SCHIZOPHRENIC SYMPTOMATOLOGY IN MENTALLY RETARDED CHILDREN
Abstract
In summary, I think we should make a break with the facile generalizations that seem to simplify but really complicate and distort our work. There is no single entity of mental retardation: there are a great variety of factors, medical, psychological and social, which may impede mental growth and development. Similarly, there is no simple entity of schizophrenia: here too we encounter a variety of medical, social and psychological factors which induce bizarre distortions and disorganized patterns of behavior and development. Where the intellectual retardation dominates the picture, we are justified in labeling it descriptively as mental retardation: where the distortion and disorganization dominate the picture, we are justified in calling its schizophrenia. But we must recognize that there are many intermediate and overlapping types where we must be satisfied to describe the picture as retardation, with more or less prominent schizophrenic features. Moreover, in point of time, the clinical picture may change in any one case and latent or secondary features may become dominant. There is much to recommend Benda's(3) suggestion that cerebral defect or dysfunction present at birth is more likely to produce a picture of retarded development, while the same process superimposed later, after a period of normal development, is more likely to induce a pattern of disorganization that is called psychotic. This may be compared to the building of a small structure with a few bricks, or the later undermining or demolition of a good-sized building by removing bricks after the building is completed.
In terms of research and scientific interest, it is reasonable to expect that some common etiologic factors may induce both syndromes; it can be regarded as already established that certain kinds of cerebral pathology or dysfunction can induce both retardation and schizophrenia. Post-anoxic, post-encephalitic, and phenylketonuric cerebral dysfunction can all demonstrably induce psychoses, mental retardation, or combinations of both. It is proper to suspect that other etiologic agents can do the same. At the same time, it would not be at all surprising to find that the hard core of schizophrenic cases, and the hard core of retarded cases, tend to have different types of etiology, with ganglion cell destruction and cerebral defect dominant in retardation, and toxic inhibitory factors dominant in schizophrenia. This was Kraepelin's view when he first propounded the concept of dementia praecox and there is much new work to indicate that his view may prove to be correct.
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