Acute motor and sensory axonal neuropathy (AMSAN) is a rare and more severe variant of Guillain-Barre syndrome (GBS) characterized by axonal degeneration. Acute nutritional axonal neuropathy (ANAN) can occur as a complication of thiamine deficiency. We describe a case of AMSAN following a household diarrheal illness combined with thiamine deficiency following bariatric surgery.

A 31-year-old woman with history of idiopathic intracranial hypertension (IIH) status-post bariatric surgery six months prior presenting with 2-3 weeks of progressive bilateral lower extremity weakness and numbness. Examination showed bilateral distal lower extremity weakness and sensory loss to all modalities associated with sinus tachycardia. Patellar and ankle reflexes were absent. Cerebrospinal fluid analysis was normal. Nerve conduction study showed evidence of bilateral symmetric small CMAP amplitudes and absent SNAP amplitudes; findings compatible with diagnosis of AMSAN. Thiamine and albumin levels were low. Work-up for other causes of neuropathy was unremarkable. Patient was treated with IVIg and thiamine with significant improvement.

The incidence of GBS in North America and Europe is between 0.84 and 1.91/100,000 according to a review of the literature with 5% of these patients having an axonal sub-type. CSF cyto-albuminologic dissociation is seen in ≥75% after 3rd week of symptom onset. ANAN is a well recognized but rare consequence of thiamine deficiency seen with alcohol abuse, following bariatric surgery and with malnutrition. This patient's clinical presentation as well as improvement with IVIg therapy were suggestive of a variant of GBS. However, low thiamine and albumin levels following bariatric surgery were indicative of a likely concomitant nutritional etiology.