Schizophrenia: an etiological speculation.

Abstract

����� In his book, An Adaptive Competence Theory ofNeurosis, this author has formulated a theory of neurosis in the following terms [I]. Neurosis is a life-style manifestation of inadequate mentation that results from the partial failure offunctional maturation ofthe neomammillary, or cortical, brain. As a consequence, paleomammillary, or limbic, mentation retains an unwarranted degree of input into wholebrain function and behavioral choice. The failure of full functional maturation of the neomammalian brain is a result of deficient postnatal training rather than inadequate nurturance and is expressed in defective cognitive control of the whole mind and in consequent adaptive malfunctioning. While the psychopathology of schizophrenia may be explained in terms of the same psychobiological constructs, the etiology points in quite another direction. Schizophrenia is not, in this author's view, at one end of a spectrum of mental disorder, the other end of which is occupied by the neuroses. The derangements that make up the clinical picture of schizophrenia reach so much more deeply into the mental processes that they cannot be explained in terms of degree of neurobiological maturation. What are these derangements, and how may they be accounted for in terms ofemerging psychobiological understanding? There are five principal characteristics of schizophrenia that are essential to this overview. These are (1) schizophrenia, the split between affect and ideation; (2) thought disorder; (3) hallucinations; (4) catatonia and other motor manifestations; and (5) the praecox onset of the dementia. Before examining these in detail, perhaps it would be helpful to review, albeit briefly, the psychobiological constructs we shall be using to formulate our etiological speculation.