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The previous chapter focused on depressive and anxiety disorders. Those disorders can disrupt people’s lives, yet they generally leave two psychological qualities intact. One is that people are in touch with reality. For example, a socially anxious person’s level of worry about social relationships may be excessive, but the relationships really do exist. Another quality is that thinking is organized logically. A depressed person may say, “I just feel I’m wasting everyone’s time. No one can help me” (see Chapter 15), but is unlikely to say, “I have a sort of silver bullet which held me by my leg, that one cannot jump in, where one wants, and that ends beautifully like the stars” (McKenna & Oh, 2005, p. 2)—a disorganized jumble of ideas.

In psychotic disorders, people lose these basic mental abilities. Psychotic disorders are psychological disorders whose core symptoms are that people’s thoughts and actions are disorganized and their thinking loses touch with reality; people see and worry about things that do not exist (Heckers et al., 2013).

A particularly severe psychotic disorder, which we will focus on first, is schizophrenia. The Diagnostic and Statistical Manual of Mental Disorders (DSM, discussed in Chapter 15) defines schizophrenia as a disorder in which people exhibit multiple psychotic symptoms (detailed below) for a period of at least one month. Schizophrenia is prevalent globally. A meta-analysis of nearly 200 studies from 46 different nations indicated that schizophrenia occurs in 4.6 out of 1000 people (i.e., about 1 out of every 200; Saha et al., 2005). Rates do not vary across countries or between genders (Eranti et al., 2013); wherever you go, between 4 and 7 people out of 1000 experience the disease. Schizophrenia is costly not only to sufferers and their families, but also to society as a whole. In a wide range of industrialized countries, between 1.5 and 3% of nations’ overall healthcare budgets are expended on schizophrenia treatment and care (Knapp, Mangalore, & Simon, 2004).

Let’s first learn about schizophrenia at a person level of analysis. We’ll examine symptoms that haunt the lives of people with schizophrenia, as well as the illness’s typical development across the course of people’s lives. Next, we’ll move “down” to mind and brain levels of analysis to show how schizophrenia affects information processing in the mind and physiological functioning in the brain. The study of mind and brain, as you’ll see, helps to explain the symptoms experienced by people with schizophrenia. Finally, you’ll learn how mental health professionals treat this mental illness.

People with schizophrenia face exceptional challenges. Schizophrenia symptoms severely disrupt their experience of the world and their sense of self (Estroff, 1989). The symptoms are of three types (National Institute of Mental Health, 2009):

Let’s examine these in detail, beginning with positive symptoms.

POSITIVE SYMPTOMS. One positive symptom of schizophrenia is delusional beliefs, which are personal convictions that contradict known facts about the world but that a person clings to even when faced with conflicting evidence (Heckers et al., 2013). You read some delusional beliefs in the quotes above. The idea that one’s family has been replaced by androids or that one is receiving messages from the CIA through the TV is typical of the delusional beliefs experienced by people with schizophrenia (Elgie et al., 2005). Such beliefs are so bizarre that you can’t help but wonder how anyone could take them seriously. Yet, to people with schizophrenia, they are vivid, compelling, and convincing. Some common delusional beliefs are somatic delusions (e.g., believing that one has been injured, is ill, or has been poisoned) and delusions of grandeur (believing one has special abilities or powers; Tateyama et al., 1998).

A second positive symptom of schizophrenia is hallucination. Hallucinations are experiences—sights, sounds, smells, tastes, or feelings (touch)—of people or things that are not really there. A person with schizophrenia may, for instance, hallucinate an evil demon. He may have the experience of seeing and hearing the demon, standing right there in front of him, issuing orders. The majority of people with schizophrenia experience hallucinations, which often recur across decades of life (Goghari et al., 2013).

Some people with schizophrenia experience delusions and hallucinations, yet otherwise retain their normal thinking abilities. For example, when they express strange beliefs (e.g., “The demon is telling me what to do”), they do so in sentences that are organized logically. But others with the disease suffer a third positive symptom of schizophrenia: disorganized thinking. In disorganized thinking, people cannot structure their thoughts and spoken words in a manner consistent with standard rules of language use. Their thoughts are garbled and unintelligible.

Sometimes disorganized thinking is evident in sentence-to-sentence connections within a conversation. In normal dialogue, ideas flow logically from one sentence to the next. In conversation marked by disorganized thinking, however, ideas jump illogically. Consider this interview with a patient with schizophrenia, who begins by discussing his fear of other people:

“I’m so scared I could tell you that picture’s got a headache.”

“Can you tell me more about that?” the interviewer asks.

“When a sperm and an egg go together to make a baby, only one sperm goes up the egg and when they touch there are two contact points touched before the other two then it’s carried up in the air. When they fuse it’s like nuclear fusion except it’s human fusion. There’s a mass loss of the proton. When heat abstraction goes up in the electron, spins around, comes back down into the proton to form the mind. And the mind could be reduced to one atom.”

—Neuroslicer (2007, April 18)

It’s not merely that the content of the person’s beliefs is bizarre (e.g., “picture’s got a headache”). In addition, the sentence-to-sentence flow of thoughts does not follow normal rules of conversation. The interviewer asks about the picture. In response, the patient discusses human conception.

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Disorganized thinking can also occur at the level of sentences and individual words. Patients’ sentences may be schizophrenic word salads: seemingly random jumbles of words that are meaningless to listeners. When talking to someone with schizophrenia, you may hear sentences such as, “Tramway flogging into my question, are you why is it thirty letters down under peanut butter, what is it” (an example frequently cited online).

A final positive symptom of schizophrenia is disorders of motor movement (Arango & Carpenter, 2011). Patients may display odd mannerisms, such as a strange grimace on their face. Others engage in repeated movements, such as spinning a lock of hair over and over again. Still others exhibit catatonia, which is a lack of motor movement. Some people with schizophrenia display little movement throughout the day and thus appear withdrawn from the outside world. “No movement from me,” one writes. “It’s as if I was an old oak tree, the blank stare, the silent face” (www.schizophrenia.com posting).

NEGATIVE SYMPTOMS. The negative symptoms of schizophrenia consist of emotional and behavioral deficits (Kirkpatrick et al., 1989). People with schizophrenia lack emotional experiences enjoyed by others and fail to engage in valuable social behaviors. These deficits in emotion and behavior reduce schizophrenic individuals’ overall sense of well-being (Blanchard et al., 2011); in fact, their quality of life is reduced even more by the negative symptoms of schizophrenia than the positive ones (Rabinowitz et al., 2012).

One negative symptom is flat affect (pronounced AFF-ect), an absence of normal emotional expression (Kring & Moran, 2008). Rather than the typical “ups” and “downs” of emotion—a smile, a frown, a look of interest, a look of annoyance—people with schizophrenia may display no emotions at all; they may appear lethargic and emotionless. When asked by researchers, people with schizophrenia do report experiencing emotions—yet, at the same time, they may show little or no sign of emotion on their faces (Kring et al., 1993). Not all persons with schizophrenia display flat affect. However, those who do display it report lower quality of life and, in the long run, are less likely to see their schizophrenic symptoms improve (Gur et al., 2006).

Another negative symptom is a lack of interest in social activities. Normally, people find some daily activities interesting. You might look forward to lunch, or meeting friends, or shopping, or playing video games—or maybe even learning about psychology! However, many people with schizophrenia experience little pleasure in any everyday activity. As a result, they are not motivated to plan or engage in them (Kirkpatrick et al., 1989). This lack of interest can extend to behaviors that seem like necessities of life, such as hygiene and overall personal care.

People with schizophrenia often are well aware of this neglect: “Lately I’ve noticed that my personal hygiene has been (expletive),” one person writes. “I only shower once every two weeks, I don’t shave my face, I just don’t care how I look anymore” (www.schizophrenia.com posting). They also may possess insight into why they lack motivation for personal care: “When we discover that our futures are impacted by an incurable disease, we give up on it.”

COGNITIVE IMPAIRMENTS. On top of the positive and negative symptoms of schizophrenia, individuals with the disease also experience cognitive impairments, which, as noted previously, are reduced abilities to execute mental skills that are simple for most people (Kuperberg & Heckers, 2000). We’ll look at three, which involve concentration, memory, and social cognition —that is, thinking about other people and social interactions (see Chapter 12).

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Table 16.1 summarizes the range of symptoms—positive, negative, and cognitive impairments—experienced in schizophrenia. Not all patients experience all symptoms; people with schizophrenia can exhibit different patterns of symptomatology.

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Why do people with schizophrenia experience this broad range of symptoms? Some answers come from research on how the illness affects information-processing systems of the mind and the biological machinery of the brain. One key information-processing system is working memory.

WORKING MEMORY. Working memory (see Chapter 6) is the mental system you use to store information in mind for brief periods (e.g., a phone number you keep in mind until you have time to write it down), to manipulate stored information (e.g., adding up a set of digits), and, importantly, to control your own mental activities. Working memory contains a “central executive” that people use to focus attention on tasks. When you concentrate on solving a problem while avoiding distractions from nearby sounds and sights, you’re employing the central executive component of your working memory system.

In schizophrenia, working memory is impaired (Barch, 2005). Individuals with schizophrenia perform less well than others on laboratory tasks that assess working memory ability (Barch, 2005). This working memory impairment helps to explain symptoms experienced by people with schizophrenia, discussed earlier, such as disorganized thinking (where words and sentences are not connected logically). Working memory is the “executive” mental system that enables people to organize their thoughts. Breakdowns in this component of the mind thus contribute to a positive symptom of schizophrenia, disorganized thought.

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An additional information-processing problem in schizophrenia is information-processing speed. Individuals with schizophrenia do not process information as quickly as others. They take longer to complete various timed laboratory tasks (Mesholam-Gately et al., 2009).

EMOTION AND DECISION MAKING. In addition to affecting working memory, schizophrenia impairs mental systems that are needed for decision making. These systems involve both thinking and emotion. When people who are not affected by schizophrenia make decisions, their emotions often improve the quality of their decision making (see Chapter 10). Specifically, negative emotions experienced after bad decisions help people avoid making those same poor decisions in the future. Key evidence of this comes from research where people played a gambling task in which participants’ emotional reactions and decisions were recorded. Negative emotions after bad gambling decisions helped people improve the decisions they made on future gambles (Bechara et al., 1994).

What happens when people with schizophrenia play this gambling game? Unlike most others, they show little improvement across trials of the task (Shurman, Horan, & Nuechterlein, 2005). Even after big gambling losses, schizophrenic patients do not have the emotion-induced changes in decision making that nonpatients exhibit. As a result, they perform poorly on the task.

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We’ve now seen what life is like for people with schizophrenia. They experience delusions and flat affect, and they have difficulty focusing on tasks and planning daily events. We’ve also seen how schizophrenia affects information-processing systems of the mind. It impairs the central executive system of working memory, as well as the thinking and emotional systems involved in decision making.

Let’s now move to a biological level of analysis. How does schizophrenia affect the brain and how do these biological effects explain the psychological ones?

As discussed in Chapters 2 and 3, the brain contains both neurons (the cells of the brain) and neurotransmitters (the chemical substances through which neurons communicate). We’ll look at both, starting with the role of a specific neurotransmitter, dopamine, in schizophrenia.

DOPAMINE. The brain contains a variety of neurotransmitters. When searching for biochemical bases of schizophrenia, then, two questions arise: Which neurotransmitter is most central to schizophrenia? And why do high or low levels of that neurotransmitter cause schizophrenic symptoms?

Most researchers agree that the answer to the first question is dopamine. Dopamine is a neurotransmitter found in multiple regions of the brain (Figure 16.1). Thanks to its widespread presence, it can affect multiple aspects of mental life.

More than half a century ago, researchers discovered that dopamine and schizophrenia were linked. The discovery originated with an unexpected finding: Some drugs originally designed to treat other medical problems were found to reduce symptoms of schizophrenia (Valenstein, 1998). The drugs, it turned out, were those that blocked the neuron-to-neuron transmission of dopamine. This finding fueled the dopamine hypothesis of schizophrenia, which states that abnormal levels of dopamine are responsible for the symptoms of schizophrenia. According to the hypothesis, positive symptoms of schizophrenia, such as delusions, result from unusually high levels of dopamine-based communication among neurons in lower (subcortical) regions of the brain (Stahl, 2002; Figure 16.2). Schizophrenia’s negative symptoms and cognitive impairments result from unusually low levels of dopamine in the brain’s cortex (Abi-Dargham, 2004).

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Research has provided support for the dopamine hypothesis. For example, individuals with schizophrenia have relatively high levels of dopamine in subcortical regions of their brains; they may also have excess dopamine receptors, the molecules on the surface of neurons that receive dopamine signals (Kapur, 2003).

FROM DOPAMINE TO DELUSIONS. Two key facts about schizophrenia, then, are that (1) people have delusional beliefs and (2) the brain has excess dopamine. How can we put together these person-level and brain-level facts? Dopamine is just a chemical substance; it can’t, by itself, create a delusional belief.

One theory connects the person-level and brain-level facts by considering an in-between level of analysis: the mind (Kapur, 2003). Dopamine affects mental processes. In particular, it alters attention and motivation. Suppose, for example, that you’re hungry and are driving past road signs. You hardly notice most of them—but one that says “EAT” grabs your attention. You concentrate on it and are motivated to find the restaurant ahead. Dopamine contributes to this attention grabbing. It converts the EAT sign from “cold” information to a “hot,” motivating, attention-grabbing stimulus (Berridge & Robinson, 2003).

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What does this have to do with schizophrenia? In schizophrenia, excess dopamine causes even trivial stimuli—a picture on the wall, a TV commercial—to grab people’s attention. Objects and events that once seemed irrelevant now seem deeply significant. This is confusing to people with schizophrenia, who struggle to understand the profound change in their everyday experience (“Why does this TV commercial feel so important?”). To make sense of their experiences, they invent explanations. Because the experiences are weird, the explanations are, too (“The TV commercial must be a message directly to me!”). The strange, delusional beliefs seen in schizophrenia, then, are created by people trying to understand the alterations in mental life caused by excess dopamine (Kapur, 2003).

BRAIN STRUCTURES AND SCHIZOPHRENIA. Let’s now turn from neurotransmitters to brain structures, to examine activity in the various parts of the brain, each of which contains millions of neurons (Chapter 3).

Which brain structures does schizophrenia affect? You name it—“Almost every cortical and subcortical brain structure has been found to be abnormal in schizophrenia” (Antonova et al., 2004, p. 118). Schizophrenia affects not only individual brain regions, but also the brain as a whole. Brain volume—that is, the overall amount of cellular material in the brain—is reduced among people with the disorder.

One brain area is enlarged, rather than reduced, in people with schizophrenia: the brain’s ventricles (Palmer, Dawes, & Heaton, 2009). The ventricles are spaces in the brain filled with a fluid that supports the brain’s functioning. These spaces do not contain neurons. Larger ventricles mean that a smaller percentage of the brain’s overall volume contains the neurons that power thinking.

Although schizophrenia affects the whole brain, some brain regions are likely to be more central to the disease than others. How could you find them? The search has benefited from a strategy you see often in this book: using research on the mind to guide research on the brain. Earlier, you saw that one aspect of mind that schizophrenia strongly impairs is working memory. This mind-level finding suggests a strategy for brain research: Compare the brain activity of people with and without schizophrenia while they perform a task that places great demands on the working memory system. When researchers do this (Glahn et al., 2005; Figure 16.3), they find that brain activity in people with schizophrenia differs in two ways:

Once again, one can connect these brain-level findings to person-level symptoms of schizophrenia. You’ll recall that people with schizophrenia have difficulty concentrating on tasks and planning daily events. Schizophrenia and planning events are connected through a three-step process involving the brain, the mind, and the person’s ability to plan (Figure 16.4): (1) Schizophrenia impairs neural communication in the frontal cortex; (2) impaired communication in the frontal cortex reduces working memory; and (3) impaired working memory makes it difficult for people to perform tasks that require concentration, such as planning daily events.

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Now that we’ve seen how schizophrenia affects people, the mind, and the brain, let’s look at how it develops. One factor to consider in the development of the disease is genetics (Riley, 2011).

GENES AND THE ENVIRONMENT. When asking about genes and the development of schizophrenia, two scientific questions require answers: (1) Do genes have an effect? (2) If so, why? Which genes are important, and how do they contribute to the disease’s development?

The first question can be answered through twin studies, which compare identical to fraternal twins (see Chapter 4). In a twin study of schizophrenia, researchers determined whether twin pairs differ in concordance, that is, whether the two individuals in a twin pair have the same outcome (i.e., schizophrenia or not). Figure 16.5 shows the results. As you can see, identical, or monozygotic (MZ), twins—who share 100% of their genes—are far more concordant for schizophrenia than are any other pairs of relatives. Fraternal, or dizygotic (DZ), twins are far less similar. They share the same prenatal environment and grow up together in the same household, as is the case for MZ twins. But (like any pair of siblings), on average, they share only 50% of their genes and, as a result, are less concordant for schizophrenia than are MZ twins.

This finding establishes that genetic factors have an effect; specifically, they are a diathesis for schizophrenia (Fowles, 1992). For any medical or psychological disorder, a diathesis is any factor that predisposes a person to experience the disorder.

With that established, one can turn to the second question: Which genes are important, and why? Answering this requires more than twin studies. Researchers must identify (1) specific genes that predict the development of schizophrenia (see Research Toolkit) and (2) the biological processes through which they affect the brain.

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Finding genes that make people susceptible to developing schizophrenia is very difficult (Duan, Sanders, & Gejman, 2010). The number of potential genes (more than 1000) is large (Xu et al., 2013). Furthermore, studies require the participation of large numbers of people with schizophrenia—a challenge, since 99% of the population does not have the disease. In general, “progress in the identification of susceptibility genes has been slow” (Xu et al., 2013, p. 1). For example, a large-scale study in China involving thousands of participants was able to identify general regions of the genome that differ in people with and without the illness, but it could not pinpoint specific genes or explain how they contribute to the disease (Cyranoski, 2011).

RESEARCH TOOLKIT

Some recent progress has come from a change in strategy. Rather than studying the presence or absence of the disease as a whole, researchers have related genetic material to specific symptoms of schizophrenia. A meta-analysis (Xu et al., 2013) has identified five points along the genome at which variations in genetic material were strongly associated with the disease’s negative symptoms (the impaired emotional reactions and social behavior discussed earlier). Initial evidence suggests that the genetic variations may influence the growth of brain cells and the speed with which the brain processes information.

Whatever their precise role in schizophrenia, genes alone will never tell the whole story of how this mental illness develops. You can see this for yourself if you look back at Figure 16.6. How similar were identical twins? Their concordance for schizophrenia was not 100% or 99% or 98%. It was only 48%. This means that more than half the time, if one member of an identical twin pair has schizophrenia, the other twin—who of course is genetically identical—does not. Genes by themselves, then, do not determine who develops this mental illness.

What other factors are important? It’s hard to say; science does not fully understand the causes of schizophrenia. However, some research points to the prenatal environment. A vast amount of brain development occurs before a child’s birth, and prenatal events may interfere with this development in a way that, later in life, results in schizophrenia. Harmful prenatal factors include bodily infections and exposure to lead (Opler & Susser, 2005). Another is poor nutrition. Research conducted in China examined the life outcomes of children conceived in the years 1959 to 1961, a time of catastrophic famine (Xu et al., 2009). These children were twice as likely to develop schizophrenia as were children conceived in other, non-famine historical periods.

SCHIZOPHRENIA ACROSS THE LIFE COURSE. It is rare for anyone to develop schizophrenia in early childhood. It is very rare for individuals to develop schizophrenia in their 40s or later in life if they have not had it previously. Among people who have the mental illness, schizophrenia usually first develops between the ages of 16 and 30 (Mueser & McGurk, 2004). Biological changes occurring during puberty may explain why the disease does not develop until the teenage years (Galdos, van Os, & Murray, 1993).

Bad news for sufferers is that schizophrenia persists. The disease generally lasts throughout a person’s lifetime (Mueser & McGurk, 2004), although the severity of positive symptoms of schizophrenia often decreases in older adulthood (Schultz et al., 1997). The vast majority of people who experience an initial episode of schizophrenia will relapse (i.e., will have another such period) subsequently; studies report relapse rates of 95% (Emsley et al., 2013). Treatments for schizophrenia, which we’ll learn about next, help people manage the symptoms, but do not eradicate the disease.

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Schizophrenia exerts a huge cost on individuals and society at large. Treating the disorder is thus one of the greatest challenges for psychological science. Let’s see how it’s done.

DRUG THERAPY. You’ve learned enough about schizophrenia that, when it comes to the question of how to treat it, you can take an educated guess. Excess dopamine-based signals in the brain produce symptoms of schizophrenia. What’s the treatment? Drugs that reduce these dopamine-based signals.

To treat schizophrenia, psychiatrists prescribe antipsychotic drugs, which are medications that alter the action of neurotransmitters in the brain in a manner that reduces psychotic symptoms. The drugs generally target the neurotransmitter dopamine.

Two types of antipsychotic drugs are available: typical and atypical antipsychotics. Their names indicate the historical time of their development. Typical antipsychotics are those developed first, in the 1950s. Atypical antipsychotics were developed in the 1990s, by which time use of the previously developed drugs was “typical.” One commonly used typical antipsychotic is chlorpromazine (which has the trade name thorazine). A common atypical antipsychotic is the drug clozapine.

Both typical and atypical antipsychotics lower dopamine-based communication among neurons. How? They do not lower the brain’s overall amount of dopamine. Instead, they block dopamine receptor sites. With the sites already filled, dopamine molecules thus cannot land there and deliver their signals. This reduction of dopamine-based neural activity alleviates the positive symptoms—the delusions and hallucinations—of schizophrenia (Stahl, 2002; see Figure 16.2).

Although typical and atypical antipsychotics both affect dopamine in this manner, in other ways they differ. Atypical antipsychotics affect not only dopamine signaling, but also signaling by a second neurotransmitter, serotonin. Serotonin contributes to emotional feelings that occur when people pursue activities that they find rewarding (Kranz, Kasper, & Lanzenberger, 2010). By influencing serotonin, atypical antipsychotic drugs thus may benefit not just positive symptoms of schizophrenia, but negative symptoms such as flat affect and lack of motivation, too (Stahl, 2002). A second difference is that the typical antipsychotics have a side effect that is not usually produced by the atypical drugs (Geddes et al., 2000), namely, uncontrollable, “shaking” muscular movements.

Unfortunately for patients with schizophrenia, both types of antipsychotic medication can produce a side effect known as tardive dyskinesia. Tardive dyskinesia consists of repetitive, involuntary movements of facial muscles. These movements result in odd symptoms such as repeated grimacing and lip smacking. For some patients, tardive dyskinesia is irreversible; it continues even after they stop taking the antipsychotic medication that triggered it (Muench & Hamer, 2010). Tardive dyskinesia rates are lower with atypical than typical antipsychotics (Kane, 2004).

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EFFECTIVENESS OF ANTIPSYCHOTIC DRUGS. The good news is that antipsychotic drugs work for many patients, substantially reducing their positive symptoms of schizophrenia. As a result, people who otherwise might be hospitalized can live in their regular community. One study finds that, among patients treated for schizophrenia, 40% experience significant periods of recovery, that is, periods during which they are free from schizophrenic symptoms and can hold a job and take part in social activities (Harrow et al., 2005). The scholar you read about in this chapter’s opening, Dr. Elyn Saks, is an example. She lives with schizophrenia yet leads an exceptionally productive professional life, in part thanks to antipsychotic drugs (Saks, 2007).

There are, however, two pieces of bad news. First, antipsychotic drugs do not always work. Reviews indicate that at least half the patients taking the drugs do not experience substantial long-term reductions in schizophrenic symptoms (Hegarty et al., 1994). Second, the drugs have side effects that include not only tardive dyskinesia, as just noted, but also sluggishness, sexual dysfunction, and weight gain (Muench & Hamer, 2010). The side effects cause many patients to stop taking the medications—which results in their losing out on the drugs’ potential benefits. In one large study (Lieberman et al., 2005), the majority of schizophrenic patients—between two-thirds and four-fifths, depending on the drug—stopped taking their medication after either experiencing side effects or concluding that the drug didn’t work. A major challenge is to develop antipsychotic drugs that are both effective and tolerable for more patients.

PSYCHOTHERAPY. Drugs can reduce the delusions and hallucinations of schizophrenia, but these symptoms are only part of the story. Schizophrenia affects the person as a whole. People with schizophrenia question themselves—their capabilities, their identity, their purpose in life. “It’s hard for us,” one person with schizophrenia writes, “because we lose everything that we thought we were. Our identity is taken from us in a sense” (www.schizophrenia.com posting). Psychotherapy (i.e., psychological therapy) can help people cope with the distress that schizophrenia brings (Lysaker et al., 2010).

A key question about psychotherapies for schizophrenia is which ones work. Which therapies, in other words, are empirically supported? (Also see Chapter 15.) One approach with empirical support is cognitive therapy. Cognitive therapists engage in a dialogue with patients about their delusional beliefs (Beck & Rector, 2002). They encourage patients to question the accuracy of the beliefs—to think of them as ideas they have about the world, rather than as statements of fact. (For example, they might encourage a patient to think, “It seems to me that the TV is sending a message directly to me, but that might not be true.”) Patients learn how to question the evidence behind their beliefs and to cope with distress that the beliefs create. Evidence indicates that cognitive therapy can reduce both positive and negative symptoms of schizophrenia (Dickerson et al., 2002).

Some therapists employ cognitive strategies while also emphasizing the usefulness of humanistic approaches. The humanistic approach to therapy for schizophrenia focuses on the person as a whole: the individual who must cope not only with symptoms of schizophrenia, but also with the changes in lifestyle and self-concept that schizophrenia brings. In the humanistic approach, the quality of the personal relationship between therapist and client is seen as integral to therapy. The job of the therapist is not merely to teach clients but to collaborate with them (Chadwick, 2006); therapist and client work together to reduce the distress of mental illness.

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We have examined schizophrenia in depth for two reasons. One, as noted earlier, is that its personal cost to individuals and its economic cost to society—estimated at more than $60 billion in the United States in any given year (Wu et al., 2005)—are so large that the disease demands attention. Second, its symptoms are so diverse and severe that, in schizophrenia, one sees the range of psychotic symptoms that people with psychotic disorders may experience.

Schizophrenia, however, is not the only psychotic disorder. There are other psychological disorders in which people experience psychotic symptoms, but not with the severity and duration seen in schizophrenia. Two of them are brief psychotic disorder and delusional disorder.

In brief psychotic disorder, people experience the same types of symptoms as in schizophrenia (delusions, hallucinations, etc.). However, they experience them—as you can guess from the disorder’s name—for only a brief period of time. DSM-5 classifies people as having brief psychotic disorder if they exhibit these symptoms for at least one day but less than one month.

In delusional disorder, people experience only one psychotic symptom, delusions, which may persist indefinitely. People with the disorder may believe, without evidence, that they are being spied upon, that someone is trying to poison them, or that they have made some profoundly important discovery that society has not recognized. Some beliefs held by people with delusional disorder may be wildly implausible (DSM-5 gives the example of the belief that a stranger has removed one’s internal organs and replaced them with somebody else’s).

Brief psychotic disorder and delusional disorder illustrate that psychoses exist on a continuum. There is, in other words, a dimension—ranging from low to high severity—along which psychoses vary. Schizophrenia is at the high end of the severity dimension; brief psychotic disorder and delusional disorder are lower in severity. At the very low end are the experiences of people who occasionally exhibit one of the symptoms of psychosis, yet do not have any psychological disorder at all. Such people are not all that rare. Surveys indicate that about 10% of people experience a hallucination (e.g., hearing voices) at least once in their life, and that much larger numbers of people hold beliefs that qualify as delusional. For example, a belief in ghosts was expressed by 25% of survey respondents in Great Britain (a nation where, unlike some parts of the world, the existence of ghosts is not a culturally accepted belief; Johns & van Os, 2001). In a large-scale survey conducted in 52 countries, an average prevalence rate of about 5% was found for the belief that one’s thoughts were sometimes controlled by another person or other outside force (Nuevo et al., 2010).

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These survey findings can help reduce the social stigma associated with psychotic disorders. Social stigma refers to widespread negative beliefs about a group. Societies around the world stigmatize people with psychotic disorders (Lee, 2002). The stigma portrays them as “lunatic, “crazy” individuals who differ fundamentally from “normal” members of society. In surveys of people with schizophrenia, 4 in 5 individuals report overhearing hurtful, offensive comments about mental illness from other people or the media, and the majority indicate that people sometimes try to avoid them (Wahl, 1999). These experiences can create stress, lower self-esteem, and thus make it even harder for individuals to cope with the disorder. “People attempting to recover from mental illnesses … often feel that they suffer as much from being labeled mentally ill as they do from mental illnesses itself” (Link & Phelan, 2009, p. 571).