Atypical demyelination, a clinical challenge: sero-negative MOGAD. About a case.

Abstract

INTRODUCTION: MOGAD is an autoimmune demyelinating disorder of the CNS that is associated with a serological antibody directed against MOG, a glycoprotein located on the surface of myelin and found exclusively in the CNS. The clinical spectrum includes optic neuritis, myelitis, acute demyelinating encephalomyelitis, cortical encephalitis, brainstem syndromes and hyperintense FLAIR lesions in encephalitis with associated seizures. CLINICAL CASE: 59-year-old female patient with 03 months of evolution: thermal increases, ophthalmoplegia, dysphagia and left hemicranial headache, later, paresthesias in the right hemibody; she came to the emergency department with decreased visual acuity, ataxic gait, diplopia, dysarthria and right hemiparesis hours prior to admission. Brain MRI: diffuse hyperintense lesions in T2 and FLAIR, hypointense in T1 that restrict diffusion, with high cervical medullary involvement, anterolateral region of the bulb, posterior bridge and mesencephalic with predominance of cerebral peduncles. Cerebrospinal fluid studies: non-infectious inflammatory fluid. Serum AQP4-IgG and Ac-Anti MOG negative. Glucocorticoid is administered, obtaining satisfactory therapeutic response. DISCUSSION: The positivity of serum antibodies is directly related to the time of sampling in view of the kinetics of disease evolution; however, it should be taken into account that not all patients present these antibodies and that there may be other factors involved in their pathogenesis. CONCLUSION: MOGAD is a relatively new and still poorly understood disease with a wide variety of phenotypes, which constitutes a diagnostic challenge due to its clinical and paraclinical difficulty.