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We studied 71 patients (NMOSD, 37; SCS, 34). Sixteen (47%) SCS cases were initially diagnosed as NMOSD or idiopathic transverse myelitis. Median delay to diagnosis was longer for SCS than NMOSD (5 vs 1.5 months, p<0.01). NMOSD myelitis patients were more commonly women, had concurrent or prior optic neuritis or intractable vomiting episodes more frequently, had shorter time to maximum deficit, and had systemic autoimmunity more often than SCS (p<0.05). SCS patients had constitutional symptoms, cerebrospinal fluid (CSF) pleocytosis, and hilar adenopathy more frequently than NMOSD (p<0.05); CSF hypoglycorrhachia (11%, p=0.25) and elevated angiotensin-converting enzyme (18%, p = 0/30) were exclusive to SCS. Dorsal cord subpial gadolinium enhancement extending �2 vertebral segments and persistent enhancement <2 months favored SCS, and ringlike enhancement favored NMOSD (p<0.05). Maximum disability was similar to both disorders. SCS is an under-recognized cause of longitudinally extensive myelitis that commonly mimics NMOSD. We identified clinical, laboratory, systemic, and radiologic features that, taken together, help discriminate SCS from NMOSD. |
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angiotensin-converting enzyme delay in diagnosis differential diagnosis heralding manifestation hypoglycorrhachia lymphadenopathy lymphadenopathy,hilar mimics misdiagnosis MRI,abnormal MRI,contrast enhanced MRI,spinal cord MRI,spinal cord,increased intramedullary cord signal myelitis myelitis,longitudinal myelitis,transverse neuromyelitis optica (Devic's disease) neuromyelitis optica spectrum disorder pleocytosis of cerebrospinal fluid sarcoidosis sarcoidosis,CNS spinal cord,biopsy spinal cord,dorsal subpial enhancement spinal cord,lesion of treatment of neurologic disorder
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