Ketamine activates psychosis and alters limbic blood flow in schizophrenia.
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.
Lahti
A C
AC
Maryland Psychiatric Research Center, University of Maryland, Department of Psychiatry, Baltimore 21228, USA.
Holcomb
H H
HH
Medoff
D R
DR
Tamminga
C A
CA
D001519:Behavior / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D006801:Humans; D007649:Ketamine / Q000494:pharmacology*; D008032:Limbic System / Q000098:blood supply*; D008279:Magnetic Resonance Imaging; D011569:Psychiatric Status Rating Scales; D012559:Schizophrenia / Q000503:physiopathology*; D012565:Schizophrenic Psychology; D014055:Tomography, Emission-Computed
D007649:Ketamine