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Iatrogenic injury to the sciatic nerve during surgical repair of proximal hamstring avulsion

tive. Tests for Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, hepatitis A, B, and C, and HIV excluded concomitant infections. Brain and spinal cord MRI were unremarkable. He was treated with 5 sessions of alternateday plasmapheresis. Nine months after onset, he could walk 0.5 miles independently, but impaired proprioception was still present. The differential diagnosis of (sensory) ataxic neuropathy includes metabolic disorders (e.g., diabetes), toxicity (alcohol, drugs), nutritional deficiencies, infectious disease, autoimmune disease, paraneoplastic disorders, vasculitis, amyloidosis, cryoglobulinemia, and hereditary causes, all of which were excluded by history and appropriate ancillary testing. The clinical presentation of this patient is consistent with AAN according to published criteria. Anti-GQ1b and GD1b antibodies are absent in 47% of patients with AAN. There have been 3 reports of patients with ataxia and HEV. In contrast to our patient, they presented with severe weakness. GBS and AAN share an antecedent infection with C. jejuni. Together with the report of 10 patients with GBS and 5 patients with neuralgic amyotrophy, HEV may be a trigger for GBS and related conditions.