This case report highlights the clinical presentation and electrodiagnostic findings of botulism, emphasizing that diagnosis relies on identifying the toxin in the patient's serum.
May aid NMJ localization via modest M-wave increment on rapid RNS when findings are nonspecific; leaves open validation in larger cohorts.
Botulinal toxin causes a marked reduction in the number of quanta released by autonomic and motor nerve terminals. As a result it causes blurred vision, inability to move the eyes, weakness of other cranial nerve-innervated muscles, dyspnea progressing to apnea, and generalized weakness. Electrodiagnostic findings in severe botulism can be relatively nonspecific, with low amplitude and short duration motor unit action potentials and small M wave amplitudes. A modest increment in M wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction. Identification of the toxin in the patient's serum is diagnostic. The treatment of botulism is mainly supportive.
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Jackson B. Pickett (1988) studied this question.
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