Acute arsenic intoxication presenting as guillainbarréa‐like syndrome

Abstract

Arsenic‐induced polyneuropathy is traditionally classified as an axonal‐loss type, electrodiagnostically resulting in low amplitude or absent sensory and motor responses, relatively preserved proximal and distal motor conduction rates, and distal denervation. We report four patients with a subacute onset progressive polyradiculoneuropathy following high‐dose arsenic poisoning. In three patients, early electrodiagnostic testing demonstrated findings suggestive of an acquired segmental demyelinating polyradiculoneuropathy. Serial testing confirmed evolution into features of a distal dying‐back neuropathy. We hypothesize that arsenic toxicity and the resultant biochemical derangement of the peripheral nerve cell leads to subtle changes in axonal function that produce, initially, segmental demyelination and eventually distal axonal degeneration. Acute arsenic toxicity must be suspected in patients with clinical and electrodiagnostic features supporting Guillain‐Barré syndrome.