The notion that psychosocial factors play an important role in the genesis of schizophrenia was a recurrent theme in older psychiatric writings, but is now given less credence. Prominent in these early writings was Freud’s view that the schizophrenic process represents a fixation at an early autoerotic stage of sexual development. There is no way of affirming or refuting this proposition. The same can be said for the many suggestions that disturbed intrafamily relationships engender schizophrenic traits or possibly provoke psychosis in persons who are genetically vulnerable. Behind all these suggestions was the notion that disturbed interpersonal relations in the family in some way interfered with the normal maturation of personality. The extent to which these aberrations of family relationships are primary or secondary cannot be ascertained.
The often-cited observations of Harlow on the deleterious effects of maternal and peer deprivation in primates opened the possibility that similar deprivations in humans may be responsible for the development of schizophrenia. However, such severe degrees of familial deprivation have rarely been documented in humans and when they were, as in some orphans, the effects were only transitory.
From a neurologic standpoint, the main initial distinction to be made is between an acute schizophrenia-like psychosis and the chronic disease, schizophrenia. The acute schizophreniform illness takes the form of a delusional-hallucinatory syndrome in which there is little if any disturbance of consciousness. Although such a syndrome is characteristic of schizophrenia, it may occur in the manic phase of bipolar disease, encephalitis, temporal lobe epilepsy, chronic amphetamine intoxication, withdrawal from alcohol after a sustained period of intoxication, and most often in the emergency department, from PCP, angel dust, LSD, and other drug intoxications. On rare occasions it is seen with postpartum psychosis (see further on) and with certain endocrine and metabolic disorders in which consciousness is not impaired. Thus whenever this syndrome is recognized, these several causes need to be differentiated. On our services, less than 1 of 5 of the acute schizophreniform psychoses has proved to be a result of the disease schizophrenia. This distinction is made by the premorbid history and the course of the illness. If the patient had been reclusive, withdrawn, and socially maladapted and does not seem to recover fully from the acute psychosis, then the diagnosis of schizophrenia is more likely. Lacking these features, and in particular with a full remission, one assumes the occurrence of hypomania or of a toxic-metabolic psychosis, which can be detected by laboratory screening for drugs and endocrine diseases. Only 10 percent of patients with classic schizophrenia will have such an acute episode. Adherence to the criteria enumerated earlier, particularly to those devised by Feighner and colleagues will avoid most errors in diagnosis.
It is the present authors’ opinion that the status of acute schizophrenia and of the so-called schizothymic and schizoaffective states brings to light a crucial nosologic problem. Is the traditional separation of depressive disease, bipolar disease, and schizophrenia biologically sound? The suggestion is that they are linked in some way by these transitional forms. Neurologists should keep an open mind about these and other theoretical problems that lack a firm genetic and neuropathologic basis.