Schizophrenia researchFeb 18, 2014

Brain chemical changes linked to methamphetamine use and methamphetamine-induced psychosis

Updated Jan 13, 2026

Abstract

Methamphetamine use is associated with decreased neuronal integrity in specific brain regions.

Methamphetamine dependence is linked to lower concentrations of n-acetyl-aspartate (NAA) in the right anterior cingulate cortex (ACC) and right dorsolateral prefrontal cortex (DLPFC) compared to healthy controls.
The methamphetamine dependent group exhibited significantly reduced choline metabolites in the right DLPFC relative to controls.
In individuals with methamphetamine-induced psychotic disorder (MAP), NAA concentrations correlated significantly with the age of initial methamphetamine use and duration of use, which was not observed in the methamphetamine dependent group.
Active neurodegeneration appears to be present in the right DLPFC of the methamphetamine dependent group but not in the MAP group, possibly due to antipsychotic medication.
Findings suggest that early onset of methamphetamine use may disrupt neuronal plasticity in frontal brain regions.

Simplified

BACKGROUND: Methamphetamine (MA) use has been shown to decrease n-acetyl-aspartate (NAA), a marker of neuronal integrity and viability, on (1)H magnetic resonance spectroscopy ((1)H-MRS). However, little work has compared (1)H-MRS in MA dependent individuals and MA dependent individuals with MA induced psychotic disorder (MAP).

METHODS: Twenty six participants with MA dependence (sixteen without psychosis, ten with psychosis - MAP) and nineteen healthy controls underwent 2D-chemical shift imaging (1)H-MRS, which included voxels in the anterior cingulate cortices (ACC), dorsolateral prefrontal cortices (DLPFC), and frontal white matter. We compared metabolite concentrations relative to phosphocreatine+creatine (PCr+Cr) for n-acetyl-aspartate (NAA), n-acetyl-aspartate+n-acetyl-aspartyl-glutamate (NAA+NAAG), glutamate (Glu), glutamate+glutamine (Glu+Gln), myo-inositol, and glycerophosphocholine+phosphocholine (GPC+PCh) across groups.

RESULTS: The MA groups showed significantly decreased relative NAA metabolite concentrations for right ACC and right DLPFC, compared with control group. The MA dependent group only showed significantly decreased choline metabolites for right DLPFC, compared with control group. The MAP group's relative NAA metabolite concentrations were significantly correlated with age of initial use and duration of MA use, these correlates were not apparent in MA dependent group.

CONCLUSION: MA use is associated with decreased neuronal integrity and viability, specifically in the right ACC and right DLPFC. MA dependence showed active neurodegeneration in the right DLPFC, this was not apparent in the MAP group and may be related to the use of antipsychotic medication in the MAP group. The effects of MA use in MAP suggest that age of initial use presents a mismatch of neuronal plasticity, in frontal white vs. gray matter and duration of use relates to decreased neuronal integrity and viability. Further study is warranted from this initial study of (1)H-MRS in MAP, in particular longitudinal assessment of these individuals both neurobiologically ((1)H-MRS) and clinically - to determine disease progression.

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