Published online by Cambridge University Press: 17 September 2025
Autoimmune psychosis (AP) and other autoimmune psychiatric syndromes (APS) are associated with central nervous system antibodies. This study investigated related magnetic resonance spectroscopic imaging (MRSI) signatures and their correlations with electroencephalography (EEG), cerebrospinal fluid (CSF), and psychometric/neuropsychological measures.
Twenty-eight adults with suspected antibody-positive AP spectrum syndromes were compared with 28 matched healthy controls. Inclusion in the patient group was based on the APS concept, resulting in a heterogeneous group with uniform autoimmunity. MRSI was performed using a spiral-encoded Mescher-Garwood localized adiabatic selective refocusing 3D-MRSI sequence. Glutamate+glutamine (Glx), gamma-aminobutyric acid (GABA), total N-acetylaspartate (tNAA), and total creatine (tCr) were reported as ratios to tNAA and/or tCr. EEG was analyzed for intermittent rhythmic delta/theta activity (IRDA/IRTA) using independent component analysis.
No significant differences in Glx, GABA, tNAA, or tCr ratios were observed between patients and controls. Correlation analyses in patients showed a trend for a negative association of the IRDA/IRTA rate before hyperventilation with the GABA/tCr ratio in both hippocampi and with the GABA/tNAA ratio in the left hippocampus and Glx/tCr ratio in the right putamen and pallidum. Significant positive correlations were observed between inflammatory CSF markers (white blood cell count and IgG Index) and GABA/tCr and GABA/tNAA ratios in the left caudate nucleus and right isthmus cingulate and thalamus, as well as between negative symptoms in PANSS and higher GABA/tCr ratios in the right putamen.
No group differences were identified; however, correlations suggest a link between neuroinflammatory CSF markers and negative symptoms with GABAergic signaling in patients. Multimodal diagnostic approaches may provide a better understanding of the link between neuroinflammation, neurochemistry, and EEG slowing.
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