The genesis and history of the term “schizotypal” must be understood within the context of the history of schizophrenia as a diagnostic category. This is because schizotypal personality disorder is seen as a less severe point on a spectrum, on which schizophrenia itself is the most severe manifestation. An English neurologist, Willis (1668; 1684/1912) reported observing “young persons who, lively and spirited, and at times even brilliant in their childhood, passed into obtuseness and hebetude during adolescence.” Likewise, the Belgian psychiatrist MOrel (1852-1853) described “a 14-year-old boy who had been a cheerful and good student, but who progressively lost his intellectual capacities and increasingly became melancholy and withdrawn.” He believed that this downward spiral resulted from neurobiological deterioration, and thus, presented the clinician with a pessimistic prognosis. He referred to it as “dementia praecox,” thinking it a form of early dementia. It was this label that would be used of schizophrenia until the early 20th century, when the term was first coined.
K.L. Kahlbaum (1863) and E. Hecker (1871) referred to such deterioration as “hebephrenia” when it began in adolescence. Theodore Millon notes that they perceived it as starting with “a quick succession of erratic moods followed by a rapid enfeeblement of all functions, and finally progressed to an unalterable psychic decline.” The term “catatonic” came to be used to represent what was known as “tension insanity.” In such cases, the patient exhibited a lack of reactivity to sensory stimuli and lacked “self-will,” frozen into place, having withdrawn entirely from contact and interaction with the social world.
Kraepelin (1896) equated hebephrenia and dementia praecox, presumably in an effort to eradicate diagnostic confusion and bring the disparate phenomena under a single head. He believed that either metabolic or sexual dysfunctions caused these symptoms, as opposed to the German psychiatric tradition in general, which focused primarily on the neurobiological roots of medical illness, as resulting from cerebral or anatomical lesion.
“Among the major signs that Kraepelin considered central, in addition to the progressive and inevitable decline, were discrepancies between thought and emotion, negativism, and stereotyped behaviors, wandering or unconnected ideas, hallucinations, delusions, and a general mental deterioration.”
His ideas were engaged by Eugen Bleuler and Adolf Meyer in America. In 1911, Bleuler denied that the type of mental deterioration which they exhibited was comparable to metabolic problems or genuine dementia. He insisted that his patients were oftentimes quite creative, and exhibited a degree of complexity one would not expect from someone with serious brain degeneration. Many of them exhibited psychosis in adulthood, rather than adolescence, such that it could no longer be properly termed “hebephrenia,” and they did not necessarily present with unalterable or progressive cognitive deterioration.
Instead, Bleuler noted disturbances in the association between thoughts, as well as the link between affect and intellect, and an “autistic” detachment from the reality of the external world. In 1911, Bleuler was led “to term them “the group of schizophrenias,” a label selected to signify what he saw to be a split (schism) within the mind (phrenos) of these patients. Although he considered schizophrenia to be a diverse set of disorders, he retained the Kraepelinian view that the impairment stemmed from a unitary disease process that was attributable to a physiological pathology.” He noted secondary symptoms such as delusions and hallucinations, and Bleuler related these back to the distinctive life experiences of his patients. While the content of the delusions and hallucinations were unique to the life experiences and environment of the schizophrenic individual, he denied that the syndrome could be seen as psychogenic.
Adolf Meyer, in 1906, differed from a purely neurobiological view, and saw it as a way of reacting to intense stress. He referred to the syndrome as a set of “progressive habit deteriorations” which mirrored “inefficient and faulty attempts to avoid difficulties.” He referred to schizophrenia as “paregasia.” Of special note for those studying schizotypal personality disorder, he believed that it could be manifested in less severe, non-psychotic forms, in which hallucinations, deterioration and delusions were absent and he believed, furthermore, that these sets of tendencies could stabilize at this pre-psychotic point. Meyer located the genesis of schizophrenia in a maladaptive and self-defeating response to stress.
Thus, Meyer and Bleuler repudiated Kraepelin’s understanding of schizophrenia as a condition of inevitable decline and deterioration. Kraepelin himself later accepted this criticicsm (1919) and articulated schizophrenic pathology in the language of the “autistic personality.” Others, such as Langfeldt (1937), however, retained Kraepelin’s earlier conception of schizophrenia as a degenerative dementia. It was he who would coin the term “schizophreniform” for “reactive” responses, in whom symptoms were more related to affect than disordered thinking, and which were acute responses to intense precipitants. On the other hand, true schizophrenics, he believed, suffered from a “process” illness, anticipated by premorbid schizoid personalities, “that would progress insidiously to the clinical state with minimal external promptings. As this deterioration progresses, previously inchoate signs of “ego-boundary disturbances,” associative thought defects, and feelings of depersonalization gain in increasing prominence.”