1. CLONAZEPAM (Ro 5-4023) IN THE TREATMENT OF MYOCLONUS EPILEPSY
- Author
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E. Toivakka and L. Laitinen
- Subjects
Adult ,Myoclonus ,medicine.drug_class ,Photic Stimulation ,Thiazines ,Progressive myoclonus epilepsy ,Electroencephalography ,Chlorobenzenes ,Myoclonus epilepsy ,Epilepsy ,Pharmacotherapy ,medicine ,Humans ,Fatigue ,Benzodiazepinones ,Benzodiazepine ,Diazepam ,medicine.diagnostic_test ,Genetic Diseases, Inborn ,General Medicine ,Nitro Compounds ,medicine.disease ,Clonazepam ,Neurology ,Phenytoin ,Anesthesia ,Anticonvulsants ,Drug Therapy, Combination ,Female ,Epilepsies, Partial ,Neurology (clinical) ,Psychology ,Primidone ,medicine.drug - Abstract
Progressive hereditary myoclonus epilepsy is a relentless disease which responds poorly to conventional drug therapy. Clonazepam (Ro 5-4023) a new benzodiazepine derivative, was given to 3 patients with progressive myoclonus epilepsy (Unverricht-Lundborg), and to 1 with focal myoclonus epilepsy (Kojewnikow). All 4 were females. Their ages ranged from 19 to 21 years. The duration of symptoms varied from 5 to 12 years. The duration of the trial was 30, 19, 3, and 4 months, respectively. With a daily dose of 6–8 mg, clonazepam effectively reduced the number of jerks in all patients; this effect appeared after 1 month of treatment. The duration of the effect looks promising. Intratrial EEG showed a clear decrease in spike-and-wave paroxysms. Photic stimulation provoked less jerks than before the trial; the amplitude of evoked activity was also reduced. There was some drowsiness when clonazepam was first given, but it disappeared after some weeks of treatment.
- Published
- 2009
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