Ketamine activates psychosis and alters limbic blood flow in schizophrenia
Adrienne C. Lahti, Henry H. Holcomb, Deborah R. Medoff, Carol A. Tamminga
Neuroreport April 1, 1995 DOI: 10.1097/00001756-199504190-00011 via OpenAlex
Summary
AI-generated from the abstractA subanesthetic dose of the NMDA antagonist ketamine temporarily activated psychotic symptoms in people with schizophrenia, closely resembling their usual episodes. In a PET study using radioactive water, ketamine increased blood flow in the anterior cingulate cortex and decreased flow in the hippocampus and primary visual cortex. These findings support the idea that altered glutamate transmission may contribute to schizophrenia and PCP-induced psychosis.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Schizophrenic individuals |
| Intervention | Ketamine |
| Dose | 0.3 mg kg-1 |
| Citations | 440 |
| Key finding | Ketamine increased cerebral blood flow in the anterior cingulate cortex and reduced it in the hippocampus and primary visual cortex in people with schizophrenia. |
Abstract
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 H2(15)O 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.