PSYCH 14

Misconceptions about abnormal behavior are common. Consequently, we need to clear up some preliminary issues before we describe the various types of disorders. In this section, we will discuss (1) the medical model of abnormal behavior, (2) the criteria of abnormal behavior, and (3) the classification of psychological disorders.

The Medical Model Applied to Abnormal Behavior

There’s no question that Howie Mandel’s extreme fear of germs is abnormal. But does it make sense to view his unusual and irrational behavior as an illness? This is a contro- versial question. The medical model proposes that it is useful to think of abnormal behavior as a disease. This point of view is the basis for many of the terms used to refer to abnormal behavior, including mental illness, psychological disorder, and psychopathology (pathology refers to manifestations of disease). The medical model gradually became the dominant way of thinking about abnormal behavior during the 18th and 19th centuries. Its influence remains very strong today.

The medical model clearly represented progress over earlier models of abnormal be- havior. Prior to the 18th century, most conceptions of abnormal behavior were based on superstition. People who behaved strangely were thought to be possessed by demons, to be witches in league with the devil, or to be victims of God’s punishment. The rise of the medical model brought improvements in the treatment of those who exhibited abnor- mal behavior. As victims of an illness, they were viewed with more sympathy and less hatred and fear. Although living conditions in early asylums were often deplorable, grad- ual progress was made toward more humane care of the mentally ill.

However, in recent decades, some critics have suggested that the medical model may have outlived its usefulness (Deacon, 2013; Vanheule, 2017). Some critics are troubled be- cause medical diagnoses of abnormal behavior pin potentially derogatory labels on people. Being labeled as psychotic, schizophrenic, or mentally ill carries a social stigma that can be difficult to shake. Those characterized as mentally ill are viewed as erratic, dangerous, incompetent, and inferior (Corrigan & Larson, 2008). These stereotypes promote distanc- ing, disdain, and rejection. This prejudice is a significant source of stress for people who endure mental illness (Rüsch et al., 2014). Perhaps even more important, the stigma asso- ciated with psychological disorders prevents many people from seeking the mental health care they need and could benefit from (Schomerus et al., 2018; Stolzenburg et al., 2017).

Unfortunately, the stigma associated with psychological disorders appears to be deeply rooted. In recent decades, research has increasingly demonstrated that many psychologi- cal disorders are at least partly attributable to genetic and biological factors, making them appear more similar to physical illnesses, which carry far less stigma (Pescosolido, 2010). These findings have been registered by a sizable portion of the general public (Schomerus et al., 2012). You would think that these trends would lead to a reduction in the stigma as- sociated with mental illness, but reviews of recent research suggest that the stigmatization of psychiatric disorders has actually increased (Larkings & Brown, 2018). How can we make sense of this perplexing paradox? Haslam and Kvaale (2015) review evidence that the rise of biogenetic explanations for mental illness have led to a decreased tendency to blame people with psychological disorders for their problems, which should reduce the stigma of mental illness. But biogenetic explanations have also led to increased tendencies to view psychological disorders as untreatable, and to view affected individuals as unpredictable and dangerous, thus leading to greater stigma. Unfortunately, in the eyes of the general pub- lic, the negative implications of biogenetic views may outweigh the favorable implications.

Another line of criticism has been voiced by Thomas Szasz (1974, 1990). He asserts that “strictly speaking, disease or illness can affect only the body; hence there can be no mental illness. . . . Minds can be ‘sick’ only in the sense that jokes are ‘sick’ or economies are ‘sick’” (1974, p. 267). He further argues that abnormal behavior usually involves a deviation from social norms rather than an illness. He contends that such deviations are “problems in liv- ing” rather than medical problems. According to Szasz, the medical model’s disease analogy converts moral and social questions about what is acceptable behavior into medical questions.

The criticism of the medical model clearly has merit, and it is important to recognize the social roots and ramifications of the medical model. However, the bottom line is that the medical model continues to dominate thinking about psychological disorders. Medical concepts such as diagnosis, etiology, and prognosis have proven valuable in the treatment and study of abnormality. Diagnosis involves distinguishing one illness from another. Etiology refers to the apparent causation and developmental history of an illness. A prognosis is a forecast about the probable course of an illness. These medi- cally based concepts have widely shared meanings that permit clinicians, researchers, and the public to communicate more effectively in their discussions about abnormal behavior.

Criteria of Abnormal Behavior

If your next-door neighbor scrubs his front porch twice every day and spends virtually all his time cleaning and recleaning his house, is he normal? If your sister-in-law goes to one physician after another seeking treatment for ailments that appear imaginary, is she psychologically healthy? How are we to judge what’s normal and what’s abnormal? More important, who’s to do the judging?

These are complex questions. In a sense, all people make judgments about normality in that they all express opinions about others’ (and perhaps their own) mental health. Of course, formal diagnoses of psychological disorders are made by mental health profes- sionals. In making these diagnoses, clinicians rely on a variety of criteria, the foremost of which are the following:

1. Deviance. As Szasz pointed out, people are often said to have a disorder because their behavior deviates from what their society considers acceptable. What constitutes normality varies somewhat from one culture to another. However, all cultures have such norms. When people violate these standards and expectations, they may be labeled mentally ill. For exam- ple, transvestic fetishism is a sexual disorder in which a man achieves sexual arousal by dress- ing in women’s clothing. This behavior is regarded as disordered because a man who wears a dress, brassiere, and nylons is deviating from our culture’s norms. This example illustrates the somewhat arbitrary nature of cultural standards regarding normality, as the same overt behavior (cross-sex dressing) is considered acceptable for women but deviant for men.

2. Maladaptive behavior. In many cases, people are judged to have a psychological dis- order because their everyday adaptive behavior is impaired. This is the key criterion in the diagnosis of substance use (drug) disorders. In and of itself, alcohol and drug use is not terribly unusual or deviant. However, when the use of cocaine, for instance, begins to interfere with a person’s social or occupational functioning, a substance use disorder ex- ists. In such cases, it is the maladaptive quality of the behavior that makes it disordered.

3. Personal distress. Frequently, the diagnosis of a psychological disorder is based on an individual’s report of great personal distress. This is usually the criterion met by people who are troubled by depression or anxiety disorders. Depressed people, for in- stance, may or may not exhibit deviant or maladaptive behavior. Such people are usually labeled as having a disorder when they describe their subjective pain and suffering to friends, relatives, and mental health professionals.

Although two or three criteria may apply in a particular case, people are often viewed as disordered when only one criterion is met. As you may have already noticed, diag- noses of psychological disorders involve value judgments about what represents normal or abnormal behavior (Sadler, 2005). These judgments reflect prevailing cultural values, social trends, and political forces, as well as scientific knowledge (Frances & Widiger, 2012; Kirk, Gomory, & Cohen, 2013).

Antonyms such as normal versus abnormal and mental health versus mental illness imply that people can be divided neatly into two distinct groups: those who are normal and those who are not. In reality, it is often difficult to draw a line that clearly separates nor- mality from abnormality (Wakefield, 2016). On occasion, everyone acts in deviant ways, everyone displays some maladaptive behavior, and everyone experiences

personal distress. People are judged to have psychological disorders only

when their behavior becomes extremely deviant, maladaptive, or dis-

tressing. Thus, normality and abnormality exist on a continuum. It’s a

matter of degree, not an either–or proposition (see Figure 14.1).

Psychodiagnosis: The Classification of Disorders

Lumping all psychological disorders together would make it extremely difficult to understand them better. A sound taxonomy of mental disorders can facilitate empiri- cal research and enhance communication among scientists and clinicians (First, 2015; Widiger & Crego, 2018). Thus, a great deal of effort has been invested in devising an elaborate system for classifying psychological disorders. This classification system, pub- lished by the American Psychiatric Association, is outlined in a book titled the Diagnostic and Statistical Manual of Mental Disorders. The current, fifth edition, titled DSM-5 was released in 2013. It was the product of more than a decade of research and sometimes heated debates (Kupfer, Kuhl, & Regier, 2013).

One major issue in the development of DSM-5 was whether to reduce the system’s commitment to a categorical approach. In recent years, many critics of the DSM system have questioned the fundamental axiom that the diagnostic system is built on: the as- sumption that people can reliably be placed in discontinuous (nonoverlapping) diag- nostic categories (Helzer et al., 2008). These critics note that there is enormous overlap among various disorders’ symptoms, making the boundaries between diagnoses much fuzzier than would be ideal. Critics have also pointed out that people often qualify for more than one diagnosis (Lilienfeld & Landfield, 2008).

Because of problems such as these, some theorists argue that the traditional categori- cal approach to diagnosis should be replaced by a dimensional approach. A dimensional approach would describe disorders in terms of how people score on a limited number of continuous dimensions, such as the degree to which they exhibit anxiety, depression, agitation, anger, hypochondria, rumination, paranoia, and so forth (Kraemer, 2008; Widiger, Livesley, & Clark, 2009). The practical logistics of shifting to a dimensional approach to psychological disorders proved formidable and controversial (Blashfield et al., 2014; Wakefield, 2016). Experts would have had to agree about which dimensions to assess and how to measure them. Because of difficulties such as these, the authorities developing DSM-5 chose to retain a categorical approach, although they supplemented the traditional system with dimensional approaches in some areas (Burke & Kraemer, 2014; Zachar, Krueger, & Kendler, 2016).

Another area of concern related to the DSM has been its nearly exponential growth (Escobar & Marin, 2017). The number of specific diagnoses in the DSM increased from 128 in the first edition to 541 in the current edition (Blashfield et al., 2014) (see Figure 14.2). Some of this growth was due to splitting existing disorders into narrower subtypes, but much of it was due to adding entirely new

disorders. Some of the new disorders encompass behavioral patterns that used to be regarded as mundane, everyday adjustment problems, rather than mental disorders. For ex- ample, DSM-5 includes diagnoses for caffeine intoxication (getting really buzzed from coffee), tobacco use disorder (inability to control smoking), disruptive mood dysregula- tion disorder (problems with recurrent temper tantrums in youngsters), binge-eating disorder (gluttonous over- eating more than once a week for at least 3 months), and gambling disorder (inability to control gambling). Some of these syndromes can be serious problems for which peo- ple might want to seek treatment, but should they merit a formal designation as a mental illness? Some critics of the DSM argue that this approach “medicalizes” everyday problems and casts the stigma of pathology on normal self- control issues (Frances, 2013; Kirk et al., 2013). Critics also worry that turning everyday problems into mental disor- ders could trivialize the concept of mental illness We are now ready to start examining the specific types of psychological disorders. Obviously, in this chapter, we cannot cover all of the hundreds of specific diagnoses listed in DSM-5. However, we will introduce most of the major categories of disorders to give you an overview of the many forms abnormal behavior takes. In discussing each set of disorders, we will begin with brief descriptions of the specific subtypes that fall in the cat- egory. If data are available, we will discuss the prevalence of the disorders in that category (how common the disorders are in the population). Then we’ll focus on the etiology of that set of disorders.

In the previous edition of the DSM, anxiety disorders was a very broad category of disor- ders, including generalized anxiety disorder, specific phobia, panic disorder, obsessive– compulsive disorder (OCD), and posttraumatic stress disorder (PTSD). In DSM-5, OCD was removed from the anxiety disorders category and put in its own special category with other compulsive problems, such as hoarding disorder. Similarly, PTSD was shifted into a new category for trauma-related disorders. There were compelling reasons for this reorganization (Stein et al., 2014), but for our level of analysis, it still makes sense to cover these anxiety-dominated disturbances together.

Generalized Anxiety Disorder

Generalized anxiety disorder is marked by a chronic, high level of anxiety that is not tied to any specific threat. People with this disorder worry constantly about yesterday’s mistakes and tomorrow’s problems. They worry about minor matters related to family, finances, work, and personal illness (Kimmel & Roy-Byrne, 2017). Their anxiety is often accompanied by physical symptoms, such as trembling, muscle tension, diarrhea, dizzi- ness, faintness, sweating, and heart palpitations. They hope their worrying will prepare them for the worst that could possibly happen, but the net result is they just generate negative emotions and prolonged physiological arousal (Newman & Llera, 2011). Peo- ple with generalized anxiety disorder sound like the “worried well,” but the disorder can be very disabling and is associated with an increased risk for a variety of physical health problems (Newman et al., 2013). Generalized anxiety disorder has a lifetime prevalence of about 5% and is seen about twice as much in females as males (Schneier et al., 2014). The typical age of onset is midlife, which is later than most other anxiety-related disor- ders (Rodebaugh, Weisman, & Tonge, 2018).

Specific Phobia

In a specific phobic disorder, an individual’s troublesome anxiety has a precise focus.

A specific phobia involves a persistent and irrational fear of an object or situation that presents no realistic danger. The following case provides an example of a specific phobia:

Hilda is 32 years of age and has a rather unusual fear. She is terrified of snow. She cannot go outside in the snow. She cannot even stand to see snow or hear about it on the weather report. Her phobia severely constricts her day-to-day behavior. Probing in therapy revealed that her phobia was caused by a traumatic experience at age 11. Playing at a ski lodge, she was buried briefly by a small avalanche of snow. She had no recollection of this experience until it was recov- ered in therapy. (Adapted from Laughlin, 1967, p. 227) As Hilda’s unusual snow phobia illustrates, people can develop phobic responses to virtually anything. Nonetheless, certain types of phobias are relatively common, includ- ing acrophobia (fear of heights), claustrophobia (fear of small, enclosed places), bron- tophobia (fear of storms), hydrophobia (fear of water), and various animal and insect phobias (McCabe, Hood, & Antony, 2015) (see Figure 14.3). People troubled by phobias typically realize that their fears are irrational, but still are unable to calm themselves when confronted by a phobic object. Phobic fears appear to be quite common, as the lifetime prevalence of specific phobias is estimated to be around 10%; two-thirds of the victims are females (Sadock, Sadock, & Ruiz, 2015).

Panic Disorder

A panic disorder is characterized by recurrent attacks of overwhelming anxiety that usually occur suddenly and unexpectedly. These paralyzing attacks are accompanied by physical symptoms of anxiety and are sometimes misinterpreted as heart attacks. After a number of anxiety attacks, victims often become apprehensive and hypervigilant, wondering when their next panic attack will occur. About two-thirds of people who are diagnosed with panic disorder are female, and the onset of the disorder typically occurs during late adolescence or early adulthood (Schneier et al., 2014).

Agoraphobia

People with panic disorder often become increasingly concerned about exhibiting panic in public, to the point where they are afraid to leave home. This fear can create a condition called agoraphobia, which is a fear of going out to public places (its literal meaning is “fear of the marketplace or open places”). In particular, agoraphobics tend to experience great discomfort in shopping malls, theaters, and restaurants and when using buses, trains, and subways. The crux of the problem is that in these situations they fear that it may be difficult to escape or get help if they panic. Some agoraphobics manage to venture out with a trusted companion, but they endure crowds with intense dread (Asmundson, LeBouthillier, & Taylor, 2015). Agoraphobia tends to coexist with a variety of other disorders, especially panic disorder.

Obsessive–Compulsive Disorder

Obsessions are thoughts that repeatedly intrude on one’s consciousness in a distressing way. Compulsions are actions one feels forced to carry out. Thus, obsessive–compulsive disorder (OCD) is marked by persistent, uncontrollable intrusions of unwanted thoughts (obsessions) and urges to engage in senseless rituals (compulsions). To illustrate, let’s examine the bizarre behavior of a man once reputed to be the wealthiest person in the world:

The famous industrialist Howard Hughes was obsessed with the possibility of being contaminated by germs. This led him to devise extraordinary rituals to minimize the possibility of such contamination. He would spend hours methodically cleaning a single telephone. He once wrote a three-page memo instructing assistants on exactly how to open cans of fruit for him. (Adapted from Barlett & Steele, 1979, pp. 227–237)

Obsessions often center on inflicting harm on others, personal failures, suicide, or sexual acts. People troubled by obsessions may feel they have lost control of their mind. Compulsions usually involve stereotyped rituals that may temporarily relieve the anxi- ety produced by one’s obsessions. As we saw at the beginning of the chapter, common examples include constant handwashing; repetitive cleaning and ordering of things; and endless rechecking of locks, faucets, and such. Most people with this disorder have mul- tiple obsessions and compulsions (Pato et al., 2015). People with OCD vary considerably in regard to how much insight they have into their disorder. Some are keenly aware that their obsessions and compulsions are irrational, whereas others are convinced that their behavior is rational (Abramowitz & Jacoby, 2015).

Many of us can be compulsive at times. Indeed, in samples of people without a mental disorder, many individuals report significant obsessions or compulsions (Clark et al., 2014). However, full-fledged obsessive–compulsive disorders occur in roughly 2%–3% of the population, with a mean age of onset of 19–20 (Tolin & Springer, 2018). Although OCD is often trivialized in the media (Pavelko & Myrick, 2015), it can be a very severe disorder and is often associated with serious social and occupational im- pairments (Dougherty, Wilhelm, & Jenike, 2014). The disorder’s severity was highlight- ed in research that found that OCD is associated with a tenfold elevation in the risk for suicide (de la Cruz et al., 2017). OCD is unusual among anxiety-related problems in that it is seen in males and females in roughly equal numbers (Gallo et al., 2013).

Clinicians are concerned that the coronavirus pandemic may lead to an increase in the prevalence of OCD (Rivera & Carballea, 2020; Shafran, Coughtrey, & Whittal, 2020). Contamination fears and cleaning rituals are common in OCD. It is possible that rational infection worries and hygienic practices related to the pandemic may gradually grow into pathological fears and rituals that become chronic problems in some people who are vulnerable to obsessive–compulsive disorder (Pozza, Mucci, & Marazziti, 2020).

Posttraumatic Stress Disorder

Posttraumatic stress disorder (PTSD) involves enduring psychological disturbance attributed to the experience of a major traumatic event. PTSD was first recognized as a disorder in the 1970s in the aftermath of the Vietnam War, when a great many veterans were traumatized by their combat experiences (Shalev & Marmar, 2017). Research eventually showed that PTSD can be caused by a variety of traumatic events besides harrowing war experiences. For example, PTSD is often seen after a rape or as- sault, a severe automobile accident, a natural disaster, or the witnessing of someone’s death. Although people tend to assume that such events are relatively uncommon, research shows that a majority of adults have been exposed to one or more seri-

ous traumatic events (Ogle et al., 2013). Common symptoms of PTSD include reexperiencing the event in the form of nightmares and flashbacks; emotional numbing; alienation; problems in social relations; an increased sense of vul- nerability; and elevated arousal, anxiety, anger, and guilt (Stoddard, Simon, & Pitman, 2014). Research has generally suggested that some 7%–8% of people are diagnosed with PTSD at some point in their lives, but studies using newer DSM- 5 diagnostic criteria have yielded even higher estimates (Fulton, Calhoun, & Beckham, 2015). PTSD is another disorder that may spike in the aftermath of the COVID-19 pandemic (Dutheil, Mondillon, & Navel, 2020). It is easy to envision how some people may be traumatized by the pandemic. Moreover, studies of previous, more localized epidemics have found that they led to elevated rates of PTSD in the areas where the outbreaks occurred (Boyraz & Legros, 2020).

Etiology of Anxiety-Related Disturbances

Like most psychological disorders, anxiety-dominated disorders develop out of compli- cated interactions between a variety of biological and psychological factors.

Biological Factors

In studies that assess the impact of heredity on psychological disorders, investigators look at concordance rates. A concordance rate indicates the percentage of twin pairs or other pairs of relatives who exhibit the same disorder. If relatives who share more genetic similarity show higher concordance rates than relatives who share less genetic overlap, this finding supports the genetic hypothesis. The results of both twin studies (see Figure 14.4) and family studies (see Chapter 3 for discussions of both methods) sug- gest a moderate genetic predisposition to anxiety disorders (Hettema & Otowa, 2017).

Research suggests that a link may exist between anxiety disorders and neurochemi- cal activity in the brain. Neurotransmitters are chemicals that carry signals from one neuron to another. Therapeutic drugs (such as Valium or Xanax) that reduce excessive anxiety appear to alter neurotransmitter activity at synapses that release a neurotrans- mitter called GABA. This finding and other lines of evidence suggest that disturbances in the neural circuits using GABA may play a role in some types of anxiety disorders (Naragon-Gainey, Lawrence, & Brown, 2015). Abnormalities in neural circuits using serotonin have been implicated in obsessive–compulsive disorders (Pato et al., 2015).

Conditioning and Learning

Many anxiety responses can be acquired through classical conditioning and maintained through operant conditioning (see Chapter 6). According to Mowrer (1947), an originally neutral stimulus (the snow in Hilda’s case, for instance) can be paired with a frighten- ing event (the avalanche) so that it becomes a conditioned stimulus eliciting anxiety (see Figure 14.5). Once a fear is acquired through classical conditioning, the person may start avoiding the anxiety-producing stimulus. The avoidance response is negatively reinforced because it is followed by a reduction in anxiety. This process involves operant conditioning (see Figure 14.5). Thus, separate conditioning processes can create and then sustain spe- cific anxiety responses. Consistent with this view, studies find that a substantial portion of people reporting phobias can identify a traumatic conditioning experience that probably contributed to their anxiety disorder (McCabe et al., 2015). The acquisition of conditioned fears is far from automatic, however. For a variety of reasons, people vary in how easily they develop conditioned fears that may evolve into anxiety problems (Mineka, 2013).

The tendency to develop phobias of certain types of objects and situations can be explained by Martin Seligman’s (1971) concept of preparedness. Like many theorists, Seligman believes that classical conditioning creates most phobic responses. However, he suggests that people are biologically prepared by their evolutionary history to acquire some fears much more easily than others. His theory would explain why people develop phobias of ancient sources of threat (such as snakes and spiders) much more readily than modern sources of threat (such as electrical outlets or hot irons). Arne Öhman and Susan Mineka (2001) updated the notion of preparedness, which they call an evolved module for fear learning. They maintain that this evolved module is automatically activated by stimuli related to past survival threats in evolutionary history and that it is relatively resistant to intentional efforts to suppress the resulting fears. Consistent with this view, when stimuli associated with evolutionary threats (pictures of snakes or spiders) are paired with mild electric shock in a classical conditioning procedure, they tend to produce stronger fear responses than when neutral stimuli (pictures of flowers or mushrooms) are paired with the same shock (Öhman, Fredrikson, Hugdahl, & Rimmo, 1976).

Distortions in the process of generalization in classical conditioning may also con- tribute to anxiety disorders. Research suggests that patients with panic disorder and those with PTSD both have a tendency to overgeneralize—that is, to have broader general- ization gradients than control subjects—when exposed to stimuli that trigger anxiety (Kaczkurkin et al., 2017; Lissek et al., 2010).

Cognitive Factors

Cognitive theorists maintain that certain styles of thinking make some people particularly vulnerable to anxiety disorders (McKay, 2016). According to these theorists, some people are especially vulnerable to anxiety problems because they tend to (1) misinterpret harm- less situations as threatening, (2) focus excessive attention on perceived threats, and (3) se- lectively recall information that seems threatening (Clark & Beck, 2010). In one intriguing test of the cognitive view, anxious and nonanxious subjects were asked to read thirty-two sentences that could be interpreted in either a threatening or a nonthreatening manner (Ey- senck et al., 1991). For instance, one such sentence was “The doctor examined little Emma’s growth,” which could mean that the doctor checked her height or the growth of a tumor. As Figure 14.6 shows, the anxious participants interpreted the sentences in a threatening way more often than the nonanxious participants did. Thus, consistent with our theme that human experience is highly subjective, the cognitive view holds that some people are prone to anxiety disorders because they see threat in every corner of their lives (Riskind, 2005). Researchers have also linked OCD to deficits in what is called executive function. Execu- tive function refers to the basic cognitive processes that underlie self-regulation, planning, and decision making. In an influential meta-analysis of 110 relevant studies, Snyder et al. (2015) found broad impairments in executive function among OCD patients.

Stress

Obviously, cases of posttraumatic stress disorder are attributed to individuals’ expo- sure to extremely stressful incidents. Research has also demonstrated that various types of anxiety disorders can be stress related (Beidel & Stipelman, 2007). For instance, Faravelli and Pallanti (1989) found that patients with panic disorder had experi- enced a dramatic increase in stress in the month prior to the onset of their disorder. Other studies found that stress levels are predictive of the severity of OCD patients’ symptoms (Morgado et al., 2013). Thus, there is reason to believe that high stress often helps to precipitate or to aggravate anxiety related disorders

What do Abraham Lincoln, Marilyn Monroe, Kurt Cobain, Vincent van Gogh, Ernest

Hemingway, Winston Churchill, Ted Turner, Alec Baldwin, Catherine Zeta-Jones, Sting, Billy Joel, Jim Carrey, Jon Hamm, Ben Stiller and Anne Hathaway have in com- mon? Yes, they all achieved great prominence, albeit in different ways at different times. But, more pertinent to our interest, they all experienced severe emotional dysfunc- tion, or mood disorders. Although emotional disorders can be crippling, people with mood disorders can still achieve greatness because such disorders tend to be episodic. In other words, mood disturbances often come and go, interspersed between periods of normality.

In earlier versions of the DSM, major depressive disorder and bipolar disorder were lumped together in a category called mood disorders. In DSM-5, they each get their own chapter or category, but we will discuss them together here. Figure 14.7 depicts the main way in which these disorders differ. People with major depressive disorder experience emotional extremes at just one end of the mood continuum because they experience pe- riodic bouts of depression. People with bipolar disorder generally experience emotional extremes at both ends of the mood continuum, going through periods of both depression and mania (excitement and elation). Actually, although the name for the disorder suggests that all individuals with bipolar illness experience both depression and mania, a minority of people with bipolar disorder do not report episodes of depression (Johnson, Cuellar, & Peckham, 2014). Major Depressive Disorder

The line between normal and abnormal depres- sion can be difficult to draw (Bebbington, 2013). The depressive disorders category includes a num- ber of milder syndromes, but the most common disorder in this domain is major depressive disor- der. In major depressive disorder, people show persistent feelings of sadness and despair and a loss of interest in previous sources of pleasure. Negative emotions form the heart of this syn- drome, but many other symptoms can also appear. The most common symptoms of depression are summarized and compared with the symptoms of mania in Table 14.1. A central feature of major depression is anhedonia —a diminished ability to experience pleasure. Depressed people lack energy and motivation. Hence, they often give up things they used to enjoy, such as hobbies, favor- ite foods, or spending time with friends. Reduced appetite and insomnia are common. They tend to

CHAPTER 14

move sluggishly and talk slowly. Anxiety, irritability, and brooding are commonly observed. Depression plunges people into feelings of hopelessness, dejection, and boundless guilt.

The onset of depression can occur at any point in the life span. However, the average age of onset is around 30–35 and a substantial majority of cases emerge before age 40 (Merikangas & Rihmer, 2017). Depression occurs in children and adolescents, as well as adults, although rates of depression are notably lower in children and somewhat lower in adolescents (Hankin, 2017). Most estimates suggest that some two-thirds of the people who are diagnosed with major depression experience more than one episode over the course of their lifetime (Akiskal, 2017), although Monroe and Cummins (2017) argue that the recurrence rate is closer to 40%–50%. Among those with recurrent depression the average number of depressive episodes is five to six. The average length of these epi- sodes is about 6 months (MacKinnon, 2015). An earlier age of onset is associated with more recurrences, more severe symptoms, and a worse prognosis (Hammen & Keenan- Miller, 2013). Although depression tends to be episodic, some people endure persistent major depression that may last for many years. Persistent depression is associated with a particularly severe impairment of functioning (Klein & Black, 2017). Depression is as- sociated with an elevated risk for a variety of health problems and increases mortality by about 50% (Cuijpers et al., 2014; Hopko, Melndoo, & File, 2017).

How common are depressive disorders? Lifetime prevalence is estimated to be around 13%–16% (Hammen & Keenan-Miller, 2013). At the low end, that estimate suggests that roughly 40 million people in the United States have or will experience depression! If this news isn’t sufficiently depressing, there is evidence that the prevalence of depression may be on the rise in recent birth cohorts (Twenge, 2015). That said, some theorists believe that a substantial portion of the people who meet the DSM criteria for major depression would be better characterized as experiencing normal, although intense and unpleasant, reactions to severe stressful events (Wakefield, Horwitz, & Lorenzo-Luaces, 2017). Studies of “uncompli- cated depression” suggest that these individuals eventually recover and are no more likely to have a recurrence of depression than people with no history of a depressive disorder. The im- plication is that the diagnostic criteria for depression have been expanded to the point of in- cluding normal sadness, which, of course, would inflate the apparent prevalence of depression.

Research indicates that the prevalence of depression is about twice as high in women as it is in men (Hatzenbuehler & McLaughlin, 2017). This disparity is apparent in adoles- cence and then declines slightly and remains stable throughout adulthood (Salk, Hyde, & Abramson, 2017). The many possible explanations for this gender gap are the subject of considerable debate. The gap does not appear to be attributable to differences in genetic makeup (Franić et al., 2010). A portion of the disparity may be the result of women’s ele- vated vulnerability to depression at certain points in their reproductive life cycle (Hilt & Nolen-Hoeksema, 2014). Obviously, only women have to worry about postpartum and postmenopausal depression. Susan Nolen-Hoeksema (2001) argues that women experi- ence more depression than men because they are far more likely to be victims of sexual abuse and somewhat more likely to endure poverty, sexual harassment, and excessive pressure to be thin and attractive. In other words, she attributes a portion of the higher prevalence of depression among women to their experience of greater stress and adver- sity. Nolen-Hoeksema also believes that women have a greater tendency than men to ruminate about setbacks and problems. Evidence suggests that this tendency to dwell on one’s difficulties elevates vulnerability to depression, as we will discuss momentarily.

Bipolar Disorder

Bipolar disorder is marked by the experience of both depressed and manic periods. The symptoms seen in manic periods generally are the opposite of those seen in depression (see Table 14.1 for a comparison). In a manic episode, a person’s mood becomes elevated to the point of euphoria. Self-esteem skyrockets as the person bubbles over with optimism, energy, and extravagant plans. He or she becomes hyperactive and may go for days without sleep. The individual talks rapidly and shifts topics wildly, as his or her mind races at break- neck speed. Judgment is often impaired. Some people in manic periods gamble impulsively, spend money frantically, or become sexually reckless. DSM-5 distinguishes between bipo- lar I disorder, which involves full manic episodes, and bipolar II disorder, which involves milder hypomanic episodes marked by shorter duration and less impairment (Akiskal, 2017).

You may be thinking that the euphoria in manic episodes sounds appealing. If so, you are not entirely wrong. In their milder forms, manic states can seem attractive. The increases in energy, self-esteem, and optimism can be deceptively seductive (Goodwin & Jamison, 2007). However, manic periods often carry a paradoxical negative undercurrent of uneasiness, irri- tability, and anger (El-Mallakh & Bauer, 2015). Moreover, mild manic episodes often escalate to higher levels that become scary and disturbing. Impaired judgment leads many victims to do things they greatly regret later, as you can see in the following case history:

Robert, a dentist, awoke one morning with the idea that he was the most gifted dental surgeon in his tri-state area. He decided that he should try to provide services to as many people as possible, so that more people could benefit from his talents. Thus, he decided to remodel his two-chair dental office so that he could simultaneously attend to twenty patients. That same day, impatient to get rolling on his remodeling, he rolled up his sleeves, got himself a sledgehammer, and began to knock down the walls in his office. Annoyed when that didn’t go so well, he smashed his dental tools, washbasins and X-ray equipment. Later, Robert’s wife became concerned about his behavior and summoned two of her adult daughters for assistance. The daughters responded quickly, arriving at the family home with their husbands. In the ensuing discussion, Robert made sexual advances toward his daughters. He had to be sub- dued by their husbands. (Adapted from Kleinmuntz, 1980, p. 309).

Although not rare, bipolar disorder is much less common than depression. Bipolar I and II disorders each affect about 1% of the population (Strunk & Sasso, 2017). Unlike depression, bipolar disorders are seen equally often in males and females (Merikangas & Rihmer, 2017). The typical age of onset for bipolar disorder is in the late teens or early twenties (Ketter & Chang, 2014).

Mood Dysfunction and Suicide

A tragic, heartbreaking problem associated with mood disorders is suicide. Suicide is the tenth leading cause of death in the United States, accounting for some 45,000 deaths annu- ally, a 25% increase since 2000 (Simon et al., 2018). Official statistics may underestimate the scope of the problem. Many suicides are disguised as accidents, either by the suicidal person or by the survivors, who try to cover up afterward. Moreover, experts estimate that suicide attempts may outnumber completed suicides by a ratio of as much as 25 to 1 (Roth- berg & Feinstein, 2014). Women attempt suicide three times more often than men, but men are more likely to actually kill themselves in an attempt, so they complete four times as many suicides as women. With the luxury of hindsight, it is recognized that about 90% of the people

who complete suicide manifest some type of psychological disorder, although this disorder may not be readily apparent beforehand in some cases (Rihmer & Pompili, 2017). As you might expect, suicide rates are highest for people with depressive and bipolar disorders. They account for about 50%–60% of completed suicides (Nock et al., 2014). The likelihood of a suicide attempt increases as the severity of individuals’ depression increases (MacLeod, 2013). Still, suicide is no- toriously difficult to predict. Perhaps the best predictor is when one expresses a sense of hopelessness about the future, but even that can be difficult to gauge (Ma- cLeod, 2013). Unfortunately, there is no foolproof way to prevent suicidal persons from taking their own lives. But some useful tips are compiled in Figure 14.8.

Suicide is another mental health issue that experts think may be increased by the coronavirus pandemic (Gunnell et al., 2020; Klomek, 2020). People who are already battling depression or other psychological disorders may experience worsening symptoms, and other people, severely stressed by the pandemic, may develop entirely new disorders that fuel suicidal ideation or behavior. Unfortunately, research evidence suggests that suicidal risk is elevat- ed by unemployment and by feelings of social isolation, both of which appear to be common hardships caused by the pandemic (Kawohl & Nordt, 2020; Levi-Belz & Aisenberg, 2020). It is far from inevitable, as people often show remarkable resilience, but a rise in suicide may be another form of pestilence inflicted by the coronavirus pandemic.

Etiology of Depressive and Bipolar Disorders

Quite a bit is known about the etiology of depressive and bipolar disorders, although the puzzle hasn’t been assembled completely. There appear to be a number of routes into these disorders, involving intricate interactions among psychological and biological factors.

Genetic Vulnerability

The evidence strongly suggests that genetic factors influence the likelihood of developing major depression and bipolar disorder (Kelsoe & Greenwood, 2017). Twin studies have found a huge disparity between identical and frater- nal twins in concordance rates for mood disorders. The concordance rate for identical twins is much higher (see Figure 14.9). Overall, the data suggest that the heri- tability of bipolar disorder is around 65%–80%, whereas the heritability of depression is around 40% (Berrettini & Lohoff, 2017). This evidence suggests that heredity can create a predisposition or vulnerability to mood dysfunction.

Neurochemical and Neuroanatomical Factors

Correlations have been found between mood disorders and abnormal levels of two neu- rotransmitters in the brain—norepinephrine and serotonin—although other neurotrans- mitter disturbances may also contribute (Thase, 2017). The details remain elusive, but low levels of serotonin appear to be a factor underlying most forms of depression.

Studies have also found some interesting correlations between mood disorders and a variety of structural abnormalities in the brain (Newman et al., 2017). Perhaps the best- documented correlation is the association between depression and reduced hippocampal volume, especially in the dentate gyrus of the hippocampus (Mathias et al., 2016). A rela- tively new theory of the biological bases of depression may be able to account for this find- ing. The springboard for this theory is the discovery that the human brain continues to generate new neurons (neurogenesis) in adulthood, especially in the hippocampal forma- tion (Kozorovitskiy & Gould, 2007, 2008) (see Chapter 3). The relevant evidence suggests that depression occurs when major life stress causes neurochemical reactions that sup- press this neurogenesis, resulting in reduced hippocampal volume (Mahar et al., 2014).

Other lines of research have implicated abnormally high reactivity in the amygdala as a factor in depression. The amygdala is a small structure in the brain that is known to play a key role in the learning of fear responses and may contribute to the regulation of other emotions (LeDoux & Damasio, 2013). Brain-imaging studies indicate that depressed subjects show heightened reactivity in the amygdala to negative emotional stimuli, which may contribute to vulnerability to depression (Swartz, Williamson, & Hairi, 2015). An- other line of research has related depression to reduced activation in specific areas of the brain that process the anticipation and experience of reward and reinforcement (Keren et al., 2018). This blunted sensitivity to reward may be the neural basis for the anhedonia seen in depression.

Cognitive Factors

A variety of theories emphasize how cognitive processes contribute to depressive disor- ders (Alloy et al., 2017). For example, based largely on animal research, Seligman (1974) proposed that depression is caused by learned helplessness—passive “giving up” behavior produced by exposure to unavoidable aversive events (such as uncontrollable shock in the lab). He originally considered learned helplessness to be a product of conditioning, but eventually revised his theory to give it a cognitive slant. The reformulated theory of learned helplessness asserts that the roots of depression lie in how people explain the setbacks and other negative events they experience (Abramson, Seligman, & Teasdale, 1978). According to Seligman (1990), people who exhibit a pessimistic explanatory style are especially vulnerable to depression. These people tend to attribute their setbacks to their personal flaws instead of to situational factors. Moreover, they tend to draw global, far-reaching conclusions about their personal inadequacies based on these setbacks.

In accord with this line of thinking, Susan Nolen-Hoeksema (1991, 2000) found that people with depression who ruminate about their depression remain depressed longer than those who try to distract themselves. People who respond to depression with rumination repetitively focus their attention on their feelings of depression. They think constantly about how sad, lethargic, and unmotivated they are. Excessive rumination tends to foster and am- plify episodes of depression by increasing negative thinking, impairing problem solving, and undermining social support (Lyubomirsky et al., 2015). As we noted earlier, evidence sug- gests that women have a greater tendency to ruminate than men, and that this disparity may be a major reason depression is more prevalent in women. Interestingly, research suggests that rumination may contribute to other disorders besides depression, including generalized anxiety disorder, eating disorders, and substance-abuse disorders (Johnson et al., 2016).

Hindsight bias—the tendency to mold one’s recall of the past to fit with how events turned out (see Chapters 7 and 11)—may also help to fuel depression. People with de- pression tend to view negative outcomes as more foreseeable and inevitable than they actually were (Groß, Blank, & Bayen, 2017). Thoughts about setbacks such as “I saw it coming, I knew things would turn out poorly” promote self-blame for negative outcomes, which may increase the emotional impact of the negative outcomes.

In sum, cognitive models of depression maintain that negative thinking is what leads to depression in many people. The principal problem with cognitive theories is their difficulty in separating cause from effect. Does negative thinking cause depres- sion? Or does depression cause negative thinking (see Figure 14.10)? Strong evi- dence favoring a causal role for negative thinking comes from a study by Alloy and colleagues (1999), who assessed explanatory style in first-year college students who were not depressed at the outset of the study, which followed students for 2.5 years. They compared 173 high-risk students who scored high on negative thinking against 176 low-risk students who scored low on negative thinking. They found that a nega- tive explanatory style predicted vulnerability to depression, with major depression emerging in 17% of students who exhibited negative thinking, but only 1% of those who did not.

Interpersonal Roots

Some approaches to understanding depression emphasize how social difficulties put peo- ple on the road to depressive disorders (see Figure 14.11) (Whisman, 2017). According to this notion, depression-prone people tend to lack the social finesse needed to acquire many important kinds of reinforcers, such as good friends, top jobs, and desirable spouses. This lack of reinforcers could understandably lead to negative emotions and depression. Consistent with this theory, researchers have found correlations between poor social skills and depression (Petty, Sachs-Ericsson, & Joiner, 2004). Evidence also suggests that de- pressed people unintentionally court rejection from others because they tend to be irri- table, pessimistic, unpleasant companions (Joiner & Timmons, 2009). They also alienate people by constantly asking for reassurances about their relationships and their worth. This excessive reassurance seeking ends up fostering rejection and is predictive of depression (Hames, Hagan, & Joiner, 2013). Yet another issue is that complicated and difficult social relations can greatly increase the level of stress in one’s life. Insofar as depressed people are prone to experience awkward, tense, stormy, and frustrating interactions with family, friends, and colleagues, they are likely to generate chronic stress for themselves (Hammen & Shih, 2014), and as we will discuss next, stress can be a factor in mood dysfunction.

Precipitating Stress

Mood disorders sometimes appear mysteriously in people who are leading benign, nonstressful lives (Monroe & Cummins, 2017). For this reason, ex- perts used to believe that stress had little influence on mood disorders. How- ever, advances in the measurement of personal stress altered this picture. The evidence available today suggests the existence of a moderately strong link between stress and the onset of both major depression (Monroe, Slavich, & Georgiades, 2014) and bipolar disorder (Johnson et al., 2014). Severe, highly aversive stressors appear to be more likely to trigger depression than less severe stressors (Monroe & Cummins, 2017). Still, the majority of people who experience significant stress do not develop a mood disorder, so one’s vulner- ability to both stress and mood disorders must play a role. Unfortunately, vulnerability to depression seems to increase as people go through more recurrences of depressive episodes. Studies show that stress is less of a factor in triggering depression as episodes of depression accumulate over the years (Monroe et al., 2014). Literally, schizophrenia means “split mind.” However, when Eugen Bleuler coined the term in 1911, he was referring to the fragmentation of thought processes seen in the disorder—not to a “split personality.” Unfortunately, writers in the popular media often assume that the split-mind notion, and thus schizophrenia, refers to the rare syndrome in which a person manifests two or more personalities. As you have already learned, this syndrome is actually called dissociative identity disorder. Schizophrenia is a much more common, and altogether different, type of disorder.

Schizophrenia is a disorder marked by delusions, hallucinations, disorganized thinking and speech, and deterioration of adaptive behavior. Schizophrenia usually emerges during adolescence or early adulthood. About 75% of cases manifest by the age of 30 (Perkins, Miller-Anderson, & Lieberman, 2006). Prevalence estimates suggest that about 1% of the population may be diagnosed with schizophrenia over the course of their lives (Mueser & Roe, 2016). That may not sound like much, but it means that in the United States alone, several million people may be troubled by schizophrenic disturbances. Schizophrenia is an extremely costly illness for society because it is a severe, debilitating illness that tends to have an early onset and often requires lengthy hospital care (Jablensky, 2017). Moreover, in- dividuals diagnosed with schizophrenia show an increased risk for suicide and for premature mortality (early death) from quite a variety of physical diseases (Newcomer et al., 2017).

Symptoms

Schizophrenia is a serious disorder that wreaks havoc in victims’ lives. Many of the key symptoms of schizophrenia are apparent in the following case history, adapted from Sheehan (1982). Sylvia was first diagnosed as schizophrenic at age 15. She has been in and out of many types of psychiatric facilities since then. She has never been able to hold a job for any length of time. During severe flare-ups of her disorder, her personal hygiene de- teriorates. She rarely washes, she wears clothes that neither fit nor match, and she smears makeup on heavily but randomly. Sylvia occasionally hears voices talking to her. She tends to be argumentative, aggressive, and emotionally volatile. Over the years, she has been involved in innumerable fights with fellow patients, psychiatric staff members, and strangers. Her thoughts can be highly irrational, as is apparent from the following quote:

“Mick Jagger wants to marry me. If I have Mick Jagger, I don’t have to covet Geraldo Rivera. Mick Jagger is St. Nicholas and the Maharishi is Santa Claus. I want to form a gospel rock group called the Thorn Oil, but Geraldo wants me to be the music critic on Eyewitness News, so what can I do? Got to listen to my boyfriend. Teddy Kennedy cured me of my ugliness. I’m pregnant with the son of God. They’re eating the patients here. I’m Joan of Arc. I’m Florence Nightingale. The door be- tween the ward and the porch is the dividing line between New York and California. Forget about zip codes. I need shock treatments. The body is run by electricity. My wiring is all faulty.” (Adapted from Sheehan, 1982; quotation from pp. 104–105).

Sylvia’s case clearly shows that schizophrenic thinking can be bizarre, and that schizo- phrenia can be a severe and crippling disorder. Although no single symptom is inevita- bly present, the following symptoms are commonly seen in schizophrenia (Arango & Carpenter, 2011; Lewis, Escalona, & Keith, 2017).

Delusions and Irrational Thought

Cognitive deficits and disturbed thought processes are the central, defining feature of schizophrenia (Heinrichs et al., 2013). Various kinds of delusions are common. Delusions are false beliefs that are maintained even though they clearly are out of touch with reality. For example, one patient’s delusion that he was a tiger (with a deformed body) persisted for 15 years (Kulick, Pope, & Keck, 1990). More typically, affected persons believe that their private thoughts are being broadcast to other people, that thoughts are being in- jected into their mind against their will, or that their thoughts are being controlled by some external force (Maher, 2001). Delusions of persecution are seen in some 80% of patients with schizophrenia (Lewis et al., 2017). These delusions can range from brief suspicions about strangers’ behavior to enduring concerns about elaborate plots attributed to family or friends. In delusions of grandeur, people maintain that they are famous or important. Sylvia expressed an endless array of grandiose delusions, such as thinking that Mick Jagger wanted to marry her, that she had dictated the hobbit stories to J. R. R. Tolkien, and that she was going to win the Nobel Prize for medicine. In addition to delusions, the schizophrenic person’s train of thought deteriorates. Thinking becomes chaotic rather than logical and linear. A “loosening of associations” occurs, as the person shifts topics in disjointed ways. The quotation from Sylvia illustrates this symptom dramatically. The entire quote involves a wild flight of ideas in which the thoughts mostly have no apparent connection to each other.

Deterioration of Adaptive Behavior

Schizophrenia usually involves a noticeable deterioration in the quality of the person’s routine functioning in work, social relations, and personal care (Harvey & Bowie, 2013). Friends often make remarks such as “Hal just isn’t himself anymore.” This deterioration is readily apparent in Sylvia’s inability to get along with others or to function in the work world. It’s also apparent in her neglect of personal hygiene.

Distorted Perception

A variety of perceptual distortions can occur with schizophrenia, the most common being auditory hallucinations, which are reported by about 70% of patients (Lewis et al., 2017). Hallucinations are sensory perceptions that occur in the absence of a real, external stimulus or are gross distortions of perceptual input. People with schizophre- nia commonly report that they hear voices of nonexistent or absent people talking to them. Sylvia, for instance, said she heard messages from former Beatle Paul McCartney. These voices often provide an insulting, running commentary on the person’s behavior (“You’re an idiot for shaking his hand”). They may be argumentative (“You don’t need a bath”), or they may issue commands (“Prepare your home for visitors from outer space”).

Disturbed Emotion

Normal emotional tone can be disrupted in a variety of ways. Some individuals with schizophrenia show a flattening of emotions. In other words, they show little emotional responsiveness. Others show inappropriate emotional responses that don’t jell with the situation or with what they are saying. People with schizophrenia can also become emo- tionally volatile. Because of this volatility, acts of aggression can be a problem with some schizophrenic patients (Serper, 2011).

Traditionally, four subtypes of schizophrenic disorders were recognized: paranoid, catatonic, disorganized, and undifferentiated schizophrenia (Minzenberg, Yoon, & Carter, 2008). As its name implies, paranoid schizophrenia was thought to be dominated by delu- sions of persecution, along with delusions of grandeur. Catatonic schizophrenia was marked by striking motor disturbances, ranging from the muscular rigidity seen in a withdrawn state called a catatonic stupor to random motor activity seen in a state of catatonic excite- ment. Disorganized schizophrenia was viewed as a particularly severe syndrome marked by frequent incoherence, obvious deterioration in adaptive behavior, and virtually complete social withdrawal. People who clearly exhibited schizophrenic symptoms but who could not be placed into any of the three previous categories were said to have undifferentiated schizophrenia, which involved idiosyncratic mixtures of schizophrenic symptoms.

However, in a radical departure from tradition, DSM-5 discarded the four subtypes of schizophrenia. Why? For many years, researchers pointed out that there were not mean- ingful differences between the classic subtypes in etiology, prognosis, or response to treat- ment. The absence of such differences cast doubt on the value of distinguishing among the subtypes. Critics also noted that the catatonic and disorganized subtypes were rarely seen in contemporary clinical prac- tice, and that undifferentiated cases did not represent a subtype as much as a hodge- podge of “leftovers” (Braff et al., 2013).

Another approach to understanding

and describing schizophrenia is to distin-

guish between the positive symptoms and

negative symptoms of the disorder (Stroup

et al., 2014; see Figure 14.12). Negative

symptoms involve behavioral deficits, such

as flattened emotions, social withdrawal,

apathy, impaired attention, poor groom-

ing, lack of persistence at work or school,

and poverty of speech. Positive symptoms

involve behavioral excesses or pecu-

liarities, such as hallucinations, delusions,

incoherent thought, agitation, bizarre

behavior, and wild flights of ideas. Most people with the disorder exhibit both types of symptoms, but they vary in the degree to which positive or negative symptoms dominate (Andreasen, 2009). A relative predominance of negative symptoms is associated with less effective social functioning (Robertson et al., 2014), and poorer overall

treatment outcomes (Fervaha et al., 2014).

Etiology of Schizophrenia

You can probably identify, at least to some extent, with people who struggle with mood disorders and anxiety disorders. You can probably imagine events that could unfold that might leave you struggling with depression or grappling with anxiety. But what could possibly account for Sylvia’s thinking that she was Joan of Arc or had dictated the hobbit novels to Tolkien? As mystifying as these delusions may seem, you’ll see that the etiology of schizophrenic disorders is not all that different from the etiology of other psychologi- cal disorders. We’ll begin our discussion by examining the matter of genetic vulnerability.

Genetic Vulnerability

Evidence is plentiful that hereditary factors play a role in the development of schizo- phrenic disorders. For instance, in twin studies, concordance rates average around 48% for identical twins, in comparison with about 17% for fraternal twins (Gottesman, 1991, 2001). Studies also indicate that a child born to two parents with schizophrenia has about a 46% probability of developing a schizophrenic disorder (as compared with the probability in the general population of about 1%). These and other findings that show the genetic roots of schizophrenia are summarized in Figure 14.13. Some theorists sus- pect that genetic factors may account for as much as 80% of the variability in susceptibil- ity to schizophrenia (Hilker et al., 2018; Kendall, Kirov, & Owen, 2017).

Research suggests that genetic vulnerability may be heightened when it is accompa- nied by relatively low general intelligence. A large-scale study in Sweden found that low IQ scores were associated with an increased prevalence of schizophrenia (Kendler et al., 2015). The data suggested that IQ moderated the effect of genetic vulnerability, as low IQ amplified genetic risk, whereas high IQ provided some protection against genetic risk.

Neurochemical Factors

Like depressive and bipolar disorders, schizophrenic disorders appear to be accompanied by changes in the activity of one or more neurotransmitters in the brain. The dopamine hy- pothesis asserts that excess dopamine activity is the neurochemical basis for schizophrenia. This hypothesis makes sense because most of the drugs that are useful in the treatment of schizophrenia are known to dampen dopamine activity in the brain (Stroup et al., 2014). In recent years, the dopamine hypothesis has become more nuanced and complex. Some researchers believe that elevated dopamine activity in certain areas of the brain may foster positive symptoms and that reduced dopamine activity in other neural circuits may foster negative symptoms (Bobo et al., 2015; Maia & Frank, 2017). Moreover, it has become appar- ent that dopamine dysregulation is intertwined with disturbances in other neurotransmitter systems including serotonin, GABA, and glutamate (Lawrence, First, & Lieberman, 2015). Thus, the neurochemical bases of schizophrenia appear to involve complicated interactions among many neurotransmitter systems and different types of dys- regulation in different regions of the brain (Bobo et al., 2015).

Accumulating research has suggested that marijuana use during adoles- cence may help precipitate schizophrenia in young people who have a genetic vulnerability to the disorder (van Winkel & Kuepper, 2014). For example, a meta-analysis of eighty-three studies found that the onset of psychotic dis- order tended to occur 2.7 years earlier in cannabis users than in non-users (Large et al., 2011). This unexpected finding has generated considerable debate about whether and how cannabis might contribute to the emergence of schizophrenia. Some theorists suggest that schizophrenia could lead to canna- bis use, rather than vice versa. In other words, emerging psychotic symptoms may prompt young people to turn to marijuana to self-medicate. Recent stud- ies have provided some support for the self-medication explanation (Aas et al., 2018; Gage et al., 2017; Hiemstra et al., 2018). But many studies also suggest that there is a causal link between marijuana use and the emergence of schizo- phrenia (Hamilton, 2017; Nesvåg et al., 2017; Shahzade et al., 2018).

Structural Abnormalities in the Brain

Right ventricle

Left ventricle

Third ventricle

Fourth ventricle

Individuals with schizophrenia exhibit a variety of deficits in attention, per-

ception, working memory, and speed of information processing (Harvey,

Keefe, & Eesley, 2017). These cognitive deficits suggest that schizophrenic

disorders may be caused by neurological defects. Brain-imaging studies

have yielded intriguing findings that are consistent with this idea. The most

reliable finding is that CT scans and MRI scans (see Chapter 3) suggest an association between enlarged brain ventricles (the hollow, fluid-filled cavities

in the brain depicted in Figure 14.14) and schizophrenic disturbance (Lyall,

Kubicki, & Shenton, 2017). Enlarged ventricles are assumed to reflect the degeneration of nearby brain tissue. Consistent with this assumption, a meta-analysis of MRI studies of more than 2000 schizophrenia patients found shrinkage in several crucial subcortical structures. The patients were found to have a smaller hippocampus, thalamus, and amyg- dala than comparable control subjects (van Erp et al., 2015). This structural deterioration could be a consequence of schizophrenia, or it could be a contributing cause of the illness.

One line of thinking about this structural deterioration in the brain is that it might be partly the result of synaptic pruning going awry. Synaptic pruning involves the selective elimination of synapses by certain types of glial cells (see Chapter 3). It is a normal pro- cess that plays a role in the sculpting of neural pathways in the brain. But some evidence suggests that indiscriminate elimination of healthy, functional synapses in adolescence may contribute to the brain abnormalities seen in schizophrenia (Costandi, 2019; De Picker et al., 2017; Notter & Meyer, 2017).

The Neurodevelopmental Hypothesis

The neurodevelopmental hypothesis of schizophrenia asserts that schizophrenia is caused in part by various disruptions in the normal maturational processes of the brain before or at birth (Rapoport, Giedd, & Gogtay, 2012). According to this hypothesis, insults to the brain during sensitive phases of prenatal development or during birth can cause subtle neurological damage that elevates individuals’ vulnerability to schizophrenia years later in adolescence and early adulthood (see Figure 14.15). What are the sources of these ear- ly insults to the brain? Thus far, research has focused on viral infection or malnutrition during prenatal development and on obstetrical complications during the birth process.

Quite a number of studies have found a link between exposure to influenza and other in- fections during prenatal development and an increased prevalence of schizophrenia (Brown & Derkits, 2010), with inflammation thought to be the critical process that disrupts neural mat- uration (Miller, Culpepper et al., 2013). Additionally, a study that investigated the possible impact of prenatal malnutrition found an elevated incidence of schizophrenia in a group of people who were prenatally exposed to a severe famine in 1944–1945, resulting from a Nazi blockade of food deliveries in the Netherlands during World War II (Susser et al., 1996). Other research has shown that people with schizophrenia are more likely than control subjects to have experienced obstetrical complications when they were born (van Os & Reininghaus, 2017). Finally, research suggests that minor physical anomalies (slight anatomical defects of the head, hands, feet, and face) that would be consistent with prenatal neurological damage are more common in people with schizophrenia than in others (Akabaliev, Sivkov, & Mantarkov, 2014). Collectively, these diverse studies argue for a relationship between early neurological trauma and a vulnerability to schizophrenia (Rapoport et al., 2012).

Expressed Emotion

Research on expressed emotion has primarily focused on how this element of family dynamics influences the course of schizophrenic illness, after the onset of the disorder (Leff & Vaughn, 1985). Expressed emotion is the degree to which a relative of a schizo- phrenic patient displays highly critical or emotionally overinvolved attitudes toward the patient. Audiotaped interviews of relatives’ communication have been carefully evaluated for critical comments; resentment toward the patient; and excessive emotional involvement (overprotective, overconcerned attitudes) (Hooley, 2004). Studies show that a family’s expressed emotion is a good predictor of the course of a schizophrenic patient’s illness (Hooley, 2007). After release from a hospital, schizophrenic patients who return to a family high in expressed emotion show relapse rates three times those of patients who return to a family low in expressed emotion (Hooley, 2009) (see Figure 14.16). Part of the problem for patients returning to homes high in expressed emotion is that their families probably are sources of stress rather than of social support (Bebbington & Kuipers, 2011).

Stress

Many theories of schizophrenia assume that stress plays a key role in triggering schizophrenic disorders (Pruessner et al., 2017). According to this notion, various biological and psycho- logical factors influence individuals’ vulnerability to schizophrenia. High stress may then serve to precipitate a schizophrenic disorder in someone who is vulnerable (Bebbington & Kuipers, 2011). Research indicates that high stress can also trigger relapses in patients who have made progress toward recovery (Walker, Mittal, & Tessner, 2008).

14.6 Autism Spectrum Disorders

Many of the disorders we have discussed can be seen in children. For example, pho- bic disorders, obsessive–compulsive disorders, and depression are routinely seen among children, as well as adults. However, our next disorder, autism, is diagnosed almost exclusively during childhood, and usually very early childhood at that. Autism, or autism spectrum disorder (ASD), is a neurodevelopmental disorder characterized by deficits in social interaction and communication and restricted, repetitive interests and activities. Originally called infantile autism, this disorder was first described by child psychiatrist Leo Kanner in the 1940s. In DSM-5, several related and milder disorders such Asperger’s syndrome, which were described individually in the previous DSM, were lumped together with classic autism in one category with the variety in symptom pre- sentations reenvisioned as variations in severity along an autism spectrum. Although there were some sound reasons for this change, it proved to be a controversial decision (Parsloe & Babrow, 2016; Solomon, 2017; Tsai, 2013). Critics pointed out that it created a diagnostic category characterized by enormous diversity, ranging from severe disorders requiring hospitalization to subtle manifestations that can go undetected (Szatmari, 2016; Syriopoulou-Delli & Papaefstathiou, 2019). Some critics also argued that the new scheme applied a stigmatizing diagnostic label to some relatively mild conditions (Gamlin, 2017). In this section, we will mostly focus on the original syndrome of autism, but we will try to address some of the diversity incorporated into the new spectrum diagnosis.

Symptoms and Prevalence

Early symptoms of autism include minimal eye contact with others and declining social interest and social smiling. Delays in the development of language are one of the first things that spark concern in parents. Repetitive body movements and manipulations of objects, as well as hyperreactivity to stimuli, are also common manifestations of autism. Verbal communication can be greatly impaired, as about 30%–40% of children with clas- sic autism fail to develop functional speech (Volkmar et al., 2017). Among those who do develop speech, their ability to initiate and sustain a conversation can be limited, and their use of language tends to be marked by peculiarities, such as echolalia, which in- volves rote repetition of others’ words. Children with autism can be extremely inflexible and minor changes in their environment can trigger meltdowns and shutdowns. Some children with ASD exhibit self-injurious behavior, such as banging their heads or bit- ing themselves. About one-half of children with autism exhibit subnormal IQ scores (Volkmar et al., 2017). Many children with autism are easily overwhelmed by crowds, have difficulties processing others’ emotions, have difficulties regulating their emotions, and find it challenging to build friendships (Lerner et

al., 2018). Parents of children who develop autism typi- cally become concerned about their child’s development by about 15–18 months of age and usually seek profes- sional consultation by about 24 months. Earlier versions of the DSM assumed that all children with autism were diagnosed by age 3. In conjunction with DSM-5’s in- clusion of milder syndromes under the autism um- brella, this assumption was discarded in DSM-5.

Until relatively recently, the prevalence of au- tism was thought to be well under 1% (Newschaffer, 2007). Since the mid-1990s, however, there has been a dramatic increase in the diagnosis of autism, with prevalence estimates approaching and then exceeding 1% (Zahorodny et al., 2014). The most recent preva- lence estimates are around 1.5% (Lerner et al., 2018). Most experts believe that this surge in ASD is largely due to greater awareness of the syndrome and the use of broader diagnostic criteria (Abbeduto et al., 2014). Males account for about 80% of autism diagnoses (Friedman et al., 2015). Research on long-term outcomes for those with ASD has mostly focused on individuals with the classic, more severe autism syndrome. The findings of these studies may not be ap- plicable to the burgeoning number of people diagnosed in more recent years using broader diagnostic criteria. One meta-analysis of outcome research (Steinhausen, Jensen, & Lauritsen, 2016) reported that 20% of individuals with autistic disorders experienced a good outcome (a high level of independence), 31% a fair outcome (some independence, but support and supervision are needed), and 48% a poor outcome (needing residential supervision or hos- pital care). More favorable findings seem likely in future research focusing on the broader ASD diagnosis. There already is research showing that individuals with ASD are increasingly enrolling in college (Jackson et al., 2018) and entering the workforce (Hedley et al., 2018).

However, individuals with autism and their families may face new challenges in the wake of the coronavirus pandemic (Eshraghi et al., 2020). Many crucial therapeutic pro- grams may be shut down, perhaps for long periods, due to social distancing require- ments. Plus, as already noted, children with autism tend to struggle with disruptions to their routines and the COVID-19 pandemic has proven enormously disruptive.

Etiology of ASD

Autism was originally blamed on cold, aloof parenting (Bettelheim, 1967), but that view was discredited by research decades ago (Bhasin & Schendel, 2007). Given its appearance so early in life, most theorists today view autism as a disorder that originates in biological dysfunctions. Consistent with that viewpoint, twin studies and family studies have demon- strated that genetic factors make a major contribution to ASD (Abbeduto et al., 2014; Tick et al., 2016). Many theorists believe that autism must be attributable to some sort of brain abnormality, but until recently there was relatively little progress in pinpointing the nature of this abnormality. The most reliable finding has been that ASD is associated with general- ized brain enlargement that is apparent by age 2 (Hazlett et al., 2011). This brain overgrowth can be seen in many areas of the cortex (Friedman et al., 2015). MRI studies suggest that this overgrowth begins sometime around the end of the first year, which, with the luxury of hindsight, is right around the time that autistic symptoms usually start to surface. However, a more recent study found evidence that this overgrowth may begin during the second and third trimesters of prenatal development (Bonnet-Brilhault et al., 2018). Theorists speculate that this overgrowth probably produces disruptions in neural circuits.

One hypothesis that has garnered a great deal of publicity is the idea that autism may be caused by the mercury used as a preservative in some childhood vaccines (Kirby, 2005). However, the 1998 study that first reported a link between vaccinations and autism has been discredited as fraudulent (Deer, 2011; Godlee, Smith, & Marcovitch, 2011). Moreover, inde- pendent efforts to replicate the purported association between vaccinations and ASD have consistently failed (Hviid et al., 2019; Jain et al., 2015; Paul, 2009). Widespread belief in the apparently spurious relationship between autism and vaccinations may simply be due to the fact that children get scheduled vaccinations around the same age (12–15 months) that par- ents first start to realize their children are not developing normally (Doja & Roberts, 2006). Most people don’t seem to take eating disorders as seriously as they take other types of psychological disorders. Yet, you will see that these disorders are dangerous and debili- tating, and that no other types of psychological disorders are associated with a greater elevation in mortality.

Description

Eating disorders are severe disturbances in eating behavior characterized by preoc- cupation with weight concerns and unhealthy efforts to control weight. The three syndromes are: anorexia nervosa, bulimia nervosa, and a new syndrome added to DSM-5 called binge-eating disorder.

Anorexia Nervosa

Anorexia nervosa involves intense fear of gaining weight, disturbed body image, re- fusal to maintain normal weight, and use of dangerous measures to lose weight. Two subtypes have been observed. In restricting type anorexia nervosa, people drastically re- duce their intake of food, sometimes literally starving themselves. In binge-eating/purging type anorexia nervosa, individuals attempt to lose weight by forcing themselves to vomit after meals, by misusing laxatives and diuretics, and by engaging in excessive exercise.

Individuals with anorexia tend to have a disturbed body image. No matter how frail they become, they insist that they are too fat. Their morbid fear of obesity means that they are never satisfied with their weight. If they gain a pound or two, they panic. The only thing that makes them happy is to lose more weight. The common result is a relentless decline in body weight. Ironically, in light of their minimal eating, people with anorexia often report that they wake up thinking about food and continue to do so all day long, but they set strict rules for their food intake (Attia, 2017).

Because of their disturbed body image, individuals with anorexia generally do not appreciate the maladaptive quality of their behavior. Hence, they rarely seek treatment on their own. They are typically coaxed or coerced into treatment by friends or family mem- bers who are alarmed by their appearance. Anorexia nervosa eventually leads to a cascade of medical problems. These problems may include amenorrhea (a loss of menstrual cycles in women), gastrointestinal problems, low blood pressure, osteoporosis (a loss of bone density), and metabolic disturbances that can lead to cardiac arrest or circulatory collapse (Call, Attia, & Walsh, 2017; Mehler, 2018). Anorexia is a debilitating illness that is associ- ated with a tenfold elevation in premature death (Keel, 2018).

Bulimia Nervosa

Bulimia nervosa involves habitually engaging in out-of-control overeating, followed by unhealthy compensatory efforts, such as self-induced vomiting, fasting, abuse of laxa- tives and diuretics, and excessive exercise. The eating binges are usually carried out in secret and are followed by intense guilt and concern about gaining weight. These feelings motivate ill-advised strategies to undo the effects of the overeating. However, vomiting prevents the absorption of only about half of recently consumed food, and laxatives and diuretics have negligible impact on caloric intake. So, individuals with bulimia nervosa typically maintain a reasonably normal weight (Fairburn, Cooper, & Murphy, 2009). Medical problems associated with bulimia nervosa include cardiac arrythmias, dental problems, metabolic deficiencies, and gastrointestinal problems (Mehler, 2018; Mitchell & Wonderlich, 2014).

Obviously, bulimia nervosa shares many features with anorexia nervosa, such as a morbid fear of becoming obese; preoccupation with food; and rigid, maladaptive ap- proaches to controlling weight that are grounded in naïve all-or-none thinking. However, the syndromes also differ in crucial ways. First and foremost, bulimia is a much less life-threatening condition. Second, although their appearance is usually more “normal” than that seen with anorexia, people with bulimia are much more likely to recognize that their eat- ing behavior is pathological and are more likely to cooperate with treatment (Guarda et al., 2007). Nonetheless, like anorexia, bulimia is associated with elevated mortality rates, although this elevation is only about one-third as great as that seen for anorexia (Arcelus et al., 2011).

Binge-Eating Disorder

Binge-eating disorder involves distress-inducing eating binges that are not accompa- nied by the purging, fasting, and excessive exercise seen in bulimia. Obviously, this syndrome resembles bulimia, but it is a less severe disorder. Still, this disorder creates great distress, as these people tend to be disgusted by their bodies and distraught about their overeating. Their excessive eating is often triggered by stress (Gluck, 2006). This comparatively mild syndrome is more common than anorexia or bulimia (Keel & Forney, 2015). Unfortunately, many individuals with this disorder progress onto a diagnosis of bulimia (Bohon, 2018), while others develop problems with obesity (Devlin, 2017).

Prevalence and Cultural Roots

Eating disorders have been viewed as a product of modern, affluent Western culture, in which food is generally plentiful and the desirability of being thin is widely en- dorsed. Until recent decades, these disorders were not seen outside of Western cultures (Hoek, 2002), and they remain rare in countries where food insecurity is predominant (Anderson-Fye, 2018). However, advances in communication have exported modern Western culture to far-flung corners of the globe. Hence, eating disorders have started showing up in many non-Western societies, especially affluent Asian countries (Pike, Dunne, & Grant, 2015; Szabo, 2015).

There are huge gender gaps in the likelihood of developing eating disorders. About 90%–95% of individuals with anorexia nervosa and bulimia nervosa are female, and about 60% of those with binge-eating disorder are female (Devlin & Steinglass, 2014). The stag- gering gender disparities in the prevalence of the more serious eating disorders appear to be a result of cultural pressures rather than biological factors (Murnen & Smolak, 2015). Western standards of attractiveness emphasize slenderness more for females than for males, and women generally experience greater pressure to be physically attractive than men do (Levine & Murnen, 2015). Eating disorders mostly afflict young women. The typi- cal age of onset for anorexia is 15–19; for bulimia it is 15–21 (see Figure 14.17). How common are eating disorders in Western societies? Research suggests that among females, about 1% develop anorexia nervosa, roughly 1.5% develop bulimia nervosa, and about 3.5% exhibit binge-eating disorder (Keel, 2018). In some respects, these figures may only scratch the surface of the problem (Keel et al., 2012). Evidence suggests that another 2%–4% of people may struggle with serious eating problems that do not quite qualify for a formal diagnosis (Swanson et al., 2011). People with eating dis- orders often manifest other psychological disorders, showing elevated rates of depressive disorders, anxiety disorders, OCD, personality disorders, and substance abuse disorders (Coelho, Thaler, & Steiger, 2015; Halmi, 2018).

Etiology of Eating Disorders

Like other types of psychological disorders, eating disorders are caused by multiple deter- minants that work interactively. Let’s take a brief look at some of the factors that contrib- ute to the development of anorexia nervosa and bulimia nervosa.

Genetic Vulnerability

The stockpile of research findings is not as large as it is for many other types of psy- chopathology (such as anxiety, mood, and schizophrenic disorders), but studies sug- gest that some people may inherit a genetic vulnerability to eating disorders (Wade & Bulik, 2018). There is convincing evidence for a hereditary component in both an- orexia nervosa and bulimia nervosa, with genetics probably playing a stronger role in anorexia (Bulik & Breen, 2017). A genetic predisposition also appears to contribute to binge-eating disorder, but there are fewer studies of this newer diagnosis (Baker et al., 2015).

Personality Factors

The interrelated traits of anxiety, negative emotionality, and neuroticism are associat- ed with elevated rates of eating disorders (Halmi, 2018). Research also suggests that a high level of perfectionism is a risk factor for eating disorders, especially anorexia (Keel et al., 2012; Lavender, Young, & Wonderlich, 2015). Given these personality traits, it is not surprising that people with eating disorders often have difficulties in effectively regulat- ing their emotions, especially negative emotions (Wonderlich & Lavender, 2017). These deficits in emotional regulation may contribute to both the development and mainte- nance of eating disorders.

Cultural Values

The contribution of cultural values to the increased prevalence of eating disorders can hardly be overestimated (Striegel-Moore & Bulik, 2007). In Western society, young wom- en are socialized to believe they must be attractive. To be attractive, they think they must be as thin as the actresses and fashion models who dominate the media (Ata, Schaefer, & Thompson, 2015). Thanks to this cultural milieu, many young women are dissatisfied with their weight because the societal ideals promoted by the media are unattainable for most of them (Anderson-Fye, 2018). Unfortunately, in a small portion of these women, the pressure to be thin, in combination with genetic vulnerability, family pathology, and other factors, leads to unhealthy efforts to control weight.

The Role of the Family

Quite a number of theorists stress how family dynamics can contribute to the develop- ment of anorexia and bulimia in young women. One issue appears to be that some moth- ers contribute to eating disorders simply by endorsing society’s message that “you can never be too thin” and by modeling unhealthy dieting behaviors of their own (Crowther, Smith, & Wiliams, 2015). In conjunction with media pressures, this role modeling leads many daughters to internalize the idea that the thinner you are, the more attractive you are. Of course, peers can also endorse beliefs and model behaviors that promote eating disorders (Lunde & Frisén, 2015). Another potential family-related issue is that there is an association between childhood sexual and physical abuse and an elevated risk for eating disorders (Brewerton, 2015; Coelho et al., 2015).

Cognitive Factors

Many theorists emphasize the role of disturbed thinking in the etiology of eating dis- orders (Williamson et al., 2001). For example, anorexic patients’ typical belief that they are fat when they are really wasting away is a dramatic illustration of how thinking goes awry. Patients with eating disorders display rigid, all-or-none thinking and many maladaptive beliefs (Roberts, Tchanturia, & Treasure, 2010). Such thoughts may in- clude “I must be thin to be accepted”; “If I am not in complete control, I will lose all control”; “If I gain one pound, I’ll go on to gain enormous weight.” Additional research is needed to determine whether distorted thinking is a cause or merely a symptom of eating disorders.

Answer the following “true” or “false.”

1 Insanity is frequently used as a

defense in criminal proceedings.

2 When the insanity defense is used,

it is successful fairly often.

3 Final decisions about involuntary commitment to a mental hospi- tal are made by psychiatrists and

psychologists.

All of the above statements are false, as you will see in this Application. Societies use laws to enforce their norms regarding appropriate behavior. Given this function, the law in our society has something to say about many issues related to abnor- mal behavior. In this section, we examine the concepts of insanity, competency, and involuntary commitment.

Insanity

Insanity is not a diagnosis; it’s a legal con- cept. Insanity is a legal status indicating that a person cannot be held responsible for his or her actions because of mental illness. Why is this an issue in the court- room? Because criminal acts must be intentional. The law reasons that people who are “out of their mind” may not be able to appreciate the significance of what they’re doing. The insanity defense is used in criminal trials by defendants who ad- mit they committed the crime, but claim they lacked intent.

No simple relationship exists between specific diagnoses of mental disorders and court judgments of insanity, or what is sometimes called criminal responsibil- ity. The vast majority of people with diag- nosed psychological disorders would not qualify as insane. The people most likely to qualify are those troubled by severe dis- turbances that display delusional behavior. The courts apply various rules in making udgments about a defendant’s sanity, depending on the jurisdiction (Packer, 2015). According to one widely used rule, called the M’naghten rule, insanity exists when a mental disorder makes a person unable to distinguish right from wrong. As you can imagine, evaluating insanity as defined in the M’naghten rule can be dif- ficult for judges and jurors, and even for the psychologists and psychiatrists who are called into court as expert witnesses.

Although highly publicized and con- troversial, the insanity defense is actually used less frequently and less successfully than widely believed (see Figure 14.18). One study found that the general public estimates the insanity defense is used in 37% of felony cases, when in fact it’s used in less than 1% (Silver, Cirincione, & Steadman, 1994). Another study of over 60,000 indictments in Baltimore found that only 190 defendants (0.31%) pleaded insanity. Of these, only eight were suc- cessful (Janofsky et al., 1996).

Competency

Competency (or fitness in some states) refers to a defendant’s capacity to stand trial. To be competent, defendants must

be able to understand the nature and pur- pose of the legal proceedings and be able to assist their attorney. If they’re not able, they’re declared incompetent and can’t be brought to trial unless they become com- petent once again.

What’s the difference between insan- ity and incompetence? Insanity refers to a defendant’s mental state at the time of the alleged crime. Competency refers to a defendant’s mental state at the time of the trial. Given the potential for delay in our legal system, the crime and the trial may take place many months or even years apart. Insanity can’t even become an issue unless a defendant is competent to stand trial. Far more people are found to be incompetent than insane. As with insan- ity, no simple relationship exists between specific diagnoses and being declared incompetent (Benedek & Grieger, 2015).

What happens to defendants who are declared incompetent or insane? Essen- tially, they’re turned over to the mental health system for treatment. However, this simple statement masks immense variability in the handling of their cases. What happens to a defendant depends on the nature of the offense, the rules applied in the specific jurisdiction, the nature of the mental disorder, the likelihood of re- covery and a return to competence, and a host of other factors.

Involuntary Commitment

The issue of insanity surfaces only in criminal proceedings. Far more people are affected by civil proceedings relating to involuntary commitment. In invol- untary commitment, people are hospi- talized in psychiatric facilities against their will. What are the grounds for such a dramatic action? They vary some from state to state. Generally, people are sub- ject to involuntary commitment when mental health professionals and legal au- thorities believe that a mental disorder makes them (1) dangerous to themselves (usually suicidal), (2) dangerous to oth- ers (potentially violent), or (3) unable to provide for their own basic care (Simon & Shuman, 2014). Commitment typically becomes an issue in emergency situations when family members, police, or medical personnel are concerned about suicide or violence. In these situations calling for immediate action, psychologists and psychiatrists can authorize temporary commitment, usually for 24–72 hours (Watson, Eth, & Leong, 2017). Orders for long-term involuntary commitment are usually set up for renewable 6-month

periods and can only be issued by a court after a formal hearing. Mental health professionals provide extensive input in these hearings. The courts, however, make the final decisions.

Most involuntary commitments occur because people appear to be dangerous to themselves or others. The real difficulty, though, is in predicting dangerousness (Freedman et al., 2007). Studies suggest that clinicians’ short-term predictions about which patients are likely to become violent are only moderately accurate. Moreover, their long-term predictions of violent behavior are largely inaccu- rate (Simon & Shuman, 2008). Most of the general public (75%), influenced by news reports linking psychological disor- ders to incidents of violence, believe that people with serious disorders are dan- gerous, but in reality they only account for 5%–10% of violent crime (Elbogen, Dennnis, & Johnson, 2016). Most psychi- atric symptoms are not associated with gun violence (Lu & Temple, 2019). People with serious mental illness are somewhat more likely to be violent than the general population. For example, in one specific year, 2.9% of people with serious mental illness committed violent acts, compared with 0.8% of people without mental disor- ders (Swanson et al., 2014). But a history of violent behavior is a much stronger predictor of future violence than any psychiatric diagnosis.

This inaccuracy in predicting danger- ousness is unfortunate. Detaining a per- son is no small matter. And involuntary commitment involves the detention of people for what they might do in the fu- ture, not necessarily for what they did do. Such detention goes against the grain of the American legal principle that people are innocent until proven guilty. The inher- ent difficulty in predicting dangerousness makes involuntary commitment a com- plex and controversial issue.