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 schizo-phrenogenic 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 over-arousal. 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 1940's 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 con ditions observed is called the schizophrenia spectrum of illness; schizotypal personality 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.
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