Margaret, a 39-year-old mother, believed that God was punishing her for marrying a man she did not love and bringing two children into the world. As her punishment, God had made her and her children immortal so that they would have to suffer in their unhappy home life forever—a realization that came to her one evening when she was washing dishes and saw a fork lying across a knife in the shape of a cross. Margaret found further support for her belief in two pieces of evidence: First, a local television station was rerunning old episodes of The Honeymooners, a 1950s situation comedy in which the main characters often argue and shout at each other. She saw this as a sign from God that her own marital conflict would go on forever. Second, she believed (falsely) that the pupils of her children’s eyes were fixed in size and would neither dilate nor constrict—a sign of their immortality. At home, she would lock herself in her room for hours and sometimes days. The week before her diagnosis, she kept her 7-year-old son home from school so that he could join her and his 4-year-old sister in reading aloud from the Bible (Oltmanns et al., 1991). Margaret was suffering from the most well-known and widely studied psychotic disorder: schizophrenia. Schizophrenia is one of the most mystifying and devastating of all the mental disorders.

Schizophrenia is a psychotic disorder (psychosis is a break from reality) characterized by the profound disruption of basic psychological processes; a distorted perception of reality; altered or blunted emotion; and disturbances in thought, motivation, and behaviour. Traditionally, schizophrenia was regarded primarily as a disturbance of thought and perception, in which the sense of reality becomes severely distorted and confused. However, this condition is now understood to take different forms affecting a wide range of functions. According to the DSM–5, schizophrenia is diagnosed when two or more symptoms emerge during a continuous period of at least 1 month with signs of the disorder persisting for at least 6 months. The symptoms of schizophrenia are often separated into positive, negative, and cognitive symptoms.

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Positive symptoms of schizophrenia include thoughts and behaviours not seen in those without the disorder, such as

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Negative symptoms are deficits or disruptions to normal emotions and behaviours. They include emotional and social withdrawal; apathy; poverty of speech; and other indications of the absence or insufficiency of normal behaviour, motivation, and emotion. These symptoms refer to things missing in people with schizophrenia. Negative symptoms may rob people of emotion, for example, leaving them with flat, deadpan responses, their interest in people or events may be undermined, or their capacity to focus attention may be impaired.

Cognitive symptoms are deficits in cognitive abilities, specifically in executive functioning, attention, and working memory. These are the most difficult symptoms to notice because they are much less bizarre and public than the positive and negative symptoms. However, these cognitive deficits often play a large role in terms of preventing people with schizophrenia from achieving a high level of functioning, such as maintaining friendships and holding down a job (Green et al., 2000).

Schizophrenia occurs in about 1 percent of the population (Jablensky, 1997) and is slightly more common in men than in women (McGrath et al., 2008). Early versions of the DSM suggested that schizophrenia might have a very early onset—in the form of infantile autism—but more recent studies suggest that these disorders are distinct and that schizophrenia rarely develops before early adolescence (Rapoport et al., 2009). The first episode typically occurs in late adolescence or early adulthood (Gottesman, 1991). Despite its relatively low frequency, schizophrenia is the primary diagnosis for nearly 40 percent of all admissions to American state and county mental hospitals; it is the second most frequent diagnosis for inpatient psychiatric admission at other institutions (Rosenstein, Milazzo-Sayre, & Manderscheid, 1990). The disproportionate rate of hospitalization for schizophrenia is a testament to the devastation it causes in people’s lives.

In 1899, when German psychiatrist Emil Kraepelin first described the syndrome we now know as schizophrenia, he remarked that the disorder was so severe that it suggested “organic,” or biological, origins. Over the years, accumulating evidence for the role of biology in schizophrenia has come from studies of genetic factors, biochemical factors, and neuroanatomy.

Family studies indicate that the closer a person’s genetic relatedness to a person with schizophrenia, the greater the likelihood of developing the disorder (Gottesman, 1991). As shown in FIGURE 15.4, concordance rates increase dramatically with biological relatedness. The rates are estimates and vary considerably from study to study, but almost every study finds the average concordance rates higher for identical twins (48 percent) than for fraternal twins (17 percent), which suggests a genetic component for the disorder (Torrey et al., 1994).

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Although genetics clearly have a strong predisposing role in schizophrenia, considerable evidence suggests that environmental factors, such as the prenatal and perinatal environments, also affect concordance rates (Jurewicz, Owen, & O’Donovan, 2001; Thaker, 2002; Torrey et al., 1994). For example, because approximately 70 percent of identical twins share the same prenatal blood supply, toxins in the mother’s blood could contribute to the high concordance rate. More recent studies (discussed in the earlier section on bipolar disorder) are contributing to a better understanding of how environmental stressors can trigger epigenetic changes that increase susceptibility to this disorder.

During the 1950s, major tranquilizers were discovered that could reduce the symptoms of schizophrenia by lowering levels of the neurotransmitter dopamine. The effectiveness of many drugs in alleviating schizophrenic symptoms is related to the drugs’ capacity to reduce dopamine’s role in neurotransmission in certain brain tracts. This finding suggested the dopamine hypothesis, the idea that schizophrenia involves an excess of dopamine activity. The hypothesis has been invoked to explain why amphetamines, which increase dopamine levels, often exacerbate symptoms of schizophrenia (Iverson, 2006).

If only things were so simple. Considerable evidence suggests that this hypothesis is inadequate (Moncrieff, 2009). For example, many individuals with schizophrenia do not respond favourably to dopamine-blocking drugs (e.g., major tranquilizers), and those who do seldom show a complete remission of symptoms. Moreover, the drugs block dopamine receptors very rapidly, yet individuals with schizophrenia typically do not show a beneficial response for weeks. Finally, research has implicated other neurotransmitters in schizophrenia, suggesting that the disorder may involve a complex interaction among a host of different biochemicals (Risman et al., 2008; Sawa & Snyder, 2002). In sum, the precise role of neurotransmitters in schizophrenia has yet to be determined.

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When neuroimaging techniques became available, researchers immediately started looking for distinctive anatomical features of the brain in individuals with schizophrenia. The earliest observations revealed enlargement of the ventricles, hollow areas filled with cerebrospinal fluid, lying deep within the core of the brain (see FIGURE 15.5) (Johnstone et al., 1976). In some individuals (primarily those with chronic, negative symptoms), the ventricles were abnormally enlarged, suggesting a loss of brain tissue mass that could arise from an anomaly in prenatal development (Arnold et al., 1998; Heaton et al., 1994).

Understanding the significance of this brain abnormality for schizophrenia is complicated by several factors, however. First, such enlarged ventricles are found in only a minority of cases of schizophrenia. Second, some individuals who do not have schizophrenia also show evidence of enlarged ventricles. Finally, this type of brain abnormality can be caused by the long-term use of some types of antipsychotic medications commonly prescribed in schizophrenia (Breggin, 1990; Gur et al., 1998).

Neuroimaging studies provide evidence of a variety of brain abnormalities in schizophrenia. Paul Thompson and his colleagues (2001) examined changes in the brains of adolescents whose MRI scans could be traced sequentially from the onset of schizophrenia. By morphing the images onto a standardized brain, the researchers were able to detect progressive tissue loss beginning in the parietal lobe and eventually encompassing much of the brain (see FIGURE 15.6). All adolescents lose some grey matter over time in a kind of normal “pruning” of the brain, but in the case of those developing schizophrenia, the loss was dramatic enough to seem pathological. A variety of specific brain changes found in other studies suggests a clear relationship between biological changes in the brain and the progression of schizophrenia (Shenton et al., 2001).

With all these potential biological contributors to schizophrenia, you might think there would be few psychological or social causes of the disorder. However, several studies do suggest that the family environment plays a role in the development of and recovery from the condition. One large-scale study compared the risk of schizophrenia in children adopted into healthy families and those adopted into severely disturbed families (Tienari et al., 2004). (Disturbed families were defined as those with extreme conflict, lack of communication, or chaotic relationships.) Among children whose biological mothers had schizophrenia, the disturbed environment increased the likelihood of developing schizophrenia—an outcome that was not found among children who were also reared in disturbed families but whose biological mothers did not have schizophrenia. This finding provides support for the diathesis–stress model described earlier.

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