Autoimmune encephalitis and demyelinating diseases: intersections

This article examines the growing conceptual and clinical convergence between autoimmune encephalitis (AE) and demyelinating diseases (DD) of the central nervous system. The author emphasizes that the traditional boundaries between these disease groups are becoming increasingly blurred due to shared immunopathological mechanisms leading to autoimmune damage to the central nervous system. The article begins with clear definitions: AE are characterized by an immune attack on neuronal antigens (synaptic receptors, intracellular proteins), which clinically manifests as acute neuropsychiatric symptoms such as psychosis, seizures, cognitive impairment, and dyskinesias. Meanwhile, DD, a classic example of which is multiple sclerosis, primarily affect the myelin sheath, leading to focal neurological deficits (paresis, sensory disturbances, optic neuritis).

The focus is on the intersection points and overlap syndromes, where patients exhibit features of both disease groups simultaneously. Key examples include:

• myelin oligodendrocyte glycoprotein antibody-associated disease, which can manifest as both a demyelinating disease (e.g., optic neuritis) and an encephalitis with cortical lesions;
• anti-NMDAR encephalitis, which in rare cases can coexist with or precede multiple sclerosis;
• AQP4-positive neuromyelitis optica, severe forms of which, involving the brainstem or hypothalamus, can phenotypically mimic encephalitis.

The author provides a detailed comparative table, highlighting the differences and similarities between AE and DD in terms of parameters such as the primary immune target, leading symptoms, magnetic resonance imaging findings, laboratory markers, prognosis, and triggers.

The section on treatment notes that in the acute phase, therapy for both groups is similar and includes pulse corticosteroid therapy, plasmapheresis, and intravenous immunoglobulin aimed at suppressing the autoimmune response. However, maintenance therapy differs fundamentally: in AE, the focus is on identifying and eliminating the trigger (e.g., tumor) and using second-line drugs (rituximab), whereas in DD, the primary goal is long-term relapse prevention with disease-modifying therapies specific to each disease (e.g., ocrelizumab in multiple sclerosis, eculizumab in AQP4-positive neuromyelitis optica).

The paper concludes that AE and DD represent a continuum of immune-mediated central nervous system lesions. The importance of comprehensive diagnostics using expanded antibody panels and neuroimaging methods to identify overlap syndromes is emphasized, as early and adequate treatment is critical to improving prognosis and minimizing irreversible damage. Future research should be aimed at developing personalized therapeutic approaches.