Cephalic tetanus studied with single fibre EMG.

Abstract

SUMMARY In a case of cephalic tetanus with left facial spasms and trismus, the repetitive stimulation of the left facial nerve at 3, 10 and 20 Hz showed no facilitation or decrement. The amplitudes of the blink reflex were 50% lower on the affected side. The silent period of the masseter muscles was shortened. Concentric needle examination of the masseters and left facial muscles disclosed an almost continuous involuntary firing of motor unit potentials. Single fibre EMG of the left frontalis muscle showed increased jitter and blocking in a significant proportion of the recorded potentials. Both jitter and blocking improved on higher innervation rates. All electrophysiological findings were normal on the second examination when the patient was asymptomatic. The single fibre EMG findings point to a presynaptic defect in the neuromuscular transmission in human tetanus.The clinical manifestations of tetanus in mammals are mainly characterised by spasms produced by the central action of the tetanus toxin which provokes abnormal motoneuron activity.' However, experimental studies have demonstrated that, in addition to its central effects, tetanus toxin also blocks neuromuscular transmission in rat,23 mouse45 and goldfish-fin67 muscle by impairing the acetyl choline release at nerve terminals. In April 1983 Presented in part at the Advanced EMG and SFEMG Course and Symposium, Newcastle upon Tyne, 8-13 July 1982. can be seen with repetitive nerve stimulation.'-'9 However, no single fibre EMG studies have been published in human tetanus to our knowledge. We report a case of cephalic tetanus in which single fibre EMG findings provided further evidence of a presynaptic defect. Case reportA 58-year-old farmer was in good health until one month before admission when he had a car accident and lacerated the left side of his forehead. He had never had tetanus prophylaxis and antitoxin was not given at the time of the accident. Two days later, he developed stiffness and spasm of the left facial and neck muscles, difficulty in opening his mouth, dysphagia, insomnia and headache. As the symptoms persisted, he was referred for evaluation. On examination he was an alert and oriented patient with normal vital signs. Spasms of all the left facial muscles and trismus were prominent. The jaw jerk was brisk. Upon repeated volitional contraction of the facial muscles, the left facial spasm increased. On maximal effort there was no clear facial asymmetry. The remaining neurological examination including tone and stretch reflexes was normal. EEG, serum calcium and magnesium levels and cerebrospinal fluid also were normal. The diagnosis of tetanus was established and he was given active and passive tetanus immunisation, a short course of penicillin and 20 mg diazepam every six hours. Four weeks later the symptoms had subsided. 862

Brainstem myoclonus in generalised tetanus

“…The toxin binds specifically to two gangliosides, GT1 and GD1b, on the membranes of motor, sensory, and autonomic nerve terminals, and is carried toward the spinal cord or brainstem by retrograde axonal transport. After reaching the perikarya of motor neurones, it is transferred trans‐synaptically to abutting presynaptic terminals,2 producing a pre‐synaptic block. As a consequence, the amount of glycine and γ‐aminobutyric acid (GABA) released from the inhibitory terminals of spinal interneurones is reduced, and post‐synaptic inhibition of motor neurones by interneurones is blocked,3 producing tetanic rigidity.…”

Tetanus toxin reduces local and descending regulation of the H-reflex

“…25,26 Nerve conduction velocities were not measured directly by the recording procedure, but the latency between the stimulation artifact and the initiation of the M-or H-waves showed no differences after injection of the toxin, similar to studies using analogous human peripheral nerves. 27,28 The total duration of the M-and Hwaves waves, which might be altered if tetanus toxin interfered directly with the intrinsic excitability of a-motor neurons 29 or neuromuscular transmission, 30,31 was similarly unaffected by the toxin. The slopes of the recruitment curves for the M- Table 1.…”

Intraoperative Diagnosis and Use of Glidescope<sup>t</sup><sup>m</sup> Video Laryngoscope for Cephalic Tetanus

“…Although the exact mechanism remains unclear, cephalic tetanus pathology has been studied with a single fiber EMG and points to a pre-synaptic defect in neuromuscular transmission [16]. Another clinical and electrophysiological study of 15 cases proposed that paralysis is due to high local concentrations of toxin in the brainstem while lesser concentrations cause spasm by abolishing inhibition.…”