Paranoia in the “Normal” Population (Psychiatry – Theory, Applications and Treatments)

PSYCHIATRY - THEORY, APPLICATIONS AND TREATMENTS SERIES

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PSYCHIATRY - THEORY, APPLICATIONS AND TREATMENTS SERIES

PARANOIA IN THE “NORMAL” POPULATION

ANTONIO PRETI AND

MATTEO CELLA

Nova Science Publishers, Inc. New York

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Published by Nova Science Publishers, Inc.   New York

CONTENTS

Preface

xi

Introduction

xiii

Chapter 1

The Clinical Picture

1

Chapter 2

The Symptoms of Psychosis: Structure and Epidemiology

7

Chapter 3

A Dimensional View on Psychosis

13

Chapter 4

The Concept of Psychosis Proneness

19

Chapter 5

Models of Paranoia

21

Chapter 6

Cognition and Paranoia

25

Chapter 7

Mood, Anxiety and Paranoia

31

Chapter 8

Emotions and Affects in Paranoia

37

Chapter 9

The Heuristics of Paranoia

41

Chapter 10

The Tipping Point: When Suspiciousness Becomes Paranoia

45

How Understanding Persecutory Thinking Can Help Prevention

49

Chapter 11 Conclusion

53

References

55

x Index

Contents 73

PREFACE This chapter reviews the dimensional conceptualization of persecutory delusion in the attempt to elucidate the transition from suspicious thinking to clinically relevant paranoia. For a better understanding of psychosis, a study of non-clinical population would prove useful: to this aim this chapter reviews some research works and proposed ideas. The first section reviews the epidemiological studies on psychotic features in the general population, and frames the findings in the dimensional and quasidimensional models of psychotic symptoms distribution. The concept of paranoia is described according to the clinical diagnosis used in the current classificatory system and then approached as a dimensional construct: the validity of the dimensional model is investigated by reviewing clinical, epidemiological and experimental research involving the psychological factors recently associated to paranoia. In particular we will focus on the relevance of the affective system, which contributes to determining psychopathological severity within paranoia. We will then formulate a heuristic concept of paranoia in order to support the dimensional view on psychosis with the empirical finding. In the final part of this chapter we will use this concept expressed to explore the boundaries between pathological and normal paranoia and evaluate the relevance of this conceptualization for the treatment and the prevention of psychosis.

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Keywords: paranoia; paranoid ideation; psychosis; schizophrenia; early intervention; psychosis proneness; persecutory delusion; dimensionality psychosis

INTRODUCTION The term psychosis refers to the most severe end of the psychiatric disorders spectrum, where individuals are believed to be out of touch with reality. The deficit of reality testing typically observed in psychosis is expressed by symptoms such as delusions, hallucinations, and disorganized behavior. The term delusion describes a belief that is held true and real, but it is actually false, fanciful or completely bizarre; hallucinations are vivid perceptions experienced in the absence of a stimulus occurring in a conscious state. Hallucinations can involve any sense (e.g. sight, hearing, or smell) and are located in the external objective space. Disorganized behavior is often, but not always, a consequence of delusions and/or hallucinations: it can be defined as any unpredictable or unusual action or conduct whereby the individual violates the rules of behavior expected in the specific social circumstances. Delusions and hallucinations are hallmarks of psychosis: the contemporary classifications of mental disorders give delusions and hallucinations a particular place in the diagnosis of psychosis, in both the affective and the non-affective spectrums of mental illness (Berrios, 1991; Chen and Berrios, 1996). Although delusion and hallucination are typically considered signs of mental disorder, particularly when they are characterized by persecutory thinking, they are not specific to psychotic psychopathologies (Ohayon, 2000; Verdoux and van Os, 2002).

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In clinical practice psychotic disorders are rather uncommon: even when considering all the different diagnostic categories expressing psychotic features (i.e. schizophrenia, schizoaffective disorder, chronic delusional disorder, bipolar disorder, and major depression with psychotic features), the prevalence rate of psychotic disorders in the general population is rarely above 2-3% (Kessler et al., 1994; Perälä et al., 2007). As for the prototypical expression of psychotic features – schizophrenia – a recent systematic metaanalysis on epidemiological data reported a median yearly incidence of 15.2/100,000 persons (80%C.I.=7.7-43.0), and a median prevalence of 4.0/1,000 persons (80%C.I.=1.8-11.6), with a lifetime morbidity risk of 7.2/1,000 persons (McGrath et al., 2008). Despite this, a number of epidemiological surveys presented evidence that those experiences and beliefs that can be ascribed to the psychotic dimension are quite common in non-clinical populations (Aleman et al., 2001; Allardyce et al., 2007; Kendler et al., 1996; Poulton et al., 2000; Verdoux and van Os, 2002). In the United States, for example, up to 25% of the general population endorsed at least one item out of the survey questions exploring psychotic symptoms, while in the country the prevalence of clinically-defined psychosis is under 1% (Kendler et al., 1996). In the Netherlands, 17.5% of the population endorsed at least one of the psychosis-screening items (Bijl et al, 1998), but the prevalence of ascertained psychoses is 2.1%. In 2000, the British National Survey of Psychiatric Morbidity found that 5.5% of the respondents not diagnosed with a psychosis endorsed one or more items of the Psychosis Screening Questionnaire (Johns et al., 2004). Regardless of the discrepancies in the figures, most likely due to different measurement criteria, these studies showed that psychotic features are significantly present in the general population. On the whole, there is clear evidence that the rate of delusional beliefs in the general population is higher than that of diagnosed psychotic disorders (Freeman, 2006). Moreover the reporting of delusional subjective experiences, although largely clinically asymptomatic, proved to be related to increased chances of the future onset of a mental disorder that falls in the “psychosis” spectrum, such as schizophrenia, manic-depression, or schizoaffective disorder (Chapman et al., 1994; Krabbendam et al., 2005; Kwapil et al., 1997).

Introduction

xv

In psychopathology, delusions are defined as firmly held beliefs despite evidence to the contrary, with unfounded content according to shared evidence and cultural beliefs, and typically resistant to change despite plausible alternative explanations. Cultural acceptability is an important element in the definition of delusions; for example in early Western civilizations, the implications of malevolent dark forces in personal experiences would have been understood and accepted (O'Connor, 2009). People holding delusional beliefs generally present high distress and preoccupation levels, poor social functioning and a self-centered perception of events (i.e. personal reference ideation). Although clinicians and researchers basically agree on what typically defines a delusion, the evidence from epidemiological studies that found delusion-related convictions more widespread in the community than previously thought, challenged the idea that delusional beliefs must always be related to some level of disability. A dimensional approach to the conceptualization of psychotic features is therefore considered more appropriate to appreciate psychotic presentation, since it is able to account for the presence of delusional beliefs in the general population. Before exploring the concept of dimensionality and its relevance for delusional ideation, it is worth defining the concept of paranoia and the clinical disorders associated with it. The etymology of the term “paranoia” has a long history. The word comes from the Greek parãnoia1 (=paranoia), which can be roughly translated with the term madness or crazyness, from “para”=outside and “nous”=mind. Kraepelin (1899) introduced the term in the psychiatric classification system to define an unshakable type of delusional disorder of non-bizarre quality not accompanied by hallucinations. Paranoia was then reframed by US psychiatrists during the Second World War to define a class of persecutory delusions that are not necessarily pathological. As Bentall (2003) noticed the definition given to the term paranoia in the Oxford English Dictionary tends to reflect an ordinary process rather than a psychiatric classification: Paranoia: “A tendency to suspect or distrust other or to believe oneself unfairly used”. Since the introduction of the DSM-III-R paranoid disorder was replaced by 1

Font: Athenian

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delusion disorder, leaving the term “paranoia” featuring in two diagnoses: paranoid personality disorder and paranoid schizophrenia. More recently this term has been used to describe delusions where the affected persons specifically believe they are being persecuted. According Freeman and Garety‟s formulation (2004) paranoid delusion can be defined with two characteristics: 1. The individual thinks that harm is occurring, or is going to occur, to him or her. 2. The individual thinks that the persecutor has the intention to cause harm. In spite of a less common use of the term in psychopathological classifications, the current diagnostic classification recognizes three types of mental disorders characterized by paranoia: paranoid schizophrenia, delusional disorder (persecutory type), and paranoid personality disorder (PPD). However, paranoid disposition and behavior appear in a large number of mental disorders, including depression and dementia.

Chapter 1

THE CLINICAL PICTURE The clinical disorders featuring paranoia can be organized by the degree of symptom severity and consequent level of disability. The following section will describe the milder form of paranoid disorder first, i.e. the paranoid personality disorder, then the delusional disorder and, finally, the most severe end of the paranoia spectrum: paranoid schizophrenia.

PARANOID PERSONALITY DISORDER (PPD) DSM-IV defines personality disorder as "an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the culture of the individual who exhibits it" (APA, 1994). This pattern of behavior is relatively stable, generally inflexible and rigidly pervasive across situations and circumstances. Although it causes significant distress or negative consequences in many areas of personal life, this pattern is enduring because the individual perceives it as ego-syntonic, hence appropriate to his/her own goals and aims. Onset is often in adolescence, but personality disorders can develop at any age after brain lesions that modify the personal style of thinking. To be diagnosed with a personality disorder, individuals must present symptoms in at least two of these areas: thought (i.e. ways of

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thinking about the world, the self or the others), emotions (i.e. appropriateness, intensity and display), interpersonal functioning, and/or impulse control. PPD is a personality disorder characterized by a long-standing pattern of suspiciousness and generalized mistrust of others. The personality trait is believed to be recognizable since early adulthood by characteristic maladaptive behaviors, style of thinking and social oddity, but the disorder is diagnosed when these behaviors become persistent and disabling, or distressing. Any established psychotic disorder, such as schizophrenia, mood disorder with psychotic features, psychosis due to the direct physiological effects of a neurological condition (e.g., temporal lobe epilepsy) or other general medical condition, is an exclusion criterion (APA, 1994). Individuals with PPD have problems with close relationships because of their excessive suspiciousness and hostility that at times may elicit a hostile response in others which, in turn, is often interpreted as evidence supporting the delusion. Rigidness and difficulty in engaging in collaborative and social situations are also common of this personality type. It is not rare that people with PPD exhibit unrealistic grandiose fantasies, often linked to a longing for power and rank – with the most severely affected individuals being perceived as fanatics, or as gurus or leaders by the individuals who share their paranoid beliefs. In response to stress, individuals with PPD may experience very brief psychotic episodes, lasting from a few minutes to some hours. Anxiety, mood and substance abuse-related disorders can co-occur. The PPD tends to exhibit a chronic course. Prevalence estimates of PPD in the general population range from 0.7% (Lenzenweger et al., 1997) to 5.1% (Crawford et al., 2005), according to the method of assessment. In the recent World Mental Health Survey (WMHS), the overall prevalence estimates of personality disorders in cluster A, including the PPD, the schizoid personality disorder (SPD) and the schizotypal personality disorder (STPD), stood at 3.6%, with large variations across countries, from 1.1% in Western Europe to 4.6% in Mexico and 5.3% in Colombia, and

The Clinical Picture

3

consistent high co-morbidity with pretty all Axis I disorders (Huang et al., 2009).

DELUSIONAL DISORDER On a clinical ground, paranoia (now delusional disorder) is an uncommon chronic condition, characterized by the presence of delusions and the relative absence of other psychopathologies. Despite the usual chronic course of the disorder, usually encompassing persecutory delusional themes, personality deterioration is absent. Unlike schizophrenia, paranoia-type delusions are nonbizarre and concern experiences that can possibly occur in real life: to be arbitrarily persecuted by a real person, to be fraudulently betrayed by the partner, to be intensely loved by a stranger. The epidemiology and other clinical evidence support the hypothesis that paranoia is a distinct nosologic entity from schizophrenia. Moreover, nonschizophrenic delusional disorders are more sensitive to incisive antipsychotic drugs, such as pimozide and (less often) haloperidol (Manschreck & Khan, 2006), and their onset is more often in middle-aged adults than in schizophrenia, with a course that rarely goes into severe deterioration of functioning. Psychometric studies investigating the distribution and formation of paranoid thinking in clinical samples showed that the development of the disorder progresses by stages, beginning with hostile attitude to end with delusions of influence (e.g. Romney, 1987). A number of researchers and clinicians deem it artificial to consider paranoid personality, delusional disorder, and paranoid schizophrenia as separate diagnostic entities: according to this view paranoid schizophrenia should be regarded as a more severe form of paranoia that, in turn, is a more severe form of paranoid personality (Romney, 1987). Data from non-clinical samples also provide some evidence on a continuum of paranoid ideas between deluded and healthy individuals (Green et al., 2008).

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PARANOID SCHIZOPHRENIA Paranoid schizophrenia is a psychotic illness characterized by the presence of not less than three delusion-related symptoms, with the active symptoms and functional deterioration lasting 6 months minimum (APA, 1994). The diagnosis of paranoid schizophrenia was introduced to account for persecutory, grandiose and jealous delusional themes, or for hallucinations with similar content. However various diagnostic classification manuals inform that the prevalence of paranoid schizophrenia may vary, when adopting additional criteria. For example a study conducted 20 years ago applied ICD-9 criteria to 200 patients diagnosed with schizophrenia, and found that the paranoid subtype was the most prevalent, with an incidence up to 51.5%. But when DSM-III criteria were applied to the same sample, only 36.5% of the patients did fulfill the criteria for the diagnosis of paranoid schizophrenia. Finally, by applying an even more restrictive set of criteria, only 19% of the patients were diagnosed as paranoid schizophrenic (Kendler and Tsuang, 1981, p. 603-604). In this study, complete congruence between different sets of criteria was found in scant 3% of the sample. In paranoid schizophrenia, hallucinations are almost always present, delusions are rarely systematized and often have a bizarre content, and the course is generally chronic, with a trend towards development of thought disorders and deterioration of the pre-morbid personality. In 1896 Kraepelin, the influential German psychiatrists who mostly contributed to the (still shared) Western diagnostic criteria for the classification of mental disorders, was the first to use the term “dementia paranoids” to group a subset of cases that belonged to a more general class, which he thereafter named “dementia praecox”. According to Kraepelin, “dementia paranoids” are “a small group of patients who after rapidly developing nonsensical and incoherent persecutory and grandiose delusions, tend to quickly progress from slight agitation to permanent confusion” (Kraepelin, 1896, p. 463). It was not until 1899 that he distinguished “paranoia” as a “chronic, progressive psychosis […] characterized by the gradual development of a stable progressive system of delusions, without marked mental deterioration, clouding of consciousness or involvement of the

The Clinical Picture

5

coherence of thought” (Kraepelin, 1904, p. 316). The concept of paranoia was repeatedly changed across the different editions of Kraepelin‟s textbook on psychiatry, but essentially he attributed some kind of autonomy to the disorder, since the patients with this disorder tend to preserve a sense of consistency in behavior, and sometimes they may end up with full remission (Kendler and Tsuang, 1981). The boundaries between paranoid schizophrenia and paranoia become less clear when Bleuler revolutionized the concept of dementia praecox by grouping under a common term, the still used “schizophrenia”, all the conditions expressing delusions and/or hallucinations, which he believed to be secondary to abnormal thought associations (Bleuler, 1908/1950). Nevertheless many European psychiatrists, and Kretschmer among them, firmly held the distinction between paranoid schizophrenia and paranoia. According to Kretschmer (1927/1974), psychologically understandable delusions of a paranoid type always develop in persons who are vulnerable because of their personality: when some specific kind of stress affects crucial areas of self-esteem, paranoid delusions might occur.

Chapter 2

THE SYMPTOMS OF PSYCHOSIS: STRUCTURE AND EPIDEMIOLOGY Symptoms of psychosis can be grossly distinguished into three clusters: positive, negative and affective symptoms. The symptoms of the three clusters can aggregate in various forms, eventually producing an additional set of symptoms called the disorganized cluster (Table 1). The aggregation of positive and negative symptoms prevails in the group of schizophrenia and schizophrenia-related psychoses, which also can display affective symptoms in the form of depression and maniac excitement, depending on the phase. The aggregation of positive and affective symptoms prevails in mood disorders, especially in bipolar disorder and in the variant of major depression with psychotic features (Morgan et al., 2005; Haro et al., 2006). Purely affective symptoms are observed in mood disorders only, while purely positive symptoms, in the form of a non-bizarre systematized chronic delusion, are more typical of delusional disorder (formerly paranoia).

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Antonio Preti and Matteo Cella Table 1. The symptoms of psychosis: major clusters

Positive symptoms

Negative symptoms

Affective symptoms

Disorganized behavior

They are florid sensory perceptions and thoughts impacting on the mental status and resulting in behavioral, emotional and mental alteration. Examples of positive symptoms are hallucinations (seeing, hearing, or smelling in the absence of external stimuli), delusions (incorrect belief sustained despite incontrovertible proofs), disorganized speech (loose association of ideas, derailment of sentences, incoherence, excessive detail) and bizarre behavior (walking backward, talking to one‟s self, sudden and unexpected laugh). They are defined as the loss or absence of thoughts, feelings or behaviors as a consequence of psychosis. Examples of negative symptoms are social withdrawal, apathy (decreased motivation), poverty of speech (laconic replies), anhedonia (inability to experience pleasure) and limited emotional expression. Others, more severe negative symptoms are alogia (poverty of speech), avolition (loss of motivation and participative desire) and affective flattering (restricted emotional manifested by poor eye contact and minimal body language). They are noticeably dissonant mood or emotional responses to a normal situation, usually accompanied by inappropriate behaviors. In psychosis, irritability (excessive reactivity to environmental stimuli) is a typical affective symptom. Other affective symptoms include depression, anger outbursts, and anxiety. Affective symptoms are distinct from negative symptoms and respond to different treatments. It is any unpredictable or unusual action or conduct whereby the individual violates the rules of behavior expected in the specific social circumstances. It is a general feature of psychosis that can range from simple problems

The Symptoms of Psychosis …

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such as sustaining targeted self-care behaviors (e.g. personal hygiene) to unpredictable and bizarre socially inappropriate outbursts (e.g. agitation). A further and foremost severe example of disorganized behavior is introverted catatonia, a condition characterized by total lack of spontaneous movements. Disorganization is also found in verbal and communicative behavior often as a result of the influence of positive symptoms such as delusion and hallucinations.

DELUSIONAL THEMES Although every delusion can be considered unique for circumstances of its emergence and the personal story of the individual, a number of overreaching themes can be reliably identified. Believing of being part of some kind of malevolent plot is the most common theme. A study on the delusional themes of schizophrenic patients showed that paranoia was present in 42% of an inpatient cohort (Jørgensen & Jensen, 1994). Individuals with paranoia would generally attribute the role of imaginary persecutors to politicians and authorities (e.g. the president, the communists), religious and supernatural entities (e.g. god, aliens), criminals and mysterious congregations (e.g. criminal gang, satanic sect) or ethnic groups. Another common theme is delusion of reference, when the patient perceives that events have a special significance. In this context a message on the radio, a newspaper title or even a random object disposition can be interpreted as having a particular meaning: hence it reinforces the underlying delusional theme. Delusions of reference are often seen in association with the grandiose theme where the individual thinks to possess special powers, to be an important person, or well known by the others, or to be part to a very important mission. Confirmatory evidence is sought after in the environment to confirm the grandiose theme, based on the ideas of reference.

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A less common theme of delusion is the somatic or hypocondriacal delusion; patients with this delusion complain about various symptoms that can not be ascertained by medical examination. Bentall (2003) suggests that this form of delusion may be under-recorded because it is difficult to identify clearly, due to the still largely unknown side effects of psychotic medication and to ubiquity of other confounding symptoms. Other less common delusion themes are: delusion of jealousy (the loved person is believed unfaithful), parasitosis delusion (believed to be infested by parasites), dismorpophobic delusion (believe to be disfigured or ugly), erotomanic delusion (believe to be loved by someone famous, usually a singer or an actor) and the Capgras delusion (believe that a loved person has been replaced by an impostor).

EPIDEMIOLOGY A recent meta-analysis of community based studies found that the median prevalence of positive symptoms (delusions and hallucinations) was 5.3% (interquartile range: 1.9-14.4%), while the median 1-year incidence rate was 3.1% (interquartile range: 1.1-8.6%) (van Os et al., 2009). This is suggesting that, regardless of phenotype assessment (e.g. self-report or interview), both prevalence and annual incidence rates are higher than the expected prevalence and incidence of clinical diagnoses, which rarely record prevalence above 23%, and annual incidence never exceeds 0.01-0.05%. Among individuals reporting sub-clinical positive symptoms only half (i.e. 4%) of those rating the experience as distressing (8%) would activate a help-seeking behavior (van Os et al., 2000; Hanssen et al., 2005). These results are congruent with epidemiological surveys conducted in the US and the Netherlands, where the prevalence of positive symptoms based on selfreport was largely above the rates of clinically diagnosable non-affective disorders, respectively 28% as against 0.7% in the US National Comorbidity Study (Kendler et al., 1996), and 17.5% as against 0.4% in the Netherlands Mental Health Survey and Incidence Study (NEMESIS) (van Os et al., 2001).

The Symptoms of Psychosis …

11

Overall, the data support the idea that the threshold to diagnose psychotic illness is influenced by subjective reactions to the symptoms, the patient‟s consequent perception of the illness, and also depend upon what the clinician considers a condition in need of treatment. Prevalence data are not the sole indicators of a continuum in psychotic symptoms, at least for positive symptoms. Indeed, in the quoted metaanalysis, the prevalence of sub-clinical psychosis resulted higher among males, migrants, ethnic minorities, the unemployed, the unmarried, and lower in educated people (Verdoux et al. 1998; Agerbo et al. 2004; McGrath et al. 2004), all these being oft-reported socio-demographic correlates of schizophrenia. Other indicators of epidemiological validity for the continuum hypothesis of psychosis are to be found in the association between sub-clinical psychotic experiences and exposure to cannabis, alcohol, or psychoactive drugs (van Os et al., 2009). There is some limited evidence on the familial clustering of both positive and negative sub-clinical symptoms in community samples (Hanssen et al., 2006). In the general population the distribution of the cognitive deficits seen in psychosis, e.g. mentalizing ability (Langdon & Coltheart, 2004) and bias in probabilistic reasoning (Linney et al., 1998), is also consistent with the psychosis continuum hypothesis, while there is less evidence on other, more severe cognitive deficits observed in patients with non-affective psychosis (van Os et al., 2009). Overall there is robust evidence on the increased risk of transition to clinical psychotic disorder for individuals with sub-clinical psychosis proneness features. This was initially reported by Chapman et al., (1994), who demonstrated high rates of psychosis in those scoring higher on the scales of magical ideation and perceptual aberration when examined 10 years later. In the Dunedin Multidisciplinary Health and Development Study, the children who reported psychotic-like experiences when assessed at age 11, were 16 times more likely to be screened positive for schizophreniform disorder, an attenuated form of schizophrenia, when assessed at 26 years of age (Poulton et al., 2000). More recently, in the Netherlands the transition to mental illness in those reporting sub-clinical symptoms of psychosis at inception was 8% after

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a 2-year follow-up, this figure being about 60 times higher than in those without psychotic-like experiences (Hanssen et al., 2005). Overall, these studies cannot be considered conclusive since they used different criteria in the definition of the outcomes, and were not replicated in other countries. Nevertheless their results are greatly important for the early recognition and phase-focused treatment of psychosis according to the early intervention paradigm (Cocchi et al., 2008; Edwards and McGorry, 2002).

Chapter 3

A DIMENSIONAL VIEW ON PSYCHOSIS The dimensional approach to psychopathological traits originates from two seemingly distant sources: one is more theoretical, rooted in the personality theory of Hans Eysenck and the other is more clinical, grounded in the anomaly of psychiatric diagnosis compared to other braches of medicine. Eysenck proposed that, as with other personality dimensions, psychoticism could be reduced to a fully continuous dimension measured with questionnaires at the descriptive level (Eysenck & Eysenck, 1985). Using factor analysis techniques he reduced personality traits to four dimensions and two continuums: introversion-extroversion and neuroticism-psychoticism. According to this theory, an individual who would score at the extremes of these continuums could be affected by psychopathological disorders. For instance schizophrenia was considered the result of high psychoticism and high introversion, while maniac depression would equally present high psychoticism, but show high extrovert traits. The Eysenck model is traditionally referred to as the full dimensional model, as clinical diagnosis and sanity lay on the same continuum. The concept that a clinical relevant disorder results from the worsening of a normal function/trait had been already widely accepted for the diagnosis of systemic diseases. The diagnosis of hypertensive condition, for example, would follow the measurement of blood pressure at an abnormal and

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dangerous level. In this framework the role of biological and environmental factors can be taken into account as they contribute to modifying the level of the continuous variable. In the example of hypertension, aspects such as a biological predisposition (e.g. relatives with hypertension) and precipitating factors (e.g. eating habits) contribute to the rise of the trait to clinical severity. The conceptualization of psychosis as a systemic disease would therefore suit the full dimensional view proposed by Eysenck. Roughly at the same time when Eysenck was working on his theory of personality, Paul Meehl (1962) advanced the “diseased” model of schizophrenia, more widely referred to as the quasi-dimensional model. Following the phenotypic and genotypic heterogeneity observed in psychosis, Meehl argued that schizophrenia arises from inherited vulnerability to the disorder rather than being a disorder itself. Meehl used the term schizotaxia to define the vulnerability and proposed this trait to be quasi-dimensionally distributed or, in other words, that not every individual would have a level of schizotaxia. Also within the individuals carrying the schizotaxon only a minority would develop the full-blown disease, with the remaining proportion showing milder symptoms or no symptoms at all. The disease model developed by Meehl (1962; 1989) uses the dimensional concept only on a small proportion of the general population presenting the genetic vulnerability to psychosis. Up to this point, the two models illustrate the application of the dimensional framework to the problem of psychotic traits distribution, as against the dichotomous classification. The quasi-dimensional model proposed a compressed dimensionality accounting for a proportion of the general population, whereas the full dimensional models attempted, more ambitiously, to explain psychopathology in the frame of personality. The empirical evidence collected in recent years has shown a degree of support to both models; on one side the studies conducted on the genetic vulnerability related to psychosis confirmed the role of genes in the underpinning of psychosis (Raine, 2006), on the other hand epidemiological studies showed that a larger and larger proportion of the general population has schizotypal traits (Hanssen et al 2005). The two models also diverge in the consideration of psychotic trait aptness. According to the full dimensional model, a

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moderate level of psychoticism is perfectly tolerable, and does not compromise adaptation, whereas for the quasi-dimensional model the signs of psychoticism are always conceived as risk factors. Gordon Claridge (1997) tried to incorporate the dimensional and quasidimensional views into a single model. In this model the full dimensional and the quasi-dimensional models overlap non-linearly at the high end of the psychoticism scale. According to Claridge there is a discontinuity between psychoticism, as intended by Eysenck, and the psychopathological continuum of schizophrenia, the schizotaxon, as hypothesized by Meehl. High psychotic traits, therefore, do not lead necessarily to the development of psychosis. In order to develop pathology an individual with high psychotic traits needs to be exposed to adverse environmental events that would discontinue the psychotic trait on the personality axis and shift it to the psychopathological continuum where the trait become a risk factor to develop psychosis. The idea that delusion-proneness might be distributed in the general population along a continuum from sub-clinical expression to full-blown psychosis resurrected the interest in the “reactive” or “psychogenic” psychoses (Strömgren 1974), and in the role that protective and precipitating factors could play in the passage from psychosis-proneness to clinical psychosis (D'Souza, 2007; Gracie et al., 2007; Scott et al., 2007). Current classifications already recognize a specific class of conditions characterized by symptoms of psychosis, and the related decline in psychosocial functioning that stem from a stressful event. Individuals with brief psychotic disorder experience delusions, hallucinations, and/or disorganized speech and behavior that last for at least one day and fully remit within a month. In this case a past severe mental disorder with psychotic features, or the symptoms attributable to substance abuse or to a co-existing physical illness or to head trauma, are exclusion criteria. The continuum dimensional view of psychosis has now more ambitious goals than to identify a subgroup of clinical conditions. A diagnosable psychosis is now thought as the most severe variant of a phenotype, which is distributed in the general population more widely than its clinical manifestations would suggest. According to the psychosis continuum, the symptoms observable in patients diagnosed with psychosis could be measured

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in non-clinical populations in less severe, but clearly recognizable forms (van Os et al., 2009). A radical take on the dimensional model would therefore assume that the difference between a clinically diagnosable psychosis and its sub-clinical features does not coincide with the presence of delusions or hallucinations, but it depends upon the impact associated to features as intrusiveness, preoccupation, distress, and tolerance to deviancy (van Os et al., 2009). A continuum dimensional view of psychosis underlies the possibility that the production of delusions and hallucinations originates from psychobiological dynamics common to all humans, and does not arise from brain damage or genetically impaired neurodevelopment, as currently thought (Lewis & Levitt, 2002; Preti & Miotto, 2005). Therefore delusion would be the result of automatic processes, activated by specific circumstances and based on evolutionary mechanics rooted in our ancestral history. The psychosis continuum hypothesis rests essentially on epidemiological data and on the evidence that both affective and non-affective psychoses do not depend on single genes, but seems to result from the accumulating effects of multiple interacting causes, both genetic and epigenetic ones, as in the two/three hit model of schizophrenia (Figure 1). According to this view, complex and interacting mechanisms would lead to the symptoms of psychosis by an interaction between biologically-based processes and environmental events, including exposition to brain-activating substances (for example, cannabis) and the neural and hormonal consequences of stressful life events (increasing levels of dopamine and corticosteroids). Indeed, the administration of dopamine agonists can induce paranoid beliefs, whereas antipsychotic drugs (dopamine-blocking agents) are able to abolish threat anticipation in animals, as measured using a conditioned avoidance paradigm (Moutoussis et al., 2007).

Step one Genetically-based anomaly

Step two Anomalous brain reorganization under normal endocrine stimuli during adolescence [?]a

Onset

Effects of protective and aggravating genes Increased dopaminergic sensitivity to stress [?]b

Stress [?]c Drug use [? Cannabis]d

Abnormal brain development

Perinatal insult

Effects genes a) b) c) d)

of protective and aggravating

Effects of protective and aggravating genes

Feinberg, 1982; Walker & Bollini, 2002 Davis et al., 1991; Kapur, 2003 Gracie et al., 2007; Scott et al., 2007 Moore et al., 2007; D'Souza, 2007

Figure 1. The “two/three-hit” developmental hypothesis of schizophrenia (modified from Preti and Miotto, 2005)

Chapter 4

THE CONCEPT OF PSYCHOSIS PRONENESS The idea that there is a pre-psychotic phase whereupon someone runs a higher risk of transition to full-blown psychosis renewed the interest in the measurement of psychosis proneness (Allardyce et al., 2007). To date, psychosis proneness is conceived alongside two different approaches. One approach assumes that a subgroup in the population is constitutionally at risk of developing a psychosis, for genetic or epigenetic reasons that impact on development and lead to the so-called schizotaxia, as first described by Meehl (1962), or schizotypy, as described by others (Claridge, 1997; Raine, 2006; Vollema and Hoijtink, 2000), schizotypy refers to a construct that does not fully overlap with Meehl‟ schizotaxia. The other approach takes a more radical view: this model assumes a complete symptomatic continuum between normalcy and patients with psychosis, whereby hallucinatory and delusion-like experiences and beliefs in non-clinical and clinical samples would share an underlying etiologic influence, including socio-demographic factors and neurocognitive mechanisms (Claridge, 1997; Garety et al., 2001). In a dimensional view, the distress caused by the pre-delusional belief, the preoccupation raised by it, intended as the time spent thinking about the unusual belief, and the conviction, the force with which the pre-delusional

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belief is held, would all contribute to the course and severity of anomalous subjective experiences (Peters et al., 1999; 2004). Indeed, patients diagnosed with psychosis tend to score higher on the measures of distress and preoccupation related to their delusional beliefs (Peters et al., 1999; 2004, Rocchi et al., 2008). The level of conviction is less likely to discriminate patients with delusions from healthy controls (Peters et al. 1999; Rocchi et al., 2008). Apparently, when a firm belief has settled, it is held with the same level of conviction by people with and without a diagnosed psychosis. An alternative hypothesis is that, above a certain level of psychological distress, delusions reflect perceptual abnormalities that lead to a mistaken conclusion even through normal reasoning (Maher, 1988). This interpretation is congruent with a continuum-threshold approach to psychosis-proneness. This model assumes that certain unusual subjective experiences and beliefs exist along a continuum (i.e. the multifaceted beliefs shared by a culture), but beyond a critical threshold of intensity/severity, or of distress and preoccupation, they become psychopathological symptoms and cause functional impairment (Hafner, 1988; Preti et al., 2007; van Os et al., 2009).

Chapter 5

MODELS OF PARANOIA Being prudent and cautious in the social encounters of everyday life is an approach that folklore and popular wisdom suggest as appropriate and advisable. Indeed, suspicion feelings and thoughts are frequent, and in general most of them do not cause particular concern, distress or interference in social activities. However, the strongest of these feelings and thoughts can upsurge to persecutory delusion. Paranoia can be considered a central symptom of psychosis; indeed, delusions of persecution occur in about 50% of cases of schizophrenia (Sartorius et al. 1986), and are widespread in clinical samples of patients diagnosed with bipolar disorder (Goodwin and Jamison, 1990), or major depression (Haltenhof et al., 1999). The high prevalence of paranoid delusions in clinical samples has been confirmed across different cultures (Ndetei and Vadher, 1984; Stompe et al., 1999). Persecutory thoughts are relatively distributed in the general population with percentages up to 30% and even 50%, according to the different studies and assessment methods (Verdoux et al., 1998; Peters et al. 1999; Martin & Penn, 2001; Ellett et al., 2003). Thoughts with high levels of threat (e.g., “There is a conspiracy against me”) are endorsed by a large proportion of the general population, too (Green et al., 2008). In all likelihood, current investigations on delusion underestimate the true frequency of paranoid

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thoughts, because large epidemiological studies from a psychiatric perspective generally phase out the most plausible instances of paranoid thinking (Freeman, 2007). Paranoid thinking appears related to instances of safety and integrity, concerning both physical and personal psychosocial identity. In experiments using virtual reality, people with higher levels of anxiety and interpersonal sensitivity were more likely to be suspicious during the test. This was interpreted as a relationship between anticipation of danger and concerns about inadequacy, and/or inferiority or rejection from others (i.e. feelings of vulnerability) and the chance that persecutory ideation could occur (Freeman, 2006; 2007). Paranoid thinking is strictly related, although it does not overlap, with ideas of reference: in these instances the person “holds the belief that some neutral event has special personal significance to him or her personally, by means of observation or communication by another” (Startup and Startup, 2005). Gossip and the circulation of information about him/herself are central to reputation building: behaviors supporting the individual‟s social image and reputation, such as altruism, cooperation and fairness, are subjected to important selective forces (Nowak and Sigmund, 1998; Stevens and Hauser, 2004). Some studies also reported evidence on brain areas involved in public image scoring (Rilling et al., 2004; Singer et al., 2004). Therefore, there is evidence for normal brain processes being involved in the formation of ideas of references: people are expected to scan social cues related to their own public image, such as scoring their status as far as reputation is concerned, and this is thought to impact on self-esteem, too (Leary et al., 1995). Recent studies indicate that ideas of persecution rarely occur in the absence of ideas of reference, while ideas of social reference may be present without ideas of persecution (Green et al., 2008); this suggests that the social monitoring of one‟s public image is a mechanism normally active in the general population, contributing to the onset of paranoid thinking. The pervasive feeling of “being at the center” is related to the formation of paranoid delusions in many models (e.g. Maggini and Raballo, 2004). A vague and unstable feeling of reference, which coexists with the critical

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awareness of its implausibility, often precedes the onset of psychotic breakdown. In the Basic Symptoms (BS) Model this experience is categorized as a second level BS, at an intermediate level between pre-clinical and fullblown psychosis (Huber and Gross, 1995). Indeed, subjective self-centrality is a feature occurring in schizophrenia, often in the initial prodromal phase of the disorder (Klosterkoetter et al., 2001). As for patients in stable maintenance treatment, about 72% report one or more self-centrality experiences (Maggini and Raballo, 2004). Finally, measures of self-centrality are related to both positive (i.e. cognitive-perceptual) and negative (i.e. interpersonal) factors of schizotypy (Raballo and Maggini, 2004).

Chapter 6

COGNITION AND PARANOIA Along with epidemiological studies demonstrating the high incidence of psychotic-prone features in the general population, the dimensional approach has sought to establish whether the cognitive impairments seen in schizophrenia are present, to a lesser degree, in individuals showing schyzotypal traits. Paranoia has been studied extensively in this respect and has provided evidence that some cognitive abnormalities are common, although different in intensity, between schizophrenia and healthy individuals with high delusion proneness.

REASONING BIAS Suggesting the existence of a reasoning bias in psychiatric patients involves the assumption that a correct or unbiased form of reasoning can be identified. Reasoning is a heterogeneous process that humans apply differently in order to solve problems. The nature of the process renders a normative definition of reasoning impossible, therefore any attempt to study this process leads to make some level of assumption about what reasoning is. Hemsley and Garety (1986) studied reasoning in persecutory delusion using as a Bayesian reference model of decision-making. According to the Bayesian theory of decision-making, optimal decision results form the mathematical computation of event probabilities. Therefore every occurring

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event has a probability attached to it that changes the probability of the event re-occurring and may modify the probability of related events. The hypothesis of Hemsley and Garety was that individuals with paranoid delusion are more prone to draw firm conclusions based on less evidence compared to control participants. To test this hypothesis, participants were shown two jars, each containing beads of the same two colours. In one jar the ratio of one colour outnumbered the other, whereas in the other, the proportion was reversed (the ratio was 85:15). Once this information was explained to the participants, the jars were hidden away and participants were told that they had to guess from which jar the experimenter was drawing beads. The result of the first and subsequent studies showed that deluded patients made guesses based on less information compared to other psychiatric patients (non-deluded) and control participants (Hemsley & Garety, 1986; Huq et al., 1988; Garety et al., 1991). This effect was subsequently named “jumping-to-conclusions” (JTC) reasoning style and was also observed in individuals with delusion proneness (Linney et al., 1998). Similarly, Young and Bentall (1995; 1996) conducted a series of investigations on deluded patients with a slightly different paradigm and suggested that persecutory delusion, rather than being associated with a probabilistic reasoning bias, has a data-gathering bias i.e. seeking less information before making a decision (Blackwood et al. 2001). Studies in this area have also confirmed that reasoning bias in deluded patients is not associated with memory impairment or lower IQ (Dudley, John, Young & Over, 1997), supporting the idea that reasoning bias is characteristic of paranoid thinking style and not a consequence of it.

ATTENTIONAL BIAS Patients with persecutory delusions overvalue threatening stimuli, and preferentially attend to them. Latent inhibition, for example, a physiological mechanism involved in the filtering of irrelevant environmental stimuli, is typically disrupted in acute psychosis (Baruch et al., 1988), as it is in healthy people scoring high on measures of schizotypy (Braunstein-Bercovitz &

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Lubow, 1998). Patients with paranoid delusions tend to overestimate the likelihood of future threatening events (Corcoran et al., 2006; Kaney et al., 1997), even when their recall of past threatening events is controlled for. Deluded patients show a high susceptibility to environmental threatening stimuli that they preferentially attend to and recall (Bentall & Kaney, 1989; Leafhead, 1996). In the context of visual attention, paranoid patients are quicker to identify threatening stimuli although they are less efficacious than controls and other psychiatric disorders to identify target stimuli (Phillips et al., 2000). Similar visual detection paradigms have been applied to schyzotypal individuals, showing that proneness to psychosis can alter the attention pattern, especially in a situation where the amount of stimulation is scarce and time constraint applies (Cella et al., 2007)

ATTRIBUTION STYLE Attributional biases are not pathological per se and healthy individuals tend to display a self-serving bias in explaining events, which is taking credit for success (internal attribution) and deflecting responsibilities for failure (external attribution). It has been argued that such a bias may serve to preserve and enhance self-esteem (Mezulis et al., 2004). Early studies conducted on paranoid patients showed an exaggerated self-serving bias with marked internal attribution for positive events and external attribution for negative events (Kaney & Bentall, 1989; Sharp & Healy, 1997). Freeman and coworkers (Freeman et al., 1998) found lower levels of self-esteem in schizophrenic patients. Bowins and Shugar (1998) reported lower levels of self-esteem in deluded patients, too. The studies reviewed so far used questionnaire measures to assess selfesteem. Bentall (2003) argued that the use of questionnaires can only inform about the nature of explicit beliefs and that paranoid levels of self-esteem can be better understood at the implicit level. Implicit beliefs are automatic judgments about one‟s own self that cannot be readily accessed. Evidence from self-reported measures of self-esteem and experimental tasks measuring implicit association highlighted that paranoid patients showed an accentuated

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self-serving bias for explicit attribution, but a pattern similar to depression for implicit attribution (Lyon et al., 1994). The implicit attribution task showed paranoid patients with low internal positive and high internal negative attributions. We are not aware of studies reporting on implicit and explicit self-esteem levels in individuals with delusion proneness, but association between low mood, delusion and hallucination proneness has already been suggested by several studies (e.g. Cella et al., 2008; Verdoux et al., 1999).

THEORY OF MIND (TOM) The ability to attribute desires, knowledge and beliefs to other individuals is generally described as “Theory of Mind” (ToM). Inference about other people‟s mind is a cognitive ability that humans constantly apply to make sense of social situations and understand other people‟s beliefs and behavior. Interest in studying the theory of mind in the frame of psychopathology was prompted by the findings that children with autism have a specific difficulty in understanding other people‟s mind (Baron-Cohen et al., 1985). Autistic people have often been described as lacking a ToM, as a consequence of a neurodevelopmental pattern resulting in withdrawal from social situations. The concept of abnormal mentalizing function in schizophrenia was first suggested by Frith and co-workers (Frith & Corcoran, 1996). Unlike autism, schizophrenia does not show problems in mentalizing function up to the insurgence of the disorder. Paranoid patients have no problem in ascribing intentions to other people: their problem is that they tend to ascribe the wrong intentions (Frith, 2004). It has been suggested that paranoia does not affect the ability to mentalize other people‟s states of mind but alters the contents ascribed to other minds. Research has shown that people with paranoia tend to ascribe the wrong intentions in ToM tasks but, unlike autism, rather than being confused about what emotion or belief might lie behind a situation, they tend to ascribe it to other intentions that support their delusion (Doody et al 1998; Pickup & Frith, 2001). Blakemore and colleagues (2003) suggested that the problem with

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paranoid individuals is a tendency to over-mentalize and therefore ascribe intentions to situations that would go unnoticed by most people. More recently, Langdon and Coltheart (2004) found that high-schizotypal adults were significantly impaired in their ability to appreciate metaphors and ironic utterance, suggesting a theory of mind problem in the psychotic-prone individuals. Similarly, Pickup (2006) found that positive schizotypal traits in the normal population are associated with subtle impairments in ToM tasks; the deficit was found to be independent from reasoning ability, executive function and verbal IQ. Bentall and co-workers (2001) purported a model in which delusions arise as a “psychological defence” or attempt to separate negative affect from consciousness. Freeman and Garety (2004), instead, suggested that delusions are induced by an attempt to gain an explanation for an unusual experience, and they are maintained by cognitive biases which collect confirmatory evidence and avoid disconfirming evidence. Epidemiological longitudinal studies showed that states of negative affect, when associated with hallucinations or intrusive perceptions, greatly increase the chances of later developing a delusion (Krabbendam et al., 2002; Lewandowski et al., 2006). In a recent study using a mixed sample (i.e. patients with schizophrenia spectrum disorders, major depression and healthy controls), the depressive or pessimistic thinking style, characterized by low self-esteem and high levels of depression and anxiety, was found to be strongly related to the presence of persecutory beliefs (Bentall et al., 2009). In the same study cognitive performance, including the ability to understand the mental states of others, and the ability to formulate hypotheses on the basis of sequentially presented information, was related to paranoid thinking, too, but less strongly and with less explained variance than the affective dimensions. The authors concluded by pointing at affective processing as a necessary factor in the development of paranoid thinking, and suggesting the need specifically to address affective symptoms in patients with psychosis. This subject is of absolute relevance to the debate concerning treatment of the affective component of psychosis, especially considering the poor effectiveness of pharmacological treatment for this cluster. The use of psychological therapies and in particular cognitive

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behavioral therapy (CBT) for first-episode psychosis is showing promising results and, in future years, it may become the elective treatment to tackle affective components in psychosis (Cocchi et al., 2008; Edwards and McGorry, 2002). As we have seen, the role of affective components has been recently reevaluated and included in several conceptualizations of psychotic symptoms as a factor contributing to the insurgence, maintenance and remission of psychotic symptoms. The following section will expand and clarify the relevance of affective factors to paranoia.

Chapter 7

MOOD, ANXIETY AND PARANOIA The term “affect” defines the transition in brain states expressed through stable changes in the readiness to undertake behaviors. The term derives from the Latin “affectus” = ad + facio, which means “tendency to do”.

MOOD The term “mood” refers to the affect involved in the control of voluntarily initiated processes: depression is the mood state which relates to a general decrease in behavioral activation, while excitement or mania is the mood state which increases behavioral activation. In humans, mood alteration can influence behavior, thoughts and the experience of emotions. There is robust evidence that the neural circuits involved in the control of mood were primarily established as a mechanism to tune animal behavior to climatically based seasonal changes in the environment (Reinberg & Ashkenazi, 2003; Sherman, 2001). A “spontaneous” depression would have led the animal to decrease behavioral involvement during the cold season, when the chances of getting food were too low; on the contrary, excitement would have increased the number of actions during the “good season”, leading the animal to hunting and mating behaviors. In social animals, including

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humans, additional processes reinforce the use of depressive withdrawal as a way to deal with failure and defeat, thus linking mood variations to nonseasonally related events (Price, 1967; Stevens & Price, 1996). Pathological activations of the circuits that control mood, secondary to genetic polymorphisms (Canli et al., 2006; Willis-Owen and Flint, 2007) or brain damage during early development (Preti et al., 2000), are likely to result in mood disorders such as major depression or bipolar disorder. Internal psychodynamic conflicts related to the social environment are instead thought to be involved in “neurotic” depression (LeCroy, 2000). Adjustment disorders with depressive mood are normal occurrences, which can require treatment when they impair social and occupational functioning, but should not be considered pathological per se.

ANXIETY Anxiety is basic affect involved in the control and allocation of attention necessary to orient behavior. People with high levels of anxiety are more likely to deploy attention to both external and internal cues. Highly anxious individuals are more reactive to environmental stimuli indicating potential threats and tend to respond more readily to internal bodily symptoms interpreted as signals of dysfunction. The term anxiety is defined as a complex psycho-physiological state expressed with feelings of uneasiness, fear or worry. It includes an array of specific cognitive, somatic and behavioral components. Anxious patients tend to report a large number of symptoms most commonly with a somatic basis, such as heart palpitations, fatigue, nausea, chest pain, shortness of breath, stomachaches, or headaches. External signs of anxiety include pale skin, sweating, trembling, and pupillary dilation. Blood pressure and heart rate are often increased, as are sweating and blood flow to the major muscle groups; on the contrary, immune and digestive system functions are inhibited. Individuals suffering from anxiety might also experience panic and feel to be about to die. Stress is the classic activator of anxiety, given its evolutionary role in helping to deal with tense situations and maintaining the focus on

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relevant actions. Overall, this profile corresponds to the “fight or flight” reaction, also observed in animals. All the symptoms of anxiety are the sub-product of mechanisms aimed at progressively controlling actions during their execution. This mechanism controls the execution of motor behavior via a feedback loop connected with the programmed action. Our brain can program many actions, though never acted before; it is also capable of planning without the need for execution. When a programmed action is carried out, the peripheral sensory system records the execution and muscle sensors record the state of tension. Other sensors record every minimal change, such as the distribution of weight over the foothold or the body position in space. Any minimal discrepancy between the expected outcome of the action and the actual perceived outcome produces changes in muscle tension, to adjust the movement, and also resets the allocation of oxygen and blood to the involved parts of the body. As a consequence, respiratory and heart rates can change, especially when the readaptation is intense and/or sudden. This change in muscle tension, and the concurrent changes in respiratory and heart rates are what we experience as “anxiety”, particularly when the action‟s execution is in the planning stage, as often occurs when planning social actions (e.g. meeting a good-looking person at a party, taking an exam). The larger the discrepancy between the programmed and the currently executed action is, the bigger the changes in muscle tension and in respiratory and heart rates will be. This discrepancy creates the feeling of anxiety. While the motor and visceral system continually adapts, the attention demand for the planned action is also reallocated to bodily sensations. It is obvious that large discrepancies in executing actions entail the risk of negative outcomes and increase the perception of vulnerability: therefore more attention is paid to threat or menace cues, signaling potential perils or dangers. In our view, this is the main reason for anxiety being linked to hypochondria (Creed & Barsky, 2004) on the one hand, and to paranoid thinking on the other: indeed, in both clinical and non-clinical samples anxiety is predictive of the occurrence and persistence of paranoid thoughts (Freeman, 2007). In patients diagnosed with a mental disorder, anxiety is specifically linked to depression. Depression is the mood state of the “bad season”, deputed to

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rest (Foster & Roenneberg, 2008; Goodwin & Jamison, 1990; Hazlerigg & Loudon, 2008); on the other hand, contingent depression is linked to negative life events, when the person is more exposed to the most negative consequences of loss or defeat (Stevens & Price, 1996). In general, when the brain experiences a “depressed” state, the individual feels an enhanced risk of negative outcome, because the feeling of depression is associated with a lower availability of resources: thus higher levels of anxiety develop as the levels of depression rise. The increased allocation of attention to bodily sensations and environmental cues of threat and menace may also favor the development of paranoid thinking: the interplay of anxiety and paranoia can be observed in major depressive patients, who often report somatization problems and persecutory delusion (Bentall et al., 2008; Kamara et al., 2009).

AFFECTS AND PSYCHOSIS Neurosis and psychosis have traditionally been studied as separate entities. At the basis of this distinction, there is the assumption that psychotic disorders have an organic etiology and neurotic disorders have a psychological etiology (Freeman & Garety, 2003). In the last twenty years there has been an increasing interest in the study of the psychological components associated with psychotic symptoms (e.g. Bentall, 1994; Chadwick and Birchwood, 1994). One of the major achievements of the psychological investigations has been the reconsideration of the role played by affects and emotions (i.e. anxiety, anger, mood and mania) in the formation and maintenance of psychotic symptoms, especially delusion and hallucinations. Longitudinal studies conducted on risk factors contributing to the development of schizophrenia found that children who went on to develop schizophrenia were significantly more anxious, at age fifteen, than their pairs who did not develop schizophrenia (Jones et al., 1994). In a 3-year populationbased study, Krabbendam and colleagues (2002) reported that low levels of self-esteem and high neuroticism could predict the onset of psychotic positive symptoms. Similarly, Tien and Eaton (1992) showed that the presence of

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anxiety, but not depression, was a significant risk factor for the subsequent development of psychosis. Anxiety and mood disturbances have been shown to precede the insurgence of psychotic episodes. Clinical and retrospective studies have shown that irritability, anxiety and depression precede by two to four weeks the appearance of positive symptoms (Birchwood et al., 1992; Yung & McGorry, 1996). Finally, it has been ascertained that depression and anxiety accompany positive symptoms during the acute and remittance phases. Comorbidity between depression and schizophrenia has been found as high as 45% in a sample of first admitted patients (Leff et al.,, 1988). In consecutive admitted patients with a diagnosis of schizophrenia, the rate of anxiety disorders was as high as 43% (Cosoff & Hafner, 1998). Norman and Malla (1994) conducted a longitudinal study on more than fifty patients with schizophrenia and monthly assessed depression and anxiety: results showed that anxiety and depression were more related to positive than to negative symptoms. Emotional deregulation and dysphoria have also been observed in crosssectional studies as associated with delusion and hallucination proneness (Cella et al 2008; van 't Wout et al., 2004).

Chapter 8

EMOTIONS AND AFFECTS IN PARANOIA Anxiety and depression are not the sole affects linked to paranoia. As a matter of fact, mania, anger, fear, guilt and shame all present a considerable level of association with paranoid thinking Excitement, which is the motor correlate of mania, is triggered by seasonal cues of the “good season”, and in evolutionary terms relates to a higher chance of successful mating. Contingent excitement is also triggered by joy, the emotion of cheerfulness, which is often associated with the achievement of resources necessary for survival. We experience excitement when presented with the prospect of a nice meal, in the presence of pleasant company, when winning a competition or by proxy when our favorite team wins a game. When people experience joy, they are likely to become excited, and this leads to higher sociability. Excited people are also more likely to allocate attention to social cues predicting the opportunity of further achievements. Paranoid thinking does not necessarily relate to menace and threats: people can experience “positive” paranoid thinking, leading them to believe in their “effectiveness” as achievers. This “positive” paranoid thinking is likely to be involved in grandiosity or erotomanic delusions, often occurring in patients with bipolar disorder during the manic phase, and it is also associated with hypomania in the form of fixed ideas or pre-delusional conviction.

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As for anger and fear, it is intuitive to understand their links with anxiety and depression, on one side, and paranoia on the other. Anger is the emotion signaling a social menace to one‟s own personal properties. When someone, or something, threatens the integrity of their own properties, people become angry, and prepare to fight for the defense of their threatened property. Anxiety and anger show a close relation depending on the chances of an anger-related behavior being acted. People who are reluctant to get involved in a fight, will be more likely to experience a gap between the imagined outcome of the necessary action and the foreseen outcome of what they expect to do, therefore they will experience anxiety. Fear occurs in face of peril and danger, particularly when it involves the actual risk of being harmed or killed. The experience of fear is accompanied by willingness to fight for life or to fly away from danger. Again, deviancy between the perception of imagined and effectively executed behaviors can trigger anxiety in relation to fear. This is the reason why people suffering from anxiety disorder can report fear as specifically linked to their anxiety. Panic attacks can be triggered by imaginary situations or thoughts of doing or having done something wrong. We often have these thoughts, but they are mostly subconscious and do not reach a level of full awareness. People with inner conflicting beliefs towards others (e.g. powerful figures, attitudes towards different races, sexual orientation) can experience fear related to thoughts of sexual or aggressive behavior. People often become aware of the consequences of these thoughts, feeling anxious and fearful, but they cannot precisely link this feeling to the surrounding environment, as initially suggested by Freud (1926/1936). Depression is the affect associated with scarcity of resources, failure and defeat. Depressed people feel more vulnerable to threats and danger, they are more likely to experience anxiety and react with anger or fear to the negatively perceived environment. Anxiety and depression are often comorbid conditions, to the extent that identifying one of the two disorders makes the second more likely to be present than not (Kessler et al., 1994; Kessler, 2007); moreover, patients with major depression are more likely than controls to experience anger (Luutonen, 2007; Painuly et al., 2005). Fear, per

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se, is less often investigated in patients with mental disorders, since it is mistaken with anxiety. As we have seen, both anger and fear relate to anxiety, and anxiety can trigger paranoid thinking by increasing attention towards environmental cues. On the other hand, we have also seen that paranoid thinking tends to allocate attention specifically to stimuli perceived as holding some degree of threat or menace. Cullari (1994) measured the level of anger in a schizophrenic inpatient sample and found significantly higher levels of state anger in patients, compared to non-patients. In a sample of patients diagnosed with schizophrenia, Lysaker et al. (2009) found that those who reported low levels of self-esteem also made significantly more misattributions of anger than comparison groups. Guilt and shame are two of the most important affects involved in the selfmonitoring of social behavior, also erroneously referred to as “moral emotions” (Kroll & Egan, 2004; Tangney et al., 2007). Guilt is the affect that drives people to repay a damage done to someone else. When people feel guilty, they become aware of the damage they caused and also enter in a state of distress which depends on the fear of losing the love of the damaged and/or being exposed to retaliation. Guilty people exhibit rituals of reparation (e.g. begging pardon, and so on), and specifically aim at regaining bonds with the offended person. When experiencing shame, people become aware of having broken some social rule, and expect or fear the chance of being exposed to punishment. This affect prompts people to rituals of humiliation in order to regain consideration by the group they belong to, by publicly admitting being aware of their mistake and accepting reproof. Shame, indeed, usually triggers visible markers, such as blush spreading over one‟s face, and people who exhibit these markers are more likely to gain acceptance than those who show arrogance and defy public disapproval. Evolutionarily, guilt and shame are used to avoid retaliation, with guilt more linked to social bonding, which is critical in helping and support, and shame associated with public image scoring, which is critical in trades and alliances.

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Guilty or ashamed people can experience fear and anger for easily understandable reasons. They can be forced to repay even for involuntary damages, they can be exposed to public discredit or suffer ostracism. Anger and fear lead to anxiety, which might be intensified by depression, when defeat follows retaliation: all these emotions and affects can precipitate paranoid thinking, especially when punishment is expected. Research has shown that shame and guilt are associated with higher chances of experiencing paranoid thinking (Stanghellini & Ballerini, 1992) although to date the findings have not been replicated.

Chapter 9

THE HEURISTICS OF PARANOIA What has been illustrated so far is a range of psychological phenomena that can explain the genesis of paranoid thinking not only in psychopathology but also in normal experiences. We embraced the view that paranoid thinking is not pathological per se but it becomes pathological only when it reaches the extreme of its distribution. The conceptualization of paranoid thinking as a dimensionally distributed style of thinking would allow its reformulation as human heuristic or a shortcut used by the cognitive system to deal with uncertainty during stressful situations. In computer science, a heuristic is an algorithm (i.e. a sequence of calculations) designed to reach an acceptable solution to a problem, in a rapid but poorly controllable way (Pearl, 1983). A heuristic produces solutions that cannot be formally proved to be correct, or optimal (i.e., with the best allocation of resources), nevertheless they are practical and can be effectively used. Heuristics use exploratory problem-solving techniques based on feedback to improve performance: more specifically, heuristics stand for “strategies using readily accessible, though loosely applicable, information to control problem solving in human beings and machines” (Pearl, 1983, p. vii). Through a variety of experiments, Kahneman and Tversky (1982) have shown that heuristic and decision-making biases are far from uncommon in humans, particularly in an uncertain environment. Although susceptible to

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errors, heuristics can generally simplify the complexity of the environment, be accurate and reach advantageous decisions. Damasio (1994) proposed that the organism can simplify the environmental complexity by using emotional signals arising from the body: the process of using emotions to assist decision has been increasingly referred to with the concept of “emotion-based learning” (Damasio, 2003; LeDoux, 1996). The emotion-based learning system appears to provide knowledge about the outcome of decisions, on the basis of previous experience on the emotional consequences of interactions with specific stimuli (Damasio, 1994). Bowman and Turnbull (2004) suggested that the emotion-learning system is an aggregate of learning principles, so much so that they provide information about the often long and complex reinforcement history that the individual has had with an object. The addition of emotions is claimed to be particularly helpful in uncertain conditions where individuals are required to make rapid decisions while not clearly understanding the situation, or when the advantageous outcomes of a decision do not result in an immediate gain (Damasio, 1996; LeDoux, 1996). The sub-threshold activation of an emotion adds information on past interaction with that specific situation: when the reenacted emotion signals a bad outcome (as for fear, disgust or anger), the individual will avoid the situation. There is mixed evidence showing that patients with schizophrenia have difficulties in performing emotion-based learning tasks and in deploying emotions to support the cognitive system (Dunn et al., 2006; Sevy et al., 2007). By increasing the chance of perceiving neutral stimuli as threatening, paranoid individuals could prevent the chance of missing a real menace in the surrounding environment when they are under stress. Clearly, in order to be effective, this heuristics should be activated only when the level of perceived stress is high enough to signal relevant deviations from normalcy in social interactions. However, paranoid thinking can also be activated when stress arises from the risk of losing a good chance: in this case, paranoid thinking acts by resetting the threshold for reaction to environmental stimuli, so that the risk of missing an available resource is prevented. This “positive” paranoid thinking

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increases the allocation of attention to stimuli such as potential mating or other achievements, and can end up in grandiose or erotomanic delusions. When specifically investigated (Peters et al. 1999; Martin & Penn, 2001; Ellett et al., 2003), the high prevalence of paranoid thinking in the general population favored this model. Clearly, more detailed studies will be necessary to conceive elements of paranoid thinking as a normal feature of our cognitive system, and not as the result of pathological processes. The first step in this process will be to understand when and how the threshold of normalcy is passed and paranoid thinking steps into clinical ground.

Chapter 10

THE TIPPING POINT: WHEN SUSPICIOUSNESS BECOMES PARANOIA Considering paranoid thinking as heuristic leaves space to a more detailed consideration of activating factors. Among the factors considered in the previous section, stress is likely to be the most relevant element. Individuals who are more likely to expose themselves to stressful situations should also be more likely to develop paranoid thinking, up to delusional paranoia. Indeed, there is evidence that stress is specifically linked to the onset of psychosis (Gracie et al., 2007), and it is related to positive symptoms of psychosis in non-clinical populations (Scott et al., 2007). Anxiety and depression could be influential in linking stress to paranoid thinking: people with dysphoria, experiencing distress, or presenting anxious and depressive features are prone to report positive symptoms of psychosis (Cella et al., 2008; Preti et al., 2007). People prone to impulsive behavior are also more likely to be involved in stressful situations (Compton & Kaslow, 2005; O'Boyle & Barratt, 1993), but the links between impulsivity, stress and symptoms of psychosis are poorly investigated. However, people with personality disorders associated with impulsivity, such as borderline personality disorder, sometimes develop a mental breakdown with psychotic features, as a reaction to stressful situations they have caused to themselves.

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Cognitive biases can influence the way anxiety and depression activates paranoid thinking: a constitutional propensity to attribute threatening intentions to others can favor the activation of paranoid thinking when in distress. In a recent study, participants whose anxiety was experimentally induced significantly reported more paranoid thoughts and also made more “jumping-to-conclusions” inferences than those in the control condition (Lincoln et al., 2009). More interestingly to the hypothesis summarized beforehand, there was an interaction of anxiety and reasoning biases in the development of paranoid beliefs. These constitutional cognitive biases can depend on genetic vulnerability (Iarocci et al., 2007), brain damage occurring during early life stages (Preti and Miotto, 2005) or they can be the result of learning when exposed to a discriminating social environment (Morgan et al., 2009). The abuse of psychotogenic substances, such as dopamine-stimulating agents (cocaine, amphetamine) or cannabis, can precipitate paranoid thinking in predisposed persons (Kaye & Darke, 2004; Miettunen et al., 2008; Rounsaville, 2007). Brain damage in adulthood results in delusion formation, too: brain lesions in the right hemisphere or in the bifrontal areas are often at stake in neurologic patients with delusions (Devinsky, 2009). Some malfunctioning of the amygdala, which is involved in the detection of fearful stimuli and activated in anger, can contribute to the cognitive biases that activate paranoid thinking when this is not necessary (Reuter et al., 2009). Other potential areas involved in the improper activation of the paranoid heuristics are those implied in brain networks supporting empathy (Singer & Lamm, 2009). Paranoid thinking could also be a relic of the past, when the world was much more violent and dangerous than today. The most important threat to personal integrity in the civilized world (i.e. living in a town together with people who are not genetically related with one other) is not violence but social exclusion from bargaining. For this reason, public image scoring is very important in current life, and people might be more concerned about other people‟s attitudes towards them than in the early environment of adaptation (EEA). However, a psychological process able to detect threats of violence in the environment might have been adaptive in the

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EEA, but less advantageous in the current world: being ready to react to someone who might kill us could have been advantageous in a world where this was a real threat, but it is no longer adaptive in a world where other people can be dangerous in a less violent, but not less dreadful way. A further hypothesis on the development of paranoia can stem from the adaptive challenges faced by the anxiety system. In the past, being able to correct an ongoing action, in order to compensate for deviancy in execution, would have been adaptive when facing the risk of confrontation with a dangerous animal or an aggressor. Now, we are more likely to imagine actions, rather than execute them: we imagine meeting someone we are in love with, or facing a bullying boss. In these imagined scenarios we do not execute actions, nevertheless we strive to correct the imagined execution of an action which is going wrong with a distressing result. Living with strangers is the rule in our modern civilized world: necessity and the longer duration of life expose people to social encounters with other people they do not know very well. During these encounters, individuals may experience an unexpected breaking of the social rules, followed by an alteration in affect due to shame, embarrassment and guilt. These “moral affects”, as already said, are involved in the protection from the risk of retaliation, but they are activated at the cost of greater distress, with a greater chance of experiencing anxiety, and depression creating a fertile ground for paranoid thinking. Within the framework of emotion-based learning, paranoid thinking can be interpreted as the result of an overactivation of the emotional system assisting a higher cognitive function. When pondering options in a complex environment, paranoid individuals may experience high levels of emotional arousal before making a choice. In the case of an inflated emotional response to a large number of options in the environment, the individual may experience threat. The behavior resulting from this highly threatening experience of the environment is likely to carry a high degree of bias and give rise to paranoid thinking. Recent research has also shown that paranoid thinking is less sensitive to drugs than other positive symptoms (Manschreck & Khan, 2006). This can

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depend on paranoia being a heuristic not amenable to modifications, and it suggests that paranoia can be a trait deeply rooted in the individual.

Chapter 11

HOW UNDERSTANDING PERSECUTORY THINKING CAN HELP PREVENTION The conceptualization of paranoid thinking in a dimensional fashion has suggested the idea that there are different degrees of persecutory delusion intensities. The distinction between pathological and non-pathological lies in the dysfunction caused by paranoia to the individual and to his/her social environment. As the dysfunctional levels are likely to increase proportionally to the severity level of paranoia, interventions can be designed for different stages. Preventive interventions for psychosis are in their early days, but if further studies confirmed a positive effect, in the near future they could be incorporated in common practice (de Koning, et al., 2009). The reason for the increased popularity of preventive treatments is the fact that this intervention can greatly influence the future course of psychotic illness and avoid transition to a full-blown psychosis (French et al., 2007). Among others, CBT has shown to be effective in treating prone-to-psychosis individuals and firstepisode psychosis (Addington & Gleeson, 2005). The issue of treating individuals in pre-clinical phases relies on the assumption that those people are at a high risk of developing a highly debilitating illness (e.g. schizophrenia). Although this can be thought true for the majority of cases, a proportion of those who show psychosis proneness do

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not develop a psychotic illness (Hanssen et al., 2005). Peters et al (1999), for example, found that the followers of new religious movements (e.g. Hare Krishnas and Druids) reported levels of delusional proneness that were comparable to those of deluded patients: the only distinction between the deluded patient and the new religious movement was in the level of distress associated with delusion. Preventive intervention would therefore need to incorporate the fact that delusional ideation per se may not be pathological, and it should target only those individuals showing a high degree of distress and preoccupation attached to their delusional ideation. Considering distress as the precipitating factor to pathological delusion fits the overall idea presented in this contribution, i.e. suggesting the affective factor to be a moderator in the clinical severity of paranoia. Whether paranoid thinking is a heuristic that we all have, the pathological end of a chain of circumstances, the consequence of a constitutional low selfesteem that needs to be re-balanced, a pathological propensity to develop depression or anxiety, the result of a stressful strain not amenable to correction or even the product of cognitive biases with a developmental component, intervention can be undertaken. Stress can be buffered by social support, therefore offering institutional social support (e.g. social workers, social security cards) can prevent the exacerbation of distress in those who are exposed to unavoidable stress. In patients with an already developed mental disorder, stress can precipitate anxiety and depression, which could be aggressively treated, also because untreated distress is often complicated with substance abuse for the purpose of self-medication (Khantzian, 1985). Moreover, in patients with schizophrenia, depression and paranoia are strictly related over time (Drake et al., 2004); treating depression, the principal risk factor for suicide, can decrease paranoid thinking, too, suspicion and diffidence being factors involved in the psychotic patients‟ poor attendance to care services. Psychoeducation can decrease faulty appraisal and attribution errors, with more focused cognitive strategies aimed at improving problem solving and social skills in people who are defective in these fields. There is some evidence on CBT being effective in reducing stress and transition to psychosis

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in people at higher risk, but well-conducted replication studies are still lacking (O'Connor, 2009).

CONCLUSION We have summarized information on a model depicting paranoid thinking as the first stage in delusion formation. Paranoid thinking can be conceived as a heuristic aimed at dealing with uncertainty under pressure of stress: it is activated by anxiety, depression and hypomania, and by anger, fear, shame and guilt. Preventive interventions aimed at reducing transition to psychosis in people at risk, and in reducing the most impairing consequences of paranoia in those who have already developed a psychosis, must appreciate the dimensional nature of paranoid thinking, and effective treatments will be developed once we are successful in defining more precisely the subcomponents involved in the transition from mild paranoid thinking, characterized by suspiciousness and alarmed diffidence, to the more severe paranoia which is typical of PPD, chronic delusion and paranoid schizophrenia.

REFERENCES Addington, J. & Gleeson, J. (2005). Implementing cognitive-behavioural therapy for first-episode psychosis. British Journal of Psychiatry, (Suppl.) 48, s72-76. Agerbo, E., Byrne, M., Eaton., W.W., & Mortensen, P.B. (2004). Marital and labor market status in the long run in schizophrenia. Archives of General Psychiatry, 61, 28-33. Aleman, A., Nieuwenstein, M.R., Bocker, K.B.E., & De Haan, E.H.F. (2001). Multi-dimensionality of hallucinatory predisposition: factor structure of the Launay-Slade Hallucination Scale in a normal sample. Personality and Individual Differences, 30, 287-292. Allardyce, J., Suppes, T., & van Os, J. (2007). Dimensions and the psychosis continuum. International Journal of Methods in Psychiatric Research, 16, S34-S40. APA (American Psychiatric Association). (1994). DSM–IV. Diagnostic and Statistical Manual of mental disorders. Fourth Edition. Washington, DC: American Psychiatric Association Press. Baron-Cohen, S., Leslie, A.M., & Frith, U. (1985). Does the autistic child have a "theory of mind"? Cognition, 21, 37-46. Baruch, I., Hemsley, D.R., & Gray, J.A. (1988). Differential performance of acute and chronic schizophrenics in a latent inhibition task. Journal of Nervous and Mental Disorders, 176, 598-606.

56

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Bentall, R.P. & Kaney, S. (1989). Content specific information processing and persecutory delusions: an investigation using the emotional Stroop test. British Journal of Medical Psychology, 62, 355-364. Bentall, R.P. (1994). Cognitive biases and abnormal beliefs: toward a model of persecutory delusion. In David, A.S., & Cutting, J. eds. The neuropsychology of schizophrenia (pp. 337-360). London, UK: LEA. Bentall, R.P. & Young, H.F. (1996) Sensible hypothesis testing in deluded, depressed and normal subjects. British Journal of Clininical Psychology168(3):372-5. Bentall, R.P. (2003). Madness explained. London, UK: Allen Lane. Bentall, R.P., Rowse, G., Kinderman, P., Blackwood, N., Howard, R., Moore, R., Cummins, S., & Corcoran, R. (2008). Paranoid delusions in schizophrenia spectrum disorders and depression: the transdiagnostic role of expectations of negative events and negative self-esteem. Journal of Nervous & Mental Disease,196, 375-383. Bentall, R.P., Rowse, G., Shryane, N., Kinderman, P., Howard, R., Blackwood, N., Moore, R., & Corcoran, R. (2009). The cognitive and affective structure of paranoid delusions: A transdiagnostic investigation of patients with schizophrenia spectrum disorders and depression. Archives of General Psychiatry, 66, 236-247. Bentall, R.P., Corcoran, R., Howard, R., Blackwood, N., & Kinderman, P. (2001). Persecutory delusions: a review and theoretical integration. Clinical Psychological Reviews, 21, 1143-1192. Berrios, G.E. (1991) Delusions as „wrong beliefs‟: A conceptual history. British Journal of Psychiatry, 14(suppl.), 6-13. Birchwood, M., Macmillan, F. & Smith, J. (1992). Innovations in the psychological management of schizophrenia (pp. 115-145). London, UK: John Wiley & Sons. Bijl, R.V., van-Zessen, G., Ravelli, A., de-Rijk, C., Langendoen, Y. (1998). The Netherlands mental health survey and incidence study (NEMISIS): objectives and design. Social Psychiatry & Psychiatric Epidemiology, 33, 581-586.

References

57

Blackwood N, Howard R, Bentall RP & Murray RM (2001) Cognitive neuropsychiatric models of persecutory delusions. American Journal of Psychiatry, 158, 527-539 Blakemore, S.J., Sarfati, Y., Bazin, N., & Decety, J. (2003). The detection of intentional contingencies in simple animations in patients with delusions of persecution. Psychological Medicine, 33, 1433-1441. Bleuler, E. (1950). Dementia Praecox or the Group of Schizophrenias. (1908). Translated by J. Ainkia. New York: International Universities Press. Bowman, C.H, & Turnbull, O.H. (2004). Emotion-based learning on a simplified card game: the Iowa and Bangor Gambling Tasks. Brain & Cognition, 55, 277-282. Braunstein-Bercovitz, H., & Lubow, R.E. (1998). Are high-schizotypal normal participants distractible or limited in attentional resources? A study of latent inhibition as a function of masking task load and schizotypy level. Journal of Abnorm Psychology, 107, 659-670. Bowins, B. & Shugar, G. (1998). Delusions and self-esteem. Canadian Journal of Psychiatry. 43(2):154-8. Canli, T., Qiu, M., Omura, K., Congdon, E., Haas, B.W., Amin, Z., Herrmann, M.J., Constable, R.T., & Lesch, K.P. (2006). Neural correlates of epigenesis. Proceedings of the National Academy of Sciences - USA, 103, 16033-16038. Cella, M., Cooper, A., Dymond, S.O., & Reed, P. (2008). The relationship between dysphoria and proneness to hallucination and delusions among young adults. Comprehensive Psychiatry 49, 544-550. Cella, M., Taylor, K., & Reed, P (2007).Violation of expectancies produces more false positive reports in a word detection task in people scoring high in unusual experiences scale. Personality and Individual Differences, 43, 59-70. Chadwick, P., & Birchwood, M. (1994).The omnipotence of voices. A cognitive approach to auditory hallucinations. British Journal of Psychiatry, 164, 190-201. Chapman, L.J., Chapman, J.P., Kwapil, T.R., Eckblad, M., & Zinser, M.C. (1994). Putatively psychosis-prone subjects 10 years later. Journal of Abnormal Psychology 103, 171–183.

58

Antonio Preti and Matteo Cella

Chen, E., & Berrios, G.E. (1996) Recognition of hallucinations: a new multidimensional model and methodology. Psychopathology, 29, 54-63. Claridge, G. (1997). Schizotypy : Implications for Illness and Health. Oxford, UK: Oxford University Press. Cocchi, A., Meneghelli, A., & Preti, A. (2008). “Programma 2000”: Celebrating ten years of activity of an Italian pilot program on early intervention in psychosis. Australian & New Zealand Journal of Psychiatry, 42, 1003-1012. Compton, M. T., & Kaslow, N.J. (2005). Self-reported psychotic symptoms predict impulsivity among African-American patients in an urban nonpsychiatric medical setting. Psychiatry Research, 135, 35-44. Corcoran, R., Ciummins, S., Rowse, G., Moore, E., Blackwood, N., Howard, R., Kinderman, P., & Bentall, R.P. (2006). Reasoning under uncertainty: heuristic judgments in patients with persecutory delusions or depression. Psychological Medicine, 36, 1109-1118. Cosoff, S.J., & Hafner, R.J. (1998). The prevalence of comorbid anxiety in schizophrenia, schizoaffective disorder and bipolar disorder. Australian & New Zealand Journal of Psychiatry, 32, 67-72. Crawford, T.N., Cohen, P., Johnson, J.G., Kasen, S., First, M.B., Gordon, K., & Brook, J.S. (2005). Self-reported personality disorder in the children in the community sample: convergent and prospective validity in late adolescence and adulthood. Journal of Personality Disorders, 19, 30-52. Creed, F., & Barsky, A. (2004). A systematic review of the epidemiology of somatisation disorder and hypochondriasis. Journal of Psychosomatic Research, 56, 391-408. Cullari, S. (1994). Levels of anger in psychiatric inpatients and normal subjects. Psychological Reports, 75, 1163-1168. Damasio, A. R. (2003). Looking for Spinoza: joy, sorrow and the feeling brain. New York: Harcourt Brace & Co. Damasio, A. R. (1994). The Descartes error: emotion, reason and the human brain. New York: Avon. Davis, K.L., Kahn, R.S., Ko, G., & Davidson, M. (1991). Dopamine in schizophrenia: a review and reconceptualization. American Journal of Psychiatry 148, 1474-1486.

References

59

de Koning, M.B., Bloemen, O.J., van Amelsvoort, T.A., Becker, H.E., Nieman, D.H., van der Gaag, M., & Linszen, D.H. (2009). Early intervention in patients at ultra high risk of psychosis: benefits and risks. Acta Psychiatr Scand. In press. Devinsky, O. (2009) Delusional misidentifications and duplications: Right brain lesions, left brain delusions. Neurology, 72, 80–87. Doody, G.A., Götz, M., Johnstone, E.C., Frith, C.D., & Owens, D.G. (1998). Theory of mind and psychoses. Psychological Medicine, 28, 397-405. Drake, R.J., Pickles, A., Bentall, R.P., Kinderman, P., Haddock, G., Tarrier, N., & Lewis, S.W. (2004) The evolution of insight, paranoia and depression during early schizophrenia. Psychological Medicine, 34, 285292. D'Souza, D.C. (2007). Cannabinoids and psychosis. International Reviews of Neurobiology, 78, 289-326. Dudley, R.E., John, C.H., Young, A.W. & Over, D.E. (1997). Normal and abnormal reasoning in people with delusions. British Journal of Clinical Psychology, 36, 243-258. Dunn, B. D., Dalgleish, T., & Lawrence, A. D. (2006). The somatic marker hypothesis: a critical evaluation. Neuroscience & Biobehavioral Reviews, 30, 239-271. Edwards, J., & McGorry, P.D. (2002). Implementing early intervention in psychosis. A guide to establishing early psychosis services. London, UK: Dunitz. Eysenck, H. J., & Eysenck, M. W. (1985). Personality and individual differences: A natural science approach. New York: Plenum. Ellett, L., Lopes, B., & Chadwick, P. (2003) Paranoia in a nonclinical population of college students. Journal of Nervous & Mental Disorders, 191, 425-430. Fear, C., Sharp, H., & Healy, D. (1996). Cognitive processes in delusional disorders. British Journal of Psychiatry, 168, 61-67. Feinberg, A. (1982) Schizophrenia: caused by a fault in programmed synaptic elimination during adolescence? Journal of Psychiatric Research 17, 319334. Foster, R.G., Roenneberg, T. (2008). Human responses to the geophysical daily, annual and lunar cycles. Current Biology, 18, R784-R794.

60

Antonio Preti and Matteo Cella

Freeman, D. (2006). Delusions in the non-clinical population. Current Psychiatry Reports, 8, 191-204. Freeman, D. (2007) Suspicious mind: the psychology of persecutory delusions. Clinical Psychological Reviews, 27, 425-457. Freeman, D., Garety, P., Fowler, D., Kuipers, E., Dunn, G., Bebbington, P., & Hadley, C. (1998). The London-East Anglia randomized controlled trial of cognitive-behaviour therapy for psychosis. IV: Self-esteem and persecutory delusions. British Journal of Clinical Psychology, 37, 415-430. Freeman, D. & Garety, P.A. (2003). Connecting neurosis and psychosis: the direct influence of emotion on delusions and hallucinations. Behavioral Research & Therapy, 41, 923-947. Freeman, D. & Garety, P.A. (2004). Paranoia: The Psychology of Persecutory Delusions. Hove: Psychology Press. French, P., Shryane, N., Bentall, R.P., Lewis, S.W. & Morrison AP. (2007). Effects of cognitive therapy on the longitudinal development of psychotic experiences in people at high risk of developing psychosis. British Journal of Psychiatry, 51 (suppl.), s82-87. Freud, S. (1936). Inhibitions, Symptoms and Anxiety (1926). London, UK: Hogarth Press. Frith, C.D. (2004). Schizophrenia and theory of mind. Psychological Medicine, 34, 385-389. Frith, C.D. & Corcoran, R. (1996) Exploring 'theory of mind' in people with schizophrenia. Psychological Medicine, 26, 521-530. Garety, P.A., Hemsley, D.R. & Wessely, S. (1991). Reasoning in deluded schizophrenic and paranoid patients. Biases in performance on a probabilistic inference task. Journal of Nervous & Mental Disorders, 179, 194-201. Garety, P.A., Kuipers, E., Fowler, D., Freeman, D., & Bebbington, P.E. (2001). A cognitive model of the positive symptoms of psychosis. Psychological Medicine, 31, 189-195. Goodwin, F.K., & Jamison, K.R. (1990). Manic-Depressive Illness. Oxford, UK: Oxford University Press. Gracie, A., Freeman, D., Green, S., Garety, P.A., Kuipers, E., Hardy, A., Ray, K., Dunn, G., Bebbington, P., & Fowler, D. (2007). The association

References

61

between traumatic experience, paranoia and hallucinations: a test of the predictions of psychological models. Acta Psychiatrica Scandinavica, 116, 280-289. Green, C.E,. Freeman, D., Kuipers, E., Bebbington, P., Fowler, D., Dunn, G., & Garety, P.A. (2008). Measuring ideas of persecution and social reference: the Green et al. Paranoid Thought Scales (GPTS). Psychological Medicine, 38, 101-111. Häfner, H. (1988), What is schizophrenia? Changing perspectives in epidemiology. European Archives of Psychiatry & Neurological Sciences, 238, 63-72. Haltenhof, H., Ulrich, H., & Blanenburg, W. (1999). Themes of delusion in 84 patients with unipolar depression. Krankenhauspsychiatrie, 10, 87-90. Hanssen, M., Bak, M., Bijl, R., Vollebergh, W., & van Os, J. (2005). The incidence and outcome of subclinical psychotic experiences in the general population. British Journal of Clinical Psychology, 44, 181-191. Hanssen, M., Krabbendam, L., Vollema, M., Delespaul, P., & van Os, J. (2006). Evidence for instrument and family-specific variation of subclinical psychosis dimensions in the general population. Journal of Abnormal Psychology, 115, 5-14. Haro, J.M., van Os, J., Vieta, E., Reed, C., Lorenzo, M., Goetz, I. and the EMBLEM Advisory Board. (2006). Evidence for three distinct classes of typical, psychotic and dual mania: results from the EMBLEM study. Acta Psychiatrica Scandinavica, 113, 112–120. Hazlerigg, D., Loudon, A. (2008). New insights into ancient seasonal life timers. Current Biology, 18, R795-R804. Hemsley, D.R., & Garety, P.A. (1986). The formation of maintenance of delusions: a Bayesian analysis. British Journal of Psychiatry, 149, 51-6. Huang, Y., Kotov, R., de Girolamo, G., Preti, A., Angermeyer, M., Benjet, C., Demyttenaere, K., de Graaf, R., Gureje, O., Karam, A.N., Lee, S., Lépine, J.P., Matschinger, H., Posada-Villa, J., Suliman, S., Vilagut, G., & Kessler, R.C. (2009). DSM-IV Personality Disorders in the WHO World Mental Health Surveys. British Journal of Psychiatry, 2009; in press. Huber, G., & Gross, G. (1995). The concept of basic symptoms and basic stages and its meaning for schizophrenia and schizoaffective psychoses; in

62

Antonio Preti and Matteo Cella

Maggini C (ed): Psicopatologia e Clinica della Schizofrenia. Pisa, ETS, pp 41–58. Huq, S.F., Garety, P.A. & Hemsley, D.R. (1988). Probabilistic judgements in deluded and non-deluded subjects. Quarterly Journal of Experimental Psychology, 40, 801-12. Iarocci, G., Yager, J., & Elfers, T. (2007). What gene-environment interactions can tell us about social competence in typical and atypical populations. Brain & Cognition, 65, 112-127. Johns, L.C., Cannon, M., Singleton, N., Murray, R.M., Farrell, M., Brugha, T., Bebbington, P., Jenkins, R., & Meltzer, H. (2004) Prevalence and correlates of self-reported psychotic symptoms in the British population. British Journal of Psychiatry, 185, 298-305. Jones, P., Rodgers, B., Murray, R., & Marmot M. (1994). Child development risk factors for adult schizophrenia in the British 1946 birth cohort. Lancet, 344, 1398-1402. Jørgensen, P., & Jensen, J. (1994). Delusional beliefs in first admitters. A clinical description. Psychopathology, 27, 100-112. Kahneman, D., Tversky, A., & Slovic, P. eds. (1982). Judgment under Uncertainty: Heuristics & Biases. Cambridge, UK, Cambridge University Press. Kamara, T.S., Whyte, E.M., Mulsant, B.H., Peasley-Miklus, C., Rothschild, A.J., Flint, A.J., Heo, M., Papademetriou, E., Mathis, E.R., Meyers, B.S.; STOP-PD Study Group. (2009). Does major depressive disorder with somatic delusions constitute a distinct subtype of major depressive disorder with psychotic features? Journal of Affective Disorders, 112, 250255. Kaney, S., & Bentall, R.P. (1989). Persecutory delusions and attributional style. British Journal of Medical Psychology, 62, 191-198. Kaney, S., Bowen-Jones, K., Dewey, M.E., Bentall, R.P. (1997). Two predictions about paranoid ideation: deluded, depressed and normal participants‟ subjective frequency and consensus judgments for positive, neutral and negative events. British Journal of Clinical Psychology, 36, 349-364.

References

63

Kapur, S. (2003) Psychosis as a state of aberrant salience: A framework linking biology, phenomenology, and pharmacology in schizophrenia. American Journal of Psychiatry, 160, 13-23. Kaye, S., & Darke, S. (2004). Injecting and non-injecting cocaine use in Sydney, Australia. Physical and psychological morbidity. Drug & Alcohol Reviews, 23, 391-398. Kendler, K.S., Gallagher, T.J., Abelson, J.M., & Kessler, R.C. (1996). Lifetime prevalence, demographic risk factors, and diagnostic validity of nonaffective psychosis as assessed in a US community sample. The National Comorbidity Survey. Archives of General Psychiatry, 53, 10221031. Kendler, K.S., & Tsuang, M.T. (1981). Nosology of paranoid schizophreniua and other paranoid psychoses. Schizophrenia Bulletin, 7, 594-610. Kessler, R.C. (2007). The global burden of anxiety and mood disorders: putting the European Study of the Epidemiology of Mental Disorders (ESEMeD) findings into perspective. Journal of Clinical Psychiatry, 68 (Suppl 2), 10-9. Kessler, R.C., McGonagle, K.A., Zhao, S., Nelson, C.B., Hughes, M., Eshleman, S., Wittchen, H.-U., & Kendler, K.S. (1994). Lifetime and 12month prevalence of DSM-III-R psychiatric disorders in the United States. Archives of General Psychiatry, 51, 8-19. Khantzian, E.J. (1985). The self-medication hypothesis of addictive disorders: focus on heroin and cocaine dependence. American Journal of Psychiatry, 142, 1259-1264. Klosterkoetter, J., Hellmich, M., Steinmeyer, E., & Schultze-Lutter, F. (2001). Diagnosing schizophrenia in the initial prodromal phase. Archives of General Psychiatry, 58, 158–164. Krabbendam, L., Janssen, I., Bak, M., Bijl, R.V., de Graaf, R., & van Os, J. (2002). Neuroticism and low self-esteem as risk factors for psychosis. Social Psychiatry & Psychiatric Epidemiology, 37, 1-6. Krabbendam, L., Myin-Germeys, I., Bak, M., & van Os, J. (2005) Explaining transitions over the hypothesized psychosis continuum. Australian & New Zealand Journal of Psychiatry, 39, 180-186.

64

Antonio Preti and Matteo Cella

Kraepelin, E. (1904). Clinical Psychiatry: A Textbook for Students and Physicians. (1899). Edited and translated by A.R. Diefendorf from 6th edition of Kraepelin's textbook. New York, NY: MacMillan. Kraepelin, E. (1896). Psychiatrie: Ein Lehrbuch fur Studirende und Aerzte. Leipzig, East Germany: Ambrosius Barth. Kretschmer, E. (1974). The sensitive delusion of reference (1927). In: Hirsch, SR, & Shepherd, M, eds. Themes and Variations in European Psychiatry (pp. 153-196). Charlottesville: University Press of Virginia. Kroll J, Egan E. (2004). Psychiatry, moral worry, and the moral emotions. Journal of Psychiatric Practice, 10, 352-360. Kwapil, T., Miller, M., Zinser, M., Chapman, J., & Chapman, L. (1997). Magical ideation and social anhedonia as predictors of psychosis proneness: a partial replication. Journal of Abnormal Psychology, 106, 491495. Langdon, R., & Coltheart, M. (2004). Recognition of metaphor and irony in young adults: the impact of schizotypal personality traits. Psychiatry Research, 125, 9-20. Leafhead, K.M. (1996). Delusions demand attention. Cognitive Neuropsychiatry, 1, 5-16. Leary, M.R., Tambor, E.S., Terdal, S.K., & Downs, D.L. (1995). Self-esteem as an interpersonal monitor: The sociometer hypothesis. Journal of Personality and Social Psychology, 68, 518-530. LeCroy, D. (2000). Freud: The first evolutionary psychologist? Annals of the New York Academy of Sciences, 907, 182-190. LeDoux, J., (1996). The emotional brain: the mysterious underpinnings of emotional life. New York, NY: Simon and Schuster. Leff, J., Tress, K., & Edwards, B. (1988) The clinical course of depressive symptoms in schizophrenia. Schizophrenia Research, 1, 25-30. Lenzenweger, M.F., Loranger, A.W., Korfine, L., & Neff, C. (1997). Detecting personality disorders in a nonclinical population. Application of a 2-stage procedure for case identification. Archives of General Psychiatry, 54, 345-351.

References

65

Lewandowski, K.E., Barrantes-Vidal, N., Nelson-Gray, R.O., Clancy, C., Kepley, H.O., & Kwapil, T.R. (2006). Anxiety and depression symptoms in psychometrically identified schizotypy. Schizophrenia Research, 83, 225-235. Lewis, D.A., & Levitt, P. (2002). Schizophrenia as a disorder of neurodevelopment. Annual Reviews of Neuroscience, 25, 409-432. Lincoln, T.M., Lange, J., Burau, J., Exner, C., Moritz, S. (2009) The Effect of State Anxiety on Paranoid Ideation and Jumping to Conclusions. An Experimental Investigation. Schizophrenia Bulletin, 2009 May 8. [Epub ahead of print] Linney, Y.M., Peters, E.R., & Ayton, P. (1998). Reasoning biases in delusionprone individuals. British Journal of Clinical Psychology, 37, 285-302. Luutonen, S. (2007). Anger and depression--theoretical and clinical considerations. Nordic Journal of Psychiatry, 61, 246-251. Lyon, H.M., Kaney, S., & Bentall, R.P. (1994) The defensive function of persecutory delusions. Evidence from attribution tasks. British Journal of Psychiatry, 164, 637-646. Lysaker, P.H., Davis, L.W., & Tsai, J. (2009). Suspiciousness and low selfesteem as predictors of misattributions of anger in schizophrenia spectrum disorders. Psychiatry Research, 166, 125-131. Maggini, C, & Raballo, A. (2004). Self-centrality, basic symptoms model amd psychopathology in schizophrenia. Psychopathology, 37, 69-75. Maher, B.A. (1988), Anomalous experiences and delusional thinking: the logic of explanations. In: Oltmanns, T.F., & Maher, B.A.,eds. Delusional beliefs. New York, NY: Wiley. Manschreck, T.C., & Khan, N.L. (2006). Recent advances in the treatment of delusional disorder. Canadian Journal of Psychiatry, 51, 114-119. Martin, J.A., & Penn, D.L. (2001). Social cognition and subclinical paranoid ideation. British Journal of Clinical Psychology, 40, 261–265. McGrath, J, Saha, S, Welham, J, El Saadi, O, MacCauley, C, & Chant, D. (2004). A systematic review of the incidence of schizophrenia : the distribution of rates and the influence of sex, urbanicity, migrant status and methodology. BMC Medicine, 2, 13.

66

Antonio Preti and Matteo Cella

McGrath, J., Saha, S., Chant, D., Welham, J. (2008). Schizophrenia: A concise overview of incidence, prevalence, and mortality. Epidemiological Reviews, 30, 67-76. Meehl, P.E. (1962). Schizotaxia, schizotypy, schizophrenia. American Psychologist, 17, 827–838. Meehl, P.E. (1989). Schizotaxia revisited. Archives of General Psychiatry, 46, 935-944. Messerli, F.H., Williams, B., & Ritz, E. (2007) Essential hypertension. Lancet, 370, 591-603. Mezulis, A.H., Abramson, L.Y., Hyde, J.S., & Hankin, B.L. (2004). Is there a universal positivity bias in attributions? A meta-analytic review of individual, developmental, and cultural differences in the self-serving attributional bias. Psychological Bulletin, 130, 711-747. Miettunen, J., Törmänen, S., Murray, G.K., Jones, P.B., Mäki, P., Ebeling, H., Moilanen, I., Taanila, A., Heinimaa, M., Joukamaa, M., & Veijola, J. (2008). Association of cannabis use with prodromal symptoms of psychosis in adolescence. British Journal of Psychiatry, 192, 470–471. Moore, T.H.M., Zammit, S., Lingford-Hughes, A., Barnes, T.R., Jones, P.B., Burke, M., & Lewis, G. (2007). Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet, 370, 319328. Morgan, V.A., Mitchell, P.B., & Jablensky, A.V. (2005). The epidemiology of bipolar disorder: sociodemographic, disability and service utilization data from the Australian National Study of Low Prevalence (Psychotic) Disorders. Bipolar Disorders, 7, 326-337. Morgan, C., Fisher, H., Hutchinson, G., Kirkbride, J., Craig, T.K., Morgan, K., Dazzan, P., Boydell, J., Doody, G.A., Jones, P.B., Murray, R.M., Leff, J., Fearon, P. (2009). Ethnicity, social disadvantage and psychotic-like experiences in a healthy population based sample. Acta Psychiatrica Scandinavica, 119, 226-235. Moutoussis, M., Williams, J., Dayan, P., & Bentall, R.P. (2007). Persecutory delusions and the conditioned avoidance paradigm: towards an integration of the psychology and biology of paranoia. Cognitive Neuropsychiatry, 12, 495-510.

References

67

Ndetei, D.M., & Vadher, A. (1984). Frequency and clinical significance of delusions across cultures. Acta Psychiatrica Scandinavica, 70, 73-76. Norman, R.M., Malla, A.K. (1994). Correlations over time between dysphoric mood and symptomatology in schizophrenia. Comprehensive Psychiatry, 35, 34-38. Nowak, M.A., & Sigmund, K. (1998). Evolution of indirect reciprocity by image scoring. Nature, 393, 573-577. O'Boyle, M.. & Barratt, E. S. (1993). Impulsivity and DSM-III-R personality disorders. Personality and Individual Differences, 14, 609-611. O'Connor, K. (2009) Cognitive and meta-cognitive dimensions of psychoses. Canadian Journal of Psychiatry, 54, 152-159. Ohayon, M.M. (2000) Prevalence of hallucinations and their pathological associations in the general population. Psychiatry Research, 97, 153-164. Painuly, N., Sharan, P., & Mattoo, S.K. (2005). Relationship of anger and anger attacks with depression: a brief review. European Archives of Psychiatry & Clinical Neuroscience, 255, 215-222. Pearl, J. (1983). Heuristics: Intelligent Search Strategies for Computer Problem Solving. New York, NY: Addison-Wesley. Perälä, J., Suvisaari, J., Saarni, S.I., Kuoppasalmi, K., Isometsa, E., Pirkola, S., Partonen, T., Tuulio-Henriksson, A., Hintikka, J., Kieseppa, T., Harkanen, T., Koskinen, S., & Lonnqvist, J. (2007), Lifetime prevalence of psychotic and bipolar I disorders in a general population. Archives of General Psychiatry, 64, 19-28. Peters, E., Day, S., McKenna, J., & Orbach, G. (1999). Delusional ideation in religious and psychotic populations. British Journal of Clinical Psychology, 38, 83-96. Peters, E., Joseph, S., Day, S., Garety, P. (2004) Measuring delusional ideation: the 21-item Peters et al. Delusions Inventory (PDI). Schizophrenia Bulletin, 30, 1005-1022. Peters, E.R., Joseph, S.A., Garety, P.A. (1999) The measurement of delusional ideation in the normal population: Introducing the PDI (Peters et al. Delusions Inventory). Schizophrenia Bulletin, 25, 553-576.

68

Antonio Preti and Matteo Cella

Phillips, M.L., Senior, C. & David, A.S. (2000). Perception of threat in schizophrenics with persecutory delusions: an investigation using visual scan paths. Psychological Medicine, 30, 157-167. Pickup, G.J. (2006). Theory of mind and its relation to schizotypy. Cognitive Neuropsychiatry, 11, 177-192. Pickup, G.J., & Frith, C.D. (2001). Theory of mind impairments in schizophrenia: symptomatology, severity and specificity. Psychological Medicine, 31, 207-220. Poulton, R., Caspi, A., Moffitt, T.E., Cannon, M., Murray, R., & Harrington, H. (2000). Children‟s self-reported psychotic symptoms and adult schizophreniform disorder: a 15-year longitudinal study. Archives of General Psychiatry, 57, 1053-1058. Preti, A., Bonventre, E., Ledda, V., Petretto, D.R., & Masala, C. (2007). Hallucinatory experiences, delusional thought proneness and psychological distress in a nonclinical population. Journal of Nervous & Mental Disorders, 195, 484-491. Preti, A., & Miotto, P. (2005). Genetics, perinatal insult, and schizophrenia: The mechanism underlying an increased prevalence of perinatal complications among individuals with a diagnosis of schizophrenia? Current Psychiatry Reviews, 1, 139-150. Preti, A., Cardascia, L., Zen, T., Pellizzari, P., Marchetti, M., Favaretto, G., & Miotto, P. (2000). Obstetric complications in patients with depression. A population-based case-control study. Journal of Affective Disorders, 61, 101-106. Price, J.S. (1967). Hypothesis: the dominance hierarchy and the evolution of mental illness. Lancet, ii, 243-246. Raballo, A., & Maggini, C. (2004). Personality and psychosis: Subjective experiences, self-centrality and schizotypal dimensions in 1st degree relatives of schizophrenics. European Psychiatry, 19 (suppl 1), 49s. Raine, A. (2006). Schizotypal personality: neurodevelopmental and psychosocial trajectories. Annual Reviews of Clinical Psychology, 2, 291– 326. Reinberg, A., & Ashkenazi, I. (2003). Concepts in human biological rhythms. Dialogues in Clinical Neuroscience, 5, 327-342.

References

69

Reuter, M., Weber, B., Fiebach, C.J., Elger, C., Montag, C. (2009). The biological basis of anger: associations with the gene coding for DARPP32 (PPP1R1B) and with amygdala volume. Behavioral & Brain Research, 202, 179-183. Rilling, J.K., Sanfey, A.G., Aronson, J.A., Nystrom, L.E., Cohen, J.D. (2004). The neural correlates of theory of mind within interpersonal Interactions. NeuroImage, 22, 1694-1703 Rocchi, M.B.L., Sisti, D., Manca, S., Siddi, S., Mura, T., Preti, A. (2008). Latent class analysis of delusion-proneness: Exploring the latent structure of the Peters et al. Delusions Inventory. Journal of Nervous & Mental Disease, 196, 620-629. Romney, DM. (1987). A simplex model of the paranoid process: implications for diagnosis and prognosis. Acta Psychiatrica Scandinavica, 75, 651-655. Rounsaville, B.J. (2007). DSM-V research agenda: substance abuse/psychosis comorbidity. Schizophrenia Bulletin, 33, 947-952. Sartorius, N., Jablensky, A., Korten, A., Ernberg, G., Anker, M., Cooper, J.E., Day, R. (1986). Early manifestations and first-contact incidence of schizophrenia in different cultures. A preliminary report on the initial evaluation phase of the WHO Collaborative Study on determinants of outcome of severe mental disorders. Psychological Medicine, 16, 909-928. Scott, J., Chant, D., Andrews, G., Martin, G., & McGrath, J. (2007). Association between trauma exposure and delusional experiences in a large community-based sample. British Journal of Psychiatry, 190, 339343. Sevy, S., Burdick, K.E., Visweswaraiah, H., Abdelmessih, S., Lukin, M., Yechiam, E. & Bechara, A. (2007). Iowa gambling task in schizophrenia: a review and new data in patients with schizophrenia and co-occurring cannabis use disorders. Schizophrenia Research, 92, 74-84. Sharp, H.M. & Healey, D. (1997). Attributional style and delusions: An investigation based on delusional content. European Psychiatry 12, 1–7. Sherman, J.A. (2001). Evolutionary origin of bipolar disorder (EOBD), Psycoloquy, 12(028). http://www.cogsci.soton.ac.uk/psyc-bin/newpsy?12.028 Singer, T., Kiebel, S.J., Winston, J.S., Dolan, R.J., & Frith, C.D. (2004). Brain responses to the acquired moral status of faces. Neuron, 41, 653-662.

70

Antonio Preti and Matteo Cella

Singer, T., Lamm, C. (2009). The social neuroscience of empathy. Annals of the New York Academy of Sciences, 1156, 81-96. Stanghellini, G., & Ballerini, A. (1992). Ossessione e rivelazione. Torino, IT: Bollati Boringhieri. Startup, M., & Startup, S. (2005). On two kinds of delusions of reference. Psychiatry Research, 137, 87–92. Stevens, A., & Price, J. (1996). Evolutionary psychiatry. A new beginning. London and New York, Routledge. Stevens, J.R., & Hauser, M.D. (2004). Why be nice? Psychological constraints on the evolution of cooperation. Trends in Cognitive Sciences, 8, 60-65. Stompe, T., Friedman, A., Ortwein, G., Strobl, R., Chaudhry, H.R., Najam, N., & Chaudhry, M.R. (1999). Comparisons of delusions among schizophrenics in Austria and Pakistan. Psychopathology, 32, 225-234. Strömgren, E. (1974). Psychogenic psychoses. In: Hirsch, SR, & Shepherd, M, eds. Themes and Variations in European Psychiatry (pp. 97-120). Charlottesville, VI: University Press of Virginia. Tangney, J.P., Stuewig, J., & Mashek, D.J. (2007). Moral emotions and moral behavior. Annual Reviews of Psychology, 58, 345-372. Tien, A.Y., & Eaton, W.W. (1992). Psychopathologic precursors and sociodemographic risk factors for the schizophrenia syndrome. Archives of General Psychiatry, 49, 37-46. van Os, J., Hanssen, M., Bijl, R.-V., & Ravelli, A. (2000). Straus (1969) revisited : a psychosis continuum in the general population? Schizophrenia Research, 45, 11-20. van Os, J., Hanssen, M., Bijl, R.V., & Vollebergh, W. (2001). Prevalence of psychotic disorder and community level of psychotic symptoms: an urban–rural comparison. Archives of General Psychiatry, 58, 663-668. van Os, J., Linscott, R.J., Myin-Germeys, I., Delespaul, P., & Krabbendam, L. (2009). A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness–persistence–impairment model of psychotic disorder. Psychological Medicine, 39, 179-195. van 't Wout, M., Aleman, A., Kessels, R.P., Larøi, F., & Kahn, R.S. (2004). Emotional processing in a non-clinical psychosis-prone sample. Schizophrenia Research, 68, 271-281

References

71

Verdoux, H., van Os, J., Maurice-Tison, S., Gay, B., Salamon, R., & Bourgeois, M. (1998). Is early adulthood a critical developmental stage for psychosis proneness ? A survey of delusional ideation in normal subjects. Schizophrenia Research, 29, 247-254. Verdoux, H., van Os, J., Maurice-Tison, S., Gay, B., Salamon, R., & Bourgeois M.L. (1999). Increased occurrence of depression in psychosisprone subjects: A follow-up study in primary care settings. Comprehensive Psychiatry, 40, 462-468 Verdoux, H., & van Os, J. (2002). Psychotic symptoms in non-clinical populations and the continuum of psychosis. Schizophrenia Research, 54, 59-65. Vollema, M.G., & Hoijtink, H (2000). The multidimensionality of self-report schizotypy in a psychiatric population: an analysis using multidimensional Rasch models. Schizophrenia Bulletin, 26, 565–575. Walker, E., & Bollini, A. (2002). Pubertal neurodevelopment and the emergence of psychotic symptoms. Schizophrenia Research, 54, 17-23. Willis-Owen, S.A.G., Flint, J. (2007). Identifying the genetic determinants of emotionality in humans; insights from rodents. Neuroscience & Biobehavioral Reviews, 31, 115-124. Young, H.F. & Bentall, R.P. (1995). Hypothesis testing in patients with persecutory delusions: comparison with depressed and normal subjects. British Journal of Clininical Psychology, 34 (3):353-369. Yung, A.R. & McGorry, P.D. (1996). The prodromal phase of first-episode psychosis: past and current conceptualizations. Schizophrenia Bulletin, 22, 353-370.

INDEX

A abnormalities, 20, 25 achievement, 37 activation, 31, 42, 46 acute, 26, 35, 55 adaptation, 15, 33, 46 ADHD, ii, v administration, 18 adolescence, 1, 17, 58, 59, 66 adulthood, 2, 46, 58, 71 adults, 3, 29, 57, 62, 64, 68 affective dimension, 29 affective disorder, 10 African-American, 58 age, 1, 11, 34 agents, 18, 46 aggregation, 7 aggressive behavior, 38 alcohol, 11 algorithm, 41 alternative hypothesis, 20 alters, 28

altruism, 22 American Psychiatric Association, 55 amphetamine, 46 amygdala, 46, 69 anger, 8, 34, 37, 38, 39, 40, 42, 46, 53, 58, 65, 67, 69 animals, 18, 31, 33 animations, 57 anomalous, 20 antipsychotic, 3, 18 antipsychotic drugs, 3, 18 anxiety, 2, 8, 22, 29, 31, 32, 33, 34, 35, 37, 38, 39, 40, 45, 46, 47, 50, 53, 58, 60, 63, 65 anxiety disorder, 35, 38 APA, 1, 2, 4, 55 apathy, 8 application, 14 arousal, 47 assessment, 2, 10, 21 asymptomatic, xiv attacks, 38, 67 Attention Deficit Hyperactivity Disorder, ii

74

Index

attitudes, 38, 46 attribution, 27, 28, 50, 65 auditory hallucinations, 57 autism, 28 automatic processes, 16 autonomy, 5 availability, 34 avoidance, 18, 66 awareness, 23, 38

B bargaining, 46 Bayesian, 25, 61 behavior, xiii, xvi, 1, 5, 8, 10, 15, 28, 31, 32, 33, 38, 39, 45, 47, 70 beliefs, xiv, xv, 2, 18, 19, 20, 27, 28, 29, 38, 46, 56, 62, 65 benefits, 59 bias, 11, 25, 26, 27, 28, 47, 66 biological rhythms, 68 bipolar disorder, xiv, 7, 21, 32, 37, 58, 66, 69 birth, 62 blood, 13, 32, 33 blood pressure, 13, 32 body language, 8 bonding, 39 borderline personality disorder, 45 brain, 1, 16, 17, 18, 22, 31, 32, 33, 34, 46, 58, 59, 64 brain damage, 16, 32, 46 brain development, 17 breakdown, 23, 45 bullying, 47

C cannabis, 11, 18, 46, 66, 69 catatonia, 8

children, 11, 28, 34, 58 circulation, 22 classes, 61 classification, xv, xvi, 4, 14 clinical diagnosis, xi, 13 clinical disorders, xv, 1 clinical symptoms, 11 clinician, 11 close relationships, 2 clusters, 7, 8, 11 cocaine, 46, 63 coding, 69 cognition, 65 cognitive ability, 28 cognitive behavioral therapy, 30 cognitive biases, 29, 46, 50 cognitive deficit, 11 cognitive dimension, 67 cognitive function, 47 cognitive impairment, 25 cognitive performance, 29 cognitive system, 41, 42, 43 cognitive therapy, 60 coherence, 5 cohort, 9, 62 college students, 59 communication, 22 community, xv, 10, 11, 58, 63, 69, 70 comorbidity, 69 competence, 62 competition, 37 complexity, 42 complications, 68 components, 30, 32, 34 computation, 25 computer science, 41 conceptualization, xi, xv, 14, 30, 41, 49, 71 confrontation, 47 confusion, 4

Index congruence, 4 consciousness, 4, 29 consensus, 62 conspiracy, 21 constraints, 70 control, 2, 26, 31, 32, 41, 46, 68 conviction, 19, 20, 37 corticosteroids, 18 credit, 27 criminals, 9 cross-sectional, 35 cues, 22, 32, 33, 34, 37, 39 cultural differences, 66 culture, 1, 20 cycles, 59

75

disorder, xiii, xiv, xv, xvi, 1, 2, 3, 5, 7, 11, 13, 14, 15, 21, 23, 28, 32, 33, 37, 38, 45, 50, 58, 62, 65, 66, 68, 69, 70 disposition, xvi, 9 distress, xv, 1, 16, 19, 20, 21, 39, 45, 46, 47, 50, 68 distribution, xi, 3, 11, 14, 33, 41, 65 dominance, 68 dopamine, 18, 46 dopaminergic, 17 drugs, 3, 11, 18, 47 DSM, xv, 1, 4, 55, 61, 63, 67, 69 duration, 47 dysphoria, 35, 45, 57

E D danger, 22, 38 decisions, 42 defense, 29, 38 deficit, xiii, 11, 29 definition, xv, 12, 25 dementia, xvi, 4 demographic factors, 19 depressed, 34, 56, 62, 71 depression, xiv, xvi, 7, 8, 13, 21, 28, 29, 31, 33, 35, 37, 38, 40, 45, 46, 47, 50, 53, 56, 58, 59, 61, 65, 67, 68, 71 depressive disorder, 62 depressive symptoms, 64 deregulation, 35 detection, 27, 46, 57 diagnostic criteria, 4 dilation, 32 dimensionality, xii, xv, 14, 55 disability, xv, 1, 66 discontinuity, 15 disease model, 14

eating, 14 EEA, 46 ego, 1 emotion, 2, 8, 28, 31, 34, 37, 38, 39, 40, 42, 47, 56, 58, 60, 64, 70 emotionality, 71 empathy, 46, 70 endocrine, 17 environment, 9, 31, 38, 41, 42, 46, 47, 49, 62 environmental factors, 14 environmental stimuli, 8, 26, 32, 42 epidemiology, 3, 58, 61, 66 epigenetic, 16, 19 epilepsy, 2 ethnic groups, 9 etiology, 34 evolution, 59, 68, 70 exclusion, 2, 15, 46 execution, 33, 47 executive function, 29 expert, viii exposure, 11, 69

76

Index

extroversion, 13 extrovert, 13 eye contact, 8

F factor analysis, 13 failure, 27, 32, 38 fairness, 22 false positive, 57 familial, 11 family, 61 fatigue, 32 fear, 32, 37, 38, 39, 40, 42, 53 feedback, 33, 41 feelings, 8, 21, 22, 32 flow, 32 food, 31

G gambling, 69 genes, 14, 16, 17, 62, 69 geophysical, 59 goals, 1, 15 grandiose delusions, 4 groups, 5, 9, 32, 39 guilt, 37, 39, 40, 47, 53

H hallucinations, xiii, xv, 4, 5, 8, 10, 15, 16, 29, 34, 57, 58, 60, 61, 67 haloperidol, 3 hanging, 61 harm, xvi head trauma, 15 health, 56, 66 hearing, xiii, 8

heart rate, 32, 33 hemisphere, 46 heroin, 63 heterogeneity, 14, 25 heuristic, xi, 41, 45, 48, 50, 53, 58 high risk, 49, 59, 60 hostility, 2 human brain, 58 humans, 16, 25, 28, 31, 32, 41, 58, 68, 71 humiliation, 39 hunting, 31 hygiene, 8 hypertension, 13, 14, 66 hypochondriasis, 33, 58 hypothesis, 3, 11, 16, 17, 20, 26, 46, 47, 56, 59, 63, 64

I ICD, 4 identification, 64 identity, 22 impairments, 25, 29, 68 impulsivity, 45, 58 incidence, xiv, 4, 10, 25, 56, 61, 65, 66, 69 indicators, 11 individual differences, 59 inferences, 46 inferiority, 22 information processing, 56 inherited, 14 inhibition, 26, 55, 57 injury, viii insight, 59 integration, 56, 66 integrity, 22, 38, 46 intentions, 28, 46 interaction, 18, 42, 46, 62 interference, 21

Index intervention, xii, 12, 49, 50, 58, 59 interview, 10 introversion, 13 irritability, 8, 35

L labor, 55 language, 8 latent inhibition, 55, 57 LEA, 56 learning, 42, 46, 47, 57 lesions, 1, 46, 59 lifetime, xiv likelihood, 21, 27 links, 38, 45 longitudinal study, 29, 35, 68 love, 39, 47

M machines, 41 magnetic, viii maintenance, 23, 30, 34, 61 major depression, xiv, 7, 21, 29, 32, 38, 62 maladaptive, 2 males, 11 management, 56 mania, 31, 34, 37, 61 manic, xiv, 37 market, 55 masking, 57 measurement, xiv, 13, 19, 20, 23, 26, 27, 67 median, xiv, 10 medication, 10, 50, 63 medicine, 13 memory, 26 mental disorder, xiii, xiv, xvi, 4, 15, 33, 39, 50, 55, 69

77

mental health, 56, 66 mental illness, xiii, 11, 68 mental state, 29 meta-analysis, xiv, 10, 11, 70 metaphor, 29, 64 middle-aged, 3 migrant, 11, 65 minorities, 11, 14 models, xi, 14, 15, 22, 57, 61, 71 mood, 2, 7, 8, 28, 31, 33, 34, 35, 63, 67 mood disorder, 2, 7, 32, 63 moral behavior, 70 morbidity, xiv, 3, 63 mortality, 66 motivation, 8 motor behavior, 33 movement, 33, 50 multidimensional, 58, 71 muscle, 32, 33

N National Academy of Sciences, 57 natural science, 59 nausea, 32 negative consequences, 1, 34 negative life events, 34 negative outcomes, 33 neurological condition, 2 neuropsychology, 56 neuroscience, 70 neurotic, 32, 34 neuroticism, 13, 34 non-clinical, xi, xiv, 3, 16, 19, 33, 45, 60, 70, 71 non-clinical population, xi, xiv, 16, 45, 60, 71 normal, xi, 8, 13, 17, 20, 22, 29, 32, 41, 43, 55, 56, 57, 58, 62, 67, 71

78

Index O

occupational, 32 organic, 34 organism, 42 orientation, 38 oxygen, 33

P pain, 32 palpitations, 32 paranoia, xi, xii, xv, xvi, 1, 3, 4, 7, 9, 28, 30, 34, 37, 38, 45, 47, 48, 49, 50, 53, 59, 61, 66 Paranoid Ideation, 65 paranoid personality disorder, xvi, 1 paranoid schizophrenia, xvi, 1, 3, 4, 5, 53 parasites, 10 pathology, 15 patients, 4, 9, 10, 11, 15, 19, 20, 21, 23, 25, 26, 27, 28, 29, 32, 33, 34, 35, 37, 38, 39, 42, 46, 50, 56, 57, 58, 59, 60, 61, 68, 69, 71 PDI, 67 perceived outcome, 33 perceptions, xiii, 8, 11, 29, 33, 38 perinatal, 68 persecutory delusion, xi, xii, xv, 3, 21, 25, 26, 34, 49, 56, 57, 58, 60, 65, 68, 71 personal hygiene, 8 personal life, 1 personality, xvi, 1, 2, 3, 4, 5, 13, 14, 15, 45, 58, 64, 67, 68 personality disorder, xvi, 1, 2, 45, 58, 64, 67 personality traits, 13, 64 pharmacological treatment, 29 pharmacology, 63 phenomenology, 63 phenotype, 10, 15 phenotypic, 14

physicians, 64 physiological, 2, 26, 32 planned action, 33 pleasure, 8 politicians, 9 polymorphisms, 32 poor, xv, 8, 29, 50 population, xi, xiv, xv, 2, 11, 14, 15, 19, 21, 22, 25, 29, 34, 43, 59, 60, 61, 62, 64, 66, 67, 68, 70, 71 poverty, 8 power, 2, 9 PPD, xvi, 1, 2, 53 pre-clinical, 23, 49 predictors, 64, 65 pressure, 13, 32, 53 prevention, xi, 49 primary care, 71 probabilistic reasoning, 11, 26 problem solving, 41, 50 prodromal symptoms, 66 production, 16 prognosis, 69 program, 33, 58 property, viii, 38 protection, 47 psychiatric disorders, xiii, 13, 27, 63 psychiatric patients, 25, 26 psychiatrists, xv, 4 psychoactive drug, 11 psychological distress, 20, 68 psychological phenomena, 41 psychology, 60, 64, 66 psychopathology, xv, 14, 28, 41, 65 psychoses, xiv, 7, 15, 16, 59, 61, 63, 67, 70 psychosis, xi, xii, xiii, xiv, 2, 4, 7, 8, 11, 12, 14, 15, 16, 18, 19, 20, 21, 23, 26, 27, 29, 34, 35, 45, 49, 50, 53, 55, 57, 58, 59, 60, 61, 63, 64, 66, 68, 69, 70, 71

Index psychosocial functioning, 15 psychosomatic, 58 psychotic, xi, xiii, xiv, xv, 2, 4, 7, 10, 11, 14, 15, 19, 23, 25, 29, 30, 34, 35, 45, 49, 50, 58, 60, 61, 62, 66, 67, 68, 70, 71 psychotic symptoms, xi, xiv, 11, 30, 34, 58, 62, 68, 70, 71 psychoticism, 13, 15 PTSD, ii, iii public, 22, 39, 40, 46 punishment, 39, 40

Q questionnaires, 13, 27

R radio, 9 random, 9 range, 2, 8, 10, 41 reactivity, 8 reality, xiii, 22 reasoning, 11, 20, 25, 26, 29, 46, 59 recall, 27 reciprocity, 67 recognition, 12 reinforcement history, 42 rejection, 22 relationship, 2, 22, 57 relatives, 14, 68 relevance, xi, xv, 29, 30 remission, 5, 30 reparation, 39 replication, 51, 64 reputation, 22 resources, 34, 37, 38, 41, 57 respiratory, 33 responsibilities, 27

79

retaliation, 39, 40, 47 rhythms, 68 right hemisphere, 46 risk, xiv, 11, 15, 19, 33, 34, 38, 42, 47, 49, 50, 51, 53, 59, 60, 62, 63, 66, 70 rodents, 71 rural, 70

S safety, 22 scarcity, 38 schizoaffective disorder, xiv, 58 schizoid personality disorder, 2 schizophrenia, xii, xiv, xvi, 1, 2, 3, 4, 5, 7, 11, 13, 14, 15, 16, 17, 21, 23, 25, 28, 29, 34, 35, 39, 42, 49, 50, 53, 55, 56, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70 schizophrenic patients, 9, 27 schizotypal personality disorder, 2 schizotypy, 19, 23, 26, 57, 65, 66, 68, 71 security, 50 self-care, 8 self-esteem, 5, 22, 27, 28, 29, 34, 39, 50, 56, 57, 63, 65 self-monitoring, 39 self-report, 10, 27, 62, 68, 71 sensations, 33, 34 sensitivity, 17, 22 sensors, 33 sensory perceptions, 8 series, 26 services, viii, 50, 59 severity, xi, 1, 14, 20, 49, 50, 68 sex, 65 sexual orientation, 38 shame, 37, 39, 40, 47, 53 shortness of breath, 32 side effects, 10

80

Index

signaling, 32, 33, 38, 42 signs, xiii, 15, 32 skills, 50 skin, 32 sociability, 37 social activities, 21 social behavior, 39 social competence, 62 social environment, 32, 46, 49 social exclusion, 46 social rules, 47 social security, 50 social situations, 2, 28 social skills, 50 social support, 50 social withdrawal, 8 social workers, 50 somatic marker, 59 somatization, 34 speech, 8, 15 stages, 3, 46, 49, 61 stimulus, xiii strain, 50 strategies, 41, 50 stress, 2, 5, 17, 42, 45, 50, 53 stressful life events, 18 students, 59 subjective, xiv, 11, 20, 23, 62 substance abuse, 2, 15, 50, 69 substances, 18, 46 suffering, 32, 38 suicide, 50 supernatural, 9 survival, 37 susceptibility, 27 symptoms, xi, xiii, xiv, 1, 4, 7, 8, 10, 11, 14, 15, 18, 20, 21, 29, 30, 32, 33, 34, 35, 45, 47, 58, 60, 61, 62, 64, 65, 66, 68, 70, 71 syndrome, 70

T target stimuli, 27 task load, 57 temporal lobe epilepsy, 2 tension, 33 therapy, 30, 55, 60 thinking, xi, xiii, 1, 2, 3, 19, 22, 26, 29, 33, 34, 37, 39, 40, 41, 42, 43, 45, 46, 47, 49, 50, 53, 65 threat, 18, 21, 26, 27, 32, 33, 34, 37, 38, 39, 42, 46, 47, 68 threshold, 11, 20, 42, 43 time, 14, 19, 27, 50, 67 tolerance, 16 traits, 13, 14, 15, 25, 29, 64 transition, xi, 11, 19, 31, 49, 50, 53, 63 trauma, 15, 69 trial, 60 triggers, 39

U uncertainty, 41, 53, 58 unusual experiences, 57 urbanicity, 65

V validity, xi, 11, 58, 63 variation, 29, 61 violent, 46, 47 virtual reality, 22 visible, 39 visual attention, 27 vulnerability, 14, 22, 33, 46

Index W walking, 8 Western Europe, 2 WHO, 61, 69 winning, 37 wisdom, 21 withdrawal, 8, 28, 32

81

workers, 27, 28, 29, 50 World War, xv worry, 32, 64

Y young adults, 57, 64