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Objectives: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 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).Conclusions: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.

Immunoglobulin G (IgG) autoantibodies targeting myelin oligodendrocyte glycoprotein (MOG) have recently been associated with autoimmune CNS demyelination. We present the case of a 35-year-old patient who was seronegative for MOG-IgG (as confirmed by means of three independent immunoassays) during two corticosteroid-responsive attacks of brainstem encephalitis and optic neuritis, respectively, but turned positive for MOG-IgG under treatment with interferon-beta (IFN-beta), which was commenced 6 months after onset of the first attack. MOG-IgG serum levels declined after therapy was switched to glatiramer acetate. The fact that seroconversion was first observed under treatment with IFN-beta is in accordance with previous evidence suggesting a role of IFN-beta in disease exacerbation in antibody-mediated disorders.

Myelin basic protein (MBP) is one of the most abundant proteins in the human brain. Active immunization with MBP induces experimental autoimmune encephalomyelitis, and anti-MBP antibodies have been repeatedly described in MS.1 However, its role in MS pathogenesis or prediction of disease progression is still unclear.2,3 Previous studies utilized enzyme-linked immunosorbent assay or immunoblot assays with linear epitopes of MBP, thus potentially overlooking autoantibodies that bind to MBP's natural conformation. These initial studies also included antibodies against another myelin protein, myelin oligodendrocyte glycoprotein (MOG). As happened for MBP, conflicting results stimulated the discussion of whether MOG antibodies contribute to MS pathogenesis.2,3 More recent work demonstrated that there are presumably pathogenic MOG antibodies defining the new entity of MOG antibody-associated disease;4 however, they bind to conformational MOG only. The authors are grateful to Professor Brian Popko, Department of Neurology, University of Chicago, for providing MBP knockout mouse brains.