Infant botulism: exacerbation by aminoglycosides.
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We performed in vitro microelectrode studies in the anconeus muscle biopsy of a 6-week-old infant intoxicated with Clostridium botulinum toxin B. The most striking abnormalities were the severe reduction of the endplate potential (EPP) quantal content and the marked variability of EPP latencies. The increased variability was often limited to a "single quantum" component of the EPP. Neither the amplitudes nor the frequencies of spontaneous miniature endplate potentials (MEEPs) were decreased. However, there was a wide range of amplitudes and frequencies of MEPPs. This unique combination of electrophysiologic findings indicates a severe presynaptic failure of neuromuscular transmission, which appears to result from an impairment of the process of synaptic vesicle release taking place after the stimulus induced influx of calcium into the motor nerve terminals.
Four cases of mild botulinus type B intoxication are reported with the clinical neurophysiological studies. Electromyographically tetanic stimulation of the N. ulnaris initially led to tetanic potentiation of the muscle action potential. After an interval without any symptoms tetanic reduction became apparent between the fourth and seventh week of the illness. The electroneurographic finding was normal during the observation period of three months. Infrared reflex pupillographic studies revealed that the cholinergic autonomous synapses were disturbed for a period much longer than the symptoms clinically established. The speed at which the pupillographic findings returned to normal varied considerably according to the patient. Electroencephalographic results indicated generalized groups of slow high amplitude waves in three of the four cases during the period of observation. The pathophysiology of botulinus intoxication is discussed with a consideration of the literature and the results of this study.
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