The Dopamine Hypothesis: An Overview of Studies With Schizophrenic Patients

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.

Frontal Auditory-Evoked Potential Augmenting-Reducing and Urinary Homovanillic Acid

“…. 1984 and central dopaminergic dysfunctioning [see re view in Haracz, 1982] have been hypothesized.…”

Reservasjonsrett i psykiatrien nå!

“…However, after being put on an antipsychotic, their dopamine metabolites increased to abnormal levels, for at least a short period of time. 17,18,19 This finding led researchers to put together a new understanding of how the brain responded to the drug's blockade of dopamine receptors. The drug acted as a brake on dopamine transmission, and in compensatory response, the brain's presynaptic neurons, trying to maintain the normal functioning of their dopaminergic pathways, increased their output of dopamine.…”

Analysis of Physiological Mechanism in Psychopharmacology

“…Because most drugs antidote only a fraction of the symptomatology that characterizes the disease, a direct analysis of etiological determinants in patients is required. It must be shown, for example, that schizophrenics have an excess of DA activity [see Haracz, 1982] or that depressed patients are uniquely characterized by monoamine deficits. The analysis of efficacious drug effect is thus only a part of the analysis of etiology.…”