Relationship between reactive psychosis and the depressive disorders

The diagnostic validity of acute schizophrenia has come under close scrutiny since 1970, when Robins and Guze¹ disclosed that clinical symptomatology, family history, and treatment outcome consistently differentiate between schizophrenics who recover and schizophrenics who follow a chronic, deteriorating course. Not only have recent clinical and empirical investigations into prognosis in schizophrenia confirmed Robins and Guze's hypothesis that good prognosis schizophrenia,^2–5 acute schizophrenia,^6,7 and schizoaffective psychoses^8,9 bear little relation to poor prognosis schizophrenia, studies have also demonstrated that the phenomenology of these good prognosis disorders generally coincide with patterns typically associated with the depressive disorders.^2–7,9 In fact, one-half to two-thirds of the patients receiving admission diagnoses of acute schizophrenia have met strict research criteria for bipolar mania, while less than 5% have fulfilled strict requirements for a diagnosis of schizophrenia.^2–7,9McCabe has recently proposed that many of the remaining third of recovered schizophrenics suffer from a reactive, psychogenic psychosis that is different from both schizophrenia and depressive disorder.^10–14 In a series of studies, he has suggested that certain genetically and/or developmentally vulnerable individuals manifest an abrupt, acute psychosis when subjected to overwhelming psychologic trauma. However, the results of his symptomologic and genetic study do not equivocally support the thesis of a third functional disorder masquerading as acute schizophrenia.^10,11 Rather, much of the data on reactive psychoses overlap with typical phenomenology of the depressive disorders.The congruence of these disorders, one predominantly biologic, the other psychologic in etiology, lends additional support to the integrated models of depressive disorder recently proposed by Akiskal and McKinney^15,16 and Depue and Evans,¹⁷ which suggest that depressive behaviors must be understood as occurring on several levels simultaneously, and that a multiplicity of genetic, developmental, pharmacologic, and interpersonal factors converge in the midbrain and lead to a reversible functional derangement of the mechanisms of reinforcement.¹⁵