To the Editor.—
In several neurological disorders, myoclonus appears as a disturbing and persistent symptom. Presently, these involuntary and repetitive movements of the skeletal muscle are being controlled by the administration of the serotonin precursor carubicin hydrochloride in combination with a peripheral decarboxylase inhibitor1 or by the benzodiazepine muscle relaxant clonazepam.2 While these two drug treatments have been found to be effective, their long-term administration could lead to undesirable side effects. Dependence liability of the benzodiazepines is well documented.Because of the nonavailability of a suitable animal model for myoclonus in the past, introduction of new drugs for the management of clinical myoclonus was not possible. Recently we introduced a valid animal model for clinical myoclonus.3 This is based on our observation that intraperitoneal (IP) administration of muscimol, 3 mg/kg, a γ-aminobutyric acid agonist, induces involuntary and repetitive myoclonic jerks in a particular strain of mice that
Menon MK. Antimyoclonic Effect of Sodium Oxybate: Clinical Implications. JAMA. 1981;245(24):2495–2496. doi:10.1001/jama.1981.03310490013011
Customize your JAMA Network experience by selecting one or more topics from the list below.