News in autoimmune myelitis in the oncological context

Autoimmune myelitis represents a heterogeneous group of disorders whose classification has evolved substantially over the past decade. Advances in antibody diagnostics and the widespread use of immune checkpoint inhibitors (ICIs) in oncology have reshaped current concepts, revealing mechanistic and clinical overlaps between antibody-mediated, paraneoplastic, and treatment-induced myelopathies.

Antibody-associated myelitis, including myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), aquaporin-4 (AQP4)-immunoglobulin G (IgG)-positive NMOSD and glial fibrillary acidic protein (GFAP) astrocytopathies, accounts for many cases previously labeled idiopathic. Paraneoplastic myelitis is rare but severe, possibly overlapping with NMOSD or GFAP astrocytopathies. In parallel, ICIs have emerged as a novel trigger of immune-mediated myelitis, capable of inducing de novo inflammatory spinal cord syndromes or unmasking latent autoimmune diseases, including AQP4-IgG-positive NMOSD and GFAP astrocytopathies but not MOGAD.

Autoimmune myelitis is best conceptualized within an etiological and context-dependent framework integrating antibody status, oncological evaluation, and exposure to immunotherapies. The expanding interface between astrocytopathies, paraneoplastic syndromes, and ICI-associated myelitis has important diagnostic and therapeutic implications, underscoring the need for systematic antibody testing and cancer screening in patients with inflammatory myelopathy.