Neurophysiological patterns of acute and post‐acute foodborne botulism.

Introduction/Aims: Neurophysiological patterns in patients with foodborne botulism are rarely described after the acute phase. We report data from a large Italian outbreak of botulism, with patients evaluated at different timepoints after poisoning. Methods: Eighteen male patients (mean age 47 ± 8.4 y) underwent 22 clinical and neurophysiological evaluations (4 patients were re‐evaluated). The resting compound muscle action potential (CMAP) amplitude, postexercise CMAP amplitude, CMAP change after high‐frequency (50 Hz) repetitive nerve stimulation (HFRNS), and motor unit action potentials (MUAPs) were assessed in the acute (4–8 days after poisoning; 5 patients), early post‐acute (32–39 days after poisoning; 5 patients), and late post‐acute (66–80 days after poisoning; 12 patients) phases. Results: In the acute, early post‐acute, and late post‐acute phases, respectively, reduced CMAP amplitudes were found in 100%, 20%, and 17% of patients; abnormal postexercise CMAP facilitation was observed in 100%, 40%, and 0% of patients; and pathological incremental responses to HFRNS were found in 80%, 50%, and 8% of patients. Baseline CMAP amplitudes, postexercise CMAP facilitation, and CMAP increases in response to HFRNS differed significantly between the acute and post‐acute phases. Small MUAPs were found in 100% of patients in the acute and early post‐acute phases and in 50% of patients in the late post‐acute phase. Discussion: The neurophysiological findings of foodborne botulism vary considerably according to the evaluation time point. In the post‐acute phase, different neurophysiological techniques must be applied to support a diagnosis of botulism. [ABSTRACT FROM AUTHOR]