"The dopamine hypothesis: An overview of studies with schizophrenic patients": Erratum

Reports an error in the original article by John L. Haracz (Schizophrenia Bulletin, 1982, Vol 8[3], 438-469). The article contains a misplaced section of text that should be deleted. The misplaced text begins on p. 452 with the paragraph "The failure to find a universal biochemical ..." and extends to p. 453 including the paragraph which begins with "A nondopaminergic etiology. ..." Furthermore, a sentence on p. 456 should be deleted. This sentence begins at the bottom of the second column and reads as follows: "Schizophrenics with a positive family history of schizophrenia did not differ in platelet MAO activity from schizophrenics with no such family history (Belmaker et al. 1978)." (The following abstract of this article originally appeared in record 1983-08019-001). For the past decade, the dopamine hypothesis of schizophrenia has been the predominant biochemical theory of schizophrenia. Despite the extensive study of tissue samples obtained from schizophrenics, indirect pharmacological evidence still provides the major support for the hypothesis. Direct support is either uncompelling or has not been widely replicated. The dopamine hypothesis is limited in theoretical scope and in the range of schizophrenic patients to which it applies, and no comprehensive biological scheme has yet been proposed to draw together the genetic, environmental, and clinical features of schizophrenia. Recent refinements of the dopamine hypothesis may aid in the delineation of biologically homogeneous subgroups. Positive symptoms (e.g., hallucinations and delusions) and negative symptomatology (e.g., affective flattening and social withdrawal) may result from different pathophysiological processes. Schizophrenia research might benefit from an increased attention to neurophysiological adaptations. (PsycINFO Database Record (c) 2016 APA, all rights reserved)