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10649900

Source:http://linkedlifedata.com/resource/pubmed/id/10649900

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pubmed-article:10649900pubmed:dateCreated2000-2-10lld:pubmed
pubmed-article:10649900pubmed:abstractTextAtaxia is defined as a disturbance which, quite independent of any motor weakness, alters direction and extent of voluntary movement and impairs the sustained voluntary of reflex muscle contraction necessary for maintaining postiue and equilibrium [1]. Since pathophysiological basis of cerebeller ataxia is still not completely clear, the current therapeutic attempts are mainly symptom-oriented [3]. One possible approach could be a modification of potentially involved neurotransmitter systems of the cerebellum, where particularly interesting is the serotonergic system. However, attempts with levorotatory form of tryptophan (5-HT precursors) proved to be ineffective [4, 5]. Since receptors in the cerebellum are mainly of 5-HTIA subtype, the use of specific agonists might be a more reasonable therapy [6]. The study initially involved 11 patients, but only 9 completed the protocol due to unfavorable side effects. Our open label prospective study lasted for 15 weeks. The patients were tested before the beginning of the treatment (initial visit), at 7th (first visit) and 11th week (second visit) of continuous therapy, and eventually at 15th week (final visit). The daily dose was 40 mg at the first and 60 mg at the second visit. We used the evaluation scale gurposed for cerebellar functions testing (speech, gait, coordination and ocular movements). Significant improvement of cerebellar ataxia in patients under buspiron therapy has been noted. We analyzed the results obtained from our 9 patients (4 females and 5 males), of which 6 patients suffered from cerebellar degeneration, one from multiple sclerosis, one from Ramsey-Hunt syndrome, and one from pontine myelinolysis. At the initial visit the patient score was 18.9 (SD = 7.3), subsequently, at the iirst visit the score was 15.4 (SD = 8), while the second visit yielded the score of 12.9 (SD = 8.2), and finally, after a two-weeks lasting wash-out period, it was 17.7 (SD = 7.1) (Table 1). It was found that patients exhibiting mild ataxia showed a better improvement in comparison to the patients who had marked cerebellar symptoms at the beginning of the treatment (Table 2). In conclusion, our prospective study shows that buspiron treatment improves cerebellar symptoms.lld:pubmed
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pubmed-article:10649900pubmed:authorpubmed-author:Vojvodi?NNlld:pubmed
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pubmed-article:10649900pubmed:authorpubmed-author:Filipovi?S...lld:pubmed
pubmed-article:10649900pubmed:authorpubmed-author:Dragasevi?NNlld:pubmed
pubmed-article:10649900pubmed:authorpubmed-author:SvetelMMlld:pubmed
pubmed-article:10649900pubmed:issnTypePrintlld:pubmed
pubmed-article:10649900pubmed:volume127lld:pubmed
pubmed-article:10649900pubmed:ownerNLMlld:pubmed
pubmed-article:10649900pubmed:authorsCompleteYlld:pubmed
pubmed-article:10649900pubmed:pagination312-5lld:pubmed
pubmed-article:10649900pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:10649900pubmed:articleTitle[Buspirone in the treatment of cerebellar ataxia].lld:pubmed
pubmed-article:10649900pubmed:affiliationInstitute of Neurology, Clinical Centre of Serbia, Belgrade.lld:pubmed
pubmed-article:10649900pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10649900pubmed:publicationTypeClinical Triallld:pubmed
pubmed-article:10649900pubmed:publicationTypeEnglish Abstractlld:pubmed