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 localised 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 analysed 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 signalling in patients. Multimodal diagnostic approaches may provide a better understanding of the link between neuroinflammation, neurochemistry, and EEG slowing.

Autoimmune mechanisms are related to disease development in a subgroup of patients with psychosis. The contribution of immunoglobulin G (IgG) antibodies against myelin oligodendrocyte glycoprotein (MOG) is mainly unclear in this context.

Therefore, two patients with psychosis and anti-MOG antibodies – detected in fixed cell-based and live cell-based assays – are presented.

Patient 1 suffered from late-onset psychosis with singular white matter lesions in magnetic resonance imaging (MRI) and intermittent electroencephalography (EEG) slowing. Patient 2 suffered from a chronic paranoid–hallucinatory disorder with intermittent confusional states, non-specific white matter alterations on MRI, a disorganised alpha rhythm on EEG, and elevated cerebrospinal fluid protein. Both patients had anti-MOG antibody titres of 1 : 320 in serum (reference < 1 : 20).

The arguments for and against a causal role for anti-MOG antibodies are discussed. The antibodies could be relevant, but due to moderate titres, they may have caused a rather ‘subtle clinical picture’ consisting of psychosis instead of ‘classical’ MOG encephalomyelitis.