However, in our case, the cervical cord was more extensively involved. While patients with AQP4-IgG usually present cervical (with or without brainstem involvement) and thoracic lesions, patients with MOG-IgG may present lesions of the lower cord, including the conus medullaris. Both patient groups show cervical myelitis as the most frequent spinal cord involvement, but lumbosacral myelitis is more common in patients with anti-MOG-Ab. Radiologically it is difficult to differentiate between NMOSD & MOG Antibody Disease with certainty but there are some imaging features that can help to point towards a certain diagnosis. Recovery from attacks is also reported as better in MOG Antibody Disease than in AQP4-IgG-seropositive NMOSD. It is also known by several other terminologies like MOG-IgG-associated Optic Neuritis, Encephalitis, and Myelitis (MONEM), Anti-MOG associated encephalomyelitis, and anti-MOG encephalitis.įeatures suggestive of MOG Antibody Disease as opposed to NMOSD include male gender, single or few attacks, bilateral or recurrent optic neuritis sparing the optic chiasma, LETM involving the conus medullaris, and good recovery after attacks. It has overlap with acute disseminated encephalomyelitis (ADEM), neuromyelitis optica spectrum disorder (NMOSD), and multiple sclerosis (MS). MOG Antibody associated disease is an inflammatory demyelinating disorder characterized by the presence of IgG antibodies to myelin oligodendrocyte glycoprotein. MOG antibody disease is now recognized as a distinct clinical entity with specific management and therapeutic requirements. Myelin oligodendrocyte glycoprotein (MOG) is a glycoprotein located on the myelin surface and found exclusively in the central nervous system. In these patients, autoantibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been identified.
However, some patients with clinical presentations suggestive of NMOSD do not show anti-aquaporin 4 antibodies. The presence of an NMO-specific antibody (Anti-aquaporin 4) in the CSF and serum has allowed these patients to be distinguished from those with multiple sclerosis. Neuromyelitis optica spectrum disorders are demyelinating disorders associated with attacks on the optic nerves and spinal cord. In comparison with the previous study, the follow-up scan showed a significant reduction in the cervico-dorsal intramedullary T2 hyperintensities (Fig 8,9) and relative reduction in the size of the left midbrain T2 hyperintensity (Fig 10), reflecting a good response to treatment. Repeat MRI brain and spine was done after 2 weeks. The patient was treated with intravenous immunoglobulin & Azathioprine following which his symptoms gradually improved. NMO Antibody (Serum and CSF) and oligoclonal bands were negative. CSF Anti-MOG (Myelin oligodendrocyte glycoprotein) antibody was positive. CSF analysis showed a total count of 60 cells with lymphocyte predominance, glucose - 86 mg/dl, and protein - 51.1mg/dl. Nerve conduction study was done which showed a mild delay in latencies. Based on the above finding, the possibility of neuromyelitis optica spectrum disorder (NMOSD) was suggested and the patient was subjected to laboratory workup for the same. Both optic nerves appeared relatively thickened with T2/ STIR hyperintensities in the left optic nerve (Fig 3,7). Discrete T2 hyperintensities were also noted in the left anterior midbrain (Fig 6). The nerve roots of the cauda equina appeared normal. Post-contrast administration, the cervico-dorsal lesion showed patchy enhancement (Fig 5). The hyperintensities were seen predominantly involving the central and posterior parts of the spinal cord with relative sparing of the anterior portion (Fig 4).
Subtle intramedullary T2 hyperintensities were also noted in the lower dorsal cord and conus medullaris (Fig 2). 3 Tesla MRI of Brain & spine was done which showed long segment intramedullary T2 hyperintensities in the spinal cord extending from the cervico-medullary region to D1 level (Fig 1,2), with expansion of the cervical cord.
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