Comparison of schizophrenia and methamphetamine-induced psychosis: a
proton magnetic resonance spectroscopy and cytokine study.
Abstract
Background: There is similarity in schizophrenia and
methamphetamine-induced psychosis neurobiology. Few studies have
directly compared neurometabolites in thalamo-cortical circuitry across
these disorders or assessed the relationship with peripheral cytokines.
This study compared neurometabolites and neuronal integrity in
thalamo-cortical circuitry, and investigated associations with
peripheral cytokine levels in both disorders. Methods: Ninety-five
participants were recruited – 36 with schizophrenia, 27 with
methamphetamine-induced psychosis, and 32 healthy controls. All
participants underwent a magnetic resonance imaging scan, which included
magnetic resonance spectroscopy. Glutamatergic and neuroinflammatory
neurometabolites were examined. Serum cytokine concentrations included
Interleukin 1-beta, Interleukin-8, Interleukin-10, Tumor Necrosis Factor
alpha and Interferon gamma. Parametric data were analyzed with one-way
analysis of variance and non-parametric data were analyzed with Kruskal
Wallis tests. Associations were determined using Spearman’s rank-order
coefficient. Results: The methamphetamine-induced psychosis group had
lower n-acetyl aspartate with n-acetyl-aspartyl glutamate in left
dorsolateral prefrontal cortex and left frontal white matter, compared
to controls. In schizophrenia, positive associations were found between
glutamate and n-acetyl aspartate and n-acetyl aspartate with
n-acetyl-aspartyl glutamate in the anterior cingulate cortex. In the
methamphetamine-induced psychosis group, positive relationships were
found between myo-inositol in the left thalamus and bilateral anterior
cingulate cortex. Conclusion: In schizophrenia, there is suggestion of
dysfunction in neuronal tissues in the glutamate-glutamine cycle within
the thalamo-cortical circuit. In methamphetamine-induced psychosis,
there is evidence of compromised neuronal integrity associated with
chronic disease progression, and suggestion of aberrant
neuroinflammatory regulation in the thalamus-ACC circuit. This study
highlights similarities and differences in the psychobiology of the two
disorders