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Neuromechanism of Developing Methamphetamine Psychosis: A Neuroimaging Study
Author(s) -
IYO MASAOMI,
SEKINE YOSHIMOTO,
MORI NORIO
Publication year - 2004
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1316.036
Subject(s) - methamphetamine , psychosis , dopamine transporter , nucleus accumbens , putamen , medicine , psychology , endocrinology , cerebral blood flow , dopamine , psychiatry , dopaminergic
A bstract : The long‐term use of methamphetamine (MAP) induces a psychotic state, called MAP psychosis. To understand the neuromechanisms of the persistent psychosis, we used SPECT, MR spectroscopy (MRS), and PET on the MAP users. The SPECT study showed a high incidence of multiple patchy deficits in cerebral blood flow among the users. The MRS study MAP users showed a significantly reduced ratio of creatine plus phosphocreatine (Cr + PCr)/choline‐containing compounds (Cho) in the brain compared with the healthy control subjects. In addition, the reduction in the ratio of Cr + PCr/Cho was significantly correlated with the duration of MAP use and with the severity of residual psychiatric symptoms. PET revealed no significant differences between the ex‐users of MAP and the healthy controls in the density of striatal dopamine D2 receptors. On the other hand, the density of dopamine transporter in the nucleus accumbens and caudate/putamen in the MAP users was significantly less compared with the controls. This reduction was significantly correlated with the length of use and severity of psychotic symptoms. These findings suggest that long‐term use of MAP causes abnormal cerebral blood flow patterns, reduction of brain dopamine transporter density, and metabolite alteration, which may be closely related to a susceptibility to MAP psychosis.