Abstract
A 44-year-old Japanese woman was referred to our hospital complaining of progressive weakness of limbs over the prior 2 days. A neurological examination showed oculomotor disturbance, bilateral facial nerve palsy, dysarthria, dysphagia, limb muscle weakness, diminished deep tendon reflexes, bilateral positive Babinski’s sign, sensory disturbance in limbs and bladder or bowel dysfunction. Nerve conduction studies revealed decreased F-wave frequencies in median and ulnar nerves. The motor evoked potential (MEP) induced in the abductor pollicis brevis muscle (APB) showed prolonged latency (26.9 ms), and the calculated central motor conduction time (CMCT) was delayed at 13.6 ms. A cerebrospinal fluid analysis revealed elevated protein level (103 mg/dL) and mild pleocytosis (8/μL). Antiganglioside antibodies were positive for GM1, GD1b, GD3, GT1b, GQ1b, and GT1a. Brain and spinal MRI showed no abnormal findings. She was treated with high-dose intravenous immunoglobulin, and on the 19th day of her illness, the Babinski’s sign had disappeared. Post-treatment, the MEP latency and CMCT in the APB were improved at 20.5 and 7.9 ms, respectively. This case suggests that patients with Guillain–Barre syndrome can present Babinski’s sign as a result of pyramidal tract dysfunction caused by antiganglioside antibodies.
Published Version
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