Dissociative Disorders And Trauma chapter 8

Dissociative Disorders And Trauma

Chapter 8 

Discuss the relationship of trauma to dissociative amnesia and dissociative identity disorder. 

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 Schizophrenia Chapter 13

Dissociative Disorders And Trauma

 Review the changes in the diagnosis of schizophrenia that have occurred historically and the changes in the current definition due to the DSM 5 publication. How has brain research advanced the understanding of schizophrenia? 

8 somatic symptom and dissociative disorders

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learning objectives 8

·  8.1 What are somatic symptom disorders?

·  8.2 What is illness anxiety disorder?

·  8.3 What is conversion disorder (functional neurological symptom disorder)?

·  8.4 What is the difference between a factitious disorder and malingering?

·  8.5 What are the primary features of dissociative disorders?

·  8.6 What is depersonalization/derealization disorder?

·  8.7 What is dissociative amnesia?

·  8.8 What is dissociative identity disorder?

Have you ever had the experience, particularly during a time of serious stress, when you felt like you were walking around in a daze or like you just weren’t all there? Or have you known people who constantly complained about being sure they had a serious illness even though medical tests failed to show anything wrong? Both of these are examples of mild dissociative and somatic symptoms experienced at least occasionally by many people. However, when these symptoms become frequent and severe and lead to significant distress or impairment, a somatic symptom or dissociative disorder may be diagnosed. Somatic symptom disorders (formerly known as  somatoform disorders ) and dissociative disorders appear to involve more complex and puzzling patterns of symptoms than those we have so far encountered. As a result, they confront the field of psychopathology with some of its most fascinating and difficult challenges. Unfortunately, however, we do not know much about them—in part because many of them are quite rare and difficult to study.

As we have seen ( Chapter 6 ), both somatic symptom and dissociative disorders were once included with the various anxiety disorders (and neurotic depression) under the general rubric neuroses, where anxiety was thought to be the underlying cause of all neuroses whether or not the anxiety was experienced overtly. But in 1980, when DSM-III abandoned attempts to link disorders together on the basis of hypothesized underlying causes (as with neurosis) and instead focused on grouping disorders together on the basis of overt symptomatology, the anxiety, mood, somatic symptom, and dissociative disorders each became separate categories.

Somatic Symptom and Related Disorders

The somatic symptom disorders lie at the interface between abnormal psychology and medicine. They are a group of conditions that involve physical symptoms combined with abnormal thoughts, feelings, and behaviors in response to those symptoms (APA,  2013 ).  Soma  means “body,” and somatic symptom disorders involve patterns in which individuals complain of bodily symptoms that suggest the presence of medical problems but where there is no obvious medical explanation that can satisfactorily explain the symptoms such as paralysis or pain. Despite a wide range of clinical manifestations, in each case the person is preoccupied with some aspect of her or his health to the extent that she or he shows significant impairments in functioning.

In DSM-IV a great deal of emphasis was placed on the idea that the symptoms were medically unexplained. In other words, although the patient’s complaints suggested the presence of a medical condition no physical pathology could be found to account for them (Allen & Woolfolk,  2012 ; Witthöft & Hiller,  2010 ). In DSM-5 this idea is less prominent, because it is recognized that medicine is fallible and that a medical explanation for symptoms cannot always be provided. Nonetheless, medically unexplained symptoms are still a key part of some disorders (such as conversion disorder) that we will describe later.

Equally key to these disorders is the fact that the affected patients have no control over their symptoms. They are also not intentionally faking symptoms or attempting to deceive others. For the most part, they genuinely believe something is terribly wrong with them. Not surprisingly, these patients are frequent visitors to their primary-care physicians.

Sometimes, of course, people do deliberately and consciously feign disability or illness. Also placed in the somatic symptoms and related disorders category in DSM-5 is factitious disorder. In  factitious disorder  the person intentionally produces psychological or physical symptoms (or both). Although this may strike you as strange, the person’s goal is to obtain and maintain the benefits that playing the “sick role” (even to the extent of undergoing repeated hospitalizations) may provide, including the attention and concern of family and medical personnel. However, there are no tangible external rewards. In this way factitious disorder differs from malingering. In  malingering  the person is intentionally producing or grossly exaggerating physical symptoms and is motivated by external incentives such as avoiding work or military service or evading criminal prosecution (APA,  2013 ; Maldonado & Spiegel,  2001 ).

In our discussion, we will focus on four disorders in the somatic symptom and related disorders category. These are (1) somatic symptom disorder; (2) illness anxiety disorder; (3) conversion disorder; and (4) factitious disorder.

Somatic Symptom Disorders

This new diagnosis includes several disorders that were previously considered to be separate diagnoses in DSM-IV. The old disorders of (1) hypochondriasis, (2) somatization disorder, and (3) pain disorder have all now disappeared from DSM-5. Most of the people who would in the past have been diagnosed with any one of these disorders will now be diagnosed with a somatic symptom disorder. In each case, individuals must be experiencing chronic somatic symptoms that are distressing to them and they must also be experiencing dysfunctional thoughts, feelings, and/or behaviors. In the past, the diagnosis required evidence that the symptoms were medically unexplained. However, as we noted earlier, this is no longer required for the diagnosis (in part because it is very difficult to prove something is medically unexplainable). Instead the focus in DSM-5 is on there being at least one of the following three features: (1) disproportionate and persistent thoughts about the seriousness of one’s symptoms; (2) persistently high level of anxiety about health or symptoms; and/or (3) excessive time and energy devoted to these symptoms or health concerns (Allen & Woolfolk, 2013). Symptoms have to have persisted for at least six months.

Patients with somatic symptom disorder are usually seen in medical clinics. They are more likely to be female, nonwhite, and less educated than are people with symptoms that have an obvious medical basis. Patients with somatic symptom disorder frequently engage in illness behavior that is dysfunctional, such as seeking additional medical procedures or diagnostic tests when the physician fails to find anything physically wrong with them. Whereas most of us are relieved when tests do not reveal any problems, people with somatic symptom disorder are likely to think something was missed and therefore seek help from another physician, leading to needlessly high medical bills due to unnecessary tests, hospitalizations, and even surgeries. High levels of functional impairment are common, as is comorbid psychopathology—especially depression and anxiety.

Research suggests that people with somatic symptom disorders tend to have a cognitive style that leads them to be hyper-sensitive to their bodily sensations. They also experience these sensations as intense, disturbing, and highly aversive. Another characteristic of such patients is that they tend to think catastrophically about their symptoms, often overestimating the medical severity of their condition.

In the following sections, we will be discussing hypochondriasis, pain disorder, and somatization disorder. It’s important to note that in DSM-5, these disorders were technically dropped and are now part of the somatic symptom disorders. However, the history of and the research on these disorders is still important to understand.

Hypochondriasis

DSM-5 criteria for: Somatic Symptom Disorder

·  A. One or more somatic symptoms that are distressing or result in significant disruption of daily life.

·  B. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns as manifested by at least one of the following:

·  1. Disproportionate and persistent thoughts about the seriousness of one’s symptoms.

·  2. Persistently high level of anxiety about health or symptoms.

·  3. Excessive time and energy devoted to these symptoms or health concerns.

·  C. Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months).

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Approximately 75 percent of people previously diagnosed with hypochondriasis will be diagnosed with somatic symptom disorder in DSM-5 (APA,  2013 ). In  hypochondriasis  the person is preoccupied either with fears of contracting a serious disease or with the idea that of having that disease even though they do not. These very distressing preoccupations are thought to all be based on a misinterpretation of one or more bodily signs or symptoms (e.g., being convinced that a slight cough is a sign of lung cancer). Of course the decision that a complaint is hypochondriacal and is based on a misinterpretation of bodily signs or symptoms can only be made after a thorough medical evaluation has failed to find a medical condition that could account for the signs or symptoms. Another typical feature of hypochondriasis is that the person cannot be reassured by the results of a medical evaluation. In other words, the fear or idea of having a disease persists despite lack of medical evidence. Indeed, these individuals are sometimes disappointed when no physical problem is found. The condition has to persist for at least 6 months for the diagnosis to be made so as to not diagnose relatively transient health concerns.

Not surprisingly, people with hypochondriasis usually first see a medical doctor for their physical complaints. Because they are never reassured for long and are inclined to suspect that their doctor has missed something, they sometimes shop for additional doctors, hoping one might discover what their problem really is. Because they repeatedly seek medical advice (e.g., Bleichhardt & Hiller,  2006 ; Fink et al.,  2004 ), it is hardly surprising that their annual medical costs are much higher than average (e.g., Fink et al.,  2010 ; Hiller et al.,  2004 ). People with hypochondriasis are generally resistant to the idea that their problem is a psychological one that might be best treated by a psychologist or psychiatrist.

Prior to DSM-5, hypochondriasis was one of the two most commonly seen somatic symptom disorders with a prevalence in general medical practices of 2 to 7 percent (APA,  2000 ). Hypochondriasis occurs about equally often in men and women and can start at almost any age, although early adulthood is the most common age of onset. Hypochondriasis is regarded as a persistent disorder if left untreated, although its severity can fluctuate over time. Individuals with hypochondriasis often also suffer from mood disorders, panic disorder, or other types of somatic symptom disorders (Creed & Barsky,  2004 ). This is one reason why hypochondriasis is now not differentiated from other somatic symptom disorders in DSM-5.

MAJOR CHARACTERISTICS

Individuals with hypochondriasis tend to be highly preoccupied with bodily functions (e.g., heart beats or bowel movements), or with minor physical abnormalities (e.g., a small sore or an occasional cough), or with vague and ambiguous physical sensations (such as a “tired heart” or “aching veins”). They attribute these symptoms to a particular disease and often have intrusive thoughts about it. The diagnoses they make for themselves include cancer, exotic infections, AIDS, and numerous other diseases.  image2 Watchthe Video Henry: Hypochondriasis on MyPsychLab

Although people with hypochondriasis are usually in good physical condition, they are sincere in their conviction that the symptoms they detect represent real illness. In other words, they are not malingering—consciously faking symptoms to achieve a specific goals such as winning a personal injury lawsuit. Not surprisingly, given their tendency to doubt the soundness of their doctors’ conclusions (i.e., that they have no medical problem) and recommendations, the relationships they have with their doctors are often marked by conflict and hostility.

The following case captures the typical clinical picture in hypochondriasis. It also demonstrates that a high level of medical sophistication does not necessarily protect someone from developing this or a related disorder.

An “Abdominal Mass” This 38-year-old physician/radiologist initiated his first psychiatric consultation after his 9-year-old son accidentally discovered his father palpating (examining by touch) his own abdomen and said, “What do you think it is this time, Dad?” The radiologist describes the incident and his accompanying anger and shame with tears in his eyes. He also describes his recent return from a 10-day stay at a famous out-of-state medical diagnostic center to which he had been referred by an exasperated gastroenterologist colleague who had reportedly “reached the end of the line” with his radiologist patient. The extensive physical and laboratory examinations performed at the center had revealed no significant physical disease, a conclusion the patient reports with resentment and disappointment rather than relief.

The patient’s history reveals a long-standing pattern of overconcern about personal health matters, beginning at age 13 and exacerbated by his medical school experience. Until fairly recently, however, he had maintained reasonable control over these concerns, in part because he was embarrassed to reveal them to other physicians. He is conscientious and successful in his profession and active in community life. His wife, like his son, has become increasingly impatient with his morbid preoccupation about life-threatening but undetectable diseases.

In describing his current symptoms, the patient refers to his becoming increasingly aware, over the past several months, of various sounds and sensations emanating from his abdomen and of his sometimes being able to feel a “firm mass” in its left lower quadrant. His tentative diagnosis is carcinoma (cancer) of the colon. He tests his stool for blood weekly and palpates his abdomen for 15 to 20 minutes every 2 to 3 days. He has performed several X-ray studies of himself in secrecy after hours at his office.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 88–90). Washington, DC: (Copyright © 2002). American Psychiatric Association.

CAUSAL FACTORS

Our knowledge of causal factors involved in somatic symptom disorders, including hypochondriasis, is quite minimal. This is especially true when compared to knowledge about the mood and anxiety disorders discussed in the preceding chapters. Currently, cognitive-behavioral views of hypochondriasis are perhaps most widely accepted. These have as a central tenet that it is a disorder of cognition and perception. Misinterpretations of bodily sensations are currently a defining feature of the syndrome, but in the cognitive-behavioral view these misinterpretations also play a causal role. It is believed that an individual’s past experiences with illnesses (in both him- or herself and others, and as observed in the mass media) lead to the development of a set of dysfunctional assumptions about symptoms and diseases that may predispose a person to developing hypochondriasis (Marcus et al.,  2007 ; Salkovskis & Warwick,  2001 ). These dysfunctional assumptions might include notions such as, “Bodily changes are usually a sign of serious disease, because every symptom has to have an identifiable physical cause” or “If you don’t go to the doctor as soon as you notice anything unusual, then it will be too late” (Salkovskis & Bass,  1997 , p. 318; see also Marcus et al.,  2007 ).

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Individuals with hypochondriasis are preoccupied with unrealistic fears of disease. They are convinced that they have symptoms of physical illness, but their complaints typically do not conform to any coherent symptom pattern, and they usually have trouble giving a precise description of their symptoms.

Because of these dysfunctional assumptions, individuals with hypochondriasis seem to focus excessive attention on symptoms, with experimental studies showing that these individuals do in fact have an attentional bias for illness-related information (Owens et al.,  2004 ; see also Jasper & Witthöft,  2011 ). Although their physical sensations probably do not differ from those in normal controls (Marcus et al.,  2007 ), they perceive their symptoms as more dangerous than they really are and judge a particular disease to be more likely or dangerous than it really is. Once they have misinterpreted a symptom, they tend to look for confirming evidence and to discount evidence that they are in good health; in fact, they seem to believe that being healthy means being completely symptom-free (Rief et al.,  1998a ). They also perceive their probability of being able to cope with the illness as extremely low (Salkovskis & Bass,  1997 ) and see themselves as weak and unable to tolerate physical effort or exercise (Rief et al.,  1998a ). All this tends to create a vicious cycle in which their anxiety about illness and symptoms results in physiological symptoms of anxiety, which then provide further fuel for their convictions that they are ill.

If we also consider the secondary reinforcements that individuals with hypochondriasis obtain by virtue of their disorder, we can better understand how such patterns of thought and behavior are maintained in spite of the misery these individuals often experience. Most of us learn as children that when we are sick special comforts and attention are provided and, furthermore, that we may be excused from a number of responsibilities. Barsky and colleagues ( 1994 ) found that their patients with hypochondriasis reported much childhood sickness and missing of school. People with hypochondriasis also tend to have an excessive amount of illness in their families while growing up, which may lead to strong memories of being sick or in pain (Pauli & Alpers,  2002 ), and perhaps also of having observed some of the secondary benefits that sick people sometimes reap (Cote et al.,  1996 ; Kellner,  1985 ).

Interestingly, one study retested patients with hypochondriasis 4 to 5 years later and found that those who had remitted at follow-up had acquired significantly more (real) major medical problems than their nonremitting counterparts (Barsky et al.,  1998 ). In other words, it appears that hypochondriacal tendencies were reduced by the occurrence of serious medical conditions. The authors suggested that having a serious medical illness “served to legitimize the patients’ complaints, sanction their assumption of the sick role, and lessen the skepticism with which they had previously been regarded …. As one noted, ‘Now that I know Dr. X is paying attention to me, I can believe him if he says nothing serious is wrong’” ( p. 744 ).

TREATMENT OF HYPOCHONDRIASIS

More than a dozen studies on cognitive-behavioral treatment of hypochondriasis have found that it can be a very effective treatment for hypochondriasis (e.g., Barsky & Ahern,  2004 ; Tyrer,  2011 ; see also Hedman et al.,  2011 , for an example of Internet-based Cognitive Behavioral Therapy). The cognitive components of this treatment approach focus on assessing the patient’s beliefs about illness and modifying misinterpretations of bodily sensations. The behavioral techniques include having patients induce innocuous symptoms by intentionally focusing on parts of their body so that they can learn that selective perception of bodily sensations plays a major role in their symptoms. Sometimes they are also directed to engage in response prevention by not checking their bodies as they usually do and by stopping their constant seeking of reassurance. The treatment is relatively brief (6 to 16 sessions) and can be delivered in a group format. In these studies such treatment produced large changes in hypochondriacal symptoms and beliefs as well as in levels of anxiety and depression.

Somatization Disorder

The DSM-IV diagnosis of somatization disorder is another disorder that has now been subsumed into the broader category of somatic symptom disorder in DSM-5 Somatization disorder  is characterized by many different physical complaints. To qualify for the diagnosis, these had to begin before age 30, last for several years, and not be adequately explained by independent findings of physical illness or injury. They also had to have led to medical treatment or to significant life impairment. Not surprisingly, somatization disorder has long been seen most often among patients in primary medical care settings (Guerje et al.,  1997 ; Iezzi et al.,  2001 ). Indeed, patients with this variant of somatic symptom disorder are enormously costly to health care systems because they often have multiple unnecessary hospitalizations and surgeries (Barsky et al.,  2005 ; Hiller et al.,  2003 ).

The DSM-IV-TR (APA,  2000 ) criteria required that patients report a large number of symptoms across a wide range of domains (e.g., 4 pain symptoms, two gastrointestinal symptoms, one sexual symptom and one neurological-type symptom). Thus, to qualify for a diagnosis of somatization disorder, a patient had to have experienced at least 8 out of 33 specified symptoms (Rief & Barsky,  2005 ). Over time, the rather arbitrary nature of this became increasing apparent and the formal diagnostic criteria began to be modified by many researchers and clinicians (e.g., Rief & Broadbent,  2007 ). Following suit, in DSM-5 the long and complicated symptom count is no longer required and somatization disorder is now considered to be just another variant of somatic symptom disorder.

Another advantage of the recent change in DSM-5 is that it is no longer necessary for us to be concerned about whether somatization disorder and hypochondriasis are really two different and distinct disorders. There are indeed significant similarities between the two conditions. They also sometimes co-occur (Mai,  2004 ). Some years ago leading researchers in this area expressed concerns about whether somatization disorder and hypochondriasis could really be regarded as separate disorders (e.g., Creed & Barsky,  2004 ). Combining them both into a common category in DSM-5 and considering them to be variants of somatic symptom disorder is probably a wise move.

The main features of somatization disorder are illustrated in the following case summary, which also involves a secondary diagnosis of depression.

Not-Yet-Discovered Illness This 38-year-old married woman, the mother of five children, reports to a mental health clinic with the chief complaint of depression, meeting diagnostic criteria for major depressive disorder …. Her marriage has been a chronically unhappy one; her husband is described as an alcoholic with an unstable work history, and there have been frequent arguments revolving around finances, her sexual indifference, and her complaints of pain during intercourse.

The history reveals that the patient … describes herself as nervous since childhood and as having been continuously sickly beginning in her youth. She experiences chest pain and reportedly has been told by doctors that she has a “nervous heart.” She sees physicians frequently for abdominal pain, having been diagnosed on one occasion as having a “spastic colon.” In addition to M.D. physicians, she has consulted chiropractors and osteopaths for backaches, pains in her extremities, and a feeling of anesthesia in her fingertips. She was recently admitted to a hospital following complaints of abdominal and chest pain and of vomiting, during which admission she received a hysterectomy. Following the surgery she has been troubled by spells of anxiety, fainting, vomiting, food intolerance, and weakness and fatigue. Physical examinations reveal completely negative findings.

DEMOGRAPHICS, COMORBIDITY, AND COURSE OF ILLNESS

Somatization disorder usually begins in adolescence and is believed by many to be about three to ten times more common among women than among men. It also tends to occur more among less educated individuals and in lower socioeconomic classes. The lifetime prevalence has been estimated to be between 0.2 and 2.0 percent in women and less than 0.2 percent in men (APA,  2000 ). Somatization disorder very commonly co-occurred with several other disorders including major depression, panic disorder, phobic disorders, and generalized anxiety disorder. It has generally been considered to be a relatively chronic condition with a poor prognosis, although sometimes the disorder remits spontaneously (e.g., Creed & Barsky,  2004 ).

CAUSAL FACTORS IN SOMATIZATION DISORDER

Despite its prevalence in medical settings, researchers are still not certain about the developmental course and specific etiology of somatization disorder. There is evidence that somatization disorder runs in families and that there is a familial linkage between antisocial personality disorder in men (see  Chapter 10 ) and somatization disorder in women. That is, one possibility is that some common, underlying predisposition, probably at least partly genetically based, leads to antisocial behavior in men and to somatization disorder in women (Cale & Lilienfeld,  2002b ; Guze et al.,  1986 ; Lilienfeld,  1992 ). Moreover, somatic symptoms and antisocial symptoms in women tend to co-occur (Cale & Lilienfeld,  2002b ). However, we do not yet have a clear understanding of this relationship. One possibility is that the two disorders are linked through a common trait of impulsivity.

It has also become clear that people with somatization disorder selectively attend to, and show perceptual amplification of, bodily sensations. They also tend to see bodily sensations as somatic symptoms (Martin et al.,  2007 ). Like patients with hypochondriasis, they tend to catastrophize about minor bodily complaints (taking them as signs of serious physical illness) and to think of themselves as physically weak and unable to tolerate stress or physical activity (Martin et al.,  2007 ; Rief et al., 1998).

TREATMENT OF SOMATIZATION DISORDER

Somatization disorder was long considered to be extremely difficult to treat, and general practitioners experienced a great deal of uncertainty and frustration in working with these patients. However, in the past 15 years some treatment research has begun to suggest that a certain type of medical management along with cognitive-behavioral treatments may be quite helpful and that general practitioners can be educated in how to better manage and treat somatization patients and be less frustrated by them (Rosendal et al.,  2005 ; see also Edwards & Edwards,  2010 ). One moderately effective treatment involves identifying one physician who will integrate the patient’s care by seeing the patient at regular visits (thereby trying to anticipate the appearance of new problems) and by providing physical exams focused on new complaints (thereby accepting her or his symptoms as valid). At the same time, however, the physician avoids unnecessary diagnostic testing and makes minimal use of medications or other therapies (Looper & Kirmayer,  2002 ; Mai,  2004 ). Several studies have found that these patients show substantial decreases in health care expenditures over subsequent months and sometimes an improvement in physical functioning (although not necessarily in psychological distress; e.g., Rost et al.,  1994 ). This type of medical management can be even more effective when combined with cognitive-behavioral therapy that focuses on promoting appropriate behavior, such as better coping and personal adjustment, and discouraging inappropriate behavior such as illness behavior and preoccupation with physical symptoms (e.g., Bleichhardt et al.,  2004 ; Mai,  2004 ).

Pain Disorder

The third DSM-IV diagnosis subsumed into the new category of somatic symptom disorder is pain disorder.  Pain disorder  is characterized by persistent and severe pain in one or more areas of the body that is not intentionally produced or feigned. Although a medical condition may contribute to the pain, psychological factors are judged to play an important role. Indeed psychological factors play a role in all forms of pain. The pain disorder may be acute (duration of less than 6 months) or chronic (duration of over 6 months). When working with patients with pain disorder it is very important to remember that the pain that is experienced is very real and can hurt as much as pain that comes from other sources. It is also important to note that pain is always, in part, a subjective experience that is private and cannot be objectively identified by others.

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When one physician integrates a patient’s care, the physical functioning of patients with somatization disorder may improve. Why should this be?

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The experience of pain is always subjective and private, making pain impossible to assess with pinpoint accuracy. Pain does not always exist in perfect correlation with observable tissue damage or irritation. Psychological factors influence all forms of pain.

The prevalence of pain disorder in the general population is unknown. It is definitely quite common among patients at pain clinics. It is diagnosed more frequently in women than in men and is very frequently comorbid with anxiety or mood disorders, which may occur first or may arise later as a consequence of the pain disorder. People with pain disorder are often unable to work (they sometimes go on disability) or to perform some other usual daily activities. Their resulting inactivity (including an avoidance of physical activity) and social isolation may lead to depression and to a loss of physical strength and endurance. This fatigue and loss of strength can then exacerbate the pain in a kind of vicious cycle (Bouman et al.,  1999 ; Flor et al.,  1990 ). In addition, the behavioral component of pain is quite malleable in the sense that it can increase when it is reinforced by attention, sympathy, or avoidance of unwanted activities (Bouman et al.,  1999 ). Finally, there is suggestive evidence that people who have a tendency to catastrophize about the meaning and effects of pain may be the ones most likely to progress to a state of chronic pain (Seminowicz & Davis,  2006 ).

TREATMENT OF PAIN DISORDER

Perhaps because it is a less complex and multifaceted disorder than somatization disorder, pain disorder is usually easier to treat. Indeed, cognitive-behavioral techniques have been widely used in the treatment of both physical and more psychological pain syndromes. Treatment programs generally include relaxation training, support and validation that the pain is real, scheduling of daily activities, cognitive restructuring, and reinforcement of “no-pain” behaviors (Simon,  2002 ). Patients receiving such treatments tend to show substantial reductions in disability and distress, although changes in the intensity of their pain tend to be smaller in magnitude. In addition, antidepressant medications (especially the tricyclic antidepressants) and certain SSRIs have been shown to reduce pain intensity in a manner independent of the effects the medications may have on mood (Aragona et al.,  2005 ; Simon,  2002 ).

ILLNESS ANXIETY DISORDER

Illness anxiety disorder is new to DSM-5. In this newly identified disorder, people have high anxiety about having or developing a serious illness. This anxiety is distressing and/or disruptive but there are very few (mild) somatic symptoms. (see the DSM-5 criteria box below).

It is estimated that around 25 percent of people who would have been diagnosed with hypochondriasis in DSM-IV will be diagnosed with illness anxiety disorder in DSM-5 (APA,  2013 ).

Conversion Disorder (Functional Neurological Symptom Disorder)

DSM-5 criteria for: Illness Anxiety Disorder

·  A. Preoccupation with having or acquiring a serious illness.

·  B. Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is present or there is a high risk for developing a medical condition (e.g., strong family history is present), the preoccupation is clearly excessive or disproportionate.

·  C. There is a high level of anxiety about health, and the individual is easily alarmed about personal health status.

·  D. The individual performs excessive health-related behaviors (e.g., repeatedly checks his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals).

·  E. Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may change over that period of time.

·  F. The illness-related preoccupation is not better explained by another mental disorder, such as somatic symptom disorder, panic disorder, generalized anxiety disorder, body dysmorphic disorder, obsessive-compulsive disorder, or delusional disorder, somatic type.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Conversion disorder  is one of the most intriguing and baffling patterns in psychopathology, and we still have much to learn about it. It involves a pattern in which symptoms or deficits affecting the senses or motor behavior strongly suggest that the patient has a medical or neurological condition. However, upon a thorough medical examination, it becomes apparent that the pattern of symptoms or deficits cannot be fully explained by any known medical condition. A few typical examples include partial paralysis, blindness, deafness, and pseudoseizures. The person is not intentionally producing or faking the symptoms, Rather, psychological factors are often judged to play an important role because symptoms usually either start or are exacerbated by preceding emotional or interpersonal conflicts or stressors.

Early observations dating back to Freud suggested that most people with conversion disorder showed very little of the anxiety and fear that would be expected in a person with a paralyzed arm or loss of sight. This seeming lack of concern (known as la belle indifférence—French for “the beautiful indifference”) in the way the patient describes what is wrong was thought for a long time to be an important diagnostic criterion for conversion disorder. However, more careful research later showed that la belle indifférenceactually occurs in only about 20 percent of patients with conversion disorder, so it was dropped as a criterion from recent editions of the DSM (Stone et al.,  2006 , 2011).

The term conversion disorder is relatively recent. Historically this disorder was one of several disorders that were grouped together under the term  hysteria .

Freud used the term conversion hysteria for these disorders (which were fairly common in his practice) because he believed that the symptoms were an expression of repressed sexual energy—that is, the unconscious conflict that a person felt about his or her repressed sexual desires. However, in Freud’s view, the repressed anxiety threatens to become conscious, so it is unconsciously converted into a bodily disturbance, thereby allowing the person to avoid having to deal with the conflict. For example, a person’s guilty feelings about the desire to masturbate might be solved by developing a paralyzed hand. This is not done consciously, of course, and the person is not aware of the origin or meaning of the physical symptom. Freud also thought that the reduction in anxiety and intrapsychic conflict was the “primary gain” that maintained the condition, but he noted that patients often had many sources of “secondary gain” as well, such as receiving sympathy and attention from loved ones. Authors of DSM-5 had many suggestions for changing the name of this disorder (e.g., to psychogenic, functional, and dissociative). In the end, a conservative approach was taken and the term conversion disorder was retained, although this is now followed in parentheses by “Functional neurological symptom disorder” (Stone et al., 2011).

PRECIPITATING CIRCUMSTANCES, ESCAPE, AND SECONDARY GAINS

Freud’s theory that conversion symptoms are caused by the conversion of sexual conflicts or other psychological problems into physical symptoms is no longer accepted outside psychodynamic circles. However, many of Freud’s astute clinical observations about primary and secondary gain are still incorporated into contemporary views of conversion disorder. Although the condition is still called a conversion disorder, the physical symptoms are usually seen as serving the rather obvious function of providing a plausible bodily “excuse” enabling an individual to escape or avoid an intolerably stressful situation without having to take responsibility for doing so. Typically, it is thought that the person first experiences a traumatic event that motivates the desire to escape the unpleasant situation, but literal escape may not be feasible or socially acceptable. Moreover, although becoming sick or disabled is more socially acceptable, this is true only if the person’s motivation to do so is unconscious.

Thus, in contemporary terms, the  primary gain  for conversion symptoms is continued escape or avoidance of a stressful situation. Because this is all unconscious (i.e., the person sees no relation between the symptoms and the stressful situation), the symptoms go away only if the stressful situation has been removed or resolved. Relatedly, the term  secondary gain , which originally referred to advantages that the symptom(s) bestow beyond the “primary gain” of neutralizing intrapsychic conflict, has also been retained. Generally, it is used to refer to any “external” circumstance, such as attention from loved ones or financial compensation, that would tend to reinforce the maintenance of disability.

DSM-5 criteria for: Conversion Disorder

·  A. One or more symptoms of altered voluntary motor or sensory function.

·  B. Clinical findings provide evidence of incompatibility between the symptom and recognized neurological or medical conditions.

·  C. The symptom or deficit is not better explained by another medical or mental disorder.

·  D. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Given the important role often attributed to stressful life events in precipitating the onset of conversion disorder, it is unfortunate that little is actually known about the exact nature and timing of these psychological stress factors (Roelofs et al.,  2005 ). However, one study compared the frequency of stressful life events in the recent past in patients with conversion disorder and depressed controls and did not find a difference in frequency between them. Moreover, the greater the negative impact of the preceding life events, the greater the severity of the conversion disorder symptoms (Roelofs et al.,  2005 ). Another study compared levels of a neurobiological marker of stress (lower levels of brain-derived neurotropic factor) in individuals with conversion disorder versus major depression versus no disorder. Both those with depression and those with conversion disorder showed reduced levels of this marker relative to the nondisordered controls (Deveci et al.,  2007 ). This also provides support for the link between stress and the onset of conversion disorder.

DECREASING PREVALENCE AND DEMOGRAPHIC CHARACTERISTICS

Conversion disorders were once relatively common in civilian and (especially) military life. In World War I, conversion disorder was the most frequently diagnosed psychiatric syndrome among soldiers; it was also relatively common during World War II. Conversion disorder typically occurred under highly stressful combat conditions and involved men who would ordinarily be considered stable. Here, conversion symptoms—such as paralysis of the legs—enabled a soldier to avoid an anxiety-arousing combat situation without being labeled a coward or being subject to court-martial.

Conversion disorders are found in approximately 50 percent of people referred for treatment at neurology clinics. The prevalence in the general population is unknown, but even the highest estimates have been around only 0.005 percent (APA,  2013 ). Interestingly, this decreased prevalence seems to be closely related to our growing sophistication about medical and psychological disorders: A conversion disorder apparently loses its defensive function if it can be readily shown to lack a medical basis. When it does occur today, it is most likely to occur in rural people from lower socioeconomic circles who are medically unsophisticated. For example, a highly unusual “outbreak” of cases of severe conversion disorder involving serious motor weakness and wasting symptoms was reported in five 9- to 13-year-old girls living in a small, poor, rural Amish community. Each of these girls had experienced substantial psychosocial stressors including behavioral problems, dys-functional family dynamics, and significant community stress from a serious local church crisis (see Cassady et al.,  2005 ). Fortunately, after the caregivers of these girls were educated regarding the psychological nature of the symptoms and given advice to stick with one doctor, minimize stress, and avoid reinforcement of the “sick role,” four of the five girls showed significant improvement over the next 3 months. In the fifth case, the family refused to acknowledge the psychological component of the illness, holding to the belief that the symptoms were caused by parasites.

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Conversion disorders were fairly common during World War I and World War II. The disorder typically occurred in otherwise “normal” men during stressful combat conditions. The symptoms of conversion disorder (e.g., paralysis of the legs) enabled a soldier to avoid high-anxiety combat situations without being labeled a coward or being court-martialed.

Conversion disorder occurs two to three times more often in women than in men (APA  2013 ). It can develop at any age but most commonly occurs between early adolescence and early adulthood (Maldonado & Spiegel,  2001 ). It generally has a rapid onset after a significant stressor and often resolves within 2 weeks if the stressor is removed, although it commonly recurs. In many other cases, however, it has a more chronic course. Like most other somatic symptom disorders, conversion disorder frequently occurs along with other disorders, especially major depression, anxiety disorders, and other forms of somatic symptom or dissociative conditions.

RANGE OF CONVERSION DISORDER SYMPTOMS

The range of symptoms for conversion disorder is practically as diverse as it is for physically based ailments. In describing the clinical picture in conversion disorder, it is useful to think in terms of four categories of symptoms: (1) sensory, (2) motor, (3) seizures, and (4) a mixed presentation of the first three categories (APA,  2013 ).

Sensory Symptoms or Deficits Conversion disorder can involve almost any sensory modality, and it can often be diagnosed as a conversion disorder because symptoms in the affected area are inconsistent with how known anatomical sensory pathways operate. Today the sensory symptoms or deficits are most often in the visual system (especially blindness and tunnel vision), in the auditory system (especially deafness), or in the sensitivity to feeling (especially the anesthesias). In the anesthesias, the person loses her or his sense of feeling in a part of the body. One of the most common is glove anesthesia, in which the person cannot feel anything on the hand in the area where gloves are worn, although the loss of sensation usually makes no anatomical sense.

With conversion blindness, the person reports that he or she cannot see and yet can often navigate about a room without bumping into furniture or other objects. With conversion deafness, the person reports not being able to hear and yet orients appropriately upon “hearing” his or her own name. Such observations lead to obvious questions: In conversion blindness (and deafness), can affected people actually not see (or hear), or is the sensory information received but screened from consciousness? In general, the evidence supports the idea that the sensory input is registered but is somehow screened from explicit conscious recognition (explicit perception).

Motor Symptoms or Deficits Motor conversion reactions also cover a wide range of symptoms (e.g., Maldonado & Spiegel,  2001 ; see also Stone et al., 2010). For example, conversion paralysis is usually confined to a single limb such as an arm or a leg, and the loss of function is usually selective for certain functions. For example, a person may not be able to write but may be able to use the same muscles for scratching, or a person may not be able to walk most of the time but may be able to walk in an emergency such as a fire where escape is important. The most common speech-related conversion disturbance is aphonia, in which a person is able to talk only in a whisper although he or she can usually cough in a normal manner. (In true, organic laryngeal paralysis, both the cough and the voice are affected.) Another common motor symptom, called globus hystericus, is difficulty swallowing or the sensation of a lump in the throat (Finkenbine & Miele,  2004 ).

Seizures Conversion seizures, another relatively common form of conversion symptom, involve pseudoseizures, which resemble epileptic seizures in some ways but can usually be fairly well differentiated via modern medical technology (Bowman & Markand,  2005 ; Stonnington et al.,  2006 ). For example, patients with pseudoseizures do not show any EEG abnormalities and do not show confusion and loss of memory afterward, as patients with true epileptic seizures do. Moreover, patients with conversion seizures often show excessive thrashing about and writhing not seen with true seizures, and they rarely injure themselves in falls or lose control over their bowels or bladder, as patients with true seizures frequently do.

The following case of conversion disorder clearly shows how “functional” a conversion disorder may be in the overall life circumstances of a patient despite its exacting a certain cost in illness or disability.

A Wife with “Fits” Mrs. Chatterjee, a 26-year-old patient, attends a clinic in New Delhi, India, with complaints of “fits” for the last 4 years. The “fits” are always sudden in onset and usually last 30 to 60 minutes. A few minutes before a fit begins, she knows that it is imminent, and she usually goes to bed. During the fits she becomes unresponsive and rigid throughout her body, with bizarre and thrashing movements of the extremities. Her eyes close and her jaw is clenched, and she froths at the mouth. She frequently cries and sometimes shouts abuses. She is never incontinent of urine or feces, nor does she bite her tongue. After a “fit” she claims to have no memory of it. These episodes recur about once or twice a month. She functions well between the episodes.

Both the patient and her family believe that her “fits” are evidence of a physical illness and are not under her control. However, they recognize that the fits often occur following some stressor such as arguments with family members or friends …. She is described by her family as being somewhat immature but “quite social” and good company. She is self-centered, she craves attention from others, and she often reacts with irritability and anger if her wishes are not immediately fulfilled. On physical examination, Mrs. Chatterjee was found to have mild anemia but was otherwise healthy. A mental status examination did not reveal any abnormality … and her memory was normal. An electroencephalogram showed no seizure activity.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 469–70). Washington, DC. (Copyright © 2002). American Psychiatric Association.

IMPORTANT ISSUES IN DIAGNOSING CONVERSION DISORDER

Because the symptoms in conversion disorder can simulate a variety of medical conditions, accurate diagnosis can be extremely difficult. It is crucial that a person with suspected conversion symptoms receive a thorough medical and neurological examination. Unfortunately, however, misdiag-noses can still occur. Nevertheless, as medical tests (especially brain imaging) have become increasingly sophisticated, the rate of misdiagnoses has declined substantially from in the past, with estimates of misdiagnoses in the 1990s at only 4 percent down from nearly 30 percent in the 1950s (e.g., Stone et al.,  2005 ).

Several other criteria are also commonly used for distinguishing between conversion disorders and true neurological disturbances:

·  • The frequent failure of the dysfunction to conform clearly to the symptoms of the particular disease or disorder simulated. For example, little or no wasting away or atrophy of a “paralyzed” limb occurs in conversion paralyses, except in rare and long-standing cases. image7

Virtually all the symptoms of conversion disorder can be temporarily reduced or reproduced by hypnotic suggestion.

·  • The selective nature of the dysfunction. As already noted, in conversion blindness the affected individual does not usually bump into people or objects, and “paralyzed” muscles can be used for some activities but not others.

·  • Under hypnosis or narcosis (a sleeplike state induced by drugs), the symptoms can usually be removed, shifted, or re-induced at the suggestion of the therapist. Similarly, a person abruptly awakened from a sound sleep may suddenly be able to use a “paralyzed” limb.

TREATMENT OF CONVERSION DISORDER

Our knowledge of how best to treat conversion disorder is very limited because few well-controlled studies have yet been conducted (e.g., Bowman & Markand,  2005 ; Looper & Kirmayer,  2002 ). However, it is known that some hospitalized patients with motor conversion symptoms have been successfully treated with a behavioral approach in which specific exercises are prescribed in order to increase movement or walking, and then reinforcements (e.g., praise and gaining privileges) are provided when patients show improvements. Any reinforcements of abnormal motor behaviors are removed in order to eliminate any sources of secondary gain. In one small study using this kind of treatment for 10 patients, all had regained their ability to move or walk in an average of 12 days, and for seven of the nine patients available at approximately 2-year follow-up, the improvements had been maintained (Speed,  1996 ). At least one study has also used cognitive-behavior therapy to successfully treat psychogenic seizures (LaFrance et al.,  2009 ). Some studies have used hypnosis combined with other problem-solving therapies, and there are some suggestions that hypnosis, or adding hypnosis to other therapeutic techniques, can be useful (Looper & Kirmayer,  2002 ; Moene et al.,  2003 ).

Distinguishing Somatization, Pain, and Conversion Disorders from Malingering and Factitious Disorder

DSM-5 criteria for: Factitious Disorder

Factitious Disorder Imposed on Self

·  A. Falsification of physical or psychological signs or symptoms, or induction of injury or disease, associated with identified deception.

·  B. The individual presents himself or herself to others as ill, impaired, or injured.

·  C. The deceptive behavior is evident even in the absence of obvious external rewards.

·  D. The behavior is not better explained by another mental disorder, such as delusional disorder or another psychotic disorder.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Earlier we mentioned that the DSM distinguishes between malingering and factitious disorder on the basis of the feigning person’s apparent goals. Malingering is diagnosed if the person is intentionally producing or grossly exaggerating physical symptoms and is motivated by external incentives such as avoiding work or obtaining financial compensation. Factitious disorder is diagnosed if the person intentionally produces psychological or physical symptoms, the person’s goal being simply to obtain and maintain the personal benefits that playing the “sick role” (even undergoing repeated hospitalizations) may provide, including the attention and concern of family and medical personnel. In factitious disorder, frequently these patients surreptitiously alter their own physiology—for example, by taking drugs—in order to simulate various real illnesses. Indeed, they may be at risk for serious injury or death and may even need to be committed to an institution for their own protection. The World Around Us box above describes a particularly pathological variation on this theme. In the past, severe and chronic forms of factitious disorder with physical symptoms were called “Munchausen’s syndrome,” where the general idea was that the person had some kind of “hospital addiction” or a “professional patient” syndrome.

the WORLD around us: Factitious Disorder Imposed on Another (Munchausen’s Syndrome by Proxy)

In a somewhat bizarre variant of factitious disorder called factitious disorder imposed on another (or Munchausen’s syndrome by proxy), the person seeking medical help or consulting a mental health professional has intentionally produced a medical or psychiatric illness (or appearance of an illness) in another person who is under his or her care (usually a child; e.g., Pankratz,  2006 ). In a typical instance, a mother presents her own child for treatment of a medical condition she has deliberately caused, disclaiming any knowledge of its origin. Of course, the health of such victims is often seriously endangered by this repeated abuse, and the intervention of social service agencies or law enforcement is sometimes necessary. In as many as 10 percent of cases, this atypical form of child abuse may lead to a child’s death (Hall et al.,  2000 ).

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Over a period of 20 months, Jennifer, 8, shown here with her mother, Kathy Bush, was taken to the hospital more than 130 times, underwent 40 surgeries, and amassed over $3 million in medical expenses. Doctors and nurses testified that Jennifer’s condition always worsened after her mother visited her daughter at the hospital behind closed doors. In addition, Jennifer’s health had significantly improved since being removed from her mother’s care. The jury was convinced that Kathy Bush was responsible for causing Jennifer’s illnesses. Bush was arrested and diagnosed with Munchausen’s syndrome by proxy.

This disorder may be indicated when the victim’s clinical presentation is atypical, when lab results are inconsistent with each other or with recognized diseases, or when there are unduly frequent returns or increasingly urgent visits to the same hospital or clinic. The perpetrators (who often have extensive medical knowledge) tend to be highly resistant to admitting the truth (McCann,  1999 ), and it has been estimated that the average length of time to confirm the diagnosis is 14 months (Rogers,  2004 ). If the perpetrator senses that the medical staff is suspicious, he or she may abruptly terminate contact with that facility, only to show up at another one to begin the entire process anew. Compounding the problem of detection is the fact that health care professionals who realize they have been duped may be reluctant to acknowledge their fallibility for fear of legal action. Misdiagnosing the disorder when the parent is in fact innocent can also lead to legal difficulties for the health care professionals (McNicholas et al.,  2000 ; Pankratz,  2006 ). One technique that has been used with considerable success is covert video surveillance of the mother and child during hospitalizations. In one study, 23 of 41 suspected cases were finally determined to have factitious disorder by proxy, and in 56 percent of those cases video surveillance was essential to the diagnosis (Hall et al.,  2000 ).

It is sometimes possible to distinguish between a conversion (or other somatic symptom) disorder and malingering, or factitiously “sick-role-playing,” with a fair degree of confidence, but in other cases it is more difficult to make the correct diagnosis. Persons engaged in malingering (for which there are no formal diagnostic criteria) and those who have factitious disorder are consciously perpetrating frauds by faking the symptoms of diseases or disabilities, and this fact is often reflected in their demeanor. In contrast, individuals with conversion disorders (as well as with other somatic symptom disorders) are not consciously producing their symptoms, feel themselves to be the “victims of their symptoms,” and are very willing to discuss them, often in excruciating detail (Maldonado & Spiegel,  2001 , p. 109). When inconsistencies in their behaviors are pointed out, they are usually unperturbed. Any secondary gains they experience are byproducts of the conversion symptoms themselves and are not involved in motivating the symptoms. On the other hand, persons who are feigning symptoms are inclined to be defensive, evasive, and suspicious when asked about them; they are usually reluctant to be examined and slow to talk about their symptoms lest the pretense be discovered. Should inconsistencies in their behaviors be pointed out, deliberate deceivers as a rule immediately become more defensive. Thus conversion disorder and deliberate faking of illness are considered distinct patterns.

in review

·  ● What are the primary characteristics of hypochondriasis, and how does the cognitive-behavioral viewpoint explain their occurrence?

·  ● What are the symptoms of somatization disorder and of pain disorder?

·  ● What are sources of primary and secondary gains involved in conversion disorders, and how is conversion disorder distinguished from malingering and from factitious disorder?

Dissociative Disorders

Dissociative disorders  are a group of conditions involving disruptions in a person’s normally integrated functions of consciousness, memory, identity, or perception (APA,  2013 ; Spiegel et al.,  2013 ). Included here are some of the more dramatic phenomena in the entire domain of psychopathology: people who cannot recall who they are or where they may have come from, and people who have two or more distinct identities or personality states that alternately take control of the individual’s behavior.

The term  dissociation  refers to the human mind’s capacity to engage in complex mental activity in channels split off from, or independent of, conscious awareness (Kihlstrom,  1994  2001  2005 ). The concept of dissociation was first promoted over a century ago by the French neurologist Pierre Janet (1859–1947). We all dissociate to a degree some of the time. Mild dissociative symptoms occur when we daydream or lose track of what is going on around us, when we drive miles beyond our destination without realizing how we got there, or when we miss part of a conversation we are engaged in. As these everyday examples suggest, there is nothing inherently pathological about dissociation itself. Dissociation only becomes pathological when the dissociative symptoms are “perceived as disruptive, invoking a loss of needed information, as producing discontinuity of experience” or as “recurrent, jarring involuntary intrusions into executive functioning and sense of self” (Spiegel et al., 2011, p. E19).

Much of the mental life of all human beings involves automatic nonconscious processes that are to a large extent autonomous with respect to deliberate, self-aware direction and monitoring. Such unaware processing extends to the areas of implicit memory and implicit perception, where it can be demonstrated that all persons routinely show indirect evidence of remembering things they cannot consciously recall ( implicit memory ) and respond to sights or sounds as if they had perceived them (as in conversion blindness or deafness) even though they cannot report that they have seen or heard them ( implicit perception ; Kihlstrom,  2001  2005 ; Kihlstrom et al.,  1993 ). As we learned in  Chapter 3 , the general idea of unconscious mental processes has been embraced by psychodynamically oriented clinicians for many years. But only in the past 30 years has it also become a major research area in the field of cognitive psychology (though without any of the psychodynamic implications for why so much of our mental activity is unconscious).

In people with dissociative disorders, however, this normally integrated and well-coordinated multichannel quality of human cognition becomes much less coordinated and integrated. When this happens, the affected person may be unable to access information that is normally in the forefront of consciousness, such as his or her own personal identity or details of an important period of time in the recent past. That is, the normally useful capacity of maintaining ongoing mental activity outside of awareness appears to be subverted, sometimes for the purpose of managing severe psychological threat. When that happens, we observe the pathological dissociative symptoms that are the cardinal characteristic of dissociative disorders. Like somatic symptom disorders, dissociative disorders appear mainly to be ways of avoiding anxiety and stress and of managing life problems that threaten to overwhelm the person’s usual coping resources. Both types of disorders also enable the individual to deny personal responsibility for his or her “unacceptable” wishes or behavior. In the case of DSM-defined dissociative disorders, the person avoids the stress by pathologically dissociating—in essence, by escaping from his or her own autobiographical memory or personal identity. The DSM-5 recognizes several types of pathological dissociation. These include depersonalization/derealization disorder, dissociative amnesia, dissociative fugue (a subtype of dissociative amnesia) and dissociative identity disorder.

Depersonalization/Derealization Disorder

Two of the more common kinds of dissociative symptoms are derealization and depersonalization. We mentioned these in  Chapter 6  because they sometimes occur during panic attacks. In  derealization  one’s sense of the reality of the outside world is temporarily lost, and in  depersonalization  one’s sense of one’s own self and one’s own reality is temporarily lost. As many as 50-74 percent of us have such experiences in mild form at least once in our lives, usually during or after periods of severe stress, sleep deprivation, or sensory deprivation (e.g., Khazaal et al.,  2005 ; Reutens et al.,  2010 ). But when episodes of depersonalization or derealization become persistent and recurrent and interfere with normal functioning,  depersonalization  derealization disorder  may be diagnosed.

In this disorder, people have persistent or recurrent experiences of feeling detached from (and like an outside observer of) their own bodies and mental processes. They may even feel they are, for a time, floating above their physical bodies, which may suddenly feel very different—as if drastically changed or unreal. During periods of depersonalization, unlike during psychotic states, reality testing remains intact. The related experience of derealization, in which the external world is perceived as strange and new in various ways, may also occur. As one leader in the field described it, in both states “the feeling puzzles the experiencers: the changed condition is perceived as unreal, and as discontinuous with his or her previous ego-states. The object of the experience, self (in depersonalization) or world (in derealization), is commonly described as isolated, lifeless, strange, and unfamiliar; oneself and others are perceived as ‘automatons,’ behaving mechanically, without initiative or self-control” (Kihlstrom,  2001 , p. 267). Often people also report feeling as though they are living in a dream or movie (Maldonado et al.,  2002 ). In keeping with such reports, research has shown that emotional experiences are attenuated or reduced during depersonalization—both at the subjective level and at the level of neural and autonomic activity that normally accompanies emotional responses to threatening or unpleasant emotional stimuli (Lemche et al.,  2007 ; Phillips & Sierra,  2003 ; Stein & Simeon,  2009 ). After viewing an emotional video clip, participants with depersonalization disorder showed higher levels of subjective and objective memory fragmentation than controls (Giesbrecht et al.,  2010 ). Memory fragmentation is marked by difficulties forming an accurate or coherent narrative sequence of events, which is consistent with earlier research suggesting that time distortion is a key element of the experience of depersonalization (Simeon et al.,  2008 ).

DSM-5 criteria for: Depersonalization/Derealization Disorder

·  A. The presence of persistent or recurrent experiences of depersonalization, derealization, or both:

·  1. Depersonalization: Experiences of unreality, detachment, or being an outside observer with respect to one’s thoughts, feelings, sensations, body, or actions (e.g., perceptual alterations, distorted sense of time, unreal or absent self, emotional and/or physical numbing).

·  2. Derealization: Experiences of unreality or detachment with respect to surroundings (e.g., individuals or objects are experienced as unreal, dreamlike, foggy, lifeless, or visually distorted).

·  B. During the depersonalization or derealization experiences, reality testing remains intact.

·  C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

·  D. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, medication) or another medical condition (e.g., seizures).

·  E. The disturbance is not better explained by another mental disorder, such as schizophrenia, panic disorder, major depressive disorder, acute stress disorder, posttraumatic stress disorder, or another dissociative disorder.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

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People with derealization symptoms experience the world as hazy and indistinct.

A number of researchers have noted elevated rates of comorbid anxiety and mood disorders as well as avoidant, borderline, and obsessive-compulsive personality disorders (e.g., Hunter et al.,  2003 ; Mula et al.,  2007 ; Reutens et al.,  2010 ). Another study of over 200 cases found that the disorder had an average age of onset of 23. Moreover, in nearly 80 percent of cases, the disorder has a fairly chronic course (with little or no fluctuation in intensity; Baker, Hunter, et al.,  2003 ).

The case of the foggy student below is fairly typical.

A Foggy Student A 20-year-old male college student sought psychiatric consultation because he was worried that he might be going insane. For the past 2 years he had experienced increasingly frequent episodes of feeling “outside” himself. These episodes were accompanied by a sense of deadness in his body. In addition, during these periods he was uncertain of his balance and frequently stumbled into furniture; this was more apt to occur in public, especially if he was somewhat anxious. During these episodes he felt a lack of easy, natural control of his body, and his thoughts seemed “foggy” as well ….

The patient’s subjective sense of lack of control was especially troublesome, and he would fight it by shaking his head and saying “stop” to himself. This would momentarily clear his mind and restore his sense of autonomy, but only temporarily, as the feelings of deadness and of being outside himself would return. Gradually, over a period of several hours, the unpleasant experiences would fade …. At the time the patient came for treatment, he was experiencing these symptoms about twice a week, and each incident lasted from 3 to 4 hours. On several occasions the episodes had occurred while he was driving his car and was alone; worried that he might have an accident, he had stopped driving unless someone accompanied him.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 270–71). Washington, DC. (Copyright © 2002). American Psychiatric Association.

The lifetime prevalence of depersonalization/derealization disorder is unknown but has been estimated at 1 to 2 percent of the population (Reutens et al.,  2010 ). Moreover, occasional depersonalization/derealization symptoms are not uncommon in a variety of other disorders such as schizophrenia, borderline personality disorder, panic disorder, acute stress disorder, and posttraumatic stress disorder (PTSD) (Hunter et al.,  2003 ). Although severe depersonalization/derealization symptoms can be quite frightening and may make the victim fear imminent mental collapse, such fears are usually unfounded. Sometimes, however, feelings of depersonalization are clearly early manifestations of impending decompensation and the development of psychotic states ( Chapter 13 ). In either case, professional assistance in dealing with the precipitating stressors and in reducing anxiety may be helpful. Unfortunately, however, as of yet there are no clearly effective treatments—either through medication or psychotherapy.

Dissociative Amnesia and Dissociative Fugue

Retrograde amnesia is the partial or total inability to recall or identify previously acquired information or past experiences; by contrast, anterograde amnesia is the partial or total inability to retain new information (Gilboa et al.,  2006 ; Kapur,  1999 ). Persistent amnesia may occur in several disorders, such as dissociative amnesia and dissociative fugue. It may also result from traumatic brain injury or diseases of the central nervous system. If the amnesia is caused by brain pathology, it most often involves failure to retain new information and experiences (anterograde amnesia). That is, the information contained in experience is not registered and does not enter memory storage (Kapur,  1999 ).

On the other hand,  dissociative amnesia  is usually limited to a failure to recall previously stored personal information (retrograde amnesia) when that failure cannot be accounted for by ordinary forgetting. The gaps in memory most often occur following intolerably stressful circumstances—wartime combat conditions, for example, or catastrophic events such as serious car accidents, suicide attempts, or violent outbursts (Maldonado & Spiegel,  2007 ; Spiegel et al., 2011). In this disorder, apparently forgotten personal information is still there beneath the level of consciousness, as sometimes becomes apparent in interviews conducted under hypnosis or narcosis (induced by sodium amytal, or so-called truth serum) and in cases where the amnesia spontaneously clears up.  image10 Watch the Video Sharon: Dissociative Amnesia on MyPsychLab

Amnesic episodes usually last between a few days and a few years. Although many people experience only one such episode, some people have multiple episodes in their lifetimes (Maldonado & Spiegel,  2007 ; Staniloiu & Markowitsch,  2010 ). In typical dissociative amnesic reactions, individuals cannot remember certain aspects of their personal life history or important facts about their identity. Yet their basic habit patterns—such as their abilities to read, talk, perform skilled work, and so on—remain intact, and they seem normal aside from the memory deficit (Kihlstrom,  2005 ; Kihlstrom & Schacter,  2000 ). Thus the only type of memory that is affected is episodic (pertaining to events experienced) or autobiographical memory (pertaining to personal events experienced). The other recognized forms of memory—semantic (pertaining to language and concepts), procedural (how to do things), and short-term storage—seem usually to remain intact, although there is very little research on this topic (Kihlstrom,  2005 ; Kihl-strom & Schacter,  2000 ). Usually there is no difficulty encoding new information (Maldonado & Spiegel,  2007 ).

DSM-5 criteria for: Dissociative Amnesia

·  A. An inability to recall important autobiographical information, usually of a traumatic or stressful nature, that is inconsistent with ordinary forgetting.

Note: Dissociative amnesia most often consists of localized or selective amnesia for a specific event or events; or generalized amnesia for identity and life history.

·  B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

·  C. The disturbance is not attributable to the physiological effects of a substance (e.g., alcohol or other drug of abuse, a medication) or a neurological or other medical condition (e.g., partial complex seizures, transient global amnesia, sequelae of a closed head injury/traumatic brain injury, other neurological condition).

·  D. The disturbance is not better explained by dissociative identity disorder, posttraumatic stress disorder, acute stress disorder, somatic symptom disorder, or major or mild neurocognitive disorder.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

In rare cases a person may retreat still further from real-life problems by going into an amnesic state called a  dissociative fugue , which, as the term implies (the French word fugue means “flight”), is a defense by actual flight—a person is not only amnesic for some or all aspects of his or her past but also departs from home surroundings. This is accompanied by confusion about personal identity or even the assumption of a new identity (although the identities do not alternate as they do in dissociative identity disorder). During the fugue, such individuals are unaware of memory loss for prior stages of their life, but their memory for what happens during the fugue state itself is intact (Kihlstrom,  2005 ; Kihlstrom & Schacter,  2000 ). Their behavior during the fugue state is usually quite normal and unlikely to arouse suspicion that something is wrong. However, behavior during the fugue state often reflects a rather different lifestyle from the previous one (the rejection of which is sometimes fairly obvious). Days, weeks, or sometimes even years later, such people may suddenly emerge from the fugue state and find themselves in a strange place, working in a new occupation, with no idea how they got there. In other cases, recovery from the fugue state occurs only after repeated questioning and reminders of who they are. In either case, as the fugue state remits, their initial amnesia remits—but a new, apparently complete amnesia for their fugue period occurs. In DSM-5 dissociative fugue is considered to be a subtype of dissociative amnesia rather than a separate disorder as it was in DSM-IV.

The pattern in dissociative amnesia and dissociative fugue is essentially similar to that in conversion symptoms, except that instead of avoiding some unpleasant situation by becoming physically dysfunctional, a person unconsciously avoids thoughts about the situation or, in the extreme, leaves the scene (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Thus people experiencing dissociative amnesia and fugue are typically faced with extremely unpleasant situations from which they see no acceptable way to escape. Eventually the stress becomes so intolerable that large segments of their personalities and all memory of the stressful situations are suppressed.

Several of these aspects of dissociative fugue are illustrated in the following case.

A Middle Manager Transformed into a Short-Order Cook Burt Tate, a 42-year-old short-order cook in a small-town diner, was brought to the attention of local police following a heated altercation with another man at the diner. He gave his name as Burt Tate and indicated that he had arrived in town several weeks earlier. However, he could produce no official identification and could not tell the officers where he had previously lived and worked. Burt was asked to accompany the officers to the emergency room of a local hospital so that he might be examined ….

Burt’s physical examination was negative for evidence of recent head trauma or any other medical abnormality …. He was oriented as to current time and place, but manifested no recall of his personal history prior to his arrival in town. He did not seem especially concerned about his total lack of a remembered past ….

Meanwhile, the police … discovered that Burt matched the description of one Gene Saunders, a resident of a city some 200 miles away who had disappeared a month earlier. The wife of Mr. Saunders … confirmed the real identity of Burt, who … stated that he did not recognize Mrs. Saunders.

Prior to his disappearance, Gene Saunders, a middle-level manager in a large manufacturing firm, had been experiencing considerable difficulties at work and at home. A number of stressful work problems, including failure to get an expected promotion, the loss of some of his key staff, failure of his section to meet production goals, and increased criticism from his superior—all occurring within a brief time frame—had upset his normal equanimity. He had become morose and withdrawn at home and had been critical of his wife and children. Two days before he had left, he had had a violent argument with his 18-year-old son, who had declared his father a failure and had stormed out of the house to go live with friends.

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (pp. 254–55). Washington, DC. (Copyright © 2002). American Psychiatric Association.

MEMORY AND INTELLECTUAL DEFICITS IN DISSOCIATIVE AMNESIA AND FUGUE

Unfortunately, very little systematic research has been conducted on individuals with dissociative amnesia and fugue. What is known comes largely from intensive studies of the memory and intellectual functioning of isolated cases with these disorders, so any conclusions should be considered tentative pending further study of larger samples with appropriate control groups. What can be gathered from a handful of such case studies is that these individuals’ semantic knowledge (assessed via the vocabulary subtest of an IQ test) seems to be generally intact. The primary deficit these individuals exhibit is their compromised episodic or autobiographical memory (Kihlstrom,  2005 ; Kihlstrom & Schacter,  2000 ). Indeed, several studies using brain-imaging techniques have confirmed that when people with dissociative amnesia are presented with autobiographical memory tasks, they show reduced activation in their right frontal and temporal brain areas relative to normal controls doing the same kinds of tasks (Kihlstrom,  2005 ; Markowitsch,  1999 ). In a recent review of nine cases of dissociative amnesia for which brain imaging data were available, the authors concluded there was evidence of significant changes in the brains of these patients, mostly centered on subtle loss of function in the right anterior hemisphere—changes similar to those seen in the brains of patients with organic memory loss (Staniloiu & Markowitsch,  2010 ).

However, several cases (some nearly a century old) have suggested that implicit memory is generally intact. For example, Jones (1909, as cited in Kihlstrom & Schacter,  2000 ) studied a patient with dense amnesia and found that although he could not remember his wife’s or daughter’s names, when asked to guess what names might fit them, he produced their names correctly. In a more contemporary case (Lyon, 1985, as cited in Kihlstrom & Schacter,  2000 ), a patient who could not retrieve any autobiographical information was asked to dial numbers on a phone randomly. Without realizing what he was doing, he dialed his mother’s phone number, which then led to her identifying him. In one particularly fascinating contemporary case of dissociative fugue, Glisky and colleagues ( 2004 ) describe a German man who had come to work in the United States several months before he had experienced a traumatic incident in which he had been robbed and shot. After the trauma, he wandered along unfamiliar streets for an unknown period of time. Finally, he stopped at a motel and asked if the police could be called because he did not know who he was (and had no ID because he’d been robbed) and could not recall any personal details of his life. He spoke English (with a German accent) but could not speak German and did not respond to instructions in German (which he denied that he spoke). In spite of his extensive loss of autobiographical memory (and the German language), when given a variety of memory tasks, he showed intact implicit memory. Especially striking was his ability to learn German–English word pairs, which he learned much faster than did normal controls, suggesting implicit knowledge of German even though he had no conscious knowledge of it.

Some of these memory deficits in dissociative amnesia and fugue have been compared to related deficits in explicit perception that occur in conversion disorders. This has convinced many people that conversion disorder should be classified with dissociative disorders rather than with somatic symptom disorders. This issue is discussed in more detail in the Thinking Critically About DSM-5 box below.

Dissociative Identity Disorder (Did)

DSM-5 THINKING CRITICALLY about DSM-5: Where Does Conversion Disorder Belong?

Starting with Freud and Janet, and for a large portion of the twentieth century prior to the publication of DSM-III in 1980, conversion disorders were classified together with dissociative disorders as subtypes of hysteria. When it was determined that DSM-III would rely heavily on overt behavioral symptoms rather than on presumed underlying etiology (namely, repressed anxiety) for classifying disorders, the decision was made to include conversion disorder with the other somatic symptom disorders. This was because its symptoms were physical ones with no demonstrable medical basis. However, as Kihlstrom ( 1994  2001  2005 ) and others have pointed out, this ignores some very important differences between conversion disorders and other somatic symptom disorders. The most important overall difference is that conversion symptoms (but not those of the other somatoform disorders) are nearly always pseudoneurological in nature (blindness, paralysis, anesthesias, deafness, seizures, etc.), mimicking some true neurological syndromes, just as most of the dissociative disorders do.

The disorders we currently classify as dissociative disorders (such as dissociative amnesia and DID) involve disruptions in explicit memory for events that have occurred, or who or what one’s identity is, or both. However, it is clear that events occurring during a period of amnesia or in the presence of one identity are indeed registered in the nervous system because they influence behavior indirectly even when the person cannot consciously recollect them (i.e., implicit memory remains at least partially intact in dissociative disorders). Similarly, Kihlstrom and others have argued that the conversion disorders involve disruptions in explicit perception and action. That is, people with conversion disorders have no conscious recognition that they can see or hear or feel, or no conscious knowledge that they can walk or talk or feel. However, patients with conversion disorder can see, hear, feel, or move when tricked into doing so or when indirect physiological or behavioral measures are used (see Janet,  1901  1907 ; Kihlstrom,  1994  2001  2005 ). Thus Kihlstrom ( 1994  2001  2005 ) and others made a compelling argument that in future editions, the term conversion disorder should be dropped and the sensory and motor types of the syndrome should be reclassified as forms of dissociative disorders. This way, the central feature of all dissociative disorders would be a disruption of the normally integrated functions of consciousness (memory, perception, and action). Such a proposal is also consistent with observations that dissociative symptoms and disorders are quite common in patients with conversion disorder (e.g., Sar et al.,  2004 ). This proposal was seriously considered and heavily debated by the DSM-5 task force. In the end, the proponents for moving conversion disorder into the dissociative disorders category did not succeed and in DSM-5 conversion disorder (at least for now) is still listed as a somatic symptom disorder.

Dissociative identity disorder (DID) , formerly known as multiple personality disorder is a dramatic dissociative disorder in which a patient manifests two or more distinct identities that alternate in some way in taking control of behavior. There is also an inability to recall important personal information that cannot be explained by ordinary forgetting. Each identity may appear to have a different personal history, self-image, and name, although there are some identities that are only partially distinct and independent from other identities. In most cases the one identity that is most frequently encountered and carries the person’s real name is the  host identity . Also in most cases, the host is not the original identity, and it may or may not be the best-adjusted identity. The  alter identities  may differ in striking ways involving gender, age, handedness, handwriting, sexual orientation, prescription for eyeglasses, predominant affect, foreign languages spoken, and general knowledge. For example, one alter may be carefree, fun-loving, and sexually provocative, and another alter quiet, studious, serious, and prudish. Needs and behaviors inhibited in the primary or host identity are usually liberally displayed by one or more alter identities. Certain roles such as a child and someone of the opposite sex are extremely common.

Much of the reason for abandoning the older diagnostic term multiple personality disorder in favor of DID was the growing recognition that it had misleading connotations, suggesting multiple occupancy of space, time, and people’s bodies by differing, but fully organized and coherent, “personalities.” In fact, alters are not in any meaningful sense personalities but rather reflect a failure to integrate various aspects of a person’s identity, consciousness, and memory (Spiegel, 2006). The term DID better captures this. Indeed Spiegel (one prominent theorist in this area) has argued that “the problem is not having more than one personality, it is having less than one” (Spiegel, 2006, p. 567).

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Chris Sizemore was the inspiration for the book and movie Three Faces of Eve, which explore her multiple personality disorder (now known as DID). After her recovery, Sizemore worked as an advocate for the mentally ill.

DSM-5 criteria for: Dissociative Identity Disorder

·  A. Disruption of identity characterized by two or more distinct personality states, which may be described in some cultures as an experience of possession. The disruption in identity involves marked discontinuity in sense of self and sense of agency, accompanied by related alterations in affect, behavior, consciousness, memory, perception, cognition, and/or sensory-motor functioning. These signs and symptoms may be observed by others or reported by the individual.

·  B. Recurrent gaps in the recall of everyday events, important personal information, and/or traumatic events that are inconsistent with ordinary forgetting.

·  C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

·  D. The disturbance is not a normal part of a broadly accepted cultural or religious practice.

Note: In children, the symptoms are not better explained by imaginary playmates or other fantasy play.

·  E. The symptoms are not attributable to the physiological effects of a substance (e.g., blackouts or chaotic behavior during alcohol intoxication) or another medical condition (e.g., complex partial seizures).

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Alter identities take control at different points in time, and the switches typically occur very quickly (in a matter of seconds), although more gradual switches can also occur. When switches occur in people with DID, it is often easy to observe the gaps in memories for things that have happened—often for things that have happened to other identities. But this amnesia is not always symmetrical; that is, some identities may know more about certain alters than do other identities. Sometimes one submerged identity gains control by producing hallucinations (such as a voice inside the head giving instructions). In sum, DID is a condition in which normally integrated aspects of memory, identity, and consciousness are no longer integrated. Additional symptoms of DID include depression, self-mutilation, frequent suicidal ideation and attempts, erratic behavior, headaches, hallucinations, posttraumatic symptoms, and other amnesic and fugue symptoms (APA,  2013 ; Maldonado et al.,  2002 ). Depressive disorders, PTSD, substance-use disorders, and borderline personality disorder are the most common comorbid diagnoses (Maldonado & Spiegel,  2007 ). One recent study found that among patients with diagnoses of DID, the average number of comorbid diagnoses (based on structured diagnostic interviews) was five, with PTSD being the most common (Rodewald et al.,  2011 ).

DID usually starts in childhood, although most patients are in their teens, 20s, or 30s at the time of diagnosis (Maldonado & Spiegel,  2007 ). Approximately three to nine times more females than males are diagnosed as having the disorder, and females tend to have a larger number of alters than do males (Maldonado & Spiegel,  2007 ). Some believe that this pronounced gender discrepancy is due to the much greater proportion of childhood sexual abuse among females than among males (see  Chapter 12 ), but this is a highly controversial point.

Many of these features are illustrated in the case of Mary Kendall below.

the WORLD around us: DID, Schizophrenia, and Split Personality: Clearing Up the Confusion

The general public has long been confused by the distinction between DID and schizophrenia. It is not uncommon for people diagnosed with schizophrenia to be referred to as having a “split personality.” We have even heard people say such things as, “I’m a bit schizophrenic on this issue” to mean that they have more than one opinion about it!

Although this misuse of the term split personality actually began among psychiatric professionals, today it reflects the public’s general misunderstanding of schizophrenia, which does not involve a “split” or “Jekyll and Hyde” personality at all. The original confusion may have stemmed from the term schizophrenia, which was first coined by a Swiss psychiatrist named Bleuler. Schizien is German for “split,” and phren is the Greek root for “mind.” The notion that schizophrenia is characterized by a split mind or personality may have arisen this way (see McNally,  2007 , for a historical review of how this confusion arose).

However, this is not at all what Bleuler intended the word schizophrenia to mean. Rather, Bleuler was referring to the splitting of the normally integrated associative threads of the mind—links between words, thoughts, emotions, and behavior. Splits of this kind result in thinking that is not goal-directed or efficient, which in turn leads to the host of other difficulties known to be associated with schizophrenia.

It is very important to remember that people diagnosed with schizophrenia do not have multiple distinct identities that alternately take control over their mind and behavior. They may have a delusion and believe they are someone else, but they do not show the changes in identity accompanied by changes in tone of voice, vocabulary, and physical appearance that are often seen when identities “switch” in DID. Furthermore, people with DID (who are probably closer to the general public’s notion of “split personality”) do not exhibit such characteristics of schizophrenia as disorganized behavior, hallucinations coming from outside the head, and delusions, or incoherent and loose associations (e.g., Kluft,  2005 ).

Mary and Marian Mary, a 35-year-old divorced social worker, had … in her right forearm and hand … chronic pain. Medical management of this pain had proved problematic, and it was decided to teach her self-hypnosis as a means whereby she might control it. She proved an excellent hypnotic subject and quickly learned effective pain control techniques.

Her hypnotist/trainer, a psychiatrist, describes Mary’s life in rather unappealing terms. She is said to be competent professionally but has an “arid” personal and social life …. She spends most of her free time doing volunteer work in a hospice ….

In the course of the hypnotic training, Mary’s psychiatrist discovered that she seemed to have substantial gaps in her memory. One phenomenon in particular was very puzzling: She reported that she could not account for what seemed an extraordinary depletion of the gasoline in her car’s tank. She would arrive home from work with a nearly full tank, and by the following morning as she began her trip to work would notice that the tank was now only half-full. When it was advised that she keep track of her odometer readings, she discovered that on many nights on which she insisted she’d remained at home the odometer showed significant accumulations of up to 100 miles. The psychiatrist, by now strongly suspecting that Mary had a dissociative disorder, also established that there were large gaps in her memories of childhood. He shifted his focus to exploring the apparently widespread dissociative difficulties.

In the course of one of the continuing hypnotic sessions, the psychiatrist again asked about “lost time,” and was greeted with a response in a wholly different voice tone that said, “It’s about time you knew about me.” Marian, an apparently well-established alter identity, went on to describe the trips she was fond of taking at night … Marian was an extraordinarily abrupt and hostile “person,” the epitome in these respects of everything the compliant and self-sacrificing Mary was not. Marian regarded Mary with unmitigated contempt, and asserted that “worrying about anyone but yourself is a waste of time.”

In due course some six other alter identities emerged …. There was notable competition among the alters for time spent “out,” and Marian was often so provocative as to frighten some of the more timid others, which included a 6-year-old child ….

Mary’s history, as gradually pieced together, included memories of physical and sexual abuse by her father as well as others during her childhood …. Her mother was described … as having abdicated to a large extent the maternal role, forcing Mary from a young age to assume these duties in the family.

Four years of subsequent psychotherapy resulted in only modest success in achieving a true “integration” of these diverse trends in Mary Kendall’s selfhood.

Source: Adapted with permission from DSM-IV-TR Casebook (pp. 56–57). Washington, DC. (Copyright © 2002). American Psychiatric Association.

The number of alter identities in DID varies tremendously and has increased over time (Maldonado & Spiegel,  2007 ). One early review of 76 classic cases reported that two-thirds of these cases had only two personalities and most of the rest had three (Taylor & Martin,  1944 ). More recent estimates are that about 50 percent now show over 10 identities with some respondents claiming as many as a hundred. This historical trend of increasing multiplicity suggests the operation of social factors, perhaps through the encouragement of therapists, as we discuss below (e.g., Kihlstrom,  2005 ; Lilienfeld et al.,  1999 ; Piper & Merskey,  2004a  2004b ). Another recent trend is that many of the reported cases of DID now include more unusual and even bizarre identities than in the past (such as being an animal) and more highly implausible backgrounds (e.g., ritualized satanic abuse in childhood).

PREVALENCE—WHY HAS DID BEEN INCREASING?

Owing to their dramatic nature, cases of DID receive a great deal of attention and publicity in fiction, television, and motion pictures. But in fact, until relatively recently, DID was extremely rare—or at least rarely diagnosed—in clinical practice. Prior to 1979, only about 200 cases could be found in the entire psychological and psychiatric literature worldwide. By 1999, however, over 30,000 cases had been reported in North America alone (Ross,  1999 ), although as we will discuss later, many researchers believe that this is a gross overestimate (e.g., Piper & Merskey,  2004b ). Because their diagnosed occurrence in both clinical settings and in the general population increased enormously in recent years, prevalence estimates in the general population vary. One study of 658 people in upstate New York estimated a 1.5 percent prevalence (Johnson et al.,  2006 ), but it is possible that no such estimates are valid, given how hard it is to make this diagnosis reliably. (For example, recall that Mary’s DID was uncovered only in the course of hypnotic sessions for pain management.)

Many factors probably have contributed to the drastic increase in the reported prevalence of DID (although in an absolute sense it is still very rare, and most practicing psychotherapists never see a person with DID in their entire careers). For example, the number of cases began to rise in the 1970s after the publication of Flora Rhea Schreiber’s Sybil ( 1973 ) This increased public awareness of the condition. (Ironically, however, the case has now been thoroughly discredited (see Borch-Jacobsen,  1997 ; Paris,  2012 ; Rieber,  1999 ). At about the same time, the diagnostic criteria for DID (then called multiple personality disorder) were clearly specified for the first time with the publication of DSM-III in 1980. This seems to have led to increased acceptance of the diagnosis by clinicians, which may have encouraged reporting of it in the literature. Clinicians were traditionally (and often still are today) somewhat skeptical of the astonishing behavior these patients often display.

Another reason why the diagnosis was made more frequently after 1980 is that the diagnostic criteria for schizophrenia were tightened in DSM-III. People who had perhaps been inappropriately diagnosed with schizophrenia could now receive the more appropriate diagnosis of multiple personality disorder. In addition, beginning in about 1980, prior scattered reports of instances of childhood abuse in the histories of adult patients began building into what would become a crescendo. As we will see later, many controversies arose regarding how to interpret such findings, but it is definitely true that these reports of abuse in patients with DID drew a great deal of attention to this disorder, which in turn may have increased the rate at which it was being diagnosed.

Finally, it is almost certain that some of the increase in the prevalence of DID is artifactual and has occurred because some therapists looking for evidence of DID in certain patients may suggest the existence of alter identities (especially when the person is under hypnosis and very suggestible; e.g., Kihlstrom,  2005 ; Piper & Merskey,  2004b ). The therapist may also subtly reinforce the emergence of new identities by showing great interest in these new identities. Nevertheless, such factors cannot account for all cases of diagnosed DID, which has been observed in most parts of the world, even where there is virtually no personal or professional knowledge of DID, including rural Turkey (Akyuz et al.,  1999 ; see also Maldonado & Spiegel,  2007 ) and Shanghai, China (Xiao et al.,  2006 ).

EXPERIMENTAL STUDIES OF DID

Much of what is known about DID comes from patients’ self-reports and from therapists’ or researchers’ clinical observations. Indeed, only a small number of experimental studies of people with DID have been conducted to corroborate clinical observations. Moreover, most of these studies have been conducted on only one or a few cases, although very recently a few larger studies have been done that include appropriate control groups (e.g., Dorahy et al.,  2005 ; Huntjens et al.,  2003  2007 ). In spite of such shortcomings, most of the findings from these studies are generally consistent with one another and reveal some very interesting features of DID.

The primary focus of these studies has been to determine the nature of the amnesia that exists between different identities. As we have already noted, most people with DID have at least some identities that seem completely unaware of the existence and experiences of certain alter identities, although other identities may be only partially amnesic of some alters (e.g., Elzinga et al.,  2003 ; Huntjens et al.,  2003 ). This feature of DID has been corroborated by studies showing that when one identity (Identity 1) is asked to learn a list of word pairs, and an alter identity (Identity 2) is later asked to recall the second word in each pair using the first word as a cue, there seems to be no transfer to Identity 2 of what was learned by Identity 1. This interpersonality amnesia with regard to conscious recall of the activities and experiences of at least some other identities has generally been considered a fundamental characteristic of DID (Kihlstrom,  2001  2005 ; Kihlstrom & Schacter,  2000 ). Nevertheless, several interesting recent studies, each with about 20 DID patients, have challenged any idea that this interpersonality amnesia is complete, instead sometimes finding partial transfer of explicit memory across identities in certain tasks (Huntjens et al.,  2003  2007 , 2012; see also Dorahy & Huntjens,  2007 , for a review).

As noted earlier, there are kinds of memory other than simply what can be brought to awareness (explicit memory). As with dissociative amnesia and fugue, there is evidence that Identity 2 has some implicit memory of things that Identity 1 learned. That is, although Identity 2 may not be able to recall consciously the things learned by Identity 1, these apparently forgotten events may influence Identity 2’s experiences, thoughts, and behaviors unconsciously (Kihlstrom,  2001  2005 ). This might be reflected in a test asking Identity 2 to learn the list of words previously learned by Identity 1. Even though Identity 2 could not consciously recall the list of words, Identity 2 would learn that list more rapidly than a brand-new list of words, an outcome that suggests the operation of implicit memory (e.g., Eich et al.,  1997 ; Elzinga et al.,  2003 ; see Kihlstrom,  2001  2005 , for reviews).

Related studies on implicit transfer of memories have shown that emotional reactions learned by one identity often transfer across identities, too. Thus, even though Identity 2 may not be able to recall an emotional event that happened to Identity 1, a visual or auditory reminder of the event (a conditioned stimulus) administered to Identity 2 may elicit an emotional reaction even though Identity 2 has no knowledge of why it did so (e.g., Ludwig et al.,  1972 ; Prince,  1910 ). Moreover, one study by Huntjens and colleagues ( 2005 ) had 22 DID patients in Identity 1 learn to reevaluate a neutral word in a positive or negative manner through a simple evaluative conditioning procedure in which neutral words are simply paired with positive or negative words; the neutral words then come to take on positive or negative connotations. When Identity 2 was later asked to emerge, he or she also categorized the formerly neutral word in the same positive or negative manner as learned by Identity 1, showing implicit memory for the reevaluation of the word learned by Identity 1 (although complete subjective amnesia was reported by Identity 2). Nevertheless, other sophisticated studies have made it clear that implicit memory transfer across personalities does not always occur, particularly with certain kinds of implicit memory tasks where memory performance may be strongly influenced by the identity currently being tested (e.g., Dorahy,  2001 ; Eich et al.,  1997 ; Nissen et al.,  1988 ). However, the results that do show implicit memory transfer are very important because they demonstrate that explicit amnesia across identities cannot occur simply because one identity is trying actively to suppress any evidence of memory transfer. If this were possible, there would be no leakage of implicit memories across identities (Dorahy,  2001 ; Eich et al.,  1997 ).

An even smaller number of experimental studies have examined differences in brain activity when individuals with DID are tested with different identities at the forefront of consciousness. For example, in an early classic study, Putnam ( 1984 ) investigated EEG activity in 11 DID patients during different identities, and in 10 control subjects who were simulating different personality states, in order to determine whether there were different patterns of brain wave activity during different identities (real or simulated), as would be found if separate individuals were assessed. The study found that there were indeed differences in brain wave activity when the patients with DID were in different personality states and that these differences were greater than those found in the simulating subjects (see Kihlstrom et al.,  1993 ; Putnam,  1997 ).

One particularly interesting study by Reinders and colleagues ( 2006 ) examined subjective and cardiovascular activation patterns to both neutral and traumatic memories in 11 people diagnosed with DID. Each patient had one alter with a neutral identity such as the one active when they were functioning in everyday life, and each had another alter with a traumatic identity who had access to traumatic memories. As expected, when exposed to a script of neutral personal memories neither identity displayed much subjective or cardiovascular reactivity. However, when exposed to a script of personal memories of traumatizing events, responding differed in the two identity states. Specifically, the traumatic identity state (but not the neutral identity state) showed subjective and cardiovascular reactivity reflecting emotional distress to the personal traumatic memory. Such results could be seen as providing support for the idea that one function of certain alters is to protect the person from traumatic memories that a traumatic identity state has access to.

CAUSAL FACTORS AND CONTROVERSIES ABOUT DID

There are at least four serious, interrelated controversies surrounding DID and how it develops. First, some have been concerned with whether DID is a real disorder or is faked, and whether, even if it is real, it can be faked. The second major controversy is about how DID develops. Specifically, is DID caused by early childhood trauma, or does the development of DID involve some kind of social enactment of multiple different roles that have been inadvertently encouraged by careless clinicians? Third, those who maintain that DID is caused by childhood trauma cite mounting evidence that the vast majority of individuals diagnosed with DID report memories of an early history of abuse. But are these memories of early abuse real or false? Finally, if abuse has occurred in most individuals with DID, did the abuse play a causal role, or was something else correlated with the abuse actually the cause?

DID: Real or Faked? The issue of possible factitious or malingering origins of DID has dogged the diagnosis of DID for at least a century. One obvious situation in which this issue becomes critical is when it has been used by defendants and their attorneys to try to escape punishment for crimes (“My other personality did it”). For example, this defense was used, ultimately unsuccessfully, in the famous case of the Hillside Strangler, Kenneth Bianchi (Orne et al.,  1984 ), but it has probably been used successfully in other cases that we are unaware of (unaware because the person is not sent to prison but rather to a mental hospital in most cases). Bianchi was accused of brutally raping and murdering 10 young women in the Los Angeles area. Although there was a great deal of evidence that he had committed these crimes, he steadfastly denied it, and some lawyers thought perhaps he had DID. He was subsequently interviewed by a clinical psychologist, and under hypnosis a second personality, “Steve,” emerged. Steve confessed to the crimes, thereby creating the basis for a plea of “not guilty by reason of insanity” (see  Chapter 17 ). However, Bianchi was later examined even more closely by a renowned psychologist and psychiatrist specializing in this area, the late Martin Orne. Upon closer examination, Orne determined that Bianchi was faking the condition. Orne drew this conclusion in part because when he suggested to Bianchi that most people with DID have more than two identities, Bianchi suddenly produced a third (Orne et al.,  1984 ). Moreover, there was no evidence of multiple identities existing prior to the trial. When Bianchi’s faking the disorder was discovered, he was convicted of the murders. In other words, some cases of DID may involve complete fabrication orchestrated by criminal or other unscrupulous persons seeking unfair advantages, and not all prosecutors have as clever and knowledgeable an expert witness as Martin Orne to help detect this. Nevertheless, most researchers think that factitious and malingering cases of DID (such as the Bianchi case or cases in which the person has a need to be a patient) are relatively rare.

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FIGURE 8.1 Reported childhood abuse in five separate studies of DID patients (Total n = 843).

If DID Is Not Faked, How Does It Develop: Posttraumatic Theory or Sociocognitive Theory? Many professionals acknowledge that, in most cases, DID is a real syndrome (not consciously faked), but there is marked disagreement about how it develops and how it is maintained. In the contemporary literature, the original major theory of how DID develops is  posttraumatic theory  (Gleaves,  1996 ; Maldonado & Spiegel,  2007 ; Ross,  1997  1999 ). The vast majority of patients with DID (over 95 percent by some estimates) report memories of severe and horrific abuse as children (see  Figure 8.1  below). According to this view, DID starts from the child’s attempt to cope with an overwhelming sense of hopelessness and powerlessness in the face of repeated traumatic abuse. Lacking other resources or routes of escape, the child may dissociate and escape into a fantasy, becoming someone else. This escape may occur through a process like self-hypnosis (Butler et al.,  1996 ), and if it helps to alleviate some of the pain caused by the abuse it will be reinforced and occur again in the future. This notion is consistent with recent evidence that inducing a dissociative state in research participants can lead to decreased pain sensitivity (Ludascher et al.,  2009 ). Sometimes the child simply imagines the abuse is happening to someone else. If the child is fantasy prone, and continues to stay fantasy prone over time, the child may unknowingly create different selves at different points in time, possibly laying the foundation for multiple dissociated identities.

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Kenneth Bianchi, known as the “Hillside Strangler,” brutally raped and murdered 10 women in the Los Angeles area. Hoping to create a plea of “not guilty by reason of insanity,” Bianchi fabricated a second personality—“Steve”—who “emerged” while Kenneth was under hypnosis. A psychologist and psychiatrist specializing in DID determined he was faking the diagnosis, and Bianchi was subsequently convicted of the murders.

But only a subset of children who undergo traumatic experiences are prone to fantasy or self-hypnosis, which leads to the idea that a diathesis-stress model may be appropriate here. That is, children who are prone to fantasy and those who are easily hypnotizable may have a diathesis for developing DID (or other dissociative disorders) when severe abuse occurs (e.g., Butler et al.,  1996 ; Kihlstrom et al.,  1993 ). However, it should also be emphasized that there is nothing inherently pathological about being prone to fantasy or readily hypnotizable (Kihlstrom et al.,  1994 ).

Increasingly, those who view childhood abuse as playing a critical role in the development of DID are beginning to see DID as perhaps a complex and chronic variant of posttraumatic stress disorder, which by definition is caused by exposure to some kind of highly traumatic event(s), including abuse (e.g., Brown,  1994 ; Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Anxiety symptoms are more prominent in PTSD than in DID, and dissociative symptoms are more prominent in DID than in PTSD. Nevertheless, both kinds of symptoms are present in both disorders (Putnam,  1997 ). Moreover, some (but not all) investigators have estimated that a very high percentage of individuals diagnosed with DID have a comorbid diagnosis of PTSD, suggesting the likelihood of some important common causal factors (Vermetten et al., 2006; see also Rodewald et al.,  2011 ).

At the other extreme from posttraumatic theory is  sociocognitive theory , which claims that DID develops when a highly suggestible person learns to adopt and enact the roles of multiple identities, mostly because clinicians have inadvertently suggested, legitimized, and reinforced them and because these different identities are geared to the individual’s own personal goals (Lilienfeld & Lynn,  2003 ; Lilienfeld et al.,  1999 ; Spanos,  1994  1996 ). It is important to realize that at the present time, the sociocognitive perspective maintains that this is not done intentionally or consciously by the afflicted individual but, rather, occurs spontaneously with little or no awareness (Lilienfeld et al.,  1999 ). The suspicion is that overzealous clinicians, through fascination with the clinical phenomenon of DID and unwise use of such techniques as hypnosis, are themselves largely responsible for eliciting this disorder in highly suggestible, fantasy-prone patients (e.g., Giesbrecht et al.,  2008 ; Piper, Merskey,  2004a  2004b ; Spanos,  1996 ).

Consistent with the sociocognitive hypothesis, Spanos et al. ( 1985 ) demonstrated that normal college students can be induced by suggestion under hypnosis to exhibit some of the phenomena seen in DID, including the adoption of a second identity with a different name that shows a different profile on a personality inventory. Thus people can enact a second identity when situational forces encourage it. Related situational forces that may affect the individual outside the therapist’s office include memories of one’s past behavior (e.g., as a child), observations of other people’s behavior (e.g., others being assertive and independent, or sexy and flirtatious), and media portrayals of DID (Lilienfeld et al.,  1999 ; Piper & Merskey,  2004b ; Spanos,  1994 ).

Sociocognitive theory is also consistent with evidence that most DID patients do not show unambiguous signs of the disorder before they enter therapy and with evidence that the number of alter identities often increases (sometimes dramatically) with time spent in therapy (Piper & Merskey,  2004b ). It is also consistent with the increased prevalence of DID since the 1970s, when the first popular accounts of DID reached the general public, and since 1980, when therapist awareness of the condition increased as well (Lilienfeld et al.,  1999 ; Piper & Merskey,  2004a ).

However, there are also many criticisms of sociocognitive theory. For example, Spanos and colleagues’ demonstration of role-playing in hypnotized college students is interesting, but it does not show that this is the way DID is actually caused in real life. For example, someone might be able to give a convincing portrayal of a person with a broken leg, but this would not establish how legs are usually broken. Moreover, the hypnotized participants in this and other experiments showed only a few of the most obvious symptoms of DID (such as more than one identity) and showed them only under short-lived, contrived laboratory conditions. No studies have shown that other symptoms such as depersonalization, memory lapses for prolonged periods, or auditory hallucinations can occur under similar laboratory conditions. Thus, although some of the symptoms of DID could be created by social enactment, there is no evidence that the disorder can be created this way (e.g., Gleaves,  1996 ).

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Former Georgia football star Herschel Walker has written a book, Breaking Free: My Life with Dissociative Identity Disorder (2008), in which he tells about his struggle with this disorder.

Are Recovered Memories of Abuse in DID Real or False? Case reports of the cruelty and torture that some DID patients suffered as children are gut-wrenching to read or hear. However, the accuracy and trustworthiness of these reports of widespread sexual and other forms of childhood abuse in DID have become a matter of major controversy. Critics (who are often proponents of sociocognitive theory) argue that many of these reports of DID patients, which generally come up in the course of therapy, may be the result of false memories, which are in turn a product of highly leading questions and suggestive techniques applied by well-meaning but inadequately skilled and careless psychotherapists (Lilienfeld et al.,  1999 ; Loftus & Davis,  2006 ; Yapko,  1994 ). It seems quite clear to many investigators that this sort of thing has happened, often with tragic consequences. Innocent family members have been falsely accused by DID patients and have sometimes been convicted and imprisoned. But it is also true that brutal abuse of children occurs far too often and that it can have very adverse effects on development, perhaps encouraging pathological dissociation (e.g., Maldonado & Spiegel,  2007 ; Nash et al.,  1993 ). In such cases, prosecution of the perpetrators of the abuse is indeed appropriate. Of course, the real difficulty here is in determining when the recovered memories of abuse are real and when they are false (or some combination of the two). This bitter controversy about the issue of false memory is more extensively considered in the Unresolved Issues section at the end of this chapter.

One way to document that particular recovered memories are real might be if some reliable physiological test could be developed to distinguish between them. Thus, some researchers are currently trying to determine whether there are different neural correlates of real and false memories that could be used to make this determination reliably. Another somewhat easier way to document whether a particular recovered memory is real would be to have independent verification that the abuse had actually occurred, such as through physician, hospital, and police records. A number of studies have indeed reported that they have confirmed the reported cases of abuse, but critics have shown that the criteria used for corroborating evidence are almost invariably very loose and suspect as to their validity. For example, Chu and colleagues ( 1999 ) simply asked their subjects, “Have you had anyone confirm these events?” (p. 751) but did not specify what constituted confirmation and had no way of determining if subjects were exaggerating or distorting the information they provided as confirming evidence (Loftus & Davis,  2006 ; Piper & Merskey,  2004a ). In another example of a flawed study, Lewis and colleagues ( 1997 ) studied 12 convicted murderers and then confirmed through medical, social service, and prison records that all 12 had been severely abused as children. Unfortunately, this study did not include a control group of otherwise comparable murderers who did not exhibit DID symptoms. Hence we cannot be certain that the childhood abuse of these subjects is not as much (or more) associated with violence or conviction for murder as with the development of DID specifically. Moreover, Lewis and colleagues should have carefully assessed for the possibility that some of the murderers might have been malingering (i.e., faking DID; Lilienfeld et al.,  1999 ). Thus, although this study may have been one of the most impressive attempts yet to document abuse independently in people with DID, it was significantly flawed and therefore highly inconclusive.

If Abuse Has Occurred, Does It Play a Causal Role in DID? Let us put the previous controversy about the reality of recovered memories of abuse aside for a moment and assume that severe abuse has occurred in the early childhood backgrounds of many people with DID. How can we determine whether this abuse has played a critical causal role in the development of DID (e.g., Piper & Merskey,  2004a )? Unfortunately, many difficulties arise in answering this question. For example, child abuse usually happens in family environments plagued by many other sources of adversity and trauma (e.g., various forms of psychopathology and extreme neglect and poverty). One or more of these other, correlated sources of adversity could actually be playing the causal role (e.g., Lilienfeld et al.,  1999 ; Nash et al.,  1993 ). Another difficulty of determining the role of abuse is that people who have experienced child abuse as well as symptoms of DID may be more likely to seek treatment than people with symptoms of DID who did not experience abuse. Thus the individuals in most studies on the prevalence of child abuse in DID may not be representative of the population of all people who suffer from DID. Finally, childhood abuse has been claimed by some to lead to many different forms of psychopathology including depression, PTSD, eating disorders, somatic symptom disorders, and borderline personality disorder, to name just a few. Perhaps the most we will ever be able to say is that childhood abuse may play a nonspecific role for many disorders, with other, more specific factors determining which disorder develops (see  Chapters 10  and  12 ).

Comments on a Few of These Controversies About DID As we have seen, numerous studies indicate that the separate identities harbored by DID patients are somewhat physiologically and cognitively distinct. For example, EEG activity of various alters may be quite different. Because such differences cannot in any obvious way be simulated (e.g., Eich et al.,  1997 ), it seems that DID must, in at least some cases, involve more than simply the social enactment of roles. Moreover, this should not be too surprising, given the widespread evidence of separate (dissociated) memory subsystems and nonconscious active mental processing, which indicates that much highly organized mental activity is normally carried on in all of us in the background, outside of awareness (e.g., Kihlstrom,  2005 ). Moreover, some people seem to be especially prone to pathological variants of these dissociative processes (Waller et al.,  1996 ; Waller & Ross,  1997 ).

We should also note that each of these controversies has usually been stated in a dichotomous way: Is DID real or faked? What causes DID—spontaneous social enactment of roles or repeated childhood trauma? Are recovered memories of abuse real or false? If abuse occurs, does it play a primary causal role? Unfortunately, however, such dichotomously stated questions encourage oversimplified answers. The human mind does not seem to operate in these dichotomous ways, and we need to address the complex and multifaceted nature of the dissociated mental processes that these often miserable and severely stressed patients are experiencing. Fortunately, theorists on both sides have begun to soften their positions a little, acknowledging that multiple different causal pathways are likely to be involved. For example, Ross ( 1997  1999 ), a long-time advocate for a strong version of posttraumatic theory, later acknowledged that some cases are faked and that some may be inadvertently caused by unskilled therapists in the course of treatment. In addition, other advocates of posttraumatic theory have recently acknowledged that both real and false memories do occur in these patients, noting that it is critical that a method for determining which is which be developed (e.g., Gleaves & Williams,  2005 ; Gleaves et al.,  2004 ). From the other side, Lilienfeld et al.,  1999 , who have been vocal advocates for Spanos’ sociocognitive theory since his death in  1994 , have acknowledged that some people with DID may have undergone real abuse, although they believe it occurs far less often, and is less likely to play a real causal role, than the trauma theorists maintain (see also Kihlstrom,  2005 ).

Sociocultural Factors in Dissociative Disorders

There seems little doubt that the prevalence of dissociative disorders, especially their more dramatic forms such as DID, is influenced by the degree to which such phenomena are accepted or tolerated either as normal or as legitimate mental disorders by the surrounding cultural context. Indeed, in our own society, the acceptance and tolerance of DID as a legitimate disorder have varied tremendously over time. Compared to relatively high reported rates of DID in Western cultures, a recent study of 893 patients diagnosed with some type of dissociative disorder over 10 years at a psychiatric hospital in India found no cases of DID (Chaturvedi et al.,  2010 ). Nevertheless, although its prevalence varies, DID has now been identified in all racial groups, socioeconomic classes, and cultures where it has been studied. For example, outside North America it has been found in countries ranging from Nigeria and Ethiopia to Turkey, India, China, Australia, and the Caribbean, to name a few (Maldonado et al.,  2002 ; Xiao et al.,  2006 ).

Many seemingly related phenomena, such as spirit possession and dissociative trances, occur very frequently in many different parts of the world where the local culture sanctions them (Krippner,  1994 ; Spiegel et al., 2011). When entered into voluntarily, trance and possession states are not considered pathological and should not be construed as mental disorders. But some people who enter into these states voluntarily because of cultural norms develop distress and impairment. In DSM-5, the diagnostic criteria for DID have been modified to that they now include certain phenomena associated with possession. A trance is said to occur when someone experiences a temporary marked alteration in state of consciousness or identity (but with no replacement by an alternative identity). It is usually associated with either a narrowing of awareness of the immediate surroundings, or stereotyped behaviors or movements that are experienced as beyond one’s control. A possession trance is similar except that the alteration of consciousness or identity is replaced by a new identity that is attributed to the influence of a spirit, deity, or other power. In both cases there is typically amnesia for the trance state. One study of 58 individuals from Singapore with this diagnosis, as well as 58 individuals with a diagnosis of major depression, found that conflicts over religious or cultural issues, prior exposure to trance states, and being a spiritual healer or healer’s helper were most predictive of who had dissociative trance disorder relative to major depression (Ng & Chan,  2004 ). A recent review of 402 cases of dissociative trance and possession disorders indicates that migration and struggles with acculturation are associated with these disorders (During et al.,  2011 ).

There are also cross-cultural variants on dissociative disorders, such as Amok, which is often thought of as a rage disorder. Amok occurs when a dissociative episode leads to violent, aggressive, or homicidal behavior directed at other people and objects. It occurs mostly in men and is often precipitated by a perceived slight or insult. The person often has ideas of persecution, anger, and amnesia, often followed by a period of exhaustion and depression. Amok is found in places such as Malaysia, Laos, the Philippines, Papua New Guinea, and Puerto Rico and among Navajo Indians.

Treatment and Outcomes in Dissociative Disorders

Unfortunately, virtually no systematic, controlled research has been conducted on treatment of depersonalization disorder, dissociative amnesia, and dissociative fugue, and so very little is known about how to treat them successfully. Numerous case histories, sometimes presented in small sets of cases, are available, but without control groups who are assessed at the same time or who receive nonspecific treatments it is impossible to know the effectiveness of the varied treatments that have been attempted (Kihlstrom,  2005 ).

As noted earlier depersonalization/derealization disorder is generally thought to be resistant to treatment (e.g., Simeon et al.,  1997 ), although treatment may be useful for associated psycho-pathology such as anxiety and depressive disorders. Some think that hypnosis, including training in self-hypnosis techniques, may be useful because patients with depersonalization disorder can learn to dissociate and then “reassociate,” thereby gaining some sense of control over their depersonalization and derealization experiences (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Many types of antidepressant, antianxiety, and antipsychotic drugs have also been tried and sometimes have modest effects. However, one randomized controlled study showed no difference between treatment with Prozac versus with placebo (Simeon et al.,  2004 ). One recent treatment showing some promise for the treatment of dissociative disorders involves administering rTMS (repetitive transcranial magnetic stimulation) to the temporo-parietal junction, an area of the brain highly involved in the experience of a unified self and body (Mantovani et al.,  2011 ). After three weeks of treatment, half of the subjects showed significant reductions in depersonalization, with nonresponders showing symptom reduction after an additional three weeks of treatment. In dissociative amnesia and fugue, it is important for the person to be in a safe environment, and simply removing her or him from what he or she perceives as a threatening situation sometimes allows for spontaneous recovery of memory. Hypnosis, as well as drugs such as benzodiazepines, barbiturates, sodium pentobarbital, and sodium amobarbital, is often used to facilitate recall of repressed and dissociated memories (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). After memories are recalled, it is important for the patient to work through the memories with the therapist so that the experiences can be reframed in new ways. However, unless the memories can be independently corroborated, they should not be taken at their face value (Kihlstrom,  2005 ).

For DID patients, most current therapeutic approaches are based on the assumption of posttraumatic theory that the disorder was caused by abuse (Kihlstrom,  2005 ). Most therapists set integration of the previously separate alters, together with their collective merging into the host personality, as the ultimate goal of treatment (e.g., Maldonado & Spiegel,  2007 ). There is often considerable resistance to this process by the DID patients, who often consider dissociation as a protective device (e.g., “I knew my father could get some of me, but he couldn’t get all of me”; Maldonado & Spiegel,  2007 , p. 781). If successful integration occurs, the patient eventually develops a unified personality, although it is not uncommon for only partial integration to be achieved. But it is also very important to assess whether improvement in other symptoms of DID and associated disorders has occurred. Indeed, it seems that treatment is more likely to produce symptom improvement, as well as associated improvements in functioning, than to achieve full and stable integration of the different alter identities (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ).

Typically the treatment for DID is psychodynamic and insight-oriented, focused on uncovering and working through the trauma and other conflicts that are thought to have led to the disorder (Kihlstrom,  2005 ). One of the primary techniques used in most treatments of DID is hypnosis (e.g., Kluft,  1993 ; Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ). Most DID patients are hypnotizable and when hypnotized are often able to recover past unconscious and frequently traumatic memories, often from childhood. Then these memories can be processed, and the patient can become aware that the dangers once present are no longer there. (One problem here is that such patients are suggestible under hypnosis, so much of what is recalled may not be accurate; see Kihlstrom,  2005 ; Loftus & Davis,  2006 ). Through the use of hypnosis, therapists are often able to make contact with different identities and reestablish connections between distinct, seemingly separate identity states. An important goal is to integrate the personalities into one identity that is better able to cope with current stressors. Clearly, successful negotiation of this critical phase of treatment requires therapeutic skills of the highest order; that is, the therapist must be strongly committed as well as professionally competent. Regrettably, not all therapists are.

Most reports in the literature are treatment summaries of single cases, and reports of successful cases should always be considered with caution, especially given the large bias in favor of publishing positive rather than negative results. Treatment outcome data for large groups of DID patients have been reported in only four studies we are aware of, and none of these included a control group, although it is clear that DID does not spontaneously remit simply with the passage of time, nor if a therapist chooses to ignore DID-related issues (Kluft,  1999 ; Maldonado et al.,  2002 ). For example, Ellason and Ross ( 1997 ) reported on a 2-year postdischarge follow-up of DID patients originally treated in a specialized inpatient unit. Of the original 135 such patients, 54 were located and systematically assessed. All these patients, and especially those who had achieved full integration, generally showed marked improvements in various aspects of their lives. However, only 12 of the 54 had achieved full integration of their identities. Such results are promising, but we must wonder about the clinical status of the 81 “lost” patients who may likely have done less well. Another 10-year follow-up study reported similar results in a smaller sample of 25 treated DID patients. Only 12 were located 10 years later; of these, six had achieved full integration, but two of those had partially relapsed (Coons & Bowman,  2001 ). In general it has been found that (1) for treatment to be successful, it must be prolonged, often lasting many years, and (2) the more severe the case, the longer that treatment is needed (Maldonado & Spiegel,  2007 ; Maldonado et al.,  2002 ).

in review

·  ● Describe the symptoms known as depersonalization and derealization, and indicate which disorder is primarily characterized by their appearance.

·  ● Describe dissociative amnesia and dissociative fugue, and indicate what aspects of memory are affected.

·  ● What are the primary symptoms of dissociative identity disorder (DID), and why is its prevalence thought to have increased?

·  ● Review the four major controversies surrounding DID that were discussed in this chapter.

UNRESOLVED issues: DID and the Reality of “Recovered Memories”

As we have seen in this chapter, many controversies surround the nature and origins of DID. None have been more bitter than those related to the truth value of “recovered” memories of childhood abuse, particularly sexual abuse, which posttraumatic theorists assert is the major causal factor in the development of DID. Indeed, a virtual chasm has developed between the “believers” (mostly but not exclusively private practitioners who treat people with DID) and the “dis-believers” (mostly but not exclusively the more academic and science-oriented mental health professionals). The disbelievers are very sympathetic to people suffering DID symptoms, but they have tended to doubt that the disorder is usually caused by childhood abuse and have challenged the validity or accuracy of recovered memories of abuse (see Loftus & Davis,  2006 , for a review of the recovered memory debate).

For 20 years, these controversies have moved beyond professional debate and have become major public issues, leading to countless legal proceedings. DID patients who recover memories of abuse (often in therapy) have often sued their parents for having inflicted abuse. But ironically, therapists and institutions have also been sued for implanting memories of abuse that they later came to believe had not actually occurred. Some parents, asserting they had been falsely accused, formed an international support organization—the False Memory Syndrome Foundation—and have sometimes sued therapists for damages, alleging that the therapists induced false memories of parental abuse in their child. Many families have been torn apart in the fallout from this remarkable climate of suspicion, accusation, litigation, and unrelenting hostility.

Whether DID originates in childhood abuse and whether recovered memories of abuse are accurate are basically separate issues, but they have tended to become fused in the course of the debate. Hence those who doubt the validity of memories of abuse are also likely to regard the phenomenon of DID as stemming from the social enactment of roles encouraged or induced—like the memories of abuse themselves—by misguided therapy (e.g., see Bjorklund,  2000 ; Lilienfeld et al.,  1999 ; Lynn et al.,  2004 ; Piper & Merskey,  2004a  2004b ). Believers, on the other hand, have usually taken both DID and the idea that abuse is its cause to be established beyond doubt (e.g., see Gleaves,  1996 ; Gleaves et al.,  2001 ; Ross,  1997  1999 ).

Much of the controversy about the validity of recovered memories is rooted in disagreements about the nature, reliability, and malleability of human autobiographical memory. With some exceptions, evidence for childhood abuse as a cause of DID is restricted to the “recovered memories” (memories not originally accessible) of adults being treated for dissociative experiences. Believers argue that before treatment such memories had been “repressed” because of their traumatic nature or had been available only to certain alter identities that the host identity was generally not aware of. Treatment, according to this view of believers, dismantles the repressive defense and thus makes available to awareness an essentially accurate memory recording of the past abuse.

Disbelievers counter with several scientifically well-supported arguments. For example, scientific evidence in support of the repression concept is quite weak (e.g., Kihlstrom,  2005 ; Loftus & Davis,  2006 ; Piper,  1998 ). In many alleged cases of repression, the event may have been lost to memory in the course of ordinary forgetting rather than repression, or it may have occurred in the first 3 to 4 years of life, before memories can be recorded for retrieval in adulthood. In many other cases, evidence for repression has been claimed in studies where people may simply have failed to report a previously remembered event, often because they were never asked or were reluctant to disclose such very personal information (Kihlstrom,  2005 ; Loftus & Davis,  2006 ; Pope et al.,  1998 ).

Even if memories can be repressed, there are very serious questions about the accuracy of recovered memories. Human memory of past events does not operate in a computer-like manner, retrieving with perfect accuracy an unadulterated record of information previously stored and then repressed. Rather, human memory is malleable, constructive, and very much subject to modification on the basis of events happening after any original memory trace is established (Loftus & Bernstein,  2005 ; Loftus & Davis,  2006 ; Schacter et al.,  2000 ).

Indeed, there is now good evidence that in certain circumstances, people are sometimes very prone to the development of false memories (see Wade et al.,  2007 , for a review). For example, a number of studies have now shown that when normal adult subjects are asked to imagine repeatedly events that they are quite sure had not happened to them before age 10, they later increase their estimate of the likelihood that these events actually had happened to them (Tsai et al.,  2000 ). Moreover, even in a relatively short time frame, adult subjects sometimes come to believe they have performed somewhat bizarre acts (e.g., kissing a magnifying glass), as well as common acts (e.g., flipping a coin), after simply having imagined they had engaged in these acts several times 2 weeks earlier (Thomas & Loftus,  2002 ). These and other studies clearly show that repeated imagining of certain events (even somewhat bizarre events) can lead people to have false memories of events that never happened (Loftus & Bernstein,  2005 ; Loftus & Davis,  2006 ). In addition, an experimental study by McNally and colleagues ( 2005 ) looked at individuals who reported either repressed or recovered memories of childhood sexual abuse and found some evidence that they had greater difficulty on at least some measures than normal controls in distinguishing between words that they had seen versus words that they had only imagined. This suggests that people with repressed or recovered memories of abuse may have greater difficulty distinguishing between what has actually happened to them and what they have imagined happened to them. However, a different study found that those who report recovered memories of childhood sexual abuse did not show increased difficulty retrieving non-abuse-related autobiographic memories compared to those who reported continuous memories of childhood sexual abuse or a control group reporting no childhood sexual abuse (Raymaekers et al.,  2010 ).

One fascinating study compared a group of people who had continuous memories of childhood abuse with two groups who had recovered memories of abuse. In one of the latter groups the memories had been recovered during therapy and in the other the memories had been recovered out of therapy. The researchers then attempted to corroborate these recovered memories, and found corroborative evidence for over half of those who had recovered memories outside of therapy and for none in the group who recovered their memories during therapy (Geraerts et al.,  2007 ).

Recently, McNally and Geraerts ( 2009 ) offered a different perspective on recovered memories, one that attempts to bridge the gap between the conviction that repression underlies recovered memories and the alternate conviction that all recovered memories are false. Their third perspective suggests that some recovered memories are genuine but were never actually repressed. Instead, some abuse victims may simply not have thought about their abuse for a long period of time, have been deliberately attempting to forget the abuse (suppression rather than repression), or may have forgotten prior instances when they did recall the abuse, resulting in the false impression that a recently surfaced memory had been repressed for years.

8 summary

·  8.1 What are somatic symptom disorders?

·  • Somatic symptom disorders lie at the interface of abnormal psychology and medicine. These are disorders in which psychological problems are manifested in physical symptoms. In response to the symptoms the person also experiences abnormal thoughts, feelings, and behaviors.

·  • Somatic symptom disorder occurs in individuals who have had multiple somatic complaints lasting at least 6 months. Even if the symptoms do not seem to have a medical explanation, the person’s suffering is regarded as authentic.

·  8.2 What is illness anxiety disorder?

·  • Illness anxiety occurs in individuals who are very anxious about having an illness even though there are no apparent symptoms.

·  8.3 What is conversion disorder (functional neurological symptom disorder)?

·  • Conversion disorder involves patterns of symptoms or deficits affecting sensory or voluntary motor functions leading one to think there is a medical or neurological condition, even though medical examination reveals no physical basis for the symptoms.

·  8.4 What is the difference between a factitious disorder and malingering?

·  • Individuals with factitious disorder intentionally produce medical or psychological symptoms (or both). They do this in the absence of external rewards in order to take on an illness role.

·  • Malingering involves the intentional production of symptoms or the exaggeration of symptoms. This is motivated by external factors such as a wish to claim insurance money, avoid work or military service, or to get leniency in a criminal prosecution.

·  8.5 What are the primary features of dissociative disorders?

·  • Dissociative disorders occur when the processes that normally regulate awareness and the multichannel capacities of the mind apparently become disorganized, leading to various anomalies of consciousness and personal identity.

·  8.6 What is depersonalization/derealization disorder?

·  • Depersonalization/derealization disorder occurs in people who experience persistent and recurrent episodes of derealization (losing one’s sense of reality of the outside world) and/or depersonalization (losing one’s sense of oneself and one’s own reality).

·  8.7 What is dissociative amnesia?

·  • Dissociative amnesia involves an inability to recall previously stored information that cannot be accounted for by ordinary forgetting and seems to be a common initial reaction to highly stressful circumstances. The memory loss is primarily for episodic or autobiographical memory.

·  8.8 What is dissociative identity disorder?

·  • In dissociative identity disorder, the person manifests at least two or more distinct identities that alternate in some way in taking control of behavior. Alter identities may differ in many ways from the host identity.

key terms

·  alter identities  281

·  conversion disorder  270

·  depersonalization  276

·  depersonalization/derealization disorder  276

·  derealization  276

·  dissociation  276

·  dissociative amnesia  278

·  dissociative disorders  276

·  dissociative fugue  278

·  dissociative identity disorder (DiD)  280

·  factitious disorder  264

·  factitious disorder imposed on another  275

·  host identity  281

·  hypochondriasis  265

·  hysteria  271

·  implicit memory  276

·  implicit perception  276

·  malingering  264

·  pain disorder  269

·  posttraumatic theory (of DID)  285

·  primary gain  271

·  secondary gain  271

·  sociocognitive theory (of DID)  286

·  soma  264

·  somatic symptom disorders  264

·  somatization disorder  268

·  somatoform disorders  264

13 schizophrenia and other psychotic disorders

image1

learning objectives 13

·  13.1 What are the symptoms of schizophrenia?

·  13.2 What is the prevalence of schizophrenia and when does it begin? Who is most affected?

·  13.3 What are the risk and causal factors associated with schizophrenia?

·  13.4 How is the brain affected in schizophrenia?

·  13.5 What neurotransmitters are implicated in schizophrenia?

·  13.6 Why is the family environment important for the well-being of patients with schizophrenia?

·  13.7 What is the clinical outcome of schizophrenia and how is it treated?

Emilio: “Eating Wires and Lighting Fires” Emilio is a 40-year-old man who looks 10 years younger. He is brought to the hospital, his 12th hospitalization, by his mother because she is afraid of him. He is dressed in a ragged overcoat, bedroom slippers, and a baseball cap, and he wears several medals around his neck. His affect ranges from anger at his mother (“She feeds me shit … what comes out of other people’s rectums”) to a giggling, obsequious seductiveness toward the interviewer. His speech and manner have a childlike quality, and he walks with a mincing step and exaggerated hip movements. His mother reports that he stopped taking his medication about a month ago and has since begun to hear voices and to look and act more bizarrely. When asked what he has been doing, he says “eating wires and lighting fires.” His spontaneous speech is often incoherent and marked by frequent rhyming and clang associations (where sounds, rather than meaningful relationships, govern word choice).

Emilio’s first hospitalization occurred after he dropped out of school at age 16, and since that time he has never been able to attend school or hold a job. He has been treated with neuroleptics (medications used to treat schizophrenia) during his hospitalizations, but he doesn’t continue to take his medications when he leaves, so he quickly becomes disorganized again. He lives with his elderly mother, but he sometimes disappears for several months at a time and is eventually picked up by the police as he wanders the streets. (Modified from Spitzer et al.,  2002 , pp. 189–90.)

The disorder that Emilo has is called schizophrenia. Schizophrenia is a severe disorder that is often associated with considerable impairments in functioning. This chapter describes the pieces of the schizophrenia puzzle as we currently know them. Keep in mind from the outset that not all of the pieces or their presumed interconnections have been found, so our puzzle is far from being solved. As you read through this chapter you will learn just how complex and challenging this disorder is—not only for patients who suffer from it and for their families who try to care for them, but also for the clinicians who attempt to treat it and the researchers who are determined to understand it.

Schizophrenia

Schizophrenia  occurs in people from all cultures and from all walks of life. The disorder is characterized by an array of diverse symptoms, including extreme oddities in perception, thinking, action, sense of self, and manner of relating to others. However, the hallmark of schizophrenia is a significant loss of contact with reality, referred to as  psychosis . Although the clinical presentation of schizophrenia differs from one patient to another, the case of Emilio is quite typical.

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The internal suffering of the person with schizophrenia is often readily apparent, as are bizarre behavior and unusual appearance.

Origins of the Schizophrenia Construct

The first detailed clinical description of what we now recognize to be schizophrenia was offered in 1810 by John Haslam, the apothecary at the Bethlem Hospital in London, England. Haslam described the case of a patient who appears to have suffered from a variety of symptoms—including delusions—that are typical of schizophrenia (see Carpenter,  1989 ). Fifty years later, the Belgian psychiatrist Benedict Morel described the case of a 13-year-old boy who had formerly been the most brilliant pupil in his school but who gradually lost interest in his studies; became increasingly withdrawn, lethargic, seclusive, and quiet; and appeared to have forgotten everything he had learned. Morel thought the boy’s intellectual, moral, and physical functions had deteriorated as a result of brain degeneration of hereditary origin. He used the term démence précoce (mental deterioration at an early age) to describe the condition and to distinguish it from the dementing disorders associated with old age.

It is the German psychiatrist Emil Kraepelin (1856–1926) who is best known for his careful description of what we now regard as schizophrenia. Kraepelin used the Latin version of Morel’s term (dementia praecox) to refer to a group of conditions that all seemed to feature mental deterioration beginning early in life. Kraepelin, an astute observer of clinical phenomena, described the patient with dementia praecox as someone who “becomes suspicious of those around him, sees poison in his food, is pursued by the police, feels his body is being influenced, or thinks that he is going to be shot or that the neighbours are jeering at him” (Kraepelin,  1896 ). Kraepelin also noted that the disorder was characterized by hallucinations, apathy and indifference, withdrawn behavior, and an incapacity for regular work.

It was a Swiss psychiatrist named Eugen Bleuler (1857–1939) who gave us the diagnostic term we still use today. In 1911, Bleuler used schizophrenia (from the Greek roots of sxizo, pronounced “schizo” and meaning “to split or crack,” and phren, meaning “mind”) because he believed the condition was characterized primarily by disorganization of thought processes, a lack of coherence between thought and emotion, and an inward orientation away (split off) from reality. Although the term is often thought to reflect a “Jekyll and Hyde” split personality, this is a major misconception. The splitting does not refer to multiple personalities (an entirely different form of disorder, now called dissociative identity disorder). Instead, in schizophrenia there is a split within the intellect, between the intellect and emotion, and between the intellect and external reality. Interestingly, the subtitle of Bleuler’s monograph (Bleuler, 1911/1950) was “The Group of Schizophrenias,” indicating that he believed this disorder was not a single diagnostic entity.

Epidemiology

The risk of developing schizophrenia over the course of one’s lifetime is a little under 1 percent—actually around 0.7 percent (Saha et al.,  2005 ). What this means is that approximately 1 out of every 140 people alive today who survive until at least age 55 will develop the disorder. Of course, a statistic like this does not mean that everyone has exactly the same risk. This is an average lifetime risk estimate. As we shall see later, some people (e.g., those who have a parent with schizophrenia) have a statistically higher risk of developing the disorder than do others (e.g., people who come from families where there has never been a case of schizophrenia).

There are also other groups of people who seem to have an especially high risk of developing schizophrenia. For example, people whose fathers were older (aged 45 to 50 years or more) at the time of their birth have two to three times the normal risk of developing schizophrenia when they grow up (Byrne et al.,  2003 ; Malaspina et al.,  2001 ). Having a parent who works as a dry cleaner is also a risk factor (Perrin, Opler et al.,  2007 ). Moreover, people of Afro-Caribbean origin living in the United Kingdom have higher-than-expected rates of schizophrenia (Harrison et al.,  1997 ). Although the reasons for these differences are not well understood, they are of great interest to researchers.

The vast majority of cases of schizophrenia begin in late adolescence and early adulthood, with 18 to 30 years of age being the peak time for the onset of the illness (Tandon et al.,  2009 ). Although schizophrenia is sometimes found in children, such cases are rare (Green et al.,  1992 ; McKenna et al.,  1994 ). Schizophrenia can also have its initial onset in middle age or later, but again, this is not typical.

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Children whose fathers are older at the time of their birth have two to three times the normal risk of developing schizophrenia.

The characteristic age of onset of schizophrenia differs in men and women. In men, there is a peak in new cases of schizophrenia between ages 20 and 24. The incidence of schizophrenia in women peaks during the same age period, but the peak is less marked than it is for men (see  Figure 13.1 ). After about age 35, the number of men developing schizophrenia falls markedly, whereas the number of women developing schizophrenia does not. Instead, there is a second rise in new cases that begins around age 40, as well as a third spike in onset that occurs when women are in their early sixties (Abel et al.,  2010 ).

In addition to being more likely to have an early age of onset, males also tend to have a more severe form of schizophrenia (Leung & Chue,  2000 ). Brain-imaging studies show that schizophrenia-related anomalies of brain structure (discussed later) are more severe in male patients than they are in female patients (Nopoulos et al.,  1997 ). Gender-related differences in illness severity may also explain why schizophrenia is more common in males than it is in females. The male-to-female sex ratio is 1.4:1. So for every three men who develop the disorder, only two women do so (Aleman et al.,  2003 ; Kirkbridge et al.,  2006 ). If women have a less severe form of schizophrenia, and if they also have more symptoms of depression (see Leung & Chue,  2000 ), they may either not be diagnosed at all or else be diagnosed with other disorders, thus giving rise to the sex ratio imbalance.

What might explain the better clinical outcome of women with schizophrenia? One possibility is that female sex hormones play some protective role. When estrogen levels are low (as is true premenstrually) or are falling, psychotic symptoms in women with schizophrenia often get worse (Bergemann et al.,  2007 ). The protective effect of estrogen may therefore help explain both the delayed onset of schizophrenia and the more favorable clinical course of the disorder in females. Declining levels of estrogen around menopause might also explain why late-onset schizophrenia is much more likely to strike women than men. There is some evidence that this late-onset pattern in women is associated with a more severe clinical presentation (Haffner et al.,  1998 ).

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FIGURE 13.1 Onset of Schizophrenia. Age distribution of onset of schizophrenia (first sign of mental disorder) for men and women.

Source: From Haffner, H., et al. ( 1998 ). Causes and consequences of the gender difference in age at onset of schizophrenia. Schizophrenia Bulletin24(1), 99–114.

in review

·  • What did Kraepelin mean by the term dementia praecox? How accurate is this description?

·  • What was Bleuler’s use of the term schizophrenia meant to convey?

·  • Is schizophrenia the same thing as split personality?

·  • What is the prevalence of schizophrenia? What groups of people show lower or higher rates of schizophrenia than expected?

·  • How does the age of onset of schizophrenia vary by gender?

·  • How does gender influence the severity of schizophrenia? Why might this be?

Clinical Picture

As we have mentioned earlier, the DSM is a work in progress. Diagnostic criteria are not fixed and immutable but instead change subtly over time as new research findings become available. We show the current DSM-5 criteria for the diagnosis of schizophrenia in the DSM-5 table on page 447. These are broadly similar to those used in DSM-IV and to the diagnostic criteria in the ICD (WHO, 2003), which is the diagnostic system used in Europe and other parts of the world. One change that has occurred in DSM-5 is the elimination of the requirement that only one other symptom is necessary if delusions are bizarre or if the auditory hallucinations are of a certain type.

In isolation, however, lists of symptoms convey little about the clinical essence of schizophrenia. In the sections that follow, we elaborate on the hallmark symptoms of this major form of psychotic disorder.

Delusions

 delusion  is essentially an erroneous belief that is fixed and firmly held despite clear contradictory evidence. The word delusion comes from the Latin verb ludere, which means “to play.” In essence, tricks are played on the mind. People with delusions believe things that others who share their social, religious, and cultural backgrounds do not believe. A delusion therefore involves a disturbance in the content of thought. Not all people who have delusions suffer from schizophrenia. However, delusions are common in schizophrenia, occurring in more than 90 percent of patients at some time during their illness (Cutting,  1995 ). In schizophrenia, certain types of delusions or false beliefs are quite characteristic. Prominent among these are beliefs that one’s thoughts, feelings, or actions are being controlled by external agents (made feelings or impulses), that one’s private thoughts are being broadcast indiscriminately to others (thought broadcasting), that thoughts are being inserted into one’s brain by some external agency (thought insertion), or that some external agency has robbed one of one’s thoughts (thought withdrawal). Also common are delusions of reference, where some neutral environmental event (such as a television program or a song on the radio) is believed to have special and personal meaning intended only for the person. Other strange propositions, including delusions of bodily changes (e.g., bowels do not work) or removal of organs, are also not uncommon.

DSM-5 criteria for: Schizophrenia

·  A. Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these must be (1), (2), or (3):

·  1. Delusions.

·  2. Hallucinations.

·  3. Disorganized speech (e.g., frequent derailment or incoherence).

·  4. Grossly disorganized or catatonic behavior.

·  5. Negative symptoms (i.e., diminished emotional expression or avolition).

·  B. For a significant portion of the time since the onset of the disturbance, level of functioning in one or more major areas, such as work, interpersonal relations, or self-care, is markedly below the level achieved prior to the onset (or when the onset is in childhood or adolescence, there is failure to achieve expected level of interpersonal, academic, or occupational functioning).

·  C. Continuous signs of the disturbance persist for at least 6 months. This 6-month period must include at least 1 month of symptoms (or less if successfully treated) that meet Criterion A (i.e., active-phase symptoms) and may include periods of prodromal or residual symptoms. During these prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or by two or more symptoms listed in Criterion A present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences).

·  D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either 1) no major depressive or manic episodes have occurred concurrently with the active-phase symptoms, or 2) if mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness.

·  E. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.

·  F. If there is a history of autism spectrum disorder or a communication disorder of childhood onset, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations, in addition to the other required symptoms of schizophrenia, are also present for at least 1 month (or less if successfully treated).

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

Sometimes delusions are not just isolated beliefs. Instead they become elaborated into a complex delusional system. The next case study provides an example of this. This material was printed on a flier and handed to one of the authors by a man who appeared to be in his 30s. Any errors of grammar are errors in the original flier.

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The inner world of people with schizophrenia is often confused, punctuated by alien voices, paranoia, and illogical thoughts.

Are You Being Mind Controlled? Are you being or were you mind controlled to do something very stupid? Twenty-five percent of our population have what is called electronic hearing. This 25 percent can hear a silent radio and do not hear it. You might be one. In hearing pitch the average person hears from zero to sixteen thousand cycles. Twenty-five percent can hear up to thirty thousand cycles. The silent radio can be heard by these high hearing frequency persons. The silent radio sounds the same as thoughts in their minds.

This silent radio tricks these persons into every crime imaginable. It tricks them into bad decisions, to quit jobs, to divorce, to run away, to be sheriff saled and any stupidity possible. The broadcasters over this silent radio are government, medical, psychiatrists, religious and educational. This is an enormous budget used to destroy the innocent and helpless. The media is scared to cover this up.

This minority, which can be in any ethnic or race, has lost all rights under law because the Russians do it everywhere. It is shocking to discover very large corporations and all colleges have mind control departments. If you and your family constantly make bad decisions and have ruinous problems, you probably are mind controlled. Every year these mind controlled people are going down the economic ladder as they cannot be trusted. No company knows when one will be selected as a guinea pig. Who could risk a sizeable work force of persons with electronic hearing for your competitor could easily wipe you out?

Hallucinations

 hallucination  is a sensory experience that seems real to the person having it, but occurs in the absence of any external perceptual stimulus. This is quite different from an illusion, which is a misperception of a stimulus that actually exists. The word comes from the Latin verb hallucinere or allucinere, meaning to “wander in mind” or “idle talk.” Hallucinations can occur in any sensory modality (auditory, visual, olfactory, tactile, or gustatory). However, auditory hallucinations (e.g., hearing voices) are by far the most common. In a sample recruited from 7 different countries, auditory hallucinations were found in 75 percent of patients with schizophrenia (Bauer et al.,  2011 ). In contrast, visual hallucinations were reported less frequently (39 percent of patients), and olfactory, tactile, and gustatory hallucinations were even more rare (1–7 percent). Even deaf people who are diagnosed with schizophrenia sometimes report auditory hallucinations (Aleman & Larøi,  2008 ). As “The World Around Us” box on the next page illustrates, hallucinations can even be induced in healthy people if they are under a lot of stress and drink a lot of caffeine. image6 Watch the Video Larry: Schizophrenia on MyPsychLab.

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Hallucinations often have relevance for the patient at some affective, conceptual, or behavioral level. Patients can become emotionally involved in their hallucinations, often incorporating them into their delusions. In some cases, patients may even act on their hallucinations and do what the voices tell them to do. People who consider themselves to be socially inferior tend to perceive the voices they hear as being more powerful than they are and to behave accordingly (Paulik,  2011 ).

In an interesting study of the phenomenology of auditory hallucinations, Nayani and David ( 1996 ) interviewed 100 hallucinating patients and asked them a series of questions about their hallucinatory voices. The majority of patients (73 percent) reported that their voices usually spoke at a normal conversational volume. Hallucinated voices were often those of people known to the patient in real life, although sometimes unfamiliar voices or the voices of God or the Devil were heard. Most patients reported that they heard more than one voice and that their hallucinations were worse when they were alone. Most commonly, the hallucinated voices uttered rude and vulgar expletives or else were critical (“You are stupid”), bossy (“Get the milk”), or abusive (“Ugly bitch”), although some voices were pleasant and supportive (“My darling”).

Are patients who are hallucinating really hearing voices? Neuroimaging studies of hallucinating patients are providing answers to this interesting question. Several research groups have used PET and fMRI to look at activity in the brains of patients when they are actually experiencing auditory hallucinations (Cleghorn et al.,  1992 ; McGuire et al.,  1996 ). Although it might be expected that patients hearing voices would show an increase of activity in areas of the brain involved in speech comprehension (e.g., Wernicke’s area in the temporal lobe), imaging studies reveal that hallucinating patients show increased activity in Broca’s area—an area of the temporal lobe that is involved in speech production. In some cases, the pattern of brain activation that occurs when patients experience auditory hallucinations is very similar to that seen when healthy volunteers are asked to imagine that there is another person talking to them (Shergill et al.,  2000 ). Overall, the research findings suggest that auditory hallucinations occur when patients misinterpret their own self-generated and verbally mediated thoughts (inner speech or self-talk) as coming from another source. Indeed, if transcranial magnetic stimulation (in which a magnetic field passing through the skull temporarily disrupts activity in underlying brain areas) is used to reduce activity in speech production areas, hallucinating patients actually show a reduction in their auditory hallucinations (Hoffman et al.,  2005 )! Modern research approaches are thus supporting a very old idea: Auditory hallucinations are really a form of misperceived subvocal speech (Gould,  1949 ).

Disorganized Speech and Behavior

Delusions reflect a disorder of thought content. Disorganized speech, on the other hand, is the external manifestation of a disorder in thought form. Basically, an affected person fails to make sense, despite seeming to conform to the semantic and syntactic rules governing verbal communication. The failure is not attributable to low intelligence, poor education, or cultural deprivation. Years ago, Meehl ( 1962 ) aptly referred to the process as one of “cognitive slippage”; others have referred to it as “derailment” or “loosening” of associations or, in its most extreme form, as “incoherence.”

the WORLD around us: Stress, Caffeine, and Hallucinations

Do you feel that you are under a lot of stress? Do you drink a lot of caffeinated beverages each day? If so, you may be interested in the findings from a recent study that was conducted using healthy volunteers who had no history of psychiatric disorders (Crowe et al.,  2011 ). Ninety-two participants were recruited into what they believed was a study of auditory perception. As participants entered the testing room to begin the experiment, the song “White Christmas” by Bing Crosby was playing. After the song ended, participants were given headphones and asked to listen to white noise. They were told that the White Christmas song they had just heard might be embedded in the white noise at a subthreshold level. Every time they thought they heard a fragment of the song during the 3 minutes of white noise, participants were told to note this using a hand counter.

In reality, no sound fragments of White Christmas were embedded in the sound at all. Participants only heard white noise. However, those participants who reported that they had been under a high level of stress in the past year and who were high caffeine users (five or more drinks per day) reported hearing significantly more embedded song fragments than participants in the low-stress and low-caffeine group did. Moreover, it was the combination of high stress and high caffeine intake that was important. In participants who reported high stress but low caffeine intake or in participants who reported low stress but high caffeine intake, the number of false alarms or “hallucinations” (hearing a song fragment that was not there) was not elevated. The associations also remained when variables such as age, creativity, social desirability, mental imagery ability, and hallucination-proneness were taken into account.

Overall the results of this study demonstrate that, under certain conditions, the combination of high caffeine consumption and high stress can render normal people vulnerable to auditory hallucinations. Caffeine is known to increase how much cortisol is produced in response to a stressor. Caffeine consumption has also been found to correlate with hallucination proneness in other studies of healthy people (Jones & Fernyhough, 2009). It is also important to note that patients with schizophrenia typically drink a great deal of coffee. During times of high stress, this might perhaps increase their risk of having an exacerbation in hallucinatory symptoms.

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The combination of high stress levels and high caffeine intake is associated with hallucinations in psychiatrically healthy people.

In disorganized speech, the words and word combinations sound communicative, but the listener is left with little or no understanding of the point the speaker is trying to make. In some cases, completely new, made-up words known as neologisms (literally, “new words”) appear in the patient’s speech. An example might be the word detone, which looks and sounds like a meaningful word but is a neologism. Formal thought disorder (a term clinicians use to refer to problems in the way that disorganized thought is expressed in disorganized speech) is well illustrated in the following example. It is taken from a letter written by a man with schizophrenia and addressed to Queen Beatrix of the Netherlands.

Disorganized Speech: A Letter to Queen Beatrix I have also “killed” my ex-wife, [name], in a 2.5 to 3.0 hours sex bout in Devon Pennsylvania in 1976, while two Pitcairns were residing in my next room closet, hearing the event. Enclosed, please find my urology report, indicating that my male genitals, specifically my penis, are within normal size and that I’m capable of normal intercourse with any woman, signed by Dr. [name], a urologist and surgeon who performed a circumcision on me in 1982. Conclusion: I cannot be a nincompoop in a physical sense (unless Society would feed me chemicals for my picture in the nincompoop book).

Disorganized behavior can show itself in a variety of ways. Goal-directed activity is almost universally disrupted in schizophrenia. The impairment occurs in areas of routine daily functioning, such as work, social relations, and self-care, to the extent that observers note that the person is not himself or herself anymore. For example, the person may no longer maintain minimal standards of personal hygiene or may exhibit a profound disregard of personal safety and health. In other cases, grossly disorganized behavior appears as silliness or unusual dress (e.g., wearing an overcoat, scarf, and gloves on a hot summer day). Many researchers attribute these disruptions of “executive” behavior to impairment in the functioning of the prefrontal region of the cerebral cortex (Lenzenweger & Dworkin,  1998 ).

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A person with catatonia may maintain an odd position for minutes or even hours.

Catatonia is an even more striking behavioral disturbance. The patient with catatonia may show a virtual absence of all movement and speech and be in what is called a catatonic stupor. At other times, the patient may hold an unusual posture for an extended period of time without any seeming discomfort.

Positive and Negative Symptoms

Since the days of Bleuler, two general symptom patterns, or syndromes, of schizophrenia have been differentiated. These are referred to as positive- and negative-syndrome schizophrenia (e.g., Andreasen,  1985 ; Andreasen et al.,  1995 ). Statistical procedures have further indicated that some symptoms like disordered speech and disorganized behavior that were previously thought to reflect positive symptoms might be better separated from “true” positive symptoms like hallucinations and delusions. A  disorganized symptom  pattern is now also recognized (Lenzenweger et al.,  1991 ). These symptom types are illustrated in  Table 13.1 .

Positive symptoms  are those that reflect an excess or distortion in a normal repertoire of behavior and experience, such as delusions and hallucinations.  Negative symptoms , by contrast, reflect an absence or deficit of behaviors that are normally present. Important negative symptoms in schizophrenia include  flat affect , or blunted emotional expressiveness, and  alogia , which means very little speech. Another negative symptoms is  avolition , or the inability to initiate or persist in goal-directed activities. For example, the patient may sit for long periods of time staring into space or watching TV with little interest in any outside work or social activities.

TABLE 13.1 Positive, Negative, and Disorganized Symptoms of Schizophrenia

Positive SymptomsNegative SymptomsDisorganized Symptoms
HallucinationsEmotional flatteningBizarre behavior
DelusionsPoverty of speechDisorganized speech
 Asociality 
 Apathy 
 Anhedonia 
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Positive, negative, and disorganized symptoms can co-occur in the same patient. This woman appears to exhibit marked social withdrawal (a negative symptom) in addition to showing bizarre behavior (a disorganized symptom).

Although most patients exhibit both positive and negative symptoms during the course of their disorders (Breier et al.,  1994 ; Guelfi et al.,  1989 ), a preponderance of negative symptoms in the clinical picture is not a good sign for the patient’s future outcome (e.g., Fenton & McGlashan,  1994 ; Milev et al.,  2005 ).

Not all negative symptoms are exactly what they seem, however. Kring and Neale ( 1996 ) studied unmedicated male patients with schizophrenia while they were watching film clips. Three different types of film clips were used, the scenes in them being very positive, very negative, or neutral in terms of the emotions they were designed to elicit in the viewers. Videotapes of how the patients looked while they were watching the films were then coded by trained raters. As might be expected, the patients with schizophrenia showed less facial expressiveness than a group of healthy controls.

What was surprising was that when the patients were asked about their emotional experiences during the films, they reported as many emotional feelings as the controls—and sometimes slightly more. Measures of autonomic arousal also showed that when they were watching the films, the patients exhibited more physiological reactivity than the controls did. What these findings suggest, therefore, is that even though patients with schizophrenia may sometimes not look very emotionally expressive, they are nonetheless experiencing plenty of emotion.

Subtypes of Schizophrenia

There is a great deal of heterogeneity in the presentation of schizophrenia, and patients with this disorder often look quite different clinically. In consideration of this, the DSM-IV-TR recognized several subtypes of schizophrenia. The most clinically meaningful of these were  paranoid schizophrenia  (where the clinical picture is dominated by absurd and illogical beliefs that are often highly elaborated and organized into a coherent, though delusional, framework),  disorganized schizophrenia  (which is characterized by disorganized speech, disorganized behavior, and flat or inappropriate affect) and  catatonic schizophrenia (which involves pronounced motor signs that reflect great excitement or stupor). Unfortunately, research using the subtyping approach did not yielded major insights into the etiology or treatment of the disorder. Reflecting this, subtypes of schizophrenia are no longer included in DSM-5.

Other Psychotic Disorders

SCHIZOAFFECTIVE DISORDER

The DSM-5 recognizes a diagnostic category called  schizoaffective disorder  (see the DSM-5 table for diagnostic criteria). This diagnosis is conceptually something of a hybrid, in that it is used to describe people who have features of schizophrenia and severe mood disorder. In other words, the person not only has psychotic symptoms that meet criteria for schizophrenia but also has marked changes in mood for a substantial amount of time. Because mood disorders can be unipolar or bipolar in type, these are recognized as subtypes of schizoaffective disorder.

The reliability of schizoaffective disorder tends to be quite poor, and clinicians often do not agree about who meets the criteria for the diagnosis (Maj et al.,  2000 ; Vollmer-Larsen et al.,  2006 ). In an effort to improve this, in DSM-5 it is specified that mood symptoms have to meet criteria for a full major mood episode and also have to be present for more than 50% of the total duration of the illness. This clarification should help improve the reliability of this diagnosis and possibly also decrease the number of people who receive it.

DSM-5 criteria for: Schizoaffective Disorder

·  A. An uninterrupted period of illness during which there is a major mood episode (major depressive or manic) concurrent with Criterion A of schizophrenia.

Note: The major depressive episode must include Criterion A1: Depressed mood.

·  B. Delusions or hallucinations for 2 or more weeks in the absence of a major mood episode (depressive or manic) during the lifetime duration of the illness.

·  C. Symptoms that meet criteria for a major mood episode are present for the majority of the total duration of the active and residual portions of the illness.

·  D. The disturbance is not attributable to the effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

In general, the prognosis for patients diagnosed with schizoaffective disorder is somewhere between that of patients with schizophrenia and that of patients with mood disorders (Walker et al.,  2004 ). Research suggests that the long-term (10-year) outcome is much better for patients with schizoaffective disorder than it is for patients with schizophrenia (Harrow et al.,  2000 ).

SCHIZOPHRENIFORM DISORDER

Schizophreniform disorder  is a category reserved for schizophrenia-like psychoses that last at least a month but do not last for 6 months and so do not warrant a diagnosis of schizophrenia (see the DSM-5table for diagnostic criteria). It may include any of the symptoms described in the preceding sections. Because of the possibility of an early and lasting remission after a first psychotic breakdown, the prognosis for schizophreniform disorder is better than that for established forms of schizophrenia.

DSM-5 criteria for Schizophreniform Disorder

·  A. Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these must be (1), (2), or (3):

·  1. Delusions.

·  2. Hallucinations.

·  3. Disorganized speech (e.g., frequent derailment or incoherence).

·  4. Grossly disorganized or catatonic behavior.

·  5. Negative symptoms (i.e., diminished emotional expression or avolition).

·  B. An episode of the disorder lasts at least 1 month but less than 6 months. When the diagnosis must be made without waiting for recovery, it should be qualified as “provisional.”

·  C. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either 1) no major depressive or manic episodes have occurred concurrently with the active-phase symptoms, or 2) if mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness.

·  D. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

DSM-5 criteria for: Delusional Disorder

·  A. The presence of one (or more) delusions with a duration of 1 month or longer.

·  B. Criterion A for schizophrenia has never been met.

Note: Hallucinations, if present, are not prominent and are related to the delusional theme (e.g., the sensation of being infested with insects associated with delusions of infestation).

·  C. Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and behavior is not obviously bizarre or odd.

·  D. If manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periods.

·  E. The disturbance is not attributable to the physiological effects of a substance or another medical condition and is not better explained by another mental disorder, such as body dysmorphic disorder or obsessive-compulsive disorder.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

DSM-5 criteria for: Brief Psychotic Disorder

·  A. Presence of one (or more) of the following symptoms. At least one of these must be (1), (2), or (3):

·  1. Delusions.

·  2. Hallucinations.

·  3. Disorganized speech (e.g., frequent derailment or incoherence).

·  4. Grossly disorganized or catatonic behavior.

Note: Do not include a symptom if it is a culturally sanctioned response.

·  B. Duration of an episode of the disturbance is at least 1 day but less than 1 month, with eventual full return to premorbid level of functioning.

·  C. The disturbance is not better explained by major depressive or bipolar disorder with psychotic features or another psychotic disorder such as schizophrenia or catatonia, and is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric Association.

DELUSIONAL DISORDER

Patients with  delusional disorder , like many people with schizophrenia, hold beliefs that are considered false and absurd by those around them. Unlike individuals with schizophrenia, however, people given the diagnosis of delusional disorder may otherwise behave quite normally. Their behavior does not show the gross disorganization and performance deficiencies characteristic of schizophrenia, and general behavioral deterioration is rarely observed in this disorder, even when it proves chronic (see the DSM-5table for criteria for delusional disorder). One interesting subtype of delusional disorder is erotomania. Here, the theme of the delusion involves great love for a person, usually of higher status. One study suggests that a significant proportion of women who stalk are diagnosed with erotomania (Purcell et al.,  2001 ).

BRIEF PSYCHOTIC DISORDER

Brief psychotic disorder  is exactly what its name suggests. It involves the sudden onset of psychotic symptoms or disorganized speech or catatonic behavior. Even though there is often great emotional turmoil, the episode usually lasts only a matter of days (too short to warrant a diagnosis of schizophreniform disorder). After this, the person returns to his or her former level of functioning and may never have another episode again (see the DSM-5 table for criteria for brief psychotic disorder). Cases of brief psychotic disorder are infrequently seen in clinical settings, perhaps because they remit so quickly. Brief psychotic disorder is often triggered by stress, as illustrated in the following case.

Four Days of Symptoms and Rapid Recovery Ronald was 32 years old and had worked successfully as a lawyer for 6 years. He was married with two young children and he had many close friends. One day he returned home early from work and was shocked to find his wife in bed with his best friend. His initial reaction was anger, followed by depression. However, within 2 days he began to hear voices that called his name and that said, “Love, love, love.” Ronald began to express odd ideas, speaking of fusing with God and dispensing peace on Earth. He also talked about needing to fight what he called the “giant conspiracy.” During this time his affect was flat and he spoke in a slow and distinct manner. Ronald was admitted to hospital and was given medication. He and his wife also began marital therapy. Ronald showed rapid improvement of his symptoms and within 5 days of the onset of his initial symptoms he was back at work again. (Based on Janowsky et al.,  1987 )

in review

·  • What are the major symptoms of schizophrenia?

·  • How is a hallucination different from a delusion?

·  • Explain the differences among positive, negative, and disorganized symptoms.

·  • Why were the subtypes of schizophrenia not included in DSM-5?

·  • In what ways are schizophrenia and schizoaffective disorder different?

·  • How will the change to the criteria for schizoaffective disorder in DSM-5 improve the reliability of this diagnosis?

·  • What are the major differences between schizophreniform disorder and brief psychotic disorder?

Risk and Causal Factors

What causes schizophrenia? Despite enormous efforts by researchers, this question still defies a simple answer. In the sections that follow, we discuss what is currently known about the etiology of schizophrenia. What is clear is that no one factor can fully explain why schizophrenia develops. The old dichotomy of nature versus nurture is as misleading as it is simplistic. Psychiatric disorders are not the result of a single genetic switch being flipped. Rather, a complex interplay between genetic and environmental factors is responsible.

Genetic Factors

It has long been known that disorders of the schizophrenia type are “familial” and tend to “run in families.” There is overwhelming evidence for higher-than-expected rates of schizophrenia among biological relatives of index cases; that is, the diagnosed group of people who provide the starting point for inquiry (also called pro-bands).  Figure 13.2  shows the percentage risk of developing schizophrenia given a specific genetic relationship with someone who has the disorder. As you can see, there is a strong association between the closeness of the blood relationship (i.e., level of gene sharing or consanguinity) and the risk for developing the disorder. For example, the prevalence of schizophrenia in the first-degree relatives (parents, siblings, and offspring) of a proband with schizophrenia is about 10 percent. For second-degree relatives who share only 25 percent of their genes with the proband (e.g., half-siblings, aunts, uncles, nieces, nephews, and grandchildren), the lifetime prevalence of schizophrenia is closer to 3 percent.

Of course, just because something runs in families does not automatically implicate genetic factors. The terms familial and genetic are not synonymous, and a disorder can run in a family for nongenetic reasons (if I am obese and my dog is also obese, the reasons for this are clearly not genetic!). As we have repeatedly emphasized, the interpretation of familial concordance patterns is never completely straightforward, in part because of the strong relationship between the sharing of genes and the sharing of the environments in which those genes express themselves. Although they are indispensable in providing a starting point for researchers, family studies cannot, by themselves, tell us why a disorder runs in families. To disentangle the contributions of genes and environment, we need twin and adoption studies.

TWIN STUDIES

We discussed twin studies in general in  Chapter 3  and again more specifically in relation to anxiety and mood disorders. As with the mood disorders, schizophrenia concordance rates for identical twins are routinely and consistently found to be significantly higher than those for fraternal twins or ordinary siblings. The most famous case of concordance for schizophrenia is summarized in “The World Around Us” box, and describes the Genain Quadruplets.

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FIGURE 13.2 Risk of Developing Schizophrenia by Genetic Relationship. Lifetime age-adjusted, averaged risks for the development of schizophrenia-related psychoses in classes of relatives differing in their degree of genetic relatedness.

Source: Compiled from family and twin studies in European populations between 1920 and 1987. From Gottesman, I. I. ( 1991 ). Schizophrenia Genesis: The Origins of Madness (p. 96). Copyright © 1991 by Irving I. Gottesman. Used with permission of W. H. Freeman and Company/Worth Publishers.

the WORLD around us: The Genain Quadruplets

The Genain quadruplets, born sometime in the early 1930s, were rare MZ quadruplets who each developed schizophrenia, an outcome that would be expected to occur by chance only once in approximately 1.5 billion births. The genetically identical girls, given the pseudonym Genain (from the Greek for “dreadful gene”), were hospitalized at the National Institute of Mental Health in the mid-1950s and studied intensively by lead researcher David Rosenthal (see Rosenthal,  1963 ; see also Mirsky & Quinn,  1988 ). Rosenthal also selected first names for the girls using the initials of the institution, NIMH. Accordingly, the women are known to us as Nora (the firstborn), Iris, Myra, and Hester. They are all concordant for schizophrenia. However, they are discordant with regard to the severity of their illnesses.

The most severely ill Genain is Hester, who was born last and had the lowest birth weight. Hester was always the slowest to develop, and she was removed from school after 11th grade. She has never held a job outside the home and has suffered from chronic and unremitting severe symptoms since age 18. Neurocognitive testing at NIMH revealed that, along with Nora, Hester showed a great deal of evidence of brain disturbance.

Nora was always considered by the family to be the best of the four girls. She had the highest IQ and was the first to get a job. Nonetheless, after she was hospitalized at the age of 22 with hallucinations, delusions, and withdrawal, she had a long history of hospitalizations and has never been able to live independently or hold a job for an extended period of time.

In contrast, third-born Myra, despite having some problems in her 20s (when she was questionably diagnosed as having schizophrenia), does not appear to have experienced delusions and paranoia until her mid-40s. The only one of the Genains to marry and have children, she has a clinical picture that suggests schizoaffective disorder (a blend of psychotic symptoms and mood symptoms). Although she is not psychiatrically well by any means, she was able to go off medications and eventually went into remission.

Finally, there is Iris. Like Nora, Iris had her first psychiatric hospitalization at age 22. She spent 12 years in a state hospital and suffered from hallucinations, delusions, and motor abnormalities. Although neurocognitive testing did not reveal any obvious brain disturbance, it is clear that she has suffered from a severe form of schizophrenia.

Why do these identical quadruplets not have identical illnesses? We do not know. Did Nora and Hester, being born first and last, experience more traumatic birth complications? Has Iris done less well than might have been expected from her neuro-cognitive test results because her parents insisted on treating the quads as though they were two sets of twins—a superior and talented set consisting of Nora and Myra, and an inferior, problematic set consisting of Iris and Hester? Did being paired with Hester somehow compromise Iris’s development? Has Myra done so well (relatively) because she was the most favored and because she did not sustain any brain damage?

And why did the quadruplets develop schizophrenia at all? In all probability, there was a family history of the disorder. Mr. Genain’s mother (the girls’ grandmother) had a nervous breakdown in her teens and appears to have had some symptoms of paranoid schizophrenia. It is also clear that the family environment was far from healthy and may have provided the stress that acted on the quadruplets’ genetic predispositions to induce full-blown illness. Mr. Genain was very disturbed and spent most of his time drinking and expressing his various fears and obsessions to his family. He imposed extreme restrictions and surveillance on the girls until the time of their breakdowns. He was sexually promiscuous and was reported to have sexually molested at least two of his daughters. Mrs. Genain seems to have ignored the sexual exploitation occurring in the home. In short, nothing about the family environment can be considered to have been normal.

Although being a twin does not increase one’s risk for developing schizophrenia (the incidence of schizophrenia among twins is no greater than it is for the general population), study after study has shown a higher concordance for schizophrenia among identical, or monozygotic (MZ), twins than among people related in any other way, including fraternal, or dizygotic (DZ), twins.

E. Fuller Torrey is a noted schizophrenia researcher who has a sister with the disorder. He and his colleagues (1994) have published a review of the major literature worldwide on twin studies of schizophrenia. The overall pairwise concordance rate is 28 percent in MZ twins and 6 percent in DZ twins. This suggests that a reduction in shared genes from 100 percent to 50 percent reduces the risk of schizophrenia by nearly 80 percent. Also note that sharing 50 percent of one’s genes with a co-twin with schizophrenia is associated with a lifetime risk for schizophrenia of 6 percent. Although this is low in absolute terms, it is markedly higher than the baseline risk of less than 1 percent found in the general population.

If schizophrenia were exclusively a genetic disorder, the concordance rate for identical twins would, of course, be 100 percent. Although MZ concordance rates vary from one twin study to another, and although some researchers report higher rates than the 28 percent reported by Torrey and colleagues ( 1994 ), they are never even close to 100 percent. Two conclusions can therefore be drawn: First, genes undoubtedly play a role in causing schizophrenia. Second, genes themselves are not the whole story. Twin studies provide some of the most solid evidence that the environment plays an important role in the development of schizophrenia. But why one MZ twin should develop schizophrenia when his or her co-twin does not is a fascinating question.

A great deal of research attention is now being directed at studying people with a known genetic liability for schizophrenia. Historically, the most important subjects to study in this regard have been MZ twins who are discordant for schizophrenia. This investigative strategy was pioneered many years ago by Fischer ( 1971  1973 ) in an ingenious study. Fischer reasoned that genetic influences, if present, would be just as likely to show up in the offspring of the twins without schizophrenia in discordant pairs (see  Figure 13.3 ) as they would be to show up in the offspring of the twins with schizophrenia (because they share all their genes in common). And, in a search of official records in Denmark, Fischer found exactly that. Subsequent to this, in a follow-up of Fischer’s subjects, Gottesman and Bertelson (1989) reported an  age-corrected incidence rate  for schizophrenia of 17.4 percent for the offspring of the MZ twins without schizophrenia (i.e., the well MZ twins). This rate, which far exceeds normal expectancy, was not significantly different from that for offspring of the twins with schizophrenia in discordant pairs or from that for offspring of DZ twins with schizophrenia. Assuming that exposure to an aunt or uncle with schizophrenia would have, at most, limited etiologic significance, these results lend impressive support to the genetic hypothesis. They also, as the authors note, indicate that a predisposition to schizophrenia may remain “unexpressed” (as in the twins without schizophrenia in discordant pairs) unless “released” by unknown environmental factors.

research CLOSE-UP: Age-Corrected Incidence Rate

Incidence is the number of new cases that develop. An age-corrected incidence rate takes into account predicted breakdowns for subjects who are not yet beyond the age of risk for developing the disorder.

ADOPTION STUDIES

One major assumption that twin studies make is that any differences found between MZ and DZ twins are attributable to genes. At the heart of this assumption is the idea that the environments of MZ twins are no more similar than the environments of DZ twins. But it is very reasonable to expect that, because MZ twins are identical (and always of the same gender), their environments will actually be more similar than the environments of DZ twins. To the extent that this is true, twin studies will overestimate the importance of genetic factors (because some similarities between MZ twins that actually occur for nongenetic reasons will be attributed to genetic factors). In some cases, of course, MZ twins go to a great deal of effort to try to be different from one another. The bottom line, however, is that the assumption that MZ and DZ twins have equally similar environments can create some problems when we try to interpret the findings of twin studies.

Several studies have attempted to overcome the shortcomings of the twin method in achieving a true separation of hereditary from environmental influences by using what is called the adoption strategy. Here, concordance rates for schizophrenia are compared for the biological and the adoptive relatives of people who have been adopted out of their biological families at an early age (preferably at birth) and have subsequently developed schizophrenia. If concordance is greater among the patients’ biological than adoptive relatives, a hereditary influence is strongly suggested; the reverse pattern would argue for environmental causation.

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FIGURE 13.3 Fischer’s Study. Because MZ twins have identical genes, the children of the well twin will have an elevated risk of schizophrenia even if their parent did not suffer from the disorder.

The first study of this kind was conducted by Heston in 1966. Heston followed up 47 children who had been born to mothers who were in a state mental hospital suffering from schizophrenia. The children had been placed with relatives or into foster homes within 72 hours of their birth. In his follow-up study, Heston found that 16.6 percent of these children were later diagnosed with schizophrenia. In contrast, none of the 50 control children (selected from among residents of the same foster homes whose biological mothers did not have schizophrenia) developed schizophrenia. In addition to the greater probability of being diagnosed with schizophrenia, the offspring whose mothers had schizophrenia were also more likely to be diagnosed as mentally retarded, neurotic, or psychopathic (i.e., antisocial). They also had been involved more frequently in criminal activities and had spent more time in penal institutions. These findings are often taken to suggest that any genetic liability conveyed by the mothers is not specific to schizophrenia but also includes a liability for other forms of psychopathology. But we must be careful about drawing such a conclusion. Heston’s study provided no information about psychopathology in the fathers of the children. We therefore cannot know to what extent some of the problems the children had were due to genetic liability conveyed by their fathers.

Heston’s study began by identifying mothers with schizophrenia and then traced what had happened to their adopted-away offspring. An alternative approach involves locating adult patients with schizophrenia who were adopted early in life and then looking at rates of schizophrenia in their biological and adoptive relatives. A large-scale and multifaceted adoption study of this type was undertaken in Denmark, with Danish and American investigators working in collaboration (Kendler & Gruenberg,  1984 ; Kendler et al.,  1994 ; Kety et al.,  1978  1994 ). As would be expected on the basis of a genetic model, the data showed a preponderance of schizophrenia and “schizophrenia-spectrum” problems (e.g., schizotypal and paranoid personality disorder) in the biological relatives of adoptees with schizophrenia. More specifically, 13.3 percent of the 105 biological relatives had schizophrenia or schizophrenia-spectrum disorders themselves. In contrast, only 1.3 percent of the 224 adoptive parents showed such problems.

THE QUALITY OF THE ADOPTIVE FAMILY

The Danish adoption studies did not include independent assessments of the child-rearing adequacy of the adoptive families into which the index children (those who developed schizophrenia) and the control children (those who did not) had been placed. It remained for Tienari and colleagues (Tienari et al.,  1987  2000  2004 ) to add this feature to their research design. The Finnish Adoptive Family Study of Schizophrenia, as it is known, followed up the adopted-away children of all women in Finland who were hospitalized for schizophrenia between 1960 and 1979. As they grew to adulthood, the functioning of these index children was compared with the functioning of a control sample of adoptees whose biological mothers were psychiatrically healthy. Over the course of a 21-year follow-up, the index adoptees developed more schizophrenia and schizophrenia-related disorders than did the controls (Tienari et al.,  2000  2003 ). What sets this study apart, however, is what it tells us about the interaction between genes and environment.

One measure of the family environment that the researchers looked at was communication deviance (Wahlberg et al.,  1997 ). Communication deviance is a measure of how understandable and “easy to follow” the speech of a family member is. Vague, confusing, and unclear communication reflects high communication deviance. What Wahlberg and colleagues found was that it was the combination of genetic risk and high communication deviance in the adopted families that was problematic. Children who were at genetic risk and who lived in families where there was high communication deviance showed high levels of thought disorder at the time of the follow-up. In contrast, the control adoptees who had no genetic risk for schizophrenia showed no thought disorder, regardless of whether they were raised in a high- or a low-communication-deviance family. Perhaps what was most remarkable, though, was the outcome for the high-risk children who were raised by adopted families low in communication deviance. These children were healthier at follow-up than any of the other three groups! In other words, if they are raised in a benign environment, even children who are at genetic risk for schizophrenia appear to do very well.

Tienari and colleague have provided further evidence of a genotype–environment interaction in schizophrenia (Tienari et al.,  2004 ). (If you are unsure what these terms mean, check back to  Chapter 3 .) Using interviews, the researchers first looked at the quality of the family environment in which the adopted children were raised. They then looked at what happened to the children who were raised in healthy versus dysfunctional families. The degree of adversity in the family environment predicted later problems in the adopted children. However, only those children who were raised in dysfunctional families and had high genetic risk for schizophrenia went on to develop schizophrenia-related disorders themselves. Children at high genetic risk who were raised in healthy family environments did not develop problems any more frequently than did children at low genetic risk.

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Even if children are at genetic high risk for schizophrenia they are less likely to develop the disorder if they are raised in a healthy family environment.

These findings are important because they suggest that our genetic makeup may control how sensitive we are to certain aspects of our environments. If we have no genetic risk, certain kinds of environmental influences may not affect us very much. But if we have high genetic risk, we may be much more vulnerable to certain types of environmental risks such as high communication deviance or adverse family environments. Findings such as these also raise the exciting possibility that certain kinds of environments may protect people with a genetic susceptibility to schizophrenia from ever developing the illness.

In summary, these findings indicate a strong interaction between genetic vulnerability and an unfavorable family environment in the causal pathway leading to schizophrenia. Of course, it could be argued that the children who went on to develop problems caused the disorganization of their adoptive families. However, there is little support for this alternative interpretation (see Tienari et al.,  2004 ; Wahlberg et al.,  1997 ). Some independent work reported by Kinney and colleagues (1997) also fails to show diminished mental health in adoptive parents raising children who later developed schizophrenia. Everything considered, the Finnish Adoptive Family Study has provided strong confirmation of the diathesis-stress model as it applies to the origins of schizophrenia.

MOLECULAR GENETICS

Family studies tell us that schizophrenia runs in families, and twin and adoption studies help us explore the relative contributions of genes and environment. These approaches also tell us about the genetic heterogeneity of schizophrenia. For example, in addition to higher rates of schizophrenia, higher rates of schizotypal personality disorder are also found in the relatives of patients with schizophrenia (Kendler et al.,  1993 ). This supports the idea of the schizophrenia spectrum and suggests that a genetic liability to schizophrenia can sometimes manifest itself in a form of pathology that is “schizophrenia-like” but not exactly schizophrenia itself (see Lenzenweger,  2010 ).

Researchers no longer believe that schizophrenia will, like Huntington’s disease (see  Chapter 14 ), be explained by one mutated gene on one specific chromosome. Rather, in most cases, schizophrenia probably involves many genes working together to confer susceptibility to the illness. The individual’s “dose” of schizophrenia genes may explain why one person develops schizophrenia and another develops a milder variant within the schizophrenia spectrum, such as schizotypal personality disorder.

Researchers are now trying to locate and identify the genes that are involved in schizophrenia using the techniques of molecular genetics. In one approach, they are using known DNA markers to try to learn where aberrant genes might lie. As Faraone and colleagues (1999) aptly state, DNA markers are the “milemarkers” on our chromosomal highways. Molecular geneticists capitalize on the fact that we know the locations of some important genes that are associated with observable traits (such as genes for color blindness, for blood group, and for the human leukocyte antigen). Because genes that are close together on the same chromosome tend to stay together when genetic information is shuffled (as happens during reproduction), researchers can see whether a disorder like schizophrenia tends to co-occur with any known DNA marker traits. This is the rationale behind  linkage analysis . Linkage analysis has been very successful in helping locate the genes associated with diseases that have well-defined models of inheritance. Even newer approaches such as genome-wide association methods (which may be able to detect genes that have very small effects) are also now being used to identify susceptibility genes.

In much of the research to date, failures to replicate previously reported findings have been more the rule than the exception. Nonetheless, studies are suggesting specific regions on certain chromosomes that may contribute to schizophrenia. Currently, there is a great deal of interest in regions on chromosomes 1, 2, 6, 8, 13, and 22 among others (Karoutzou et al.,  2008 ; Maier,  2008 ; O’Donovan et al.,  2008 ; Pogue-Geile & Yokley,  2010 ; Stefansson et al.,  2008 ).

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Many genes, each with a small effect, probably contribute to the development of schizophrenia. Genes that play a role in brain development may be especially implicated.

Why are these chromosomes of such interest? The reason is that, in some cases, they host genes that are known to be involved in processes that are believed to be aberrant in schizophrenia. These genes are known as  candidate genes . An example is the COMT (catechol-O-methyltransferase) gene. This gene is located on chromosome 22 and is involved in dopamine metabolism. As you will soon learn, dopamine is a neurotransmitter that has long been implicated in psychosis (impaired reality testing). Interestingly, children who have a genetic syndrome (called velocardiofacial syndrome) that involves a deletion of genetic material on chromosome 22 are at high risk for developing schizophrenia as they move through adolescence (Gothelf et al.,  2007 ). Prior to the onset of any disorder, they often report transient psychotic symptoms (such as auditory hallucinations) and have poor social functioning and reduced IQ (Debbané et al.,  2006 ). Furthermore, as we shall see later, people with a particular variant of the COMT gene are much more likely to become psychotic as adults if they use cannabis during adolescence. For obvious reasons, schizophrenia researchers are very interested in chromosome 22 and in the COMT gene in their search to understand the origins of the disorder. Other genes implicated in schizophrenia are the neuregulin 1 gene (located on chromosome 8), the dysbindin gene (on chromosome 6), the DISC1 (which stands for “disrupted in schizophrenia”) gene on chromosome 1, and several dopamine receptor genes (Gejman et al.,  2011 ; Pogue-Geile & Yokley,  2010 ). These genes are involved in various neurobiological processes that are thought to have gone awry in schizophrenia.

ENDOPHENOTYPES

Although we are certain that schizophrenia has a genetic basis, we are still a long way from understanding which genes are involved and what effects they have. Progress has been frustratingly slow because schizophrenia appears to be very complex genetically. A major collaborative study that examined 14 genes thought to be involved in schizophrenia has found no association between these genes and schizophrenia, disappointing many researchers (Sanders et al.,  2008 ). However, it is possible that the genes involved may have only weak effects or else may be relevant in only certain population subgroups. A robust finding in one segment of the sample could therefore be washed out in a very large and mixed overall sample (Hamilton,  2008 ). Another difficulty is that researchers are still not sure exactly what phenotype (i.e., measurable characteristic of interest) they should be looking for (remember Bleuler’s idea of “the schizophrenias”?). Because genetic analysis requires that we know who is “affected” and who is not, this is a big problem.

To simplify things, researchers are now focusing on less complex and more homogenous phenotypes (such as specific symptom clusters) that may potentially be under the control of a smaller number of genes. They are also exploring  endophenotypes —discrete, stable, and measurable traits that are thought to be under genetic control. By studying different endophenotypes, researchers hope to get closer to specific genes that might be important in schizophrenia (Gottesman & Gould,  2003 ; Lenzenweger,  2010 ). Accordingly, researchers are interested in people who score high on certain tests or measures that are thought to reflect a predisposition to schizophrenia. One example is subjects who score high on a self-report measure of schizotypic traits involving perceptual aberrations and magical ideation (the Per-Mag Scale; see Chapman et al.,  1982 ; Chapman et al.,  1994 ). Examples of items from these scales are shown in  Table 13.2 . Other endophenotypic risk markers for schizophrenia include abnormal performance on measures of cognitive functioning such as tests of working memory (see Barch,  2005 ; Lenzenweger,  2010 ). By studying these traits rather than the disorder itself, researchers hope to speed up progress in the search for the genes related to schizophrenia. Major collaborative studies designed to explore different endophenotypes are now under way (Greenwood et al.,  2007 ).

Prenatal Exposures

Whether or not a genotype is expressed depends on biological and environmental triggers. We now know that a range of environmental factors, including such things as maternal exposure to stress, are capable of influencing patterns of gene expression in the developing offspring. In the sections below we highlight some environmental risk factors that might either cause schizophrenia or trigger it in a genetically vulnerable person.

VIRAL INFECTION

The idea that schizophrenia might result from some kind of virus is not new. Kraepelin ( 1919 ) suggests that “infections in the years of development might have a causal significance” for schizophrenia. We also know that in the Northern Hemisphere, more people with schizophrenia are born between January and March than would be expected by chance (Waddington et al.,  1999 ). Could some seasonal factor, such as a virus, be implicated?

TABLE 13.2 Sample Items Measuring Psychosis-Proneness

Magical Ideation
TFThings seem to be in different places when I get home, even though no one has been there.
TFI have sometimes felt that strangers were reading my mind.
TFAt times, I have felt that a professor’s lecture was meant especially for me.
Perceptual Aberration
TFSometimes people whom I know well begin to look like strangers.
TFOrdinary colors sometimes seem much too bright for me.
TFNow and then, when I look in the mirror, my face seems quite different than usual.

Sources: Eckbald & Chapman (1983); Chapman et al. (1978). Answering “true” to these items is more indicative of psychosis–proneness.

In 1957 there was a major epidemic of influenza in Finland. Studying the residents of Helsinki, Mednick and colleagues (1988) found elevated rates of schizophrenia in children born to mothers who had been in their second trimester of pregnancy at the time of the influenza epidemic. The link between maternal influenza and subsequent schizophrenia in the grown offspring has now been well replicated using influenza epidemic information from other countries (see Wright et al.,  1999 ). Risk of schizophrenia seems to be greatest when the mother gets the flu in the fourth to seventh month of gestation. Although the size of the effect is small and influenza clearly does not account for very many cases of schizophrenia, the fact that this association exists is very provocative. But how can maternal influenza set the stage for schizophrenia in a child two or three decades later? One possibility is that the mother’s antibodies to the virus cross the placenta and somehow disrupt the neurodevelopment of the fetus (Waddington et al.,  1999 ). Other maternal infections such as rubella (German measles) and toxoplasmosis (a parasitic infection) that occur during this time have also been linked to increased risk for the later development of schizophrenia (Brown,  2011 ).

RHESUS INCOMPATIBILITY

The idea that the mother’s immune system might somehow damage the developing brain of the fetus is not as far-fetched as it might sound. Rhesus (Rh) incompatibility occurs when an Rh-negative mother carries an Rh-positive fetus. (Rhesus-positive or -negative is a way of typing a person’s blood.) Incompatibility between the mother and the fetus is a major cause of blood disease in newborns. Interestingly, Rh incompatibility also seems to be associated with increased risk for schizophrenia. Hollister, Laing, and Mednick ( 1996 ) have shown that the rate of schizophrenia is about 2.1 percent in males who are Rh-incompatible with their mothers. For males who have no such incompatibility with their mothers, the rate of schizophrenia is 0.8 percent—very near the expected base rate found in the general population. Hollister is another example of a schizophrenia researcher who has a family member with the disorder, in this case a sister who was Rh-incompatible with her mother.

How might Rh incompatibility increase the risk for schizophrenia? One possibility is that the mechanism involves oxygen deprivation, or hypoxia. This suggestion is supported by studies that have linked the risk for schizophrenia to birth complications. Recent research also suggests that incompatibility between the blood of the mother and the blood of the fetus may increase the risk of brain abnormalities of the type known to be associated with schizophrenia (Freedman et al.,  2011 ).

PREGNANCY AND BIRTH COMPLICATIONS

Patients with schizophrenia are much more likely to have been born following a pregnancy or delivery that was complicated in some way (Cannon et al.,  2002 ). Although the type of obstetric complication varies, many delivery problems (e.g., breech delivery, prolonged labor, or the umbilical cord around the baby’s neck) affect the oxygen supply of the newborn. Although we still have much to learn, the research again points toward damage to the brain at a critical time of development.

EARLY NUTRITIONAL DEFICIENCY

Yet another piece of evidence that supports the idea that schizophrenia might be caused or triggered by environmental events that interfere with normal brain development comes from a tragedy that occurred in the Netherlands toward the end of World War II. In October 1944, a Nazi blockade resulted in a severe famine that affected people living in Amsterdam and other cities in the west of the country. The Dutch Hunger Winter (as it was known) continued until the Netherlands was liberated in May 1945. The population was severely malnourished during this time, and many died of starvation. Not surprisingly, fertility levels fell and the birth rate dropped precipitously. However, some children were born during this time. Those who were conceived at the height of the famine had a twofold increase in their risk of later developing schizophrenia (Brown,  2011 ). Early prenatal nutritional deficiency appears to have been the cause. Whether the problem was general malnutrition or the lack of a specific nutrient such as folate or iron is not clear. But again, something seems to have compromised the development of the fetus during a critical stage.

MATERNAL STRESS

If a mother experiences an extremely stressful event late in her first trimester of pregnancy or early in the second trimester the risk of schizophrenia in her child is increased (King et al.,  2010 ). For example, in a large population study conducted in Denmark, the death of a close relative during the first trimester was associated with a 67 percent increase in the risk of schizophrenia in the child (Khashan et al.,  2008 ). Currently, it is thought that the increase in stress hormones that pass to the fetus via the placenta might have negative effects on the developing brain, although the mechanisms through which maternal stress increases risk for schizophrenia are not yet well understood.

Genes and Environment in Schizophrenia: A Synthesis

Without question, schizophrenia has a strong genetic component. Current thinking is that genetic risk for schizophrenia emerges in one of two ways. The first is from large numbers (perhaps thousands) of common genes. The individual contribution of each of these genes is likely very small. However, when all of these genetic variants interact together, they set the stage for the development of the illness. The other way that schizophrenia may arise is because of very rare genetic mutations. These could be highly specific to certain people or to certain families (see Crow,  2007 ; McClellan, Susser, & King,  2007 ). These genetic events might involve microdeletions (bits of the DNA sequence that are missing in some places) or problems in the DNA sequence itself (such as repetitions of specific sections; St. Clair, 2009).

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FIGURE 13.4 Chorionic Arrangements in Twins. (A) Dichorionic twins, who can be either dizygotic or monozygotic, have separate placentas and separate fetal circulation. (B) Monochorionic twins, who are always monozygotic, have a single placenta and shared circulation.

Source: From Davis, J. O., Phelps, J. A., & Bracha, H. S. ( 1995 ). Prenatal development of monozygotic twins and concordance for schizophrenia. Schizophrenia Bulletin, 21(3), 357–66.

It is also possible that the focus on MZ concordance rates has caused us to overestimate the heritability of schizophrenia. This is because some MZ, and all DZ, twins do not have equally similar prenatal environments. Around two-thirds of MZ embryos are monochorionic, which means they share a placenta and blood supply. The remaining MZ twins and all DZ twins are dichorionic; they have separate placentas and separate fetal circulations. This is shown in  Figure 13.4  above. The higher concordance rate for schizophrenia in MZ than in DZ twins might therefore be a consequence, at least in part, of the greater potential for monochorionic MZ twins to share infections. Davis, Phelps, and Bracha ( 1995 ) have found that MZ twins who are monochorionic are much more likely to be concordant for schizophrenia (around 60 percent concordance) than MZ twins who are dichorionic (around 11 percent concordance). The concordance figure for dichorionic MZ twins is very similar to that generally reported for DZ twins. Monochorionic MZ twins may therefore have inflated concordance rates in schizophrenia, which may have caused us to overattribute to genetics what might more accurately be attributed to environmental influences.

Finally, we need to keep in mind that genes get “turned on” and “turned off” in response to environmental changes. MZ twins who are discordant for schizophrenia show differences in their gene expression (Petronis et al.,  2003 ). Perhaps some environmental “hits” turn on the genes for schizophrenia in one twin and not in the other. And perhaps some environments can keep the genes for schizophrenia from ever being turned on at all. Unfortunately, consistent with the diathesis-stress perspective, being at genetic risk does seem to make people more susceptible to environmental insults. In a study looking at the consequences of birth complications, Cannon and colleagues (1993) found that only the people who had a parent with schizophrenia and who had birth complications later showed brain abnormalities in adulthood such as enlarged ventricles (fluid-filled spaces in the brain). Moreover, for people who had two parents with schizophrenia, the problems were even worse. In contrast, people with no family history of schizophrenia did not show enlarged ventricles regardless of whether they experienced delivery complications when they were born. The message seems to be clear: A genetic liability to schizophrenia may predispose an individual to suffer more damage from environmental insults than would be the case in the absence of the genetic predisposition.

A Neurodevelopmental Perspective

Earlier in this chapter you learned that schizophrenia typically strikes people in late adolescence or early adulthood. Yet in the sections above, we saw that some of the factors thought to cause schizophrenia occur very early in life—in some cases before birth. How can this be? Current thinking is that schizophrenia is a disorder in which the development of the brain is disturbed very early on. Risk for schizophrenia may start with the presence of certain genes that, if turned on, have the potential to disrupt the normal development of the nervous system. Exposure to environmental insults in the prenatal period may turn on these genes or may create problems in other ways, independently of genotype. What this means is that the stage for schizophrenia, in the form of abnormal brain development, may be set very early in life. Nonetheless, problems may not be apparent until other triggering events take place or until the normal maturation of the brain reveals them. This may not occur until the brain is fully mature, typically late in the second decade of life (Conklin & Iacono,  2002 ; Weinberger,  1987 ).

What goes wrong? We are not yet certain. Brain development is a complex process that involves a programmed, orderly, and progressive sequence of events (Romer & Walker,  2007 ). Interestingly, some of the genes that have been implicated in schizophrenia are known to play a role in brain development and neural connections. (And organic solvents used in the dry cleaning business might disrupt fetal neurodevelopment and so explain why having a parent who works as a dry cleaner triples the risk of schizophrenia in the offspring.) If there were a disruption in cell migration some cells might fail to reach their target destinations, greatly affecting the “internal connectivity” of the brain. Neuronal migration is known to occur during the second trimester—exactly the period in development during which the consequences of maternal influenza seem to be most devastating.

If the seeds of schizophrenia are sown so early in life, can we see early indications of vulnerability to the disorder before the illness itself strikes? An ingenious series of studies reported by Walker and colleagues nicely illustrates the association between early developmental deviation and schizophrenia risk. These investigators gathered family home movies made during the childhoods of 32 people who eventually developed schizophrenia. Trained observers made “blind” ratings (i.e., the observers were uninformed of outcomes) of certain dimensions of the emotional (Grimes & Walker,  1994 ) and facial expressions (Walker et al.,  1993 ), motor skills, and neuromotor abnormalities (Walker et al.,  1994 ) of these children and their healthy-outcome siblings from the same movie clips. The facial and emotional expressions and the motor competence of the “pre-schizophrenia” and the healthy-outcome children were found by the raters to differ significantly. The “preschizophrenia” children showed more motor abnormalities including unusual hand movements than their healthy siblings; they also showed less positive facial emotion and more negative facial emotion. In some instances these differences were apparent by age 2. Of course, we must keep in mind that these early problems do not characterize all children who will later develop schizophrenia. But they do tell us that subtle abnormalities can be found in children who are vulnerable to the disorder. We should also note that a major advantage of Walker’s research design was that it avoided the problem of retrospective bias. Rather than asking parents or siblings what patients were like when they were growing up, the study used home movies to provide an objective behavioral record.

Another way to explore childhood indicators without the problem of retrospective bias is to use a prospective research design (see  Chapter 1 ). Jones and colleagues (1994) and Isohanni and colleagues (2001) studied whole cohorts of children born in particular years and followed them up over time. Both groups of researchers found evidence of delayed speech and delayed motor development at age 2 in children who later went on to develop schizophrenia.

Yet another approach is to follow children who are known to be at high risk for schizophrenia by virtue of their having been born to a parent with the disorder. This strategy, pioneered by Mednick and Schulsinger ( 1968 ), has led to several other studies of high-risk children (for reviews, see Cornblatt et al.,  1992 ; Erlenmeyer-Kimling & Cornblatt,  1992 ; Neale & Oltmanns,  1980 ; Watt et al.,  1984 ). Obviously, research of this kind is both costly and time consuming. It also requires a great deal of patience on the part of researchers because children at risk have to be identified early in their lives and then followed into adulthood. Moreover, because the majority of people with schizophrenia do not have a parent with the disorder (in fact, 89 percent of patients have no first- or second-degree relatives with schizophrenia [Gottesman,  2001 ]), high-risk samples are not particularly representative. Nonetheless, they have provided us with some valuable information about what people at risk look like prior to developing the full illness.

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Ratings of clips of old home movies revealed that children who went on to develop schizophrenia showed more unusual hand movements than their healthy siblings, even when they were just 2 years old.

Source: Walker ( 1994 ).

One of the most consistent findings from high-risk research is that children with a genetic risk for schizophrenia are more deviant than control children on research tasks that measure attention (Erlenmeyer-Kimling & Cornblatt,  1992 ). Adolescents at risk for schizophrenia are also rated lower in social competence than adolescents at risk for affective illness (Dworkin et al.,  1994 ; Hooley,  2010 ). Some of the social problems that these high-risk children have may result from underlying attentional problems (Cornblatt et al.,  1992 ).

Echoing the findings from Walker’s home movie study is evidence that early motor abnormalities might be an especially strong predictor of later schizophrenia. Using data from the New York High-Risk Study, Erlenmeyer-Kimling and colleagues (1998) reported that, of an initial group of 51 high-risk children, 10 developed schizophrenia or schizophrenia-like psychosis as adults. Of these, 80 percent had shown unusual motor behavior when they were between 7 and 12 years of age. In another study, adolescents at high risk for schizophrenia showed more movement abnormalities (e.g., facial tics, blinking, tongue thrusts) than either nonclinical controls or adolescents with personality or behavioral problems (Mittal et al.,  2008 ). Moreover, these movement abnormalities became more marked with time and also became more strongly correlated with psychotic symptoms as the children got older. Although we might have suspected that schizophrenia would first begin to show itself via hallucinations or delusions, it may be that the first signs of the illness can instead be found in the way that children move. This could be because movement abnormalities and psychotic symptoms share some of the same neural circuitry in the brain. Problems in this neural circuitry might show themselves first via movement abnormalities. Then, as the brain matures, problems in the same neural circuits manifest themselves in psychotic symptoms (see MacManus et al.,  2011 ; Mittal et al.,  2008 ).

DSM-5 THINKING CRITICALLY about DSM-5: Attenuated Psychosis Syndrome

There was lively debate about whether a new diagnosis called attenuated psychosis syndrome should be added to the DSM-5 (Carpenter & Van Os,  2011 ). In the end it was decided that the syndrome should be included in a provisional manner and placed in a section reserved for disorders in need of further study. But what is attenuated psychosis syndrome and why is it such a controversial diagnosis?

Attenuated psychosis syndrome is characterized by mild psychotic symptoms that are not severe enough to meet clinical criteria for another full-blown psychotic disorder. People with this syndrome are thought to be at risk for later psychosis. They are also experiencing some distress or disability and are seeking help for their problems. Proponents of including the syndrome in DSM-5 argued that it would help clinicians identify these people and provide them with treatment at an early stage. This could, in theory, reduce distress in the short term and prevent the onset of a full-blown psychotic disorder in the long term. This is important because, once schizophrenia has developed, most patients are likely to experience recurring positive and negative symptoms, as well as persistent impairments in their work or social functioning for a large part of their lives (Jobe & Harrow,  2010 ).

Although these may seem like valid reasons to include the new diagnosis, there are also arguments against doing so. The potential for stigma is one problem (Yang et al.,  2013 ). Another concern is that the majority of people who are identified as being at high risk are not on their way to developing a psychotic disorder. Addington and colleagues (2011) followed 303 young adults who were showing prodromal symptoms of schizophrenia. At the end of the follow-up period the majority of these young people (71 percent) had not made the transition into psychosis. Although the follow-up period was relatively short it seems that the false positive rate here is very high (see also Fusar-Poli et al.,  2012 ).

Another concern is that the existence of the diagnosis will increase the likelihood that antipsychotic medications will be used to treat it (see Weiser,  2011 ). But is it really appropriate and ethical to prescribe antipsychotic medications to someone who has only mild psychotic symptoms? As you have learned, second-generation antipsychotic medications are not as effective as had been initially hoped. They also appear to be associated with some very undesirable changes (such as tissue loss) in the brain (Ho et al.,  2011 ; Lewis,  2011 ). When used long term, they may even perpetuate psychosis (see Unresolved Issues at the end of this chapter). Given this, it behooves us to be cautious with their use.

The inclusion of attenuated psychosis in Section III of the DSM may be a good interim solution. It will encourage more research into this new disorder. This may help us refine and improve the diagnostic criteria that are currently being used. More research may also stimulate the development of new treatment approaches capable of providing clinical benefits to patients without exposing them to unnecessary risks.

The original high-risk studies have given us many insights into the problems that characterize people at risk for schizophrenia. But researchers have now changed their strategies. A new generation of high-risk studies is focusing on young people who are at clinical (as opposed to genetic) high risk. By focusing on those who are already showing some  prodromal , or very early, signs of schizophrenia, researchers are hoping to improve their ability to detect, and also perhaps intervene with, people who appear to be on a pathway to developing the disorder (Addington et al.,  2007 ; Cannon et al.,  2007 ). Recognizing this, the new diagnosis of  attenuated psychosis syndrome  has entered DSM-5 as a disorder in need of further study (see the “Thinking Critically About DSM-5” box).

Structural and Functional Brain Abnormalities

Technological developments now allow us to study the brain in ways that used to be impossible. Positron emission tomography (PET), magnetic resonance imaging (MRI), and other even more sophisticated approaches are in wide use. They are revealing abnormalities in the structure and function of the brain as well as in neurotransmitter activity in people who suffer from schizophrenia. In the sections that follow we describe some of the problems in cognitive functioning that have long been known to characterize people with this disorder. We then consider what abnormalities in the structure and functioning of the brain might be responsible for these and other problems.

NEUROCOGNITION

Schizophrenia patients experience many problems with their neurocognitive functioning (see Cornblatt et al.,  2008 ; Green,  1997 , for reviews). For example, they perform much worse than healthy controls on a broad range of neuropsychological tests (Heaton et al.,  1994 ; Hoff et al.,  1992  2000 ). Furthermore, patients who have only recently become ill perform about the same on neuropsychological tests as patients who have been ill for many years (and both groups obviously perform worse than controls). In other words, cognitive difficulties can be seen right from the start of the illness and so are unlikely to be due to the effects of extended hospitalizations or medications.

Other cognitive deficits are also apparent. For example, when asked to respond to a stimulus as quickly and appropriately as possible (this is a measure of reaction time), schizophrenia patients do poorly compared with controls (see Nuechterlein,  1977 ). In addition, they show deficits on the Continuous Performance Task (CPT; e.g., Cornblatt et al.,  1989 ). This task requires the subject to attend to a series of letters or numbers and then to detect an intermittently presented target stimulus that appears on the screen along with the letters or numbers (e.g., “Press when you see the number 7”). There are also problems with working memory (Barch,  2005 ; Park et al.,  1995 ), which can be thought of as our “mental blackboard.” When they engage in tasks of working memory, patients with schizophrenia show less prefrontal brain activity compared to healthy controls (Cannon et al.,  2005 ).

Somewhere between 54 and 86 percent of people with schizophrenia also show eye-tracking dysfunction (see  Figure 13.5 ) and are deficient in their ability to track a moving target such as a pendulum (Cornblatt et al.,  2008 ). This is a skill referred to as smooth-pursuit eye movement (Levy et al.,  1993 ; Lieberman et al.,  1993 ). In contrast, only about 6 to 8 percent of the general population shows problems with eye tracking. Especially interesting is that around 50 percent of the first-degree relatives of schizophrenia patients also show eye-tracking problems even though they do not have schizophrenia themselves (e.g., Iacono et al.,  1992 ; Levy et al.,  1993 ; Sporn et al.,  2005 ). This suggests that disturbances in eye tracking have a genetic basis and that eye tracking may represent a viable endophenotype for genetic studies.

Perhaps the strongest finding in the area of neurocognition and schizophrenia, however, concerns a psychophysiological measure called P50 (see Heinrichs,  2001 ). When two clicks are heard in close succession, the brain (receiving the auditory signal) produces a positive electrical response to each click. This response is called P50 because it occurs 50 milliseconds after the click. In normal subjects, the response to the second click is less marked than the response to the first click because the normal brain dampens, or “gates,” responses to repeated sensory events. If this didn’t happen, habituation to a stimulus would never occur. Many patients with schizophrenia, in contrast, respond almost as strongly to the second click as to the first. This is referred to as “poor P50 suppression.” First-degree family members of patients with schizophrenia are also more likely than controls to have problems with P50 suppression (Clementz et al.,  1998 ). It has been suggested that poor P50 suppression is the result of problems with specific receptors in the hippocampus of the medial temporal lobe (Adler et al.,  1998 ). As you will soon learn, the hippocampus is one brain region that appears to be compromised in schizophrenia. Cells in the hippocampus are also especially susceptible to damage from hypoxia during brain development.

Taken together, the weight of the evidence suggests that patients with schizophrenia have problems with the active, functional allocation of attentional resources. What this means is that they are unable to attend well on demand. Although many of the findings may not be highly specific to schizophrenia (some of the neurocognitive deficits can be found in patients with mood disorders, for example), it has long been suspected that attentional dysfunctions could be indicators of a biological susceptibility to at least some forms of schizophrenia (Cornblatt et al.,  1992 ). In the following sections, we consider some of the reasons that this might be the case.

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FIGURE 13.5 Normal and Abnormal Eye Tracking of a Sinusoidal Wave. The top pattern is the target, the middle pattern is a record of normal tracking, and the lowest pattern is the kind of abnormal record produced by some patients with schizophrenia.

Source: Figure from Levy et al. ( 1993 ). Eye tracking dysfunction and schizophrenia: A critical perspective. Schizophrenia Bulletin, 19(3), 461–536. Used with permission of Oxford University Press.

LOSS OF BRAIN VOLUME

One of the most well-replicated findings concerns the brain ventricles. These are fluid-filled spaces that lie deep within the brain. Compared with controls, patients with schizophrenia have enlarged brain ventricles, with males possibly being more affected than females (Lawrie & Abukmeil,  1998 ; Shenton et al.,  2001 ). However, we must also point out that enlarged brain ventricles are apparent only in a significant minority of patients. Enlarged brain ventricles also are not specific to schizophrenia and can be seen in patients with Alzheimer’s disease, Huntington’s disease, and chronic alcohol problems.

Enlarged brain ventricles are important because they are an indicator of a reduction in the amount of brain tissue. The brain normally occupies fully the rigid enclosure of the skull. Enlarged ventricles therefore imply that the brain areas that border the ventricles have somehow shrunk or decreased in volume, the ventricular space becoming larger as a result. In fact, MRI studies of patients with schizophrenia show about a 3 percent reduction in whole brain volume relative to that in controls (Hulshoff Pol & Kahn,  2008 ). This decrease in brain volume is present very early in the illness. Even patients with a recent onset of schizophrenia have lower overall brain volumes than controls (Steen et al.,  2006 ; Vita et al.,  2006 ) or else show evidence of enlarged ventricles (Cahn et al.,  2002 ). These findings suggest that some brain abnormalities likely predate the illness rather than develop as a result of untreated psychosis or as a consequence of taking neuroleptic medications. Consistent with this, important new research shows that brain volume changes can be seen in genetically high-risk individuals as the illness is starting to develop. Indeed, it has been suggested that these changes may play a causal role in the onset of symptoms (Karlsgodt et al.,  2010 ; Sun et al.,  2009b ).

We also know that the brain changes that characterize people in the early stages of the illness progressively get worse with time. Cahn and colleagues (2002) measured changes in the overall volume of gray matter (which is made up of nerve cells) in patients who were experiencing their first episode of schizophrenia. Thirty-four patients and thirty six matched, healthy comparison subjects received MRI brain scans at the start of the study and then again 1 year later. The results showed that the volume of gray matter declined significantly over time in the patients but not in the controls. More specifically, there was almost a 3 percent decrease in the volume of gray matter in the patients in the 1-year period between the first and the second scans.  Figure 13.6  illustrates the progressive loss of gray matter over a 5-year period in another sample of adolescents with schizophrenia compared to healthy controls.

Studies of more chronically ill patients suggest that decreases in brain tissue and increases in the size of the brain ventricles are not limited to the early phases of this illness. Instead, progressive brain deterioration continues for many years. Moreover, these brain changes can also be found in MZ twins where one has schizophrenia and the other does not. The fact that brain changes are present in the discordant twin (the one without schizophrenia) suggests that they cannot be explained by the influence of antipsychotic medications and may instead be under genetic control (Brans et al.,  2008 ; Hulshoff Pol & Kahn,  2008 ). Overall, the research findings suggest that in addition to being a neurodevelopmental disorder, schizophrenia is also a neuroprogressive disorder characterized by a loss of brain tissue over time. Kraepelin’s use of the term dementia praecox may have been highly appropriate after all.

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FIGURE 13.6 Progressive Gray Matter Loss in Schizophrenia. Compared with normal adolescents, young people with early-onset schizophrenia show a progressive loss of gray matter in their brains over time. MRI scans repeated over a 5-year period show a much greater loss of brain tissue in patients with schizophrenia than in healthy controls. Gray matter loss occurs in many brain areas, beginning in the parietal cortex and spreading to the temporal cortex and the frontal cortex.

AFFECTED BRAIN AREAS

Are there regions of the brain that are especially implicated in schizophrenia? Although much remains to be learned, there is evidence of reductions in the volume of regions in the frontal and temporal lobes. These brain areas play critical roles in memory, decision making, and in the processing of auditory information. More specifically, there is a reduction in the volume of such medial temporal areas as the amygdala—which is involved in emotion, the hippocampus—which plays a key role in memory, and the thalamus—a relay center that receives almost all sensory input (Ettinger et al.,  2001 ; Keshavan et al.,  2008 ; Shenton et al.,  2001 ; Tamminga et al.,  2002 ; Weinberger,  1997 ). Again, however, remember that the alterations in brain structure that are found in schizophrenia are not specific only to this diagnosis. As you know from other chapters in this book, problems in some of these brain areas are implicated in other conditions (e.g., severe mood disorders) as well.

WHITE MATTER PROBLEMS

When we talk about volume loss in the brains of people with schizophrenia we are referring to the loss of brain cells or gray matter. However, evidence is growing that schizophrenia also involves problems with white matter. Nerve fibers are covered in a myelin sheath (which looks white in color in a chemically preserved brain). Myelin acts as an insulator and increases the speed and efficiency of conduction between nerve cells. White matter is therefore crucially important for the connectivity of the brain. If there are disruptions in the integrity of white matter, there will be problems in how well the cells of the nervous system can function. For example, imagine the problems you would have in a group of networked computers if the connections that linked them were damaged in some way.

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Nerve fibers are covered in by a fatty myelin sheath, which looks white in a preserved brain (hence the term white matter). Myelin improves the electrical conductivity of nerve cells. This image illustrates white matter tracts (shown here in color for better clarity) and shows how interconnected the brain is.

Studies of patients with schizophrenia show that they have reductions in white matter volume as well as structural abnormalities in the white matter itself. Interestingly, these abnormalities can be found in first-episode patients and also in people at genetic high risk for the disorder. This suggests that they are not a result of the disease itself or the effects of treatment.

At the clinical level, white matter abnormalities have been shown to be correlated with cognitive impairments (Kubicki et al.,  2007 ). In people at high risk of developing schizophrenia, white matter changes in the temporal areas of the brain also predict later social functioning (Karlsgodt et al.,  2009 ). Another interesting recent finding is that children of people with schizophrenia, even though they are not psychotic themselves, have a reduction in the volume of the corpus callosum—a massive tract of white matter fibers that connects the two hemispheres of the brain (Francis et al.,  2011 ). Although much remains to be learned, it is becoming increasingly clear that abnormalities in white matter, and in white matter development, may provide us with important additional insights into what goes wrong with the brain in schizophrenia.

BRAIN FUNCTIONING

Studies of brain functioning tell us what is going on in the working brain, either when it is engaged in a task or at rest. You have already learned about the structural brain abnormalities associated with schizophrenia and the problems that patients with schizophrenia have on various neurocognitive tests. Given this, you will hardly be surprised to learn that neuroimaging research is showing us just how disrupted brain functioning is in patients with this disorder.

For example, some patients show abnormally low frontal lobe activation (known as “hypofrontality”) when they are involved in mentally challenging tasks such as the Wisconsin Card Sorting Test (WCST) or in other tests generally thought to require substantial frontal lobe involvement. Essentially, this brain area does not seem to be able to kick into action when patients perform complex tasks (see  Figure 13.7 ). In other patients, hyperactivation in frontal brain areas is found, suggesting that they are having to work harder to be successful on the task. In both sets of circumstances, however, the brain is not functioning in an optimal and efficient way.

Impaired functioning of the frontal lobes during cognitive tasks is also found in patients in the early stages of schizophrenia as well as in people at high risk for developing the disorder (Fusar-Poli et al.,  2007 ). Again, however, it is important to remember that such alterations in functioning are not characteristic of all patients (e.g., Buchsbaum et al.,  1992 ; Heinrichs,  2001 ). Nonetheless, frontal lobe dysfunction is believed to account for some of the negative symptoms of schizophrenia and perhaps to be involved in some attentional-cognitive deficits (Cannon et al.,  1998 ; Goldman-Rakic & Selemon,  1997 ).

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FIGURE 13.7 The Brain in Schizophrenia. Many brain regions and systems operate abnormally in schizophrenia, including those highlighted here.

Dysfunction of the temporal lobe is also found, although here the findings are often not very consistent (Keshavan et al.,  2008 ). However, what may be most important is that there may be a problem with the way activity in different brain regions gets coordinated. When we are at rest or relaxing there is activation in a network of brain regions that comprise the “default mode network.” You can think of this as the brain on standby. Then, when we are actively engaged in a task, activity in this network of brain areas has to be suppressed in favor of activity in brain areas that are relevant to the task at hand. But imagine what might happen if it was difficult to disengage from the default mode. Performance on the task would suffer. This is what researchers now think may be happening in people with schizophrenia. Whereas healthy people find it easy to suppress activity in the default mode network (tuning their brains into the “correct station” so to speak), people with schizophrenia may not be able to do this as efficiently (Guerrero-Pedrazza et al.,  2011 ; Whitfield-Gabrieli et al.,  2009 ). This lack of ability to disengage the default mode network may help us understand why people with schizophrenia have so many difficulties with a wide range of tasks across a broad array of areas (Karlsgodt et al.,  2010 ).

CYTOARCHITECTURE

As we have seen, one hypothesis about schizophrenia is that genetic vulnerabilities, perhaps combined with prenatal insults, can lead to disruption of the migration of neurons in the brain. If this is true, some cells will fail to arrive at their final destinations, and the overall organization of cells in the brain (the brain’s cytoarchitecture) will be compromised. This is illustrated in  Figure 13.8 .

There are also other ways in which the organization of cells in the brain appears to be disrupted. Some researchers, using complex, three-dimensional counting techniques, have reported an increase in neuronal density in some areas of the brains of patients with schizophrenia (see Selemon,  2004 ). There are also abnormalities in the distribution of cells in different layers of the cortex and hippocampus (Arnold,  2000 ; Kalus et al.,  1997 ; Selemon et al.,  1995 ), as well as evidence that patients with schizophrenia are missing particular types of neurons known as “inhibitory interneurons” (Benes & Berretta,  2001 ). These neurons are responsible for regulating the excitability of other neurons. Their absence may mean that bursts of activity by excitatory neurons in the brain go unchecked. Again, research suggests that the brains of patients with schizophrenia may be less able to regulate or dampen down overactivity in certain key neural circuits (see Daskalakis et al.,  2002 ). As we will see shortly, patients with schizophrenia have difficulty handling even normal levels of stress. Given what we have just learned, this makes a great deal of sense.

BRAIN DEVELOPMENT IN ADOLESCENCE

Although we have every reason to believe that risk genes and early prenatal experiences compromise brain development in the fetus, the story may not end so early. The brain continues to develop and mature through adolescence and into young adulthood. For example, we all have an excess of synapses well into our late teens. However, normal processes that occur during adolescence prune (or reduce) these synapses, so decreasing “neuronal redundancy.” There is also a normal reduction in gray matter volume that occurs in adolescence, as well an increase both in white matter and in the volume of the hippocampus and the amygdala. In addition, the number of excitatory synapses decreases and the number of inhibitory synapses increases. All of these processes are thought to occur to enhance brain function overall and to make the brain more “adult” (Insel,  2010 ; Walker et al.,  2010 ).

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FIGURE 13.8 Cytoarchitecture and Neural Development. The upper diagram shows examples of normal and abnormal pyramidal cell orientation in the hippocampus. The lower diagram is a schematic representation of stained neurons and the “downward-shift” phenomenon. Premature arrest of cell migration during development may underlie the high frequency of cells in lower regions close to white matter and their relative paucity near the cortical surface.

Source:  Figure 7.1  from Heinrichs R. W. ( 2001 ). In search of madness: Schizophrenia and neuroscience (p. 196). Oxford University Press. Adapted from Arnold, S. E., & Trojanowski, J. Q. ( 1996 ). Recent advances in defining the neuropathology of schizophrenia. Acta Neuropathologie, 92, 217–31 and Kolb, B., & Wishaw, I. Q. (1996). Fundamentals of human neuropsychology (4th ed.). New York: Freeman.

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Major brain changes take place during adolescence as the brain matures. If problems occur during this critical phase of development schizophrenia may be the result.

But what if these processes fail to occur in a normal way? We might expect to see many of the differences (reduced gray matter volume, less white matter, reduced volume of the hippocampus) that we do actually see in schizophrenia. Of course, we still have much to learn. The etiology of schizophrenia is very complicated. But many of the answers lie in what goes wrong in the brain at critical periods of development.

SYNTHESIS

The brain is compromised in schizophrenia, although the compromise is often very subtle. Some of the brain abnormalities that are found are likely to be genetic in origin. Others may reflect environmental insults. For example, Baaré and colleagues (2001) used MRI to study the brains of MZ and DZ twins who were discordant for schizophrenia and then compared the results for these groups to results from a group of healthy twins. What these researchers found was that the patients with schizophrenia had smaller brain volumes than their well co-twins. What was interesting, however, was that these well co-twins also had smaller brains than the healthy control twins. Baaré and colleagues (2001) propose that genetic risk for schizophrenia may be associated with reduced brain development early in life. This is why the healthy twins who had a co-twin with schizophrenia had smaller brain volumes than the healthy controls. Baaré and colleagues also hypothesize that patients who develop schizophrenia suffer additional brain abnormalities that are not genetic in origin. This explains why the twins with schizophrenia had smaller brain volumes than their discordant co-twins. In people at genetic risk for schizophrenia (but not in those without genetic risk), a history of fetal oxygen deprivation has been shown to be associated with brain abnormalities in later life (Cannon et al.,  2002 ). In other words, what we may have here is an excellent example of how genes can create an enhanced susceptibility to potentially aversive environmental events. Moreover, even when both members of a twin pair have identical genes (as is the case for MZ twins), if only one of them experiences the environmental insult (i.e., a birth cord around the neck, creating hypoxia), only one twin might be pushed across the threshold into illness while the co-twin remains healthy.

Finally, we emphasize that it is unlikely that schizophrenia is the result of any one problem in any one specific region of the brain. The brain is comprised of functional circuits—regions that are linked to other regions by a network of interconnections. If there is a problem at any point in the circuit, the circuit will not function properly. The focus now is on learning how the brain is wired and what regions are functionally linked. Research on the default mode network is an example of this. Subtle brain abnormalities in some key functional circuits (or deficiencies in the ability to switch from one functional circuit to another) may wreak havoc with normal functioning. As we gain more knowledge about how the brain does its job, we will understand more about how exactly the brain is compromised in schizophrenia.

NEUROCHEMISTRY

After researchers discovered in 1943 that LSD could cause profound mental changes, those interested in schizophrenia began to consider the possible biochemical basis of the disorder. Now the idea that serious mental disorders are due to “chemical imbalances” in the brain is commonplace. This phrase is often used to provide a general explanation of why someone has a disorder like schizophrenia. But the notion of “chemical imbalance” is vague and imprecise. All it really conveys is the widely accepted notion that alterations in brain chemistry may be associated with abnormal mental states.

The most well-studied neurotransmitter implicated in schizophrenia is  dopamine . The dopamine hypothesis dates back to the 1960s and was derived from three important observations. The first was the pharmacological action of the drug chlorpromazine (Thorazine). Chlorpromazine was first used in the treatment of schizophrenia in 1952. It rapidly became clear that this drug was helpful to patients. Eventually, it was learned that the therapeutic benefits of chlorpromazine were linked to its ability to block dopamine receptors.

The second piece of evidence implicating dopamine in schizophrenia came from an entirely different direction. Amphetamines are drugs that produce a functional excess of dopamine (i.e., the brain acts as if there is too much dopamine in the system). In the late 1950s and early 1960s, researchers began to see that abuse of amphetamines led, in some cases, to a form of psychosis that involved paranoia and auditory hallucinations (Connell,  1958 ; Kalant,  1966 ; Tatetsu,  1964 ). There was thus clinical evidence that a drug that gave rise to a functional excess of dopamine also gave rise to a psychotic state that looked a lot like schizophrenia.

The third piece of indirect evidence linking dopamine to schizophrenia came from clinical studies that actually treated patients by giving them drugs that increase the availability of dopamine in the brain. An example here is Parkinson’s disease, which is caused by low levels of dopamine in a specific brain area (the basal ganglia; see  Figure 13.7  on p. 466) and is treated with a drug called L-DOPA. Psychotic symptoms are a significant complication of treatment with L-DOPA. Again, then, the circumstantial evidence pointed to the role of dopamine in inducing psychosis.

How could dopamine induce psychosis? Activity in the dopa-mine system may play a role in determining how much salience we give to internal and external stimuli. Dysregulated dopamine transmission may actually make us pay more attention to and give more significance to stimuli that are not especially relevant or important. This is called “aberrant salience” (see Kapur,  2003 ). If this is the case, it is quite easy to see why patients might develop delusions or experience hallucinations and why psychotic experiences might be so shaped by the patient’s culture and history. In the early stages of their illnesses, patients often report heightened sensory awareness (“My senses were sharpened. I became fascinated by the little insignificant things around me”) or increased meaning in events (“I felt that there was some overwhelming significance in this”). If dopamine creates aberrant salience, the person will struggle to make sense of everyday experiences that were previously in the background but that now have become inappropriately important and worthy of attention. In this way, the hum of a refrigerator could become a voice talking; or the arrival of a package could signal a threat, which then prompts the patient to look carefully at the subtle behaviors of others to see who could be a source of harm and persecution.

But how might a functional excess of dopamine in the system come about? One way is through too much dopamine available in the synapse (the gap between nerve cells that has to be “bridged” by a neurotransmitter for a nerve impulse to be carried from one neuron to another). This could come about by increasing the synthesis or production of dopamine, by releasing more of it into the synapse, by slowing down the rate at which dopamine is metabolized or broken down once it is in the synapse, or by blocking neuronal reuptake (the “recycling” of dopamine back into the neuron). Any or all of these could increase the overall availability of dopamine. There are also ways in which a functional excess of dopamine could be produced or, more accurately, mimicked. If the receptors that dopamine acts on (i.e., those on the postsynaptic membrane) are especially dense and prolific or if they are especially sensitive (or both), the effects of a normal amount of dopamine being released into the synapse would be multiplied. In other words, the system acts as though there were more dopamine available even though there really isn’t.

Before the development of highly sophisticated imaging techniques, researchers interested in learning about dopamine in the brains of people with schizophrenia could use one of two approaches. They could measure dopamine in the (postmortem) brains of decreased patients, or they could study dopamine indirectly by measuring its major metabolite (what most of it is converted into). The major metabolite of dopamine is homovanillic acid, or HVA. However, HVA is best collected in cerebrospinal fluid (CSF). This requires that the patient agree to a lumbar puncture, which involves a large needle being inserted into the spine to draw off fluid. Not only is this potentially dangerous, it also leaves the patient with a violent headache.

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After being synthesized, dopamine is stored until it is released into the synapse. Dopamine binds to receptors on the post-synaptic neuron (shown in blue) triggering other reactions. It is then recycled back into the neuron to be used again. image24 Watch the Video In the Real World: Neurotransmitters on MyPsychLab.

The early studies that examined concentrations of HVA in the CSF of patients with schizophrenia and in controls yielded generally negative results (see Heinrichs,  2001 ; Owen & Simpson,  1995 ). The same was true of postmortem studies. Researchers were forced to conclude that there was no strong evidence to support the idea that patients with schizophrenia were producing more dopamine than controls were. Research efforts therefore moved toward exploring the idea that the problem lay not in overall dopamine levels (dopamine turnover) but in receptor density and receptor sensitivity. These studies were facilitated by technological developments, such as PET scans, which allow us to study the working brain and to look at the density of dopamine receptors in living patients.

There are five subtypes of dopamine receptors (D1–D5). Of these, the D2 receptor is the most relevant clinically, and most of the research has focused on this. In general, postmortem studies show that there are about 1.4 times more D2 receptors in the brains of deceased patients with schizophrenia than there are in controls (Seeman,  2011 ). Early PET studies also found evidence for a more-than-twofold increase in D2 receptors in living patients with schizophrenia compared with controls (Wong et al.,  1986 ; Gjedde & Wong,  1987 ), although some nonsignificant findings (Farde et al.,  1987  1990 ) led to a great deal of debate and controversy.

Subsequent research, however, has now established that the density of D2 receptors is indeed increased in patients with schizophrenia (Kestler et al.,  2001 ; Seeman,  2011 ). Although some of this increase is no doubt related to medication effects (older patients, who have taken more medications over their lives, have the highest densities of D2 receptors), medication effects do not explain all the findings. Importantly, we now have evidence that D2 receptors are also elevated in the healthy co-twins of patients with schizophrenia (Hirvonen et al.,  2005 ). Not only does this tell us that the elevation in D2 receptors is not simply attributable to taking medications, but it also tells us that having more D2 receptors doesn’t necessarily mean that someone will develop psychosis.

So what else is going on? Current thinking is that people with schizophrenia are supersensitive to dopamine (Seeman,  2011 ). This arises because they have greater numbers of a form of D2 receptor (called a D2high receptor) that has a very high affinity for dopamine. What is also exciting is that animal studies suggest that anoxia (oxygen deprivation) at the time of birth can lead to dopa-mine supersensitivity. What this means is that we now have a bridge between problems with dopamine system and some of the prenatal problems (e.g., birth complications) that we discussed earlier.

But dopamine is not the only neurotransmitter implicated in schizophrenia. Before leaving our discussion of neurochemistry, we take a quick look at another key neurotransmitter that is attracting a lot of attention.

Glutamate  is an excitatory neurotransmitter that is widespread in the brain. As was the case for dopamine, there are a number of reasons why researchers suspect that a dysfunction in glutamate transmission might be involved in schizophrenia. First, PCP, or angel dust, is known to block glutamate receptors. PCP also induces symptoms (both positive and negative) that are very similar to those of schizophrenia. Moreover, when people with schizophrenia take PCP, it exacerbates their symptoms.

Second, physicians had to stop using ketamine, which is an anesthetic, because when it is given intravenously to healthy volunteers, it produces schizophrenia-like positive and negative symptoms (see Krystal et al.,  2005 ). When given to patients whose schizophrenia is stable and well controlled, ketamine exacerbates hallucinations, delusions, and thought disorder. But what is all the more remarkable about ketamine is that it does not cause any of these problems when it is administered to children, for whom it continues to be used as an anesthetic. This suggests that age (and brain maturity) determines whether ketamine causes psychosis.

Like PCP, ketamine blocks glutamate receptors. Researchers are now exploring concentrations of glutamate in postmortem brains of patients with schizophrenia and finding lower levels of glutamate in both the prefrontal cortex and the hippocampus compared with the levels in control subjects (Goff & Coyle,  2001 ). Recent results from a meta-analysis further suggest that glutamate levels are also low in the brains of living patients who have schizophrenia (Marsman et al.,  2011 ). This is exciting because, many years ago, Olney and Farber ( 1995 ) proposed that diminished activity at certain types of glutamate receptors (known as “NMDA” receptors) may not only trigger schizophrenia-like symptoms but may also cause the degeneration of neurons in key brain areas. In other words, if the NMDA receptors are not normally active (perhaps because glutamate levels are low), subtle brain damage may result.

For all of these reasons, the glutamate hypothesis of schizophrenia is now attracting a lot of research attention. It is also prompting the development of new experimental drugs that might provide additional ways to treat schizophrenia. For example, amino acids such as glycine and D-serine are now being used to enhance neurotransmission at NMDA receptor sites. This research is still in its early stages; nonetheless, the initial findings look very promising (Javitt,  2008 ; Lane et al.,  2008 ).

Finally, does the importance of glutamate challenge the importance of dopamine in the neurochemistry of schizophrenia? No. One action of dopamine receptors is to inhibit the release of glutamate. Simply stated, an overactive dopaminergic system could result in excessive suppression of glutamate, leading to the underactivity of the NMDA receptors. The dopamine hypothesis of schizophrenia is actually made all the more credible by discoveries about glutamate.

Psychosocial and Cultural Factors

DO BAD FAMILIES CAUSE SCHIZOPHRENIA?

Years ago, parents were routinely assumed to have caused their children’s disorders through hostility, deliberate rejection, or gross parental ineptitude. Many professionals blamed parents, and their feedback to them was often angry and insensitive. Mothers were particularly singled out for criticism. The idea of the “schizophrenogenic mother,” whose cold and aloof behavior was the root cause of schizophrenia, was very influential in many clinical circles (Fromm-Reichman,  1948 ). This was very distressing for families. Not only were they faced with the difficulties of coping with a son or daughter who had a devastating illness, but they suffered all the more because of the blame that was directed toward them by mental health professionals.

Today, things are very different. Theories that were popular many decades ago—for example, the idea that schizophrenia was caused by destructive parental interactions (Lidz et al.,  1965 )—have foundered for lack of empirical support. Another idea that has not stood the test of time is the double-bind hypothesis(Bateson,  1959  1960 ). A double bind occurs when the parent presents the child with ideas, feelings, and demands that are mutually incompatible (e.g., a mother may complain about her son’s lack of affection but freeze up or punish him when he approaches her affectionately). According to Bateson’s etiologic hypothesis, such a son is continually placed in situations where he cannot win, and he becomes increasingly anxious. Presumably, over time, such disorganized and contradictory communications in the family come to be reflected in his own thinking. However, no solid support for these ideas has ever been reported.

Instead, we have learned from past research that disturbances and conflict in families that include an individual with schizophrenia may well be caused by having a person with psychosis in the family (e.g., Hirsch & Leff,  1975 ). In other words, rather than causing the schizophrenia, family communication problems could be the result of trying to communicate with someone who is severely ill and disorganized (Liem,  1974 ; Mishler & Waxler,  1968 ). Of course, some families do show unusual communication patterns that we now refer to as “communication deviance” and which we described earlier. These amorphous and fragmented communications may actually reflect genetic susceptibility to schizophrenia on the part of the relative (Hooley & Hiller,  2001 ; Miklowitz & Stackman,  1992 ). However, as we know from the Finnish Adoptive Study, adverse family environments and communication deviance probably have little pathological consequence if the child who is exposed has no genetic risk for schizophrenia (Tienari et al.,  2004 ; Wahlberg et al.,  1997 ).

FAMILIES AND RELAPSE

Although schizophrenia is often a chronic disorder, its symptoms may be especially severe at some times (i.e., when there is a relapse) and less severe at other times (e.g., during a period of remission). Decades ago, George Brown and his colleagues (1958) observed that the kind of living situation patients with schizophrenia had after they left the hospital predicted how well they would fare clinically. Surprisingly, patients who returned home to live with parents or with a spouse were at higher risk of relapse than patients who left the hospital to live alone or with siblings. Brown reasoned that highly emotional family environments might be stressful to patients. Unlike his counterparts across the Atlantic, he suspected that what might be important was not the presence of markedly disturbed or pathological patient–family relationships (although those certainly existed in some families) but something much more ordinary and commonplace. Brown’s hunch was that researchers should focus on “the range of feelings and emotions to be found in ordinary families” (see Brown,  1985 , p. 22). This was an unusual insight at the time. But viewed today in the context of the diathesis-stress model, we see just how prescient Brown was.

In a series of studies, Brown and his colleagues went on to develop and refine the construct of  expressed emotion,  or  EE . Expressed emotion is a measure of the family environment that is based on how a family member speaks about the patient during a private interview with a researcher (Hooley,  2007 ). It has three main elements: criticism, hostility, and emotional over-involvement (EOI). The most important of these is criticism, which reflects dislike or disapproval of the patient. Hostility is a more extreme form of criticism that indicates a dislike or rejection of the patient as a person. Finally, EOI reflects a dramatic or overconcerned attitude on the part of the family member toward the patient’s illness.

Expressed emotion is important because it has been repeatedly shown to predict relapse in patients with schizophrenia.

In a meta-analysis of 27 studies, Butzlaff and Hooley ( 1998 ) demonstrated that living in a high-EE home environment more than doubled the baseline level of relapse risk for schizophrenia patients in the 9 to 12 months after hospitalization. Moreover, even though EE predicts relapse regardless of whether the patients studied have been ill for a short, medium, or long time, EE seems to be an especially strong predictor of relapse for patients who are chronically ill.

Of course, it could be that families simply tend to be more critical of patients who are more severely ill and that is why EE and relapse are correlated. However, a review of the literature provides no strong support for this assumption (see Hooley et al.,  1995 ). Also, EE predicts relapse even when potentially important patient variables are controlled statistically (Nuechterlein et al.,  1992 ). Finally, research shows that when EE levels in families are lowered (usually by clinical interventions), patients’ relapse rates also decrease (Falloon et al.,  1985 ; Hogarty et al.,  1986 ; Leff et al.,  1982 ; McFarlane et al.,  1995 ). This suggests that EE may play a causal role in the relapse process.

But how might EE trigger relapse? There is a great deal of evidence that patients with schizophrenia are highly sensitive to stress. Consistent with the diathesis-stress model, environmental stress is thought to interact with preexisting biological vulnerabilities to increase the probability of relapse (Nuechterlein et al.,  1992 ). We know, for example, that independent stressful life events occur more frequently just prior to psychotic relapse than at other times (Ventura et al.,  1989  1992 ) and may exert their effects over longer periods of time too. Furthermore, one of the primary manifestations of the stress response in humans is the release of cortisol (a glucocorticoid) from the adrenal cortex. Animal and human studies show that cortisol release triggers dopa-mine activity (McMurray et al.,  1991 ; Rothschild et al.,  1985 ). Glucocorticoid secretion also affects glutamate release (Walker & Diforio,  1997 ). In other words, two of the major neurotransmitters implicated in schizophrenia (dopamine and glutamate) are affected by cortisol, which is released when we are stressed.

Along these lines, Hooley and Gotlib ( 2000 ) have suggested that, to the extent that high-EE behaviors exhibited by family members are perceived as stressful by patients, these behaviors are likely to trigger the release of cortisol. In support of this idea, high-EE relatives have been found to be more behaviorally controlling of patients than low-EE relatives are (Hooley & Campbell,  2002 ). When they try to help, they seem to do so in rather intrusive ways (e.g., “She wouldn’t go to sleep so I held her head down onto the pillow”). Furthermore, controlling behaviors such as these predict relapse in patients with schizophrenia. Quite possibly, relatives’ well-meaning attempts to get patients to function better simply backfire. If patients are stressed by what their relatives do, this could increase cortisol levels, affect important neurotransmitter systems, and perhaps eventually lead to a return of symptoms.

At the present time, we have no direct evidence that this happens. However, one study is worthy of note. A group of researchers studied the behavior of patients with schizophrenia when they were involved in interactions with high-EE and low-EE relatives (Rosenfarb et al.,  1995 ). The researchers observed that when patients said something strange (e.g., “If that kid bites you, you’ll get rabies”), high-EE relatives tended to respond by being critical of the patient. What was interesting was that when this happened, it tended to be followed by another unusual remark from the patient. In other words, an increase in patients’ unusual thinking occurred immediately after the patient was criticized by a family member. Although other interpretations of the findings are possible, the results of this study are consistent with the idea that negative (stress-inducing) behaviors by relatives can trigger increases in unusual thinking in patients with schizophrenia. Although we have no way of knowing what was happening to the cortisol levels of these patients, it is intriguing to speculate that increased cortisol release might somehow be involved.

Researchers are now using functional neuroimaging techniques (see  Chapter 1 ) to learn more directly how EE affects the brain. Recent findings show that hearing criticism or being exposed to emotionally overinvolved comments leads to different patterns of brain activity in people who are vulnerable to psychopathology compared to healthy controls (Hooley et al.,  2009  2010 ). We do not yet know if people who show this pattern of brain activation are at increased risk of relapse, although this might be expected.

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Patients with schizophrenia who live in families where there is a high level of emotional tension have more than twice the risk of relapse.

URBAN LIVING

Being raised in an urban environment seems to increase a person’s risk of developing schizophrenia. Pederson and Mortensen ( 2001 ) studied a sample of 1.9 million people in Denmark, a country in which information about where people live is recorded in a national registry and people have to notify authorities when they change addresses in order to retain eligibility for benefits. The researchers found that children who had spent the first 15 years of their lives living in an urban environment were 2.75 times more likely to develop schizophrenia in adulthood than were children who had spent their childhoods in more rural settings. Other methodologically sound studies also confirm this association (Sundquist et al.,  2004 ). It has been estimated that if this risk factor could be removed (that is, if we all lived in relatively rural settings) the number of cases of schizophrenia could decrease by about 30 percent (see Brown,  2011 ).

IMMIGRATION

The findings showing that urban living raises a person’s risk for developing schizophrenia suggest that stress or social adversity might be important factors to consider with respect to this disorder. Supporting this idea, research is also showing that recent immigrants have much higher risks of developing schizophrenia than do people who are native to the country of immigration. Looking at the results of 40 different studies involving immigrant groups from many different parts of the world, Cantor-Graae and Selten ( 2005 ) found that first-generation immigrants (i.e., those born in another country) had 2.7 times the risk of developing schizophrenia; for second-generation immigrants (i.e., those with one or both parents having been born abroad), the relative risk was even higher at 4.5. In other words, there is something about moving to another country that appears to be a risk factor for developing schizophrenia. The following case study illustrates this.

Schizophrenia in an Immigrant from China After she lost her job, Lian, young Chinese woman, was sent by her parents to live in Ireland. Upon arrival, Lian lived first in a boarding house. She then moved into a house that she shared with eight other young Chinese. Lian enrolled in a language school and also began to study for a degree in business administration. She made very few friends and spent most of her time on her own reading or playing games. The people who knew her described her as being a very private person who usually preferred to be alone.

Lian’s difficulties began after she learned that two young Chinese students in Dublin had died under suspicious circumstances. She became exceedingly alarmed–so much so that she left the language school and moved back into the boarding house to be with her former landlady. She began to believe that her abdomen contained a “presence” that was living there. She also reported hearing multiple voices coming from the “presence”. These voices, which spoke both Chinese and English, included the voices of teachers from Lian’s language school, her landlady, and her family from China. Lian reported that she had received a banknote from her family and that the picture on the banknote had spoken to her saying, “You are no longer welcome here”. Lian also developed a delusion that the family who had raised her were not her real family. She rapidly cut off all contact with them and talked about wanting to find her “real mother”. Lian also said that the CIA was searching for her. When questioned about why this should be the case, she was unable to say. (Based on Feeney et al.,  2002 ).

Why should immigration be associated with an elevated risk of developing schizophrenia? One possibility is that immigrants are more likely to receive this diagnosis because of cultural misunderstandings (Sashidharan,  1993 ). However, there is no convincing evidence that this is the case (Harrison et al.,  1999 ; Takei et al.,  1998 ). Another hypothesis is that people who are genetically predisposed to develop schizophrenia are more likely to move to live in another country. However, some of the impairments associated with the early stages of schizophrenia seem incompatible with this idea because negative symptoms and frontal lobe dysfunctions may make it harder to be organized enough to emigrate (see Cantor-Graae & Selten,  2005 ).

Perhaps the strongest clue comes from the finding that immigrants with darker skin have a much higher risk of developing schizophrenia than do immigrants with lighter skin (Cantor-Graae & Selten,  2005 ). This raises the possibility that experiences of being discriminated against could lead some immigrants to develop a paranoid and suspicious outlook on the world, which could set the stage for the development of schizophrenia. In support of this idea, the results of a prospective study show that healthy people who felt discriminated against were more likely to develop psychotic symptoms over time than were healthy people who did not perceive any discrimination (Janssen et al.,  2003 ). Another possibility suggested by animal studies is that the stress that results from social disadvantage and social defeat may have an effect on dopamine release or dopamine activity in key neural circuits (Tidey & Miczek,  1996 ). Moreover, some of these biological changes could make people more sensitive to the effects of using illicit substances (Miczek et al.,  2004 ). This is especially interesting in light of evidence linking cannabis abuse to the development of schizophrenia.

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Immigration has been found to be a risk factor for developing schizophrenia. People who leave their native land to live in another country have almost 3 times the risk of developing schizophrenia compared to people who remain living in their home country. What factors may contribute to this increased risk?

CANNABIS ABUSE

People with schizophrenia are twice as likely as people in the general population to smoke cannabis (van Os et al.,  2002 ). This has prompted researchers to ask whether there is a causal link between cannabis abuse and the development of psychosis. A methodologically rigorous study of conscripts to the Swedish army shows that, compared to those who had never used cannabis, young men who were heavy cannabis users by the time they were 18 were more than 6 times more likely to have developed schizophrenia 27 years later (Zammit et al.,  2002 ). This association also remained even after people who had used other kinds of drugs were removed from the statistical analysis.

Other studies have now replicated this link (Arsenault et al.,  2002  2004 ; Fergusson et al.,  2003 ; van Os et al.,  2002 ) and highlighted early cannabis use as being particularly problematic. For example, Arsenault and colleagues ( 2002 ) report that 10.3 percent of those who used cannabis by age 15 were diagnosed with signs of schizophrenia by age 26, compared with only 3 percent of the controls who did not use cannabis. Taken together, the research findings suggest that using cannabis during adolescence more than doubles a person’s risk of developing schizophrenia at a later stage of life.

A major methodological concern in studies of this kind is whether people who are in the early stages of developing psychosis are more likely to use cannabis. If this were the case, cannabis use would simply be a correlate of schizophrenia and not a cause. However, even after childhood psychotic symptoms are considered and accounted for statistically, cannabis use has still been found to be a predictor of later schizophrenia (Fergusson et al.,  2003 ). Moreover, a meta-analysis involving 8,167 patients with psychosis has shown that those who used cannabis (but not those who used alcohol) had an earlier onset of their symptoms compared to nonusers. These findings are consistent with the idea that cannabis use might trigger or bring forward the onset of psychosis (Large et al.,  2011 ).

Of course, the vast majority of people who use cannabis do not develop schizophrenia. So can we predict who is at higher risk? Using a large population sample, Caspi and colleagues ( 2005 ) have reported that people who carry a particular form of the COMT gene (one or two copies of the valine or val allele) are at increased risk for developing psychotic symptoms (hallucinations or delusions) in adulthood if they used cannabis during adolescence. In contrast, using cannabis has no adverse influence on those who have a different form of the COMT gene (two copies of the methionine or met allele). This is an exciting finding because it illustrates the importance of gene–environment interactions in the development of schizophrenia (see  Figure 13.9  on p. 474).

Why should the val allele of the COMT gene be a risk factor? We do not know exactly. However, the finding is provocative because the COMT gene (which you may recall is on chromosome 22) codes for a protein that plays a role in the breakdown of dopamine. One of the active ingredients of cannabis (called THC) is also thought to increase the synthesis of dopamine. We further know that cannabis makes symptoms worse in patients who already have schizophrenia (D’Souza et al.,  2005 ). So again, we have evidence of the importance of dopamine in schizophrenia and of the problems associated with cannabis use, although how everything fits together remains to be discovered.

Finally, we note that new research is showing that cannabis may actually accelerate the progressive brain changes that seem to go along with schizophrenia. Rais and colleagues ( 2008 ) collected brain scan data from 51 patients with recent-onset schizophrenia and 31 healthy controls. Nineteen of the patients were using cannabis (but not other illicit drugs) and 32 patients were not. When MRI scans were conducted again 5 years later, the patients who had continued to use cannabis during this time showed more marked decreases in brain volume relative to the patients who did not use cannabis. The changes in gray matter (brain cell) volume in the healthy controls, cannabis-using patients, and patients who did not use cannabis over the 5-year period are shown in  Figure 13.10  on page 474. Although both groups of patients lost more brain tissue over time than the healthy controls did, loss of brain tissue was especially pronounced in the patients who used cannabis. The conclusion is obvious. If you have schizophrenia, cannabis is probably very bad for your brain.

A Diathesis-Stress Model of Schizophrenia

Biological factors undoubtedly play a role in the etiology of schizophrenia. But genetic predispositions can be shaped by environmental factors such as prenatal exposures, infections, and stressors that occur during critical periods of brain development. Favorable environments may also reduce the chance that a genetic predisposition will result in schizophrenia. As we have discussed, children at genetic risk who are adopted into healthy family environments do very well (Tienari et al.,  2004 ; Wahlberg et al.,  1997 ). What you should take away from this section of the chapter therefore is an understanding that schizophrenia is a genetically influenced, not a genetically determined, disorder (Gottesman,  2001 ).

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FIGURE 13.9 Cannabis Use in Adolescence and Psychosis in Adulthood in People with Different Forms of the COMT Gene. (A) People with the val/val form of the COMT gene who use cannabis in adolescence are at increased risk for early schizophrenia at age 26. (B) People with one or two val alleles who use cannabis in adolescence also report more psychotic symptoms at age 26.

Source: Figure on p. 1123 from Caspi et al. ( 2005 ). Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: Longitudinal evidence of a gene X environment interaction. Biological Psychiatry, 57 (10), 1117–27. Reprinted with permission from Elsevier.

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FIGURE 13.10 Brain Volume Changes Over 5 years in Schizophrenia Patients and Healthy Comparison Subjects. Patients with schizophrenia who also use cannabis show more loss of gray matter over the course of a 5-year follow-up than patients who do not use cannabis or healthy controls.

Source: American Journal of Psychiatry. Online by Rais. Copyright 2009 by American Psychiatric Association (Journals). Reproduced with permission of American Psychiatric Association (Journals) in the format Textbook via Copyright Clearance Center.

The diathesis-stress model, whose origins largely derive from schizophrenia research, predicts exactly these sorts of scenarios (e.g., Walker & Diforio,  1997 ; Zubin & Spring,  1977 ).  Figure 13.11  on page 475 provides a general summary of the interplay between genetic factors, prenatal events, brain maturational processes, and stress in the development of schizophrenia.

The bottom line is that there is no simple answer to the question of what causes schizophrenia. The etiology of this disorder (or group of related disorders) is complicated and complex. In the case of a person who develops schizophrenia, predisposing genetic factors must have combined in additive and interactive ways with multiple environmental risk factors, some known and some still unknown, that operate prenatally, perinatally, and also postnatally (see Gottesman,  2001 ; Walker & Tessner,  2008 ). The net result of this is that brain pathways develop abnormally. It is also very likely that these same pathways can be damaged in a host of different ways (in much the same way as a car engine can be damaged by lack of oil, lack of coolant, or from using the wrong kind of fuel). In other words, lots of roads may lead to the same end point, which is schizophrenia or a schizophrenia-like illness. This helps explain why past efforts to find the single cause of schizophrenia were doomed to fail, although no one could know this at the time. How we are born and how we live makes a major contribution. As one researcher has so aptly stated, “Schizophrenia may be the uniquely human price we pay as a species for the complexity of our brain; in the end, more or less by genetic and environmental chance, some of us get wired for psychosis” (Gilmore,  2010 , p. 9).

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FIGURE 13.11 A Diathesis-Stress Model of Schizophrenia. Genetic factors and acquired constitutional factors (such as prenatal events and birth complications) combine to result in brain vulnerability. Normal maturational processes, combined with stress factors (family stress, cannabis use, urban living, immigration, etc.), may push the vulnerable person across the threshold and into schizophrenia.

in review

·  • What evidence supports a genetic contribution to schizophrenia?

·  • What is the dopamine hypothesis? Describe the current status of this explanation for schizophrenia.

·  • What neuroanatomical abnormalities differentiate people with schizophrenia from people who do not suffer from this disorder?

·  • What environmental factors are important in the development of schizophrenia?

·  • Why is avoiding cannabis so important for people with schizophrenia?

·  • Why do we believe that schizophrenia is both a developmental and a neuroprogressive disorder?

·  • Why is the diathesis-stress perspective so appropriate for understanding schizophrenia?

Treatments and Outcomes

Before the 1950s the prognosis for schizophrenia was bleak. Treatment options were very limited. Agitated patients might be put in straitjackets or treated with electroconvulsive “shock” therapy. Most lived in remote and forbidding institutions that they were expected never to leave (Deutsch,  1948 ).

Dramatic improvement came in the 1950s when a class of drugs known as antipsychotics were introduced. Pharmacotherapy (treatment by drugs) with these medications rapidly transformed the environment of mental hospitals by calming patients and virtually eliminating their wild, dangerous, and out-of-control behaviors. A new and more hopeful era had arrived.

Clinical Outcome

Studies of clinical outcome show that 15 to 25 years after developing schizophrenia, around 38 percent of patients have a generally favorable outcome and can be thought of as being recovered (Harrison et al.,  2001 ). This does not mean that patients return to how they were before they became ill, however. Rather, it means that with the help of therapy and medications, patients can function quite well. For a minority of patients (around 12 percent), long-term institutionalization is necessary. And around a third of patients show continued signs of illness, usually with prominent negative symptoms.

When more stringent criteria are used to define recovery (i.e., remission of symptoms and good general social functioning with improvements in at least one of these areas lasting 2 years or more) rates of recovery are even more modest. Recent estimates suggest that they are around 14 percent (Jääskeläinen et al.,  2013 ). What this means is that, despite many advances in treatment over the last 50 to 60 years, a “cure” for schizophrenia has not materialized.

Interestingly, patients who live in less industrialized countries tend to do better overall than patients who live in more industrialized nations (Jablensky et al.,  1992 ). This may be because levels of EE are much lower in countries such as India than in the United States and Europe. For example, in highly industrialized cultures, more than 50 percent of families are high in EE. In contrast, studies with Mexican American and Hindi-speaking Indian samples show that only 24 percent and 41 percent of families, respectively, are high in EE (see Karno et al.,  1987 ; Leff et al.,  1987 ). These differences may help explain why the clinical outcome of patients is different in different parts of the world.

Sometimes, patients who have been very severely impaired by schizophrenia show considerable improvement late in the course of their illness. As illustrated in the case on page 476, these spontaneous improvements can occur even when there is no change in the medications that patients are taking.

MORTALITY

The health risks of having schizophrenia cannot be understated. This is a disorder that reduces life expectancy. Recent data from the United Kingdom show that men with schizophrenia die 14.6 years earlier than would be expected based on national norms. For women with schizoaffective disorder the reduction in lifespan is 17.5 years (Chang et al.,  2011 ). Some of the factors implicated in the early deaths of patients with schizophrenia and schizophrenia-related illnesses are long-term use of antipsychotic medications, obesity, smoking, poor diet, use of illicit drugs, and lack of physical activity. The risk of suicide in patients with schizophrenia is also high compared to the general population, with about 12 percent of patients ending their lives in this way (Dutta et al.,  2010 ). In general, overall mortality is lower in patients who are treated with antipsychotic medications compared to untreated patients (Tiihonen et al.,  2011 ). This no doubt reflects the extent to which people who are actively psychotic are a risk to themselves.

From Impairment to Improvement The patient is a 46-year-old man who first became ill when he was 17 years old. At the time his illness began, he was hearing voices and he had grandiose delusions. He also had delusions of being persecuted.

By the time he was 30, he was living in the hospital. He experienced continuous symptoms including delusions, hallucinations, and incoherent speech. His self-care was also very poor. His symptoms showed only minimal improvement after he was treated with clozapine.

Spontaneous clinical improvement was noted when the patient was in his 40s. He became less isolated and he began to spend more time doing activities. Although he had previously been incoherent when he spoke, he began to speak rationally, although there was still some poverty in the content of his speech. His self-care also improved. However, hospital staff still needed to prompt him to bathe and change his clothes.

Source: Adapted from Murray et al.,  2004 .

Pharmacological Approaches

Medications are widely used in the treatment of schizophrenia. Over 60 different antipsychotic drugs have been developed. The common property that they all share is their ability to block dopamine D2 receptors in the brain (Seeman,  2011 ).

FIRST-GENERATION ANTIPSYCHOTICS

First-generation  anti-psychotics  are medications like chlorpromazine (Thorazine) and haloperidol (Haldol), which were among the first to be used to treat psychotic disorders. Sometimes referred to as  neuroleptics  (literally, “seizing the neuron”), these medications revolutionized the treatment of schizophrenia when they were introduced in the 1950s and can be regarded as one of the major medical advances of the twentieth century (Sharif et al.,  2007 ). They are called first-generation antipsychotics (or typical antipsychotics) to distinguish them from a new class of antipsychotics that was developed much more recently. These are referred to as second-generation (or atypical) antipsychotics.

There is overwhelming evidence that antipsychotic medications help patients. Large numbers of clinical trials have demonstrated the efficacy and effectiveness of these drugs (Sharif et al.,  2007 ). Also, the earlier patients receive these medications, the better they tend to do over the longer term (Marshall et al.,  2005 ; Perkins et al.,  2004 ). As we discussed earlier, first-generation antipsychotics are thought to work because they are dopamine antagonists. This means that they block the action of dopamine, primarily by blocking (occupying) the D2 dopamine receptors.

Some clinical change can be seen within the first 24 hours of treatment (Kapur et al.,  2005 ). This supports the idea that these medications work by interfering with dopamine transmission at the D2 receptors because dopamine blockade begins within hours after the patient is given the medication. However, it may take several weeks or even months for maximal clinical benefit to be achieved, although how a patient does on a particular medication in the first 2 to 4 weeks of treatment is a good predictor of how much he or she will benefit overall (Tandon et al.,  2010 ).

First-generation antipsychotics work best for the positive symptoms of schizophrenia. In quieting the voices and diminishing delusional beliefs, these medications provide patients with significant clinical improvement (Tandon et al.,  2010 ). This comes at a cost, however. Common side effects of these medications include drowsiness, dry mouth, and weight gain. Many patients on these antipsychotics also experience what are known as extrapyramidal side effects (EPS). These are involuntary movement abnormalities (muscle spasms, rigidity, shaking) that resemble Parkinson’s disease.

African Americans and other ethnic minorities appear to be at increased risk of extrapyramidal side effects (Lawson,  2008 ). Such side effects are usually controlled by taking other medications. Some patients who have been treated with neuroleptics for long periods of time may also develop tardive dyskinesia. This involves marked involuntary movements of the lips and tongue (and sometimes the hands and neck). Rates of tardive dyskinesia are about 56 percent when patients have taken neuroleptics for 10 years or more, with females being especially susceptible (Bezchlibnyk-Butler & Jeffries,  2003 ). Finally, in very rare cases there is a toxic reaction to the medication that is called neuroleptic malignant syndrome (Strawn et al.,  2007 ). This condition is characterized by high fever and extreme muscle rigidity, and if left untreated it can be fatal.

SECOND-GENERATION ANTIPSYCHOTICS

In the 1980s a new class of antipsychotic medications began to appear. The first of these to be used clinically was clozapine (Clozaril). This drug was introduced in the United States in 1989, although clinicians in Europe had been using it prior to this. Although initially reserved for use with treatment-refractory patients (those who were not helped by other medications), clozapine is now used widely.

Other examples of second-generation antipsychotic medications are risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel), and ziprasidone (Geodon). More recent additions include aripiprazole (Abilify) and lurasidone (Latuda). The reason why these medications are called “second-generation anti-psychotics” is that they cause fewer extrapyramidal symptoms than the earlier antipsychotic medications such as Thorazine and Haldol. Although it was initially believed that second-generation antipsychotics were more effective at treating the symptoms of schizophrenia, recent research findings provide no support for this view (Lieberman & Stroup,  2011 ; Tandon et al.,  2010 ). The exception here concerns clozapine, which does seem to be more valuable than other medications for treatment refractory patients. Nonetheless, most patients are now treated with these newer (and more expensive) medications.

Although they are less likely to cause movement problems, the newer neuroleptic medications are not without other side effects. Drowsiness and considerable weight gain are very common. Diabetes is also a very serious concern (Sernyak et al.,  2002 ). In rare cases, clozapine also causes a life-threatening drop in white blood cells known as agranulocytosis. For this reason, patients taking this medication must have regular blood tests.

The disappointing findings about the efficacy of second-generation antipsychotic treatments mean that there is an urgent need for innovative approaches and new medications that work better than the ones currently available. This is all the more important in light of new research showing that antipsychotic medications may actually contribute to the progressive brain tissue loss we see in schizophrenia (Ho et al.,  2011 ). In the meantime, researchers continue to seek other ways to help patients.

OTHER APPROACHES

At the beginning of the chapter, you learned that women with schizophrenia tend to do better than men. They have a later age of onset and, often, seem to have a less severe form of the illness. This has prompted some researchers to explore the potentially beneficial role of estrogen in the treatment of the disorder (Begemann et al.,  2012 ).

In an interesting study, 102 young women with schizophrenia (all of whom were receiving antipsychotic medications) were randomly assigned to one of two conditions (Kulkarni et al.,  2008 ). Some were given a transdermal (skin) patch containing estrogen; the others received a similar (placebo) patch that contained no active ingredient. The women’s symptoms were assessed at baseline. They then wore the patches for a period of 28 days, receiving new patches twice a week. At the end of the study period, symptoms were reassessed.

What were the findings? Remarkably, the women who had worn the genuine (estrogen containing) patches reported significantly fewer overall symptoms at the end of the 1-month study compared to the placebo group, with the difference for positive symptoms (shown in  Figure 13.12 ) being most striking. Overall, the results suggest that estrogen has antipsychotic effects and that providing supplemental estrogen to women with schizophrenia may give them additional clinical benefits.

THE PATIENT’S PERSPECTIVE

Not all patients benefit from antipsychotic medications, and many who do show clinical improvement will still have problems functioning without a great deal of additional help. We must also not lose sight of what it is like for patients with schizophrenia to have to take medications every day, often for years or for a lifetime. Side effects that can sound trivial to someone on the outside can be so bad for patients that they refuse to take their medications, even when those medications give them relief from their hallucinations and delusions.

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FIGURE 13.12 Estrogen Treatment and Positive Symptoms. Positive symptoms at baseline (day 0) and on days 7, 14, 21, and 28 for the estrogen and placebo groups.

Source: Figure 3 from Kulkarni et al. ( 2008 ). Archives of General Psychiatry, 65(8), 958 (Copyright © 2008). American Medical Association. Reprinted with permission.

Research using PET also shows that increased blockade of D2 dopamine receptors is associated with patients reporting more negative subjective experiences such as feeling tired and depressed even when other side effects (such as movement problems) are absent (Mizrahi et al.,  2007 ). This highlights the need for better medications and for using lower dosages wherever this is clinically feasible. We also need to remember that some patients may try to avoid taking medications because, to them, needing to take medications confirms that they are mentally ill. The following comes from the mother of a daughter who suffers from schizophrenia:

·  As a parent I also know that medication is not perfect and that the side effects can be distressing. When my daughter goes back on her medication, I feel bad seeing her shuffling or experiencing involuntary arm and mouth movements. These symptoms usually subside over time; but she also gains weight, and she hates being heavy. I think she hates taking medication most of all because she is, in a sense, admitting she is mentally ill, something she very much wants to deny. (From Slater,  1986 .)

Psychosocial Approaches

Medications play a central role in the treatment of schizophrenia. But they are not the only treatment approaches that are available. Psychosocial treatments are also of value. Some of these approaches, which are typically used in conjunction with medication, are briefly described below.

FAMILY THERAPY

The literature that links relapse in patients with schizophrenia to high family levels of EE inspired several investigators to develop family intervention programs. The idea was to reduce relapse in schizophrenia by changing those aspects of the patient–relative relationship that were regarded as central to the EE construct. At a practical level, this generally involves working with patients and their families to educate them about schizophrenia, to help them improve their coping and problem-solving skills, and to enhance communication skills, especially the clarity of family communication.

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Patients with schizophrenia benefit from psychosocial treatments. These include individual therapy, case management, cognitive remediation, and family therapy.

In general, the results of research studies in this area have shown that patients do better clinically and relapse rates are lower when families receive family treatment (see Pfammatter et al.,  2006 ). Studies done in China indicate that these treatment approaches can also be used in other cultures (Xiong et al.,  1994 ). Despite this, family treatment is still not a routine element in the accepted standard of care for patients with schizophrenia (Lehman et al.,  1998 ). Given its clear benefits to patients and its considerable cost-effectiveness (Tarrier et al.  1991  calculated that family treatment results in an average cost savings of 27 percent per patient), this seems very unfortunate.

CASE MANAGEMENT

Case managers are people who help patients find the services they need in order to function in the community. Essentially, the case manager acts as a broker, referring the patient to the people who will provide the needed service (e.g., help with housing, treatment, employment, and the like). Assertive community treatment programs are a specialized and more intensive form of case management. Typically, they involve multidisciplinary teams with limited caseloads to ensure that discharged patients don’t get overlooked and “lost in the system.” The multidisciplinary team delivers all the services the patient needs (see DeLuca et al.,  2008 ; Mueser et al.,  2013 ).

Assertive community treatment programs are cost-effective because they reduce the time that patients spend in the hospital. They also enhance the stability of patients’ housing arrangements. These approaches seem to be especially beneficial for patients who are already high utilizers of psychiatric and community services (see Bustillo et al.,  2001 ).

SOCIAL-SKILLS TRAINING

Even when their symptoms are controlled by medications, patients with schizophrenia often have trouble forming friendships, finding and keeping a job, or living independently. How well patients do in their everyday lives is referred to as functional outcome. (This is in contrast to clinical outcome, which is concerned with symptoms.) Improving the functional outcomes of patients with schizophrenia is now an active area of research.

One way to help improve the functional outcomes of patients with schizophrenia is through social-skills training. Patients with schizophrenia often have very poor interpersonal skills (for a review, see Hooley,  2008 ). Social-skills training is designed to help patients acquire the skills they need to function better on a day-to-day basis. These skills include employment skills, relationship skills, self-care skills, and skills in managing medications or symptoms. Social routines are broken down into smaller, more manageable components. For conversational skills, these components might include learning to make eye contact, speaking at a normal and moderate volume, taking one’s turn in a conversation, and so on. Patients learn these skills, get corrective feedback, practice their new skills using role-playing, and then use what they have learned in natural settings (Bellack & Mueser,  1993 ). As Green ( 2001 , p. 139) has noted, engaging in social-skills training is a bit like taking dance lessons. It does not resemble traditional “talk therapy” in any obvious manner.

Although the results of some early studies were mixed, the most recent research findings look more positive. Social-skills training does seem to help patients acquire new skills, be more assertive, and improve their overall levels of social functioning. These improvements also seem to be maintained over time. Importantly, patients who receive social-skills training are less likely to relapse and need hospital treatment (Kurtz & Mueser,  2008 ; Pfammatter et al.,  2006 ).

COGNITIVE REMEDIATION

Earlier we described some of the cognitive problems that go along with having schizophrenia. Researchers are now recognizing that these cognitive problems are likely to place limits on how well patients can function in the community. Because of this, the neurocognitive deficits of schizophrenia are becoming targets for treatment in their own right. The search is on to develop new medications that will enhance cognitive functioning in patients (Green,  2007 ; Nuechterlein et al.,  2008 ).

A major treatment effort is also being devoted to  cognitive remediation  training. Using practice and other compensatory techniques, researchers are trying to help patients improve some of their neurocognitive deficits (e.g., problems with verbal memory, vigilance, and performance on card-sorting tasks). The hope is that these improvements will translate into better overall functioning (e.g., conversational skills, self-care, job skills, and so on). Overall, the findings give cause for optimism. Cognitive remediation training does seem to help patients improve their attention, memory, and executive functioning skills. Patients who receive cognitive remediation training also show improvements in their social functioning. Especially encouraging is that even when patients have been ill for many years, they still seem to benefit from this treatment approach (Pfammatter et al.,  2006 ; Wykes et al.,  2007 ). Cognitive remediation approaches may work best when they are added to other existing rehabilitation (employment skills) strategies and offered to patients who are already clinically stable (Wykes et al.,  2011 ).

COGNITIVE-BEHAVIORAL THERAPY

As you have already learned, cognitive-behavioral therapy (CBT) approaches are widely used in the treatment of mood and anxiety disorders as well as many other conditions (Beck,  2005 ). Until fairly recently, however, researchers did not consider using them for patients with schizophrenia, no doubt because patients with schizophrenia were considered too impaired. Pioneered by researchers and clinicians in the United Kingdom, cognitive-behavioral approaches have gained momentum in the treatment of schizophrenia. The goal of these treatments is to decrease the intensity of positive symptoms, reduce relapse, and decrease social disability. Working together, therapist and patient explore the subjective nature of the patient’s delusions and hallucinations, examine evidence for and against their veracity or veridicality, and subject delusional beliefs to reality testing.

Although the results from the early research studies were encouraging, whether CBT is an effective treatment for schizophrenia is now the subject of some debate. Current data suggest that CBT is not very helpful for negative symptoms (Tandon et al.,  2010 ). A recent meta-analysis also suggests that CBT is no better than control interventions (often supportive counselling) in the treatment of schizophrenia (Lynch et al.,  2010 ). Nonetheless, the possibility that CBT works very well for some subgroups of patients is still a very real possibility.

INDIVIDUAL TREATMENT

Before 1960 the optimal treatment for patients with schizophrenia was psychoanalytically oriented therapy based on a Freudian type of approach. This is what Nobel Prize–winning mathematician John Nash received when he was a patient at McLean Hospital in Massachusetts in 1958 (the movie A Beautiful Mind is based on Nash’s story). By 1980, however, things had changed. Research began to suggest that in some cases, psychodynamic treatments made patients worse (see Mueser & Berenbaum,  1990 ). This form of individual treatment thus fell out of favor.

Individual treatment for schizophrenia now takes a different form. Hogarty and colleagues ( 1997a  1997b ) have reported on a controlled 3-year trial of what they call “personal therapy.” Personal therapy is a nonpsychodynamic approach that equips patients with a broad range of coping techniques and skills. The therapy is staged, which means that it comprises different components that are administered at different points in the patient’s recovery. For example, in the early stages, patients examine the relationship between their symptoms and their stress levels. They also learn relaxation and some cognitive techniques. Later, the focus is on social and vocational skills. Overall, this treatment appears to be very effective in enhancing the social adjustment and social role performance of discharged patients.

Educating patients about the illness and its treatment (this approach is called psychoeducation) is also helpful (Xia et al.,  2011 ). Patients who receive psychoeducation in addition to standard treatment are less likely to relapse or be readmitted to the hospital compared to patients who receive standard treatment only. These patients also function better overall and are more satisfied with the treatment they receive. All of this highlights the importance of including patients in their own care and increasing their knowledge and understanding about their illness.

In summary, although rigorous psychoanalytic approaches may be too demanding and stressful for patients with schizophrenia, supportive forms of therapy that offer an opportunity to learn skills and yet are low-key and responsive to patients’ individual concerns might well be very beneficial. Just as progress in research on schizophrenia requires a partnership between scientists across many areas, progress in the treatment of schizophrenia requires balancing pharmacology with a consideration of the specific needs of the patient. For patients who are at high risk of relapse and who live with their families, family-based interventions will be required. If patients have continuing and disturbing hallucinations and delusions, CBT may be appropriate. When patients are clinically stable, social-skills training and rehabilitation efforts may be helpful. But in all of this, we must not lose sight of the need of patients (and their families) for support, validation, and respectful care. The treatment of patients with schizophrenia is not easy, and there is no “quick fix.” Although many treatment advances have occurred, we still need more effective, high quality, and clinically sensitive care.

in review

·  • What kinds of clinical outcomes are associated with schizophrenia? Is full recovery possible or typical?

·  • Why do patients with schizophrenia have increased rates of early mortality?

·  • In what ways are first- and second-generation (conventional and atypical) neuroleptic medications similar, and in what ways are they different? How effective are these treatments for patients with schizophrenia?

·  • Describe the major psychosocial approaches used in treating schizophrenia.

UNRESOLVED issues: Why are recovery rates in schizophrenia not improving?

After the introduction of the first neuroleptic medication (Thorazine) in 1955, there was great optimism that this, and other new “wonder drugs” would revolutionalize the treatment of schizophrenia. Today, many decades later, clinicians have a broad array of first- and second-generation antipsychotic medications at their disposal. But if our treatment options are so much more sophisticated, why are recovery rates in schizophrenia so low?

The standard length of a clinical trial that compares a given drug against a placebo is 6 weeks. Numerous clinical studies have demonstrated that antipsychotic medications are effective for the treatment of acute symptoms. So there is little doubt that antipsychotic medications benefit patients in the short term.

But what about the longer term? Does staying on antipsychotic medications provide long-term benefits for patients?

The answer may be no. Concerns are now being raised that long-term exposure to neuroleptics may set into play biological process that increase the likelihood that patients will remain chronically ill (Whitaker,  2010 ). This is particularly worrisome because patients who take neuroleptic medications tend to stay on them for very long periods of time.

But how could something that is clinically beneficial in the short term be potentially harmful in the longer term? Standard anti-psychotic medications block D2 receptors in the brain. This is the basis of their therapeutic action. But one result of dopamine blockade is that the density of receptors on the post-synaptic neuron increases, creating a supersensitivity to dopamine. Put more simply, neuroleptics put a brake on dopamine transmission. To compensate for this, the brain responds by pressing the dopamine accelerator (in the form of extra dopamine receptors). Withdrawal of neuroleptics removes the brake and puts the system out of balance because the system is now in an “accelerator-on” mode. Moreover, any return of symptoms is taken as evidence that the drugs were working and preventing relapse. This impression gets confirmed when the patient goes back on drugs again and the psychosis abates. As one physician noted, “The use of neuroleptics is a trap. … It is like having a psychosis-inducing agent built into the brain.” (Whitaker,  2010 , pp. 107).

As you might expect, the idea that antipsychotic medications may help psychosis in the short term but create it in the longer term is highly controversial. However, it may not be as far fetched as it might seem. Data from a 15-year follow-up study show that over time, patients with schizophrenia who are not taking antipsychotic medications fare far better than those who continue to take medications (Harrow,  2007 ). However, difference in recovery rates between the medicated and unmedicated groups only really start to be apparent after about 4.5 years. It is also the case that patients who stop taking medications tend not to see their psychiatrists. So clinicians don’t see the people who recover. This may be one reason why psychiatry as a whole has been slow to recognize that non-medicated patients might be doing far better than expected. Also relevant here is the observation that patients in less industrialized countries tend to do better clinically than those in more developed countries. And these are the very patients who are much less likely to be maintained on antipsychotic medications.

Perhaps most provocative are the following statistics about chronic mental illness. In 1955 one in every 617 Americans was hospitalized with schizophrenia in a state or county mental hospital. These were chronic long-term patients. Today, the proportion of people with chronic schizophrenia or some other psychotic disorder is much higher—1 in every 125 people. In his efforts to understand why psychiatric medications have not improved the long-term clinical outcomes for patients with severe mental illness, Whitaker (who is an investigative reporter) has caused a storm of controversy. Nonetheless, his arguments warrant serious consideration by all mental health professionals. If the medications that are so helpful in a crisis make things worse when used long term, we need to radically re-think how we manage the treatment of patients with schizophrenia.

13 summary

·  13.1 What are the symptoms of schizophrenia?

·  • Schizophrenia is the most severe form of mental illness. It is characterized by impairments in many domains. Characteristic symptoms of schizophrenia include hallucinations, delusions, disorganized speech, disorganized and catatonic behavior, and negative symptoms such as flat affect or social withdrawal.

·  13.2 What is the prevalence of schizophrenia and when does it begin? who is most affected?

·  • Schizophrenia affects just under 1 percent of the population. Most cases begin in late adolescence or early adulthood. The disorder begins earlier in men than in women. Overall, the clinical symptoms of schizophrenia tend to be more severe in men than in women. Women also have a better long-term outcome.

·  • Even though schizophrenia first shows itself clinically in early adulthood, researchers believe that it is a neurodevelopmental disorder. Problems with brain development are implicated. Some of the genes implicated in schizophrenia play a role in brain development.

·  13.3 What are the risk and causal factors associated with schizophrenia?

·  • Genetic factors are clearly implicated in schizophrenia. Having a relative with the disorder significantly raises a person’s risk of developing schizophrenia.

·  • Other factors that have been implicated in the development of schizophrenia include prenatal exposure to the influenza virus, early nutritional deficiencies, rhesus incompatibility, maternal stress, and perinatal birth complications.

·  • Urban living, immigration, and cannabis use during adolescence have also been shown to increase the risk of developing schizophrenia.

·  • Current thinking about schizophrenia emphasizes the interplay between genetic and environmental factors.

·  13.4 How is the brain affected in schizophrenia?

·  • Patients with schizophrenia have problems in many aspects of their cognitive functioning. They show a variety of attentional deficits (e.g., poor P50 suppression and deficits on the Continuous Performance Test). They also show eye-tracking dys-functions.

·  • Many brain areas are abnormal in schizophrenia, although abnormalities are not found in all patients. The brain abnormalities that have been found include enlarged ventricles (which reflects decreased brain volume), frontal lobe dysfunction, reduced volume of the thalamus, and abnormalities in temporal lobe areas such as the hippocampus and amygdala.

·  • Major changes in the brain occur during adolescence. These include synaptic pruning, decreases in the number of excitatory neurons, and increases in the number of inhibitory neurons. There is also an increase in white matter which enhances the connectivity of the brain. Some of these changes may be abnormal in people who will later develop schizophrenia.

·  • Some of the brain abnormalities that are characteristic of schizophrenia get worse over time. This suggests that, in addition to being a neurodevelopmental disorder, schizophrenia is also a neuroprogressive disorder.

·  13.5 What neurotransmitters are implicated in schizophrenia?

·  • The most important neurotransmitters implicated in schizophrenia are dopamine and glutamate. Research shows that the dopa-mine (D2) receptors of patients with schizophrenia are supersensitive to dopamine.

·  13.6 Why is the family environment important for the well-being of patients with schizophrenia?

·  • Patients with schizophrenia are more likely to relapse if their relatives are high in expressed emotion (EE). High-EE environments may be stressful to patients and may trigger biological changes that cause dysregulations in the dopamine system. This could lead to a return of symptoms.

·  13.7 What is the clinical outcome of schizophrenia and how is it treated?

·  • For many patients, schizophrenia is a chronic disorder requiring long-term treatment or institutionalization. However, when treated with therapy and medications, around 38 percent of patients can show a reasonable recovery. Only about 14 percent of patients recover to the extent that they have minimal symptoms and function well socially.

·  • Patients with schizophrenia are usually treated with first- or second-generation antipsychotic (neuroleptic) medications. Second-generation antipsychotics are about as effective as first-generation anti-psychotics but cause fewer extrapyramidal (motor abnormality) side effects. Antipsychotic drugs work by blocking dopamine receptors.

·  • Psychosocial treatments for patients with schizophrenia include cognitive-behavioral therapy, social-skills training, cognitive remediation training, and other forms of individual treatment, as well as case management. Family therapy provides families with communication skills and other skills that are helpful in managing the illness. Family therapy also reduces high levels of expressed emotion.

key terms

·  alogia  450

·  antipsychotics (neuroleptics)  476

·  attenuated psychosis syndrome  462

·  avolition  450

·  brief psychotic disorder  452

·  candidate genes  458

·  catatonic schizophrenia  451

·  cognitive remediation  478

·  delusion  446

·  delusional disorder  452

·  disorganized schizophrenia  451

·  disorganized symptoms  450

·  dopamine  468

·  endophenotypes  458

·  expressed emotion (EE)  471

·  flat affect  450

·  glutamate  470

·  hallucination  448

·  linkage analysis  457

·  negative symptoms  450

·  paranoid schizophrenia  451

·  positive symptoms  450

·  prodromal  462

·  psychosis  444

·  schizoaffective disorder  451

·  schizophrenia  444

·  schizophreniform disorder  451

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