Introduction
Schizophrenia, an illness that strikes 1 percent of adults, involves changes in all aspects of psychological functioning. Thinking disorders, perceptual distortions and hallucinations, delusions, and emotional changes are the most prominent of such changes. Although some people recover completely, in many others, the illness is chronic and deteriorative. For many years, because the causes of schizophrenia were poorly understood, a wide range of theories was proposed to account for the development of schizophrenia. These early theories about schizophrenia can be classified into four types: psychodynamic, family interaction, learning/attention, and organic. Current theories of schizophrenia focus primarily on genetic factors and their interaction with environmental conditions, particularly the environment experienced before birth and during early development.
Psychodynamic Theories Psychodynamic theories originated with Sigmund Freud, who believed that schizophrenia results when a child fails to develop an attachment to his or her parent of the opposite sex. This causes a powerful conflict (called an Oedipal conflict in males) in which unconscious homosexual desires threaten to overwhelm the conscious self. To prevent these desires from generating thoughts and feelings that cause painful guilt or behaviors that would be punished, the ego defends itself by regressing to a state in which awareness of the self as a distinct entity is lost. Thus, the person’s behavior becomes socially inappropriate; the person mistakes fantasies for reality and experiences hallucinations and delusions.
Harry Stack Sullivan, a follower of Freud, believed that failure of maternal attachment creates excessive anxiety and sets the pattern for all future relationships. Unable to cope in a world seen as socially dangerous, the individual retreats into fantasy. Having done so, the individual cannot grow socially or develop a sense of trust in or belonging with others. By late adolescence or early adulthood, the person’s situation has become so hopeless that all pretense of normality collapses and he or she withdraws totally and finally into a world of fantasy and delusion.
Family and Learning Theories Family interaction theories dwell even more intensely on parent-child, especially mother-child, relationships. Theodore Lidz and coworkers, after conducting studies on families with a schizophrenic member, concluded that one or both parents of a future schizophrenic are likely to be nearly, if not overtly, psychotic. They proposed that the psychotogenic influence of these parents on a psychologically vulnerable child is most likely the cause of schizophrenia.
Gregory Bateson and colleagues proposed a family interaction theory called the double-bind theory. Bateson suggested that schizophrenia results when parents expose a child to a family atmosphere in which they never effectively communicate their expectations, and therefore the child is unable to discover which behaviors will win approval. Scolded for disobeying, for example, the child changes his or her behavior only to be scolded for being “too obedient.” Subjected to such no-win situations constantly, the child cannot develop an attachment to the family, and this failure generalizes to all subsequent relationships.
Learning theories propose that failure of operant conditioning causes the bizarre behavior of schizophrenia. In one version, conditioning fails because mechanisms in the brain that support operant learning, such as reinforcement and attention, are faulty, thus preventing the learning of appropriate, adaptive behaviors.
For example, a person who is unable to focus attention on relevant stimuli would be unable to learn the stimulus associations and discriminations necessary for successful day-to-day behavior. Such an individual’s behavior would eventually become chaotic. This learning/attention theory proposes a defect in perceptual filtering, a function of the brain’s reticular formation. This system filters out the innumerable stimuli that impinge on one’s senses every moment but are unimportant. In schizophrenia, the theory proposes, this filtering system fails, and the individual is overwhelmed by a welter of trivial stimuli. Unable to cope with this confusing overstimulation, the person withdraws, becomes preoccupied with sorting out his or her thoughts, and becomes unable to distinguish internally generated stimuli from external ones.
Organic Theories Organic theories of schizophrenia are influenced by the knowledge that conditions known to have organic causes (that is, causes stemming from biological abnormalities) often produce psychological symptoms that mimic the psychotic symptoms of schizophrenia. Among these are vitamin-deficiency diseases, viral encephalitis, temporal-lobe epilepsy, and neurodegenerative disease such as Huntington’s disease and Wilson’s disease. In contradistinction to historical theories of schizophrenia that have little empirical support, considerable research supports the operation of genetic factors in schizophrenia; such factors are most often assumed to influence the development of the brain and its resilience to a variety of physiological and psychological stressors. In the diathesis-stress model, such a genetic defect is necessary for the development of chronic schizophrenia but is not sufficient to produce it. Stressful life events must also be present. The genetic abnormality then leaves the person unable to cope with life stresses, the result being psychosis. Research demonstrating the operation of genetic factors in schizophrenia in no way implies the absence of environmental factors that operate to influence the course of the disorder.
Many brain abnormalities have been proposed as causes of schizophrenia. One suggestion is that schizophrenia results from generalized brain pathology. For example, some researchers suggest that widespread brain deterioration caused by either environmental poisoning or infection by a virus causes schizophrenia.
Alternatively, some biochemical abnormality may be at fault. The endogenous psychotogen theory proposes that abnormal production of a chemical substance either inside or outside the brain produces psychotic symptoms by affecting the brain in a druglike fashion. Substances similar to the hallucinogenic drugs lysergic acid diethylamide (LSD) and mescaline are popular candidates for the endogenous psychotogen. The dopamine theory, however, proposes that schizophrenia results when a chemical neurotransmitter system in the brain called the dopamine system becomes abnormally overactive or when dopamine receptors in the brain become abnormally sensitive to normal amounts of dopamine. In addition to dopamine, other neurotransmitters have been proposed as important in the development and maintenance of schizophrenia.
Neurological and Genetic Studies Theories of schizophrenia are instrumental in generating experiments that provide definite knowledge of the condition. Experimental support for psychodynamic theories of the development and progression of schizophrenia has not been forthcoming. Therefore, most empirical researchers regard psychodynamic theories of schizophrenia as having little scientific merit. Family interaction theories also have not been supported by subsequent experiments. Although studies have found disturbed family relationships, the evidence suggests that these are most likely the result of, not the cause of, having a schizophrenic individual in the family. Family interaction has, however, been shown to be influential in modifying the course of illness and the risk of relapse. Studies consistently fail to find that parent-child interactions are psychotogenic, and the once-popular notion of the schizophrenogenic parent has been discarded. Only learning/attention and organic theories are strongly supported by experimental evidence. The evidence for attentional or learning deficits resulting from a fault in the reticular formation is strong, and it stems from electrophysiological and behavioral studies.
The electroencephalogram (EEG) is often found to be abnormal in schizophrenic patients, showing excessive activation that indicates overarousal. Furthermore, studies of evoked potentials, electrical events recorded from the cortex of the brain in response to specific sensory stimuli, often find abnormalities. Significantly, these occur late in the evoked potential, indicating abnormality in the brain’s interpretation of sensory stimuli rather than in initial reception and conduction.
Behavioral studies show that schizophrenic patients often overreact to low-intensity stimuli, which corresponds to their complaints that lights are too bright or sounds are too loud. In addition, patients are often unusually distractible—unable to focus attention on the most relevant stimuli. Orienting responses to novel stimuli are deficient in about half of schizophrenic patients. Patient self-reports also indicate that, subjectively, the individual feels overwhelmed by sensory stimulation.
Thus, considerable evidence suggests that, at least in many patients, there is an abnormality in the sensory/perceptual functioning in the brain, perhaps in the perceptual filtering mechanism of the reticular formation.
Franz J. Kallmann’s
twin studies
of the 1940s provided convincing evidence of a genetic factor in schizophrenia. He found that genetically identical monozygotic twins are much more likely to be concordant for schizophrenia (that is, both twins are much more likely to be psychotic) than are dizygotic twins, who are not genetically identical. Studies using genealogical techniques also showed that schizophrenia runs in families.
The criticism of these studies was that twins not only are genetically similar but also are exposed to the same family environment, and therefore genetic and environmental factors were confounded. Seymour Kety and colleagues, working with adoption records in Scandinavia, effectively answered this criticism by showing that adoptees with schizophrenia are more likely to have biological relatives with schizophrenia or related illnesses than the biological relatives of unaffected adoptees. These studies showed that schizophrenia is more closely associated with genetic relatedness than with family environment. In addition, these studies showed that the genetic liability is not a liability to psychopathology in general (that is, relatives of individuals with schizophrenia are not at elevated risk for all forms of mental disorder) but that there is a range of severity of illness observed in the relatives of individuals with schizophrenia. The range of less severe schizophrenia-like conditions observed is called the schizophrenia spectrum of illness; schizotypal personality disorder
is the most frequently studied form. Schizotypal personality disorder occurs more frequently than schizophrenia itself among the relatives of individuals with schizophrenia.
Presumably, this genetic predisposition works by producing some organic change. Studies using advanced brain-imaging techniques indicate that, in many patients, there is nonlocalized brain degeneration, which is revealed by the increased size of the ventricles, fluid-filled spaces within the brain. What causes this degeneration is unknown, but some researchers suggest that it is caused by a virus and that a genetic factor increases susceptibility to infection and the subsequent damaging effects of a viral disease. Although direct evidence of a virus has been found in a minority of patients, the viral theory is still considered speculative and unproved. There is no evidence that schizophrenia is contagious.
Biochemical Studies Experimental evidence of biochemical abnormalities in the brain’s dopamine neurotransmitter systems is, however, impressive.
Antipsychotic drugs are effective in relieving the symptoms of schizophrenia, especially positive symptoms such as hallucinations and delusions. These drugs block dopamine receptors in the brain. Furthermore, the more powerfully the drugs bind to and block dopamine receptors, the smaller the effective dose that is necessary to produce a therapeutic result.
Further evidence comes from a condition called amphetamine psychosis, which occurs in people who abuse amphetamine and similar stimulants such as cocaine. Amphetamine psychosis so closely mimics some forms of schizophrenia that misdiagnoses have been common. Furthermore, amphetamine psychosis is not an artifact of disturbed personality; experiments show that normal control subjects will develop the condition if they are given high doses of amphetamines every few hours for several days. Amphetamine psychosis, which is believed to result from the overactivation of dopamine systems in the brain, is treated with antipsychotic drugs such as chlorpromazine.
Direct evidence of abnormality in the dopamine systems comes from studies using advanced techniques such as positron emission tomography (PET) scanning. These studies show that the brains of schizophrenic patients, even those who have never been treated with antipsychotic medications, may have abnormally large numbers of dopamine receptors in an area called the limbic system, which is responsible for emotional regulation.
Dopamine-blocking drugs, however, help only a subset of patients. Studies show that those most likely to benefit from medication are patients who display primarily positive symptoms. Patients who show negative symptoms—such as withdrawal, thought blocking, and catatonia—are less likely to be helped by medication.
History of the Concept of Schizophrenia The disorders that are now called schizophrenia were first characterized in the nineteenth century. Emil Kraepelin first grouped these disorders, referring to them by the collective name dementia praecox, in 1893.
Many early neurologists and psychiatrists thought these dementias were organic conditions. This view changed, however, after Swiss psychiatrist Eugen Bleuler published his classic work on the disorder in 1911. Bleuler proposed that the primary characteristic of the condition was a splitting of intellect from emotions. He introduced the term “schizophrenia” (literally, “split mind”). Bleuler, influenced by the psychodynamic theories of Freud, believed that the bizarre content of schizophrenic thoughts and perceptions represented a breaking away from an external reality that was too painful or frightening. His ideas became especially influential in the United States.
Attempts to treat schizophrenia with traditional psychotherapies were, however, unsuccessful. Success rates rarely surpassed the rate of spontaneous recovery, the rate at which patients recover without treatment. Because medical interventions such as lobotomy, insulin shock therapy, and electroconvulsive therapy were also ineffective, psychiatric hospitals were filled with patients for whom little could be done.
The discovery of antipsychotic drugs and changing public policy about institutionalization in the 1950s changed things dramatically. Hospital populations declined. The surprising effectiveness of these medications, in concert with the discovery of amphetamine psychosis in the 1930s and the genetic studies of the 1940s, renewed the belief that schizophrenia is an organic condition.
Two problems impeded further understanding. First, techniques available for investigating the brain were primitive compared with modern techniques. Therefore, reports of organic changes in schizophrenia, although common, were difficult to confirm. Second, since the routinely administered medications powerfully influenced brain functioning, it became a problem to distinguish organic changes that were important in causing the disorder from those that were merely secondary to the action of antipsychotic drugs in the brain.
Indeed, it became common wisdom among many psychologists that organic factors identified by researchers were not primary to the disorder but were, rather, side effects of medication. Soft neurological signs such as eye-movement dysfunctions, abnormal orienting responses, and unusual movements were considered drug related even though Kraepelin and others had described them decades before the drugs were discovered. The drugs came to be called major tranquilizers, implying that medication allowed patients to function more effectively by relieving the overwhelming anxiety that accompanied the disorder but that the drugs did not influence the schizophrenic process itself.
The fact that antipsychotic drugs have little usefulness as antianxiety agents in nonschizophrenics did not shake this opinion. Neither did the discovery of more powerful antianxiety agents such as chlordiazepoxide (Librium) and diazepam (Valium), even after they were shown to be almost useless in treating schizophrenia.
The next dramatic change in understanding schizophrenia came in the 1960s with the discovery of monoamine neurotransmitters, including dopamine, and the discovery that these chemical systems in the brain are strongly affected in opposite ways by psychotogenic drugs, such as cocaine and amphetamine, and antipsychotic drugs, such as chlorpromazine. Carefully conducted twin and adoption studies confirmed the role of genetic factors in schizophrenia and encouraged the search for the mechanism by which genes influenced the risk for developing schizophrenia. In the following decades, evidence that prenatal and perinatal factors are instrumental in the development of schizophrenia has led to the emerging consensus that schizophrenia should be considered from a neurodevelopmental perspective.
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