Anti-MOG autoantibody-associated schizophreniform psychosis

Abstract

Objective: 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. Methods: Therefore, two patients with psychosis and anti-MOG antibodies—detected in fixed cell-based and live cell-based assays—are presented. Results: Patient 1 suffered from late-onset psychosis with singular white matter lesions in MRI and intermittent EEG slowing. Patient 2 suffered from a chronic paranoid-hallucinatory disorder with intermittent confusional states, non-specific white matter alterations on MRI, a disorganized alpha rhythm on EEG and elevated cerebrospinal-fluid protein. Both patients had anti-MOG antibody titers of 1:320 in serum (reference<1:20). Conclusion: The arguments for and against a causal role for anti-MOG antibodies are discussed. The antibodies could be relevant, but due to moderate titers, they may have caused a rather “subtle clinical picture” consisting of psychosis instead of “classical” MOG encephalomyelitis.

Anti-Myelin Oligodendrocyte Glycoprotein Antibody-Associated Meningitis with Psychotic Symptoms

“…To our knowledge, in previous studies, one case reported a patient with psychotic symptoms (intermittent visual hallucinations and paranoia), positive anti-MOG antibodies and anti-NMDA-R encephalitis [14]. The other two studies respectively reported two patients with anti-MOG antibody-associated psychosis, that were negative for anti-NMDA-R antibodies in both CSF and serum [1,15]. Two patients in the former study presented with acute-onset or chronic paranoid-hallucinatory syndrome [1].…”

“…This implied the importance of immunotherapy in the treatment of anti-MOG antibody-associated encephalitis or meningitis with psychotic symptoms [16]. However, the previous case which reported two patients with anti-MOG autoantibody-associated schizophreniform psychosis partly recovered due to treatment with risperidone, olanzapine, and valproate [1]. In that case, MRI analyses revealed no inflammatory lesions, but with pronounced intermittent rhythmic theta activity or disorganised alpha rhythm on EEG.…”

“…The other two studies respectively reported two patients with anti-MOG antibody-associated psychosis, that were negative for anti-NMDA-R antibodies in both CSF and serum [1,15]. Two patients in the former study presented with acute-onset or chronic paranoid-hallucinatory syndrome [1]. While the latter study reported two pediatric patients with psychiatric disorders before or concomitant with recurrent alternating ON, which is the typical clinical manifestation of MOGAD [15].…”

“…In this report, we present the case of a patient diagnosed with anti-MOG antibody-associated meningitis, whose main clinical manifestation is thinking rupture. This is the third detailed case report of the patient with psychotic symptoms as well as anti-MOG antibodies (without comorbid anti-NMDA-R encephalitis) [1] and the first wherein immunotherapy was performed according to our literature search.…”

“…However, the role of anti-MOG antibodies remained unclear, and they were usually not routine examination of patients with psychosis [1].…”