlying cortex 3. Edema 01white matter

Through rigid margins 01cranial delects

Venous and arterial inlarction

herniation

Inlarction Ophthalmoplegia (external /internal) Medullary compression anteriorly

01:

Expansive basal telencephalic, diencephalic or mesencephalic masses

Brain tissue (swollen)

Hemorrhage or inlarction in:

{thalamus, midbrain, or pons

MCA + 1- perlorators ACA (proximal) Anterior choroidal artery

Inlarction

}

"Fungus cerebri"

ACA: anterior cerebral artery; MCA: middle cerebral artery, PCA: posterior cerebral artery

Table 4.3 b

Cerebral

tissue herniations

Structure Expanding cerebellar mass with: a) Direct brainstem compression

in the infratentorial

structures

Displacement

Primaryeftect

Secondary eftect

Anterior compression 01pons and medulla against clivus

1. Distortion and obstruction 01 lourth ventricle 2. Compression 01branches 01 basilar artery, AICA, PICA

Triventricular hydrocephalus

Triventricular hydrocephalus opposes any upward herniation 01 cerebellum

Precipitate tonsillar herniation with medullary impaction and lirst respiratory arrest and then cardiovascular collapse

1. Displacement 01vein 01Galen upward against the splenium, and compression against Iree edge 01lalx

Hemorrhagic inlarction 01diencephalon and adjacent white matter

2. Compression 01branches 01 SCA against Iree edge 01tentorium

Superior cerebellar inlarction

b) Downward cerebellar herniation

1. Tonsillar herniation into and through loramen magnum

(Small tentorial incisura)

2. Dorsoventral compression 01 medulla

c) Upward transtentorial herniation

Upward displacement 01superior cerebellar vermis with distortion 01 midbrain, buckling 01quadrigeminal plate, and shift 01colliculi upwards, beneath corpus callosum

Favored by: 1. Mass near incisura (e. g., in vermis) 2. Large tentorial incisura 3. Drainage 01lateral ventricles in obstructive hydrocephalus Expanding pontine or lourth ventricular mass

Anterior and upward displacement 01pons into interpeduncular cistern

Midbrain pushed anteriorly and superiorly, with pons reaching inlundibulum

Extra-axial posterior lossa mass (e. g., cerebellopontine angle tumor)

Asymmetrical upward shift 01pons and midbrain

Distortion and obstruction 01 lourth ventricle

AICA: anterior inlerior cerebral artery; PICA: posterior inlerior cerebellar artery

Hemorrhage or inlarction

Triventricular hydrocephalus

Physiological Subsystems far more extensive (Table 4.4). In addition to these compartments, eachof the cisterns is subcompartmentalized. The cerebrum,brainstem, and cerebellum have a distinct architecture, consistingof multiple semicircular compartments (seven cerebral lobes,25gyri, numerous transverse gyri, seven cerebellar lobules, andcountless foliae) which can be subcompartmentalized into fibersystemswiththeir semispiralcourses.The CNS arterial and venousvascular systems consist of subcompartments, as does the ventricularsystem, with semispirallateral ventricles and a semicircular third ventricle-aqueduct and fourth ventricle. (see voll.m A, Figs.7.20, 7.25, 7.26, 7.29, 7.30-7.32). As a result, in reality the CNS consists of innumerable semicircular,semispiral compartments, each with its own distinct characteristics(size, shape, pressure, compressibility, elasticity, etc.).As a consequence, the expansion of a space-occupying mass withinthe CNS propaga tes a cascade of effects on a multitude of compartments,with countless responses and counter-responses fram each compartment (Fig. 4.3). This concept of a complex, interwovennetwork of compartments is at odds with the traditionalperception of herniation, but certainly better explains the variability of clinical symptoms associated with enlarging intracranialmasses (Cases 4.1-4.8). The parameters obtained fram point measurements may present important information concerningthe course of intracranial pressure gradients. With a noninvasivetechnique, which hopefully will be available in the nearfuture, different areas and compartments should be simultaneouslymeasured to compare the dynamics of the pressure gradientsof the whole CNS continuously. Each compartment in the CNS can be affected by tumorrelatedherniations. Extrinsic and intrinsic tumors can produce bothlocal and remote herniation. Local herniation involves the displacementof parenchymal tissue, tumor, or both, from their primaryspace into a surrounding free space. Remote herniation, on theother hand, occurs when parenchymal tissue located some distance fram the tumor is displaced, either directly (by tumorrelatedaxial forces) or indirectly by the occlusion of CSF pathways(hydrocephalus),strangulation of vascular structures (infarction),or edema (peritumoral).

Fig.4.3 a Intra-axialand extra-axial herniations 1a Frontalsubfalcial 1b Sulcal 2 Sylvianfissure 3 Insular 4 Intraventricular 5 Transverse fissure 6a Foraminal 6b Cerebellopontine 6c Supratentorial

d

e

Fig.4.3b In the anterior frontal areas, herniation occurs into the oppositefrontallobe e Subfacialherniation (posterior areas)

253

Fig. 4.3 d sure

Herniation of opercular and insular tissue into the Sylvian fis-

254 Table 4.4

4 Neurophysiology Accommodative

pathways

that may be associated

with

the growth 01 CNS tumors

Osseous

Cranial

Rostral

Basal

Compartmental

CSF system

Vascular system

Parenchyma

Natural and acquired bony delects allow some Ilexibility lor intracranial tumor growth without early rise in ICP Widening 01the lontanella Suture diastasis Pacchionian granulations/ arachnoid villi hypertrophy, causing bone erosion Erosion 01calvarium (Irontal, temporal, parietal, occipital) Enlargement (+ / - erosion) 01lossae (Irontal, sphenoidal, temporal, petroclival, suboccipital) Erosion 01bone over air sinuses (sphenoid, lrontal) Widening 01neural loraminae Widening 01venous sinus, cavernous sinus, jugular bulb Relative incompressibility 01fluid components within each compartment allows compensatory reductions in other compartments Loss 01CSF spaces and volume Fissural / sulcal Cisternal Ventricular Spinal Increase in CSF reabsorbtive capacity Pacchionian granulations / arachnoid villi hypertrophy Along cranial nerves or along spinal nerves Decrease in CSF production (20-30"10 reduction, with tumors causing longstanding raised ICP) Reduction in cerebral blood volume on the venous side is later replaced by an increase in cerebral blood volume on the arterial side) Venous capacitance vessels compressed Hypertrophy 01existing venous draining system Extra collaterals to venous drainage system Later, increase in cerebral blood volume (may occur with any lactor raising ICP) Compression, displacement, distortion 01 the brain and its parts (Iobes, gyri, loliae, brainstem)

Clinical experience, in relation to modern neuroimaging, teaches us that we have to distinguish between two types of herniation: 1. Herniation without clinical consequences and therefore benign, and 2. Herniation with consequent clinical signs and neurological deficits, which is therefore of a malignant type. Neuroimaging cannot distinguish between these two types and, more importantly, it cannot predict when herniation is going to be dangerous. Extrinsic tumors may herniate directly by expansion into the extracranial epidural, or intracranial spaces. The brain parenchyma, cranial nerves, and cerebral vessels can all be compressed, stretched, distorted, displaced, and / or indented. The

Table 4.5 Deciding factors in the assessment of the buffering tem reserve in intracranial space-occupying lesions

Intracranial pressure Normal Elevated Focal Global Rate 01rise 01intracranial pressure Slow Rapid Size 01lesion

sys.

Nature 01 lesion Location 01 lesion Number 01 les ion s Presence 01 brain distortion Presence 01 brain herniation Rate 01 expansion Cranial delects CSF leaks

01 the lesion

stretched Al segment may incise the optic nerve, chiasm,or optic tract (in cases of craniopharyngioma and tuberculum sellae meningioma), and both pericallosal arteries indents the callosal body over a remarkable distance and P2segment of the crus cerebri (Table 4.5). The morphologic changes associated with this herniation may reach drama tic degrees, strongly suggesting impending clinical decompensation. However, it is clear that there is very little clinical correlation between the morphology of herniation in extrinsic tumors and the resultant physiological derangements. Patients with enormous herniation and distortion may remain asymptomatic for extended periods, while conversely other patients with slight (seemingly insignificant) compression may suffer symptoms (headache, etc.), functional deficits (sensorimotor loss), or seizure episodes. Even patients with marked obstructive hydrocephalus can present without symptoms, deficits,and papilledema (Tables 4.4 and 4.5). Intrinsic tumors may herniate indirectly by the same mechanisms as those outlined for the extrinsic tumors. Direct herniation of intrinsic tumors, however, occurs by expansion or infiltration extraparenchymally into the subarachnoid (sulcal, fissural, and cisternal), intradural and extradural, mucosal, and ventricular spaces.Cranial nerves,pituitary stalk, cerebral vessels,and whitematter fiber tracts may be displaced and distorted, sometimesto an alarming degree. As with extrinsic tumors, these morphological herniation findings are frequently not associated with clinical deficits, while smalllesions may be associated with headache, mental dysfunction, or seizures. With both intrinsic and extrinsic tumors, we have been consisten tiYunable to corre late the findings on neuroimaging (degree of mass effect, herniation etc.) withthe patient's clinical status. We have observed asymptomatic patients with enormous extensions of internal or external neoplasms into the basal cisterns, into the subfalcial, transtentorial, and perimedullary classical herniation spaces, and into the brain parenchyma. We continue to search for answers as to what additional factors are responsible for the remarkable resistance, compensation, and adaptation witnessed in these situations. Clearly, part of the answer lies in the complex interactions of the CNS subsystems. which allow for compensation of the effects of the expanding mass as long as tumor growth occurs slowly and until the systemis thrown out of balance, with resultant rapid or sudden collapse. Still, a great deal of the explanation will depend on a better understanding of the uniqueness of the effects of each individual tumor and the response of each individual patient. Some examples at the end of this Chapter illustrate these important points (Cases 4.1-4.14).

Pathophysiology: Cerebral Edema

255

Pathophysiology: Cerebral Edema Intracellular and extraceIlular water content may both be increased leading to cerebral edema. Four types of cerebral edema are weIl recognized: cytotoxic, vasogenic, interstitial (Fig.4.4),and hydrostatic. Cytotoxic edema is an intraceIlular type of edema in which the ATP-dependent sodium-potassium pump fails (aIlowing sodiumand water to accumulate within the ceIls), leading to diffusebrainswellingwithloss of the normal gray-white differentiation. There is intraceIlular sweIling of neurons, glia and endothelialceIls,with a concomitant reduction of brain extraceIlular space. The infratentorial parenchyma is usuaIly spared. Hypoxiaas a result of ischemia is by far the commonest cause, usuallyfollowingacute catastrophic insults (global cerebral ischemia aftercardiac arrest, massive systemic hemorrhage, or failure of cerebral autoregulation after severe head injury). Profound anoxiafrom respiratory arrest results in an irreversibly fatal cytotoxicedema. Water intoxication (iatrogenic or self-induced) and acutehyponatremia (e. g., from inappropriate antidiuretic hormonesecretion)may also cause cytotoxic edema, with water movingfrom extraceIlular to intraceIlular sites. Cytotoxic edema mayalso accompany other forms of edema in some brain tumors (wherevasogenicedema is usuaIlyof greater significance),and in meningitisand encephalitis. Vasogenicedema is an extraceIlular edema due to disruption or defectivefunction of the blood-brain barrier, and is the type mostfrequently seen in the vicinity of brain tumors, although it can also develop adjacent to cerebral infarcts (Klatzo 1967). Generalizedvasogenic edema, as opposed to local edema characteristicaraund tumors, may be produced in craniocerebral injury, meningitis,and lead encephalopathy. The peritumoral white-matter edema associated with many intrinsic and extrinsic brain tumors probably has several pathophysiologicalmechanisms. Certainly, as it represents vasogenicedema,thereis by definitionleakage of protein-rich plasma intothe white matter through "Ieaky" capillary endothelial ceIls. In the moremalignanttumors.this "Ieakiness" may result from abnormalitiesin the permeability characteristics (lack of normal tightjunctions)of tumor-feeding vessels (Bartkowsi 1984). In otherinstances,there is an opening of the tight junctions in the endothelialceIls of normal cerebral vessels, possibly due to the production of vascular permeability factors by the neoplasm (Bruce1987,Criscuolo 1988, Ohnishi 1990) or to focal (or diffuse) ischemiafram direct tumor compression and peritumoral vascularstasis,or the production of bioactive substances with primary metabolicsuppression of the peritumoral white matter (Hino et al.1990). This peritumoral edema flows by backflow (under hydrostaticpressuregradients) and not diffusion. It extends along whitemattertracts (Caveness et al. 1978), spares the cortex (due to the tightextracellularspace), and is usuaIlysteroid-responsive.If it persistsfor some time, myelin destruction can occur. Absorption ofthisfIuidis through the ependyma into the ventricular system. Waller(1992)suggests that some absorption may occur through the lymphaticssurrounding the cribriform plate and along the perivascularspaces of penetrating leptomeningeal vessels. Extensivevasogenicedema can add significantly to the volume effect of tumormasses,leading to considerable brain displacements and

b

e

d Fig.4.4 Types of cerebral edema after Bradley(NeuroI1984; 6: 94) a Normalbrain b Vasogenic edema. Note the breakdown of the blood-brain barrier and increased extracellular space e Cytotoxicedema. Note the swollen glialcells, limitingthe backflow of extracellular fluid secondary to associated blood-brain barrier damage d Interstitialedema. Note the increased intraventricularpressure forcing CSF through the ependyma

256

4 Neurophysiology

herniations, and elevated focal or generalized intracranial pressure (ICP) above normal. Two distinct types of peritumoral changes suggestive of tumor-related vasogenic edema have been identified and distinguished (Trittmacher et al. 1988). Type 1 occurs characteristically around benign tumors, such as meningiomas. This type is confined to the immediate vicinity of the tumor, and persists indefinitely on MRI (hypointense areas). It is believed by many that this represents the permanent effects of severe edema, ischemia, and necrosis secondary to tumor compression. Type 11 occurs with both extrinsic and intrinsic tumor types, and is distinctive in its tendency to spread throughout the ipsilateral hemisphere. It may have irregular, finger-like projections, but it tends to resolve over 8-12 weeks following tumor removal, though examples of it remaining indefinitely are not uncommon. This type can occur with even a small tumor, and its presence with a small meningioma suggests the possibility of adherence or malignant change. Cerebral edema per se (apart from extensive cytotoxic edema) does not directly interfere with neuronal activity (Penn 1980). Only when it is sufficiently severe to cause cerebral ischemia or significant distortion and herniation does cerebral edema result in brain dysfunction. However, there are many confusing discrepancies betweenclinical observations (symptoms such as headache, signs such as papilledema, and neurological findings) and the degree of peritumoral edema apparent on neu-

roimaging. Some patients with MRI evidence of severe edema remain asymptomatic, while others with similar findings are critically affected. It is impossible to accurately predict clinical findings based on these neuroimaging findings. Similarly, the degree of herniation on MRI may not correlate with the amount of edema. lnterstitial edema occurs in periventricular tissue when the intraventricular pressure exceeds the ability of the ependymal cells to contain the CSF within the ventricle, which is then forced under high pressure transependymally into periventricular white matter. This occurs in acute, or subacute, hydrocephalus, and is seen most prominently (on MRI) around the frontal horns. Hydrostatic edema may occur (even with an intact vascular endothelium) following a sudden increase in intravascular pressure that is sufficient to overcome the cerebrovascular resistance, leading to flooding of the capillary bed within the brain. Congestive brain swelling occurs immediately, and is followed within minutes by extravasation of a protein-poor fluid into and through the extracellular space. This situation occurs in hypertensive encephalopathy, but may also occur when neurosurgical procedures are performed on patients with a very high intracranial pressure (Adams and Graham 1988). It can occur both during the craniotomy, if the intracranial pressure suddenly becomes high,or later in the operation, when an intracranial mass lesion causing high intracranial pressure is abruptly decompressed (Miller 1992).

Cerebrospinal Fluid System The nervous system is isolated from the blood by a barrier system that provides a stable and optimal environment for the neurons and glia. The brain environment consists of the extracellular fluid (ECF), which amounts to 15-20% of the total brain volume (Fishman 1980).This includes the interstitial fluid, a large part of which is in the form of a specialized fluid, the cerebrospinal fluid (CSF) (Fig.4.5a). The CSF is formed in two different types of capillary systems in the brain. The choroid plexuses within the ventricles account for 60-70% of CSF production (Milhorat 1975, Pollay 1975, Davson et al. 1987). The other sources of CSF are the brain capillaries themselves (20-30%) (Davson et al. 1987, Cserr 1989), and metabolically derived water (contributes around 10%). Thus, there is a significant extrachoroidal source of CSF in the white matter of the brain, which arises as a bulk flow of interstitial fluido The classical circulation of CSF through the ventricles, subarachnoid cisterns, and convexity subarachnoid space is well known. Final absorption occurs primarily into the sinus system through the arachnoid villi, although at times significant drainage may occur via cranial nerve subarachnoid space-Iymphatic connections (especially olfactory) (Weller et al. 1992) (Fig. 4.5a-d). The following passages are adapted, with the authors permission, from Cserr et al. (1992): Pathways ofinterstitial fluid (ISF) flow. The permeable membranes covering the inner (ependymal) and outer (pial and glial) surfaces of the brain permit diffusional exchange between the CSF and ISF in superficial portions of the underlying nervous tissue. The resistance to bulk flow through the narrow intercellu-

Choroid plexus Ventricles

Brain tissue

Perivas,

Perivascular

spaces

spaces

Venous blood and Iymph

Fig.4.5a A model 01interstitial Iluid (ISF) turnover in the brain, based on the secretion 01 cerebral ISF by the blood-brain barrier (open arrows) and bulk Ilow Irom the brain to cerebrospinal fluid (CSF)via perivascular spaces (curved arrows). CSF is secreted by the choroid plexus (open arrow), and drains with ISF and CSF lrom the subarachnoid space to venous blood and Iymph (Irom Cserr et al. 1992)

Cerebrospinal Fluid System

257

Sinus Arachnoid villi

Lymph node

b Fig.4.5b Outtlow pathways from the cranial and spinal subarachnoid spaceacross the arachnoid villi or along certain cranial nerves and spinal nerve roots to the Iymphatics. I Olfactory nerve, 11Optic, V trigeminal,VIII acoustic (from Cserr et al. 1992)

D D

Nervous tissue

t

~

Intraneuralliquor space (ventricles) 2

!;.:"~ Extraneuralliquor space L...c''':_-'_J (clsterns)

3 Dura mater (pachymeninx) 4 Arachnoid Pia mater

}

(Ieptomeninges)

a::=::::J

Arteries

a::=::::::::J

Veins

~

Venous sinuses

5 6

1I'¡"i;¡;'''.;,,;~ Lymph vessels

-

8

Blood

9 10 11

Liquor cerebrospinalis

Lymph A

Liquor-blood (valvelike) passage Blood-brain barrier 01nonlenestrated endothelial wali and arachnoidal barrier layer

C

Blood-liquor barrier 01nonlenestrated epithelial wali and arachnoidal barrier layer

12

Sinus sagitfalis superior and lacunae laterales Granulationes arachnoideales Cavitas subarachnoidealis Vv.cerebri (cortical and deep cerebral veins) Aa. cerebri (cortical and deep cerebral arteries) Telachoroidea (01ali ventricles) Aa. choroideae (anterior and posterior choroid arteries) Vv. choroideae (superior and inferior choroid veins) Connective tissue Sinus rectus Sinus transversus and sinus sigmoideus Aperturae (mediana and lateralis) ventriculi quarti A. carotis interna V jugularis interna Ductus thoracicus Nervi spinales Filamentum terminale

Fig.4.5c Diagram of the blood and liquor circulation in the brain. For [> reasonsof simplification only one channel represents the arterial supply insleadof the two systems that exist in reality (Cf. next figure). NiewenhuysR, Voogd S, van Huizen. The Human Central Nervous System, A Synopsisand Atlas. Berlin: Springer, 1988: 54, Fig. 50

e

lar cleftsthat characterize much of the CNS is too high, however, lo accommodate any appreciable flow of fluid via this pathway (Welch 1970). Bulk flow requires spaces of a larger caliber (Fenstermacher et al. 1976). Perivascular spaces communicate at the outer and inner surfacesof the brain, with a number of other extracellular channels (not illustrated), including the subpial space, tissue spaces within Ihearachnoid trabeculae, and the arachnoid (Krahn 1982, Krisch el al. 1984, Alcolado et al. 1988), and the subependymal zone of (he ventricular ependyma (Cserr et al. 1977). Spaces between fibertractsin the white matter may also serve as channels of ISFflow (Cserret al. 1977), especially under pathological conditions (Reulen et al. 1977).

Bulk flow aud ISF secretiou. Studies with extracellular tracers (e. g., India ink, labeled albumin, or polyethylene glycol) support the concept of ISF drainage from the normal brain. Tissueinjected tracers spread preferentially along intracerebral channels of flow, and can be traced in high concentration to perivascular spaces surrounding large vessels on the surface of the brain (Casley-Smith et al. 1976, Bradbury et al. 1981, Szentisvanyi et al. 1984, Ichimura et al. 1991, Yamada et al. 1991). In contrast, CSFinjected tracers normally fail to penetrate in the reverse direction (Davson 1956). The impermeability of the blood-brain barrier implies that the mechanism of cerebral ISF production cannot be filtered, as in other capillary beds (Cserr et al. 1991). Secretion has been pro-

B

D

Liquor-blood passage via Iymphatic system

13 14 15 16 17

/'

258

4 Neurophysiology

posed as the most likely mechanism of fluid production (Cserr et al. 1981),based on the structural and functional similarities of the cerebral endothelium to a secretory epithelium (Crone 1986). These similarities inc1ude: bands of tight junctions between adjacent endothelial cells, which impede a pass ive exchange between plasma and cerebral ISF (Brightman et al. 1969); specific transendothelial transport mechanisms for a variety of substances, inc1udingNa+ (Murphy et al. 1989) and K+ (Katzman 1973); polarization in the distribution of Na+ pumps to the albuminal border (Firth 1977);and an increased density of mitochondria (Oldendorf et al. 1977). Cerebrospinal fluido Secretion of fluid by the choroid plexus of the lateral, third, and fourth cerebral ventric1es is the major source of CSF. Drainage of ISF into CSF constitutes an additional, extrachoroidal source accounting for approximately 10% of total CSF production (Oldendorf et al. 1977). The rate of turnover of CSF (half-time of 2-3 hours) is more rapid than that of ISF (half-time of 6-18 hours) (Szentistvanyi et al. 1984, Yamada et al. 1991).

Protective Barriers Cushing (1925) recognized that an understanding of the structure and function of the blood-CSF barrier and the blood-ECF barrier is essential to an appreciation of the pathophysiology of tumoral disturbances in the CSF pathways and environment (Fig. 4.5d). The blood-CSF barrier resides in specialized ependymal calls overlying the choroidal capillaries. The choroidal epithelium is distinguishable in three ways: by the presence of surface microvilli; by the bonding of these cells together in tight junctions; and by humerous ion-transport mechanisms. The blood-ECF barrier resides in the capillary endothelial cells of the brain. These are distinguished from other capillaries in four important ways: 1. The cells are bonded by tight junctions (impermeable to large molecules). 2. There are no fenestrations, and pinocytic vesicals are rare. 3. There are highly specific enzyme transport systems (similar to those found in the choroid plexus epithelium). 4. The cells contain no actomyosin, and are thus noncontractile (a protective feature).

FIO 1.

.

Dioqrom

o

cerebro-

~

of

spinol circulotory sedor

;¡;. .....

But the existence oí another Huid besides blood which "circulated" was soon suggested by .AselIi's discovery oí the la.ctea.ls, and Picquet's of the thora.cic duct; and fina.lly William Hunter, 01' was it aga.in your Monro secundus, who first postulated that the Iymphatics represented a. system of absorbent vessels which were supposed to conduct the watery constituents oi the tissues? To be sure, the movement oí the chyle and Iymph, under this conception, is not actua.lly in a circle in a strictly Harveian sense, but rather in what one might describe as across a sector oi the blood circle. And the same is true oi the cerebro-spinal Huid which proves to be in continual movement, in a definite direction, through a highly specialised pa.thway, that cuts across the blood circle to envelop an organ in which a lymphatic apparatus oi the usual type does not e:rist (Fig. 1).

QI;amtton Jtdnrtl'í ¡,liver,d al (h, Unit'er8Íly 01 Edinburgh on Oct. 19th, Ocl. 20th, and Ocl. 22nd, 1925. By HARVEY CUSHING, C.B., F.R.C.S. ENO.. PROFESSOR

OF SUROERY

IN RARV.I.RD

UNTVmtSrrY.

Fig.4.5d Diagram used by Cushing (1925) Cameron lectures. Lecture 1. The third circulation and its channel. Lancet 2: 851-857,1925, Fig. 1

The total are a of the brain capillary bed is enormous: 150 cm2/ g of brain. This is about 100000 cm2 in a 1500 g brain (5000 times greater than that of the choroidal epithelium).

The Intracranial

Buffering System

Studies of the complexity of CSF circulation changes and, more recently, a greater understanding of the biophysical variables accompanying the parenchymal and compartmental displacements brought about by space-occupying lesions in the brain have caused many modifications to the eighteenth-century concepts of Momo (1783) and his pupil, Kellie (1824). Their hypothesis of the incompressible nature of the intracranial contents (brain, blood) within a rigid skull was broadened by Burrows (1846), who added the important modification that CSF volume could be exchanged for blood volume, and by Duret (1878) and Kocher (1901), who

promoted the important concept of spatial compensation. The idea that a volume increase in any of the intracranial "compartments" (brain, CSF, blood) must be compensated for by a corn. mensurate decrease in the volumeof one or both of the othercorn. partments continues to be useful, but is still too simplistic. The mass-volume of brain/spinal cord (1300-1500 rnL), blood (150 mL) and CSF (150 mL) per moment in time is generated by the continuous flow of blood and CSF through and around the neural parenchyma and through the intracranial and spinal compartments. A dynamic, but finely balanced, steady sta te or equilibrium exists between these three intracranial (and intraspinal) compartments (the blood volume, arterial and venous, contributing 10-15%, the CSF 10-15%, and the

Cerebrospinal Fluid System parenchymalvolume 70-80% (including capillary blood and extracellular(CSF). As expanding mass lesions increase in size, there are correspondingreductions in CSF or blood volume, or both (through a seriesof stepwise adjustments to the steady-state equilibrium) untila critical steady state is reached. This is often the stage at whichsustained elevations in ICP can be detected. Well before this stage though, many interrelated accommodative changes haveoccurred. Some of the factors underlying these changes are wellrecognized,while others rema in obscured by the complexitiesofthe interactions(Fig.4.3). As a result, there are recurring paradoxicalexamples of large tumors in cruciallocations without discernibleneurological effects, and small or moderate-sized tumorscausingall manner of physiological upset. Understanding the mechanisms responsible in these situations is a challenge; studyingthem may teach us more than the familiar textbook examples, where the failure of compensation is obvious. However,it is c1earthat in any one individual, this finely balanced mass-volume equilibrium has a unique but finite "buffering" capabilityto compensate for expanding mass lesions (Table 4.4). In addition, neurosurgeons have long been aware that the bufferingsystem reserve is different (both in capacity and in speedof accommodation), not only at different ages, but also with differentpathologies of tumor. The time-course of a volumemassacquisition is a major determinant of the capability of the inherentcompensatory mechanisms to maintain equilibrium. The bloodvolume is the most plastic of the three, able to respond withina matter of seconds to minutes. The CSF compartment is capable oflargefluctuationsin volume,but these must be effected overa longerperiod of many minutes, hours, or even days.The brainmay accept, without loss of function, some alteration of its volumeby changing contour or decreasing interstitial fluid, but theseaccommodationsrequire a prolonged state of adaptation, in the order of days to weeks. More rapid distortions or displacements of the brain parenchyma (e. g., from traumatic hemorrhagicexpanding mass lesions) usually cause loss of neurological functionand coma. Here, the compliance of the brain is poor, as the changein volume has been too rapid, causing a far steeper exponentialrise in pressure (DV /DP), than would have been the casewitha slower change in volume. In addition, we believe that the individualbuffering system reserve (given identical tumors) mayalsobe widelyvariable. In future, a noninvasive means of anaIyzingindividual buffering system reserve would, for certain tumors(especiallyrecurrent tumors), be a great asset for surgical timingand strategy.

259

cant clinical correlates than with craniocerebral injury patients, as the underlying pathophysiologies are quite different (traumageneralized, tumor-focal). What is clear is that other factors apart from the absolute value of ICP are frequently more important in deciding how much of the buffering reserve has been used up in an individual patient with an intracranial tumor (Table 4.5). This is certainly the case with large cerebral tumors, where, in many cases, the buffering reserve is nearly fully exhausted (although the level of consciousness is fully preserved), and any additional factor raising ICP can cause rapid decompensation. Most important of these deciding factors are: the rate of increase in ICP (may be rapid with new onset of hydrocephalus, or hemorrhage within a tumor), the size, nature, and location of the lesion, and the presence of brain distortion and herniation. The presence of two or more space-occupying lesions, in the context of an already elevated ICP, is particularly worrisome, as combinations of lesions frequently defy expected physiological parameters (so metimes with disastrous clinical consequences). A complete list of these factors is shown in Table 4.5, p. 254.

ICP Monitoring The routine application of intracranial pressure monitoring has found its widest application in the treatment of patients suffering from generalized ICP abnormalities, for example with brain injury. In this situation, current ICP monitoring techniques can be informative (at least academically). However, in tumor patients significant abnormalities in intracranial pressure are usually restricted to the focal area of the lesion. The generalized affects of tumor mass are the result of a cascade of effects through the tremendously compartmentalized CNS, so that the measurement of generalized ICP has little interpretive value. For focal masses, interpretation of ICP information must take into account the compartmental site of monitoring. Each compartment surrounding a focal tumor will have a different pressure associated with it, and each will respond to changes in tumor size with a different dynamic volume-pressure curve. Present ICP monitoring techniques are incapable of mea suring pressure in the spectrum of compartments surrounding a focal mass, and as a result have no practical (or academic) value in the case of brain-tumor patients. As a consequence, we have not applied these methods in the treatment of our CNS neoplasm patients. In the not too distant future it is possible that perioperative (selective and dynamic) measurement of all CNS compartments will become available (using cellular biochemical markers).

Intracranial Pressure NormallCP Muchofour knowledgeon intracranial pressure (ICP) has come fromstudiesof patients with craniocerebral injury,or with spontaneousintracerebral or subarachnoid hemorrhage, as well as fromexperimental models.Clinicalcorrelations of ICP elevations havenot proved to be as specific in the prediction of outcome as originallyhoped, except in cases of severe craniocerebral injury (Glasgowcoma score = 8). However, knowledge of the ICP and intracranialdynamicsis considered very useful by many neurosurgeons in guiding the management of severe and moderate craniocerebralinjury (GCS 8-12), in recognizing impending brainherniation.Studies of ICP in cerebral tumor patients reveal somedifferencesin threshold leve\s (Iower), but with less signifi-

Intracranial pressure can be defined as a steady-state level of CSF pressure in the cranial cavity, upon which cardiac and respiratory components are superimposed. Under normal physiological conditions, the normal range of CSF pressure is between O and 10 mmHg. In practice, however, the upper limit of normal is usually taken as 15 mmHg in adults (Miller 1992). In children under 7 years, the upper limits of normal are much lower, e. g., 5 mmHg in a 5-year-old and 3 mmHg in a newborn (Welch 1980). In the upright position, intracranial CSF falls to zero or below, and lumbar CSF pressure increases. In the recumbent position, the CSF pressure when measured in the ventricle and in the spinal sub-

/'

260

4 Neurophysiology

Table4.6 Intraeranialpressure thresholds with intraeranial expanding lesions Elevated ICP

Type Level (mmHg)

Clinical significance

Mild Moderate

15-21 21-30

Severe

37

Welltolerated Often symptomatic; may show plateau or A-waves. Merits treatment Show signs of cerebral ischemia; impaired cerebral electrical activity Usually associated with loss of cerebral autoregulation and death

Fatal

60

arachnoid space is normally equal throughout the craniospinal axis (Table 4.6). The pulsatile variation of the normal ICP is derived from the transient changes in blood volume associated with the cardiac and respiratory cycles.The pulsa tile wave form normally recorded consists of two components, one corresponding to arterial pulsations (Fig.4.6), the other, much slower, corresponding to respiratory changes brought about by changes in intrathoracic and central venous pressure. With each arterial expansion, there is a pistonlike remolding of the brain. Due to the expansion of the parenchymal component (from capillary filling) and blood volume components of the intracranial volume, a cascading wave is produced in the cisterns, sulci, and ventricles (CSF flows in), with the venting of CSF into the spinal canal as the compensatory response (Greitz et al. 1992) (Fig.4.6). Accurate measurement of ICP should include measurement of the baseline level as well as the amplitude of the rhythmic components, giving a mean ICP. At normallevels of ICP, the difference between the recorded ICP and mean ICP may not be very great, but as mean ICP rises, the amplitude of the arterial component of CSF pressure increases, while the respiratory or venous component becomes relativeiy less apparent. Thus, mean ICP is defined as the diastolic pressure plus one-third of the pulse pressure (Brock and Hartung 1972). Changes in ICP have been shown to depend on four variables: the rate of CSF production, intracranial compliance, outflow resistance, and intradural sinus pressure (Marmarou 1992). With knowledge of these parameters, the pressure response to a known volume change can be predicted. By a reverse process, methods are available to estimate these CSF parameters from sta tic and dynamic responses of ICP to known volume changes (Fig. 4.7). CT and especially MRI visualize the degree of volume changes, displacements, and herniations that may occur. These are produced in response to extrinsic or intrinsic tumors with or without peritumoral edema, metabolic fluctuations, and hydrocephalic changes (Table 4.7).

Elevated ICP Physiological elevations of ICP occur briefly, with coughing, headdown tilt, and the compression of neck veins. They may be quite high (50-80 mmHg), but as they are equally distributed throughout the spinal axis and of short duration (less than a minute), they do not cause neurological damage.

Table4.7 Classifieation of hydroeephalus aeeording to CSF dynam. ies and ICP (From Gjerris et al., Advances and Technical Standards in Neurosurgery, Vol. 14, Vienna: Springer, 1992, p. 145-177) Type of hydro- CSF production cephalus Obstructive

CSF circulation

CSF absorption ??

Normal (?)

ICP

i i or normal

Malresorptive

Normal

Normal

Atrophic Hypersecretory

Normal

Normal Normal

i i

i i or Normal Normal

normal Normal Normal

Important thresholds of elevated ICP are well recognized from craniocerebral injury data, that may be also applicable for cerebral tumors (Table 4.6), with three important provisos. First, the threshold levels of ICP are often lower than with craniocerebral injury patients. Second, although many cerebral tumor patients have normal, or only moderately elevated, ICP at rest, they are prone to transient (and frequently symptomatic) paroxysms of ICP elevation, because-third-the bufferingsystem reserve is often near to the critical point at which any new cause of rise in ICP may cause a precipitate elevation of ICP to a moderate or severe degree (Fig. 4.6). Such patients are veryprone to suffer from pressure waves, particularly A-waves. These are most common at night, particularly during REM sleep. Often it is only at a late stage, when the patient has be come drowsy or comatose, that resting ICP becomes elevated. Even before CT and MRI, it was well established that somelarge (especiallyextrinsic) tumors remain undetected for a long time owing to a paucity of symptoms, while other smaller lesions in the same location produce a myriad of symptoms. Noninvasive neuroimaging techniques allow a more accurate (in three planes) and dramatic study of volume changes in intracranial structures, and confirm the observations of our predecessors; but, in addition, they carry us one important stage further. In the past, tumors were often not diagnosed until patients presented with final (severe) symptoms (that led to an angiogram or air study). In these instances, the tumor growth process and resultant manifestations were seen and analyzed in the final or end-phase of tumor progression. It had been firmly believed that those large tumors which cause displacement and midline shift needed urgent removal,or at least decompressive treatment to avoid herniation. It was assumed that nonurgent action might lead to ischemia, infarction and hemorrhage (even resulting in death). The radiological diagnosis of "herniation" was gene rally held to be synonymous with the assumption of imminent collapse of the intracranial "steady state," followed by massive clinical deterioration. However, the remarkable local and perifocal displacement of normal brain structures that is visualized on MRI is not always commensurate with significant clinical findings. Some patientsmay have the anticipated mental and neurologicalfindings,while others may have virtually none. Identicallesions on MRI scansdo not consistently produce the same neurological symptoms. We have witnessed patients with huge brainstem gliomas and large hemispheric lesions (with large degrees of herniation) whohave declined surgery for long periods of time (months to years), and yet maintained a normallevel of activity (sometimes even includ-

Cerebrospinal

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261

e

b

d

Fluid System

Fig.4.6a-c The direetion ot the torees responsible tor remolding the brain and tor its piston aetion, during systole; they are distributed in a tunnel-like tashion d Movements in the basal ganglia, whieh arise when the ganglia and the brainstem move in opposite direetions (shearing torees) (trom Greitz Neuroradiology 1992;34:370-380)

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Fig.4.7 The pressure-volume eurve. As volume inereases and ICP [> rises,unitorm inerements ot volume (d/v) produce progressively larger increases in ICP (dP1 and dP2). Inereases or deereases in volume causecorrespondingly greater ehanges in ICP on the steep part ot the curve(from Miller T and Adams T in Greentield, Neuropathology, 1986, p. 73, Fig. 2.1)

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"262

4 Neurophysiology

ing sports). The observation of these patients has taught us that the use of radiographic herniation as evidence of impending c1inical deterioration is not correct, and should not be used as an indication of the necessity of urgent surgical intervention. As a result, it has become apparent that tumors in similar locations often present with different symptoms (or non e), both in quantitative and qualitative terms. The response of neurological function is far from being rigidly mechanical; instead, it is highly flexible. Accordingly, an accurate prediction of neurological deficits from MRI scan abnormalities alone cannot be reliably made. This has stimulated major reassessments of the underlying physiological mechanisms and their interaction. At present, neuroradiological and neurophysiological (inc1uding neuropsychological) studies give accurate information relative to localization, yet provide relatively little information about the overall effect of the tumor on the condition of the brain. Our inability to assess the early and intermediate neurophysiological effects of tumors awaits solution by further research efforts. In addition, a pronounced shifting of midline structures and impressive transsylvian, subfalcial, parachiasmal, parapineal, tentorial, or tonsillar herniations are not even always accompanied by c1inically evident increases in intracranial pressure. Also, in these situations signs of raised ICP are frequentIy absent. The adaptive capacity of the CNS to volume increases cannot be explained solely on physicallaws. The relationships between the volume and rate of growth of a space-occupying lesion and the

resulting increase in ICP are now well established in terms of mechanicalphysics,but fail to take into account the complexcascade of biophysical responses characteristic of the in-vivo CNS. We continue to be puzzled by common c1inical neurological signs and symptoms. Why do some tumor patients with elevated ICP have papilledema and others not? Why do some meningioma patients have exophthalmus and others not (despite identical tumors)? Why is there such a poor correlation between MRI findings, ICP levels, and c1inical findings? Clearly, individual tumor patients are responding to their intracraniallesion in vastIy different ways. In order to understand this biological variability of response, we must go beyound the purely physical doctrines (based on rigid, mechanical models) that have been taught, and explore the highly variable, constantIy changing dimensions of the living oganism (biophysical, biochemical). Our present knowledge and assumptions concerning unbalanced intracranial volumes, cerebral edema, the location and extension of tumors, ICP changes, and their relation to the general and specificstate of the brain, are being challengedbyconsiderable changes in our understanding, as a result of new insights from new technologies,inc1udingPET, SPECT, MRI, MRS,transcranial Doppler wave-form analysis, and continuous EEG and spectral EEG. Unfortunately, a means of noninvasive, continuous monitoring of dynamic CNS parameters that might give us the c1earest insights into tumor effects on the CNS have yet to be devised.

Cerebrovascular System An intensive review of the physiological mechanisms underlying the cerebrovascular system is beyond the scope of this work. The reader is referred to numerous publications related to these principIes and earlier publications of the senior author over the past quarter-century (Microneurosurgery, Vol. III A, 1987, pp. 284-349, Ya§argil1968). Some details of the cerebrovascular system in relation to its role as a subsystem with the CNS, as applied to an understanding of tumor patients, are presented here.

Introduction The human brain contains about 1015neurons, and probably ten times that number of supporting cells. It receives one-eighth (12.5%) of the cardiac output (750 mL/min), and consumes onefifth (20%) of the oxygen used by the body, yet constitutes only one-fortieth (2.5%) of the body weight. Both neurons and their supporting cells are highly metabolically active. Many neurons have an enormous surface area of cell membrane to maintain. They have extensive microtubular systems for fast and slow axonal transport to regulate, requiring a constant supply of energy to create the electrochemical gradients necessary for their function. Energy is provided principally by the oxidative phosphorylation of glucose. Glucose consumption is very high (0.3 mmol / min, 60 mg/min), and the immediate reserves of glucose available in

the neuronal environment are quite limited (used up within2 minutes). As there are minimal stores of glycogen within neurons and poor alternative energy-producing metabolic substrates in the brain, the susceptibility of the brain to hypoglycemia (and soon thereafter irreversible coma and death) is very real. Even

more catastrophic is hypoxia, which within 1 minute can leadto confusion,within 3 minutes to coma (with neuronal necrosis)and within 4 minutes to death. The complexity of cerebral function triumphs or fails on the competence of its cerebrovascular system in providing for all its metabolic demands. In phylogenetic terms, the human neocortex is distinguished by a great increase in the size of the associationareas of the neocortex (especially the anterior frontal, temporal, and parietal areas) and the complexity of the cortical synaptic circuitry.This increase in the complexity of the brain has been accomplishedby two parallel changes. First, there has been a relative reduction in the size of the extracellular fluid compartment (ECF) to about 15-18% of the whole brain (which is nearly half the normal ECF average of 30% for the body as a whole). Second, the infoldingof the neocortex deep into the fissuresto form the convolutedarchitecture has permitted a disproportionately large increasein neuronal cell numbers without a concomitant major increasein the overall size of the brain. It could well be that the optimum limitsof brain developmental size have been reached, as further bulk increase would be restricted by a failure to meet cerebralenergy requirements,so criticallydependent on the adequacyofthe cerebrovascular system.

Cerebrovascular System

ArterialSupply Thecerebrovascular system is remarkable in its ability to match increaseddemand with increased supply in differentially very activeandlessactiveares of the brain in a superbly integrated and rapidmanner. The anastomotic links between the four major arterial vesseistothe brain (circle of Willis) provide a rapid and usually excel¡entredistribution system in maintaining cerebral blood flow in theeventof blockage to one or more vessels. However, the "normal"circleof Willisis present in only about 50% of persons. Variationsand anomalies are very common, especial!y in the posterior circulation.Hypoplasia and aplasia of the anterior or posterior communicatingarteries are not uncommon. It is in patients with theseanomalieswho develop occlusive disorders (occasionally tumor-related)that the compensatory mechanisms of the cerebrovascularregulating system may be fully tested.

VenousDrainage Thecerebralhemispheres are drained by the superficial and deep cerebralveins, which are devoid of valves. They in turn receive blooddeeply from the thousands of microscopic intracortical veinsand from the superficial medual!ary veins. The veins of the whitematter consist of superficial and medullary veins, transcerebral veins, and anastomotic medullary veins. The superficial medullaryveinsjoin the superficial cortical veins. The deep medullaryveinsdrain into the subependymal veins of the deep venous system.Kaplan (1959) has demonstrated that there are over 4000 directanastomotic veins between the superficial cortical and deep ependymalveins. Compression of these veins by intrinsic tumors maylead to venous stasis and vasogenic edema. There are four transcranial venous connections between the intracranialsystem and the extracranial veins: via the sigmoid sinus;via emissary veins; via the basilar venous plexus; and via ophthalmicveins.Up to 30% of normal venous drainage is by way of these connections. In states of raised intracranial pressure (frequentlytumor-related), venous drainage by these routes may be over 50%. In this situation, flow from the dural sinuses into scalpveinscan be seen. The wall of a cerebral venule consists of a continuous endotheliallayer surrounded by a perithelial cell layer and by densecollagen bundles. Smooth muscle cells are uncommon in veinsup to 200¡.tm in diameter, so venous tone is only maintained inthe larger veins.The walls of both intracerebral and meningeal veinscontain noradrenergic and peptidergic nerve fibers.

CerebralBlood Flow Themeancerebral blood flow (CBF) to the adult brain is about 55mLlIOOg/minoNormal ranges for cortical blood flow (CoBF) are60-80mL! 100g/mino Mean CBF is higher in children (up to 100ml/lOOg/min). Blood flow also varies in different regions of the brain. Gray matter has rates of CBF between 80-100mLlIOOg/ min (reflecting its higher metabolic rate and vasculature), while white matter has rates of 20-25 mL/ 100g/mino

263

The crucial pressure that determines the adequacy of cerebral oxygenation and cerebral blood flow rate is the cerebral perfusion pressure (CPP). This is strictly the difference in pressure between arteries entering the cranial subarachnoid space and the veins leaving it. In practical terms, a usefui approximation of the CPP is the difference between mean arterial pressure (MAP) and mean intracranial pressure (ICP). Thus: CPP=MAP-ICP. (Normal adult range for CPP is 88-103-mmHg.) MAP is calculated as (systolic plus two times diastolic) divided by three. It is interesting to note that the major cerebral artery supply is centrifugal (leptomeningeal vessels), while only a small amount is centripetal (perforating vessels). This is similar in some ways to the venous drainage pattern, which again is largely centrifugal (deep venous system), the smaller component being centripetal (superficial venous system). However, it is the superficial arterial supply (leptomeningeal) and the deep venous drainage (deep venous system) that supply the CNS with the vast majority of its vascular supply. Perhaps the pulsating effects of the more superficial arterial system pro mote the drainage of the more deeper located venous system. The physiological relationships between the arterial and venous systems in the brain are only beginning to be revealed (Fig. 4.8a-b).

Autoregulation Autoregulation of cerebral blood flow may be defined as the intrinsic tendency of the brain cerebrovasculature, brought about by arteriolar dilation or constriction, to maintain a relatively constant blood flow in response to moderate variations in perfusion pressure (Larssen 1959). Autoregulation operates efficiently between defined upper and lower limits of mean arterial blood pressure. Between MAPs of 50 mmHg and 150 mmHg, cerebral blood flow remains relatively constant. There are two complimentary mechanisms for autoregulation, one mechanical and the other chemical. Mechanical autoregulation is a function of an intrinsic myotactic ability of the smooth muscle in cerebral arterioles to contract in response to stretching. If the MAP rises, this rise stretches the walls of the cerebral arterioles (including the smooth muscle in the arteriolar wall) and leads to an immediate arteriolar vasoconstriction. This immediately counteracts the anticipated rise in CBF (which the rise in arterial pressure would have caused). Thus, an initial rise in the MAP results in little overall change in CBF. A fal! in the MAP results in the converse sequence of responses. This system is flowsensitive, and maintains an adequate CBF to every region of the brain independently of other regions. The chemical autoregulation of CBF operates to match regional tissue needs and blood supply (flow-metabolism coupling). This is achieved with two feedback loop systems, one positive (fine balance and main control system, sensitive to rises in COz tension and H+ ion concentration) and one negative (essential failsafe control system, sensitive to a fall in Oz tension). Second-to-second increases in activity in various regions of the brain require rapid responses to meet the local increased metabolic demands for glucose and oxygen. For normal steady-state conditions, the sensitive chemical factors that trigger arteriolar dilatation are a rise in COz tension and a rise in H+ ion concentration.

/'

264

4 Neurophysiology Fig.4.8a-b The arteriovenous system of the CNS a The superficial and deep arterial and venous systems of the cerebrum

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Fig. 4.8 b The proportions of supply provided by the superficial and deep parts of both the arterial and venous systems, and their direction of flow. In this way it can be imagined that differential flow between the constantly disequal superficial and deep venous and arterial territories

has a specific function in providinga more efficientpumping effect for the brain

b

With increased focal or global metabolism, both of these factors increase at a local or globallevel, and (due to the relatively poor buffering capacity of the cerebral interstitial fluid) the increased production of CO2 (and other metabolites) maintains the rise in H+ ion concentration. This directly results in arteriolar vasodilatation, an effect confined to the active region of the brain. This lasts as long as the increased metabolic demand lasts. By this exquisitely product-sensitive mechanism, cerebral blood flow is increased very efficiently and rapidly only to those areas of increased demando Situations may arise whereby the fine-tuning mechanisms of CO2 and H+ ion concentrations alone may not be adequate to bring cerebral oxygen supply up to requirements. It is then that the second powerful CBF regulatory mechanism comes into operation. This is quite separately controlled by changes in the quantity of available oxygen delivered to the brain (and not directly to Pa02)' The arterial partial pressure of oxygen has to fall significantly, to below about 60 mmHg (corresponding to the steep part of the slope of the hemoglobin-oxygen dissociation curve) before an increase in CBF can be detected. Any cause of hypoxia (sudden apnea, chronic respiratory disease, altitud e,

etc.), with a failure of oxygen delivery to the brain, will trigger cerebral arteriolar vasodilatation. Any further fall in Pa02 below 50 mmHg elicits a very powerful dilatation of the cerebral vessels. The exact mechanism of this response to the altered delivery of oxygen is not yet known, but it is locally mediated in the smallvesseIs.

Circumventricular Organ System

Pathophysiology Thresholds At the lower threshold limit for autoregulation (an MAP of 60mmHg),the cerebral vessels are fully dilated and autoregulationstartstofail.From thispoint CBF declinesas MAP falls.Most importantto the brain is, of course, cerebral perfusion pressure (CPP).With hemorrhagic arterial hypotension, CBF starts to fall withanyfurtherfall in CPP below 60 mmHg. With drug-induced hypotension,on the other hand, CPP can fall as low as 40 mmHg beforecerebral ischemia begins. This difference in cerebral pressurethresholdsis due to sympathetic vasoconstriction of the proximalextraparenchymal and major cerebral vessels during hemorrhagic hypotension (Harper 1972). When CPP falls below 20mmHgas a result of reduced MAp, CBF virtually stops. When the CPP is reduced by raised intracranial pressure (ICP),as when an intracranial mass is present, normallevels of CBFare maintained, provided the arterial pressure is normal or elevated,until the CPP falls to 40 mmHg. There is then a progressivedecreasein flow as CPP falls to zero, but CBF does not cease completelyuntil CPP is zero. In states of very high ICP, up to 60mmHg,CBF may still be above the threshold for normal ceredue to the compensatoryincreasein arterial presbralfunctioning sure. Frequently, regionalized ICP values above 37.5 mmHg (whichwouldnot normallyreduce CPP to criticallevels) are not toleratedby patients with brain tumors.

TumorEffectson the Cerebrovascular System Thepresence of a focal intracranial mass (tumor) may produce marked disturbances in local cerebrovascular function. Both intrinsicand extrinsic tumors may be related to the involvement of: 1. Largeor medium-sized feeding arteries (extrinsic tumors only) withstenosisor occlusion. Examples: stenosis of the ICA by a skull base meningioma, or narrowing of the Al segments (stretching)by a parasellar craniopharyngioma. 2. Smallperforating arteries (both intrinsic and extrinsic tumors). Example:tumor neovascularity. 3. Fine arteriolar "autoregulatory" vessels (extrinsic tumors only). Example: loss of autoregulation, dilatation, increased focal (or regional) CBF with blood-brain barrier leakage (vasogenicedema, peritumoral edema, type 2).

265

4. Capillaries (both intrinsic and extrinsic tumors). Example: blood-brain barrier damage with leakage of fluid, focal ischemia, and metabolic paralysis (vasogenic edema, peritumoral edema, type 1). 5. Deep and anastomotic medullary veins (intrinsic tumors only) Example: Dilatation and blood-brain barrier damage with leakage of fluid (vasogenic edema, peritumoral edema, type 2). 6. Small and medium-sized venules (both intrinsic and extrinsic tumors). Example: thrombosis within the tumor (signifies malignant change). 7. Large draining veins (bridging veins) (extrinsic tumors only). Example: compression (occlusion) by a falx meningioma. 8. Dural sinuses (extrinsic tumors only). Example: compression, occlusion (with collateralization) or embolization by a falx (superior sagittal sinus), tentorial meningioma (straight sinus), or torcular meningioma (confluence). On occasion, arteriovenous compression, displacement, distortion, stretching, or total occlusion may occur from intrinsic and extrinsic tumors. With few exceptions, all of these vascular occlusions are encountered in meningiomas. We have not encountered ischemic or hemorrhagic symptoms in these situations (except indirectly, from posterior cerebral artery occlusion at the tentorial edge ). The interrelationships between a CNS tumor and the cerebrovascular system may play a vital role in determining the functional CNS disturbances related to the mass lesion (e. g., marked peritumoral edema with herniation syndromes). In addition in intrinsic gliomas, the growth characteristics of the tumor may be related to the segmental vascularity pattern of the white matter. Many questions remain as regards the pathophysiology of peritumoral edema and its real significance on neuroimaging studies. Recent studies by Hilal et al. 1983 (using sodium-gated MRI) may point the way towards a future ability to precisely define the border between tumor and peritumoral edema. In addition, the observation that striking intratumoral venous thrombosis is strongly associated with malignant change in meningiomas and gliomas remains unexplained. Mechanical compression cannot account for this phenomenon, as it is not related to tumor size. Perhaps a thrombotic substance is produced by the tumor parenchyma to prevent its transportation (via these large veins) elsewhere. Is this a biological self-defense mechanism by the tumor? Clearly, we await refinements in neuroimaging studies that will additionally permit accurate, rapid, sequential and non-invasive studies of CBF, ICP, arteriovenous topography, blood-brain barrier competence, edema, and metabolic function in these areas.

CircumventricularOrgan System The circumventricularorgans are chemosensitive and reactive zonesthat monitor and respend to the varying concentrations of circulatinghormones (among other parameters), both in the bloodand in the CSF. These zones consist of areas of specialized tissuefound in close proximity to the ventricular system (mainly the wallsof the third ventricle and the roof of the fourth ventricle).In addition, these areas are not subject to the selective pro-

tection of the blood-brain barrier, as the normal brain-capillary endothelium with tight junctions is replaced by highly vascularized capillaries with fenestrated endothelia. (The subcommissural organ is an exception, and does have a blood-brain barrier). Because of this arrangement, chemoreceptor neurons in these areas are exposed directly to the relatively large molecules that can penetrate into the interstitial space. This permits monitor-

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4 Neurophysiology

ing of thecomposition of the blood plasma and CSF, and forms the afferent loop of a comp1ex,integrated systemfor maintaining chemicalhomeostasiswithin the CNS. Parts of the efferent loop are well understood. For example, in the case of the neurohypophysis,hypothalamic neurosecretory droplets pass down the hypothalamohypophyseal tract to gain access to the venous capillary beds. Many other parts of this system have yet to be worked out. Such regions include the subfornical organ, the organum vasculosum of the lamina terminalis (OVLT) and supraoptic crest, the subcommissural organ, the area postrema, the pineal body,the medianeminenceof the hypothalamus,and the neurohypophysis (Fig. 4.9). AlI except the subcommissural organ, are highly vascularized and lack a blood-brain barrier. AlI except the area postrema, are midline, unpaired structures, closely related to the diencephalon. Although all are located very near the ventricular system, under normal physiological circumstances they do not appear to play any role in secretion into the CSF, as the bloodCSF barrier is competent with tight junctions at the ependymal surfaces. AUhough all these features characterize what are termed circumventricularorgans (CVOs),for the purposes of this discussion the functional anatomy and physiology of the hypothalamus,pituitary,and pineal body, and their role as CVOs merit separa te description. CVOs are principally concerned with the maintenance and modulation of homeostasiswithin the central nervous system environmentby integrating systemsthat have sensor and effector functions on both sides of the blood-brain barrier. These include systems concerned with water balance, intraventricular CSF volume, pressure and possibly composition, and also with cerebral vascular autoregulation. The exact mechanisms in man are complex,and their significanceis still being evaluated. Most of the experimentalevidencehas come from work in rodents, later extended to primates. Physiological functions attributed to the following CVOs are described he re briefly: the subfornical organ (SFO); the organum vasculosum of the lamina terminalis (OVLT); and the are a postrema.

The Subfornical

Organ

The subfornical organ is a midline structure between the two interventricular foramina in the wall of the telencephalon impar. It contains many receptors for angiotensin-2, and has a significant role in the body's fluid balance regulation (Johnson 1985). Stimulation of its neurones by circulating angiotensin-2 causes release of arginine vasopressin (AVP) or antidiuretic hormone (ADH) from the posterior pituitary (stimulating thirst and promoting drinking behavior). The SFO receives neural afferents from the preoptic region and the anterior hypothalamic area. Its efferents include fibers projecting to the paraventricular and supraoptic nuclei, and also to the infralimbicprefrontal cortex, the bed nucleusof the stria terminalis (appreciation of thirst), the medial hypothalamic area, the substantia innominata, the zona incerta and the lateral hypothalamic are a (behavior arousal) (Swanson and Lind 1986).

3

4

Fig. 4.9 The circumventricular organs (sagittal view) (Irom Leonhardl, T6ndury and Zilles, Rauber/Kopsch: Anatomie des Menschen, Stuttgart: Thieme, 1987, vol. 3, p. 332, Fig. 11.8) 1 Neurohypophysis 4 Choroid plexus 2 Organum vasculosum 5 Pineal body 01 the lamina terminalis 6 Subcommissural organ 3 Sublornical organ 7 Area postrema

The Organum Vasculosum of the Lamina terminalis The OVLT(supraoptic crest) lies in the midline of the laminaterminalis,which is the embryologicalsite of formation of the commissural plate (which differentiates into the anterior, callosaland hippocampal commissures). The lamina terminalis stretches inferior to the anterior commissureand down to the opticchiasm.The CSF of the prechiasmatic cistern is anterior, and posteriorly lies the ependymal lining of the anterior wall of the third ventricle. The supraoptic nuclei are lateral, and the columns of the fornixlie in the anterior wall of the hypothalamus. The OVLT and the immediately adjacent periventricular zone of the preoptic region are often together designated as the periventricular anteroventral third ventricle (AV3V) (Johnson 1985). It is also (like the SFO), a receptor site for the central effects of angiotensin-2(Philips 1978).In addition,magnicellular neurons near the OVLT have been found to contain arginine vasopressin (AVP), but the physiological role of AVP release at the OVLT has not been fully worked out in man (Reeves and Andreoli 1992). In dogs, lesions of the OVLT attenuate osmoticallyinduced drinking and vasopressin secretion (Thrasher and Keil 1982),and, in rats, section of the pathwaysbetween AV3V andthe supraoptic nucleus produces hypernatremia (Bealer 1983). It is likely that afferent fibers from the OVLT and the SFO play an important role in the osmotic stimulatin of AVP secretion. To further complica te matters, nerve-cell bodies containing atrial natriuretic peptide, which may provide negative feedback for the release of AVP, has been detected in the AV3V region. Thus, the OVLT plays an important role in homeostatic mechanisms by promoting vasopressin release to conserve waterand also, via its pressor effect, in maintaining blood pressure. In addition, it has also been implicated in the control of LHRH secretion.

Neuroendocrine System TheOVLTreceives afferents from the SFO, from the lateral preopticandlateral hypothalamic areas, from the anterior, dorsomedial,and ventromedial hypothalamic nuclei, and from the locus coeruleus.Efferents project to the dorsomedial, supraoptic, and paraventricularnuclei.

TheAreaPostrema Theareapostrema, part of the dorsal vagal complex, consists of bilateral spongy structures that protrude into the roof of the fourthventricle, rostral to the obex. It, too, functions as a chemoreceptor zone from which neural responses are generated by changesin the blood plasma. It forms part of the neurocircuitry that has been shown to have roles in water and sodium balance (Hyde1987),energy balance (Miselis et al. 1984), and also cardiovascularregulation. Its role as a sensor for circulating potential toxinsand for eliciting nausea and vomiting is well known (Borison1984).Its neurons contain many receptors for dopamine, and as a result many dopamine antagonists are effective antiemetics. Visceral afferent inputs (especially from the thoracic and abdominal viscera) are conveyed to the are a postrema via the

267

vagus nerve. Baroreceptor input is received via the carotid sinus branch of the glossopharyngeal nerve. Efferent outputs are to the nucleus of the tractus solitarius (which contains afferents from the facial, glossopharyngeal, and vagus nerves), and to the "vomiting center" (groups of neurons within an area of the medullary reticular formation near the nuclei that constitute the "swallowing center").

Pathophysiology AIthough the important regulating roles of the CVOs are now being appreciated, so little is known about their normal function that statements about the interactions betweeen tumors and CVOs seem premature. Nonetheless, it can be well imagined that this complex CNS-modulating system is affected by any process that changes the ICP, intraventricular volume, neuroendocrinological status, cerebrovascular regulating mechanisms, sodium and water balance, and so on. Clearly, many (if not all) cerebral neoplasms will prove to have a significant impact on the CVO sys-

tem (see McKinleyand Oldfield in Paxinos 1990,and Gross 1987)..

Neuroendocrine System An intensivereview of the physiology of the neuroendocrine system is beyond the scope of this book. The reader is referred to Haymakeret al. (1969) and Saper, (1990). Details of the neuroendocrinesystem and its components (the hypothalamus, pituitary, andpineal gland) in relation to their role as a subsystem within the CNS, as applied to an understanding of tumor patients, are presentedhere.

TheHypothalamus Thehypothalamus,though littIe more than a cubic centimeter in size,is the master integrative center for the neuroendocrine, autonomicnervous,and somatic nervous systems (Fig. 4.10). It is essentialfor survivaland homeostasis. Through its efferent connections to the autonomic nervous system, it mediates some of the emotionalcomponents of mood carried through the limbic systemoThe hypothalamus provides the link between the primitive partsof the forebrain (the olfactory and limbic lobes) and the brainstem.It makes up the inferior part of the diencephalon, and iscomposedof the gray matter below the thalamus. It forms the floorandventral rounded part of the third ventricle. Its nuclei are bilaterallyrepresented. Each half of the hypothalamus can be subdivided into two functionally different regions (the lateral and medialhypothalamic areas), separated by the fornix and mamillothalamictract. The "lateral hypothalamic area" is made up of fiber systems (e.g., the medial forebrain bundle) as well as diffuse lateral nuclei.It receives neural input from the brainstem, thalamus, limbicsystem,and ascending pathways from the spinal cord. Major efferentoutputs go to autonomic and somatic nuclei in the brainstemvia multisynapticpathways in the reticular formation.

The "medial hypothalamic area," with many defined nuclei, makes reciprocal neural connections with the lateral hypothalamic area. It has neurons with direct homeostatic sampling and adjustment capabilities.Regulation of plasma osmolarity, temperature, glucose and hormonal content, and changes in CSF pressure and composition, are prominent functions of this region. Central regulatory role of the hypothalamus. The importance of the hypothalamus as the central integrating center for somatic, autonomic, limbic, and endocrine function (and its integration with the level of consciousness) can be seen in its major afferent and efferent connections. In general, stimulation of the anterior nuclei is excitatory to restorative (parasympathetic) activities, while stimulation of the posterior nuclei is excitatory to preparative (sympathetic) activities. The principal hypothalamic regulatory mechanism are summarized in Table 4.8. Central autonomic control. The hypothalamus is the principal regulating center for autonomic function by means of finely balanced neural and hormonal effector mechanisms (for immediate, intermediate and longer-term system changes). Information on changes in the internal and external environments is constantly being sensed, compared and analyzed. The hypothalamus coordinates the autonomic system in conjunction with groups of neurons in the medulla and pons, which relay afferents to the hypothalamus. These medullary and pontine centers appear to be phylogenetically more primitive, and operate via neural mechanisms that bring about immediate system changes. An example is the cardiovascular integrating center in the medulla, which responds to changes in the firing rates of the arterial baroreceptors in the carotid sinuses and in the aortic arch. Increased firing of these baroreceptors (sensitive to pressure changes in the high-

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4 Neurophysiology

Table 4.8 Principal hypothalamic regulatory mechanisms (reproduced and moditied with permission lrom Ganong, Review of Medical Physiology, 14th ed. East Norwalk: Appleton and Lange, 1989, p. 195) Function

Afferents

Temperature regulation

Cutaneous cold receptors; temperature-sensitive ceils in hypothalamus

Anterior hypothalamus (response to heat) posterior hypothalamus (response to cold)

Neuroendocrine control 01catecholamines

Emotional stimuli, probably via limbic system

Dorsomedial and posterior hypothalamus

Vasopressin

Osmoreceptors, volume receptors, others

Supraoptic and paraventricular nuclei

Oxytocin

Touch receptors in breast, uterus, genitalia

Supraoptic and paraventricular nuclei

Thyroid-stimulating hormone (thyrotropin, TSH) via tyrotropin-stimulating hormone (TRH)

Temperature receptors, perhaps others

Dorsomedial nuclei and neighboring areas

Adrenocorticotropic hormone (ACTH) and ~-lipotropin (~-LPH) via corticortropin-releasing hormone (CRH)

Limbic system (emotional stímuli); reticular lormation ("systemic" stimuli); hypothalamíc or anterior pituitary ceils sensitíve to circulating blood cortisollevel; suprachiasmatíc nuclei (diurnal rhythm)

Paraventricular nuclei

Foilicle-stimulating hormone (FSH) and luteínizing hormone (LH) via luteinizing-hormonereleasing hormone (LHRH)

Hypothalamíc ceils sensitive to estrogens; eyes, touch receptors in skin and genitalia 01 rellex ovulating species

Preoptic area, other areas

Prolactin via prolactin-inhibiting hormone (PIH) and prolactin-releasing hormone (PRH)

Touch receptors in breasts, other unknown receptors

Arcuate nucleus, other areas (hypothalamus inhibits secretion)

Growth hormone via somatostatin and growthhormone-releasíng hormone (GRH)

Unknown receptors

Periventricular nucleus, arcuate nucleus

"Appetitive" behavior Thirst

From

Integrating Areas

Osmoreceptors, sublornical organ

Lateral superior hypothalamus

Hunger

"Glucostat" ceils sensitive to rate 01glucose utilization

Ventromedial satiety center, lateral hunger center; also limbic components

Sexual behavior

Cells sensitive to circulating estrogen and androgen, others

Anterior ventral hypothalamus plus (in the male) pirilorm cortex

Sense organs and neocortex, paths unknown

In limbic system and hypothalamus

Retina via retinohypothalamic libers

Suprachiasmatic nuclei

Delensive reactions Fear, rage Control 01various endocrine and activity rhythms

pressure, left heart arterial circulation) results in reduced sympathetic output. The converse is also tme. However, increased firing from the baroreceptors in the right atrium (reflecting changes in arterial pressure in the low-pressure, right-sided circulation) results in increased sympathetic output. Thus, the conflicting lowpressure and high-pressure baroreceptor systems require integrator control. Both the hypothalamic and the brainstem centers directly influence the level of activity in the lateral horn cells of the sympathetic system. The posterior portion of the hypothalamus is involved with sympathetic function. Stimulation of the posterior hypothalamic area produces sympathetic effects: increase in heart rate and blood pressure, vasoconstriction, pupillary dilatation, and reduced peristalsis, and hyperglycemia. The anterior region of the hypothalamus functions as a parasympathetic activating center. Stimulation here produces: slowing of the heart, pupillary constriction, salivation and increased peristalsis. The descending pathways from both regions are via the posterior longitudinal fasciculus to the autonomic centers in the medulla and spinal cord. Temperature control. Temperature is very strictly controlled in mano The hypothalamic set-point is slightly below 37 degrees Celsius. All enzyme systems operate optimally at specific temperatures. Neurological function is also particularly temperaturedependent. The hypothalamus is the most important central regulator of temperature balance. The anterior hypothalamic are a has a center that prevents a rise in body temperature (by regulating heat loss), while the posterior hypothalamus operates to conserve and maintain a normal body temperature.

The anterior hypothalamic center responds to information from thermoreceptors in the skin and mucous membranes, and from the increased heat of the hypothalamic blood stream, by activating heat loss mechanisms, i. e. cutaneous vasodilation, venous vasodilatation (especially in the limbs), sweating, increased respiration and behavioral adaptations (i. e., removing clothing, limiting activity, and anorexia). Tumors of the anterior hypothalamus may limit the activation of these heat-dissipating mechanisms and lead to hyperthermia and hyperpyrexia. The posterior hypothalamic are a responds to the activityof cold-sensitive peripheral nerve endings, and to cooling of the blood. Heat is then conserved by cutaneous vasoconstriction, venous vasoconstriction (to limit heat loss via the countercurrent arterial-venous heat exchange mechanisms in the limbs), and appropriate be havioral responses (such as increased voluntary activity and putting on additional clothing). Heat production is increased by increased metabolic activity, (via increased TRH production), by hunger (promoting eating) and by involuntary shivering. Bilateral destructive lesions in the posterior regions of the hypothalamus result in poikilothermia, in which body temperature varies with environmental temperature. Food intake and eating behavior. Balanced interactions between fixed programs located in the lateral and ventromedial nuclei provide a baseline for feeding behavior. These are considerably influenced by cultural, social, and familial factors, and are mediated through the limbic system and neocortex.

Neuroendocrine System

269

Lat. preoptic /;,' area Perifomical

(red band) Tuberomam.

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Fig.4.10a Hypothalamus and hypothalamie nuelei (from R. Haymaker,Anderson and Nauta:, The Hypothalamus, Springfield, Thomas, IL:1969,p. 139, Fig. 4.3). A disseeted human brain, showing the major hypothalamienuelei. Lateral to the fornix and the mamillothalamie traet is the lateral hypothalamie area (in red), in whieh the tuberomamillary nucleus(in pink) is situated. Situated rostrally in this area is the lateral preopticnucleus. Surrounding the fornix is the perifornieal nucleus (representedas a red band), whieh joins the lateral hypothalamie area with theposteriorhypothalamie nucleus. The medially situated nuelei (in yellow)fill much of the region between the mamillothalamie traet and the laminaterminalis. The nuelei tuberis laterales (in blue) are situated at the base of the hypothalamus, mostly in the lateral hypothalamie area. Thesupraoptic nucleus (in green) eonsists of three parts

Fig.4.10b The afferent and efferent eonneetions of the hypothalamus 1> (A W. Janig, In: Sehmidt and Thews, Human Physiology, Autonomie Nervous System, Berlin: Springer, 1989, p. 357, Table 16.23)

Adeno-

Neuro-

hypophysis

hypophysis

" humoral ~ neurona

270

4 Neurophysiology

The lateral hypothalamic nuclear area ("the feeding or hungercenter") is tonically active,promoting eating behavior. In an experimentalanimal, stimulation of one lateral hypothalamic nucleuscausesthe animal to search intensely for food and to eat voraciously. If both lateral nuclei are destroyed, the animal has no interest in eating (sometimes causing lethal starvation). The ventromedial nucleus (VMN) constitutes "the satiety center," with neurons that can detect a rise in the blood glucose. It also receives inhibitory inputs from vagal nerve fibers, whose afferent fibers in the liver are stimulated in response to a rise in blood glucosein the portal vein. Stimulation of one ventromedial nucleusinhibits the urge to eal. In animals,single-VMN stimulation can causethe animal to suddenly stop eating. Destructive lesions of both ventromedial nuclei result in overeating (leading to tremendous obesity). Water metabolism and drinking. Body water is regulated by the hypothalamus in two separate ways. First, an increase in osmolarity in osmoreceptor neurons constituting a "thirst center" in the lateral hypothalamus creates the sensation of thirst, and promotes drinking. Second, the excretion of water into the urine is controlled by vasopressin(antidiuretic hormone, ADH), which acts on the collectingducts of the kidneys.Vasopressinneurons in the supraoptic nucleus (SON) display phasic activity, and release ADHin response to hyperosmolarity or a fall in blood pressure. Afferent input to the SON is from the subfornical organ (which contains osmoreceptors), and also from the locus coeruleus (noradrenergic input), relaying information from the carotid chemoreceptors and baroreceptors. The efferent pathway from the SON is made up by long neurons comprising the hypothalamohypophyseal tract, which transmit droplets of the neurotransmitter hormone ADH down to the posterior lobe of the pituitary (where it is released directIy into the circulation). Lesions affecting these neurons lead to diabetes insipidus (Table 4.9). Hypothalamic-limbic connections. The hypothalamus forms part of the limbic system,and is involvedin memory,the translation of mood into autonomic outf1ow,and the expression of emotional behavior. The mamillary nuclei receive input from the hippocampus (via the fornix), from the dorsal and ventral tegmental nuclei, and from the raphe nuclei (via the mamillary peduncle). The hypothalamusprojects to the anterior nucleus of the thalamus (via the mamillothalamic tract). Damage to the mamillary nuclei may lead to loss of memory, especially short-term memory (as seen in Korsakoff psychosis).

Pathophysiologyof the hypothalamus. The effects of tumors on the hypothalamus may be direct (related to compression, ischemia, or tissue destruction) or indirect (related to the effects of focal or generalized elevations of ICP). In both instances, specificgroups of hypothalamic functions may be altered in unison, but clinical symptoms are often subtle (or so gradual that they are ignored) untillate in the course of the disease process.It is likely,given the critical importance of the hypothalamus in homeostasis,that many of the debilitating symptoms and signs associated with end-stage CNS neoplasms are due to hypothalamic abnormalities. These deserve wider recognition and correlation with the advancing field of psychoneuroimmunology. Craniopharyngiomas and hypothalamic and optic-nerve gliomas are well known for their potential to disrupt hypothalamic function.

Table 4.9 Functional disturbances resulting from damage to hypothalamus in humans (Reichlin, S. et al. The Hyothalamus. NewYork: Raven Press, 1978) Anterior hypothalamus wíth preoptíc regíon

Intermediate hypothalamus

Posterior hypothalamus

Sleepíng /waking rhythm, thermoregulation, endocríne regulation Insomnia, hyperthermia, diabetes insípidus

Perceptíon, caloric and Iluíd balance, endocrine regulabon

Perception, consciousness, thermoregulatíon, complex endocrine regulation Hypersomnia, emotíonal and autonomic disturbances, poikílothermia Amnesia, emotional disturbances poíkilothermia,autonomic disturbances, complex endocrine disturbances (e. g. pubertas praecox)

Insomnía, complex endocríne disturbances (e. g., pubertas praecox), endocrine disturbances resulting lrom damage to median eminence, hypothermia, no leeling 01thirst

Hyperthermía, diabetes insipidus, endocrine disorders Medial: impaired memory, emotíonal disturbances, hyperphagia and obesity, endocrine disturbances Lateral:emotional disturbances, emaciation and loss 01appetíte, no leeling 01thirst

The Pituitary Gland Normal functioning of the pituitary is governed by the hypothalamus. The tuberohypophyseal tract carries releasing factors from the arcuate nucleus of the median eminence of the hypothalamus to the hypophyseal portal system and to the anterior pituitary. Long neurons run directIy down from the supraoptic and paraventricular nuclei into the posterior pituitary, via the hypophyseal portal system. Details of the physiology of individual hypothalamic stimulating and inhibitory hormones and pituitary hormones are well covered in the textbooks of neuroendocrine physiology

mentioned

at the beginning

of this Chapter.

The Pineal Gland The pineal gland is the principal structure that comprises the epithalamus.The epithalamus lies below the splenium of thecorpus callosumand above and medial to the thalamus (in the dorsal wall of the posterior rim of the third ventricle). The other structures of the epithalamus include the posterior commissure, the habenular commissure, the habenula, and the stria terminalis (the latter three also being components of the limbic system). The pineal gland is an endocrine gland that synthesizes the amine hormone melatonin from paraneuronal cells-the pinealocytes.These cells are characterized by originating from neuroectoderm, by their paucity of neurites, and by their abilityto synthesize hormonal peptides and transmitters (which are released fram secretory granules or vesicles). The pinealocytes are grouped in cords, separated by connective tissue and supported by glialcells. Secretory vesicles empty into a rich surrounding capillary bed. The endothelium of these capillaries is fenestrated. The pineal (like the other CVOs) is outside the blood-brain barrier. Thisis important for its secretory function (and also permits better

Neuroendocrine System access for chemotherapy in the treatment of malignant pineal tumors).The arterial blood supply is from the posterior cerebral arteryvia posterior choroidal branches, and the venous drainage is mainlyto the basal veins of Rosenthal and the great cerebral vem. The innervation of the pineal is through postganglionic sympatheticnerve fibers, whose cell bodies are located in the superior cervicalganglion. Descending nerves from the suprachiasmatic nuclei(pairednuc1eiin the anterior hypothalamus) influencepreganglionicfibers in the superior sympathetic chain (arising in the lateralcolumn of the spinal cord). The suprachiasmatic nuc1ei receive afferentsfrom the retina via the retinohypothalmictracts (thusprovidingthe pathway for light input that is thought to influencepineal secretory rhythms in man). Melantoin is derived from the conversion of tryptophan into serotoninby the enzyme tryptophan hydroxylase in the pinealocytes.The postganglionic sympathetic nerves at night release norepinephrine,which promotes melatonin synthesis (by activating~ -receptor on the surface of the pinealocytes). The pineal glandis also rich in other biologically active amines (dopamine, histamine),peptides (LHRH, TRH, somatostatin, vasotocin), an inhibitoryneurotransmitter (GABA), and other peptide factors thatmay have an antigonadotropic function. In man, secretion of melatonin into the general circulation occursalmost immediately after exposure to darkness and ceases uponexposureto light. Long-term exposure to darkness alters circadianrhythms by lengthening the sleep-wake cyc1e. Injecting melatoninin normal individuals results in lowered LH levels and in suppressed GH secretion. Melatonin induces sleepiness, changesthe EEG (increases a -rhythm), and increases REM sleep.

Pathophysiology of the Pineal Gland ThecIinicalfeatures of pineal region tumors result from the compressionor invasion of adjacent structures or from metas tases in CSF(or,rarely, metastases outside the neuraxis). Compression of theaqueductmay cause triventricular hydrocephalus, with a symptomaticraised intracranial pressure (and complaints of headache, lethargy,unsteadiness and incontinence). Coma may ensue. Compressionor infiltration of the tectum of the midbrain at the level of the superior colliculi will interfere with the decussating lightreflexfibers in the periaqueductal area. This characteristically givesriseto Parinaud's syndrome, with impairment of upward gaze, dilatedpupils(whichare fixed to light), and loss of convergence.A complete Parinaud's syndrome usually indica tes a large, malignanttumor. A pineal tumor exerting pressure at the level of the inferior colliculimay result in loss of downward gaze, normal pupil reactions.and loss of convergence. Suprasellar extension may lead to visualfielddefects, particularly an insidiously developing inferior bitemporalhemianopia (with difficulties walking downstairs). Posteriorcompression or invasion of the cerebellum may cause dysmetria,intention tremor, ataxia and hypotonia. Diabetes insipidus is a frequent occurrence with all types of pinealtumors (and does not necessarily imply invasion of the hypothalamus).Alterations in the timing of puberty occur in less than10%ofmalepatients with pineal region tumors. Precocious pubertyis more common than delayed puberty. The tumor markers alpha-fetoprotein (AFP) and betachorionicgonadotropin (13HCG) have proved more usehuman

271

fui in the follow-up of tumors of germ-cell origin (germinomas and teratomas, the commonest pineal region tumors) than in diagnosis. Attempts to use assays of melatonin or its precursor enzyme hormones as tumor markers in the diagnosis of true pineal parenchymal tumors (about 20% of pineal region tumors) have been disappointing.

Pathophysiology of the Neuroendocrine System as a Whole Extrinsic and intrinsic tumors can affect the neuroendocrine system directly or indirectly. Tumor producing direct hormonal effects are: 1. Primary neuroendocrine tumors that actively produce pituitary or pineal hormones, hypothalamic releasing or inhibitory factors, or pineal neuropeptides (pituitary adenomas, hypothalamic gliomas, pinealocytomas). 2. Nonendocrine tumors (especially meningiomas) that actively produce neuroendocrine substances. Tumors producing indirect (compressive) effect are: 1. Primary or metastatic tumors of the neuroendocrine system that displace, compress, or destroy the pituitary, hypothalamic, pineal, or interconnecting tracts, resulting in the partial or complete loss of neuroendocrine function. 2. Neighboring tumors that displace, compress, or destroy efferent and afferent neuroendocrine connections to the mesencephalon, thalamus, and limbic system, resulting in a disturbance of neuroendocrine function. 3. Tumors located some distance from the neuroendocrine system that produce focal or generalized increases in ICP that secondarily affect the neuroendocrine system (through edema, hemorrhage, hydrocephalus, or herniation). Future understanding of the complex interrelationships between the neuroendocrine organs and the other CNS subsystems will certainly expose other important and still unrecognized effects between cerebral neoplasms and the neuroendocrine system.

272

4 Neurophysiology

Neurotransmitters (Fig.4.11). The theory that neurons are nothing more than secretory cells acting upon one another by the passage of chemical substances has been well known since the early 1900s. Only since the introduction of the neurotechniques of immunohistochemistry (Coons 1958,Steinberger 1979) has an investigation of humoral transmission been possible. Initially, much work centered on the production and release of neurotransmitters across synaptic junctions, either an excitatory or inhibitory influence. By the end of the 1960s, astrocholin, noradrenalin, dopamine, adrenalin, and histamine had been identified as synaptically acting substances and termed neurotransmitts. Additional work over the last 20 years in the field of chemical neuroanatomy has further elucidated an increasing number of neurotransmitters (Table 4.10), their localization, their synthesiz-

ing places and their widespread effects upon the CNS. It is c1ear that neurons throughout the CNS communicate with each other by releasing these chemical transmitters. The c1assical notion regarding the activity of neurotransmitters across synaptic junctions is far too simplistic to explain the complexity of these interactions. As a result, neurotransmitters are presently described as neuromodulators, neuromediators, or neuroregulators. It is certain that future work will add to the list of known neurotraosmitters and improve our understanding of just how complex the ioteractions within the CNS really are. Detailed information about the present state of knowledge in this field can be gained from the publications of Emson (1983), Hockfelt et al. (1984), Leonhard et al. (1984), Niewenhuys (1985), and Paxinos (1990).

Fig.4.11a Neurotransmitters(from Morrisonand Hof, Neuroscience

Fig. 4.11 b

2:1993;9(2):1-80). A lateral view of a macaque monkey brain, illustrat-

aminergic transmitters (from Zilles and Rehkamper, FunktionelleNeuro-

ing three general correlations between neurotransmitters and types of cortical circuits. Note that circuits depicted by A are locally projecting, while circuits depicted by B are point-to-point, topographically organized circuits, and those represented by C are highly divergent, global

chirurgie, Berlin: Springer, 1993, p. 381, Fig. 20.1) Cholinergic system (red) 1 Basal forebrain with medial septal nuclei, diagonal band of Broca, innominate substance with basal nucleus of Meynert (Ch1-Ch4) 2 Dorsolateral tegmental area with parabrachial area and central griseum (Ch5-Ch6) 3 Periolivary nuclei 7 Olivocochlear fasciculars (Rasmussen fibers) 8 Septohippocampal tract 9 Stria terminalis 10 Fibers to thalamus Dopaminergic system (blue) 4 Ventral tegmental area with substantia nigra (pars compacta) and retrorubral field (A8-A 10) 11 Nigrostriatal tract 12 Mediallongitudinal fasciculus Noradrenergic system (black) 5 Locus coeruleus with ventrolateral reticular formation, solitary nucleus, superior olivary and subcoeruleus nucleus (A1-A7) Serotoninergic system (yellow) 6 Raphe nucleus (B1-B9)

~ffi~ A) Interneuron B) Corticocortical, thalamocortical C) Extrathalamic subcortical afferents GABA (Peptides) Glutamate, aspartate Norepinephrine, serotonin, dopamine, acetylcholine

.

The origin and projections pathway of cholinergic and mono-

Central Nervous and Immune Systems Hg.4.11a and b are taken from the latest publications, which demonstratethe current state of research in this field. Hopefully, inthenot too distant future, it will be possible to evaluate these biochemicalpathways as clinical parameters. The known transmitters are listed in Table 4.10 in order to providean overview. This is taken from Chapter 14 of Leonhardt H.,KrischB.,and Zilles K., Vol. 3, Human Anatomy Leonhardt et al.,ed, 1987,where a more detailed discussion can be found.

Table 4.10

273

Neurotransmitters of the CNS

Acetylcholine Amino acid Glutamic acid and asparagine system y-Aminobutyric acid system Glycine system Biogenic amines Dopamine Noradrenaline Adrenaline system Serotonin Histamine Neuropeptide system Vasoactive intestinal Polypeptide Endocrine opioids and neuropeptides Neurotensin Cholecystokinin Substance-P

}

Somatostatin Luliberin Corticoliberin Vasopressin and oxytocin Renin and angiotensin

r system

CentralNervous and Immune Systems Theanalogiesbetween the nervous system and the immune systemhavebeen apparent for some time. It is not only the superficialsimilarities,such as the fact that both systems have the same weightand have memory, that raised interest. Rather, the realiza!ionnow is that the two systems make use of extensive network interactions,that molecules considered to be unique to each systemhave multiple effects on the other system (i. e., the nervous system, through the production of neuroregulators-neurotransmitters,neuropeptides, and neuromodulators-and the immunesystem, through the production of immunoregulatorsimmunopeptidesand immunomodulators). The circuits that connectthe immune system and the CNS are complicated, and include neuroendocrine pathways as well as the autonomic nervoussystem. The CNS is not an immunologically privileged site (Fontanaet al. 1987).

sensitive to CSF (similar to the retinal and pineal photoreceptors in the optic ventricle and pineal recess). The peculiar localization, polarization, and synaptic connections of the CSF-contacting neurons suggest receptor and integrative functions (among which is a role in immune system neuroregulation). Significant immunoreactive serotonin (5-HT) has been found on the dense core vesicles of subependymal CSF-contacting neurons of the paraventricular organ, while y -aminobutyric acid (GABA) immunoreaction has been localized in the cytoplasm of distal infundibular CSF-contacting neurons. It is thought that these specialized neurons synthesize and release their bioactive substances directIy into the CSF in response to information received by their dendrites from the internal CSF and by afferent fiber connections from various brain are as. For further information see Roit et al. 1993.

IrnmuneCells

Immunoregulators

Inorderto protect the CNS, the immune system requires an interfacebetweenthe brain vascular system and the neuronal network. Thisinterconnecting system is provided by glial cells, namely astrocytesand brain macrophages: the so-called microglial cells. Hypertrophyof astrocytes and microglial cells is conspicuous among thecellularchangesin the lesions of multiple sclerosisand viralencephalitis.Upon activation with cytokines such as IFN-y , secretedby activated T-cells (that have invaded the CNS tissue), bothmicroglialcellsand astrocytes express major histocompatibility complexantigens and can act as antigen presenting cells (Fontana et al. 1984,Frei et al. 1984). Specialneurons called "cerebrospinal fluid-contacting neurons"are located periventricularly or intraventricularly. These neuronsare in contact with the CSF via their dendrites, perikarya, or axons.Most of these neurons form ciliated terminals that are

The presence of immunoregulators in the brain and CSF is the result of local synthesis by resident and blood-derived macrophages, by activated T-lymphocytes (that cross the blood-brain barrier), by endothelial cells of the cerebrovasculature, by microglia, by astrocytes, and by CSF-contacting neurons. In addition, uptake from the peripheral blood through the blood-brain barrier (in specific cases) and from the circumventricular organs has been found (Plata 1991. Immunoregulators play key roles in the coordination of host defence mechanisms (and repair), and induce a series of immunological, endocrinological, metabolic and neurological responses. Plata (1991) has summarized the roles of immunoregulators (including the interleukins, the tumor necrosis factors, the interferons, the transforming growth factors, the thymic peptides, tuftsin, and platelet-activating factor).

274

4 Neurophysiology

The direct actions of cytokines on the CNS are responsible for many c1inicaleffects, such as fever, altered sleep, pain perception, appetite, activity level (reduced) and pituitary hormone release. One well established immunomodulatory neuroendocrine circuit is the hypothalamic-pituitary-adrenal axis. At high concentrations, glucocorticoids are able to suppress the activity of thymicdependent immune responses, inc1uding the production of Iymphokines by T-cells and antibodies by B-cells, while at low concentrations, they can be stimulatory. The autonomic system provides an additional pathway for information originating in the CNS to influence the immune systemo Neuronal projections from the brain innervate several immunological tissues, inc1uding the bone marrow and thymus gland. Certain brainstem and spinal nuc1ei have been implicated. Furthermore, cholinergic receptors are present on thymosin-producing thymic epithelial cells and ~ -adrenergic receptors have been identified on Iymphocytes. Surgical and pharmacological manipulations of sympathetic or parasympathetic pathways have been correlated with an altered state of immunity. Many investigations support the hypothesis that ~ -adrenergic stimulation serves to depress immune responsiveness, while cholonergic stimulation enhancesit. There is evidence that brain immunomodulation may have cerebral lateralization. Unilateral ablation of the cortex on the left side (in rodents) is followed by depression of Iymphocyte and macrophage function, whereas the same functions are unchanged or enhanced after symmetrical right-sided ablation. In humans, an association between left-handedness and immune disorders has been described. Present work in the area of neuroimmunotherapy for glioblastomas has demonstrated that these neoplasms produce TGFB2(transformation growth factor B2), which suppresses cytotoxic T-cells,interleukin-lO, which suppresses nontransformed (nonactivated) astrocytes, and MCSF (macrophage colony-stimulation factors) that attracts healthy macrophages into the tumor and stimulates their proliferation. It has also been shown in tissue cultme that glioblastoma cells produce a protease enzyme that permits their migration through white-matter fiber tracts (optic

nerve). An understanding of the full significance of these glial tumor derangements in the neuroimmune system, and techniques for manipulating this system in favor of the host, are on the horlzon. The glioma and its interaction with the cells within the CNS and the immune system have been and remain a challenging problem (de Tribolet 1989).

Pathophysiology and Future Implications The ancient observation (even before Galen) that personality. mental attitude, and emotional state can influence the balance between health and disease now has strong confirmation on both a physiological and an immunological basis. New subdisciplines, such as neuroimmunology and psychoneuroimmunology have progressed in the last decade to reflect this research. Clearly,the immune system receives signals from the brain, and the neuroendocrine system in turn sends afferent information to the brain via cytokines. The scope and importance of tumor-related effects upon the neuroimmunological system (and vice versa) remain to be fully explained. It is certainly reasonable to assume that both extrinsic and intrinsic tumors affect, and are in turn affected by, the CNS immunological system. In addition, the tumor itself may possess its own unique immune system, which it regulates (for its own protective interests) by mechanisms different than those producinga tumoral response ot the CNS immune system. This very complex tumor-CNS inverse relationship may in future be demonstrated as perhaps the key mechanism accounting for the profound growth of some tumors and the chronic, quiescent state of others. Much more remains to be unraveled as we attempt not only to understand these neuro-systemic-tumor immunological interrelationships (reviewed in Fontana et al. 1992), but also as we attempt to manipulate the neuroimmunological factors to act as an adjuvant treatment for residual tumors cells. We may indeed come to find that microsurgical total gross removal, followedby neuroimmunointerstitial tumoricidal therapy is the treatment of choice for gliomas.

Pathophysiology 01 CNS Disease Processes Interactions Between Neurological Diseases and Physiological Systems Neurological c1inicians have long been intrigued by the mechanisms that might account for many of the well-recognized c1inical presentations, but remain puzzled by the all-too-frequent exceptions. It has also long been c1ear that different disease processes interact differently with the CNS physiological systems (Fig. 4.12), each process having its own pattern of effects on the CNS. Specific disorders can be c1assified only in a general way as to their pattern of effects on the CNS. For example, we recognize the general way subarachnoid bleeding or meningitis affects the brain. We may even identify distinguishable characteristics to different processes within each disorder (e. g., aneurysmal subarachnoid hemorrhage is different from that of an AVM or caver-

noma, and bacterial meningitis is different from viral or parasitic meningitis). The same applies to the different extrinsic and instrinsic tumors. Each tumor type, even those arising from identical sites, may present similar symptoms and neurological deficits.but beyond this has a characteristic c1inicalpicture (eg., meningiomas of tuberculum sellae as compared to craniopharyngioma, and adenoma, or astrocytoma and glioblastoma in any localisation). This concept may seem like nonsense, and maybe in thisera it is. But in the not too distant future, advanced imaging studies may provide a new dimension of detail, enabling us to visualize the individuality of each and every disease process. Angiography permitted us to look beyond subarachnoid hemorrhage and see aneurysm, AVMs, cavernomas, and more. CSF analysis led to the recognition of bacterial, viral, and parasitic sources. Futuristic imaging (perhaps by the end of this century) may well open our eyes to the concept that aneurysms, AVMs, cavernomas, bacteria.

Pathophysiology

of CNS Disease Processes

Fig.4.12 The spectrum of possible effects on the CNSproduced by a variety of disease processes. A current hypothetical representation to illustrate the lactthat different diseases at the same CNS locations mayhavean entirely different effect on the CNS. Future neuroimaging techniques may help to understand these basic neurophysiological changes and their importantinteractions

Normal

Ischemic infarct

Hematoma

SAH and Vasospasm

Meningioma

Glioblastoma

Astrocytoma

Abscess

Degenerative disease e.g. multiple sclerosis

Meningitis

Metabolic

diseases

AVM

Hamartomadermoid-epidermoid

Encephalitis

Lues and Tbc

Epilepsy

Trauma

275

--

276

4 Neurophysiology

viruses, parasites, and neoplasms are totally and distinctly unique in their effects on the CNS. Only then will we begin to understand the wide diversity that exists in CNS tumor clinical presentation, growth, response to therapy, recurrence, etc. (Table 4.11). Current neuropathological efforts to understand why different neurological disease processes have predilections for disturbing particular physiological systems have not been as revealing as similar studies in general pathology. Unlike many of the morphological changes seen in general pathology, neuropathological morphological findings are often disappointingly nonspecific, reflecting conditions of widely different etiology and clinical course that result in similar neurocellular responses. The reasons for this lie in the differences in basic reactive capabilities of the neuronal, glial, and mesenchymal components of the CNS. One of the striking contrasts in the neurocellular reactions to CNS diseases is the richness of morphological of neurons to disease states, compared with the limited responses of oligodendroglia, ependymal cells, epithelial cells of the choroid plexus and, to a lesser extent, astrocytes (Tables 4.12, 4.13). General cellular reactions fall into two broad groups: 1. regressive / degenerative (with decline in function, and cell death); and 2. progressive/ hyperplastic (with defensive or restorative "reactive" responses). Neoplastic processes give rise to special cellular reactions, which characteristically involve all cell types (interstitial, mesodermal and neuronal), in varying proportions. Despite the greater range of morphological diversity shown by neurons affected by various disease processes, relatively few of these changes are diagnostic by themselves (Table 4.13). Astrocytes show hyperplasia and hypertrophy as their most florid cellular response, leading to scar formation. Neovascularization and mesenchymal proliferation can also be prominent as part of an astrocytic stimulated (benign) reparative process. Microglial changes are significant in infectious and autoimmune CNS processes. However, some fatal diseases show minimal morphological evidence of an aetiology. These include rapidly fatal processes (often where there are no clear-cut morphological changes), such as can occur with fulminant infections, severe head injuries with a precipitate rise in ICP, or following profound hypoxia. The same can be found with extremely chronic diseases (accompanied only by a minimal, poorly cellular gliosis). The advent of reliable markers for each of the main cell types (interstitial, mesodermal and neuronal) quickly resolved uncertainties about the individual functions of each cell type, and revolutionized the study of their interactions. However, an understanding of the "macrophysiology" of the early and intermediate changes that a lesion occasions still could not be inferred on pure pathological criteria. Apart from the microglia (which can mount impressive inflammatory responses by recruiting help from the systemic immune system via circulating T-cells and B-cells), the limited response of the rest of the CNS-supporting cells is in contrast to the greater range of responses seen in disease processes that affect neurons themselves. Intrinsic neoplastic disease processes in the CNS primarily affect glial (and microglial) physiology and immunology early on, and only at a very much later stage is neuronal functioning per se directly compromised. (This occurs only when the maintenance functioning of the relevant neuronal supporting astrocytes is severely compromised). Similarly, extrinsic processes or tumors may be well tolerated if only causing purely mechanical effects (location and size are important pro visos). However, if the same tumor is also active biologically, an

Table 4.11 Factors influencing interactions disease processes and CNS Systems

between

neurological

General health of the individual patient Nature of the specific neurological disease process Primary location of the disease within the CNS Effects of the lesion: Local Perifocal Global (within the brain) General (systemic)

Table 4.12

Range of morphological expression of neurons to diseased states (from Okazaki, Fundamentals of Neuropathology, New York: Igaku-Shoin, 1989, p. 11) General categories

Individual types

Reactions to axonal damage (chromatolytic changes)

a. Central chromatolysis b. Peripheral chromatolysis

Acute necrosis

a. Ischemic nerve-cell change b. Liquefaction or severe cell change c. Acute swelling d. Conglutination

Atrophic changes

a. Cell sclerosis; simple atrophy b. Retrograde degeneration c. Transsynaptic degeneration

Destruction and disappearance of neurons

a. Neuronalloss ("dropping out")

Abnormal accumulations

a. Lipofuscin excess b. Alzheimer's neurofibrillary degeneration c. Pick's argentophilic inclusion and ballooned cell d. Simchowicz's granular vacuolar degeneration e. Eosinoophilic rodlike structure f. Intracytoplasmic hyalin body g. Bunina body h. Lewy body i. Marinesco body j. Lafora's amyloid inclusion k. Abnormal accumulation 01 storage diseases 1. Inclusion bodies (cytoplasmic and /or nuclear) of viral diseases a. Hematin pigment b. Ferrugination or iron incrustation a. Binucleated or multinucleated neuron b. Monster neuron

Deposition of extraneous pigment

Hypertrophic changes

array of physiological subsystems are invariably altered (and it is these alterations that can create operative and perioperativedifficulties). It is the quantification, characterization,and comprehension of these multiple alterations that will in the future diminish the uncertainties surrounding tumor pathophysiology. Yet, nowhere in the body is it more difficult to establish parameters for criticallevels of functioning than in the individual physiological systems of the central nervous system. Due to the close integration of these systems, it has proved difficult to isolate parameters that reflect function in one system alone. Some success has been achieved in correlating neuronal functionand cerebral perfusion pressure (CPP) in craniocerebral injury and

Pathophysiology hydrocephalus. Similarly, cerebral activity can be related to cerebralbloodflowin cerebral ischemic states followinginfarction, subarachnoidhemorrhage (using Doppler, PET, or SPECT), and inbriefcarotid occlusion (Wada test). Pressure/volume changes (PVI)andICP wave-form analyses can predict impending herniationinexpandingintracranial mass lesions,and EEG abnormalities can usefully reflect seizures, interictal events, encephalopathicstates, and brain death. Noninvasive techniques suggesting accurate

assessment of cerebral perfusion pressure (CPP)fromDoppler wave-form analysis look promising, but a fullunderstandingof these parameters remains elusive. In addition,thesepresentparameters cannot be reliably,routinely,continuouslyand noninvasively measured. The development of methods

to assess other physiological systems awaits future

research. It is our hope that, before the end fo the century, it will be possiblenot only to better image the CNS directly, but also to simultaneouslyand noninvasively display measured parameters ofallthe associated local, perifocal, global and general physiological changesbrought about by tumors. In this way, the unique characteristicsof each individual tumor (and its effects on the CNS),andthe cascade of responses (by the individual CNS subsystems)willbe accessible to all those caring for CNS tumor patients.

Table 4.13 Patterns of cellular response to injuries within the central nervous system (Irom Okazaki, Fundamentals of Neuropathology, New York: Igaku-Shoin, 1989, p. 10) Cell types

Functional Neuron

Interstitial (Glia) Oligodendroglia (Schwann Cell) Astrocyte Ependymal cell Epithelial cell 01 choroid plexus Microglia*

Types 01reaction Regressive I degenerative

Progressive I Hypertrophichyperplastic (excluding neoplasia)

Many specilic and nonspecilic alterations

None

Limited

None (Iimited)

Limited

Scar lormation (astrocytosis) None

Limited

Neoplasia Limited

(mesenchymal) connective tissue

Blood vessel and connective tissue

Tumorsare dynamic entities with their own metabolic agendas. In additionto their properties as space-occupying masses, tumors (evenapparently histologically identical ones) have unique physiologies,includingindividual neurochemical and neuropharmacologicalproperties (nonmechanical aspects). As they are pathological processes,these intrinsic aspects are also inconsistently expressed,with the tumor frequently passing through variable phasesof activity (growth with rapid metabolism) and inactivity (dormantstate with reduced metabolism). The tumor-brain interactionis also a highly variable phenomenon, based on a combinationof both mechanicaland nonmechanical factors. The effects onbrainfunctionof varyingpermutations of these factors may be globalor local,and may occur during the tumor's active or inactivephases. The mechanical relationships proposed by the Monro-Kellie hypothesis of brain-tumor interaction considers only mass effects.Thisis at the expense of possibly more important nonmechanicalinteractionsbetween these two separate physiological systems(that of the tumor versus that of the CNS). For instance, imagingconfirmsthe mechanical significanceof neural herniations,butprovidesno explanationas to whyall herniations are not necessarilysymptomatically equivalent. In addition, it fails to explainwhysome fiber bundle s (such as the optic radiations) can be extremelyresistent to displacement. The uniqueness of each brain-tumor interaction is also reflectedin the wide variability of functional preservation or deficit production.Manyinvestigators,since the

time of Broca, have

soughtto strictly correlate structure with function. This has resultedin a debate (that still continues) between those favoring the precise localization of function and others who assert that functionis basedon diffusecerebral interactions. Increasing evidenceexists that the actual situation lies somewhere between theseextremes. Certainly,well defined functions confined to certainareasofthe brain are accepted facts (motor and sensorycor-

Inllammatory reactions, phagocytosis

Mesodermal

Hematogenous cells (Ieukocytes)

Tumorsas Dynamic Systems

277

of CNS Disease Processes

Limited (edema)

Infiammatory reactions, phagocytosis Scar lormation (limited)

* Microglia also have mesodermal leatures.

tices); but there are exceptions to precise localization (personality, memory, and motivation) that ha ve yet to be fully clarified. Along these lines, language is known to have at least three main component are as, but their location in a particular individual is surprisingly variable (Ojemann 1990), as predicted by von Monakow in 1914. The remarkable "maps" of cortical functional topography based on direct cortical stimulation experiments and pathological extrapolations (Brodmann, Penfield) are very familiar. Yet, it is a common experience for ciinicians to witness the great ability of the central nervous system for functional accommodation-the so-called "plasticity of the CNS" in response to various insults, including birth injury, accidental trauma, cerebral infarction, infection, and, of course, neoplasia. Functions lost or impaired may be resto red or regained (to various degrees), often through the assumption of these functions by other are as in the CNS. The phenomenal back-up capacities afforded by parallel processing account for the resilience of the brain to all but the most devasting insults. Experimentally, much is currently being learned about this redundancy of function. With the new computer-aided technologies of the 1990s, interest in brain mapping is undergoing a long-overdue resurgence. At present, however, with the possible exceptions of continuous EEG and EEG spectral analysis, there are no adequate means of continuously monitoring these physiological subsystems and their dynamic interplay in the clinical setting. Lesions of the temporallobe may produce hemiparesis and language deficit in one patient, but not in another, despite the similarity of pathology and anatomical site. Similar lesions in the frontal lobe may not produce the same degree or even type of personality or intellectual change in different patients. A lesion in the

278

4 Neurophysiology

posterior temporal or parietal region may produce a visual field defect in one patient, but not in another, or a tumor in the medial frontal region may produce motor apraxia. In addition, patients with recurrrent tumors may slowly succumb to the "paraneoplastic" effects of the tumor with no evidence of mass effect or significant herniation. The significant point is that, even after considering the variation in functional plasticity between individuals, the physiological effects of the tumor (as a separate neurophysiological entity) are as unique as are the reverse effects of the system (CNS) on the tumor. Neurological deficits and pathophysiological responses cannot be reliably predicted by imaging appearances. cr and MRI may suggest edema around a cerebral tumor, yet upon tumor

removal, the surrounding brain may become very slack, though the imaging appearance of this brain tissue remains unchanged. lt is common to witness dramatic and immediate symptomatic improvement in patients started on steroids for "cerebral edema." while no change can be seen on MRI or CT for days or weeks.It is clear that direct correlations between tumor histological type and size, the degree of peritumoral density changes, and the amount of displacement, midline shift and herniation cannot be made. Methods of distinguishing and monitoring these nonmechanical factors must be developed. These observations will provide important physiological data that will help uncover why there are striking differences in illness manifestations between patients with otherwise similar pathologies.

Final Remarks Despite the wealth of knowledge available from anatomical, physiological, radiographic, imaging, and laboratory studies, surgeons remain preoccupied with judging the response of the nervous system to tumors largely in mechanical terms. The effects of parenchymal compression or displacement, CSF blockage or malabsorption, or vascular occlusion are familiar to us, yet our knowledge of changes in the circumventricular and immunological systems, the role of neurotransmitter circuits, and the behavior of tumors themselves as dynamic entities are largely unresolved. As a result our basic understanding of brain-tumor interactions fails to explain fully the small multisymptomatic lesion, the large asymptomatic mass, or the identically positioned but variably presenting tumor in different patients. In addition, we remain in large measure confused with the MRI depictions as to the true extent of some tumors and as to the real significance and cause of perilesional changes (in terms of edema, infiltration, and altered function). A certain stern, iconoclastic spirit is necessary to break the surgical constraints imposed by outdated physiological ideas. We must continue to explore the unknown neurophysiological factors involved, so that both our understanding of the tumor disease

process and our treatment of patients with tumors is enhanced. Neurosurgeons exhibited this spirit when the dictum of the inoperability of spinal intramedullary lesions was disproved. Similar revisionist thinking dismisses the notion that lesions are surgically "off-limits" in primary sensorimotor, limbic, paralimbic (and other so-called "eloquent") areas. Most important in these situations are the patient's preoperative deficit and the surgeon's skill in microtechniques. The maximal preservation of peritumoral tissue (where both real and theoretical neural mechanisms for functional accommodation reside) must be achieved at surgery.ln other words, the surgical effort must ensure the preservation of adjacent but uncompromized cortical areas (whether "silent" or "eloquent"). Coupled with the inherent capacity of the brain for dramatic homeostaticrestoration, this surgicalprincipIewillmaximize the quality of survival for every patient. As a result, it is imperative that specialist tumor surgeonsbe fully trained in microtechniques and thoroughly versed in the anatomy of lesion topography (sulcal, fissural, gyral segmental. peduncular and vascular). In addition, a flexible, discerning,and inquisitive mind concerning brain physiology and brain-tumor pathophysiology is mandatory.

Conclusions The physiologyof the CNS has been well delineated as regards subsystems generally and specifically. Generally. In terms of intracranial pressure (ICP), the dynamic interactions and changes (acute and chronic) between the brain-parenchymal, CSF, and vascular components of the intracranial cavity in relation to a space-occupying mass have been extensively studied and described over the past 100 years. Specifically. Parenchymal functional topography (i. e. cortical, basal ganglia, white matter, connecting fibers) as related to traumatic, vascular, infectious, and neoplastic processes has been analyzed utilizing EEG (and recently neuroimaging modalities such as PET and MEG) since 1925.

These studies have provided respectable advances whencom-

pared to the state of knowledgea century ago.However,wemust not ignore the information gained over the past 2000-3000years (such as the correlation between left-sided and right-sidedinjuries with sensorimotor, visual, hearing, and language difficulties) as represented in the Edwin Smith papyrus, or illustrated by Hippocrates. We must put our recent discoveries, as good as they are. into proper historical perspective. Our present knowledge is relative.Neurophysiologicalstudies have taught us the directrelationships between the size, position, and growth of an intracranial mass and the surrounding brain. These principIes, derived fram trauma experiences,are wellknown to all of us,andclearlyshould be applicable to tumor cases as well. But this is not so.

Conclusions Tumors of the same size, location, and extension do not alwaysresult in the expected (temporary or permanent) dysfunctionsordeficits.A vast majority of tumors exist for a long period withoutproducing any symptoms, even in highly functional are as. The explanation cannot simply be that the lesion developed slowly(CNS compensation and adaptability), beca use acute hemorrhages(tumoral or not) do not always cause symptoms and defieitseither. Other factors must be important: 1. Thestructural organization of the CNS does not allow noxious invadersto destroy neurons, white-matter fibers, vascular structures,or the immune system. 2. Thereis natural structural elasticity within the CNS enabling it to aeeeptmass lesions by spreading apart. 3. Herniationas a radiographic finding should not be considered to suggest clinical symptomatology. Two types of herniation exist:benign and malignant. Neuroimaging cannot distinguish betweenthese two types, and more importantly, it cannot predietwhen herniation is going to be dangerous. 4. Thelocationof certain functions within the CNS is well known, but the eell groups in these areas are not isolated from surroundingcell groups, remo te systems, the whole brain, or even the whole body.

279

5. The CNS subsystems (neuronal, vascular CSF, endocrine, immunologic) are related in a complex, network-like system. The intensity of physical, chemical, and biological noxious effects, and the irritability potential of the subsystem network are responsible for the severity and duration of dysfunction and deficits (diaschisis). The following 40 Cases in this chapter, as well as all of the other cases in this book and also in Vol. IVB, are presented to illustrate the topics discussed within this chapter on neurophysiology. Case 4.1-4.14

Controversial cases showing neuroradiological evidence of severe brain displacement and herniations, but without the expected concomitant clinical deficits 4.15-4.24 Cases with lesions in (so-called) eloquent areas without expected concomitant neurological deficits 4.25-4.31 Cases with contaversial effects of chronic or subacute tumor growth and acute hemorrhage 4.32-4.40 Cases to show the discrepancies between neuroradiological findings and the clinical state in cases with brainstem or cervical cord tumors

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4 Neurophysiology

Cases

Case 4.1

A 42-year-old

female with a 1Q-yearhis-

a

tory of progressive personality changes and headaches. Upon presentation, she was noted to have papilledema, nystagmus, and a left homonymous hemianopsia. Her sensorimotor and reflex examinations, however, were entirely normal. MRI views: a horizontal (T2), b sagittal (T1), e coronal (T1), d coronal (T1). There is a large, poorly delineated right temporallobe lesion, extending throughout the entire hemisphere. Note the severe herniation into the parachiasmal and paramesencephalic cisterns. There is severe distortion of the midline structures and the dorsal mesencephalon. There is extension, subtentorially into the cerebellar hemisphere in the area of the cerebellar mesencephalic fissure, and corresponding subsplenial extension. Post-

operative views (T1)-(7 months postoperatively) e horizontal, f sagittal. The tumor (anaplastic astrocytoma) can now be better localized in the medial basal temporal d region. It arose from the right parahippocampal gyrus. The patient made an uneventful recovery, and received radiotherapy.

e

Cases

a

b

e

d

Case 4.2 A 48-year-old female, suffering from headache. 4 weeks after a hysterectomy. Sensorimotor findings were normal. No visual field defect. The left optic radiation is displayed (e, d). MRI views: a horizontal (T1),b horizontal (T2),e horizontal (T1),d horizontal (T1).e coronal (T1)posteroanterior view. A relatively smalllesion in the left occipitallobe, with a large amount of surrounding edema (b). Note the severe tentorial and subfalcial herniation (e-e). There is severe distortion of the ipsilaterallateral ventricular system, and the mesencephalon is distorted and shifted (e) coronal (postero-anterior view). There is obliteration of the paramesencephalic cisterns. The patient is fullyalert, communicative, and rational. The tumor (metastatic adenocarcinoma) was extirpated. Postoperative radiotherapy.

281

282

4 Neurophysiology

a

b

e

d Case 4.3 A 28-year-old female with partial complex epilepsy and a left upper quandrantanopsia. There were no other neurological abnormalities. MRI views: a horizontal (T1), b sagittal (T1). A large lesion is delineated, involving the entire right temporallobe. The tumor involves the parahippocampal gyrus, with expansion in all directions. There is severe herniation and compression of the paramesencephalic cisterns (a). Note the severe compression and displacement of the upper brainstem (b). The patient was alert and had no neurological deficit. Postoperative MRI (T1) (8 months postoperatively): e horizontal, d coronal, e sagittal. The precise location of the tumor (astrocytoma, Grade 1/)is now well seen in the right parahippocampal gyrus. The patient continues to do well, nearly 3 years after surgery, and drives a car. No visual field defect.

Cases

283

a

e Case4.4 A 49-year-old male with a head injury after a fall. Neurologically,therewas no deficit, and the visual fields were normal. The patientwas mentally slow, but cooperative. MRI views: a horizontal (T2),b sagittal (T1),e coronal (T1). Two well circumscribed lesions areseen,one in the right middle fossa and the other in the right occipitalpole. Note the degree of ventricular distortion, with herniationinto the paramesencephalic cisterns. Distortion of the brain-

d stem (e). Postoperative views: d horizontal (T2). The larger right middle fossa tumor (meningioma) arose from the base of the middle fossa with indentation into the inferior temporal gyrus. The occipital tumor remains (it was removed 10 months later in a separate procedure). One wonders how a patient could remain mentally clear despite such significant herniation. Visual fields normal.

284

4 Neurophysiology

a

e

e Case 4.5 A 61-year-old female with generalized seizures and headaches, and visual field troubles, (homonymous hemianopsia). Sensorimotor findings were normal. MRI views (T1): a horizontal, b sagittal, e coronal. The is a large, right mediobasal temporallobe lesion in the area of the parahippocampal gyrus, with severe herniation into the paramesencephalic cisterns. Note the severe midline

herniation and the distortion of the mesencephalon. The patientwas fuliy alert. Postoperative views (2 weeks posteratively): d coronal, e horizontal, f sagittal. The location of the tumor (glioblastoma) is now clearly evident, with relief of the previously severe herniation. Postoperatively, the homonymous hemianopsia remains unchanged. No other neurological deficit.

Cases

a

285

b

I

e

Case 4.6 A 21-year-oldwomanwith a history of epilepsy (and a normal CT 5 years previously)

now presenting with dizziness, headaches, vomiting, memory loss, left-sided hemiparesis (minor), and a left homonymous hemianopsia, MRI views: a horizontal, b coronal, e sagittal. A large, right middle temporal fossa les ion with paramesencephalic herniation. Note the severe compression and distortion 01the brainstem (b). Preoperative diagnosis: meningioma. The

'

d

patient was fully alert, clear, and could walk without support. Postoperative view (10 days postoperatively): d coronal. The location of the tumor (anaplastic ganglioglioma, Grade 3) is now better seen with correction of the upper brainstem compression. Postoperatively only the field defect persisted. Following radiotherapy, the patient remained in excellent condition for 1 year, but died two years later from disseminated recurrent tumor.

286

4 Neurophysiology

b

a

~. - -,

e

Case 4.7 A 29-year-old male with a 4-month history of miId headache and left anisocoria. There were no other neurological deficils.

Neuroimagingviews: a MRI (T1) horizontal, b MRI (T1) coronal,e

e

MRI (T1) sagittal, d DSA, lateral. There is a large, well-encapsulaled sphenopetroclival lesion (with significant vascularization). NOlice the herniation in the paramesencephalic and parachiasmatic cisterns, with severe compression and distortion of the upper mesencephalon. Clear consciousness. Postoperative views MRI (T2)horizontal. The tumor (meningioma) was embolized preoperatively.Al surgery (pterional approach), there was enormous adherence lo the oculomotor nerve and internal choroidal and superior cerebellar arteries. Despite preoperative embolization, very bloody lumor on exploration. Postoperatively, the patient had temporary weakness of the left third nerve, but otherwise remained neurologically inlact.

-

Cases

Case4.8 A 44-year-old woman with leftfrontal headache, but no other neurologicalabnormalities. Neuroimaging views:a MRI (T2) horizontal, b MRI (T1) coronal,e DSA. superior mesenteric veinview. A large, well-encapsulated lesionoccupying the entire floor of the leftmiddle cranial fossa, with herniation into the paramesencephalic and parachiasmatic cisterns. Note the significantcompression and shifting of the upper brainstem. d Postoperative view(2 weeks postoperatively) MRI (TI) coronal. The tumor (meningioma) wasremoved via a pterional approach, and adherence to surrounding structures was noted. The patient remainedneurologically intact.

287

b

a

e

Case4.9 A 15-year-old male with a 1-year history of progressive headachesand a 1-week history of vomiting and gait apraxia. MRI view(T1): a sagittal.A well-circumscribed lesion with large surroundingcystsin the posterior cerebellum and severe tonsillar herniation.

Note the degree of medullary compression in this asymptomatic patient. Postoperative view (2 weeks postoperatively): b sagittal. The tumor (cystic astrocytoma) has been totally removed. Full recovery, neurologically intact.

288

4 Neurophysiology Case 4.10 A 62-year-old male with gait ataxia and left-hand dysmetria, but an otherwise normal neurological examination. MRI view (T,): a sagittal. A large, well-encapsulated lesion, in the posterior inferior cerebellum, with herniation into the

a

foramen magnum. Note the severe degree of medullary compression. Postoperative view (3 weeks postoperatively): b sagittal (T1). The tumor (meningioma) has been completely removed. The patient remains neurologically normal.

b

a

d

e Case 4.11 A 30-year-old male with a 6-year history of intermittent retroauricular pain. At presentation, miId right facial hypesthesia was noted; otherwise, the neurological examination was completely normal. MRI views (T,): a horizontal, b coronal (posteranterior view). A large, well-encapsulated lesion in the right cerebellopontine angle. Note the severe compression and displacement (distortion) of the entire pontobulbar area, and the absence of peritumoral

changes (characteristic of most infratentorial lesions). Postoperative views (2 weeks postoperatively): e horizontal (T,), d coronal(T1) (posteroanterior view). The tumor (acoustic neuroma) has been totally removed. No adherence to surrounding structures was noted at surgery. The patient remains neurologically normal, with no cranial nerve deficits.

IIIIIIIIII

Cases

a

289

b

e Case4.12 A 58-year-old male with a 7-year history of progressive right hearing loss. Noted to have bilateral facial hypesthesia, a diminishedleft corneal reflex. anacusis, tinnitus. horizontal nystagmus and gait apraxia. but no pyramidal deficit. Neuroimaging views:a MRI (T1) horizontal, b MRI (T1) coronal (posteroanterior view),e OSA,horizontal. There is a large, well-encapsulated multi-

cystic lesion in the left cerebellopontine angle. with severe displacement and distortion of the pontobulbar region. Postoperative view (2 months postoperatively): d MRI (T1) horizontal. The adherent tumor (acoustic neuroma) has been completely removed, with restoration of the normal pontobulbar position. Apart from rightsided anacusis, there were no residual deficits.

290

4 Neurophysiology

a

Case 4.13 A 50-year-old male with a 10-year history of progressive hearing loss and tinnitus, eventually presenting with paresthesia on the left side of the face, vertigo, nystagmus, diplopia, andgait ataxia. Neuroimaging views: a MRI (T1) coronal, b MRI (T1)horizontal (posteroanterior view). A large, well-encapsulated left cerebellopontine lesion, with entrance into the porus acusticus. Notethe massive pontobulbar shift, but the absence of perilesional changes (edema). Postoperative view (10 days postoperatively): e CT-Scan horizontal. The adherent tumor (acoustic neurinoma) has been completely removed. Interestingly, in this patient with a historyof neurofibromatosis, a small trigeminal neurinoma was removed at the same sitting. Full recovery.

Cases

b

a

e Case4.14 A 38-year-old male with a 15-year history of hearing, loss following asevere ear infection. Recently, a 2-year history of paraesthesiason the left side of the face, gait ataxia, right sixth and seventhnerve palsies, atrophy of the right side of the tongue, troubleswallowing, and right arm ataxia, but no hemiparesis. MRI views(T,): a horizontal, b coronal (posteroanterior view). There is a large,well-delineated lesion involving the right ventral portion of the brainstemand cerebellum. Note the massive displacement of the

291

d

----

fourth ventricle and identation of the pontobulbar structures. Post-

operative views

(6 months postoperatively):

e horizontal,

d coronal

(postero-anterior view). The tumor (epidermoid) had displaced all the cranial nerves, 3-11, but demonstrated no adherence, and was completely removed. The patient's neurological abnormalities improved completely. Note the return of the pontobulbar structures to their normal midline position.

292

4 Neurophysiology Case 4.15 A 35-year-old female with a long history of well controlled seizures, but no other associated neurological abnormalities. (The patient is right-handed and has no speech deficits (she speaks two languages fluently). MRI views: a sagittal (T1), b sagittal (T1), e horizontal (T2), d (coronal (T1). A well-delineated lesion in the left posterior aspect of the inferior frontal gyrus (F3) (Broca!) Observation over the last 5 years did not reveal any tumor growth. The preliminary diagnosis is of a low grade glioma. The patient remained fully active.

a

e

Case 4.16 A 29-yearold male who presented in 1983 with occasional seizures. CT revealed a large frontal cystic lesion. The patient, who was neurologically and mentally normal, refused surgery, and the size 01 the tumor on neuroimaging remained unchanged. a horizontal b corona!. MRI1 year later, when he re-presented with a 2 week his-

a

b

tory of subacute deterioration (subclinical seizures) and accepted surgery. Exploration revealed a cystic dermoid. Neurological findings were normal throughout.

Cases

Case4.17 A 23-year-old male who had hadone generalized seizure, but had an otherwisecompletely normal neurological examination.MRI views (T,): a horizontal, b sagittal, e coronal. A large, well-circumscribedcystic les ion in the left middle and inferiorfrontal gyri (just in front of Broca's area).The lesion appears to be parenchymal,with no perilesional changes. Postoperativeviews (1 year postoperatively): d coronal, e horizontal, f sagittal. The tumor (meningioma) has been completely removed.No adherence was noted at

a

surgery.Note the absence of any imaging changesto account for the location of the tumor.He is neurologically normal and was ableto travel around the world in a small sailboatwith his wife some 6 months later.

e

e

293

4 Neurophysiology

a

Case 4.18 A 35-year-old male who had had several generalized

e

seizures over eight years. Biopsy in 1985 in another center revealed an astrocytoma, and despite treatment (interstitial radiation) the seizures continued. Five years later, the patient began to develop speech difficulties and minor paresis of his right hand. (Otherwise his neurological examination was unremarkable). MRI views: a horizontal (T2), b sagittal (T1),e coronal (T1).A large cystic lesion in Ihe posterior parts of the left middle (F2) and inferior (F3) frontal gyri. Note the involvement of the pars triangularis and opercularis of F3. Postoperative views: d coronal (T1), e sagittal. The tumor (anaplastic astroeytoma) extended into the precentral area, and was radically removed. The patient's speech abnormalities improved dramatically after the operation, and he remainswell 12 monlhs after surgery.

Cases

295

a

e

Case4.19 A 33-year-old male with a lifelong history of intermittent seizures(30 years). He developed right-sided focal seizures with markedpostictal hemiparesis 4 weeks previously. Upon admission, healsohadsignificant dysphasia of a conduction type, minor weaknessof theright leg, and dysdiadochokinesia of the right armo MRI views:a horizontal(T2),b sagittal (T1), e coronal (T1). A large, wellcircumscribedlesion in the inferior parietal lobule, displacing the

d

central lobe anteriorly. Postoperative views: d coronal (T1), e horizontal (T1), f sagittal (T1). The tumor (glioblastoma, Grade IV) was very cystic and vascularized, and it had thinned the overlying bone and was infiltrative into the dura. Multiple thrombosed veins were found inside the tumor. Postoperatively, the patient had immediate speech improvement, which continued over several weeks. Following radiation therapy, he is still doing well 2 years postoperatively.

296

4 Neurophysiology

a

e

d

Case 4.20 A 59-year-old male with a 6-month history of progressive headache and minor speech abnormalities (primarily wordlinding). Note that the patient is right-handed, and has no other associated neurological abnormalities. MRI views: a horizontal, b sagittal, e coronal. A large, well-delineated lesion within the posterior part of the superior temporal gyrus, extending into the transverse temporal gyrus and adjacent insular areas. Note the displacement of the optic radiations. No visual field defect. Postoperative views:d coronal, e sagittal. The position of the tumor (glioblastoma, Grade IV) can now be better defined. The patient had immediate improvement in language function postoperatively and no visual field defect. Despite radiotherapy, unfortunately, the tumor recurred 4 months later, with the return of speech abnormalities. Followinga repeat tumor removal, the patient's speech abnormalities again resolved for 6 months, at which point the tumor recurred again. This case clearly illustrates the need for adjunctive therapy, which unfartunately does not yet exist.

Cases

a

b

e

d

e

297

Case 4.21 A 45-year-old female with occasional headaches over 6 months and acute diplopia (but no other associated neurological abnormalities). MRI views: a horizontal, b sagittal, e coronal. A large, infiltratinglesion in the area of the angular gyrus at the end of the Sylvian fissure. Note the massive displacement, compression of surrounding sturctures, and distortion of the brainstem. The perilesional changes suggest infiltrationby a glioblastoma. Postoperative views: d coronal, e sagittal. The tumor (meningioma) was totally removed, despite the moderate adherence to the transient arteries. The postoperative course was uneventful.

298

4 Neurophysiology

a

e

d

e Case 4.22 A 33-year-old female who had suffered several grand mal seizures. At presentation, this right-handed patient had no neurological abnormalities, and was fluent in seven languages. MRI views: a horizontal (T2),b sagittal (T1),e coronal (T1).A large, intrinsic tumor arising from the middle and posterior parts of the superior temporal gyrus, involving the transverse temporal gyri (Heschl). The tumor (anaplastic oligodendroglioma, Grade 111) was subradically removed. It was noted to be displacing the insular structures,

but not infiltrating into them. The patient developed, further seizures 1 year later, and MRI showed a local recurrent tumor, which was removed. Postoperative views: d coronal, e horizontal, f sagittal. Note that the optic radiations were displaced by the tumor and no! transected accounting for the patient's normal visual fields. There was no neurological deficit, and language function, in particular, remained intact.

Cases

a

299

b

d

f Case4.23 A 35-year-old female, right-handed, with a 10-year history of seizures. Earlier CT biopsy demonstrated a low-grade astrocytoma.Three years later, the CT demonstrated increasing tumorsize.The patient remained neurologically normal. She then developed a 2-week history of minor dysphasia, right-sided paresthesia,gait abnormalities, a right inferior quadrantanopsia, anddysmetria.MRI views: a horizontal (T2), b sagittal, e coronal, d corona!.A large lesion, extending from the posterior part of the superiortemporal gyrus into the parietal operculum and posterior

insula. Note the impressive midline shift with compression of the upper brainstem (c). The trigonum is filled by the tumor (d). Postoperative views (2 months postoperatively): e coronal, f sagittal. The tumor (oligoastrocytoma, Grade 1/)was completely removed, and its precise position can now be better seen. Note that the middle and anterior insula are free of involvement (f). The patient's neurological status improved significantly postoperatively, with no speech difficulties, sensorimotor functioning intact, and visual fields normal.

300

4 Neurophysiology

a

b

e

Case 4.24 A 36-year-old male, right-handed, with progressive maxillary pain, fatigue, vertigo, slight dysphasia, and a right upper quadrantanopsia (but not sensorimotor deficits). MRI views: a horizontal (T2)' b sagittal, e coronal. There is a giant parahippocampal tumor, with herniation into the parachiasmal and paramesencephalic areas and upper brainstem. Postoperative views: d sagittal, e horizontal. The tumor (anaplastic astrocytoma, Grade 11I)was

radically removed, and radiatiotherapy applied; the patient did excellently for approximately 2 years, and could work normally. There was no neurological deficit, with the exception of quadrantanopsia. One year later, he developed bulbar symptoms. f TheMRI shows dissemination along the CSF system, with involvement01the arbor vitae 01the cerebellum and the spinal cord. The patient died 3 months later.

Cases

301

Effectsof Chronic or Subacute Growth

Case4.25 A 19-yearoldfemalewith headachesand vomiting. (Shehadundergone an unremarkable lumbar puncturein another institution,withoutconsequences).Two monthslater,she developedsudden diplopiaand a left inferiorquadrantanopsia, butnoother neurologicaldeficits.MRIviews: a horizontal,b coronal, e sagittal.There is a largecystic lesion originatingin the posterior insulaand extending intothe retroinsularand retrolentiform areas. Postoperativeviews: d sagittal, e horizontal,f corona!. Thetumor (pleomorphic xanthoastrocytoma)was radicallyremoved.The preciseposition of the tumorcan now be better seen.Uneventfulpostoperativecourse.

a

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302

4 Neurophysiology

a

b

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d

Case 4.26 A 36-year-old male with a motor Jacksonian seizure (righthand,laterwithgeneralizedseizures)and postictalhemiparesis; improvementwithin 1 week. MRI views:a horizontal,b sagittal. The lesion,and associatedhematomain the middle portionsof the

precentral gyrus, can be well seen. Postoperative views: e horizontal, d sagittal. The tumor (cavernoma) and surrounding hematoma were completely removed. The patient made a complete recovery.

Cases Case4.27 A 35-yearoldfemalewith a 1Q-year historyof migrainesand progressiveleft-sidedfocal epilepsy(with postictal weakness of the left arm),withdiminished corticalsensationin the leftarmoMRI views: ahorizontal,b sagittal, ecoronal, d MRA.A welldelineatedlesion in the middlepart of the right parietallobule,with hematoma expansion. Notethe venous angiomadraining into thesubependymal venoussystem.Postoperativeviews:e horizontal,f sagittal. The tumor(cavernoma)and surroundingclot were totallyremoved(the drainingvein was saved),and the patient experienceda fuI! recovery.

303

a

b

e

d

e

f

304

4 Neurophysiology Case 4.28 A fully alert 17-year-old male with

acute developmentof

a

e

.

symptoms (headache, vomiting, right-sided hemihypesthesia, inferior quadrantanopsia to the right). MRI views: a horizontal, b corona!. These is a large hematoma within the left thalamus, with distortion of the brainstem. Via a left supracerebellar, subsplenial approach, the thalamic lesion (telangiectasia) was removed. The patient made a fuI! recovery, but the quadrantanopsia remains b unchanged. Postoperative MRI: e horizontal, d corona!.

d

Cases

a

305

b

e Case4.29 A 2-year-old boy with intermittent torticollis and ataxia. Hedevelopedacute moderate hemiparesis and loss of speech. MRIviews:a horizontal, b coronal (seen from behind), e sagittal. A largemesencephalic hematoma can be identified. It is amazing Ihalthischild did not have more neurological abnormalities. Postoperativeviews: d sagittal, e horizontal, f coronal (posteroanterior

view). The tumor (cavernoma) was removed through the pulvinar (right supracerebellar approach). It was seen to arise from the posterior third ventricle and several hematoma cavities with differing hemosiderin colors entered the mesencephalon. The patient made a full recovery.

306

4 Neurophysiology

d

e

.. ,~

\.~ Case 4.30 A 4-year-old female with congenital heart disease (a ventricular septal defect). Status after Blalock- Taussig shunt. Presented withheadache, vomiting,drowsiness, and moderate lefthemiparesis. MRI views: a horizontal, b sagittal, e coronal (anteroposterior view). A huge, well-encapsulated lesion in the right thalamus, certainly suggestive of an abscess. Postoperative views: d coronal, e horizontal, f sagittal. The abscess was approached through the interhemispheric transcallosal approach. It was aspirated, the cav-

ity was washed out witha formalinsolution,and antibioticswere given. The child made a dramatic recovery. Note the precise POSItion of the abscess in the dorsal medial thalamus. Preoperatively,it was thought that the entire thalamus is involved. This case illustrates that precise surgery is possible with intrinsic lesions indif-

ficult areas. There is a need for adjuvant therapy in gliomacases that will alow cures similar to those seen in cases of abscesses. Bacteriology revealed hemophilus parainfluencae.

Cases

a

b

e

d

Case4.31 A 40-year-old female who had been suffering from Hodgkin's disease (111B) since 1982, treated with staging laparotomy,splenectomy, chemotherapy, and radiotherapy. She suffereda sensoryJacksonian seizure in August 1992. No neurological deficits. MRI views: a horizontal, b corona!. A large parietal lesion,involving both the precentral and postcentral gyri. Surpris-

307

ingly, she had no neurological deficits. The neuroradiological diagnosis was probable local thrombophlebitis. Follow-up views (2.months later). e sagittal, d corona!. The patient had a prolonged bleeding time secondary to leukemia, and no biopsy was performed. Note the spontaneous improvement without surgical intervention.

308

4 Neurophysiology

a

b

e

Case

4.32

A 15-year-old

female

with a 2-year

history

of head-

aches and vomiting, followed by papilledema, nystagmus, ataxia, and left hemiparesis. The CT scan showed occlusive hydrocephalus due to the mesencephalic lesion. Placement of a peritoneal shunt was effective. She made a full recovery, but within a few days developed acute diplopia. MRI views: a horizontal, b coronal,

e sagittal. Postoperative views: d sagittal, e coronal (anteroposterior view). The tumor (anaplastic astrocytoma) was removed through a left paramedian supracerebellar approach. The patient remains totally symptom-free and neurologically normal 6-years postoperatively although there is residual tumor within the left thalamus and left internal capsule (1).

Cases

a

b

e

d

Case4.33 A 23-year-old man with an 8-year history of a paraspleniallesion on Cl treated by a shunt. The patient remained symptom-free,but then developed headaches, diminished concentration,and gait ataxia, but no Parinaud syndrome. MRI views: a horizontal,b coronal (posteroanterior view), e sagittal. A large dorsal mesencephaliclesion. Postoperative view: d Sagittal. The tumor

309

(piloid astrocytoma)was well cleavaged, displacing the vermis inferiorly. Through a paramedian supracerebellar approach (Ieft side), it was completely removed. Although suffering a the stigma of von Recklinghausen's disease, the patient made a full and uneventtul recovery.

310

4 Neurophysiology

a

Case 4.34 A 13-year-old male with a 3-month history of left-sided weakness, nystagmus, diminished balance, left-hand dysmetria, minor left hemiparesis, and partial sixth nerve palsy. MRI views: a horizontal(T2)'b coronal (postereoanterior view). e sagittal. A right dorsolateral pontomesencephalic lesion. Postoperative views: d sagiUal, e horizontal, f coronal (posteroanterior view). The tumor (pilocyticastrocytoma) arose in the area of the stria medullaris. and

b

extended into the mesencephalon. It was approached througha medial suboccipital craniotomy, and through the sulcus between the tonsilla and pyramis nodule fissure. The patient made a total recovery, and can ride his bicycle. The discrepancy between the clinical findings and the pontomesencephalic deficit is surprising. The patient has been doing well for 3 years.

Cases

a

b

e

d

Case4.35 A 11-year-old male with a 1-year history of headaches and progressive left sixth nerve palsy and facial weakness. MRI views:a horizontal,b sagittal. A large, pontine lesion, with surroundinghematoma.Note the size of this space-occupying mass. Postoperativeviews: e horizontal, d sagittal. The tumor (cavernoma) andsurrounding hematoma was completely removed through an

311

approach between the left tonsil and uvula from the left pontomesencephalic space. The fourth ventricle was seen to have deviated as the tumor was approached through the foramen of Magendie. The patient made a complete recovery. Again, there is a striking discrepancy between the location of the lesion and the clinical findings.

312

a

4 Neurophysiology Case 4.36 A 18-yearold female who had suffered strabismus since childhood, and had a 9-month history01 mild vertigo and within 4 weeks she developed a sixth nerve palsy and minor dysdiadochokinesia on the right side. There were no other neurological deficits. MRI views: a horizontal, b sagittal, e coronal (posteroanterior view). A large lesion within the medulla oblongata. Postoperative views: d coronal, e horizontal, f sagittal. b The tumor (piloid astrocytoma, Grade 1)was completely removed from a medial suboccipital craniotomy, and an incision was made in a somewhat swollen and very thinned portion 01 the left restiform body. The tumor extended from ventrolateral into the cisterns around cranial nerves 9,10,11, and 12. The cystic portion of the tumor was xanthochromic. The patient made a complete recovery, and continues to do well 5 years after surgery. d

e

f

Cases

313

b

a

~d

e

__

Case4.37 A 20-year-old female with right arm and hand paresthesiaand discrete weakness, but no other significant neurological abnormalities.MRI views: a horizontal, b coronal (posteroanterior view),e sagittal.A large left ventrolateral medullary lesion, extendIng into the pons. Postoperative views: d sagittal, e horizontal, f coronal(posteroanterior view). The tumor (piloid astrocytoma,

f Grade J)was removed via a suboccipital paramedian craniotomy. Exposure was gained just anterior to the olive into the ventrolateral medulla. The cyst had collapsed when entered, providing space for complete tumor removal. The patient made an excellent postoperative recovery and remains asymptomatic.

314

4 Neurophysiology

a

b

e

d

Case 4.38 A 15-year-old female with headaches, vomiting, weakness of the right arm and sensory loss in the right hand. MRI views: a horizontal, b coronal (postero-anterior view), e sagittal. A large lesion in the right dorsal medulla oblongate, more on the right side. The preoperative diagnosis was hemangioblastoma. Postoperative view: d sagittal. The tumor (hemangioblastoma) had feeding ves-

seis from the PICA in the area of the calamus scriptorius, which could be safely eliminated by bipolar coagulation. The tumorwas well encapsulated, with a cystic interface against the medulla,and adequate removal was accomplished. The patient made a full postoperative recovery.

Cases

315

Case4.39 A 32-year-old male, sufferingacutepain in both the arms (ulnar) andlegs(diffuse). There was no neurologicaldelicit. MRIviews: a An intramedullarylesion, C4-C6. Exploration(cervicalhemilaminectomy C3-C6)revealed a compact intramedullary tumor, 3 cm long, and 1.5cm in diameter.There was no hematoma. The postoperative course uneventful, and there were no no neurologicaldelicits.Sixweekslater,the patientwas able to resume work as a surgeon.Histology: ependymoma, Grade11.b Postoperative MRI.

b

a Case4.40 A 35-year-old lemale with a2-monthhistory 01dysesthesia 01the leltarm,which was particularly intense distally.Carpal tunnel syndrome was initiallyconsidered, but subsequent CTandMRIstudies, a sagittal b transverse,revealedan intramedullary cysticlesion,with an associated syrinx, extendingIrom C3-D1. Neurologically nodelicitswere lound. A left hemilaminectomy over C4-C7 was perlormedand the lesion, a solid ependy-

moma Grade11, wasexploredand completelyremoved. e Sagittal d TransversepostoperativeMRI. The cyst cavityismarkedlyreduced. Uneventful postoperative course.

a

e

d

5

Clinical Considerations Operability ".. ~. ~.'I

'.

Johannes Itten Confrontation, 1916 @VG Bild-Kunst, Bonn 1993

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318

5 Clinical Considerations

General Remarks Introduction The care of patients with CNS neoplasms has changed drama tically with the advent of modern neuroimaging techniques. No longer are these patients routinely faced with the mental anguish (and physical dangers) associated with pneumoencephalography and four-vessel cerebral angiography. Today, as soon as the first image appears on the computer screen or radiographic film, neurospecialist can reach a diagnosis, contemplate a prognosis, and discuss a treatment plan. Yet it seems clear that the evaluation and treatment of braintumor patients today presents even more difficult and perplexing problems and uncertain solutions than in years pasto It is the purpose of this Chapter to explore the present state of clinical braintumor care, and to suggest alternative concepts with regard to this current dilemma.

The Era of Neuroimaging While it is certainly true that CT and MRI have significantly reduced the morbidity associated with brain-tumor evaluation, and at the same time dramatically improved the quality and quantity of immediately discernible information, it remains questionable whether these innovations have at alllightened the burden of the decision-making process (diagnosis, treatment, prognosis). In many ways, these marvelous tests lead the investigative clinician to ask more questions than he or she can answer. As an example, the precise topographic anatomy of the tumor is illustrated in three planes (sagittal, horizontal, and coronal views), forcing one to look even closer in an attempt to better understand the neurophysiological and neuropathological aspects of the neoplasm. With the potential to see the fine detail of many abnormalities using CT and MRI, our diagnostic acumen has improved to such a point that lesions are often found prior to any manifested symptoms. Huge lesions with minimal or no deficits, and small tumors with altered peritumoral topography but normal neurologic function, pose new challenges for today's neurosurgeons. No longer are "presenting deficits" always the key to locating the diseased area (or even for speculating with regard to the function of an area). Certainly, we must continue to be pragmatic in arriving at our tentative diagnoses, yet we must also look beyond the perhaps outdated concepts that form the basis of classical syndromes. Perhaps, when confronted with a large centrallesion, we should not only ask "What is the deficit?", but more importantly, "Why does the patient not have more of a deficit?" Is the deficit due only to only the primary lesion, or is it due to alterations in the cerebrovascular, cerebrospinal, neuroendocrine, neuroimmunologic, circumventricular, and parenchymal subsystems? From our general experience, a patient with a Grade IV tumor usually has more symptoms and signs than the equivalent patient with aGrade 1-11tumor, with the same type of lesion at the same location and of the same size.

The Traditional History and Physical Examination When a patient presents with a complaint attributable to the central nervous system, the traditional investigative tools must be used. The nature of the complaint must be fully assessed. Throughout the early evaluation of all patients with neurological symptoms, the most important information necessary for the inital characterization of the suspected lesion is gained from a thorough history. This is then followed by a careful physical examination performed with the pin, reflex hammer, and ophthalmoscope. Unfortunately and tragically, these simple foundations of neurologic practice (that provide such vital information) are frequently overlooked in the modern high-technology era. Historical data and physical examination findings are fundamental for the establishment of the patient's baseline medical and neurological status, and for guiding further workup. It is important to remember that the traditional neurological diagnosis for brain tumors involves the topographicallocalization of lesions based solely on these two pieces of information. In addition, the ultimate formulation of a treatment program must take into account the patient's response to the lesion,which is best noted from repeated direct interaction between the patienl and his physician. Any second-hand reliance on historical information recorded by others dramatically interferes with attempts lo provide the best treatment option recommendations. Complacency with regard to the history and physical information, dueto the easy availability of CT and MRI "objective examination" must be condemned.

The Explosion of Neuroclinical Technology and its Impact on Clinical Neurosurgery We are presently witnessing an "explosion" of new technology that permits both morphological (topographical) and physiological (functional) assessment of CNS neoplasms. The ongoing introduction of physiological tests that permit a serial assessement (preoperative, perioperative, postoperative) of brain-tumor patienls will in the future improve our clinical treatment capabilityin these patients as much, or more, than neuroimaging has improved our morphologic' abilities. As neurosurgeons, we must not only stay abreast of these developments, but we must also jump ahead oí the pack, encouraging neuroradiologists and neurophysiologists to develop the tests necessary to improve our surgicalcapabilities (Table 5.1). Ninety years ago, Cushing propelled the speciality of neurosurgery into existence by becoming the first to do exclusively nervous system surgery.For a longtime, not everyoneagreedwith this concept of specialization (in fact, there were still generalsurgeons who performed a variety of neurosurgical procedures well

General Remarks intothe 1950sand even 1960s).Once the field of neurosurgery wascIearly defined as a speciality, though, we began to discuss whetherthere should be further subspecialization, especially for CNStumors. We wondered whether some neurosurgeons should do excIusivelypituitary adenomas, others only craniopharyngiomas,or vascular surgery, or still others only acoustic neuromas. Before a consensus could be reached, however, the entire specialitywas revolutionized by the introduction of modern neurodiagnosticand treatment techniques. These new frontiers are focusingour attention on new considerations. The advent of new diagnostic modalities (especially neuroimaging)has increased the accessibility of brain-tumor diagnosis. Asa result, almost anyone can now point out the lesiono Accord-

scope of interest in CNS neoplasms has expanded to includemany other disciplines. The clinical decision-making process for these patients (traditionally within the realm of the ingly,the

neurosurgeon)has expanded today to include: Neurology Inverventional neuroradiology Radiatiotherapy Oncology Internal medicine General practice Otolaryngology Ophthalmology Skull-basesurgery Maxillarysurgery Vascularsurgery Plasticsurgery Orthopedics,etc. At present,it is not at all uncommon for patients with newly presenting(symptomatic or asymptomatic) brain tumors to be diagnosed and treated

without a neurosurgeon being consulted. This

trendproduces dangerous consequences both for the patient with a CNSneoplasm and for the discipline of neurosurgery. First,this scenario clearly suggests that surgery is not a primeconsideration in the therapeutic decision-making process for manybraintumor patients, or, if it is, judgments regarding the indicationsare left to someone other than a neurosurgeon. Both possibilitieseliminate from the decision-making process the expertiseand experience gained in the field of neurosurgery since thetimeCushingremoved his first brain-tumor. This is certainly notin the best interest either of the patient or of our profession. Second, neurosurgery cannot totally relinquish the treatmentof brain tumors to other specialists. Our previous drive towardsneurosurgical tumor-care subspecialization has been haltedbya currentneed to redefine the role of the specialityas a whole. Still,the definitions of ever-changing specialization boundariesmustnot be allowed to impede the overall care of patients. Asneurosurgeons, we must encourage the involvement of many specialistswith these patients, facilitate an exchange of ideas and concepts, encourage further developments and techniques and assist(eachother) in providing optimal brain-tumor surgical treatmen!.At the same time, though, neurosurgery must reta in (or regain)its leadership role in the clinical evaluation and treatment of brain-tumor patients.

319

Table 5.1 History of morphological and physiological neurodiagnostics Morphological (structural) studies

Physiological (functional) studies

1900 Roentgen ray 1920 Pneumoencephalography Myelography 1930 Cerebral angiography 1950 Catheter angiography 1960 Spinal angiography 1970 Computer tomography 1980 MRI, OSA

18701900

1988 MRA 1990 3D MRI, 3D MRA

1945 1950

History Physical Neurophysiological Neuro-ophthalmological Neuro-otological

1901

Spinal fluid analysis, Laboratory tests

1935

EEG, evoked pote ntials, EMG, EPG Kety-Schmidt clearance RISA-Ventriculography CSF celiular and immunological Testing ICP monitoring SPECT, PET Regional blood flow clearance, Xenon CT Resonance spectroscopy Transcranial doppler Transcranial oxymetry Functional MRI

1960 Cerebral digital angiotomosynthesis 1965 1970 1992 Echo-planar MRI 1975 1980 1985 1991 1992

examinations

The Clinical Decision-Making Process Most patients with brain tumors come for neurosurgical evaluation on the advice of a primary care specialist (family practician, internist, etc.). Upon initial evaluation (history, physical examination, and neuroimaging), a quick, initial, and tentative (but very important) diagnosis is reached, and an immediate course of action decided upon. Simply stated, this may involve: 1) Acceptance of the patient and initiation of a treatment program 2) Referral of the patient to another physician for treatment (embolization, radiotherapy, chemotherapy, etc.) 3) Conservative treatment (back to the referring physician for symptomatic pharmacotherapy, e. g., treatment of pain, seizures, etc.)' a) Palliative Therapy (nothing surgical to do) b) Expectant policy (wait and see) This key decision as to which course of action is chosen, is based entirely on two factors: time and capability. These factors are not as much concerned with the vast scope of sophisticated neuroscientific information and expertise (that we have spent our careers learning) as with the day-to-day practical aspects of patients, doctors, hospitals, and society. As a result, this timecapability decision-making concept relates to many factors: the patient (age, condition, occupation, etc.), the tumor (asymptomatic, benign, aggressive, etc.), the treatment (observe for a while or go for immediate surgery), the operating theater team (experienced, inexperienced), the neurosurgeon (level of exper-

320

5 Clinical Considerations

tise, case load), the institution (areas of interest, available beds), and so on. These are the practical day-to-day clinical concerns that clearly always enter into the early decision-making process (see Table 5.4). As part of this decision-making process, though, we must consider several other important points: First, the hope of the patient. It is clear that many (if not all) disease processes are directly affected by the patient's sta te of mind. Certainly the same must be true of brain-tumor patients. This may even be so to such a degree that future neuropsychological research will prove that it is quite significant. With this in mind, whatever our decisions as neurosurgeons, we must not take hope away from our patients. Second, the easy decision. The nature of our speciality suggests that there are no easy decisions. Modern imaging tests have made the evaluation process easier for the patient, but not for the clinical decision making process. Third, the quality of life. As physicians, we are forced to pay attention not just to the duration of life, but also to its quality. As neurosurgeons, we must consider each case on an individual basis. Our knowledge must be advanced, comprehensive, and critical, while our care for the brain-tumor patient must be simple, individual, and compassionate. Finally, the art of medicine. Clearly, the science and technology of medicine has made great advances. But has this revolution of science helped to advance the art? To advance the art of the clinical decision-making process, we must pro be other disciplines, such as history, and philosophy and religion. We must be aware that, as neurosurgeons, our decisions for today's patients reflect the state of our artoWe must hold ourselves responsible for the final decision we reach for each and every patient.

The Decision to Operate In 1935, Cairns reviewed the long-term results in a small group of patients operated upon by Cushing, and concluded "It is justifiable to operate in suitable cases." The determination of just what are "suitable cases" remains important today. The suitability of each individual's care is related to the clinical symptomotology, tumor topography and operability.

Symptomatology The interrelationships between the size of a tumor and the resultant pathophysiological disturbances (and associated neurological symptoms and signs) remain poorly understood (Table 5.2). It is easy to imagine the effects of early tumor growth. During this initial stage, the mass of the lesion produces an increased volume in the lesion component of the intracranial compartment. At this early phase, however, the volume (though increasing) is not significant enough to affect the various physiological subsystems within the brain. Exceptions include certain small tumors that produce symptoms at an early stage by direct neural compression or occlusion of CSF pathways. During final phase, the mass (volume) of the tumor is so large that widespread pathophysiological and clinical effects are produced. It is interesting to note that many tumors present with virtually none of these effects despite a considerable size. A signifi-

cant portion of craniopharyngiomas, optic gliomas, meningiomas, acoustic neuromas, epidermoids, adenomas, chordomas, gliomas, medulloblastomas, and choroid papillomas, still come to attention when already very large. This occurs because these lesions are able to attain a large volume without producing significant pathophysiological alterations and subsequent clinical symptomatology. As we try to understand the effects of these lesions we realize just how limited our knowledge is. It is considerably more difficult to analyze the affects of tumor volume during the intermediate stages of growth. Rere, an almost unlimited number of possibilities can be encountered. Some can be reasonably predicted (obstructive hydrocephalus from certain periventricular tumors), while others remain obscure (peritumoral edema). There are no reliable laboratory tests (blood, urine, CSF) to monitor this ongoing process. Still,itis essential that those caring for these patients, attempt to both recognize and predict these occurrances. Patients suffering from CNS tumors generally present in one of the following four conditions. Tumors that are life-threatening. These lesions either present with life threatening symptoms or signs (such as malignant herniation or subacute obstructive hydrocephalus), or they suggestto the examiner that this condition will occur immanently. Clearly, the size (large, gigantic), location, and growth potential of the involved tumors are largely responsible for the grave symptomatology. Emergent surgical care should be rendered without delay in these situations. Tumors that produce persistent and intolerable brain dysfunction. At presentation, these neoplasms have already producedsignificant loss of cranial nerve function (e. g., diplopia, visual field deficit, facial pare sis, dysphonia, dysphagia, dysarthria, etc.), loss of cerebral, cerebellar (ataxia, dysmetria,gait disturbance),brainstem function, or endocrine dysfunction (amenorrhea, libido. obesity, anorexia). Based solely on these symptoms, these tumors should undergo operative intervention without long delays.

Tumors that produce intermittent but recurrent symp' toms.Though neurologically intact, these patients suffer episodic neurologic dysfunction related to their neoplasm. These symptoms may include: seizures, headache, pain (trigeminal, glossopharyngeal), vertigo, tinnitus, and other neurovegetative complaints. The intermittent but increasingly intolerable symptomatology of these individualscan seriouslyinterfere withtheirprofession or lifestyle, demanding that surgical intervention be undertaken at some point in the near future. Tumors that are totally asymptomatic. With the widespread availability of imagingstudies today, many patients are foundto have tumors on tests that are obtained for other reasons.Manyof these so-called "asymptomatic" lesions are small, but some arequite large (again forcing us to question the neurophysiological basisof functional CNS abnormalities). Decisions regarding these tumors willin future be based on the development ofnewmethodsofevaluating biologic characteristics (growth potential). It should be noted, however, that many of these lesionscan easily be followed up with repeated neuroimaging. In the asymptomatic patient, this observation of the tumor over time permits an assessment of its growth tendency.

General Remarks Table 5.2 Tumors of the CNS: Possible combinations of pathophysiological and clínical effects due to the intracranial tumors

Effeet of tumor mass (dysfunetion or defieits) No Increased volumes Perilesional edema Increased ICP Displacement Herniation Hydrocephalus Ocelusive Resorptive Neurologieal defieits Papilledema Visual failure . Numerous Crama I nerves

}

. .

vanatlons

Longtraet Neurologiealsymptoms Headache Vomiting Mentalchange Changein level of eonseiousness Epilepsy

Possible

Ves

-/+

+

-/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+ -/+

+ + + + + + + + + + + + + + + +

321

Recurrent Tumors Recurrent extrinsic tumors should, for the most part, undergo repeat surgical removal, based on the criteria proposed for primary operation. However, an alternative plan for these patients, with minimal or no symptoms, is to wait and monitor any related developmentys. In the case of recurrent gliomas, the decision regarding repeat surgery, as well as on occasions following radiotherapy, is a multifactorial decision. If the recurrent tumor is at the same site, is well circumscribed and the patient and family request it, then the subsequent second or third operation can be performed. This usually has good results, with a prolongation of the patients life for some 6-12 months, or sometimes longer.

Operability Introduction In evaluating tumor patients for the first time, we try to discern the site and nature of the lesion and assess its operability (and if so, by what surgical means). We proceed through an orderly,logical decision sequence in the determination of the operability of the tumor. This is based on whatever information we have acquired from elinical observation and neuroradiological, neuropathological, and neurophysiological investigations, as previously mentioned.

TumorTopography-Its Impact on the Decision to Operate

Decision-Making Extrinsictumors. The surgical approach should be directed at totalremovalof the tumor without injury to surrounding neural, vascular,and mucosal structures, and with no leakage of CSF. It is ourbeliefthat this can be best accomplished with a microsurgical approach.As mentioned above in relation to some asymptomatic tumors,lesions of this category may deserve a period of observationand serial imaging prior to removal (see Vol IVB). Epidural and intradurallesions, however may present severe adhesionsto surrounding nerves and vessels, such that these structuresare at risk during tumor removal. As long as modern neuroimagingstudies fail to adequately define the adhesiveness of thesetumors, the advantages and disadvantages of total and subtotalremoval must be individually discussed. Intrinsictumors. Based on the opinion that most of these lesions are not curable by surgery there is widespread reluctancy tor a standardsurgical treatment. In the opinion of the senior author, most of the intrinsic tumors canand should be considered for microsurgical excision as a first¡inetreatment. Exceptions to this rule may inelude: I. Widelydiffuse or bilateral tumors, such as callosal, limbic, mesodiencephalic and brainstem area lesions, which are fortunatelyuncommonly encountered (1%). 2 Gliomatosis,Iymphomatosis, meningiomatosis also occur very rarely(0.1%) Thegeneral strategy and the surgical techniques and results of surgeryfor intrinsic tumors will be presented, in detail, in Vol ¡VB.

With the large-scale availability and routine use of noninvasive neuroimaging techniques, our previous difficulties regarding the indication and selection of treatment have actually become more complex. High-quality CT and MRI enable us to detect, at a very early stage, suspicious changes of tissue signal or density. Consequently, small (1-2 cm) moderate-sized (2-4 cm) tumors are incidentally diagnosed. Immediately, questions arise in the minds of physicians and patients alike as to what should be done. In addition, it is sometimes difficult to make a differential diagnosis between neoplastic, vascular, infectious, parasitic, or autoimmune processes. A spectrum of opinions soon follows, questioning whether the lesion is localized in a silent or nonsilent area, whether it is diffuse or not. The neurosurgeon must develop a practical concept for decision-making that is applied on an individual basis for each patient and individual tumor. The determination of operability; whether to attempt a partial, subtotal or complete resection, versus no surgery is unique in each case. The risk to benefit ratio must also be individualized for each patient. A multitud e of factors relating to the patient, to the lesion, to the availability of surgery and other treatment options, to the surgeon's level of skill and confidence, to the capacity of the hospital, and to society weigh greatly in this decision (Tables 5.3). The flow chart (Table 5.4) incorporates a few of the major factors considered in the process of determining the operability of lesions (the possible permutations and combinations being almost unlimited). This list does not even consider perhaps the most important factor as far as the individual patient is concerned: an accurate and understandable treatment plan presented by the neurosurgeon so that his or her (and the family's) informed consent can be obtained.

322

5 Clinical Considerations

Table 5.3 Factors to consider when determiningthe operability of CNStumors Patient factors (operability 01the patient) Age General clinical condition Neurological

-

condition

Grade

I-IV and "a" or "b" (a = no neuro-

logical delicits, b = neurological delicits) Symptomatology 1 Rate 01progression 2 Duration Seizures Prior therapy Patient's and lamily's desires Tumor factors (operability 01the les ion) Location and topography Neuroimaging 1 Unilateral or bilateral, supratentorial and inlratentorial, dominant and nondominant 2 Precise location Number 01lesions - single or multiple Composition 1 Size 2 Cystic, necrotic, hemorrhagic 3 Vascularization Characteristics 1 Growth a. Diffuse (local, hemispheric, global) or demarcated (circumscribed) b. Active, inactive, or alternating, progressive or regressive c. Expansive (displacement, destructive), or infiltrative 2 Classilication (assumed) a. Benign b. Semibenign c. Malignant 3 Tumor interaction a. Edema: local, regional, general b. Shift, herniation c. Presence or absence 01occlusive hydrocephalus d. Normal or elevated intracranial pressure

Table 5.4

Flow chart relating

Patient lactors

some factors considered

tumor operability

Clinical Age

General condition

Young ~

Good

~-=

Old

Tumor lactors

in determining

~

Neurological Delicits

Mental

~~~ ~

----

~No(a)

1-11

~Yes (b)

III-IV

Poor

--

Number

Neuroimaging Characterization

Behavior

Neuropathological Nature Growth

Single

Demarcated

Silent

Benign

~

~

Multiple

~

~

==-- ---=: ~

'J>Diffuse

~ Nonsilent ~

Other lactors

Other lactors

Slow

~

>< Malign --

====--=====:

Fast

Operability Yes -

Other lactors

No-

Experience.s capable

~

Adequate

Inexperienced, reler

~

Inadequate

1-11= unchanged, III-IV = changed conscious level

Societal

Hospital

Surgeon's capacity

~

:=-

~

Care I2rovided

-:

Care denied

./

}

Treatment optlons

Treatment Option

323

TreatmentOption Current Treatment Options A tumor may be considered operable but nevertheless not be operatedupon for other therapeutic reasons. If surgery is chosen, additional intervention may be indicated (e. g., adjunctive chemotherapyor radiotherapy. The options available in treating a particulartumor may be determined by the lesion and its effect on thepatient (Table 5.5). Goals.The goals of treatment-be they palliative, ameliorative, or satisfyingly cura tive-are also largely determined by the natureof the lesion and the patient's condition. In general, the ideal,immediate aim of any form of treatment is to effect a completeablation or resolution of the tumor process with no adverseaffects on the structure and function of the CNS. Also the long-termgoal is to prevent, either by surgery alone or in conjunctionwithother modalities, recurrent growth at the same or distant sites(Table 5.6).

Table 5.5 Active treatment

options

lor patients

with CNS neoplasms

Interventional,radiological procedures e. g., embolization 01 tumor arterial supply Pharmacotherapy Palliativeprocedures

Surgery Biopsy Partial

Sub-total removal Complete } Radiotherapy Conventional (external radiotherapy) Local implantation (brachytherapy) Stereotactic Proton beam - Gammaknile (radiosurgery) Chemotherapy Traditional Experimental protocols, including: intracerebra 'nd intra-arterial (withor without blood-tumor barrier modilication, Thermophototherapy Immunotherapy Genetictherapy (investigational)

Ancillaryservices Physical and occupational therapy Psychological and social services Other hospital in-patient and out-patient

services

Table 5.6 Goals 01 surgery The etiology 01neoplasms 01the CNS is unknown. In the case 01benign tumors, surgery is effective. We have to help to patients with palliative therapy. which mayoin the case 01malignant tumor, eventually result in long-term cure. Palliative therapy For increased ICP (decompression, shunt) Tumor surgery Reduction 01tumor mass effect by tumor debulking Cytoreduction and removal 01 necrotic tissue may help to reduce metabolic and biochemical effects 01the tumor This may alter the tumor growth kinetics Re establishment 01imbalanced CNS dynamics, especially 01 CSF dynamics. to help regain normal CSF circulation Reactivation 01 immunological sell-delense 01the CNS and whole body? Reduction 01the pathological effects 01the tumor Prevention 01tumor regrowth Reduction 01the size 01tumor-brain interlace in order to increase the efficacy 01nonsurgical "multimodalitytreatment" (Chemotherapy, immunotherapy, radiotherapy) Avoidance 01iatrogenic damage

Immediatetreatment 01increased intracranial pressure Externaldrainage Shuntprocedure Preoperativeembolization

Combinedtherapy - all 01 the above in various combinations pathologyand situation dictates

Curative surgery. In 1920, Dandy wrote, "There is only one satisfactory form of treatment for brain tumors, i. e., complete operative extirpation of the tumor. It is not conceivable that neoplasms of the brain ever disappear spontaneously or are cured or even benefited by any form of medical therapy." The etiology and pathogenesis of central nervous system neoplasms is stilllargely unknown, and therefore no therapy directed at the cause is currently available. Except for certain benign tumors, our attempts at curative surgery really become only palliative surgery. Still, this frequently results in a long-term remission (or cure), even for some very aggressive lesions. Presently, even with our most sophisticating imaging modalities, the precise amount of tumor that may be safely removed can only be determined at the time of operation. While our aim should always be to safely remove all tumor tissue without damage to the surrounding structures, in many situations this is not realistic. We must, however, not content ourselves too easily with the various forms of palliation, so that possible curative procedures are not even reasonably considered.

as the

324

5 Clinical Considerations

Passive careo Supportive care only (based on the individual patient's condition and lesion) may be appropriate. This may include the amelioration of pain and other symptoms with analgesics,steroids, anticonvulsants, and antidepressants, and psychological and social support of the patient and family. Observation. A delay in the therapeutic decision may be considered for several reasons: a) uncertainty as to the lesion's behavior, b) awaiting a change or improvement in the patient's general condition, and c) the patient's indecision. The relative ease of performing noninvasive CT and MRI does allow the adoption of a conservative approach involving careful follow-up. This is particularly applicable in cases of inactive, nongrowing, or slow-

growing tumors of a benign nature or in slow-growing diffuse gliomas (Case 5.0a-b). This treatment option also involves supportive care, as indicated during the period prior to eventual option selection, or until the clinical process forces a decision (e. g., emergency situations). There are definite exceptions to the practice of observation, including: tumors of foramina of Momo and fourth ventricle masses (all of which may acutely deteriorate), hemorrhagic tumors, tumors producing intractable epilepsy (especially those arising in the limbic and paralimbic areas), cranipharyngiomas, optic gliomas, meningiomas and neurinomas with progressive symptoms, and functional adenomas.

b2 Case 5.0a-b A 38-year-old female who initially suffered a transient left-sided hemiparesis 20 years ago, at the age of 17. She recovered from this with only discrete minimal residual weakness. MRI reveals a lesion within the basal ganglia, with a large cystic lesion situated in between the insula and internal capsule. No progression was demonstrated clinically or by neuroimaging and she remains asymptomatic and very active. Differential diagnosis includes dermoid and ganglioglioma. Since no guarantee could be given to remove the lesion without any additional postb4 operative deficits, she preferred to wait and see.

Treatment Option

325

AppliedMicrosurgery forExtrinsicand Intrinsic Tumors Thedevelopmentof refined microtechniqueshas contributed substantially to the surgical treatment of aneurysms and AVMS.What,then, do we see as the role of microsurgery in the treatmentof CNS tumors? Experienceover the past 26 years, has shown the microsurgical approachto be a very effective and appropriate weapon in the assaulton virtually all forms of extrinsic tumors, permitting dramaticimprovements in operative mortality and morbidity. Extrinsic tumors,particularly those in the region of the cavernous sinus, petrousbone,and parasellar and petroclival areas, seemed for a numberof years to be almost beyond the realm of surgical treatment,evenwiththe applicationof microtechniques.However, by virtueof meticulousanatomical study and persistent refinement ofsurgicalmethods, these once apparently unsurmountable barriersare being eroded. The surgical treatment of these and other basaltumors has become commonplace. Epi- and intradurallesions may be associated with a significantriskof cranialnerve injury.It is important to remember that, if thepatienthas a good chance of being cured of the tumor, or havinga usefullife prolonged, then the loss of unilateral upper cranialnerve function (1- VIII) is acceptable. On the other hand, thelossof ninth and tenth and twelfth cranial nerve function is a serious,life-threatening neurological disability for the patient. Thedecisionto remove large lesions in this area radically,subtotally,or partially should reflect this concern. Microtechnique have permitted the routine complete removalof compact and well demarcated intrinsic tumors from everypart of the brain. The removal of these tumors from even eloquentareas of the CNS is not the problem. This can be done. Usingthe physiological, pathological, radiological, anatomical, and surgical concepts presented in these volumes, the reader shouldapproach these lesions routinely with confident microsurgicalremoval.The problem with the treatment of intrinsic tumors is the nature of the tumor, the biological characteristics of the lesionsthat cause them to extend beyond the limits of microsurgeryand grow again. Even though total tumor-cell removal is not possible with present microsurgical techniques for these lesions,this approach has proved justifiable in terms of improved patientsurvivaland quality of life, and in the production of a bettersubstrate(fewertumor cells) for adjuvant therapy (Table5.8). For diffuse, infiltrating, highly malignant, or end-stage tumors,microsurgical removal can also be good treatment option. Providedthe neurological state is acceptable, it seems entirely reasonableto attempt to increase the longevity (even if for only 3-6 months)in order for the patient to afford better organization of hisor her affairs and to allow time for an adjustment to a limited future.

Table 5.8 Factors to consider in an analysis of the results of glioma surgery Mortality Neurological Morbidity (quantity, quality)

<

Survival time Quality of life Functional outcome

General Working capacity Intellectual capacity Re-establishment of personal relationships

Duration of good results Functional hazards Seizures Cosmetic result Recurrence Interval Localization Extension Change in pathological nature Age, condition of the patient

Summary In spite of the remarkable technological advances in surgery, the final clinical decision remains an enigmatic process. In this chapter the complexity of the decision-making process is generally annotated but we have to confess that both the operability of certain types of tumors, as well as those at certain locations and in certain patients, remains an open question. This should remain so. In so doing, it allows us to keep the diagnostic and treatment process open. There are still great difficulties in the diagnosis and performance of surgery. With the combination of the presented new concepts for neuroanatomy, neuropathology, neuroradiology and neurophysiology, together with the strict application of microtechniques there is, in general, a distinct improvement in the outcome for our patients. Although neuroanesthesia has significantly contributed to this overall advancement, as has intensive care and physiotherapy, in all cases this is only seen if it forms part of a concerted management between all concerned. No individual discipline can, of its own, guarantee an outcome commensurate with expectations. The remarkable reduction seen in the mortality and morbidity will be discussed in Vol. IVE. Finally in this chapter, a further 38 cases are presented in which the individual decision of whether to operate had to be considered using the principIes of the flow-chart developed in this chapter.

326

5 Clinical Considerations

Cases 5.1-5.5 5.6-5.7 5.8 5.9-5.11 5.12 5.13 and 5.16 5.14-5.15

Sphenopetroclival meningiomas Chordomas Epidermoids Optic gliomas Hypothalamic astrocytoma Large insular oligodendroglioma Parietal astrocytomas

Cases 5.17-5.19 5.20-5.27 5.28-5.30 5.31-5.32 5.33-5.34 5.35-5.38

Limbic gliomas Intraventricular tumors Mesencephalic tumors IV Ventricular tumors Pontine tumors Inoperable tumors

Sphenopetroclival Meningiomas

a

e Case 5.1 A 28-year-old female with amenorrhea and galactorrhea for two years and progressive endocrine abnormalities (despite bromocriptine treatment). MRI views (T1):a coronal, b horizontal. A large sellar, parasellar and cavernous lesion, with erosion of the sella turcica. The lesion extends into the sphenopetroclival area, and down along the clivus. It completely surrounds the right carotid artery, with narrowing of this vessel. It also extends along the sphe-

d noid wing into the anterior and middle cranial fossa and aroundboth the anterior and posterior clinoid processes. Postoperative views (1 month postoperatively): e coronal, d horizontal. The tumor (meningioma) was subtotally removed after embolization. The cavernous sinus portion was opened, but the tumor was highly vascular and adherent. No attempt was made to radically removeit. Four years postoperatively, the patient remains neurologicallyintact and particularly without cranial nerve abnormalities.

Treatment Option

a

e Case5.2 A 59-year-old man with left-sided exophthalmus and amblyopia.The patient underwent the subtotal intrathecal removal 01aninliltrativemeningioma to decompress the left optic nerve. The patient'ssymptoms remained unchanged for 12 years, at which point progressive left eye proptosis and ophthalmoplegia and hypopituitarismdeveloped. MRIviews (T1): a horizontal, b sagittal, ccoronal.A large, parasellar sphenopetroclivallesion, with bilateral invasionof the cavernous sinus. Note the tumor encasing the carotidartery within the cavernous sinus. Despite radiotherapy, embolizationof the tumor (with ligation of the internal carotid artery andextracranial-intracranial bypass), the patient's symptoms progressed.Postoperativeviews (1 month postoperatively):d coronal, e sagittal. This infiltrating meningioma was radically (but not completely)removed. Note the second tumor focus in the area of theconfluenceof the sinuses. It is clear that careful indications must beestablishedfor radical surgery, so that neurological function is notcompromisedunnecessarily. Clearly, this patient had been able tolunctionwithout deficits for a long time; this may well have not beenthe case if radical surgery had been attempted initially. Note thesecond meningioma in the torcular herophili area, which has remainedasymptomatic to the present.

327

328

5 Clinical Considerations Case 5.3 A 59-year-old male withright partial ophthalmoplegia over nine years. CT sean view: a horizontal. A large right sphenopetroclival lesion. Postoperative view (2 months postoperatively): b horizontal. The tumor (meningotheliomatous meningioma) was removed radically.The tumor was very adherent to the basal structures, and was quite bloody (despite embolization). The patient's partial ophthalmoplegia has remained unchanged for 10 years, but there are no other deficits.

a

b

Case 5.4

a

e

A 54-year-old female with headaches and no neurologicaldeficits. Neuroimaging views: a MRI(T1)horizontal, b MRI(T1)sagittal, e carotid angiography (lateral). A large right sphenopetroclival lesion. Postoperative MRI views (T1)(3 months postoperatively): d horizontal, The intrathecal parts of this adherent tumor (meningioma) were removed, but the patient suffered a temporary postoperative diplopia (which she found disturbing). Five years later, she b remained neurologically normal, with no clinical evidence of recurrence.

Treatment Option . Cases

I \\

(

1~ d

Case5.5 A 36-year-old female with dysesthesia on the right si de 01her lace, diminished hearing in her right ear, weakness and clumsinessin her right hand, and dysphasia. Neuroimaging views: a MRI (T1)coronal, b MRI (T1) sagittal, e MRI (T1) horizontal, d OSA (superiormesenteric vein view). A large right-sided petroclivallesion with compression and deviation of the basilar artery, pons, and medulla. There are no perilesional changes. Postoperative CT (contrast) (1 monthspostoperatively): e horizontal. The tumor (meningioma) was removed via the lateral suboccipital approach. The tumor was very vascular and extremely adherent to surrounding nerves and arteries.Cranial nerves 5 through 12 were stretched and displaced dorsally and inferiorly by the tumor. Oespite this, the tumor was completely removed, and the patient made a full and complete recovery (hearing intact). In the senior author's experience, this was one01the most difficult surgical cases ever experienced.

e

329

330

5 Clinical Considerations

Chordomas

Case

5.6 A 14-year-old female with diplopia (sixth nerve palsy). Neuroimaging views: a horizontal CT (contrast), b cerebral (vertebrobasilar) angiogram (lateral view). A large bilateral clivallesion that could only be partially removed via both pterional and transnasal approaches. Histology: Chordoma. The family of the patient rejected radiotherapy.

a

MRI views

(T1) (11 years later): e horizontal, d corona!. A very large tumor extending along the clivus, with total destruction of the clivus. The tumor completely surrounds the brainstem, posterior cerebral arteries, basilar artery, and cranial nerves. Despite the tremendous extension of the tumor, the patient remains active. She is the mother of two children, and works full-time as a hospital secretary. Her only symptom is minor diplopia (1992).

e

a b Case 5.7 A 50-year-old female with 10 years of headache and diplopia (right sixth nerve palsy). MRI views (T1): a horizontal, b corona!. A large lesion arising from the clivus in the right parase llar and cavernous areas, and indenting into the mesencephalon, with obliteration of the third ventricle. Postoperative view(7 months post-

e operatively): e corona!. The tumor (chordoma) was removed viathe pterional transsylvian approach. The dura was opened in the middle fissa, and the tumor was removed from the trigeminalcavity (the fifth nerve was spared). The patient remains neurologicallynormal 4 years postoperatively.

Cases

331

Epidermoid

b

e

ffiiJlL_

_,

?i_

~ffi1liffi¡;¡¡¡iilliffiii]illjif~ 21a

,

e

_

~

d

L

Case5.8 A 20-year-old man with left-sided amblyopia, bitemparal hemianopsia, and endocrine

L

abnormalities.

MRI views

(T,):

ahorizontal,b coronal, e sagittal. A huge lesion extending from the sella turcica, filling the entire parachiasmal and paramesencephalicareas, and even extending into the mesencephalon and pons.Thebrainstem is distorted and pushed distally and inferiorly,

with partial obliteration of the third ventricle. There is asevere peduncular compression. Postoperative views (1 week postoperatively): d sagittal, e horizontal, f coronal. Via a pterional approach, the tumor (epidermoid) has been completely removed. The displacement of the chiasm, optic nerve, and carotid artery has been relieved. A full recovery was made.

Optic Gliomas

a

e

Case 5.9 An 11-yearold girl with progressive anorexia, left homonymous hemianopsia, and marked visualloss (finger counting only). MRI views (T,): a sagittal, b coronal, e horizontal. A very large lesion arising from the chiasm and extending up into the foramen of Momo in the midline, with upward displacement of the lateral ventricles and posterior displacement of the mesencephalon. Postoperative views (1 week postoperatively): d sagittal, e coronal. The tumar (optic glioma) was removed via a right pterianal approach. The tumor was seen to arise from the right posterior chiasm and optic tract, and had extended inlo the frontal orbital gyri. It was removed superior lo the carotid bifurcation.

d

Postoperatively, the patient had rapid improvement in her left visual field. Neurologically there were no olher deficits.

Case 5.10 A 5-year-old mal e with progressive drowsiness, vomiting, gait ataxia, left leg weakness bilateral blindness.

a

Neuroimaging views: a horizontal MRI (T1), b horizontal MRI (T1), e sagittal MRI (T1). A huge diencephalic lesion, extending into the foramen magnum, with displacement 01the mesencephalon backwards and upwards (bilateral, left grealer than righl). Postoperab tive contrast CT (1 months postoperatively): d horizontal. The tumor (piloid astrocytoma) has been radically removed by a combined pterional- transcallosal approach (1988). Its origin was from the righl optic trae!. Postoperatively, the patient had a 3-month course 01 endocrine abnormalilies and shunt difficulties. He remains alive and well today, despite total blindness (with no need lar hormone supplemenla-

e

d tion).

Cases

333

b

a

Case 5.11 A 10-year-old female with headaches, vomiting, endocrine abnormalities, blindness, and mental changes. MRI views (T1):a sagittal, b horizontal. A huge lesion growing from the sella into the suprasellar region and filling the thrid ventricle, with obstruction of the foramen of Momo. Note the associated obstructive hydrocephalus. Pastaperative view (3 weeks postoperatively): e sagittal. The tumor (aptic gliama) has been removed through a combined transcallosal-pterional approach. Postoperatively, the patient remains blind, with a need for permanent endocrine replacement therapy. Repeat shunt procedures required. Diseaserelated death 6 months later.

334

5 Clinical Considerations

Hypothalamic Astrocytoma

a

b

e

e Case 5.12 A 25-year-old male with amblyopia attacks (Iasting 10-20 minutes) over 5 months, but no diplopia. Gait ataxia and memory changes then developed. MRI views (T1): a horizontal, b coronal, e sagittal. An irregular multicystic lesion within the third ventricle. Postoperative views (2 weeks postoperatively): d sagittal,

e horizontal, f coronal. The tumor (astrocytoma) has been removed via the transcallosal approach. The tumor seemed to arise from the left side of the hypothalamus, but was easily dissectable. The patient remains with no visual deficits or endocrine abnormalities.

Cases

335

LargeInsular Oligodendroglioma Case 5.13 A 50-yearold male, initially presenting with discrete sensory motor dysphasia, right-sided epilepsy, and a right hemiparesis. The patient had undergone two previous operations (6 years and 3 years pre-

viously),with removal 01 anaplasticoligodendrogliomalrom the left insula,and now pre-r

.

..

..

sented with recurrent

MRI viewsr. (T1):a sagittal,

!_ .

.

"\

symptoms.

a

b coronal, e horizontal. A large recurrent left insular lesion with perilesional changes and shifting 01the midline structures. d Postoperative view (3 weeks postoperatively). The recurrentanaplastic oligodendroglioma was again removed. The patient has returned to lull work, and relused radiother-

..

..=.-&.

apy and chemotherapy. This is another example lar the need lor adjuvant therapy.

d

e

ParietalAstrocytomas Case 5.14 A 37-yearold lemale with progressive headaches and diminished mental activity,but no parietallobe syndrome. The patient had undergone resection 01a large right parietal tumor 4 years alter the onset 01 epilepsy. MRIviews: a horizontal (T2)' b sagittal (T,),

a

_l.

.,

Case 5.14c-d [>

336

5 Clinical Considerations Case 5.14c coronal (T1). A large lesion involving the middle parietal lobule, with displacement of the superior and inferior parietallobules. Distortion of the brainstem. Neurologically and mentally, there were no deficits. Postoperative MRI (2 weeks postoperatively): d coronal (T1). The tumor (anaplastic astrocytoma) was radically removed, and its originallocation can now be well visualized. Following radiotherapy the patient remains neuro-

logically intact 21/2years after surgery.

Case 5.15 A 37-year-old female with a 10-year history of headaches, and a lower left quadrantanopsia. MRI views: a horizontal (T2), b coronal (T1).A large lesion involving the right middle parietallobulus, with tremendous distortion of the brainstem (but no symptoms). The patient had undergone surgery 13 years earlier for an anaplastic astrocytoma. Postoperative views (2 weeks postoperatively): e horizontal (T1, d coronal (T1). The tumor (recurrent anaplastic astrocytoma)wasradi-

cally removed, revealing its recurrent location. Followingradiotherapy,the patient remains alive and well,for3 years and neurologically intact. a

e

b

Cases

337

Temporo-Insular Oligodendroglioma Case 5.16 A 33-year-old male with a 1-month history of epilepsy, but no neurological abnormalities. MRI views: a sagittal (T2), b horizontal (T2). A well-delineated lesion extending throughout the left insula. Postoperative views (10 days postoperatively): e sagittal, d horizontal (T1). The tumor (oligodendroglioma) was totally removed from its origin in the anterior insular area and surrounding frontal and temporal opercular gyri. Postoperatively, there were no neurological and mental deficits.

a

e

b

338

5 Clinical Considerations

Limbic Gliomas Case 5.17 A 28-year-old female with progressive headaches, distinct personality changes, and a diminished ability to concentrate. MRI views (T1):a horizontal, b coronal (posteroanterior view), e sagittal, d sagittal. A well-delineated but extensive lesion in the right posterior insular area, extending medially into the hippocampus, with severe paramesencephalic and ventricular herniation (despite no corresponding symptoms). Postoperative views (2 years postoperatively): e horizontal, f sagittal, 9 coronal (postero-anterior view). The tumor (oligodendroglioma, Grade 11)was removed via a posterior b interhemispheric approach in sitting position. The originallocation of the tumor in the right posterior parahippocampal gyrus is now well seen. The patient's only residual symptom is a left inferior quadrantanopsia. Offer of radiotherapy was rejected.

a

d

e

e

f

9

Cases

339

b

e

d

Case 5.18 A 29-year-old male with epilepsy, but no neurological abnormalities. MRI views (T1): a sagittal, b coronal (posteroanterior view). A large lesion involving the left hippocampal-parahippocampal area, with herniation into the ventricular system and surrounding cisterns (asymptomatic). Postoperative views (1 month postoperatively): e sagittal, d horizontal, e coronal (anteroposterior view). The tumor (anaplastic astrocytoma) was removed via a posterior interhemispheric and pterional approaches (two sessions, 3 weeks apart). Despite radical removal, residual tumor is apparent in the area of tumor origino Following radiotherapy, the patient remains completely neurologically intact.

e

340

5 Clinical Considerations

a

Case 5.19 A 49-year-old male with a 2-year history of intermittent thirstattacks (hypothalamic) and progressive memory loss, generalized seizures, and right hemiparesis. MRI views: a horizontal (T2), b coronal (T1),e coronal (T1),d sagittal (T1),e sagittal (T1).A large bilaterallesion involvingthe limbic lobes (right >Ieft), extending into the fronto-orbitaland septal regions. Postoperative views (5 months

b

postoperatively): f-h. The tumor (oligodendroglioma, Grade 11)was subtotally removed via a right pterional approach. Residual tumor was left along the anterior portion of the cingular gyrus. Postaperatively,the patient continues to do well, with immediate improvemenl of the hemiparesis. [>

Cases

Case 5.19g-h h coronal

341

9 horizontal

h

9

Intraventricular Tumors

a

Case5.20 A 30-year-oldfemalewith dysmenorrhea, memoryloss, and left hemiparesis. Neuroimaging views:a contrastCT (horizontal),b cerebral angiogram,venous phase (lateral). A large vascular lesion, filling the third ventricle and thalamic region. This tumorwas considered to be inoperable. Postoperative contrast CT (81/2years postoperatively): e horizontal. Thetumor (fibrillary meningioma) was removed via an interhemispheric transcallosal approach. The tumor wasvery vascular (from the postetior choroidal arteries)and collagenous.A cutting cautery loop was usedto remove the tumor, but the surgery took 81/2 hours(one of the longest operations ever experienced by the senior author). The patient made a full recovery, andwas able to have children.

e

342

5 Clinical Considerations Case 5.21

A 26-yearold female with

a 1-month history 01 headaches, vertigo, cachexia, papilledema, and epilepsy. MRI views. a horizontal (T2), b coronal (T1), e sagittal (T1). A large left intraventricular lesion, extending lrom the lateral ventricle compression. Postoperative views (6 months postoperatively): d-f. The tumor (pilocytic astrocytoma, Grade 1)was completely removed via a transcallosal approach, and the patient made a

a

e

b

complete

recovery.

Cases

343

Case 5.22 A 27 -yearold lemale with subacute evidence 01 elevated intracranial pressure (headache and vertigo). MRI views (T1): a sagittal, b coronal. A dumbbell-shaped lesion, occupying the midportion 01the third ventricle and extending to the foramen 01 Monro and into the right lateral ventricle. Postoperative views (1 week postoperatively): e sagittal, d coronal. The tumor (neurocytoma) was completely removed via an interhemispheric transcallosal approach. The patient made a complete recovery.

a

e

b

""

I

-

-

-

-...1

.

d

Case5.23 A 16-yearold male who had undergone surgery 4 years previously lor strabismus. For 4 weeks, he had had progressive headaches, vomiting, and petit mal seizures. Thepatient's neurological examination was normal. CT contrast view: a horizontal. A large intraventricular lesion, extending within the left trigone, with obstructive hydrocephalus. Postoperative view (6 years postoperatively): b horizontal:The tumor (pilocytic astrocytoma) was completely removed via a posterior interhemispheric transcallosal approach. Thepatient remained completely asymptomatic11 years postoperatively.

a

-

.....iJIIII"'"

..t..

b

344

5 Clinical Considerations

a

b

e

d

Case 5.24 A 2-year-old male with a 2-month history of vomiting and temperature elevation, but no neurological abnormalities. MRI views: a sagittal spin-echo, b coronal spin-echo (postero-anterior view), e horizontal spin-echo. A giant, well-circumscribed intraventricular lesion, extending into the left parietal lobe, with herniation of the midline structures. Postoperative view (1 month

postoperatively): d horizontal (T1). The tumor (primitive neuroectodermal tumor) was removed via a sitting interhemispheric approach. Remarkably, the patient was discharged home the day after surgery, and has remained completely neurologically normal during the following 6 months.

Cases

b

a

e Case5.25 A 9-year-old female with subacute symptoms: headache,vomiting, and homonymous hemianopsia to the left side. No sensorimotorweakness. a The MRI showed a tumor of the right pulvinarthalami.The tumor was completely removed in sitting position througha posterior interhemispheric approach. Histology revealed an oligodendroglioma, Grade 11.Postoperatively there was full recovery,and improvement of the visual field defects to a left-sided inferior quadrantanospia. b The postoperative MRI showed completeremoval of the tumor. The follow-up course was, however, interrupted9 months later by subacute symptoms (Ieft-sided hemi-

345

,. -""'"

d

paresis, homonymous hemianopsia). e The CT sean shows local recurrent tumor, and a second operation was carried out. The tumor was largely necrotic, with numerous thrombosed veins in the tumor parenchyma. The histological examination confirmed a glioblastoma, Grade IV. The d postoperative CT sean. The postoperative course was uneventful. Radiotherapy was given. Three months later, there was recurrent tumor, and the patient died within the following weeks. Unusual in this case is the unexpected change of tumor type.

346

5 Clinical Considerations

-

, ¡

,jo \

,

r \ !

Case 5.26

,

A 13-year-old male with progressive somnolence,pa-

pilledema, ocular movement disorders; and weakness 01the left

e

leg. Neuroimaging views: a MRI(T,) sagittal, b OSA, lateral,e MRI (T,) horizontal. A giant pineal lesion. Postoperative view(TI): (5 months postoperatively): d CT-Scan. The tumor (embryonalcarcinoma, teratoma, or seminoma) was totally removed via a posterior interhemispheric approach. The tumor was primarily in the subsplenial region, and appeared to arise in the neighborhood 01the right pulvinar thalami. The tumor was extremely tenacious and even the cavitron ultrasonic aspirator was 01 little value in removal.The cautery loop technique was effective. The patient remainsneurologically normal 5 years postoperatively.

Cases

347

a

e Case5.27 A 17-year-old male with gait ataxia, bilateral dysdiadochokinesia,and normal eye mitility. Sensorimotor functioning was normal.The CT showed a pineal tumor. A shunt was placed, and radiotherapyapplied. The MRI showed an increase in the size of the tumor. MRI view (T1): a coronal, b sagittal: A posterior third

ventricular lesion, extending into the mesencephalon. The preoperative diagnosis was teratoma. Postoperative views (3 years postoperatively): e coronal, d sagittal. The tumor (pilocytic astrocytoma) was totally removed via an interhemispheric subsplenial approach, and the patient remains neurologically normal.

348

5 Clinical Considerations

Mesencephalic Tumors

b

d

e

Case 5.28 A fully alert and very active 35-year-old female with progressive left oculomotor paresis and right motor hemiparesis (but no other neurological abnormalities). MRI views: a horizontal (T1), b coronal (T2), e sagittal (T2).A well-circumscribed lesion within the mesencephalon and cerebral peduncle. Note the enlarged left oculomotor nerve in b. Postoperative views (2 years postoperatively): d sagittal (T1), e horizontal (T1).The tumor (piloid astrocytoma) has been completely removed. There was remarkable improvement in the hemiparesis, but unchanged third nerve palsy. She was able to return to work as a teacher. L>

Cases Case5.28 Follow-up views(5 years later): fcoronal (T1),9 sagittal (T,).The tumor has recurredin the same location,with a return of thepatient's hemiparesisoPostoperative views (1monthafter a second operation):h, i. The tumorhas again been completelyremoved, andthe patient remains healthy2 years postoperatively.It is noteworthythat the original findingof a second left oculomotornerve was dueto tumor infiltration intothe nerve.

349

9

350

5 Clinical Considerations Case 5.29 A 6-year-old male with a 6-month history of right hemiparesis (the

a

e

e

b

arm was worse than

the leg) and tremor. MRI views:a horizontal(T1), b coronal (T2), e sagiUal (T1). A large left mesencephalic lesion, with both supratentorial and infratentorial extensions. Postoperative views (3 months postoperatively): d-f. The tumor (piloid astrocytoma) was removed via a pterional and sitting supracerebellar approaches (two se ssions over 4 weeks). The tumor extended into the crura and ambiens cisterns, and was radically removed. Postoperatively, the patient had a temporary partialleft oculomotor palsy. The child continues to do well, with an improvement in the right hemiparesis despite this the repeat MRI at 1 year revealed local recurrent tumor. The decision was made by the family to have gamma-irradiation given.

Cases

a

351

b

d Case5.30 A 4-year-old male with a 2-week subacute history of left hemiparesisand right-sided ptosis. Neuroimaging views (1983): a Contrast CT horizontal, b Contrast CT corona!. A large bilateral lesionin the anterior mesencephalon (right larger than left). PostoperativeMRI views (T1) (10 years postoperatively): e sagittal, d coronal(postero-anterior view). The tumor (fibrillaryastrocytoma)

was removed via a supracerebellar approach into the dorsal lateral mesencephalon. The tumor was visible at the surface just under the right trochlear nerve, and incision in this area revealed a hemorrhagic tumor that could be excised by suction. The child made a full recovery, and has remained asymptomatic for 11 years.

352

5 Clinical Considerations

Ventricular Tumors

a

e

Case 5.31 A 2-year-old male suffering attacks of headache, gait ataxia, and Parinaud syndrome. MRI view (T1):a sagittal. A large, infiltrative fourth ventricular lesion, extending upwards into the third ventricle. Postoperative views (2 months postoperatively): b sagittal, e coronal, d horizontal. The tumor (medulloblastoma) was totally

d removed via a median suboccipital approach, with the entrance between the tonsilla and uvula. The patient made a full postoperative recovery, and returned to his home country. Radiotherapywas recommended.

Cases

353

b

e Case5.32 A 32-year-old woman with a 6-month history of gait ataxiaand pain in both ears. The ENT specialist indicated MRI investigation. The patient's only neurological deficit was a slight left hypoacusis. MRI views (T1): a sagittal, b corona!. A large, welldelineated fourth ventricular lesion, extending into the cisterna magnaand through the foramen magnum. Postoperative views (21/2

d years postoperatively): e sagittal, d corona!. The tumor (anaplastic astrocytoma) was subtotally removed via a median suboccipital approach. The tumor vas very vascular and adherent to the base of the fourth ventricle. Residual tumor was left behind to avoid injury to the hypoglossal nuclei. Following radiotherapy, the patient remains neurologically norma!.

354

5 Clinical Considerations

Pontine Tumors

b

a

e Case 5.33 A 27-year-old male, who had developed acute symptoms 10 years previously, with headache, vertigo, vomiting, ptosis, mydriasis, nystagmus and a left sixth nerve palsy. The MRI presented a pontine cavernoma, which had been declared inoperable. The patient recovered, but had suffered episodic symptoms since, with gene rally increasing ataxia, quadriparetic (wheelchair), horizontal nystagmus, and left sixth and seventh nerve palsies. Neuroimaging views: a MRI (T1)coronal, b MRI (spin-echo) sagittal, e MRI sagittal. A large pontine lesion, extending into the fourth ventricle posteriorly, but producing no hydrocephalus. Postoperative MRIviews (T1) )1 months postoperatively): d sagittal, e horizontal. The tumor (cavernoma) was removed via a median suboccipital approach, entered between the left tonsil and uvula, then into the pons through the cleft over the stria medullaris. Postoperatively, there was a remarkable improvement in his quadriparesis and ataxia, but unchanged left sixth and seventh nerve palsies.

Cases

355

b

e

e Case5.34 A 49-year-old female with progressive dysphasia over 2 years and then rapidly advancing respiratory failure, aspiration pneumonia (requiring a tracheotomy), quadriplegia, and rightsidedsixth, seventh, ninth, tenth, and twelfth nerve palsies. Neuroimaging views: a MRI (T1) horizontal, b MRI (T1) coronal (posteroanteriorview), e DSA (lateral view). A large, vascular, well-circumscribed pontine lesion extending into the fourth ventricle. Over 6 weeks,the patient's aspiration pneumonia improved, and she was

extubated and began to move her right armo Postoperative MRI views (T1) (1 month postoperatively): d coronal (postero-anterior view), e sagittal, f horizontal. The tumor (cavernoma) was completely removed. (The operation was perfomed in sitting position, with exploration through the foramen of Magendie between the right tonsilla and uvula.) The patient's sixth and eighth cranial nerve deficits remained unchanged, but all of her other symptoms improved, and she was able to resume walking.

356

5 Clinical Considerations

Inoperable Tumors

a

b

e

d

e

Case 5.35 A 36-year-old male suffering generalized seizures. MRI views: a horizontal (T2), b horizontal, e coronal (T1), d coronal, e sagittal (T1). A diffuse lesion extending from the left mediobasal temporal region to the frontal orbital area, up to septal areas and septum pellucidum, and to the right limbic lobe. Note that there are bilateral disseminations along the CSF pathways, also infratentorially. No surgery was performed, due to the wide dissemination. Radiotherapy was recommended. The patient died 6 months later. Histology: anaplastic astrocytoma.

Cases

a

357

b

Case 5.36 A 6-year-old male with an open fontanelle and progressive apathy, dysarthria, and moderate weakness in his right arm and leg. MRI views (T1).a horizontal, b sagittal. A large, diffuse lesion with bilateral thalamic involvement and unique extension into the mesencephalon and dorsal pontine areas. The parents insisted on an exploration instead of a biopsy. Postoperative view (1 week postoperatively): e A large neuroectodermaltumor(Grade IV) was partially removedfrom the right pulvinar areas. Postoperativecondition remained unchanged.The child died at home.

e

358

5 Clinical Considerations Case 5.37 A 3-year-old male with subacute gait ataxia and diplopia. MRI views: a sagittal, b corona!. Although suffering from a large, diffuse lesion with a small hematoma in the center, the child had only left-sided sixth and seventh nerve palsies, and was able to walk. Surgical removal could not be recommended due lo the bilateral extension 01 the lesion.

a

b

T

.

..... \

,

.., 't.;

...

, . '-,

,

"J,

> ...

'.4

. r'

,

Case 5.38 Another case, but with very similar localization of the tumor within the center 01the pons, elevating the bottom 01the lourth ventricle. The tumor is partiallywell circumscribed, and the ependymallayer is intact. Biopsy was perlormed in another clinic. Histology: anaplastic astrocytoma. Clinicaldala unknown (courtesy 01 Praf. Kleihues, Neurapathologicallnstitute, University01Zurich).

Final Comments

359

Final Comments

Therecent paradigmal changes in the fields of neuroanatomy, neuropathology, neuroradiology, and neurophysiology are presented and discussed in this volume. From this knowledge essential conceptsare yielded, upon which the clinical decision making process andsurgical strategy can be based. The challenge is to evolve new visions,which may break through the present barriers and traditionalways of thinking and forge a new direction. In neuroanatomy we are eminently familiar with the centuryold sectional anatomical descriptions of topography and morphologypresented in a precise but static formo Beyond this it is becomingnecessary to develop a more interactive description of the anatomy of the central nervous system, in order to embrace the various subsystems which continually operate within the brain. This milieu is made up of the dynamic interacting components within the connective fiber tracts, vascular system, CSF pathways, neurotransmitters, immune system, neuroendocrine system,and circumventricular organs system. Only by encompassingall of the various subsystems of the brain, one can develop a more dynamic and definitive, and therefore clinically relevant neuroanatomical concept. Three-dimensional images are presentiy available, and we may soon have the advantage of a fourdimensional picture to include both time and the interwoven nature of these complex neuroanatomical concepts. A dynamic neuroanatomy will provide a basis for our understanding and interpretation of the evolving neuroimaging systems. This will surelyform the basis of the continuing evolution of modern neuroanatomy. From neuropathology we have questioned the reliability of the information given us: not from the interpretation of histopathology, but in understanding the limitations of these proceduresto impart the exact information we require as surgical specialists.We see many other characteristics of tumor systems (not onlyin malignant but also benign tumors), such as aggressiveness, invasiveness,and adhesiveness, which cannot be visualized histopathologically,but which are crucial for the surgeon as well as thepatient. Another consideration is to have reliable markers for delineation of the intrinsic tumor. In the example of intrinsic tumors,observation and experience has shown us that most of these tumors behave essentially like abscesses, in that they displace neuronal fiber systems in the early phase, rather than destroythem. Thus it is possible to often completely remove these lesions.

From neuroradiology we have witnessed an equally large eclectic spectrum of change and are excited about the accessibility and impressive resolution of these electronic photographic representations. While being enthused by the usefulness of this new technology in definition, localization, and demonstration of perilesional affects of tumors upon the brain, we have also demonstrated the limits of this present modern technology (Table 3.6, p. 202, Chapter 3). Again the most significant problem for the neurosurgeon is defining the precise margin of the lesion and understanding the significance of perilesional changes (hyperintensity of white matter) without preconceived assumptions. Furthermore the neurosurgeon should consider that only surgical exploration and dissection can reveal the real construction of a tumor and its relations to the adjacent normal structures. Not even the most sophisticated neuroimaging can demonstrate these characteristics. We all realize that the mechanical effect of tumors upon the brain is insufficient in explaining the many paradoxical situations we encounter within our daily management of patients with CNS tumors. Each generation of neurosurgeons has anecdotally shown that there is no consistent relationship between the size of a particular tumor and the clinical effects it demonstrates in a given patient. Neurophysiologists have now begun to demonstrate the many biochemical factors, which are essential for normal function at a cellular and subcellular level and how they may be influenced or usurped by disease processes such as tumors. The profound effects they bave on the individual disease process is apparent. We now realize that these cases are no longer anecdotal: they can be scientifically documented and presented as part of the CNS tumor disease process. Within this volume there are 184 case presentations, with both pre- and postoperative neuroradiological scans which demonstrate the problems we readily encounter in neuroanatomy, neuropathology, neuroradiology, and neurophysiology. An equal number will be presented in Volume IVE. Innovative concepts and ideas in fundamental and clinical neurosciences are both prerequisites and challenges for us as neurosurgeons. Many of our speciality goals have come to fruition. However, extension of our intuition and insight based on previous knowledge and experience directs us to our goal of providing the best in care for our patients. This has been the intent of Volume IVA. In Volume IVB the special surgical problems of the CNS tumors will be presented. The instrumentation, laboratory training, strategies, tactics, and techniques, as well as the approaches, results, and complications will be discussed and reviewed.

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Edwards, et al.: Treatment results of juvenile pilocytic astrocytoma. J. Neurosurg. 69: 171-176,1988 Wieser, H. G, M. G. Ya~argil: Selective amygdalohippocampectomy as a surgical treatmen! of mesiobasallimbic epilepsy. Surg. Neurol. 17:445-457,1982 Wilkins, R. H., S. S. Rengachary: Neurosurgery Update 1. Diagnosis, Operative Technique and Neuro-Oncology. McGraw-Hill, Inc.. New York, SI. Louis, San Francisco 1990 Wilson, C. B.: A decade of pituitary microsurgery. The Herbert Olivecrona Lecture. 1.Neurosurg. 61: 814-833, 1984 Wright, J. E., A. A. McNab, W. 1. McDonald: Optic nerve glioma and management of optic nerve tumous in the young. Br. J. Ophthalmol. 73: 973-874, 1989 Ya~argil, M. G: Microsurgery Applied to Neurosurgery. Thieme, Stuttgart 1969 Ya~argil, M. G: Subokzipitale-transmeatale mikrotechnische Exstirpation des AkustikusNeurinomas. In: Naumann, H. H.: Kopf- und Hals-Chirurgie. Thieme, Stuttgart 1976(pp. 545-587) Ya~argil, M. G: Mikrochirurgie der Kleinhirnbrückenwinkel-Tumoren. In: Plester, D.. S. Wende, N. Nakayama: Kleinhirnbrückenwinkel-Tumoren: Diagnostik und Therapie. Springer, Berlin, Heidelberg, New York 1978 (pp. 215-257) Ya~argil, M. G: Microsurgery. AVM of the Brain. Vol. IV. A. Thieme, Stuttgart, New York 1984- I987 Ya~argil, M. G., C. D. Abernathey, A. C. Sarioglu: Microneurosurgical treatment of intracranial dermoid and epidermoid tumours. Neurosurgery 24: 561-569,1989 Ya~argil, M. G, M. Curcic, M. Kis, et al.: Total removal of craniopharyngiomas. Approaches and long-term results in 144 patients. J. Neurosurg. 73: 3-11,1990 Ya~argil, M. G, J. L. Fox: The microsurgical approach to acustic neurinomas. Surg. Neurol. 2: 393-398, 1974 Ya~argil, M. G, R. W, Mortara, M. Curcic: Meningiomas of basal posterior cranial fossa.Adv. Tech. Stand. Neurosurg. 7: 115, 1980 Ya~argil, M. G., A. C. Sarioglu, T. E. Adamson, et al.: Surgical techniques in the management of colloid cySISof the third ventricle. Adv. 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I :t.1

I

387

Index Bold numbers refer to figure legends. Vs. (versus) indicates a differential diagnosis.

A

abducens nerve, see nerves abscess effects on CNS, 275 parasplenial area, 232 purulent, temporo-occipital area, 231 thalamus, 306 acoustic neurinoma, 226 cerebellopontine angle, 240, 241, 242,288,290 vs. meningioma, 225 acoustic radiation, 68 adenocarcinoma, occipital, metastatic, 281 adenoleukodystrophy, 245 adenoma occurrence pattern, 149 pituitary, 119, 125 adherence, 147-8 absence, epidermoid tumor, 291 cerebellopontine angle acoustic neurinoma, 241 parachiasmal craniopharyngioma, 239 sphenopetroclival meningioma, 286 adhesiveness, of tumors, 147-8 adjuvant therapy, 153, 296, 306, 335, 359 adults. most common tumors, 119 Ag-NORs (antigen nucleolar organizer regions), 120 AIDS, sequelae, and imaging techniques, 201 allocortex areas, 18 introduction of term, 7 alpha-fetoprotein, 271 amblyopia with epidermoid tumor, 331 with sphenopetroclival meningioma, 327 with third ventricular astrocytoma, 334 amenorrhea, with sphenopetroclival meningioma, 326 y-aminobutyric acid (GABA), 271, 272,273 amygdala ganglioglioma, 161 pilocytic astrocytoma, 186 relationship to basal ganglia, 138 anatomy, 1-14 brain as dynamic unit, 18 cascade structure, 26 centrallobe, 44-7 cerebellum, 81-94 cerebrum, 14-80 MRI correlation, 73-80 concluding summary, 114 frontal lo be, 39-44 gyri, 20-4 and clinical examinations, 24

and imaging techniques, 2 infratentorial, 81-94 inside-out approach, 14,26,27 insular lobe, 53-7 limbic lobe, 57-64 lobar, 39-60 and lobar terminology, 17, 114 and neuroimaging, 114 occipitallobe, 49-51 parietallobe,47-9 sulci, 19-20 and MR imaging, 20 temporal lobe, 52-3 vascular, 95-113 white matter, central zone, 65-8 Anderson, w'A., 195 aneurysm, basilar, 227 angioarchitecture, cerebral venous system, 110 angiogenesis, and tumor pathology, 121 angiography, 148-9,207 cerebral, history, 194 see also MRA angioma, 303 angular gyrus, meningioma, 297 anisocoria, with sphenopetroclival meningioma, 286 anorexia, with optic glioma, 332 anosmia, with meningioma, 236 anterior choroidal artery, supply to projection fibers, 36 anterior commissure, in embryo, 10 antigen nucleolar organizer regions (Ag-NORs),120 antilocalizationalists, 250 apathy with cingulate gyrus glioblastoma, 169 with inoperable neuroectodermal tumor, 357 with meningioma, 217 with parasplenial abscess, 232 apraxia, with insular glioma, 164 arachnoid, and imaging difficulties, 204,205,206 arachnoiditis, and pseudocapsule formation, 204 arbor vitae, cerebellum, anaplastic astrocytoma, 300 archicerebellum, 82 archicortex, insular lobe, 54 archicortical are as, 18 arcuate fibers, 32 area maps, human cortex, 277 Brodmann, 69 Duvernoy, 69 von Economo, 70-2 area postrema, 266, 267 areas, of telencephalon, 18 arginine vasopressin (AVP), 266 arm, ataxia, with brainstem and cerebellar epidermoid tumor, 291 arms, connective inferior frontal gyrus, 22 superior frontal gyrus, 22

PICA,86 and cerebral tissue herniations, 252 medulla oblongata, 106 and medullary hemangioblastoma, 314 territory, 96 territory in cerebellum, 94 pituitary gland, 104 pons, 106,106, 108 posterior cerebral, see PCA above posterior communicating, see PCoA above

Arnold, F., 16 arterial supply corpus callosum, 35 projection fibers, 36 arteries, 95, 95-108 ACA, 96 basal ganglia, 102 and cerebral tissue herniations, 252 internal AChoA

capsule,

103

basal ganglia, 102 internal capsule, 103 thalamus,I03 AICA,86 and cerebral tissue herniations, 252

posterior inferior PICA above

basal ganglia, 102-3 basilar, territory, 96 brainstem, 104, 105 central, 98 central nuclei, 102-3 cerebellar tumors, blood supply, 99-101 cerebellum, 104, 105 cerebral, supply to projection fibers, 36 and cerebral tumors, 99-101 cerebrovascular system, 263 circle of Willis, 263 CNS arteriovenous system, 264 hypothalamus, 104 ICA

internal capsule, 103 medulla oblongata, 106, 107, 108 midbrain, 105, 105, 108 middle cerebral, see MCA above PCA basal ganglia, 103 and cerebral tissue herniations, 252 internal capsule, territory, 96 PCoA

103

basal ganglia, 103 thalamus, 103

see

recurrent (Heubner), putamen, 102 SCA, 86 adherence of meningioma, 286 basal ganglia, 103 pons, 106 territory, 94, 96, 97 in sulci, 98 superior cerebellar, see SCA above thalamus, 103-4 tumor vascularity, 148 white matter, 27 see also mean arterial pressure arteriovenous malformations, 207 effects on CNS, 275 aspiration pneumonia, with pontine cavernoma, 355 association areas, structure, 18 association fibers, 32, 33 in cerebral white matter, 26 cingulum and cerebral cortex, 58 association systems, 6 astrocytoma, 119, 127 anaplastic, 217 fourth ventricle, 353 fronto-orbital region, 184 hippocampus and parahippocampus, 163 inferior and middle frontal gyri, 294

medulla oblongata, 106 pons, 106 territory, 94, 96 angiogenesis, and tumor pathology, 121 anterior cerebral, see ACA above anterior choroidal, see AChoA above anterior inferior cerebellar, see AICA above

globus pallidus, 102 internal capsule, 103 internal carotid, see ICA above internal choroidal, adherence of meningioma, 286 lenticulostriate, 56, 96 leptomeningeal, in sulcus, 98 limbic and paralimbic areas, 136 MCA, 55, 96 basal ganglia, 102 and cerebral tissue herniations,

cerebellar,

252

inferior parietal lo bu le, 159 inoperable, 356, 358 insula, 166 limbic lobe, 168, 339 vs. meningioma, 218 mesencephalon, 308 neocerebral, 154 parahippocampus, 300 posterosuperior frontal gyrus, 180 temporallobe, 161, 280 cystic, posterior cerebellum, 287 diffuse, 175 effects on CNS, 275 fibrillary inferior temporal gyrus, 181 insula, 165 and hamartoma, parahippocampus, 216 hypothalamus, 334 intermediate growth phase, 133 intraventricular, 142 neocerebral, 156

388

Index

occurrence pattern, 149 parietallobe, 335-6 pilocytic, 213, 215 amygdala, 186 with dermoid cyst, 214 infratentorial area, 229, 230 internal capsule, 171, 172 intraventricular, 342, 343 parachiasmal region, 212 pontomesencephalic area, 310 precuneus, 157 retrolenticular region, 173 piloid medulla oblongata, 312, 313 mesencephalon, 309 pleomorphic, 219 temporal lo be, 282 thalamus, 176 astroglial neoplasm, 119 astroglial network, and tumor growth, 132 ataxia with cerebellopontine angle acoustic neurinoma, 241 with infratentorial dermoid tumor, 229 with infratentoriallipoma, 229 with mesencephalic anaplastic astrocytoma, 308 with mesencephalic cavernoma, 305 with multiple lesions, 187 with septal neurocytoma, 182 with tentorial meningioma, 238 aura, olfactory, with meningioma, 237 autonomic function, 267-8 autonomic system, 274 autoregulation, cerebral blood flow, 263-4 AVP (arginine vasopressin), axial sulci, 20 axon, in neurogenesis, 12

266

B Baillarger, lO.E, balance loss with parapineal 225

4 medulloblastoma,

with pontomesencephalic pilocytic astrocytoma, 310 with retrolenticular astrocytoma, 173 barriers, protective, 258 basal ganglia, 14 arterial supply, 102-3 introduction of term, 6 movements, 261 relationship to amygdala encephalon, 138 tumors, 139-42

and pros-

blood-extracellular

fluid barrier, 258

bone scanning, iso tope, 196 borderline, brainstem, 141 borders, of telencephalon, 16 boundaries, of tumors, see demarcation brain action during systole, 261 cortical zones, 127 depictions by Ecker, 5 depictions by Retzius, 6 displacement, case studies, 280-91 divisions, 14,14-15 as dynamic unit, 18 early depictions, 3-4 embryo, 9, 10 fetus, 8, 11 immunomodulation, 274 interaction with tumor, 277 maca que, 138,272 mapping, see are a maps small, see rhinencephalon subdivisions, 15 triune, 126 use of landmarks, 24 venous drainage, 109, 110 brain plate, 8 brain scanning, isotope, 196 brainstem anatomical definition, 14 blood supply, 104, 105 distortion, 282, 283, 336 with angular gyrus meningioma, 297 with middle cranial fossa meningioma, 287 with temporal fossa ganglioglioma, 285 epidermoid tumor, 291 gliomal growth pattern, 140 place in brain structure, 15 tumors, predilection sites, 142 vascular territories, 97 brain structure, history of research, 3-7 brain-tumor interface, 147-8 Broca areas, 41 and neocortical telencephalon, 18 Brodmann areas, 69-70, 126 and cuneus, 50 and lingual gyrus, 50 and neocortical telencephalon, 18 and occipital gyri, 50 and paracentral gyrus, 46 and postcentral gyrus, 47 and temporal gyri, 52 bromodeoxyuridine labeling index, 120 bronchial carcinoma, metastatic, 243 BUDR labeling index, 120 buffering system, intracranial, 254, 258-9 Burdach, E, 4 butterfly lesions, 202

Bell,c., 4 biology CNS tumors, 117 and tumor research, 116 Blalock- Taussig shunt, status after, 306 bias toma, pineal, vs. primitive neuroectodermal tumor, 224 blindness with optic glioma, 332 with sellar optic glioma, 333 see a/so visual deficits blood cerebral flow, 263 circulation in brain, 257 blood-brain barrier, 273 blood-CSF barrier, 258

e cachexia, with intraventricular pilocytic astrocytoma, 342 calcarine sulcus, 10, 19 callosal body, in embryo, 10 callosal fibers, 34 callosal sulcus, 10, 19 capsula extrema, 68 capsula interna, 65, 66 capsula externa, 65, 68 carcinoma, bronchial, metastatic, 243

cascade structure anatomical, 26 white matter, 38 accuracy in tumor localization, 122 cases, suitable, 320 case studies clinical aspects, 326-58 neuroimaging, 209-45 neuropathology, 154-91 neurophysiology, 280-315 categorization of tumors, 122-3 caudate nucleus arterial supply, 102 gliomal growth pattern, 140, 141 cauliflower substructure, cerebral white matter, 26, 27 cautery loop, for tumor removal, 341,346 cavernoma mesencephalon, 305 neocerebral, 157 parietallobule, 303 pons,311,354,355 precentral gyrus, 302 third ven tricle, 188 CBF, see cerebral blood flow cell kinetics, tumors, 120 cellular function unit, 6 cellular response patterns, in CNS, 277 central lo be, 16, 17,45,46,47 anatomy, 44-7 gyri, 46-7 insular surface, 43 projection fibers, 36 central nuclei, tumors, 139-42 central sulcus, 23, 44 continuity rate, 19 in embryo, 9 cerebellar hemispheres, 84-5 cerebellar peduncles, 82, 88, 90, 91-2 cerebellomedullary fissure, 86 cerebellomesencephalic fissure, 86 cerebellopontine angle acoustic neurinoma, 226, 240, 241, 242,288,290 chordoma, 228 differential diagnosis, 225-8 ependymoma, 227 melanoma, 227 meningioma, 225, 226 metastatic carcinoma, 227 cerebellopontine fissure, 86 cerebellum, 14 afferent pathways, 93 anatomy, 81-94 arbor vitae, astrocytoma, 300 arterial supply, 94 blood supply, 104, 105 borders, 85 connections, 92 divisions, 81 efferent pathways, 93 embryogenesis, 8 epidermoid tumor, 291 fissures, 86-7 folia, 89 hemispheres, 84-5 intrinsic tumors, predilective sites, 93,94 lobes and lobules, 81, 82, 82-3 peduncles, 88, 90, 91-2 posterior, cystic astrocytoma, 287 posterior inferior, meningioma, 288 precentrallobule, 88 projection fibers, 90 sulci, 86, 87 surfaces, 83, 84, 84 surgical divisions, 14 vascular terri tories, 97

white matter, 88, 88-93, 90 contents,90 see a/so vermis cerebral blood flow (CBF), 263 autoregulation, 263-4 cerebral cortex, 14 connections to thalamic nuclei, 36 neurophysiology, 250-1 cerebral edema pathophysiology, 255-6 types, 255 cerebral hemispheres, 14,48,56,57 borders, 16 embryogenesis, 8 gyri, 21 cerebrallobes, 16-18 cerebral perfusion pressure (CPP), 263,265,276 cerebrospinal fluid, see CSF cerebrovascular system, 262-5 tumor effects, 265 cerebrum anatomy, 14-80 MRI correlation, 73-80 summary, 69-70 surgical conception, 17 surgical divisions, 14 tumors, symptoms and signs, 251 vascular system, 95-113 veins angioarchitecture, 110 synopsis, 109 white matter, 25, 25-39 children, most common tumors, 119 cholinergic neurotransmitters, 272 cholinergic system, 272 chondroma, occurrence pattern, 149 chordoma, 330 cerebellopontine angle, 228 occurrence pattern, 149 choroid plexus, 266 intraventricular papilloma, 142 chromosome abnormalities, and tumor, 120 chromosomes, abnormal, 153 cingulate fibers, in cerebral white matter, 26 cingulate gyrus, 62, 62 anaplastic astrocytoma, 168 connective arms, 63, 64 giant-cell glioblastoma, 169 mixed oligoastrocytoma, 170 cingulate pole, 62, 63 cingulate region, cytoarchitecture, 63,64 cingulate sulcus, 44, 47 continuity rate, 19 in embryo, 10 circle of WilIis, 263 circumventricular organs (CVOs), 265-7,266 pathophysiology, 267 Clarke and Dewhurst, on history of brain research, 3-7 classification of tumors, history, 116 claustrum, 68 cleavage of tumors, see demarcation clinical considerations, 317-59 clivus, preoperative erosion, 228 CNS (central nervous system), 273-8 arteriovenous system, 264 cellular response to injuries, 277 compartments, 253 disease pathophysiology, 274-7 patterns, 149 spectrum of effects, 275 functional subsystems, 248, 249 imaging, 277 interaction with neurological disease, 276

Index interaction with tumors, 249, 277 neurotransmitters, 273 pathophysiology,274 physiology, general conclusions, 278-9 tumors, see tumors collateral sulcus, continuity rate, 19 colloid cyst, intraventricular, 142 commissural fibers, 32, 33, 34 cascade structure in white matter, 38 in cerebral white matter, 26 coursing with projection fibers, 36 dissection, 37 commissural system, embryogenesis, 10 commissure, anterior, in embryo, 10 compartments, CNS, 253 complete sulci, 20 computed tomography, see CT connective fibers limbic lobe, 57 telencephalon, 32 in white matter sectors, 29 white matter subsystems, 32-8, 33 convergence, loss, with glioblastoma, 223-4 corneal reflex, diminished, with acoustic neuroma, 289 corpus callosum, 34, 34-5, 35 and cingulate gyrus, 63 vascularization, 35 corpus cerebelli, 82 cortex area maps, 69-73 cerebral, 14 cortical are as, functional, 250 cortical blood flow (CoBF), 263 cortical surfaces, 16 corticospinal fibers, cascade structure in white matter, 38 corticospinal tract, internal capsule, 68 corticostriopallidothalamocortical fiber system, 36 corticothalamic-thalamocortical

a

fiber system, 36 CPP, see cerebral perfusion pressure cranial nerves, see nerves craniopharyngioma adherence, 148 epidural, 210 and hypothalamic function, 270 occurrence pattern, 149 parachiasmal, without perilesional changes, 239 third ventricle, 211 crossbrain, see metencephalon CSF (cerebrospinal fluid), 256-62 circulation in brain, 257 and hydrocephalus cIassification, 260 neurons,273 outflow pathways, 257 secretion, 258 CSF pathways, transcerebral, 30 CSF rhinorrhea, and bone scanning, 196 CT (computed tomography), 318 compared with MRI, 198 current neuroimaging, 197-200 emission,196-7 and functional changes, 202 history, 194-5 peritumoral changes, 146 xenon, 196 see a/so PET, SPECT cuneus, 47, 49, 50,51,62 ganglioglioma, 160 curative surgery, 323 cure genuine vs. surgical, 153 surgical, 323

Cushing, H., 318, 319 quoted,258 CVOs, see circumventricular organs cysticercosis, and imaging techniques, 201 cytoarchitecture cingulate region, 63, 64 insular lobe, 54 cytogenetic studies, 153 cytotoxic edema, 255, 255

D

discrepancies, cIinical state vs. neurological deficit, 308-15 di sioca ti o n effect, tumor imaging, caution in interpretation, 208 disorientation with glioblastoma, 223-4 with temporo-occipital purulent abscess, 231 dizziness with amygdala tumor, 161 with encephalomalacia, 235 with incisural meningioma, 222 with infratentorial dermoid tumor, 229 with internal 171

Dandy, w., 194 da Vigevano, G., 3, 4 decision-making cIinical, 319-20, 359 operability, 321-2 time-capability approach, 319 deficits, cIinical, and neuroimaging, 318 demarcation, of tumors, 146-7, 147, 151,206-7 caution in interpretation, 208 deceptiveness, 147 imaging, 203, 204-7 demyelination, CNS, 149 density changes, in imaging, and tumor infiltration, 145 dentate gyrus, 58 dermoid cyst, with pilocytic astrocytoma, 214 dermoid tumor cystic, frontallobe, 292 effects on CNS, 275 infratentorial, 229 occurrence pattern, 149 de Vieussens, R., 3 diabetes insipidus, and pineal tumors, 271 diagnosis, traditional methods, 318 diaphragma sella e, restraining pituitary adenoma, 125 diaschisis, 250 diencephalon, 14 embryogenesis, 8 piloid astrocytoma, 332 place in brain structure, 15 differential diagnosis cerebellopontine angle, 225-8 meningioma vs. glioblastoma, 217-20 neoplastic vs. other disease processes,231-5 neuroimaging, 209-35 parapineal tumors, 221-4 perilesional changes, 235-45 diplopia with acoustic neurinoma, 290 with angular gyrus meningioma, 297 with cingulate gyrus glioblastoma, 169 with cIival chordoma, 330 with fourth ventricular tuberculoma, 233 with fronto-orbital glioblastoma, 167 with infratentoriallipoma, 229 with inoperable tumor, 358 with internal capsule astrocytoma, 171 with intraventricular lesion, 220 with pleomorphic xanthoastrocytoma, 301 with plexus papilloma, 223 with primitive neuroectodermal tumor, 224 with septal neurocytoma, 182

capsule

with parapineal 225

astrocytoma,

medulloblastoma,

with parapineal meningioma, 221 with pilocytic astrocytoma, 213 with primitive neuroectodermal tumor, 224 with temporal fossa anaplastic ganglioglioma, 285 drinking, 270 drowsiness with diencephalic piloid astrocytoma, 332 with thalamic abscess, 306 see a/so fatigue; sleep attacks; somnolence dura and imaging difficulties, 204, 205, 206 not visible on neuroimaging, 210 Duvernoy, area map, human cortex, 69 dysacusis, with limbic lobe astrocytoma, 166 dysarthria with inoperable neuroectodermal tumor, 357 with pilocytic astrocytoma, 172 dysdiadochokinesia with intraventricular astrocytoma, 347 with limbic lobe astrocytoma, 168 with medullary piloid astrocytoma, 312 with parietal glioblastoma, 295 with retrolenticular astrocytoma, 173 dysesthesia facial with cerebellopontine angle chordoma, 228 with cerebellopontine angle melanoma, 227 with cerebellopontine angle meningioma, 225, 226 with endotheliomatous meningioma, 242 with sphenopetroclival meningioma, 329 with limbic lobe astrocytoma, 166 with parietallobule cavernoma, 303 with superior parietallobule tumor, 156 dysmenorrhea, with intraventricular fibrillary meningioma, 341 dysmetria with cerebellar meningioma, 288 with infratentorial dermoid tumor, 229 with parapineal 225

medulloblastoma,

with pontomesencephalic pilocytic astrocytoma, 310 with retrolenticular astrocytoma, 173 with superior temporal gyrus oligoastrocytoma, 299

389

dysphasia with anaplastic astrocytoma, 217 improvement after surgery, 172, 214 with insular glioblastoma, 178 with neocerebral tumor, 159 with parahippocampal anaplastic astrocytoma, 300 with parietal glioblastoma, 295 with parietallobule astrocytoma, 218 with pontine cavernoma, 355 sensorimotor, with insular oligodendroglioma, 335 with sphenopetroclival meningioma, 329 with superior temporal gyrus oligoastrocytoma, 299 with Sylvian fissure meningioma, 235

E eating behavior, 268, 270 echo-planar MRI, 197 Ecker, A., 4 Economo, C. von, 6, 7, 114 area maps, human cortex, 70-2 ectoderm, 8 edema cerebral, pathophysiology, 255-6 cytotoxic, 255, 255 hydrostatic, 256 interstitial, 255, 256 neuroimaging, 200, 243-4 peritumoral,148 and tumor pathology, 121 vasogenic, 255, 255 eloquent areas, lack of expected deficits, case studies, 292-300 embryo, brain, 9, 10 embryogenesis, 8 embryology, 8-13 and cortical structure, 18 encapsulation, of tumor, 147 encephalitis, effects on CNS, 275 encephalography, contrast, history, 194 encephalomalacia, 237 vs. glioma, middle frontal gyrus, 235 encephalon, see brain endbrain, see telencephalon endocrine abnormalities with epidermoid tumor, 331 postoperative, 332 with sellar optic glioma, 333 endotheliomatous meningioma, pontomedullary junction, 242 environmental factors, and primary brain tumors, 119 ependymoma cerebellopontine angle, 227 intraventricular, 142 medulla oblongata, 315 occurrence pattern, 149 epidemiology, 119 CNS tumors, 117 and tumor research, 116 epidermoid tumor, 331 brainstem, 291 cerebellum, 291 effects on CNS, 275 occurrence pattern, 149 epilepsy effects on CNS, 275 focal, with parietallobule cavernoma, 303 with fronto-orbital anaplastic astrocytoma, 184

390

Index

grandmal with diffuse oligoastrocytoma, 175 with inferior temporal gyrus astrocytoma, 181 with multiple lesions, 188, 190 with superior frontal gyrus tumor, 154 with superior temporal gyrus oligodendroglioma, 298 with temporallobe astrocytoma, 161 with temporallobe glioblastoma, 177 with inferior parietallobule tumor, 159 with insular oligodendroglioma, 335 with intraventricular pilocytic astrocytoma, 342 lacksonian with inferior frontal gyrus tumor, 155 with local thrombophlebitis, 307 with precentral cavernoma, 302 with recurrent anaplastic astrocytoma, 180 with limbic anaplastic astrocytoma, 339 with metastatic bronchial carcinoma, 243 with oligodendroglioma, 337 with opercular glioblastoma, 179 partial complex, with temporal lobe astrocytoma, 282 petit mal with cingulate gyrus oligoastrocytoma, 170 with fourth ventricular tuberculoma, 233 with septal oligodendroglioma, 209 with temporallobe xanthoastrocytoma, 162 with temporal fossa anaplastic ganglioglioma, 285 with thalamic astrocytoma, 176 Erasistratus of Alexandria, 3 erb-b 2 oncogene amplification, 120 Ernst, R., 195 examination, 318 exophthalmus, with sphenopetroclival meningioma, 327 external capsule, 65, 68 extraceJlular fluid (ECF), 256 extrinsic tumors biology, 151 categories, 124 definition, 122 demarcation, 204-5 growth patterns, 123-5 and herniation, 253 imaging, 203 vs. in trinsic infratentorial area, 228-30 parachiasmatic area, 209-17 microsurgery, 325 neuropathology, 123-4 sudden aggression, 145 topography, clinical considerations, 321

F facial dysesthesia with cerebeJlopontine doma, 228 with cerebeJlopontine melanoma, 227

angle chorangle

with cerebeJlopontine angle meningioma, 225, 226 with endotheliomatous meningioma, 242 with sphenopetroclival meningioma, 329 facial nerve, see nerves falx, meningioma perilesional changes, 245 vs. tuberculoma, 233 fatigue with internal capsule astrocytoma, 171 with parahippocampal anaplastic astrocytoma, 300 with pulvinar thalami glioblastoma, 183 see a/so drowsiness; sleep attacks; somnolence fetus, brain, 8, 11 fibers, in cerebral white matter, 26

25,

fibrillary astrocytoma, mesencephalon, 351 fibroma, occurrence pattern, 149 fissure of Rolando, 4, 16 fissures cerebeJlar, 82, 86-7 see a/so Sylvian fissure Flechsig, P.E., 6 flocculonodular lobe, 82 flow cytometry, 120 flow voids, MRI, and tumor vascularity, 148 folia, cerebeJlum, 90 food intake, 268, 270 foramen of Magendie, 87 forebrain, see prosencephalon Forel, A., 6 forgetfulness, progressive, with multiple lesions, 186 fornix embryogenesis, variations, 35 fossa

10

middle cranial, meningioma, 287

283,

temporal, anaplastic ganglioglioma, 285 Fourier NMR spectroscopy, 195 fourth ventricle, 87 anaplastic astrocytoma, 353 deviation with pontine cavernoma, 311 displacement, 291 in embryo, 10 lipoma, 229 meduJloblastoma, 352 plexus papilloma, 228 tuberculoma, 233 tumors, 144, 352-3 frontal area, meningioma, 217 frontal gyri, 21, 40 gyrus rectus, 43, 62 variations, 44 inferior, 22, 41, 41 anaplastic astrocytoma, 294 low-grade glioma, 292 meningioma, 293 orbital part, 21, 22 specimen after removal, 43 transverse gyri, 41 triangular part, 21, 22, 294 variations, 42 see a/so opercular medial, 41, 62 middle, 22, 40, 41, 41 anaplastic astrocytoma, 294 glioma vs. encephalomalacia, meningioma, 293 variations, 42 orbital gyri, 43

parietal operculum, oligoastrocytoma, 299 superior, 22, 40, 40, 41, 45 anaplastic astrocytoma, 154, 180 transverse gyri, 41 frontal lo be, 16,17,22 anatomy, 39-44 and Brodmann areas, 69 cystic dermoid tumor, 292 insular surface, 43 MRI anatomical correlation, 78-9 projection fibers, 36 surface, 39 vascularization, 102 frontal poi e, in embryo, 10 frontal sulcus inferior, continuity rate, 19 intermedia te, incidence rate, 19 medial, incidence rate, 19 superior, continuity rate, 19 frontal syndrome, with cystic dermoid tumor, 292 fronto-orbital gyri, variations, 44 fronto-orbital region anaplastic astrocytoma, 184 glioblastoma, 167 frontopontine fibers, casca de structure in white matter, 38 functional disturbances, and hypothalamic disturbance, 270 fusiform gyrus, see temporo-occipital gyrus, lateral

G GABA (y-aminobutyric acid), 271, 272,273 gadolinium DTPA contrast, 199 gait abnormality, with oligoastrocytoma, 299 gait apraxia with cerebeJlar cystic astrocytoma, 287 with cerebeJlopontine angle acoustic neuroma, 289 gait ataxia with brainstem and cerebeJlar epidermoid tumor, 291 with cerebeJlar meningioma, 288 with cerebeJlopontine angle acoustic neurinoma, 290 with diencephalic piloid astrocytoma, 332 with fourth ventricular anaplastic astrocytoma, 353 with fourth ventricular meduJlo-

235

blastoma, 352 with infratentorial pilocytic astrocytoma, 229 with inoperable tumor, 358 with intraventricular pilocytic astrocytoma, 347 with mesencephalic piloid astrocytoma, 309 with third ventricular astrocytoma, 334 galactorrhea, with sphenopetroclival meningioma, 326 GaJl, EJ., 6 ganglioglioma amygdala anaplastic vs. meningioma, 285 temporal fossa, 285 cuneus, 160 occurrence pattern, 149 Gd-DTPA,199 genetic expression, tumors, 120-1 two-hit concept, 126, 153

genu of internal capsule, 66 germinoma, 271 Gerstmann's syndrome with inferior parietallobule tumor, 159 with parieto-occipital cerebral infarction, 234 Glasgow coma score, 259 glial cell, embryogenesis, 12-13 glia limitans, 123 glial systems, 250-4 glioblastoma vs. abscess parasplenial area, 232 parietallobe, 231 diffuse, 174 effects on CNS, 275 fronto-orbital region, 167 giant-ceJl, cingulate gyrus, 169 growth phases intermediate, 132, 133 late, 134 inferior parietallobule, 295 insula,178 vs. meningioma, 217-20 multiple, 184, 185 neuroimmunotherapy, 274 occurrence pattern, 149 peritumoral changes, 146 precuneus, perilesional changes, 244 pulvinar thalami, 183, 345 perilesional changes, 244 vs. purulent abscess, temporooccipital area, 231 superior temporal gyrus, 296 temporal lo be, 177, 284 vs. teratoma, 223-4 glioblastoma multiforme, 119, 121 histologic diagnosis, 183 survival in grade IV, 121 see a/so astrocytoma glioblastomas, adherence, 148 glioma, see tumors and specific tumor types globus paJlidus, arterial supply, 102 glomus tumor, occurrence pattern, 149 Golgi, c., 6,116 granuloma, and imaging techniques, 201 Gratiolet, L.P., 4, 46 gray matter, 14 great horizontal fissure, cerebellum, 86 growth kinetics, tumors, 119-20 gyral convolutions, embryogenesis, 8 gyralsegments,28,28,29 vascularization pattern, 30 gyralsegmentscheme,24 gyri anatomy, 20-4 and clinical examinations, 24 areas for MRI analysis, 73 centrallobe, 46 in cerebral hemisphere, 21 continuum concept, 24 frontallobe, classification, 40 hemispheric, features, 24 interdigitations,21 and lobes, 16, 17 occipital, 49-51 temporallobe, 52 transverse, 23 in frontal sulci, 22 types, 20 vascularization, 102 see a/so specific gyri gyrus rectus, 43, 62 variations, 44

Index

H

hemangioblastoma medulla oblongata, 314 occurrence pattern, 149 hematoma

Haemophilus parainfluenzae, and thalamic abscess, 306 hamartoma, effects on CNS, 275

effects on CNS, 275 thalamus, 304 hemianopsia bitemporal, with epidermoid tumor, 331 with multiple lesions, 187 with optic glioma, 332 with parachiasmal astrocytoma, 212

hamartoma-astrocytoma, parahippocampus, 216 Harvey, W., 112 headache abscess, thalamic, 306 acoustic neurinoma, 226 adenocarcinoma metastatic occipital, 281 temporal poI e, 243 astrocytoma cerebellar cystic, 287 diffuse anaplastic, 179 infratentorial pilocytic, 230 intraventricular pilocytic, 342, 343 limbic lobe, 168 mesencephalic anaplastic, 308 mesencephalic piloid, 309 parietal anaplastic, 335-6, 336 recurrent anaplastic, 180 temporal lo be, 280 cavernoma, pontine, 311, 354 chordoma, clivus, 330 craniopharyngioma, third ventricle, 211 dermoid tumor, infratentorial, 229 encephalomalacia, 235 ganglioglioma, temporal fossa, 285 glioblastoma, 223-4 cingulate gyrus, 169 diffuse, 174 fronto-orbital, 167 multiple, 184 parietal, 231 precuneus, 244 superior temporal gyrus, 296 temporallobe, 284 hemangioblastoma, medullary, 314 hypernephroma, metastatic, 243 intraventricular lesion, 220 lipoma, infratentorial, 229 medulloblastoma, fourth ventricle, 352 meningioma angular gyrus, 297 falx, 245 incisural, 222 middle cranial fossa, 287 parapineal, 221 sphenopetroclival, 286, 328 temporal pole, 244 tentorial, 238 multiple lesions, 186, 187 neurocytoma, intraventricular, 343 oligodendroglioma, 219 limbic, 338 pulvinar, 345 optic glioma, sellar, 333 plexus papilloma, 223 infratentorial, 228 primitive neuroectodermal 176,224

tumor,

telangiectasia, thalamic, 304 xanthoastrocytoma, pleomorphic, 301 hearing deficit acoustic neurinoma, cerebellopontine angle, 290 acoustic neuroma, cerebellopontine angle, 288, 289 with epidermoid tumor, brainstem and cerebellum, 291 with sphenopetroclival meningioma, 329 see a/so tinnitus

with parachiasmal craniopharyngioma, 239 with parieto-occipital cerebral infarction, 234 with pilocytic astrocytoma, 215 with pulvinar glioblastoma, 183 with pulvinar oligodendroglioma, 345 after surgery for fibrillary astrocytoma, 181 with temporal fossa anaplastic ganglioglioma, 285 with temporallobe glioblastoma, 177,284 with tentorial meningioma, 238 hemihypesthesia, with thalamic tela ngiectasia, 304 hemiparesis with cerebral infarction, 234 with insular oligodendroglioma, 335 with intraventricular fibrillary meningioma, 341 with limbic oligodendroglioma, 340 with mesencephalic anaplastic astrocytoma, 308 with mesencephalic cavernoma. 305 with mesencephalic fibrillary astrocytoma, 351 with mesencephalic piloid astrocytoma, 348-9, 350 with pilocytic astrocytoma, 215 with pontomesencephalic pilocytic astrocytoma, 310 postictal with parietal glioblastoma, 295 with precentral cavernoma, 302 with pulvinar thalami glioblastoma, 183, 244 with temporal fossa anaplastic ganglioglioma, 285 with temporo-occipital purulent abscess,231 with thalamic abscess, 306 hemispheres cerebellar,84-5 cerebral, see cerebral hemispheres hemorrhage, acute, case studies, 301-7 Henson's node, 8 herniation, 251-4, 260 extra-axial, 253 frontal areas, 253 intra-axial. 253 severe without neurological deficits, 283 with temporallobe glioblastoma, 284 syndromes, compartments involved, 201 tonsillar, with cerebellar cystic astrocytoma, 287 Heschl's gyri, 21, 23 anaplastic oligodendroglioma, 298 hindbrain, see rhombencephalon hippocampo-mamillo-thalamocingulate circuito 58

hippocampus, 18, 58 anaplastic astrocytoma, 163 embryogenesis, 8 His, w., 6 histology and cortical structure, 18 difficult cases, 188-91 primitive neuroectodermal tumor, 191 histopathology, interpretation, history brain research, 3-7

359

neurodiagnostics, 319 neuroimaging, 194-7 neuropathology, 116 see a/so patient history Hodgkin's disease, 307 human chorionic gonadotropin, 271 Huschke, E., 4, 46 Huxley, T.H., 4, 46 hydrocephalus classification, 260 with mesencephalic anaplastic astrocytoma, 308 with septal neurocytoma. 182 with third ventricle craniopharyngioma, 211 hydrostatic edema, 256 hypacusis, with cerebellopontine angle acoustic neurinoma, 240 hyperdensity, tumor imaging, caution in interpretation, 208 hyperintensity, tumor imaging, caution in interpretation. 208 hypernephroma, metastatic, 243 hypesthesia, facial with cerebellopontine angle acoustic neuroma, 289 with metastatic carcinoma, 227 hypoacusis with cerebellopontine tic neurinoma, 241 with cerebellopontine doma, 228

angle acousangle chor-

with cerebellopontine angle melanoma, 227 with cerebellopontine angle meningioma, 225 with metastatic carcinoma, 227 hypodensity. tumor imaging, caution in interpretation, 208 hypothalamic-limbic connections. 270 hypothalamus, 267-70, 269 arterial supply, 104 astrocytoma, 334 in embryo, 10 and functional disturbances, 270 lateral nuclear area, 270 pathophysiology, 270 regulatory mechanisms, 268 ventromedial nucleus, 270

391

immune response, to tumor growth, 127. 128 immune system, 273-8 pathophysiology, 274 immunohistochemistry, 153 immunomodulation, brain, 274 immunoregulators, 273-4 immunosuppressors, 121 impotence, with third ventricle craniopharyngioma, 211 incontinence, with paracentral gyrus tumor, 157 infarction, cerebral vs. glioma, 234 vs. precentral gyrus tumor, 234 infection, and imaging techniques, 201 infectious disease, CNS, 149 infiltration. of tumors, 144-5 adventitial, 148 infratentorial anatomy, 81-94 infratentorial area dermoid tumor, 229 extrinsic vs. intrinsic tumors, 228-30 lipoma, 229 pilocytic astrocytoma, 229, 230 plexus papilloma, 228 infratentorial structures, cerebral tissue herniations, 252 infundibulum, in embryo, 10 inoperable tumors, 341, 356-8 insula, 23 fibrillary astrocytoma. 165 glioblastoma, 178 mixed glioma, 164 oligodendroglioma, 335, 337 pleomorphic xanthoastrocytoma, 301 posterior, 299 insularlobe, 16,17.54,55 anatomy, 53-7 cytoarchitecture, 54 projection fibers, 36 interbrain, see diencephalon intermediate su1cus, 47 internal capsule, 65, 66-8 arterial supply, 103 genu,66 pilocytic astrocytoma, 171

topography of projection fibers, 67 tumors. case studies, 171-2 vascularization, 68 interparietal superior su1cus, 47 interstitial edema, 256 interstitial fluid, see ISF intracranial buffering system, 258-9 intracranial pressure, see ICP intraparietal su1cus, continuity rateo 19 intraventricular tumors, 142-4,341-7 sites of origin, 143,220 intrinsic tumors, 122-3 biology, 151-3 definition, 123 demarcation, 205 and herniation, 253, 254

lCP (intracranial pressure), 259-62 elevated, 260-2 with intraventricular neurocytoma, 343 and hydrocephalus classification, 260 monitoring. 259 normal, 259-60 pressure-volume curve. 261 thresholds, 260 imaging, density changes, and tumor infiltration, 145 imaging, see neuroimaging immune cells, 273

imaging, 203 initial sites, 130 microsurgery. 325 phylogenetic restriction, 135 predilection sites, 125-7 and primary sulci, 145 resembling abscesses, 359 site of origin, 135 spherical growth, 152 topography, clinical considerations, 321 ischemic infarct, effects on CNS, 275 ISF (interstitial fluid), 256-8 secretion, 257-8 turnover, 256

392

Index

island of Reil, 4 isocortex homotypical, 18 insular lobe, 54 introduction of term, 7 structure, 18

K Kolliker, R.A. von, 4

L lamina terminalis in embryo, 10 organum vasculum, 266-7 landmarks, in brain, 24 language deficit absence, with superior temporal oligodendroglioma, 298 with anaplastic astrocytoma, 217 with frontal gyrus anaplastic astrocytoma, 294 improvement after surgery, 155, 159,172,214 with insular mixed glioma, 164 with limbic lobe astrocytoma, 166, 168 with mesencephalic 305

cavernoma,

with opercular glioblastoma, 179 with parahippocampal anaplastic astrocytoma. 300 with parietal glioblastoma, 295 with parietallobule astrocytoma, 218 with pilocytic astrocytoma, 214 with sphenopetroclival meningioma, 329 with superior temporal gyrus glioblastoma, 296 with Sylvian fissure meningioma, 235 with tentorial meningioma, 238 lateral occipital sulcus, incidence rate,19 lateral ventricle and internal capsule projection fibers, 65, 66 tumors, 143 leakiness, tumor vessels, 148 lesions, see tumors leukemia, and local thrombophlebitis, 307 leukodystrophy, and imaging techniques, 201 limbic area, vascular anatomy. 136 limbic lobe, 16, 17, 18 anatomy, 57-64 and Brodmann's areas, 69 connective fibers. 60 cortical areas, 59 glioma, 338-40 nuclei, 60 projection fibers, 36 semicircular connections, 59 tumors, 136-9 case studies, 161-70 limbic-paralimbic system, cortical and nuclear connections, 137 limiting sulci, 20 lingual gyrus, see temporo-occipital gyrus, medial lingula, cerebellar, 83 lipoma, infratentorial, 229 lip smacking, with amygdala tumor, 161

lobar terminology, 17, 114, 151 inadequacy in neuroimaging, 209 lobes cerebellar. 81, 82-3 cerebral, 16-18 anatomy, 39-60 limbic.18 paralimbic. 18 vascularization, 102 lobules cerebellar. 81. 82, 82-3 parietal,47-8 localizationists, 250 localization system, stereotactic, 24 lues, effects on CNS. 275 lunate sulcus in embryo, 10 incidence rate, 19 Iymphoma B-cell, common location. 201 occurrence pattern, 149 Iymphomas, adherence, 148

perilesional changes, 245 fibrillary, intraventricular, 341 fibroblastic, 222 vs. glioblastoma, 217-20 intraventricular, 142 meningoendotheliomatous, 236 middle and inferior frontal gyri, 293 occurrence pattern, parapineal, 221 without perilesional 238

149 changes, 236,

peritumoral changes, 146 vs. pilocytic astrocytoma, 229 in planum sphenoidale, 125 posterior inferior cerebellum, 288 vs. sarcoma, 222 with severe perilesional 237

M macaque brain, 138, 272 macrophage colony-stimulation tors, 274

falx, 187

fac-

magnetic encephalography, 197 magnetic resonance, see MRA; MRI malignancy, assessing. 120 mamillary body. 58 MAP, see mea n arterial pressure maps. see area maps maxillary pain, with parahippocampal anaplastic astrocytoma, 300 mea n arterial pressure (MAP), 263. 265 medulla oblongata (myelencephalon). 14 arterial supply, 106. 107, 108 in embryo, 10 embryogenesis, 8 ependymoma, 315 hemangioblastoma, 314 piloid astrocytoma, 312, 313 place in brain structure, 15 medullary compression, 229 with cerebellar meningioma, 288 medullary substance, 14 medulloblastoma, 119 fourth ventricle, 352 occurrence pattern, 149 and primitive neuroectodermal tumor, histology, 191 MEG (magnetic encephalography), 197 melanoma, cerebellopontine angle, 227 melatonin, 271 memory loss with intraventricular fibrillary meningioma, 341 with limbic oligodendroglioma, 340 with Sylvian fissure meningioma, 235 with temporal fossa anaplastic ganglioglioma, 285 meningioma, 119 vs. acoustic neurinoma, 225 vs. anaplastic astrocytoma, 218 vs. anaplastic ganglioglioma, temporal fossa, 285 vs. anaplastic oligodendroglioma, histologic diagnosis, 189 angular gyrus, 297 cerebellopontine angle, 225 effects on CNS. 275 endotheliomatous, pontomedullary junction, 242

multiple sclerosis effects on CNS. 275 and imaging techniques, 201 and parieto-occipital cerebral infarction. 234 myc-n oncogene amplification, 120 mydriasis. with pontine cavernoma. 354 myelencephalon, see medulla oblongata myelin, 25 myelinization, in neurogenesis. myelography, 207

13

changes,

sphenoid, 188 sphenopetroclival, 286, 326-9 temporal pole, perilesional changes, 244 vs. tuberculoma, falx, 233 meningiomas, adherence, 147 meningitis, effects on CNS, 275 mesencephalon. 14 anaplastic astrocytoma, 308 arterial supply, 105, 105, 108 cavernoma, 305 compression and distortion, 286 embryogenesis, 8 piloid astrocytoma, 309 place in brain structure, 15 topography of projection fibers. 67,68 tumors, 348-51 mesocortex, areas, 18 metabolic diseases, effects on CNS, 275 metastasis, occurrence pattern. 149 metencephalon, 14 embryogenesis, 8 place in brain structure, 15 Meynert. T., 6 microglia, 276 midbrain, see mesencephalon middle cranial fossa, meningioma, 283,287 migraine with cuneus tumor, 160 with parietallobule cavernoma, 303 with septal neurocytoma, 182 Moniz, E., 194 monoaminergic neurotransmitters, 272 monoclonal antibody Ki-167, 120 Monro-Kellie hypothesis, 277 morphology CNS tumors, 117 of lesions, imaging, 200 motor function loss, with anaplastic astrocytoma, 217 MRA (magnetic resonance angiography), 148, 149, 194,197,207 MRI (magnetic resonance imaging), 318 and anatomy, 114 compared with cr, 198 contrast, 199-200 correlation with cerebral 73-80

and sulcal anatomy, 20 and three-dimensional anatomy, 25 triplanar, 208 and tumor consistency, 147 multicentric tumors. 150-1

anatomy,

disadvantages, 208 echo-planar, 197 functional studies, 199, 200, 202 history, 195 image selection, 198-9 interpreting weighted images, 199 peritumoral changes, 146 recent improvements, 200

N neck pain, with endotheliomatous meningioma, 242 neocerebellum, 82 tumors, 129-35 neocerebral tumors, 129-35 case studies, 154-60 neocortex, histogenesis, 13 nerves abducens (sixth), palsy, 223, 227. 291,310.311.312.330,354 cranial displacement, 291, 329 palsy, 355 facial (seventh), 226 palsy, 291 oculomotor (third) adherence of meningioma, 286 palsy, 213 optic (second), in embryo. 10 trigeminal (fifth) dysfunction, 226 neurinoma, 290 neuroma vs. melanoma. 227 neural plate, 8 neural systems, 250-4 neurendocrine system, 267-71 neurinoma acoustic, 226 cerebellopontine angle, 240, 241,242,290 vs. meningioma, 225 adherence, 148 occurrence pattern, 149 trigeminal, 290 neuroanatomy, and neuroimaging systems, 359 neuroclinical technology, 318-19 neurocytoma intraventricular, 142 septum pellucidum, 182 neurodiagnostics, history, 319 neuroectodermal tumor inoperable, 357 primitive, 176 neuroembryogenesis, 8-11 neuroendocrine system, pathophysiology, 271 neurogenesis, 12, 12-13 neuroglia migration pathway, 30 origin of term, 116 neuroglial cells, 250 neurohypophysis, 266 neuroimaging, 193-245,318 application to CNS tumors, 200-1 case studies, 209-45 cautions for interpretation. 208 current methods, 197-200

Index

cystic changes, 208 diagnostic accuracy, 209 differential diagnosis, 209-35 difficulties, 202-7 overreading, 203 topographic, 203 discrepancies from clinical state, case studies, 308-15 edema, 243-4 four-dimensional, 359 functional changes, 202 history, 194-7 image intensity, 208 interpretation cautions, 208 weighted MRI images, 208 limitations, 202-7 perilesional changes, 235-42 peritumoral changes, 208 postoperative, 201 specificity, 202 summary, 207-9 techniques, 2 tomographic techniques, 196 trends, 197 see u/so Cf; MRI; PET; SPECf neuroimmune system pathway, 38 neuroimmunotherapy, 274 neurological deficit, absent, with temporallobe astrocytoma, 282 neurological diseases, interactions, 274-7 neuroma, acoustic, cerebellopontine angle, 288 neuromodulators, 273 neurons, 250 cerebrospinal fIuid-contacting, 273 cytodifferentiation, 12 embryogenesis, 12-13 introduction of term, 6 morphological 276

diversity

in disease,

neuropathologists, viewpoint on tumors, 121-2 neuropathology, 115-91 features, CNS tumors, 117-19 history, 116 interpretation, 359 specific, 123-44 neuropeptides, 273 neurophysiology, 247-315, 359 case studies, 280-316 outdated ideas, 278 neuroradiology, see neuroimaging neurosurgeons iconoclastic spirit required, 278 viewpoint on tumors, 121-2 neurotransmitters, 272, 272 CNS, 273 pathways, 38 NMR (nuclear magnetic resonance), 195 norepinephrine, 271 NORs (nucleolar organizer 120 nuclear magnetic resonance 195 nucleolar organizer 120

regions), imaging,

regions (NORs),

nystagmus with cerebellopontine angle acoustic neurinoma, 241, 290 with cerebellopontine angle acoustic neuroma, 289 with infratentorial dermoid tumor, 229 with mesencephalic anaplastic astrocytoma, 308 with pontine cavernoma, 354 with pontomesencephalic pilocytic astrocytoma, 310

o observation, as treatment option, 324 occipital gyrus, 21 medial, 49 superior, 49 occipitallobe, 16,17,50,51 anatomy, 49-51 and Brodmann areas, 69 metastatic adenocarcinoma, 281 MRI anatomical correlation, 78-9 projection fibers, 36 vascularization, 102 occipital pole in embryo, 10 tumor, 283 occipitopontine fibers, 68 cascade structure in white matter, 38 occipitotemporal sulcus, continuity rate, 19 oculomotor nerve, see nerves oculomotor paresis, with mesencephalic piloid astrocytoma, 348-9 olfactory cortices, 18 olfactory sulcus, incidence rate, 19 oligoastrocytoma diffuse, 175 falx, 187 mixed, cingulate gyrus, 170 oligodendroglioma anaplastic, 219 vs. atypical meningioma, histologic diagnosis, 189 insula, 335, 337 intermediate growth phase, 132, 133 limbic lobe, 338, J40 middle parietallobule, 158 neocerebral, 155 occurrence pattern, 149 pulvinar thalami, 345 recurrence with glioblastoma, 345 septal region, 209 superior temporal gyrus, 298 oncogenes, 117 amplification, and prognosis, 120 operability, 317-59, 321-4 decision-making, 321-2 perioperative care, 322 operative treatment, decisionmaking, 320-1 opercular part, inferior frontal gyrus, 21,22,23 astrocytoma, 294 glioblastoma, 179 oligodendroglioma, 155 operculated sulci, 20 ophthalmoplegia, with sphenopetroclival meningioma, 328 optic chiasm, in embryo, 10 optic glioma, 123, 332-3 optic nerve, in embryo, 10 optic radiations, 68 displacement, 298 with superior temporal gyrus glioblastoma, 296 orbital gyri, 43 orbital sulci, incidence rate, 19 organ system, circumventricular, 265-7 organum vasculum of lamina terminalis (OVLT), 266, 266-7

p pain arms and legs, with intramedullary ependymoma, 315

aural, with fourth ventricular astrocytoma, 353 maxillary, with parahippocampal astrocytoma, 300 retroauricular, with acoustic neuroma, 288 paleocerebellum, 82 paleocortical areas, 18 palliative treatment, 319, 323, 324 papilledema with diffuse anaplastic astrocytoma, 179 with glioblastoma, 223-4 with infratentorial plexus papilloma, 228 with intraventricular lesion, 220 with intraventricular pilocytic astrocytoma, 342, 343 with meningoendotheliomatous meningioma, 236 with mesencephalic anaplastic astrocytoma, 308 with multiple lesions, 187 with primitive neuroectodermal tumor, 224 with retrolenticular astrocytoma, 173 with septal neurocytoma, 182 with temporallobe glioblastoma, 177 papilloma, intraventricular, choroid plexus, 142 paracentral gyrus, 40, 46, 62 cavernoma, 157 and centrallobe, 44 paracentrallobule, 46 paracentral sulcus, 44 parachiasmal region craniopharyngioma, 239 extrinsic vs. intrinsic tumors, 209-17 pilocytic astrocytoma, 212 parahippocampal gyrus, 61, 61 astrocytoma, 282 glioblastoma, 284 parahippocampus, 18, 51, 53, 62 anaplastic astrocytoma, 163, 300 hamartoma-astrocytoma, 216 paralimbic area, vascular anatomy, 136 paralimbic lo be, 18 tumors, 136-9 parapineal areas glioblastoma, residual, 224 meningioma, 221, 238 fibroblastic, 222 vs. sarcoma, 222 plexus papilloma, anaplastic, 223 tumors, differential diagnosis, 221-4 parasites, 201

and imaging techniques,

parasplenial area glioblastoma vs. abscess, 232 lesion treated by shunt, 309 paraterminal area, 63 paresis arm, with Sylvian fissure meningioma, 235 hand, with frontal gyrus astrocytoma, 294 paresthesia facial with brainstem and cerebellar epidermoid tumor, 291 with cerebellopontine angle acoustic neurinoma, 241, 290 with medullary piloid astrocytoma, 313 with superior temporal gyrus oligoastrocytoma, 299 parietal gyrus, 21

393

parietallobe, 16, 17,49 anatomy, 47-9 astrocytoma, 335-6 and Brodmann areas, 69 glioblastoma vs. abscess, 231 insular surface, 43 local thrombophlebitis, 307 MRI anatomical correlation, 78-9 projection fibers, 36 vascularization, 102 parietallobules, 48, 48 cavernoma, 303 inferior, 23 anaplastic astrocytoma, 159 glioblastoma, 295 middle, oligodendroglioma, 158 superior, astrocytoma, 156 parietal operculum, oligoastrocytoma, 299 parietal peduncles, 47 parieto-occipital fissure, 47 parieto-occipital sulcus, 47 cerebral infarction, vs. glioma, 234 continuity rate, 19 in embryo, 9, 10 parietopontine fibers, 68 cascade structure in white matter, 38 Parinaud syndrome absent, with mesencephalic piloid astrocytoma, 309 with fourth ventricular medulloblastoma, 352 parolfactory area, 62, 63 parolfactory sulcus, anterior, dence rate, 19

inci-

pathogenesis, 119 pathophysiology cerebral edema, 255-6 cerebrovascular system, 265 circumventricular organs, 267 CNS disease processes, 274-7 hypothalamus, 270 immune system, 274 neuroendocrine system, 271 pineal gland, 271 surgical, and MRI, 199 patient history, 318 peduncles cerebellar, 82, 88, 90, 91-2 parietal, 47 periarchicerebral areas, 18 perilesional changes, 146,208 absence acoustic neurinoma, 241, 242, 290 acoustic neuroma, 288 endotheliomatous meningioma, 242 meningiocraniopharyngioma, 239 meningioma, 236, 238 Sylvian fissure meningioma, 235 adenocarcinoma, temporal pole, 243 differential 235-45

diagnostic

problems,

glioblastoma precuneus, 244 pulvinar thalami, 244 imaging, 203-4, 235-45 meningioma meningoendotheliomatous, 236 temporal pole, 244 tuberculoma falx, 233 fourth ventricle, 233 white matter, 245 perioperative care, 322 peripaleocortex, insular lobe, 54 peripaleocortical areas, 18 persona lit y changes

394

Index

with limbic oligodendroglioma, 338 with temporallobe astrocytoma, 280 PET (positron emission tomography),196 and anatomy, 114 phylogenetic recency and initial tumor growth, 126, 128 and intrinsic tumors, 135 limbic and paralimbic are as, 136 physiological subsystems, 248-50 physiological systems, interaction with neurologic diseases, 274-7 pia, and imaging difficulties, 204, 205,206 piloid astrocytoma, mesencephalon, 348-9,350 pineal body, 266 pineal gland, 270-1 pathophysiology, 271 pineal tumors and diabetes insipidus, 271 vs. intraventricular pilocytic astrocytoma, 347 occurrence pattern, 149 pituitary adenoma, 119 growth restrained by diaphragma sellae, 125 pituitary gland, 270 arteries, 104 plexus papilloma anaplastic, 223 infratentorial, 228 occurrence pattern, 149 PNET, see primitive neuroectodermal tumor pneumoencephalography, 207 pons,14 arterial supply, 106, 106, 108 cavernoma, 311 in embryo, 10 tumors, 354-5 see a/so metencephalon pontobulbar area, distortion with acoustic neurinoma, 290 with acoustic neuroma, 288, 289 and postoperative recovery, epidermoid tumor, 291 pontomedullary junction, endotheliomatous meningioma, 242 pontomesencephalic area, pilocytic astrocytoma, 310 postcentral gyrus, 21, 23, 40, 45, 47 and Brodmann areas, 69 and centrallobe, 44 MRI anatomical correlation, 78-9 variations, 46, 47 postcentral sulcus, 23,44, 47, 49 continuity rate, 19 in embryo, 9 posterolateral fissure, cerebellum, 82 postoperative neuroimaging, 201 precentral gyrus, 21, 22, 23, 40, 42, 45,46 and Brodmann areas, 69 cavernoma, 302 and central lo be, 44 MRI anatomical correlation, 78-9 tumor vs. cerebral infarction, 234 variations, 46, 47 precentral sulcus, 23, 44 intermedia te, incidence rate, 19 interruption rate, 19 marginal, incidence rate, 19 precuneus,47,48,62 glioblastoma, perilesional changes, 244 pilocytic astrocytoma, 157 predisposition, genetic, 119 prele.nticular tumors, 134 primitive neuroectodermal tumor, 176

histology, 191 intraventricular,344 vs. pineal blastoma, 224 proisocortex, insular lobe, 54 proisocortical areas, 18 projection fibers, 32, 33, 36-8 cerebellum, 90 in cerebral white matter, 25, 26 coursing with commissural fibers, 36 dissection, 37 internal capsule and basal ganglia, 66 and central nuclei, 66 and lateral ventricle, 65, 66 topography, 67 mesencephalon, topography, 67, 68 sectorial organization, 30 projection systems, 6 proliferation rate, tumors, 120 prosencephalon,14 embryogenesis, 8 place in brain structure, 15 relationship to basal ganglia, 138 proto-oncogenes, 117 pseudocapsule formation, 147, 204 membranes, 205 ptosis with mesencephalic fibrillary astrocytoma, 351 with pontine cavernoma, 354 pulvinar thalami, 68 glioblastoma, 183, 345 perilesional changes, 244 oligodendroglioma, 345 residual glioblastoma, 224 putamen, arterial supply, 102

Q quadrantanopsia, 163, 338 with anaplastic astrocytoma, 217 with parahippocampal anaplastic astrocytoma, 300 with parietal anaplastic astrocytoma, 336 with pilocytic astrocytoma, 214 with pleomorphic xanthoastrocytoma, 301 with retrolenticular astrocytoma, 173 with superior temporal gyrus oligoastrocytoma, 299 with temporallobe astrocytoma, 282 with thalamic telangiectasia, 304 quadrigeminal plate, in embryo, 10 quadriplegia, with pontine cavernoma, 355 qua lit y of life, 320

R radical surgery, 327 radiographs, 194, 207 radiology, see neuroimaging Ram
outside anatomic borderlines, 179 at unexpected site, 179 reflex examination, normal, with temporal lo be astrocytoma, 280 Reil, le., 4 Remark, R., 4 respiratory failure, with pontine cavernoma, 355 results of surgery, analyzing, 325 retrolenticular tumors, 134 pilocytic astrocytoma, 173 Retzius, 0., 4 rhinal sulcus, incidence rate, 19 rhinencephalon, embryogenesis, 9 rhombencephalon,14 embryogenesis, 8 place in brain structure, 15 Roentgen, w.e., 194 rostral sulcus inferior, incidence rate, 19 superior, incidence rate, 19

s sarcoma, vs. meningioma, schwannoma acoustic, differentiation MRI,147 see a/so neurinoma scotoma

222 with

color, with parachiasmal astrocytoma, 212 with cuneus tumor, 160 sectors, white matter, in gyral segments, 28, 28, 29 seizures focal with diffuse astrocytoma, 175 with insular astrocytoma, 165 with superior parietallobule astrocytoma, 156 frontal, with middle parietal lobule tumor, 158 generalized with anaplastic astrocytoma, 217 with falx tuberculoma, 233 with frontal gyrus astrocytoma, 294 with frontal gyrus meningioma, 293 with inoperable 356

astrocytoma,

with insular glioblastoma, 178 with limbic oligodendroglioma, 340 with parietallobule astrocytoma, 218 with pilocytic astrocytoma, 215 with pleomorphic astrocytoma, 219 with Sylvian fissure meningioma, 235 with temporallobe glioblastoma, 284 with inferior frontal gyrus lesion, 292 intermittent, with parietal toma, 295 Jacksonian

glioblas-

with inferior frontal gyrus tumor, 155 with local thrombophlebitis, 307 with precentral cavernoma, 302 with recurrent anaplastic astrocytoma, 180 parietal, with precuneus tumor, 157 partial complex with amygdala 161

ganglioglioma,

with diffuse glioma, 174 with multiple lesions, 186 with transitional zone astrocytoma, 163 with superior temporal gyrus oligoastrocytoma, 299 temporallobe, with encephalomalacia, 235 sella, optic glioma, 333 sensorimotor examination, normal with occipital adenocarcinoma, 281 with temporallobe astrocytoma, 280 septal region, oligodendroglioma, 209 septum pellucidum embryogenesis, 10 neurocytoma, 182 serotonin, 271 sight, see visual deficits; hemianopsia; quadrantanopsia silver staining, 120 single photon emission computed tomography, 196, 197 sleep attacks with fourth ventricular tuberculoma, 233 see a/so drowsiness; fatigue; somnolence Soemmering, somnolence

S.T., 3

with embryonal tumor, 346 with pilocytic astrocytoma, 213 see a/so drowsiness; fatigue; sleep attacks SPECT (single photon emission computed tomography), 196, 197 speech,seelanguage sphenoid, meningioma, 188 sphenopetroclival meningioma, 286. 326-9 spinal cord, and divisions of brain, 14 splenium in embryo, 10 variations, 35 stereotactic localization system, 24 strabismus, and intraventricular pilocytic astrocytoma, 343 subarachnoid hemorrhage, effects on CNS, 275 subcommissural organ, 266 subfornical organ, 266, 266 subgyri, formation, 20 subparietal sulcus, 47 in embryo, 10 incidence rate, 19 substantia nigra, arterial supply, 103 subthalamic nucleus, arterial supply, 103 sulci anatomy, 19-20 arteries, 98 central lobe, 44 cerebellar, 86, 87 classification, 19-20 compression during tumor growth. 132 continuity rates, 19 frontal lo be, 40 incidence rates, 19 interhemispheric, in embryo, 9 interruption rates, 19 occipital, 49 parietallobe, 47 temporallobe, 52 types, 20 see a/so specific su/ci supratentorial structures, cerebral tissue herniations, 252 surgeon colleague 178

suffering glioblastoma.

see a/so neurosurgeon

Index surgery analyzing results, 325 curative, 323 decision to operate, 320-1 goals, 323 philosophy, 153 place in therapy, 319 planning, 359 radical, 327 surgical pathophysiology, 199

and MRl,

swallowing difficulty, with epidermoid tumor, 291 Sylvian fissure, 4, 21, 23 continuity rate, 19 in embryo, 9 fIoor, 53 and frontal gyri, 41-2 meningioma, 235 opened,43 symptomatology, 320-1 symptoms, variable responses to CNS ¡njury, 277-8 synapse, introduction of term, 7 synaptogenesis, 12 syncope, with encephalomalacia, 235 syndesm, 7

T technology, neuroclinical, 318-19 telangiectasia, thalamus, 304 telencephalon,14 borders, 16 division, 136 embryogenesis, 8 neocortical, structure, 18 place in brain structure, 15 transitional, structure, 18 temperature control,268 elevation, with primitive neuroectodermal tumor, 344 temporal fossa, anaplastic ganglioglioma, 285 temporal gyri, 21 inferior, 52, 53 fibrillary astrocytoma, 181 middle, 23, 52 superior, 23, 52 glioblastoma, 296 oligoastrocytoma, 299 oligodendroglioma, 298 transverse, anaplastic oligodendroglioma, 298 temporallobe, 16, 17,53 anatomy, 52-3 astrocytoma, 161, 280, 282 and Brodmann areas, 69 glioblastoma, 284 insular surface, 43 lesions, variation in symptoms, 277-8 pleomorphic 162

xanthoastrocytoma,

posteroinferior, glioblastoma, 177 projection fibers, 36 vascularization, 102 temporal pole adenocarcinoma, 243 meningioma, perilesional changes, 244 temporal sulcus inferior, interruption rate, 19 middle, 23 superior, 23 continuity rate, 19 temporo-occipital area, purulent abscess, 231

temporo-occipital gyrus lateral, 49, 51, 52, 62 medial, 49, 51 medial (lingual gyrus), 50, 53, 62 temporo-occipitallobe, 53 temporopontine fibers, 68 cascade structure in white matter, 38 teratoma, 271 vs. glioblastoma, 223-4 intraventricular, 142 vs. intraventricular pilocytic astrocytoma, 347 occurrence pattern, 149 terminology, for cerebrallobes, 17, 114,151 TGF (transforming growth factor) 02 121,274 thalamic nuclei, connections to cerebral cortex, 36 thalamic peduncles, 37 thalamic radiation, posterior, 68 thalamus abscess, 306 arterial supply, 103-4 astrocytoma, 176 in embryo, 10 hematoma, 304 telangiectasia, 304 tumors, predilection sites, 141 therapy, adjuvant, 153, 296, 306, 335, 359 third ventricle astrocytoma, 334 cavernoma, 188 choroidal tela, 10 craniopharyngioma, 211 tumors, 143 thirst attacks, with limbic oligodendroglioma, 340 thresholds, cerebral blood fIow autoregulation, 265 thrombophlebitis, local, parietal lobe, 307 time and capability, in clinical decision-making process, 319 tinnitus with cerebellopontine angle acoustic neurinoma, 241, 290 with cerebellopontine angle acoustic neuroma, 289 with infratentorial pilocytic astrocytoma, 229 tongue atrophy, with epidermoid tumor, 291 postoperative test, 322 tonsil of cerebellum, 87 topography extrinsic tumors, clinical considerations, 321 projection fibers internal capsule, 67 mesencephalon, 67, 68 tumors, 321 torticollis, with mesencephalic cavernoma, 305 toxoplasmosis, and imaging techniques, 201 transforming growth factor (TGF) ~2121, 274 transverse gyri, 21, 23, 48, 48, 49 lingual gyrus, 51 precuneus, 51 trauma, effects on CNS, 275 treatment options, 323-5 tremor, with mesencephalic piloid astrocytoma, 350 trigeminal nerve, see nerves triune brain, 126 tryptophan, 271 tuberculoma

fourth ventricle, 233 vs. meningioma, falx, 233 tuberculosis, effects on CNS, 275 tumor recurrence, 145, 345 clinical considerations, 321 fast growing, 176, 178 fibrillary astrocytoma, inferior temporal gyrus, 181 multiple benign, 180-2 neurocytoma, septum pellucidum, 182 outside anatomic borderlines, 179 at unexpected site, 179 tumors accommodative pathways, 254 adherence and adhesiveness. 147-8 assessing malignancy, 120 astrocytic, 127, 152 basal ganglia, 139-42 benign, multiple occurrence, 180-2 biological activity, 119-21 boundaries, imaging, 203 and buffering system reserve, 254 butterfly, 202 categorization, 122-3 cell kinetics, 120 central nuclei, 139-42 growth patterns, 140 vascularization, 100 cerebellar predilective sites, 93, 94 unique characteristics, 135 vascularization, 99-101 cerebral symptoms and signs, 251 vascularization, 99-101 cingulate, 137-8 classification, history, 116 cleavage, see demarcation be/ow CNS effects, 248 without deficits, case studies, 292-300 demarcation, 146-7, 147, 151, 206-7 deceptiveness, 147 imaging, 204-7 diffusely growing, 174 as dynamic systems, 277-8 effects on cerebrovascular system, 265 vs. encephalomalacia, middle frontal gyrus, 235 epidemiology, 119 epidural, 124 demarcation, 206 extra-axial, 123 extrinsic, see extrinsic tumors fourth ventricle, 352-3 genetic expression, 120-1 glioma, origin of term, 116 growth and progression, 122, 144, 144-5 adventitial, 148 common pattern, 128 effects, 301-7 extrinsic, 123-5 initial pattern, 127, 127-8 initial sites, 129 kinetics, 119-20 limbic and paralimbic areas, 137 limiting factors, 127 and phylogenetic recency, 126. 128 regulatory factors, 121 subgyral patterns, 131 hypothalamus, 270 imaging of lesion morphology, 200 immune response. 127 infiltration, 144-5 adventitial, 148 infratentorial, initial sites, 130 inoperable, 341, 356-8

interaction interaction

395

with CNS, 249, 277 with CNS and immune

system, 274 interface with brain, 147-8 intra-arachnoid, demarcation, 206 intra-axial, 123 intradural, 124 demarcation, 206 intraventricular, 142-4,341-7 sites of origin, 143,220 intrinsic, see intrinsic tumors limbic, 136-9 in fronto-orbital areas, 138 patterns of growth, 137 limbic lobe, vascularization, 100 localization, 129-44,251 accuracy of cascade approach, 122 locating, with imaging, 200-1 mesencephalon, 348-51 metastatic and adherence, 148 cerebellopontine angle, 227 occurrence pattern, 149 peritumoral changes, 146 mixed glioma, insula, 164 multicentric, 150-1 pathogenesis, 150 multiple, 184-8 neocerebellar, 129-35 initial growth phase, 130-1 intermediate growth phase, 131-3 late growth phase, 134 unusual patterns of spread, 134, 134 neocerebral, 129-35 case studies, 154-60 initial growth phase, 130-1 intermedia te growth phase, 131-3 late growth phase, 134 unusual patterns of spread, 134, 134 vascularization, 99 neuroectodermal, neuropathological 117-19

primitive, 176 features, range,

neurosurgical viewpoint, 121-2 nidus, 130 numbers, 149-51 occurrence patterns, 149 operability, 321-4 optic nerve, and hypothalamic function, 270 paralimbic, 136-9 patterns of growth, 137 para median cerebellar. vascularization, 101 vs. parieto-occipital cerebral infarction, 234 pathogenesis, 119 pineal area and diabetes insipidus, 271 vascularization, 101 pons, 354-5 predilection 152

sites, 125-7, 134, 151,

primitive neuroectodermal, 176, 191,224,344 proliferation rate, 120 reconstruction, with imaging techniques. 207 recurrence, see tumor recurrence residual glioblastoma, 224 and segmental blood supply, 95-6 growth restriction, 128 sites of predilection, 125-7,134, 151,152 size and pathological effects, 320 specific neuropathology, 123-44 structural consistency, 122

"'"--------

396

Index

subdural, 124 demarcation, 206 subpial-subcortical, demarcation, 207 sudden change, 145 pulvinar oligodendroglioma, 345 symptomatology, 320-1 thalamus, predilection sites, 141 topography,321 transitional, 139 types, 149-51 unicentric, 150 vascular effects, 265 vascularization, 148-9,207 vs. vascular mass lesions, MRI identification, 199 visualizing, 124 volume effects, 320 see also perilesional changes tumor-suppressor genes, and tumor etiology, 117, 120, 121, 153 Thrcot's syndrome, 150 Thrner, VV.,4, 16,46 two-hit concept, for genetic origin of tumors, 126, 153

u U fibers, 32 uncus, 51, 62 unicentric tumors, 150 uvula of cerebellum, 87

v vallecula cerebelli, 86, 87 vascular anatomy, 95-113 patterns suici, 98 white matter, 27 see also arteries; cerebrovascular system; veins vascular disease, CNS, 149 vascularization, of tumors, 148-9,207 vascular mass lesions, vs. tumors, MRI identification, 199 vasogenic edema, 255 vasospasm, effects on CNS, 275 veins, 109-13 angiogenesis, and tumor pathology, 121 angioma, 303

basal, 111 cerebral, synopsis, 109 choroid, 111 CNS arteriovenous system, 264 internal cerebral, 111 limbic and paralimbic are as, 136 posterior horn, 111 septal, 111 terminal, 111 thrombosis, 148-9, 153 thrombosis and malignancy, 124, 153 transcerebral anastomotic, 111, 111 white matter, 27,109-13 see a/so venous drainage vela, medullary, 83, 83 venous drainage, 35 cerebrovascular system, 263 and peritumoral changes, 111 projection fibers, 36 white matter anastomoses, 113 ventricles abnormalities, 201 lateral, tumors, 143 third astrocytoma, 334 cavernoma, 188 choroidal tela, 10 craniopharyngioma, 211 tumors, 143 fourth, 87 deviation with pontine cavernoma, 311 displacement, 291 in embryo, 10 lipoma, 229 plexus papilloma, 228 tuberculoma, 233 tumors, 144, 352-3 vermis, 81, 82 in embryo, 10 lobules, 81, 82 medulloblastoma, 225 uvula, 87 vertigo with cerebellopontine angle acoustic neurinoma, 242, 290 with cerebellopontine angle chordoma, 228 with encephalomalacia, 235 with infratentorial pilocytic astrocytoma, 229 with intraventricular neurocytoma, 343 with intraventricular pilocytic astrocytoma, 342 with medullary piloid astrocytoma, 312

with parahippocampal anaplastic astrocytoma, 300 with parieto-occipital cerebral infarction, 234 with pontine cavernoma, 354 Vesalius, 3 Vicq d' Azyr, F., 4 Virchow, R., 116 visual deficits with diencephalic piloid astrocytoma, 332 with intraventricular lesion, 220 with parachiasmal astrocytoma, 212 with pilocytic astrocytoma, 213 with temporallobe glioblastoma, 284 see also blindness vomiting abscess, thalamic, 306 astrocytoma cystic cerebellar, 287 diencephalic piloid, 332 mesencephalic, 308 pilocytic, 213, 230, 343 cavernoma, pontine, 354 dermoid tumor, infratentorial, 229 ganglioglioma, temporal fossa, 285 hemangioblastoma, medullary, 314 medulloblastoma, parapineal, 225 oligodendroglioma, pulvinar, 345 optic glioma, sellar, 333 plexus papilloma, 223 primitive neuroectodermal tumor, 176 intraventricular,344 telangiectasia, thalamic, 304 xanthoastrocytoma, pleomorphic, 301

with parasplenial abscess, 232 with pilocytic astrocytoma, 172 limbs, with inoperable neuroectodermal tumor, 357 postictal, with parietallobule cavernoma, 303 weight gain, with third ventricle craniopharyngioma, 211 white matter, 14,25,25-39 casca de structure, 38 accuracy in tumor localization, 122 cauliflower substructure, 26, 27 central zone, 28 anatomy, 65-8 centripetal venous drainage, 112 cerebellum, 88, 88-93, 89 contents, 90 contents,27 gyral sectors, 28, 28, 29 MRI anatomical correlation, 80 perilesional changes, 245 peripheral zone, 28 structure, and neuroimaging, 208 sublevels,28-30 clinical implications, 39 subsystems, 30-8 connective fibers, 32-8, 33 CSF pathways, 30 gyral segment vascularization, 30 neuroglial migration pathway, 30 neuroimmune system pathway, 38 neurotransmitter pathways, 38 segmental patterns, 31 veins, 109-13 venous drainage, anastomotic, 113 window of vulnerability, for neoplasm,126

w VVada test, 277 VValdeyer, vv., 6 water metabolism, weakness arm

leg with diencephalic piloid astrocytoma, 332 with fronto-orbital glioblastoma, 167 with paracentral gyrus tumor, 157

270

with intraventricular lesion, 220 with medullary hemangioblastoma, 314 facial, with pontine cavernoma, 311 with fibroblastic meningioma, hand, with hamartoma-astrocytoma, 216

222

x xanthoastrocytoma occurrence pattern, 149 pleomorphic insula, 301 temporal lo be, 162