Abstract:
:It has been suggested that dopamine/serotonin (5-HT) imbalance, with relative enhancement of serotonergic activity, might be one of the possible pathophysiological mechanisms underlying neuroleptic-induced akathisia. On the basis of preclinical data, which imply that the partial 5-HT1A agonist buspirone possesses anti-5-HT activity, in the present open-label study we examined the putative antiakathitic effect of buspirone in 10 neuroleptic-treated patients with acute neuroleptic-induced akathisia. Buspirone (up to 30 mg/day in divided doses) was administered for a trial period of 4 days (first part of the study). No significant changes in neuroleptic-induced akathisia as rated using the Barnes Akathisia Scale were detected during buspirone treatment. Buspirone was effective in only two neuroleptic-induced akathisia patients and caused worsening of akathisia in the other two patients. According to the study design, eight buspirone non-responders were switched to the 5-HT2A/2C antagonist mianserin (15 mg/day) for the other 4 days of treatment (second part of the study). Seven mianserin-treated patients improved and five revealed complete disappearance of neuroleptic-induced akathisia. It seems that the 5-HT1A partial agonist buspirone is of limited value in the treatment of acute neuroleptic-induced akathisia. It contrast, it appears that low-dose mianserin is therapeutically effective in acute neuroleptic-induced akathisia.
journal_name
Int Clin Psychopharmacoljournal_title
International clinical psychopharmacologyauthors
Poyurovsky M,Weizman Adoi
10.1097/00004850-199709000-00003subject
Has Abstractpub_date
1997-09-01 00:00:00pages
263-8issue
5eissn
0268-1315issn
1473-5857journal_volume
12pub_type
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