During their most severe periods, people with schizophrenia live in a private inner world, preoccupied with the strange ideas and images that haunt them. The word itself means “split” (schizo) “mind” (phrenia). In this disorder, however, the mind is not split into multiple personalities. Rather, the mind has suffered a split from reality that shows itself in disturbed perceptions, disorganized thinking and speech, and diminished, inappropriate emotions. Schizophrenia is the chief example of a psychosis, a broad term for a break or split from reality.

15-14 What patterns of perceiving, thinking, and feeling characterize schizophrenia?

Schizophrenia comes in varied forms. Schizophrenia patients with positive symptoms may experience hallucinations, talk in disorganized and deluded ways, and exhibit inappropriate laughter, tears, or rage. Those with negative symptoms may have toneless voices, expressionless faces, or mute and rigid bodies.

People with schizophrenia sometimes have hallucinations—they see, feel, taste, or smell things that exist only in their minds. Most often, the hallucinations are sounds, frequently voices making insulting remarks or giving orders. The voices may tell the person that she is bad or that she must burn herself with a cigarette lighter. Imagine your own reaction if a dream broke into your waking consciousness, making it hard to separate your experience from your imagination. When the unreal seems real, the resulting perceptions are at best bizarre, at worst terrifying.

Hallucinations are false perceptions. People with schizophrenia also have disorganized, fragmented thinking, which is often distorted by false beliefs called delusions. If they have paranoid tendencies, they may believe they are being threatened or pursued.

Maxine, a young woman with schizophrenia, believed she was Mary Poppins. Communicating with Maxine was difficult because her thoughts spilled out in no logical order. Her biographer, Susan Sheehan (1982, p. 25), observed her saying aloud to no one in particular, “This morning, when I was at Hillside [Hospital], I was making a movie. I was surrounded by movie stars…. Is this room painted blue to get me upset? My grandmother died four weeks after my eighteenth birthday.”

Jumbled ideas may make no sense even within sentences, forming what is known as word salad. One young man begged for “a little more allegro in the treatment,” and suggested that “liberationary movement with a view to the widening of the horizon” will “ergo extort some wit in lectures.”

One cause of disorganized thinking may be a breakdown in selective attention. Normally, we have a remarkable capacity for giving our undivided attention to one set of sensory stimuli while filtering out others. People with schizophrenia cannot do this. Thus, tiny, irrelevant stimuli, such as the grooves on a brick or the inflections of a voice, may distract their attention from a bigger event or a speaker’s meaning. As one former patient recalled, “What had happened to me … was a breakdown in the filter, and a hodge-podge of unrelated stimuli were distracting me from things which should have had my undivided attention” (MacDonald, 1960, p. 218). This selective attention difficulty is but one of dozens of cognitive differences associated with schizophrenia (Reichenberg & Harvey, 2007).

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The expressed emotions of schizophrenia are often utterly inappropriate, split off from reality (Kring & Caponigro, 2010). Maxine laughed after recalling her grandmother’s death. On other occasions, she cried when others laughed, or became angry for no apparent reason. Others with schizophrenia lapse into an emotionless flat affect state of no apparent feeling. Most also have an impaired theory of mind—they have difficulty perceiving facial emotions and reading others’ states of mind (Green & Horan, 2010; Kohler et al., 2010). These deficiencies occur early in the illness and have a genetic basis (Bora & Pantelis, 2013).

Motor behavior may also be inappropriate. Some perform senseless, compulsive acts, such as continually rocking or rubbing an arm. Others may remain motionless for hours (a condition called catatonia) and then become agitated.

As you can imagine, such disturbed perceptions, disorganized thinking, and inappropriate emotions profoundly disrupt social and work relationships. During their most severe periods, people with schizophrenia live in a private inner world, preoccupied with illogical ideas and unreal images. Many have sleep problems, which can increase night eating and obesity (Palmese et al., 2011). Given a supportive environment and medication, over 40 percent of people with schizophrenia will have periods of a year or more of normal life experience (Jobe & Harrow, 2010). Many others remain socially withdrawn and isolated or rejected for much of their lives (Hooley, 2010).

15-15 How do chronic and acute schizophrenia differ?

Nearly 1 in 100 people will experience schizophrenia this year, joining the estimated 24 million worldwide who have this disorder (Abel et al., 2010; WHO, 2011). It typically strikes as young people are maturing into adulthood. It knows no national boundaries, and it affects both males and females. Men tend to be struck earlier, more severely, and slightly more often (Aleman et al., 2003; Eranti et al., 2013; Picchioni & Murray, 2007). The risk of schizophrenia is higher for those who experience childhood abuse: They are three times more likely than their unabused counterparts to develop this disorder (Matheson et al., 2013). Other types of childhood adversity, such as bullying, also increase the risk (Varese et al., 2012).

When schizophrenia is a slow-developing process, called chronic schizophrenia, recovery is doubtful (WHO, 1979). This was the case with Maxine’s schizophrenia, which took a slow course, emerging from a long history of social inadequacy and poor school performance (MacCabe et al., 2008). Those with chronic schizophrenia often exhibit the persistent and incapacitating negative symptom of social withdrawal (Kirkpatrick et al., 2006). Men, whose schizophrenia develops on average four years earlier than women’s, more often exhibit negative symptoms and chronic schizophrenia (Räsänen et al., 2000). In one study that followed people with chronic schizophrenia over 34 years, the majority showed worsened symptoms and functioning (Newman et al., 2012).

When previously well-adjusted people develop schizophrenia rapidly following particular life stresses, this is called acute schizophrenia, and recovery is much more likely. They more often have the positive symptoms that are more likely to respond to drug therapy (Fenton & McGlashan, 1991, 1994; Fowles, 1992).

Schizophrenia is a dreaded psychological disorder. It is also one of the most heavily researched. Most studies now link it with abnormal brain tissue and genetic predispositions. Schizophrenia is a disease of the brain manifested in symptoms of the mind.

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15-16 What brain abnormalities are associated with schizophrenia?

Might chemical imbalances in the brain underlie schizophrenia? Scientists have long known that strange behavior can have strange chemical causes. The saying “mad as a hatter” refers to the psychological deterioration of British hatmakers whose brains, it was later discovered, were slowly poisoned as they moistened the brims of mercury-laden felt hats with their tongue and lips (Smith, 1983). Could schizophrenia symptoms have a similar biochemical key? Scientists continue to track the mechanisms by which chemicals produce hallucinations and other symptoms.

Dopamine Overactivity One possible answer emerged when researchers examined schizophrenia patients’ brains after death. They found an excess of receptors for dopamine—a sixfold excess for the dopamine receptor D4 (Seeman et al., 1993; Wong et al., 1986). Such a hyper-responsive dopamine system may intensify brain signals in schizophrenia, creating positive symptoms such as hallucinations and paranoia (Grace, 2010). Drugs that block dopamine receptors often lessen these symptoms. Drugs that increase dopamine levels, such as amphetamines and cocaine, sometimes intensify them (Seeman, 2007; Swerdlow & Koob, 1987).

Abnormal Brain Activity and Anatomy Brain scans show that abnormal activity accompanies schizophrenia. Some people diagnosed with schizophrenia have abnormally low brain activity in the frontal lobes, areas that help us reason, plan, and solve problems (Morey et al., 2005; Pettegrew et al., 1993; Resnick, 1992). Brain scans also show a noticeable decline in the brain waves that reflect synchronized neural firing in the frontal lobes (Spencer et al., 2004; Symond et al., 2005). Out-of-sync neurons may disrupt the integrated functioning of neural networks, possibly contributing to schizophrenia symptoms.

One study took PET scans of brain activity while people were hallucinating (Sil-bersweig et al., 1995). When participants heard a voice or saw something, their brain became vigorously active in several core regions. One was the thalamus, the structure that filters incoming sensory signals and transmits them to the brain’s cortex. Another PET scan study of people with paranoia found increased activity in the amygdala, a fear-processing center (Epstein et al., 1998).

Many studies have found enlarged, fluid-filled areas and a corresponding shrinkage and thinning of cerebral tissue in people with schizophrenia (Goldman et al., 2009; Wright et al., 2000). People often inherit these brain differences. If one affected identical twin shows brain abnormalities, the odds are at least 1 in 2 that the other twin will have them (van Haren et al., 2012). Even people who will later develop the disorder may show these symptoms (Karlsgodt et al., 2010). The greater the brain shrinkage, the more severe the thought disorder (Collinson et al., 2003; Nelson et al., 1998; Shenton, 1992).

Two smaller-than-normal areas are the cortex and the corpus callosum connecting the brain’s two hemispheres (Arnone et al., 2008). Another is the thalamus, which may explain why people with schizophrenia have difficulty filtering sensory input and focusing attention (Andreasen et al., 1994; Ellison-Wright et al., 2008). The bottom line is that schizophrenia involves not one isolated brain abnormality but problems with several brain regions and their interconnections (Andreasen, 1997, 2001).

Prenatal Environment and Risk

15-17 What prenatal events are associated with increased risk of developing schizophrenia?

What causes brain abnormalities in people with schizophrenia? Some scientists point to mishaps during prenatal development or delivery (Fatemi & Folsom, 2009; Walker et al., 2010). Risk factors for schizophrenia include low birth weight, maternal diabetes, older paternal age, and oxygen deprivation during delivery (King et al., 2010). Famine may also increase risks. People conceived during the peak of World War II’s Dutch wartime famine later developed schizophrenia at twice the normal rate. Those conceived during the famine of 1959 to 1961 in eastern China also displayed this doubled rate (St. Clair et al., 2005; Susser et al., 1996).

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Let’s consider another possible culprit. Might a midpregnancy viral infection impair fetal brain development (Brown & Patterson, 2011)? Can you imagine some ways to test this fetal-virus idea? Scientists have asked the following:

These converging lines of evidence suggest that fetal-virus infections contribute to the development of schizophrenia. They also strengthen the U.S. government recommendation that “pregnant women need a flu shot” (CDC, 2014).

Why might a second-trimester maternal flu bout put a fetus at risk? Is the virus itself the culprit? The mother’s immune response to it? Medications taken (Wyatt et al., 2001)? Does the infection weaken the brain’s supportive glial cells, leading to reduced synaptic connections (Moises et al., 2002)? In time, answers may become available.

15-18 Do genes influence schizophrenia? What factors may be early warning signs of schizophrenia in children?

Fetal-virus infections may increase the odds that a child will develop schizophrenia. But many women get the flu during their second trimester of pregnancy, and only 2 percent of them bear children who develop schizophrenia. Why are only some children at risk? Might some people be more vulnerable because they inherit a predisposition to this disorder? Some people with no family history of schizophrenia develop the disorder (Xu et al., 2011). But the evidence strongly suggests that, Yes, some may inherit a predisposition to schizophrenia. The nearly 1-in-100 odds of any person’s being diagnosed with schizophrenia become about 1 in 10 among those who have a sibling or parent with the disorder. If the affected sibling is an identical twin, the odds increase to nearly 5 in 10 (FIGURE 15.11). Those odds remain the same even when the twins are raised apart (Plomin et al., 1997). (Only about a dozen such cases are on record.)

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Remember, though, that identical twins share more than their genes. They also share a prenatal environment. About two-thirds share a placenta and the blood it supplies; the other one-third have separate placentas. Shared placentas matter. If the co-twin of an identical twin with schizophrenia shared the placenta, the chances of developing the disorder are 6 in 10. If the identical twins had separate placentas (as do fraternal twins), the co-twin’s chances of developing schizophrenia drop to 1 in 10 (Davis et al., 1995a,b; Phelps et al., 1997). Twins who share a placenta are more likely to share the same prenatal viruses. So perhaps shared germs as well as shared genes produce identical twin similarities.

Adoption studies help untangle genetic and environmental influences. Children adopted by someone who develops schizophrenia seldom “catch” the disorder. Rather, adopted children have an elevated risk if a biological parent is diagnosed with schizophrenia (Gottesman, 1991).

The search is on for specific genes that, in some combination, predispose schizophrenia-inducing brain abnormalities (Levinson et al., 2011; Mitchell & Porteous, 2011; Ripke et al., 2011; Vacic et al., 2011). (It is not our genes but our brains that directly control our behavior.) Some of these genes influence the effects of dopamine and other neurotransmitters in the brain. Others affect the production of myelin, a fatty substance that coats the axons of nerve cells and lets impulses travel at high speed through neural networks.

Although genes matter, the genetic formula is not as straightforward as the inheritance of eye color. Genome studies of thousands of individuals with and without schizophrenia indicate that schizophrenia is influenced by many genes, each with very small effects (International Schizophrenia Consortium, 2009; Xu et al., 2012). And, as we have so often seen, nature and nurture interact. Epigenetic (literally “in addition to genetic”) factors influence whether or not genes will be expressed. Like hot water activating a tea bag, environmental factors such as viral infections, nutritional deprivation, and maternal stress can “turn on” the genes that put some of us at higher risk for schizophrenia. Identical twins’ differing histories in the womb and beyond explain why only one of them may show differing gene expressions (Dempster et al., 2013; Walker et al., 2010). Our heredity and our life experiences work together. Neither hand claps alone.

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Thanks to our expanding understanding of genetic and brain influences on maladies such as schizophrenia, the general public more and more attributes psychiatric disorders to biological factors (Pescosolido et al., 2010). In 2007, one privately funded new research center announced its ambitious aim: “To unambiguously diagnose patients with psychiatric disorders based on their DNA sequence in 10 years’ time” (Holden, 2007). In 2010, $120 million in start-up funding launched a bold new effort to study the neuroscience and genetics of schizophrenia and other psychiatric disorders (Kaiser, 2010). So, can scientists develop genetic tests that reveal who is at risk? If so, will people in the future subject their embryos to genetic testing (and gene repair or abortion) if they are at risk for this or some other psychological or physical malady? Might they take their egg and sperm to a genetics lab for screening before combining them to produce an embryo? Or will children be tested for genetic risks and given appropriate preventive treatments? In this brave new twenty-first-century world, such questions await answers.

If prenatal viruses and genetic predispositions do not, by themselves, cause schizophrenia, neither do family or social factors alone. It remains true, as Susan Nicol and Irving Gottesman (1983) noted over three decades ago, that “no environmental causes have been discovered that will invariably, or even with moderate probability, produce schizophrenia in persons who are not related to” a person with schizophrenia.

Hoping to identify environmental triggers of schizophrenia, researchers have compared the experiences of high-risk children (for example, those with relatives with schizophrenia) and low-risk children. In one 2.5-year study that followed 163 teens and early-twenties adults who had two relatives with schizophrenia, the 20 percent of participants who developed schizophrenia showed social withdrawal or other abnormal behavior before the onset of the disorder (Johnstone et al., 2005). Researchers (Abel et al., 2010; Freedman et al., 1998; Schiffman et al., 2001; Susser, 1999; Welham et al., 2009) identified these other possible early warning signs:

Few of us can relate to the strange thoughts, perceptions, and behaviors of schizophrenia. Sometimes our thoughts jump around, but we rarely talk nonsensically. Occasionally we feel unjustly suspicious of someone, but we do not fear that the world is plotting against us. Often our perceptions err, but rarely do we see or hear things that are not there. We feel regret after laughing at someone’s misfortune, but we rarely giggle in response to bad news. At times we just want to be alone, but we do not live in social isolation. However, millions of people around the world do talk strangely, suffer delusions, hear nonexistent voices, see things that are not there, laugh or cry at inappropriate times, or withdraw into private imaginary worlds. The quest to solve the cruel puzzle of schizophrenia continues, more vigorously than ever.

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LEARNING OBJECTIVES

RETRIEVAL PRACTICE Take a moment to answer each of these Learning Objective Questions (repeated here from within this section). Then click the 'show answer' button to check your answers. Research suggests that trying to answer these questions on your own will improve your long-term retention (McDaniel et al., 2009).

15-14 What patterns of perceiving, thinking, and feeling characterize schizophrenia?

15-15 How do chronic and acute schizophrenia differ?

15-16 What brain abnormalities are associated with schizophrenia?

15-17 What prenatal events are associated with increased risk of developing schizophrenia?

15-18 Do genes influence schizophrenia? What factors may be early warning signs of schizophrenia in children?

TERMS AND CONCEPTS TO REMEMBER

RETRIEVAL PRACTICE Match each of the terms on the left with its definition on the right. Click on the term first and then click on the matching definition. As you match them correctly they will move to the bottom of the activity.