Vitamin B 6 treatment in acute neuroleptic-induced akathisia: A randomized, double-blind, placebo-controlled study

Mental Health Center, Faculty of Health Sciences Ben-Gurion University of the Negev, Be'er-Sheva, Israel.
The Journal of Clinical Psychiatry (Impact Factor: 5.5). 12/2004; 65(11):1550-4. DOI: 10.4088/JCP.v65n1118
Source: PubMed


Treatment strategies for acute neuroleptic-induced akathisia (NIA) contain anticholinergic (antimuscarinic) agents, dopamine agonists, gamma-aminobutyric acid (GABA)-ergic agents, beta-blockers, benzodiazepines, and serotonin antagonists. Nevertheless, many patients who suffer from acute akathisia fail to respond to treatment. In earlier studies, vitamin B6 was found to be effective in the treatment of neuroleptic-induced movement disorders. The purpose of this study was to evaluate the efficacy of vitamin B6 in the treatment of acute NIA. This is the first report of B6 as a treatment for NIA.
This study was conducted in 2 mental health centers from February 2003 to November 2003. Twenty schizophrenia and schizoaffective inpatients with a DSM-IV diagnosis of NIA were randomly divided to receive vitamin B6 600 mg/day b.i.d. (N = 10) or placebo (N = 10) twice a day for 5 days in a double-blind design. The Barnes Akathisia Scale (BAS), the Brief Psychiatric Rating Scale (BPRS), and the Clinical Global Impressions scale (CGI) were used to assess the severity of NIA and psychotic symptoms. The BAS assessment was made at baseline and every day during the study. The BPRS and CGI were completed at baseline and at the end of the study.
The vitamin B6-treated patients in comparison with the placebo group showed a significant improvement on the subjective-awareness of restlessness (p = .0004), subjective-distress (p = .01), and global (p = .004) subscales of the BAS. The objective subscale did not demonstrate significant positive results (p = .079), but there was a trend of symptom amelioration in the vitamin B6 group. A reduction of at least 2 points on the BAS global subscale was noted in 8 patients in the vitamin B6 group (80%), and in only 3 patients in the placebo group (30%) (p = .037).
Our preliminary results indicate that high doses of vitamin B6 may be useful additions to the available treatments for NIA, perhaps due to its combined effects on various neurotransmitter systems.

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    • "In addition to the medication discussed above, there are trials that show the efficacy of other agents, e.g. vitamin B6 (Lerner et al., 2004; Miodownik et al., 2006), "
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    ABSTRACT: Akathisia is a common and distressing extrapyramidal side-effect, which usually results from the use of antipsychotic medication. Previous reviews and meta-analyses have demonstrated a lack of evidence for the effectiveness of treatment strategies, which are traditionally used against neuroleptic-induced akathisia (NIA), i.e. beta-blockers, anticholinergic agents and benzodiazepines. In the last fifteen years, randomized trials have studied the effect of drugs with antiserotonergic properties on NIA. We conducted a systematic review of randomized control trials and used meta-analytic methods to quantify the overall effect size. PubMed and the Cochrane libraries were searched for eligible trials. Six randomized controlled trials were found, five of which included a placebo control group and qualified for our meta-analysis. The overall effect size in the analysis is RR = 7.10 with 95% CI 3.08-16.40 (p < 0.0001). Our findings suggest that 5-HT2A antagonists are effective in the treatment of NIA.
    The International Journal of Neuropsychopharmacology 11/2013; 17(05):1-10. DOI:10.1017/S1461145713001417 · 4.01 Impact Factor
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    Journal of Orthomolecular Medicine 06/2008; 23(2).
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    ABSTRACT: Tardive dyskinesia (TD) is characterized by repetitive, involuntary, purposeless movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonists and following exposure to L-dopa, amphetamine, metoclopramide, cinnarizine, flunarizine and other substances. The term tardive dyskinesia refers to: classical TD (bucco-lingual-masticatory triad), tardive akathisia, tardive dystonia, tardive tremor and other tardive extrapyramidal subsyndromes. The mechanisms of TD remain unclear, although pathophysiologic theories have proposed mechanisms such as dopamine receptor supersensitivity, the degeneration of cholinergic striatal interneurons, γ-aminobutyric acid (GABA) depletion, and an excess of free radicals. Though a wide range of medications for the treatment of TD has been studied, management of this distressful side effect remains a significant problem for patients and a therapeutic conundrum for physicians. According to current concepts, antioxidants such as vitamins and other antioxidative agents may be considered active components of putative therapies because antioxidants inhibit free radical distractive activities. This chapter focuses on evidence from clinical and basic science studies that support the role of antioxidants (vitamins B6 and E, omega-3, ginkgo biloba, piracetam) as potential neuroprotective compounds and effective medications for the prevention and management of TD. KeywordsNeuroprotection-Vitamin B6-Vitamin E-Omega-3-Piracetam-Ginkgo biloba-Schizophrenia-Tardive dyskinesia-Clinical trials
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