Etiologic spectrum and prognosis in noncompressive acute transverse myelopathies: An experience of 80 patients at a tertiary care facility.

INTRODUCTION: We evaluated the spectrum of acquired demyelinating and inflammatory disorders in patients presenting with an acute transverse myelopathy. We also studied differences between an acute idiopathic transverse myelitis and myelitis resulting from other etiologies. MATERIALS AND METHODS: Eighty consecutive patients with acute transverse myelopathy were included. At inclusion, clinical profile, serum and cerebrospinal fluid parameters, brain and spinal cord magnetic resonance imaging, and visual evoked potentials were obtained. All patients were given methylprednisolone therapy. Patients were followed up for 6 months. Outcome was assessed using modified Barthel index. A modified Barthel index score of ≤12 indicated a poor prognosis. RESULTS: Majority (n = 49; 61.25%) of patients had idiopathic acute transverse myelitis. Eleven cases had neuromyelitis optica spectrum disorders (8 had anti-aquaporin antibody positivity). Multiple sclerosis was diagnosed in 7 cases. Eight cases had infectious or parainfectious myelitis. Longitudinally extensive transverse myelitis was noted in 66 (82.5%) patients. Seventeen patients had abnormalities in the brain. Majority of patients improved following methylprednisolone therapy. On univariate analysis, delay in administering methylprednisolone therapy, poor modified Barthel index at discharge, and extensive cord involvement were associated with severe residual disability. On multivariate analysis, delayed initiation of methylprednisolone was identified as a poor prognostic factor. CONCLUSION: A variety of inflammatory, infective, demyelinating, and autoimmune disorders present with acute transverse myelopathy. Early institution of methylprednisolone reduces the disability in these patients.

Reversible opercular syndrome secondary to osmotic demyelination.

Opercular syndrome (OPS) is characterized by weakness of facial, masticatory, pharyngeal, laryngeal, tongue and brachial muscles on voluntary command with preservation of emotional and reflexive movements. We report a case of 45year old female who developed the features of OPS due to lesions of bilateral frontal opercular region induced by osmotic demyelination secondary to hyperosmolar hyperglycaemia. On follow up at 6 months, she had complete recovery.

Can vitamin B12 deficiency manifest with acute posterolateral or posterior cord syndrome?

Vitamin B12 deficiency can cause varied neurological manifestations which are subacute to chronic in onset. Subacute combined degeneration of spinal cord is one such characteristic neurological manifestation of vitamin B12 deficiency. We report a case series of five patients who presented with acute onset (<15 days) neurological manifestations due to vitamin B12 deficiency. Detailed history and clinical examination along with appropriate relevant investigations were done in all patients. Out of the five, two cases were of useless hand syndrome due to involvement of posterior column of the cervical spinal cord, another two patients presented with acute posterolateral cord syndrome causing gait ataxia and one acute posterior cord syndrome presented with acute sensory gait ataxia. Laboratory investigations were compatible with the diagnosis of cobalamin deficiency in all cases. All cases improved after parenteral vitamin B12 supplementation. Vitamin B12 deficiency can present with acute neurological manifestations.