A 70-year-old hypertensive woman suffered a subarachnoid haemorrhage followed by delayed vasospasm in the basal cerebral arteries. This resulted in multiple ischaemic lesions in the right middle cerebral artery region and contralateral post-ischaemic palatal myoclonus. In this setting, piracetam administered in high doses (24-36 g/day), abolished the myoclonus observed in this patient. Although there is evidence from case reports and clinical trials of the therapeutic efficacy of piracetam in patients with skeletal myoclonus of various causes, to our knowledge this is the first report indicating the beneficial effect of piracetam monotherapy on post-ischaemic palatal myoclonus.
"Karacostas, en 1999, rapporte le cas de MVP sensibles au piracétam . Son mécanisme d'action demeure incertain, l'effet bénéfique étant possiblement dû à l'action neuromodulatrice du piracétam . De nombreux auteurs ont étudié d'autres traitements des MVP sans pour autant connaître leurs mécanismes d'action : le clonazépan, les drogues anticholinergiques, la lévodopa, le baclofène, et divers anticomitiaux, avec des résultats très variables      . "
[Show abstract][Hide abstract] ABSTRACT: Introduction. – Post brainstem lesion dysphagia is frequently associated with palatal myoclonus (PM) but the correlation between these two symptoms is still unclear.Objective. – The aim of this study was to verify the relationship between PM and dysphagia, and if PM could itself induce dysphagia.Patients and methods. – Twelve patients suffering from post brainstem lesion PM and dysphagia; 10 male and two female, mean aged of 50.5 years, were assessed using clinical examination, radiological and endoscopic examination of deglutition.Results. – In three cases, PM were associated with pharyngeal area decreasing, laryngeal aspiration, and dysphagia.Discussion. – This study confirms the hypothesis of close relationship between PM and dysphagia. In these cases, specific dysphagia therapy should be recommended.Conclusion. – Post brainstem lesion dysphagia is sometimes associated with PM and in some cases, there is probably a relationship between PM and swallowing disorders of these patients.
Annales de Réadaptation et de Médecine Physique 02/2004; 47(1-47):13-19. DOI:10.1016/j.annrmp.2003.07.002
[Show abstract][Hide abstract] ABSTRACT: A 67-year-old man presented with dysphagia and difficulty breathing. Physical examination revealed palatal myoclonus. In this patient, the respiratory difficulty was caused by the fragmentation of breathing. Electromyographic examination of the cricothyroid muscle demonstrated rhythmic myoclonic jerks. Magnetic Resonance Imaging (MRI) yielded a pontine midline and right sided tegmental infarct. The patient responded to sodium valproate.
[Show abstract][Hide abstract] ABSTRACT: In this study, the temporal development of focal cerebral infarction induced by permanent middle cerebral artery occlusion (pMCAO) and the effects of piracetam, a derivative of gamma-aminobutyric acid widely used in clinical practice as a nootropic agent, on infarct area and volume were investigated. pMCAO caused a cerebral infarct whose size progressively increased after 3, 6, 9, and 24 h. Piracetam (125 mg/kg i.p.), administered 6, 9, and 22 h after pMCAO, did not reduce pMCAO-induced brain infarct area size detected at the 24th hour. By contrast, when this agent was administered at the doses of 250 and 500 mg/kg, it caused a marked reduction of the infarct area size. This reduction was observed in almost every brain slice affected by pMCAO, although statistical differences (p <0.05) were detected in slices located at 3-5.5 mm posterior to the anterior pole in animals treated with 250 mg/kg piracetam and in slices located at 3.5-5 mm in those receiving 500 mg/kg. When the mean total volumes of brain infarct resulting from pMCAO were calculated, it was observed that in animals which had received piracetam (250 or 500 mg/kg) infarction volume was markedly ( approximately 50%) and significantly (p <0.05) reduced in comparison with saline injected rats. Finally, piracetam (250 mg/kg administered i.p. 6, 9, and 22 h after the ischemic insult) significantly reduced brain infarct area evaluated 48 h and 7 days after pMCAO.
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