Pathophysiologic aspects of human botulism

Physiologic studies were carried out in six patients with botulism. Abnormalities were those of a defect of acetylcholine release. Although the most consistent findings were small, evoked muscle action potentials (MAP) and posttetanic facilitation similar to the Eaton-Lambert syndrome, there were differences. In botulism as opposed to the Eaton-Lambert syndrome, the following were true: (1) posttetanic facilitation of the amplitude of the evoked MAP was considerably less and did not approach the normal value when the block was severe; (2) posttetanic facilitation persisted at least several minutes during the postactivation cycle; (3) posttetanic depression did not occur; (4) significant tetanic facilitation of the amplitude of the MAP occurred in less than half the patients and, even then, did not approach normal (on the other hand, a decremental response, as in myasthenia gravis, is not seen); and (5) no decremental response of the MAP occurred during slow rates (two per second) of nerve stimulation. Evidence of transient physiologic denervation occurred as in experimental animals affected by botulinum toxin. All physiologic abnormalities revert to normal in association with clinical recovery.