Background

The association between demyelinating diseases and the presence of anti-N-methyl-D-Aspartate receptor antibodies (anti-NMDAR-ab) has been analyzed in recent years. This infrequent coexistence has been seen above all with neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein associated disorders (MOGAD). The overlap with multiple sclerosis (MS) has been poorly described. In most of the published cases, patients presented symptoms consistent with NMDAR encephalitis, before, after, or concomitantly with demyelinating disease.

Objectives

We present the case of a patient with newly diagnosed Relapsing Remitting Multiple Sclerosis (RRMS) and with detection of anti-NMDAR-ab, without symptoms suggestive of encephalitis.

Methods

27-year-old woman, with gender identity disorder who was admitted for distal paresthesias in her lower limbs and in her hands which had developed in the last week. The examination revealed hypoesthesia and moderate hypopalestesia in these areas, with hyperreflexia in her lower limbs, suspecting myelitis as a diagnostic possibility.

Results

We performed a lumbar puncture that showed mild pleocytosis with normal proteins, increased Ig G and the presence of oligoclonal bands Ig G in cerebrospinal fluid (CSF).

Brain and spinal cord magnetic resonance showed twelve brain lesions, as well as several lesions in the cervical and dorsal spinal cord with a typical demyelinating appearance of MS and some of them with gadolinium enhancing.

In an autoimmunity study, anti-NMDAR-ab were detected at high titers in CSF and serum, with negative anti-aquoporin 4 (AQP4) and anti-MOG Ig G antibodies (performed in two centers using cell-based assay).

Given the presence of anti-NMDAR-ab, it was decided to extend the study by conducting a screening test for occult neoplasia that was negative, as well as an electroencephalogram and a neuropsychological study that did not show data suggestive of anti-NMDAR-ab clinical expression.

In the presence of a typical clinical syndrome together with characteristic findings in the complementary tests of RRMS, we treated the sensitive spinal cord outbreak with megadoses of corticosteroids with full resolution. The review of the little published evidence shows cases similar to ours that months or years later can develop NMDAR encephalitis. Given this risk, we believed that the use of anti-CD20 therapy of proven efficacy in RRMS was justified, which in turn presents a mechanism of action similar to Rituximab, widely used in pathology secondary to anti-NMDAr-ab. Finally, after a few weeks of stability, Ocrelizumab treatment was started, with a good response.

Conclusions

The coexistence of MS and NMDAR encephalitis is an entity under study. In our case, the anti-NMDAR-ab is asymptomatic so far, but it forces us to dismiss neoplasia, to monitor symptoms in the following years, and it has also been decisive in the choice of the disease-modifying drug.