Forty schizophrenic, 20 affective-disordered, and 40 matched normal control subjects were compared on postulated marker and symptom measures of schizophrenic deficits in: (a) affect; (b) attention; (c) proprioception; and (d) thought. The schizophrenic group was significantly more impaired on all four vulnerability markers than were the other two groups, while the schizophrenic and affective-psychotic groups showed comparable impairments on three of the psychotic symptom deficits. The incidence of multiple marker deficits was significantly greater in the schizophrenic than in the affective group. The hypothesis of independence of marker deficits was supported by the absence of any significant correlations among markers in the schizophrenic sample. The data support the theory that independent markers of schizophrenic vulnerability may potentiate schizophrenic disorders when their incidence is concurrent and at deficit levels.
Research on the etiology of schizophrenia has emphasized a stress-diathesis model in which interactions between environmental stresses and genetically based, physiological vulnerabilities are viewed as causal factors (Garmezy, 1974;Heston, 1970;Meehl, 1962).
The specific nature of these vulnerabilities, their pattern of interaction, and their distribution in schizophrenia-prone individuals has not yet been ascertained. In 191 1, Bleuler (1950) proposed that there are fundamental symptoms of schizophrenia that are essential for diagnosis, namely, disturbances in the associative processes, ambivalence, autism, and affective dissociations from thought processes. The more overt symptoms, such as delusions and hallucinations, were viewed as accessory symptoms.
The early views of Bleuler have been echoed and reformulated by Zubin and Spring (1977), who proposed a view of schizophrenia that distinguishes between markers of vulnerability and markers of episodes. Markers of vulnerability are considered to be permanent , enduring behavioral expressions, whereas episodic markers are defined as those behavioral manifestations that wax and wane when the threshold is exceeded and the schizophrenic episode is activated. Similarly, Meehl(l962) proposed that phenotypic markers could be exhibited when a genetic neural integrative deficit was present. He