THE clinical picture of schizophrenia was initially labeled as a syndrome by the Belgian psychiatrist Morel, who in 1860 introduced the term dementia praecox (demence precoce) to describe an insidious, progressive personality decompensation in a 14-year-old boy. However, the formal study of schizophrenia did not receive a major impetus until Emil Kraepelin published his classical discussion of dementia praecox in 1896. Kraepelin's contribution was based on earlier descriptions of three conditions, hebephrenia, catatonia, and paranoia, that had previously been considered distinct and' unrelated syndromes. Kahlbaum in 1863 had referred ,to a condition occurring in puberty as paraphrenia hebetica, · and Hecker in 1871 had labeled this condition hebephrenia and characterized it in terms of Huctuating melancholia, mania, and confusion. In 1874 Kahlbaum had provided the first clinical description of catatonia, in which he stressed the muteness, postural rigidity, impaired volition, and occasional waxy Hexibility associated with this disorder. The term paranoia, which dates at least from Hippocrates, had been used during the eighteenth and nineteenth centuries in a variety of senses, often as a name for delusional and delirious disorders (Cameron, 1959). \)
Psychiatry, published in 1896, the first attempt to synthesize the nomen-
4 Introduction clature of schizophrenia. In this text Kraepelin concluded that because hebephrenia, catatonia, and paranoia were all characterized by progressive decay and eventual dementia they should be identified as forms of a single disorder, dementia praecox, t~e fundamental criterion for which is its outcome, dementia. Kraepelin defined dementia praecox as a syndrome consisting of hallucinations, delusions, incongruous affectivity, impaired attention, negativism, stereotyped behavior, and progressive dilapidation, anci he designated the type of dementia praecox as hebephrenic, catatonic, or paranoid, depending on which symptoms were predominant. Kraepelin believed that the clinical features of the disorder were caused either by a degenerative disease of the brain or by metabolic disturbances, and he was critical of any attempt to interpret the behavior of the afflicted person in psychological terms.