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Mog antibody disease treatment
Mog antibody disease treatment





mog antibody disease treatment

Results were all normal for eosinophil sedimentation rate (ESR), C-reactive protein (CRP), thyroid stimulating hormone (TSH), serum protein electrophoresis (SPEP), vitamin B 12, vitamin E, copper, and zinc. Serology was remarkable for mildly elevated angiotensin-converting enzyme (ACE 73 U/L). Lumbar spine axial (F) view of T1 post-contrast imaging shows focal lobular enhancement of the left S1 nerve root.Įmpiric treatment with pulse-dose intravenous (IV) steroids was initiated, and further extensive evaluation continued for potential inflammatory, infectious, and neoplastic causes of their myeloradiculitis. Lumbar spine sagittal (D, E) views of T1 demonstrate post-contrast enhancement of cauda equina nerve roots. Cervical spine sagittal (B) and axial (C) views show multiple short-segment T2 hyperintense lesions. A small T2 hyperintense brainstem lesion is viewed axially (A). These radiologic findings were most consistent with an acute or subacute inflammatory process.įigure 1 (A-F): Representative brain and spine MRI findings are shown. Brain MRI showed several small T2-hyperintense brainstem lesions, none of which displayed contrast enhancement. Enhancement in the cauda equina nerve roots and focal lobular enhancement of the left S1 nerve root was observed. None of the lesions were longitudinally extensive, although some showed trace areas of contrast enhancement. Diagnostic Studies and Initial TreatmentĬervical, thoracic, and lumbar spine MRI with and without contrast revealed multifocal short-segment T2 hyperintense lesions, diffusely central in location and involving both gray and white matter (Figure). Overall, WN’s presentation pointed to a spinal cord process as the most likely etiology of the constellation of symptoms. WN’s upper motor neuron signs, with hyperreflexia of the lower extremities and an upgoing toe on the left side, implicated the corticospinal tracts (left >right) and disfavored peripheral processes such as Guillain-Barré syndrome. The positive Romberg sign suggested dorsal column dysfunction. WN’s sensory deficits, which were distributed in a nondermatomal fashion in the left leg and right arm, suggested bilateral spinothalamic tract or multiple nerve involvement, whereas perineal numbness implied spinal cord or nerve root localization–possibly involving the conus medullaris or cauda equina. WN was able to ambulate normally but struggled with tandem gait. They exhibited an extensor plantar response on the left side and a positive Romberg sign.

MOG ANTIBODY DISEASE TREATMENT FULL

WN had full muscular strength on confrontation testing, with 2+ reflexes noted in the upper extremities and 3+ at the patella bilaterally with crossed adduction.

mog antibody disease treatment

On neurologic exam, WN’s mental status and cranial nerve function were intact, but sensation to temperature and pinprick was decreased in the right hand and left leg in a patchy, nondermatomal distribution. They did not report any weakness urinary, bowel, or sexual dysfunction fevers or other systemic symptoms. WN also reported some mid-back pain and difficulty with balance. Within several days, they noted numbness in both legs and the groin with a painful cramping and burning sensation in both legs, which was worse on the left side. Initially, WN developed insidious onset of numbness in the right arm, mostly involving the entire hand. WN, age 53, presented after 3 weeks of numbness and pain in the right arm, both legs, and perineum.







Mog antibody disease treatment