As amply illustrated, the history of the schizotypal personality disorder has been strongly influenced by a belief in its biological underpinnings and its linkage with schizophrenia. Further studies have now firmly established that some genetic relationship links the two disorders (Kendler et al., 1993), though its exact nature, the specific gene or genes, and their chromosomal location remain unclear. Presumably, research profiting from the Human Genome Project, intended to produce a complete genetic map for Homo sapiens, will eventually aid the search. For now, researchers can only say, for example, that when one family member carries a schizophrenia or schizotypal personality disorder, the risk that others do also is increased, and the positive and negative symptoms are independently heritable (Kendler & Walsh, 1995). Presumably, some forms of schizophrenia may involve a single dominant gene, as Meehl's model predicts, and other forms may involve multiple genes. The two are not mutually exclusive.
Whatever the case, the emerging view, foreshadowed by Rado and Meehl, is that the schizotype is really the fundamental disorder. In contrast, schizophrenia is simply the terminal point of a genetic predisposition, arising in conjunction with persistent environmental stress or trauma. Schizophrenia is the special case; the schizotypal personality is the general case and, therefore, the proper focus of investigation (Raine & Lencz, 1995). Accordingly, researchers have now begun to extend the classic findings of schizophrenia research downward into the range of the schizotypal personality. Although thousands of studies on schizophrenics have been published, surprisingly little is known with certainty. The hope is that the study of the schizotypal personality will clarify and extend a great many tentative findings. The most straightforward hypothesis, which need not be supported for every line of research, is simply that every schizophrenic pathology should have a less pathological parallel in the schizotypal personality.
An important research tradition focuses on structural abnormalities in the schizophrenic brain, using recently developed technologies such as computerized tomography, which passes X-rays through sections of brain tissue, and magnetic resonance imagery (MRI), which takes more precise pictures of the brain using intense magnetic fields. Findings show that the ventricles, cavities in the brain between the hemispheres that contain cerebrospinal fluid, are enlarged in many schizophrenics, suggesting either some pathology in the development of the brain or perhaps an atrophy of brain tissue as a result of the disorder. Buchsbaum, Yang, and colleagues (1997) compared the ventricular volume of schizophrenic subjects, schizotypal personality subjects, and normals. Findings suggest decreased volume of the left frontal lobe. More important, however, the degree of ventricular enlargement was not as great for schizotypals as for schizophrenics and is not found in other personality disorders (Siever, Rotter, Losonczy, & Guo, 1995).
In addition to its large-scale structural features, the brain is composed of individual neurons that communicate with one another across the synapse via chemical messengers, called neurotransmitters. Without these, the billions of neurons of the brain would be isolated, unable to do anything. Thought itself would be impossible. Because cognitive distortions are so basic to the schizotypal personality, the study of neuro-transmitters has become a natural route of investigation. Like schizophrenics, schizo-typal subjects possess ideas of reference, thought disorder, perceptual aberrations, and paranoid symptoms, the so-called positive symptoms, which respond to antipsychotic medications (Joseph, 1997), though schizotypals require lower doses than do schizophrenics. Such a similar response to similar medication again argues for continuity between the two syndromes.
Precisely which neurotransmitters are involved, however? Antipsychotics work by blocking receptor sites for dopamine. Now more than 30 years old, the "dopamine
The Schizotypal Personality hypothesis" holds simply that too much dopamine leads to the positive symptoms of schizophrenia. Indeed, any excess of dopamine should produce schizophrenic symptoms. This is exactly what occurs. Parkinson's disease, for example, is associated with a deficiency of dopamine. However, when Parkinson's patients are given drugs to increase dopamine levels, some develop positive symptoms (Celesia & Barr, 1970). Likewise, the psychosis induced by amphetamine abuse is produced through dopaminergic channels. Given such connections, it is hardly surprising that dopamine plays a role in the schizotypal personality. Research now shows that increases in the levels of chemicals in the blood that mark dopamine activity in the brain correlate with the positive symptoms of schizotypal personality disorder (Siever et al., 1993).
Combining the findings of anatomical and neurotransmitter research described previously, current thinking (Siever, 1995) is that structural brain defects account for negative symptoms in schizotypal personality disorder, and increased dopamine activity in areas of the limbic system account for the positive symptoms. Whether this reflects some hypersensitivity in the receptors or perhaps simply too many receptor sites is not yet known. Several kinds of dopamine receptors have now been identified, and their number and relative proportions are likely to become a central focus of future studies.
Another classic line of research focuses on neurovirology, an emerging subdiscipline, with the theory that at least some schizophrenics are afflicted with a viral infection of the brain during fetal development. The virus assimilates itself into the DNA and then lies dormant until somehow reactivated during puberty or early adulthood, ages when the risk for schizophrenia abruptly rises. Various studies support the viral theory. More schizophrenics are conceived in the winter months, the cold and flu season, than in summer months, for example. Machón, Huttenen, Mednick, and LaFosse (1995) compared schizophrenics born during an influenza epidemic in Finland in 1957 to control subjects born in 1955 and 1956, a relatively low influenza period. Subjects exposed to influenza during the second trimester of pregnancy were shown to be higher than controls on the cognitive-perceptual symptoms of schizotypy, with a trend toward interpersonal deficits as well. Other studies have shown that metabolites of clozapine, a relatively recently developed drug used to treat schizophrenia, inhibit the replication of human immunodeficiency virus (HIV-1), further strengthening the link between schizotypy and viral infection (Jones-Brando, Buthod, Holland, Yolken, & Torrey, 1997). Moreover, the viral hypothesis is not inconsistent with the high concordance rate of schizophrenia among identical twins, who share fetal circulation (Davis & Phelps, 1995).
Other miscellaneous but interesting findings have been reported. For example, subjects with high schizotypy scores tend to be shorter than normals (Wellman, Williams, Geaney, & Cowen, 1996). Like schizophrenics, normal subjects with high scores on schizotypy do not discriminate smells as well as normals (Park & Schoppe, 1997). Scores on cognitive measures of schizotypy predict vulnerability to nightmares (Clar-idge, Clark, & Davis, 1997). Different aspects of schizotypal personality disorder may be associated with either early or late puberty (Gruzelier & Kaiser, 1996). Schizophrenic subjects were less likely than their nonschizophrenic siblings to be breast-fed and exhibited more schizoid and schizotypal traits in childhood (McCreadie, 1997).
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