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. 1982 Nov;12(3):210-8.
doi: 10.1016/s0370-4475(82)80046-4.

[Myoclonus of toxic origin]

[Article in French]

[Myoclonus of toxic origin]

[Article in French]
F Mellerio et al. Rev Electroencephalogr Neurophysiol Clin. 1982 Nov.

Abstract

EEG, EMG and clinical correlates of myoclonus due to poisoning are reviewed. The authors propose a classification into two groups. I. Sporadic diffuse asynchronous asymmetrical myoclonic jerks, responding to treatment. These states are encountered essentially in acute intoxication by vegetal poisons (strychnine), rodenticide (chloralose) and various medications (isoniazide, tricyclic antidepressant agent, lithium). These transitory manifestations are functional and prognosis is favourable. II. Subintrant generalized synchronous symmetrical myoclonus, uncontrolled by therapeutics. These myoclonus states observed over weeks or months are frequently consecutive to organic injuries due to direct toxicity (methylbromide) or after anoxia (toxic cardiac arrest). EEG and EMG correlations are very inconstant in both groups. EEG abnormalities are a sign of cortical and/or subcortical dysfunction. Normal EEG suggests a disease of the lower central nervous structure (brain stem, medulla). Chronic bismuth and dialysis encephalopathies are also related. Withdrawal syndrome with myoclonus jerks after sudden cessation of barbiturate or benzodiazepine long-term treatment is mentioned.

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