Imagine trying to communicate with Maxine, a young woman with schizophrenia whose thoughts spill 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 .... I’m Mary Poppins. Is this room painted blue to get me upset? My grandmother died four weeks after my eighteenth birthday.”
Nearly 1 in 100 people (about 60 percent men) develop schizophrenia, with an estimated 24 million across the world suffering from this dreaded disorder (Abel et al., 2010; WHO, 2011).
Literally translated, schizophrenia means “split mind.” It refers not to a multiple-personality split but rather to a split from reality that shows itself in disturbed perceptions, disorganized thinking and speech, and diminished, inappropriate emotions. As such, it is the chief example of a psychosis, a psychotic disorder marked by irrationality and lost contact with reality.
As Maxine’s strange monologue illustrates, the thinking of a person with schizophrenia is fragmented, bizarre, and often distorted by false beliefs called delusions (“I’m Mary Poppins”). Those with paranoid tendencies are particularly prone to delusions of persecution. Even within sentences, jumbled ideas may create what is called 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.”
A person with schizophrenia may have hallucinations (sensory experiences without sensOlY stimulation). They may see, feel, taste, or smell things that are not there. Most often, however, the hallucinations are auditory, frequently voices making insulting remarks or giving orders. The voices may tell the patient that she is bad or that she must bum herself with a cigarette lighter. Imagine your own reaction if a dream broke into your waking consciousness. When the unreal seems real, the resulting perceptions are at best bizarre, at worst terrifying.
Disorganized thoughts may result from a breakdown in selective attention. Recall from Module 16 that we normally have a remarkable capacity for giving our undivided attention to one set of sensory stimuli while filtering out others. Those 20 0 f> with schizophrenia cannot do this. Thus, irrelevant, minute 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” (MacDonaid, 1960, p. 218). This selective-attention difficulty is but one of dozens of cognitive differences associated with schizophrenia (Reichenberg & Harvey, 2007).
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 state of flat affect. Most also have difficulty perceiving facial emotions and reading others’ states of mind (Green & Horan, 2010; Kohler et al., 2010).
Motor behavior may also be inappropriate. Some perform senseless, compulsive acts, such as continually rocking or rubbing an arm. Others, who exhibit catatonia, may remain motionless for hours and then become agitated.
As you can imagine, such disorganized thinking, disturbed perceptions, and inappropriate emotions profoundly disrupt social relationships and make it difficult to hold a job. Even those with dissociative identity disorder, which we’ll discuss later in this unit, may continue to function in everyday life, but less so those with schizophrenia. During their most severe periods, those with schizophrenia live in a private inner world, preoccupied with illogical ideas and unreal images. Given a supportive environment and medication, over 40 percent of schizophrenia patients will have periods of a year or more of normal life experience Gobe & Harrow, 2010). Many others remain socially withdrawn and isolated or rejected throughout much of their lives (Hooley, 2010).
Schizophrenia typically strikes as young people are maturing into adulthood. Although it only afflicts 1 in 100 people, it knows no national boundaries, and it affects both males and females - though men tend to be struck earlier, more severely, and slightly more often (Aleman et al., 2003; Picchioni & Murray, 2007).
For some, schizophrenia will appear suddenly, seemingly as a reaction to stress. For others, as was the case with Maxine, schizophrenia develops gradually, emerging from a long history of social inadequacy and poor school performance (MacCabe et al., 2008). No wonder those predisposed to schizophrenia often end up in the lower socioeconomic levels, or even homeless.
We have thus far described schizophrenia as if it were a single disorder. Actually, it varies. 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 have toneless voices, expressionless faces, or mute and rigid bodies. Thus, positive symptoms are the presence of inappropriate behaviors, and negative symptoms are the absence of appropriate behaviors.
When schizophrenia is a slow-developing process (called chronic, or process, schizophrenia), recovery is doubtful (WHO, 1979). 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). When previously well-adjusted people develop schizophrenia rapidly (called acute, or reactive, schizophrenia) following particular life stresses, recovery is much more likely. They more often have the positive symptoms that are responsive to drug therapy (Fenton & McGlashan, 1991, 1994; Fowles, 1992).
Schizophrenia is not only the most dreaded psychological disorder but also one of the most heavily researched. Most of the new research studies link it with brain abnormalities and genetic predispositions. Schizophrenia is a disease of the brain manifest in symptoms of the mind.
Might imbalances in brain chemistry 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). As we saw in Module 25, scientists are clarifying the mechanism by which chemicals such as LSD produce hallucinations. These discoveries hint that schizophrenia symptoms might have a biochemical key.
Researchers discovered one such key when they examined schizophrenia patients’ brains after death and found an excess of receptors for dopamine - a six-fold excess for the so-called D4 dopamine receptor (Seeman et al., 1993; Wong et al., 1986). They now speculate that such a hyper-responsive dopamine system may intensify brain signals in schizophrenia, creating positive symptoms such as hallucinations and paranoia (Grace, 2010). As we might therefore expect, 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).
Modern brain-scanning techniques reveal that many people with chronic schizophrenia have abnormal activity in multiple brain areas. Some have abnormally low brain activity in the frontal lobes, which are critical for reasoning, planning, and problem solving (Morey et al., 2005; Pettegrew et al., 1993; Resnick, 1992). People diagnosed with schizophrenia also display 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 (Silbersweig et al., 1995). When participants heard a voice or saw something, their brain became vigorously active in several core regions, including the thalamus, a structure deep in the brain that filters incoming sensory signals and transmits them to the 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). Some studies have even found such abnormalities in the brains of people who would later develop this disorder and in their close relatives (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). One smaller-than-normal area is the cortex. Another is the corpus callosum connection between the 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 of various studies is that schizophrenia involves not one isolated brain abnormality but problems with several brain regions and their interconnections (Andreasen, 1997, 2001).
Naturally, scientists wonder what causes these abnormalities. Some 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 the Dutch wartime famine later displayed a doubled rate of schizophrenia, as did those conceived during the famine that occurred from 1959 to 1961 in eastern China (St. Clair et al., 2005; Susser et al., 1996).
Consider another possible culprit: a midpregnancy viral infection that impairs fetal brain development (Patterson, 2007). 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 play a contributing role in the development of schizophrenia. They also strengthen the recommendation that “women who will be more than three months pregnant during the flu season” have a flu shot (CDC 2003).
Why might a second-trimester maternal flu bout put fetuses at risk? Is it the virus itself? 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.
Fetal-virus infections do appear to increase the odds that a child will develop schizophrenia. But this theory cannot tell us why only 2 percent of women who catch the flu during their second trimester of pregnancy bear children who develop schizophrenia. Might people also inherit a predisposition to this disorder? The evidence strongly suggests that, Yes, some do. The nearly 1-in-100 odds of any person’s being diagnosed with schizophrenia become about 1 in 10 among those whose sibling or parent has the disorder, and close to 1 in 2 if the affected sibling is an identical twin (FIGURE 68.1) . Although only a dozen or so such cases are on record, the co-twin of an identical twin with schizophrenia retains that 1-in-2 chance even when the twins are reared apart (Plomin et al., 1997) .
Remember, though, that identical twins also share a prenatal environment. About two-thirds also share a placenta and the blood it supplies; the other one-third have two single placentas. If an identical twin has schizophrenia, the co-twin’s chances of being similarly afflicted are 6 in 10 if they shared a placenta. If they had separate placentas, as do fraternal twins, the chances are only 1 in 10 (Davis et al., 1995a,b; Phelps et al., 1997). Twins who share a placenta are more likely to experience the same prenatal viruses. So it is possible that shared germs as well as shared genes produce identical twin similarities.
Adoption studies, however, confirm that the genetic link is real (Gottesman, 1991). 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.
With the genetic factor established, researchers are now sleuthing specific genes that, in some combination, might predispose schizophrenia-inducing brain abnormalities (Levinson et at 2011; Mitchell & Porteous, 2011; Vacic et al., 2011; Wang et al., 2010). (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 the genetic contribution to schizophrenia is beyond question, 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; Pogue-Geile & Yokley 2010). Recall from Module 14 that epigenetic (literally “in addition to genetic”) factors influence gene expression. Like hot water activating the tea bag, environmental factors such as prenatal viral infections, nutritional deprivation, and maternal stress can “turn on” the genes that predispose schizophrenia. Identical twins’ differing histories in the womb and beyond explain why only one of them may show differing gene expressions (Walker et al., 2010). As we have so often seen, nature and nurture interact. Neither hand claps alone.
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.
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Most of us can relate more easily to the ups and downs of mood disorders than to the strange thoughts, perceptions, and behaviors of schizophrenia. Sometimes our thoughts do jump around, but in the absence of disorder we do not 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 have felt 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 therefore continues, and more vigorously than ever.