Abstract
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. 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, delusions) and negative symptomatology (e.g., affective flattening, social withdrawal) may result from different pathophysiological processes. Schizophrenia research might benefit from an increased attention to neurophysiological adaptations.