Abstract

Acute idiopathic transverse myelitis (ITM) may lead to substantial disability, with almost 10% of adult and 30% of pediatric patients with ITM becoming wheelchair-bound at follow-up.1,2 Establishment of consensus definitions of subtypes of acute transverse myelitis (ATM) in 20023 allowed clinicians potentially to distinguish monophasic forms from those associated with underlying diagnoses, with one study reporting an annualized incidence of idiopathic ATM as greater than ATM with brain lesions. In this study, half of those with brain lesions and none without brain lesions eventually received a diagnosis of multiple sclerosis (MS), thus suggesting that idiopathic forms of ATM are more common than those associated with an underlying diagnosis.4 However, recent advances, including the discovery of pathogenic antibodies associated with transverse myelitis, including those to aquaporin-45 and myelin oligodendrocyte glycoprotein (MOG),6 have allowed for a shift towards greater clarity regarding etiologies of ATM. Identification of a clear etiology for a patient presenting with myelopathy is of paramount importance, given the potential for intervention and prevention of further CNS injury in recurrent inflammatory CNS disease.

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