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Ketamine activates psychosis and alters limbic blood flow in schizophrenia
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1995
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Ketamine, a non‑competitive NMDA antagonist, produces a brief, discrete activation of psychotic symptoms in schizophrenic patients that closely resembles their typical episodes. The study aimed to investigate ketamine’s psychotomimetic effects by administering 0.3 mg kg⁻¹ to schizophrenic patients during a ¹⁵O‑water cerebral blood flow PET scan. Regional cerebral blood flow was quantified with ¹⁵O‑water PET before and after ketamine to map flow alterations. Ketamine increased rCBF in the anterior cingulate cortex while decreasing it in the hippocampus and primary visual cortex, supporting a role for altered glutamatergic transmission in schizophrenia and PCP‑induced psychosis.
The non-competitive NMDA antagonist ketamine, given to schizophrenic individuals in subanesthetic doses, produced a short-lived, discrete activation of their psychotic symptoms, which had striking similarities to symptoms of their usual psychotic episodes. To further study this psychotomimetic property of ketamine, we administered 0.3 mg kg−1 of the drug to schizophrenic individuals during a [15O] water cerebral blood flow study. Regional cerebral blood flow (rCBF) was measured using H215O and positron emission tomography (PET) before and after ketamine administration to identify regions of flow change. rCBF was increased in anterior cingulate cortex and was reduced in the hippocampus and primary visual cortex (lingual and fusiform gyri). These data encourage further consideration of altered glutamatergic transmission in schizophrenic and PCP-induced psychoses.