SEROTONERGIC AGENTS IN THE TREATMENT OF ACUTE NEUROLEPTIC-INDUCED AKATHISIA - OPEN-LABEL STUDY OF BUSPIRONE AND MIANSERIN

It has been suggested that dopamine/serotonin (5-HT) imbalance, with r elative enhancement of serotonergic activity, might be one of the poss ible pathophysiological mechanisms underlying neuroleptic-induced akat hisia. 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 busp irone in 10 neuroleptic-treated patients with acute neuroleptic-induce d akathisia. Buspirone (up to 30 mg/day in divided doses) was administ ered for a trial period of 4 days (first part of the study). No signif icant changes in neuroleptic-induced akathisia as rated using the Barn es 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 tre atment (second part of the study). Seven mianserin-treated patients im proved and five revealed complete disappearance of neuroleptic-induced akathisia. It seems that the 5-HT1A partial agonist buspirone is of l imited value in the treatment of acute neuroleptic-induced akathisia. In contrast, it appears that low-dose mianserin is therapeutically eff ective in acute neuroleptic-induced akathisia.