Definition of a Psychological Disorder

Perhaps the simplest approach to conceptualizing psychological disorders is to label behaviors, thoughts, and inner experiences that are atypical, distressful, dysfunctional, and sometimes even dangerous, as signs of a disorder. For example, if you ask a classmate for a date and you are rejected, you probably would feel a little dejected. Such feelings would be normal. If you felt extremely depressed—so much so that you lost interest in activities, had difficulty eating or sleeping, felt utterly worthless, and contemplated suicide—your feelings would be atypical, would deviate from the norm, and could signify the presence of a psychological disorder. Just because something is atypical, however, does not necessarily mean it is disordered.

For example, only about 4% of people in the United States have red hair, so red hair is considered an atypical characteristic (Figure 2), but it is not considered disordered, it’s just unusual. And it is less unusual in Scotland, where approximately 13% of the population has red hair (“DNA Project Aims,” 2012). As you will learn, some disorders, although not exactly typical, are far from atypical, and the rates in which they appear in the population are surprisingly high.

If we can agree that merely being atypical is an insufficient criterion for a having a psychological disorder, is it reasonable to consider behavior or inner experiences that differ from widely expected cultural values or expectations as disordered? Using this criterion, a woman who walks around a subway platform wearing a heavy winter coat in July while screaming obscenities at strangers may be considered as exhibiting symptoms of a psychological disorder. Her actions and clothes violate socially accepted rules governing appropriate dress and behavior; these characteristics are atypical.

Cultural Expectations

Violating cultural expectations is not, in and of itself, a satisfactory means of identifying the presence of a psychological disorder. Since behavior varies from one culture to another, what may be expected and considered appropriate in one culture may not be viewed as such in other cultures. For example, returning a stranger’s smile is expected in the United States because a pervasive social norm dictates that we reciprocate friendly gestures. A person who refuses to acknowledge such gestures might be considered socially awkward—perhaps even disordered—for violating this expectation. However, such expectations are not universally shared. Cultural expectations in Japan involve showing reserve, restraint, and a concern for maintaining privacy around strangers. Japanese people are generally unresponsive to smiles from strangers (Patterson et al., 2007). Eye contact provides another example. In the United States and Europe, eye contact with others typically signifies honesty and attention. However, most Latin-American, Asian, and African cultures interpret direct eye contact as rude, confrontational, and aggressive (Pazain, 2010). Thus, someone who makes eye contact with you could be considered appropriate and respectful or brazen and offensive, depending on your culture (Figure 3).

Hallucinations (seeing or hearing things that are not physically present) in Western societies is a violation of cultural expectations, and a person who reports such inner experiences is readily labeled as psychologically disordered. In other cultures, visions that, for example, pertain to future events may be regarded as normal experiences that are positively valued (Bourguignon, 1970). Finally, it is important to recognize that cultural norms change over time: what might be considered typical in a society at one time may no longer be viewed this way later, similar to how fashion trends from one era may elicit quizzical looks decades later—imagine how a headband, legwarmers, and the big hair of the 1980s would go over on your campus today.

American Psychiatric Association (APA) Definition

Many of the features of the harmful dysfunction model are incorporated in a formal definition of psychological disorder developed by the . According to the American Psychiatric Association (APA) (2013), a psychological disorder is a condition that is said to consist of the following:

• There are significant disturbances in thoughts, feelings, and behaviors. A person must experience inner states (e.g., thoughts and/or feelings) and exhibit behaviors that are clearly disturbed—that is, unusual, but in a negative, self-defeating way. Often, such disturbances are troubling to those around the individual who experiences them. For example, an individual who is uncontrollably preoccupied by thoughts of germs spends hours each day bathing, has inner experiences, and displays behaviors that most would consider atypical and negative (disturbed) and that would likely be troubling to family members.
• The disturbances reflect some kind of biological, psychological, or developmental dysfunction. Disturbed patterns of inner experiences and behaviors should reflect some flaw (dysfunction) in the internal biological, psychological, and developmental mechanisms that lead to normal, healthy psychological functioning. For example, the hallucinations observed in schizophrenia could be a sign of brain abnormalities.
• The disturbances lead to significant distress or disability in one’s life. A person’s inner experiences and behaviors are considered to reflect a psychological disorder if they cause the person considerable distress, or greatly impair his ability to function as a normal individual (often referred to as functional impairment, or occupational and social impairment). As an illustration, a person’s fear of social situations might be so distressing that it causes the person to avoid all social situations (e.g., preventing that person from being able to attend class or apply for a job).
• The disturbances do not reflect expected or culturally approved responses to certain events. Disturbances in thoughts, feelings, and behaviors must be socially unacceptable responses to certain events that often happen in life. For example, it is perfectly natural (and expected) that a person would experience great sadness and might wish to be left alone following the death of a close family member. Because such reactions are in some ways culturally expected, the individual would not be assumed to signify a mental disorder.

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Some believe that there is no essential criterion or set of criteria that can definitively distinguish all cases of disorder from nondisorder (Lilienfeld & Marino, 1999). In truth, no single approach to defining a psychological disorder is adequate by itself, nor is there universal agreement on where the boundary is between disordered and not disordered. From time to time we all experience anxiety, unwanted thoughts, and moments of sadness; our behavior at other times may not make much sense to ourselves or to others. These inner experiences and behaviors can vary in their intensity, but are only considered disordered when they are highly disturbing to us and/or others, suggest a dysfunction in normal mental functioning, and are associated with significant distress or disability in social or occupational activities.

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Diagnostic And Statistical Manual of Mental Disorders (DSM-5)

Although a number of classification systems have been developed over time, the one that is used by most mental health professionals in the United States is the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by the American Psychiatric Association (2013). (Note that the American Psychiatric Association differs from the American Psychological Association; both are abbreviated APA.) The first edition of the DSM, published in 1952, classified psychological disorders according to a format developed by the U.S. Army during World War II (Clegg, 2012). In the years since, the DSM has undergone numerous revisions and editions. The most recent edition, published in 2013, is the DSM-5 (APA, 2013). The DSM-5 includes many categories of disorders (e.g., anxiety disorders, depressive disorders, and dissociative disorders). Each disorder is described in detail, including an overview of the disorder (diagnostic features), specific symptoms required for diagnosis (diagnostic criteria), prevalence information (what percent of the population is thought to be afflicted with the disorder), and risk factors associated with the disorder. Figure 4 shows lifetime prevalence rates—the percentage of people in a population who develop a disorder in their lifetime—of various psychological disorders among U.S. adults. These data were based on a national sample of 9,282 U.S. residents (National Comorbidity Survey, 2007).

The DSM-5 also provides information about comorbidity; the co-occurrence of two disorders. For example, the DSM-5 mentions that 41% of people with obsessive-compulsive disorder (OCD) also meet the diagnostic criteria for major depressive disorder (Figure 5). Drug use is highly comorbid with other mental illnesses; 6 out of 10 people who have a substance use disorder also suffer from another form of mental illness (National Institute on Drug Abuse [NIDA], 2007).

The DSM has changed considerably in the half-century since it was originally published. The first two editions of the DSM, for example, listed homosexuality as a disorder; however, in 1973, the APA voted to remove it from the manual (Silverstein, 2009). Additionally, beginning with the DSM-III in 1980, mental disorders have been described in much greater detail, and the number of diagnosable conditions has grown steadily, as has the size of the manual itself. DSM-I included 106 diagnoses and was 130 total pages, whereas DSM-III included more than 2 times as many diagnoses (265) and was nearly seven times its size (886 total pages) (Mayes & Horowitz, 2005). Although DSM-5 is longer than DSM-IV, the volume includes only 237 disorders, a decrease from the 297 disorders that were listed in DSM-IV. The latest edition, DSM-5, includes revisions in the organization and naming of categories and in the diagnostic criteria for various disorders (Regier, Kuhl, & Kupfer, 2012), while emphasizing careful consideration of the importance of gender and cultural difference in the expression of various symptoms (Fisher, 2010).

Some believe that establishing new diagnoses might overpathologize the human condition by turning common human problems into mental illnesses (The Associated Press, 2013). Indeed, the finding that nearly half of all Americans will meet the criteria for a DSM disorder at some point in their life (Kessler et al., 2005) likely fuels much of this skepticism. The DSM-5 is also criticized on the grounds that its diagnostic criteria have been loosened, thereby threatening to “turn our current diagnostic inflation into diagnostic hyperinflation” (Frances, 2012, para. 22). For example, DSM-IV specified that the symptoms of major depressive disorder must not be attributable to normal bereavement (loss of a loved one). The DSM-5, however, has removed this bereavement exclusion, essentially meaning that grief and sadness after a loved one’s death can constitute major depressive disorder.

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Compassionate View of Psychological Disorders

As these disorders are outlined, please bear two things in mind. First, remember that psychological disorders represent extremes of inner experience and behavior. If, while reading about these disorders, you feel that these descriptions begin to personally characterize you, do not worry—this moment of enlightenment probably means nothing more than you are normal. Each of us experiences episodes of sadness, anxiety, and preoccupation with certain thoughts—times when we do not quite feel ourselves. These episodes should not be considered problematic unless the accompanying thoughts and behaviors become extreme and have a disruptive effect on one’s life. Second, understand that people with psychological disorders are far more than just embodiments of their disorders. We do not use terms such as schizophrenics, depressives, or phobics because they are labels that objectify people who suffer from these conditions, thus promoting biased and disparaging assumptions about them. It is important to remember that a psychological disorder is not what a person is; it is something that a person has—through no fault of his or her own. As is the case with cancer or diabetes, those with psychological disorders suffer debilitating, often painful conditions that are not of their own choosing. These individuals deserve to be viewed and treated with compassion, understanding, and dignity.

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Supernatural Perspectives of Psychological Disorders

For centuries, psychological disorders were viewed from a supernatural perspective: attributed to a force beyond scientific understanding. Those afflicted were thought to be practitioners of black magic or possessed by spirits (Maher & Maher, 1985). For example, convents throughout Europe in the 16th and 17th centuries reported hundreds of nuns falling into a state of frenzy in which the afflicted foamed at the mouth, screamed and convulsed, sexually propositioned priests, and confessed to having carnal relations with devils or Christ. Although, today, these cases would suggest serious mental illness; at the time, these events were routinely explained as possession by devilish forces (Waller, 2009a). Similarly, grievous fits by young girls are believed to have precipitated the witch panic in New England late in the 17th century (Demos, 1983). Such beliefs in supernatural causes of mental illness are still held in some societies today; for example, beliefs that supernatural forces cause mental illness are common in some cultures in modern-day Nigeria (Aghukwa, 2012).

Findings such as these have led many of today’s researchers to search for specific genes and genetic mutations that contribute to mental disorders. Also, sophisticated neural imaging technology in recent decades has revealed how abnormalities in brain structure and function might be directly involved in many disorders, and advances in our understanding of neurotransmitters and hormones have yielded insights into their possible connections. The biological perspective is currently thriving in the study of psychological disorders.

Diathesis-Stress Model of Psychological Disorders

Despite advances in understanding the biological basis of psychological disorders, the psychosocial perspective is still very important. This perspective emphasizes the importance of learning, stress, faulty and self-defeating thinking patterns, and environmental factors. Perhaps the best way to think about psychological disorders, then, is to view them as originating from a combination of biological and psychological processes. Many develop not from a single cause, but from a delicate fusion between partly biological and partly psychosocial factors.

The diathesis-stress model (Zuckerman, 1999) integrates biological and psychosocial factors to predict the likelihood of a disorder. This diathesis-stress model suggests that people with an underlying predisposition for a disorder (i.e., a diathesis) are more likely than others to develop a disorder when faced with adverse environmental or psychological events (i.e., stress), such as childhood maltreatment, negative life events, trauma, and so on. A diathesis is not always a biological vulnerability to an illness; some diatheses may be psychological (e.g., a tendency to think about life events in a pessimistic, self-defeating way).

The key assumption of the diathesis-stress model is that both factors, diathesis and stress, are necessary in the development of a disorder. Different models explore the relationship between the two factors: the level of stress needed to produce the disorder is inversely proportional to the level of diathesis.

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Specific Phobia

Phobia is a Greek word that means fear. A person diagnosed with a specific phobia (formerly known as simple phobia) experiences excessive, distressing, and persistent fear or anxiety about a specific object or situation (such as animals, enclosed spaces, elevators, or flying) (APA, 2013). Even though people realize their level of fear and anxiety in relation to the phobic stimulus is irrational, some people with a specific phobia may go to great lengths to avoid the phobic stimulus (the object or situation that triggers the fear and anxiety). Typically, the fear and anxiety a phobic stimulus elicits is disruptive to the person’s life. For example, a man with a phobia of flying might refuse to accept a job that requires frequent air travel, thus negatively affecting his career. Clinicians who have worked with people who have specific phobias have encountered many kinds of phobias, some of which are shown in Table 1.

Specific phobias are common; in the United States, around 12.5% of the population will meet the criteria for a specific phobia at some point in their lifetime (Kessler et al., 2005). One type of phobia, agoraphobia, is listed in the DSM-5 as a separate anxiety disorder. Agoraphobia, which literally means “fear of the marketplace,” is characterized by intense fear, anxiety, and avoidance of situations in which it might be difficult to escape or receive help if one experiences symptoms of a panic attack (a state of extreme anxiety that we will discuss shortly). These situations include public transportation, open spaces (parking lots), enclosed spaces (stores), crowds, or being outside the home alone (APA, 2013). About 1.4% of Americans experience agoraphobia during their lifetime (Kessler et al., 2005).

Acquisition of Phobias Through Learning

Many theories suggest that phobias develop through learning. Rachman (1977) proposed that phobias can be acquired through three major learning pathways. The first pathway is through classical conditioning. As you may recall, classical conditioning is a form of learning in which a previously neutral stimulus is paired with an unconditioned stimulus (UCS) that reflexively elicits an unconditioned response (UCR), eliciting the same response through its association with the unconditioned stimulus. The response is called a conditioned response (CR). For example, a child who has been bitten by a dog may come to fear dogs because of her past association with pain. In this case, the dog bite is the UCS and the fear it elicits is the UCR. Because a dog was associated with the bite, any dog may come to serve as a conditioned stimulus, thereby eliciting fear; the fear the child experiences around dogs, then, becomes a CR.

The second pathway of phobia acquisition is through vicarious learning, such as modeling. For example, a child who observes his cousin react fearfully to spiders may later express the same fears, even though spiders have never presented any danger to him. This phenomenon has been observed in both humans and nonhuman primates (Olsson & Phelps, 2007). A study of laboratory-reared monkeys readily acquired a fear of snakes after observing wild-reared monkeys react fearfully to snakes (Mineka & Cook, 1993).

The third pathway is through verbal transmission or information. For example, a child whose parents, siblings, friends, and classmates constantly tell her how disgusting and dangerous snakes are may come to acquire a fear of snakes.

Interestingly, people are more likely to develop phobias of things that do not represent much actual danger to themselves, such as animals and heights, and are less likely to develop phobias toward things that present legitimate danger in contemporary society, such as motorcycles and weapons (Öhman & Mineka, 2001). Why might this be so? One theory suggests that the human brain is evolutionarily predisposed to more readily associate certain objects or situations with fear (Seligman, 1971). This theory argues that throughout our evolutionary history, our ancestors associated certain stimuli (e.g., snakes, spiders, heights, and thunder) with potential danger. As time progressed, the mind has become adapted to more readily develop fears of these things than of others. Experimental evidence has consistently demonstrated that conditioned fears develop more readily to fear-relevant stimuli (images of snakes and spiders) than to fear-irrelevant stimuli (images of flowers and berries) (Öhman & Mineka, 2001). Such prepared learning has also been shown to occur in monkeys. In one study (Cook & Mineka, 1989), monkeys watched videotapes of model monkeys reacting fearfully to either fear-relevant stimuli (toy snakes or a toy crocodile) or fear-irrelevant stimuli (flowers or a toy rabbit). The observer monkeys developed fears of the fear-relevant stimuli but not the fear-irrelevant stimuli.

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Social Anxiety Disorder

Social anxiety disorder (formerly called social phobia) is characterized by extreme and persistent fear or anxiety and avoidance of social situations in which the person could potentially be evaluated negatively by others (APA, 2013). As with specific phobias, social anxiety disorder is common in the United States; a little over 12% of all Americans experience social anxiety disorder during their lifetime (Kessler et al., 2005).

The heart of the fear and anxiety in social anxiety disorder is the person’s concern that he may act in a humiliating or embarrassing way, such as appearing foolish, showing symptoms of anxiety (blushing), or doing or saying something that might lead to rejection (such as offending others). The kinds of social situations in which individuals with social anxiety disorder usually have problems include public speaking, having a conversation, meeting strangers, eating in restaurants, and, in some cases, using public restrooms. Although many people become anxious in social situations like public speaking, the fear, anxiety, and avoidance experienced in social anxiety disorder are highly distressing and lead to serious impairments in life. Adults with this disorder are more likely to experience lower educational attainment and lower earnings (Katzelnick et al., 2001), perform more poorly at work and are more likely to be unemployed (Moitra, Beard, Weisberg, & Keller, 2011), and report greater dissatisfaction with their family lives, friends, leisure activities, and income (Stein & Kean, 2000).

When people with social anxiety disorder are unable to avoid situations that provoke anxiety, they typically perform safety behaviors: mental or behavioral acts that reduce anxiety in social situations by reducing the chance of negative social outcomes. Safety behaviors include avoiding eye contact, rehearsing sentences before speaking, talking only briefly, and not talking about oneself (Alden & Bieling, 1998). Other examples of safety behaviors include the following (Marker, 2013):

• assuming roles in social situations that minimize interaction with others (e.g., taking pictures, setting up equipment, or helping prepare food)
• asking people many questions to keep the focus off of oneself
• selecting a position to avoid scrutiny or contact with others (sitting in the back of the room)
• wearing bland, neutral clothes to avoid drawing attention to oneself
• avoiding substances or activities that might cause anxiety symptoms (such as caffeine, warm clothing, and physical exercise)

Although these behaviors are intended to prevent the person with social anxiety disorder from doing something awkward that might draw criticism, these actions usually exacerbate the problem because they do not allow the individual to disconfirm his negative beliefs, often eliciting rejection and other negative reactions from others (Alden & Bieling, 1998).

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People with social anxiety disorder may resort to self-medication, such as drinking alcohol, as a means to avert the anxiety symptoms they experience in social situations (Battista & Kocovski, 2010). The use of alcohol when faced with such situations may become negatively reinforcing: encouraging individuals with social anxiety disorder to turn to the substance whenever they experience anxiety symptoms. The tendency to use alcohol as a coping mechanism for social anxiety, however, can come with a hefty price tag: a number of large scale studies have reported a high rate of comorbidity between social anxiety disorder and alcohol use disorder (Morris, Stewart, & Ham, 2005).

As with specific phobias, it is highly probable that the fears inherent to social anxiety disorder can develop through conditioning experiences. For example, a child who is subjected to early unpleasant social experiences (e.g., bullying at school) may develop negative social images of herself that become activated later in anxiety-provoking situations (Hackmann, Clark, & McManus, 2000). Indeed, one study reported that 92% of a sample of adults with social anxiety disorder reported a history of severe teasing in childhood, compared to only 35% of a sample of adults with panic disorder (McCabe, Antony, Summerfeldt, Liss, & Swinson, 2003).

One of the most well-established risk factors for developing social anxiety disorder is behavioral inhibition (Clauss & Blackford, 2012). Behavioral inhibition is thought to be an inherited trait, and it is characterized by a consistent tendency to show fear and restraint when presented with unfamiliar people or situations (Kagan, Reznick, & Snidman, 1988). Behavioral inhibition is displayed very early in life; behaviorally inhibited toddlers and children respond with great caution and restraint in unfamiliar situations, and they are often timid, fearful, and shy around unfamiliar people (Fox, Henderson, Marshall, Nichols, & Ghera, 2005). A recent statistical review of studies demonstrated that behavioral inhibition was associated with more than a sevenfold increase in the risk of development of social anxiety disorder, demonstrating that behavioral inhibition is a major risk factor for the disorder (Clauss & Blackford, 2012).

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Panic Disorder

Imagine that you are at the mall one day with your friends and—suddenly and inexplicably—you begin sweating and trembling, your heart starts pounding, you have trouble breathing, and you start to feel dizzy and nauseous. This episode lasts for 10 minutes and is terrifying because you start to think that you are going to die. When you visit your doctor the following morning and describe what happened, she tells you that you have experienced a panic attack (Figure 9). If you experience another one of these episodes two weeks later and worry for a month or more that similar episodes will occur in the future, it is likely that you have developed panic disorder.

People with panic disorder experience recurrent (more than one) and unexpected panic attacks, along with at least one month of persistent concern about additional panic attacks, worry over the consequences of the attacks, or self-defeating changes in behavior related to the attacks (e.g., avoidance of exercise or unfamiliar situations) (APA, 2013). As is the case with other anxiety disorders, the panic attacks cannot result from the physiological effects of drugs and other substances, a medical condition, or another mental disorder. A panic attack is defined as a period of extreme fear or discomfort that develops abruptly and reaches a peak within 10 minutes. Its symptoms include accelerated heart rate, sweating, trembling, choking sensations, hot flashes or chills, dizziness or lightheadedness, fears of losing control or going crazy, and fears of dying (APA, 2013). Sometimes panic attacks are expected, occurring in response to specific environmental triggers (such as being in a tunnel); other times, these episodes are unexpected and emerge randomly (such as when relaxing). According to the DSM-5, the person must experience unexpected panic attacks to qualify for a diagnosis of panic disorder.

Experiencing a panic attack is often terrifying. Rather than recognizing the symptoms of a panic attack merely as signs of intense anxiety, individuals with panic disorder often misinterpret them as a sign that something is intensely wrong internally (thinking, for example, that the pounding heart represents an impending heart attack). Panic attacks can occasionally precipitate trips to the emergency room because several symptoms of panic attacks are, in fact, similar to those associated with heart problems (e.g., palpitations, racing pulse, and a pounding sensation in the chest) (Root, 2000). Unsurprisingly, those with panic disorder fear future attacks and may become preoccupied with modifying their behavior in an effort to avoid future panic attacks. For this reason, panic disorder is often characterized as fear of fear (Goldstein & Chambless, 1978).

Panic attacks themselves are not mental disorders. Indeed, around 23% of Americans experience isolated panic attacks in their lives without meeting the criteria for panic disorder (Kessler et al., 2006), indicating that panic attacks are fairly common. Panic disorder is, of course, much less common, afflicting 4.7% of Americans during their lifetime (Kessler et al., 2005). Many people with panic disorder develop agoraphobia, which is marked by fear and avoidance of situations in which escape might be difficult or help might not be available if one were to develop symptoms of a panic attack. People with panic disorder often experience a comorbid disorder, such as other anxiety disorders or major depressive disorder (APA, 2013).

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Researchers are not entirely sure what causes panic disorder. Children are at a higher risk of developing panic disorder if their parents have the disorder (Biederman et al., 2001), and family and twins studies indicate that the heritability of panic disorder is around 43% (Hettema, Neale, & Kendler, 2001). The exact genes and gene functions involved in this disorder, however, are not well-understood (APA, 2013). Neurobiological theories of panic disorder suggest that a region of the brain called the locus coeruleus may play a role in this disorder. Located in the brainstem, the locus coeruleus is the brain’s major source of norepinephrine, a neurotransmitter that triggers the body’s fight-or-flight response. Activation of the locus coeruleus is associated with anxiety and fear, and research with nonhuman primates has shown that stimulating the locus coeruleus either electrically or through drugs produces panic-like symptoms (Charney et al., 1990). Such findings have led to the theory that panic disorder may be caused by abnormal norepinephrine activity in the locus coeruleus (Bremner, Krystal, Southwick, & Charney, 1996).

Conditioning theories of panic disorder propose that panic attacks are classical conditioning responses to subtle bodily sensations resembling those normally occurring when one is anxious or frightened (Bouton, Mineka, & Barlow, 2001). For example, consider a child who has asthma. An acute asthma attack produces sensations, such as shortness of breath, coughing, and chest tightness, that typically elicit fear and anxiety. Later, when the child experiences subtle symptoms that resemble the frightening symptoms of earlier asthma attacks (such as shortness of breath after climbing stairs), he may become anxious, fearful, and then experience a panic attack. In this situation, the subtle symptoms would represent a conditioned stimulus, and the panic attack would be a conditioned response. The finding that panic disorder is nearly three times as frequent among people with asthma as it is among people without asthma (Weiser, 2007) supports the possibility that panic disorder has the potential to develop through classical conditioning.

Cognitive factors may play an integral part in panic disorder. Generally, cognitive theories (Clark, 1996) argue that those with panic disorder are prone to interpret ordinary bodily sensations catastrophically, and these fearful interpretations set the stage for panic attacks. For example, a person might detect bodily changes that are routinely triggered by innocuous events such getting up from a seated position (dizziness), exercising (increased heart rate, shortness of breath), or drinking a large cup of coffee (increased heart rate, trembling). The individual interprets these subtle bodily changes catastrophically (“Maybe I’m having a heart attack!”). Such interpretations create fear and anxiety, which trigger additional physical symptoms; subsequently, the person experiences a panic attack. Support of this contention rests with findings that people with more severe catastrophic thoughts about sensations have more frequent and severe panic attacks, and among those with panic disorder, reducing catastrophic cognitions about their sensations is as effective as medication in reducing panic attacks (Good & Hinton, 2009).

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Generalized Anxiety Disorder

Alex was always worried about many things. He worried that his children would drown when they played at the beach. Each time he left the house, he worried that an electrical short circuit would start a fire in his home. He worried that his wife would lose her job at the prestigious law firm. He worried that his daughter’s minor staph infection could turn into a massive life-threatening condition. These and other worries constantly weighed heavily on Alex’s mind, so much so that they made it difficult for him to make decisions and often left him feeling tense, irritable, and worn out. One night, Alex’s wife was to drive their son home from a soccer game. However, his wife stayed after the game and talked with some of the other parents, resulting in her arriving home 45 minutes late. Alex had tried to call his cell phone three or four times, but he could not get through because the soccer field did not have a signal. Extremely worried, Alex eventually called the police, convinced that his wife and son had not arrived home because they had been in a terrible car accident.

Alex suffers from generalized anxiety disorder: a relatively continuous state of excessive, uncontrollable, and pointless worry and apprehension. People with generalized anxiety disorder often worry about routine, everyday things, even though their concerns are unjustified (Figure 10). For example, an individual may worry about her health and finances, the health of family members, the safety of her children, or minor matters (e.g., being late for an appointment) without having any legitimate reason for doing so (APA, 2013). A diagnosis of generalized anxiety disorder requires that the diffuse worrying and apprehension characteristic of this disorder—what Sigmund Freud referred to as free-floating anxiety—is not part of another disorder, occurs more days than not for at least six months, and is accompanied by any three of the following symptoms: restlessness, difficulty concentrating, being easily fatigued, muscle tension, irritability, and sleep difficulties.

About 5.7% of the U.S. population will develop symptoms of generalized anxiety disorder during their lifetime (Kessler et al., 2005), and females are 2 times as likely as males to experience the disorder (APA, 2013). Generalized anxiety disorder is highly comorbid with mood disorders and other anxiety disorders (Noyes, 2001), and it tends to be chronic. Also, generalized anxiety disorder appears to increase the risk for heart attacks and strokes, especially in people with preexisting heart conditions (Martens et al., 2010).

Although there have been few investigations aimed at determining the heritability of generalized anxiety disorder, a summary of available family and twin studies suggests that genetic factors play a modest role in the disorder (Hettema et al., 2001). Cognitive theories of generalized anxiety disorder suggest that worry represents a mental strategy to avoid more powerful negative emotions (Aikins & Craske, 2001), perhaps stemming from earlier unpleasant or traumatic experiences. Indeed, one longitudinal study found that childhood maltreatment was strongly related to the development of this disorder during adulthood (Moffitt et al., 2007); worrying might distract people from remembering painful childhood experiences.

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Obsessive-Compulsive Disorders

People with obsessive-compulsive disorder (OCD) experience thoughts and urges that are intrusive and unwanted (obsessions) and/or the need to engage in repetitive behaviors or mental acts (compulsions). A person with this disorder might, for example, spend hours each day washing his hands or constantly checking and rechecking to make sure that a stove, faucet, or light has been turned off.

Obsessions are more than just unwanted thoughts that seem to randomly jump into our head from time to time, such as recalling an insensitive remark a coworker made recently, and they are more significant than day-to-day worries we might have, such as justifiable concerns about being laid off from a job. Rather, obsessions are characterized as persistent, unintentional, and unwanted thoughts and urges that are highly intrusive, unpleasant, and distressing (APA, 2013). Common obsessions include concerns about germs and contamination, doubts (“Did I turn the water off?”), order and symmetry (“I need all the spoons in the tray to be arranged a certain way”), and urges that are aggressive or lustful. Usually, the person knows that such thoughts and urges are irrational and thus tries to suppress or ignore them, but has an extremely difficult time doing so. These obsessive symptoms sometimes overlap, such that someone might have both contamination and aggressive obsessions (Abramowitz & Siqueland, 2013).

Compulsions are repetitive and ritualistic acts that are typically carried out primarily as a means to minimize the distress that obsessions trigger or to reduce the likelihood of a feared event (APA, 2013). Compulsions often include such behaviors as repeated and extensive hand washing, cleaning, checking (e.g., that a door is locked), and ordering (e.g., lining up all the pencils in a particular way), and they also include such mental acts as counting, praying, or reciting something to oneself (Figure 11). Compulsions characteristic of OCD are not performed out of pleasure, nor are they connected in a realistic way to the source of the distress or feared event. Approximately 2.3% of the U.S. population will experience OCD in their lifetime (Ruscio, Stein, Chiu, & Kessler, 2010) and, if left untreated, OCD tends to be a chronic condition creating lifelong interpersonal and psychological problems (Norberg, Calamari, Cohen, & Riemann, 2008).

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Body Dysmorphic Disorder

An individual with body dysmorphic disorder is preoccupied with a perceived flaw in her physical appearance that is either nonexistent or barely noticeable to other people (APA, 2013). These perceived physical defects cause the person to think she is unattractive, ugly, hideous, or deformed. These preoccupations can focus on any bodily area, but they typically involve the skin, face, or hair. The preoccupation with imagined physical flaws drives the person to engage in repetitive and ritualistic behavioral and mental acts, such as constantly looking in the mirror, trying to hide the offending body part, comparisons with others, and, in some extreme cases, cosmetic surgery (Phillips, 2005). An estimated 2.4% of the adults in the United States meet the criteria for body dysmorphic disorder, with slightly higher rates in women than in men (APA, 2013).

Hoarding Disorder

Although hoarding was traditionally considered to be a symptom of OCD, considerable evidence suggests that hoarding represents an entirely different disorder (Mataix-Cols et al., 2010). People with hoarding disorder cannot bear to part with personal possessions, regardless of how valueless or useless these possessions are. As a result, these individuals accumulate excessive amounts of usually worthless items that clutter their living areas (Figure 12). Often, the quantity of cluttered items is so excessive that the person is unable use his kitchen, or sleep in his bed. People who suffer from this disorder have great difficulty parting with items because they believe the items might be of some later use, or because they form a sentimental attachment to the items (APA, 2013). Importantly, a diagnosis of hoarding disorder is made only if the hoarding is not caused by another medical condition and if the hoarding is not a symptom of another disorder (e.g., schizophrenia) (APA, 2013).

Causes of OCD

The results of family and twin studies suggest that OCD has a moderate genetic component. The disorder is five times more frequent in the first-degree relatives of people with OCD than in people without the disorder (Nestadt et al., 2000). Additionally, the concordance rate of OCD among identical twins is around 57%; however, the concordance rate for fraternal twins is 22% (Bolton, Rijsdijk, O’Connor, Perrin, & Eley, 2007). Studies have implicated about two dozen potential genes that may be involved in OCD; these genes regulate the function of three neurotransmitters: serotonin, dopamine, and glutamate (Pauls, 2010). Many of these studies included small sample sizes and have yet to be replicated. Thus, additional research needs to be done in this area.

A brain region that is believed to play a critical role in OCD is the orbitofrontal cortex (Kopell & Greenberg, 2008), an area of the frontal lobe involved in learning and decision-making (Rushworth, Noonan, Boorman, Walton, & Behrens, 2011) (Figure 13). In people with OCD, the orbitofrontal cortex becomes especially hyperactive when they are provoked with tasks in which, for example, they are asked to look at a photo of a toilet or of pictures hanging crookedly on a wall (Simon, Kaufmann, Müsch, Kischkel, & Kathmann, 2010). The orbitofrontal cortex is part of a series of brain regions that, collectively, is called the OCD circuit; this circuit consists of several interconnected regions that influence the perceived emotional value of stimuli and the selection of both behavioral and cognitive responses (Graybiel & Rauch, 2000). As with the orbitofrontal cortex, other regions of the OCD circuit show heightened activity during symptom provocation (Rotge et al., 2008), which suggests that abnormalities in these regions may produce the symptoms of OCD (Saxena, Bota, & Brody, 2001). Consistent with this explanation, people with OCD show a substantially higher degree of connectivity of the orbitofrontal cortex and other regions of the OCD circuit than do those without OCD (Beucke et al., 2013).

The findings discussed above were based on imaging studies, and they highlight the potential importance of brain dysfunction in OCD. However, one important limitation of these findings is the inability to explain differences in obsessions and compulsions. Another limitation is that the correlational relationship between neurological abnormalities and OCD symptoms cannot imply causation (Abramowitz & Siqueland, 2013).

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Posttraumatic Stress Disorder

A Broader Definition of PTSD

PTSD was listed among the anxiety disorders in previous DSM editions. In DSM-5, it is now listed among a group called Trauma-and-Stressor-Related Disorders. For a person to be diagnosed with PTSD, she be must exposed to, witness, or experience the details of a traumatic experience (e.g., a first responder), one that involves “actual or threatened death, serious injury, or sexual violence” (APA, 2013, p. 271). These experiences can include such events as combat, threatened or actual physical attack, sexual assault, natural disasters, terrorist attacks, and automobile accidents. This criterion makes PTSD the only disorder listed in the DSM in which a cause (extreme trauma) is explicitly specified.

Symptoms of PTSD include intrusive and distressing memories of the event, flashbacks (states that can last from a few seconds to several days, during which the individual relives the event and behaves as if the event were occurring at that moment [APA, 2013]), avoidance of stimuli connected to the event, persistently negative emotional states (e.g., fear, anger, guilt, and shame), feelings of detachment from others, irritability, proneness toward outbursts, and an exaggerated startle response (jumpiness). For PTSD to be diagnosed, these symptoms must occur for at least one month.

Roughly 7% of adults in the United States, including 9.7% of women and 3.6% of men, experience PTSD in their lifetime (National Comorbidity Survey, 2007), with higher rates among people exposed to mass trauma and people whose jobs involve duty-related trauma exposure (e.g., police officers, firefighters, and emergency medical personnel) (APA, 2013). Nearly 21% of residents of areas affected by Hurricane Katrina suffered from PTSD one year following the hurricane (Kessler et al., 2008), and 12.6% of Manhattan residents were observed as having PTSD 2–3 years after the 9/11 terrorist attacks (DiGrande et al., 2008).

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Risk Factors for PTSD

Of course, not everyone who experiences a traumatic event will go on to develop PTSD; several factors strongly predict the development of PTSD: trauma experience, greater trauma severity, lack of immediate social support, and more subsequent life stress (Brewin, Andrews, & Valentine, 2000). Traumatic events that involve harm by others (e.g., combat, rape, and sexual molestation) carry greater risk than do other traumas (e.g., natural disasters) (Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). Factors that increase the risk of PTSD include female gender, low socioeconomic status, low intelligence, personal history of mental disorders, history of childhood adversity (abuse or other trauma during childhood), and family history of mental disorders (Brewin et al., 2000). Personality characteristics such as neuroticism and somatization (the tendency to experience physical symptoms when one encounters stress) have been shown to elevate the risk of PTSD (Bramsen, Dirkzwager, & van der Ploeg, 2000). People who experience childhood adversity and/or traumatic experiences during adulthood are at significantly higher risk of developing PTSD if they possess one or two short versions of a gene that regulates the neurotransmitter serotonin (Xie et al., 2009). This suggests a possible diathesis-stress interpretation of PTSD: its development is influenced by the interaction of psychosocial and biological factors.

Support for Sufferers of PTSD

Research has shown that social support following a traumatic event can reduce the likelihood of PTSD (Ozer, Best, Lipsey, & Weiss, 2003). Social support is often defined as the comfort, advice, and assistance received from relatives, friends, and neighbors. Social support can help individuals cope during difficult times by allowing them to discuss feelings and experiences and providing a sense of being loved and appreciated. A 14-year study of 1,377 American Legionnaires who had served in the Vietnam War found that those who perceived less social support when they came home were more likely to develop PTSD than were those who perceived greater support (Figure 14). In addition, those who became involved in the community were less likely to develop PTSD, and they were more likely to experience a remission of PTSD than were those who were less involved (Koenen, Stellman, Stellman, & Sommer, 2003).

Learning and Development of PTSD

PTSD learning models suggest that some symptoms are developed and maintained through classical conditioning. The traumatic event may act as an unconditioned stimulus that elicits an unconditioned response characterized by extreme fear and anxiety. Cognitive, emotional, physiological, and environmental cues accompanying or related to the event are conditioned stimuli. These traumatic reminders evoke conditioned responses (extreme fear and anxiety) similar to those caused by the event itself (Nader, 2001). A person who was in the vicinity of the Twin Towers during the 9/11 terrorist attacks and who developed PTSD may display excessive hypervigilance and distress when planes fly overhead; this behavior constitutes a conditioned response to the traumatic reminder (conditioned stimulus of the sight and sound of an airplane). Differences in how conditionable individuals are help to explain differences in the development and maintenance of PTSD symptoms (Pittman, 1988). Conditioning studies demonstrate facilitated acquisition of conditioned responses and delayed extinction of conditioned responses in people with PTSD (Orr et al., 2000).

Cognitive factors are important in the development and maintenance of PTSD. One model suggests that two key processes are crucial: disturbances in memory for the event, and negative appraisals of the trauma and its aftermath (Ehlers & Clark, 2000). According to this theory, some people who experience traumas do not form coherent memories of the trauma; memories of the traumatic event are poorly encoded and, thus, are fragmented, disorganized, and lacking in detail. Therefore, these individuals are unable remember the event in a way that gives it meaning and context. A rape victim who cannot coherently remember the event may remember only bits and pieces (e.g., the attacker repeatedly telling her she is stupid); because she was unable to develop a fully integrated memory, the fragmentary memory tends to stand out. Although unable to retrieve a complete memory of the event, she may be haunted by intrusive fragments involuntarily triggered by stimuli associated with the event (e.g., memories of the attacker’s comments when encountering a person who resembles the attacker). This interpretation fits previously discussed material concerning PTSD and conditioning. The model also proposes that negative appraisals of the event (“I deserved to be raped because I’m stupid”) may lead to dysfunctional behavioral strategies (e.g., avoiding social activities where men are likely to be present) that maintain PTSD symptoms by preventing both a change in the nature of the memory and a change in the problematic appraisals.

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What is Major Depressive Disorder?

According to the DSM-5, the defining symptoms of major depressive disorder include “depressed mood most of the day, nearly every day” (feeling sad, empty, hopeless, or appearing tearful to others), and loss of interest and pleasure in usual activities (APA, 2013). In addition to feeling overwhelmingly sad most of each day, people with depression will no longer show interest or enjoyment in activities that previously were gratifying, such as hobbies, sports, sex, social events, time spent with family, and so on. Friends and family members may notice that the person has completely abandoned previously enjoyed hobbies; for example, an avid tennis player who develops major depressive disorder no longer plays tennis (Rothschild, 1999).

To receive a diagnosis of major depressive disorder, one must experience a total of five symptoms for at least a two-week period; these symptoms must cause significant distress or impair normal functioning, and they must not be caused by substances or a medical condition. At least one of the two symptoms mentioned above must be present, plus any combination of the following symptoms (APA, 2013):

• significant weight loss (when not dieting) or weight gain and/or significant decrease or increase in appetite;
• difficulty falling asleep or sleeping too much;
• psychomotor agitation (the person is noticeably fidgety and jittery, demonstrated by behaviors like the inability to sit, pacing, hand-wringing, pulling or rubbing of the skin, clothing, or other objects) or psychomotor retardation (the person talks and moves slowly, for example, talking softly, very little, or in a monotone);
• fatigue or loss of energy;
• feelings of worthlessness or guilt;
• difficulty concentrating and indecisiveness; and
• suicidal ideation: thoughts of death (not just fear of dying), thinking about or planning suicide, or making an actual suicide attempt.

Major depressive disorder is considered episodic: its symptoms are typically present at their full magnitude for a certain period of time and then gradually abate. Approximately 50%–60% of people who experience an episode of major depressive disorder will have a second episode at some point in the future; those who have had two episodes have a 70% chance of having a third episode, and those who have had three episodes have a 90% chance of having a fourth episode (Rothschild, 1999). Although the episodes can last for months, a majority a people diagnosed with this condition (around 70%) recover within a year. However, a substantial number do not recover; around 12% show serious signs of impairment associated with major depressive disorder after 5 years (Boland & Keller, 2009). In the long-term, many who do recover will still show minor symptoms that fluctuate in their severity (Judd, 2012).

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Subtypes of Depression

The DSM-5 lists several different subtypes of depression. These subtypes—what the DSM-5 refer to as specifiers—are not specific disorders; rather, they are labels used to indicate specific patterns of symptoms or to specify certain periods of time in which the symptoms may be present. One subtype, seasonal pattern, applies to situations in which a person experiences the symptoms of major depressive disorder only during a particular time of year (e.g., fall or winter). In everyday language, people often refer to this subtype as the winter blues.

Another subtype, peripartum onset (commonly referred to as postpartum depression), applies to women who experience major depression during pregnancy or in the four weeks following the birth of their child (APA, 2013). These women often feel very anxious and may even have panic attacks. They may feel guilty, agitated, and be weepy. They may not want to hold or care for their newborn, even in cases in which the pregnancy was desired and intended. In extreme cases, the mother may have feelings of wanting to harm her child or herself. In a horrific illustration, a woman named Andrea Yates, who suffered from extreme peripartum-onset depression (as well as other mental illnesses), drowned her five children in a bathtub (Roche, 2002). Most women with peripartum-onset depression do not physically harm their children, but most do have difficulty being adequate caregivers (Fields, 2010). A surprisingly high number of women experience symptoms of peripartum-onset depression. A study of 10,000 women who had recently given birth found that 14% screened positive for peripartum-onset depression, and that nearly 20% reported having thoughts of wanting to harm themselves (Wisner et al., 2013).

People with persistent depressive disorder (previously known as dysthymia) experience depressed moods most of the day nearly every day for at least two years, as well as at least two of the other symptoms of major depressive disorder. People with persistent depressive disorder are chronically sad and melancholy, but do not meet all the criteria for major depression. However, episodes of full-blown major depressive disorder can occur during persistent depressive disorder (APA, 2013).

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Risk Factors for Bipolar Disorder

Bipolar disorder is considerably less frequent than major depressive disorder. In the United States, 1 out of every 167 people meets the criteria for bipolar disorder each year, and 1 out of 100 meet the criteria within their lifetime (Merikangas et al., 2011). The rates are higher in men than in women, and about half of those with this disorder report onset before the age of 25 (Merikangas et al., 2011). Around 90% of those with bipolar disorder have a comorbid disorder, most often an anxiety disorder or a substance abuse problem. Unfortunately, close to half of the people suffering from bipolar disorder do not receive treatment (Merikangas & Tohen, 2011). Suicide rates are extremely high among those with bipolar disorder: around 36% of individuals with this disorder attempt suicide at least once in their lifetime (Novick, Swartz, & Frank, 2010), and between 15%–19% complete suicide (Newman, 2004).

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The Biological Basis of Mood Disorders

Depression is linked to abnormal activity in several regions of the brain (Fitzgerald, Laird, Maller, & Daskalakis, 2008) including those important in assessing the emotional significance of stimuli and experiencing emotions (amygdala), and in regulating and controlling emotions (like the prefrontal cortex, or PFC) (LeMoult, Castonguay, Joormann, & McAleavey, 2013). Depressed individuals show elevated amygdala activity (Drevets, Bogers, & Raichle, 2002), especially when presented with negative emotional stimuli, such as photos of sad faces (Figure 17) (Surguladze et al., 2005). Interestingly, heightened amygdala activation to negative emotional stimuli among depressed persons occurs even when stimuli are presented outside of conscious awareness (Victor, Furey, Fromm, Öhman, & Drevets, 2010), and it persists even after the negative emotional stimuli are no longer present (Siegle, Thompson, Carter, Steinhauer, & Thase, 2007). Additionally, depressed individuals exhibit less activation in the prefrontal, particularly on the left side (Davidson, Pizzagalli, & Nitschke, 2009). Because the PFC can dampen amygdala activation, thereby enabling one to suppress negative emotions (Phan et al., 2005), decreased activation in certain regions of the PFC may inhibit its ability to override negative emotions that might then lead to more negative mood states (Davidson et al., 2009). These findings suggest that depressed persons are more prone to react to emotionally negative stimuli, yet have greater difficulty controlling these reactions.

Since the 1950s, researchers have noted that depressed individuals have abnormal levels of cortisol, a stress hormone released into the blood by the neuroendocrine system during times of stress (Mackin & Young, 2004). When cortisol is released, the body initiates a fight-or-flight response in reaction to a threat or danger. Many people with depression show elevated cortisol levels (Holsboer & Ising, 2010), especially those reporting a history of early life trauma such as the loss of a parent or abuse during childhood (Baes, Tofoli, Martins, & Juruena, 2012). Such findings raise the question of whether high cortisol levels are a cause or a consequence of depression. High levels of cortisol are a risk factor for future depression (Halligan, Herbert, Goodyer, & Murray, 2007), and cortisol activates activity in the amygdala while deactivating activity in the PFC (McEwen, 2005)—both brain disturbances are connected to depression. Thus, high cortisol levels may have a causal effect on depression, as well as on its brain function abnormalities (van Praag, 2005). Also, because stress results in increased cortisol release (Michaud, Matheson, Kelly, Anisman, 2008), it is equally reasonable to assume that stress may precipitate depression.

Diathesis-Stress Model and Major Depressive Disorders

Indeed, it has long been believed that stressful life events can trigger depression, and research has consistently supported this conclusion (Mazure, 1998). Stressful life events include significant losses, such as death of a loved one, divorce or separation, and serious health and money problems; life events such as these often precede the onset of depressive episodes (Brown & Harris, 1989). In particular, exit events—instances in which an important person departs (e.g., a death, divorce or separation, or a family member leaving home)—often occur prior to an episode (Paykel, 2003). Exit events are especially likely to trigger depression if these happenings occur in a way that humiliates or devalues the individual. For example, people who experience the breakup of a relationship initiated by the other person develop major depressive disorder at a rate more than 2 times that of people who experience the death of a loved one (Kendler, Hettema, Butera, Gardner, & Prescott, 2003).

Likewise, individuals who are exposed to traumatic stress during childhood—such as separation from a parent, family turmoil, and maltreatment (physical or sexual abuse)—are at a heightened risk of developing depression at any point in their lives (Kessler, 1997). A recent review of 16 studies involving over 23,000 subjects concluded that those who experience childhood maltreatment are more than 2 times as likely to develop recurring and persistent depression (Nanni, Uher, & Danese, 2012).

Of course, not everyone who experiences stressful life events or childhood adversities succumbs to depression—indeed, most do not. Clearly, a diathesis-stress interpretation of major depressive disorder, in which certain predispositions or vulnerability factors influence one’s reaction to stress, would seem logical. If so, what might such predispositions be? A study by Caspi and others (2003) suggests that an alteration in a specific gene that regulates serotonin (the 5-HTTLPR gene) might be one culprit. These investigators found that people who experienced several stressful life events were significantly more likely to experience episodes of major depression if they carried one or two short versions of this gene than if they carried two long versions. Those who carried one or two short versions of the 5-HTTLPR gene were unlikely to experience an episode, however, if they had experienced few or no stressful life events. Numerous studies have replicated these findings, including studies of people who experienced maltreatment during childhood (Goodman & Brand, 2009). In a recent investigation conducted in the United Kingdom (Brown & Harris, 2013), researchers found that childhood maltreatment before age 9 elevated the risk of chronic adult depression (a depression episode lasting for at least 12 months) among those individuals having one (LS) or two (SS) short versions of the 5-HTTLPR gene (Figure 18). Childhood maltreatment did not increase the risk for chronic depression for those have two long (LL) versions of this gene. Thus, genetic vulnerability may be one mechanism through which stress potentially leads to depression.

Schizophrenia and Dissociative Disorders

Schizophrenia is a severe disorder characterized by a complete breakdown in one’s ability to function in life; it often requires hospitalization. People with schizophrenia experience hallucinations and delusions, and they have extreme difficulty regulating their emotions and behavior. Thinking is incoherent and disorganized, behavior is extremely bizarre, emotions are flat, and motivation to engage in most basic life activities is lacking.

Schizophrenia is not to be confused with multiple personality disorder, which is technically termed dissociative identity disorder. The main characteristic of dissociative disorders is that people become dissociated from their sense of self, resulting in memory and identity disturbances. Dissociative disorders listed in the DSM-5 include dissociative amnesia, depersonalization/derealization disorder, and dissociative identity disorder. A person with dissociative amnesia is unable to recall important personal information, often after a stressful or traumatic experience. In this section, you’ll learn about the differences between schizophrenia and these disorders.

Symptoms of Schizophrenia

The main symptoms of schizophrenia include hallucinations, delusions, disorganized thinking, disorganized or abnormal motor behavior, and negative symptoms (APA, 2013). A hallucination is a perceptual experience that occurs in the absence of external stimulation. Auditory hallucinations (hearing voices) occur in roughly two-thirds of patients with schizophrenia and are by far the most common form of hallucination (Andreasen, 1987). The voices may be familiar or unfamiliar, they may have a conversation or argue, or the voices may provide a running commentary on the person’s behavior (Tsuang, Farone, & Green, 1999).

Less common are visual hallucinations (seeing things that are not there) and olfactory hallucinations (smelling odors that are not actually present).

Delusions are beliefs that are contrary to reality and are firmly held even in the face of contradictory evidence. Many of us hold beliefs that some would consider odd, but a delusion is easily identified because it is clearly absurd. A person with schizophrenia may believe that his mother is plotting with the FBI to poison his coffee, or that his neighbor is an enemy spy who wants to kill him. These kinds of delusions are known as paranoid delusions, which involve the (false) belief that other people or agencies are plotting to harm the person. People with schizophrenia also may hold grandiose delusions, beliefs that one holds special power, unique knowledge, or is extremely important. For example, the person who claims to be Jesus Christ, or who claims to have knowledge going back 5,000 years, or who claims to be a great philosopher is experiencing grandiose delusions. Other delusions include the belief that one’s thoughts are being removed (thought withdrawal) or thoughts have been placed inside one’s head (thought insertion). Another type of delusion is somatic delusion, which is the belief that something highly abnormal is happening to one’s body (e.g., that one’s kidneys are being eaten by cockroaches).

Disorganized thinking refers to disjointed and incoherent thought processes—usually detected by what a person says. The person might ramble, exhibit loose associations (jump from topic to topic), or talk in a way that is so disorganized and incomprehensible that it seems as though the person is randomly combining words. Disorganized thinking is also exhibited by blatantly illogical remarks (e.g., “Fenway Park is in Boston. I live in Boston. Therefore, I live at Fenway Park.”) and by tangentiality: responding to others’ statements or questions by remarks that are either barely related or unrelated to what was said or asked. For example, if a person diagnosed with schizophrenia is asked if she is interested in receiving special job training, she might state that she once rode on a train somewhere. To a person with schizophrenia, the tangential (slightly related) connection between job training and riding a train are sufficient enough to cause such a response.

Disorganized or abnormal motor behavior refers to unusual behaviors and movements: becoming unusually active, exhibiting silly child-like behaviors (giggling and self-absorbed smiling), engaging in repeated and purposeless movements, or displaying odd facial expressions and gestures. In some cases, the person will exhibit catatonic behaviors, which show decreased reactivity to the environment, such as posturing, in which the person maintains a rigid and bizarre posture for long periods of time, or catatonic stupor, a complete lack of movement and verbal behavior.

Schizophrenia has positive and negative symptoms. Positive symptoms of schizophrenia are symptoms of commission, meaning they are something that individuals do or think. Examples include the hallucinations, delusions, and bizarre or disorganized behavior describe above. Negative symptoms are those that reflect noticeable decreases and absences in certain behaviors, emotions, or drives (Green, 2001). A person who exhibits diminished emotional expression shows no emotion in his facial expressions, speech, or movements, even when such expressions are normal or expected (also known as flat affect). Avolition is characterized by a lack of motivation to engage in self-initiated and meaningful activity, including the most basic of tasks, such as bathing and grooming. Alogia refers to reduced speech output; in simple terms, patients do not say much. Another negative symptom is asociality, or social withdrawal and lack of interest in engaging in social interactions with others. A final negative symptom, anhedonia, refers to an inability to experience pleasure. One who exhibits anhedonia expresses little interest in what most people consider to be pleasurable activities, such as hobbies, recreation, or sexual activity.

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Causes of Schizophrenia

Schizophrenia: Early Warning Signs

Early detection and treatment of conditions such as heart disease and cancer have improved survival rates and quality of life for people who suffer from these conditions. A new approach involves identifying people who show minor symptoms of psychosis, such as unusual thought content, paranoia, odd communication, delusions, problems at school or work, and a decline in social functioning—which are coined prodromal symptoms—and following these individuals over time to determine which of them develop a psychotic disorder and which factors best predict such a disorder. A number of factors have been identified that predict a greater likelihood that prodromal individuals will develop a psychotic disorder: genetic risk (a family history of psychosis), recent deterioration in functioning, high levels of unusual thought content, high levels of suspicion or paranoia, poor social functioning, and a history of substance abuse (Fusar-Poli et al., 2013). Further research will enable a more accurate prediction of those at greatest risk for developing schizophrenia, and thus to whom early intervention efforts should be directed.

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Dissociative Amnesia

Amnesia refers to the partial or total forgetting of some experience or event. An individual with dissociative amnesia is unable to recall important personal information, usually following an extremely stressful or traumatic experience such as combat, natural disasters, or being the victim of violence. The memory impairments are not caused by ordinary forgetting. Some individuals with dissociative amnesia will also experience dissociative fugue (from the word “to flee” in French), whereby they suddenly wander away from their home, experience confusion about their identity, and sometimes even adopt a new identity (Cardeña & Gleaves, 2006). Most fugue episodes last only a few hours or days, but some can last longer. One study of residents in communities in upstate New York reported that about 1.8% experienced dissociative amnesia in the previous year (Johnson, Cohen, Kasen, & Brook, 2006).

Some have questioned the validity of dissociative amnesia (Pope, Hudson, Bodkin, & Oliva, 1998); it has even been characterized as a “piece of psychiatric folklore devoid of convincing empirical support” (McNally, 2003, p. 275). Notably, scientific publications regarding dissociative amnesia rose during the 1980s and reached a peak in the mid-1990s, followed by an equally sharp decline by 2003; in fact, only 13 cases of individuals with dissociative amnesia worldwide could be found in the literature that same year (Pope, Barry, Bodkin, & Hudson, 2006). Further, no description of individuals showing dissociative amnesia following a trauma exists in any fictional or nonfictional work prior to 1800 (Pope, Poliakoff, Parker, Boynes, & Hudson, 2006). However, a study of 82 individuals who enrolled for treatment at a psychiatric outpatient hospital found that nearly 10% met the criteria for dissociative amnesia, perhaps suggesting that the condition is underdiagnosed, especially in psychiatric populations (Foote, Smolin, Kaplan, Legatt, & Lipschitz, 2006).

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Depersonalization/Derealization Disorder

Depersonalization/derealization disorder is characterized by recurring episodes of depersonalization, derealization, or both. Depersonalization is defined as feelings of “unreality or detachment from, or unfamiliarity with, one’s whole self or from aspects of the self” (APA, 2013, p. 302). Individuals who experience depersonalization might believe their thoughts and feelings are not their own; they may feel robotic as though they lack control over their movements and speech; they may experience a distorted sense of time and, in extreme cases, they may sense an “out-of-body” experience in which they see themselves from the vantage point of another person. Derealization is conceptualized as a sense of “unreality or detachment from, or unfamiliarity with, the world, be it individuals, inanimate objects, or all surroundings” (APA, 2013, p. 303). A person who experiences derealization might feel as though he is in a fog or a dream, or that the surrounding world is somehow artificial and unreal. Individuals with depersonalization/derealization disorder often have difficulty describing their symptoms and may think they are going crazy (APA, 2013).

Dissociative Identity Disorder

By far, the most well-known dissociative disorder is dissociative identity disorder (formerly called multiple personality disorder). People with dissociative identity disorder exhibit two or more separate personalities or identities, each well-defined and distinct from one another. They also experience memory gaps for the time during which another identity is in charge (e.g., one might find unfamiliar items in her shopping bags or among her possessions), and in some cases may report hearing voices, such as a child’s voice or the sound of somebody crying (APA, 2013). The study of upstate New York residents mentioned above (Johnson et al., 2006) reported that 1.5% of their sample experienced symptoms consistent with dissociative identity disorder in the previous year.

Dissociative identity disorder (DID) is highly controversial. Some believe that people fake symptoms to avoid the consequences of illegal actions (e.g., “I am not responsible for shoplifting because it was my other personality”). In fact, it has been demonstrated that people are generally skilled at adopting the role of a person with different personalities when they believe it might be advantageous to do so. As an example, Kenneth Bianchi was an infamous serial killer who, along with his cousin, murdered over a dozen females around Los Angeles in the late 1970s. Eventually, he and his cousin were apprehended. At Bianchi’s trial, he pled not guilty by reason of insanity, presenting himself as though he had DID and claiming that a different personality (“Steve Walker”) committed the murders. When these claims were scrutinized, he admitted faking the symptoms and was found guilty (Schwartz, 1981).

A second reason DID is controversial is because rates of the disorder suddenly skyrocketed in the 1980s. More cases of DID were identified during the five years prior to 1986 than in the preceding two centuries (Putnam, Guroff, Silberman, Barban, & Post, 1986). Although this increase may be due to the development of more sophisticated diagnostic techniques, it is also possible that the popularization of DID—helped in part by Sybil, a popular 1970s book (and later film) about a woman with 16 different personalities—may have prompted clinicians to overdiagnose the disorder (Piper & Merskey, 2004). Casting further scrutiny on the existence of multiple personalities or identities is the recent suggestion that the story of Sybil was largely fabricated, and the idea for the book might have been exaggerated (Nathan, 2011).

Despite its controversial nature, DID is clearly a legitimate and serious disorder, and although some people may fake symptoms, others suffer their entire lives with it. People with this disorder tend to report a history of childhood trauma, some cases having been corroborated through medical or legal records (Cardeña & Gleaves, 2006). Research by Ross et al. (1990) suggests that in one study about 95% of people with DID were physically and/or sexually abused as children. Of course, not all reports of childhood abuse can be expected to be valid or accurate. However, there is strong evidence that traumatic experiences can cause people to experience states of dissociation, suggesting that dissociative states—including the adoption of multiple personalities—may serve as a psychologically important coping mechanism for threat and danger (Dalenberg et al., 2012).

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