Posted by nolvas on April 26, 2008, at 3:56:14
In reply to 1200mg of B6???, posted by iforgotmypassword on April 24, 2008, at 7:46:59
I don't think you need such a high dose, have a look at these studies. Also check Choline, Lecithin and Vitamin E as they can help with TD problems.
DeVeaugh, G. J., et al. High-dose pyridoxine in tardive dyskinesia. J Clin Psychiatry. 39(6):573-575, 1978.
The clinical similarities of tardive dyskinesia and 1-dopa intoxication lend support to the post-synaptic hypersensitivity hypothesis in tardive dyskinesia. Pyridoxine, a co-factor in the decarboxylation of dopa, reverses the movement disorder of l-dopa intoxication. Although early studies of pyridoxine in tardive dyskinesia have not been encouraging, the results of the present study suggest that high doses of pyridoxine may reduce the frequency and severity of involuntary movements in tardive dyskinesia.
·Lerner, V., et al. Vitamin B(6) in the treatment of tardive dyskinesia: a double-blind, placebo-controlled, crossover study. American Journal of Psychiatry. 158(9):1511-1514, 2001.
Division of Psychiatry, Ministry of Health Be'er Sheva Mental Health Center, Faculty of Health Sciences Ben-Gurion University of the Negev, Israel.
The authors concucted a double-blind trial of vitamin B(6) in the treatment of tardive dyskinesia in patients with schizophrenia. Fifteen inpatients with schizophrenia who met research diagnostic criteria for tardive dyskinesia were randomly assigned to treatment with either vitamin B(6) or placebo for 4 weeks in a double-blind crossover paradigm. The Extrapyramidal Symptom Rating Scale was used to assess patients weekly. Mean scores on the parkinsonism and dyskinetic movement subscales of the Extrapyramidal Symptom Rating Scale were significantly better in the third week of treatment with vitamin B(6) than during the placebo period. Vitamin B(6) appears to be effective in reducing symptoms of tardive dyskinesia.
·Lerner, V., et al. Vitamin B6 in treatment of tardive dyskinesia: a preliminary case series study. Clin Neuropharmacol. 22:241-243, 1999.
In this 4-week open-label trial, 100 mg of supplemental vitamin B6 per day was added to regular medical therapy in five patients with schizophrenia who had classic tardive dyskinesia, tardive akathisia, or tardive parkinsonism. Four of the five (80%) patients demonstrated clinically significant improvements of more than 30% on measures of involuntary movement. The authors speculate that the beneficial effects of vitamin B6 in patients with tardive dyskinesia may be due to the vitamin's antioxidant effects and/or to the effects of the vitamin B6 metabolite pyridoxal phosphate, which serves as a coenzyme for a wide variety of metabolic transformations.
Human study demonstrated that the addition of vitamin B6 (100 mg per day for four weeks) to regular treatments for tardive dyskinesia in Parkinsons disease patients improved the symptoms of tardive dyskinesia by 30% or more in 80% of subjects.
Adler, L. A., et al. Vitamin E treatment of tardive dyskinesia. Am J Psychiatry. 150(9):1405-1407,1993.
The authors studied the effects of vitamin E treatment of tardive dyskinesia; earlier studies have produced contradictory results. Twenty-eight patients with tardive dyskinesia were treated in a double-blind, parallel-group comparison study of 8-12 weeks of treatment with vitamin E (1600 IU/day) or matching placebo capsules. The Abnormal Involuntary Movement Scale scores of the patients treated with vitamin E improved significantly compared to the scores of the patients given placebo. These results support earlier findings of the efficacy of vitamin E in treating tardive dyskinesia.
·Brown, K., et al. Vitamin E, lipids and lipid peroxidation products in tardive dyskinesia. Biol Psychiatry. 43:863-867, 1998.
This study evaluated plasma levels of vitamin E and lipid peroxidation products (TBARS) in 16 schizophrenic patients with tardive dyskinesia, 16 schizophrenic patients without symptoms of tardive dyskinesia and 10 normal control subjects. Lipid-corrected plasma vitamin E levels were significantly lower in the group of patients with tardive dyskinesia than in controls. Lipid-
corrected TBARS levels did not differ significantly among the three groups. There was a significant positive association between levels of TBARS and the severity of dyskinetic movements. A chronic and sustained deficiency of vitamin E could conceivably render subjects more vulnerable to free radical damage, lipid membrane peroxidation, and ultimately tardive dyskinesia; however, the authors were unable to conclude if the lower lipid-corrected vitamin E levels in the dyskinetic group were temporary or long-standing.·Dannon, P. N., et al. Vitamin E treatment in tardive dyskinesia. Hum Psychopharmacol Clin Exp. 12(3):217-220, 1997.
·Egan, M. F., et al. Treatment of tardive dyskinesia with vitamin E. American Journal of Psychiatry. 149(6):773-777, 1992.
Neuropsychiatry Branch, NIMH, Washington, D.C., USA.
Vitamin E (alpha-tocopherol), a free-radical scavenger, has been reported to improve symptoms of tardive dyskinesia. The authors attempted to replicate this finding under more controlled conditions in a larger study group. Fifteen inpatients and six outpatients with tardive dyskinesia received up to 1600 IU/day of vitamin E for 6 weeks in a double-blind, placebo-controlled crossover study. Abnormal Involuntary Movement Scale (AIMS) examinations of these patients were videotaped and rated independently by two trained raters. Levels of neuroleptic medication and vitamin E were measured during both treatment periods. Eighteen patients who demonstrated high blood levels of vitamin E were included in the data analysis. Vitamin E levels were significantly higher while the patients were receiving vitamin E than while they were receiving placebo. For all 18 patients, there were no significant differences between AIMS scores after receiving vitamin E and AIMS scores after receiving placebo. In agreement with previous studies, however, the nine patients who had had tardive dyskinesia for 5 years or less had significantly lower AIMS scores after receiving vitamin E than after receiving placebo. There were no changes in neuroleptic levels during vitamin E treatment. Vitamin E had a minor beneficial effect on tardive dyskinesia ratings in a selected group of patients who had had tardive dyskinesia for 5 years or less. This effect was not due to an increase in blood levels of neuroleptic medications.
·Elkashef, A. M., et al. Vitamin E in the treatment of tardive dyskinesia. American Journal of Psychiatry. 147(4):505-506, 1990.
Eight subjects with persistent tardive dyskinesia were treated with vitamin E and placebo in a randomized, double-blind crossover study. Their mean score on the Abnormal Involuntary Movement Scale (AIMS) was significantly lower after treatment with vitamin E than after placebo administration.
·Lohr, J. B., et al. Alpha-tocopherol in tardive dyskinesia. Lancet. 1:913-914, 1987.
·Lohr, J. B, et al. Vitamin E in the treatment of tardive dyskinesia: The possible involvement of free radical mechanisms. Schizophrenia Bulletin. 14(2):291-296, 1988.
·Schroeder, D. J., et al. Vitamin E in tardive dyskinesia. Annals Pharmacol. 27:311-312, 1993.
Cochrane Database Systematic Review
·Soares, K. V., et al. Vitamin E for neuroleptic-induced tardive dyskinesia. Cochrane Database Syst Rev. 4:CD000209, 2001.
Antipsychotic (neuroleptic) medication is used extensively to treat people with chronic mental illnesses. However, it is associated with a wide range of adverse effects, including movement disorders such as tardive dyskinesia (TD). Vitamin E has been proposed as a treatment to prevent or decrease the severity of TD. The objective of this review was to determine the clinical effects of vitamin E for people with schizophrenia or other chronic mental illnesses who also developed neuroleptic-induced tardive dyskinesia. Electronic searches of Biological Abstracts (1982-2001), The Cochrane Schizophrenia Group's Register (January 2001), EMBASE (1980-2001), LILACS (1982-2001), MEDLINE (1966-2001), PsycLIT (1974-2001), SCISEARCH (1997), hand searching the references of all identified studies and contacting the first author of each included trial. Reports identified in the search were included if they were controlled trials dealing with people with neuroleptic-induced TD and schizophrenia or other chronic mental illness who had been randomly allocated to either vitamin E or to a placebo or no intervention. Data were independently extracted from these trials by each reviewer and relative risks (RR) or weighted mean differences (WMD), with 95% confidence intervals (CI) were estimated. The reviewers assumed that people who dropped out had no improvement. Ten studies were included. The overall results for 'clinically relevant improvement' found no benefit of vitamin E against placebo (6 trials, 256 people, RR 0.95 CI 0.89 to 1.02). For the outcome of 'any improvement in TD symptoms', again, no clear difference in favour of vitamin E was found (7 trials, 311 people, RR 0.86 CI 0.75 to 1.00). However, people who had not been allocated vitamin E, showed more deterioration of their symptoms (5 trials, 98 people, RR 0.38 CI 0.16 to 0.9). There was no difference in the incidence of adverse effects (8 trials, 163 people, RR 1.3 CI 0.5 to 3.2) or leaving the study early (medium term 5 trials, 133 people, RR 1.5 CI 0.8 to 2.7). There is no trial-based information regarding the effect of vitamin E for those with early onset of TD. Small trials with uncertain quality of randomisation indicate that vitamin E protects against deterioration of TD but there is no evidence that vitamin E improves symptoms of TD.
Gelenberg, A. J., et al. Choline and lecithin in the treatment of tardive dyskinesia: Preliminary results from a pilot study. American Journal of Psychiatry. 136(6):772-776, 1979.
Tardive dyskinesia is thought to reflect increased dopaminergic activity of the central nervous system. To compensate for this by increasing CNS cholinergic tone, the authors administered oral choline and its natural dietary source, lecithin, to 5 men with mild to severe tardive dyskinesia in a nonblind trial. Both choline and lecithin increased serum choline levels and improved abnormal movements in all patients. Lecithin had fewer adverse effects.
·Growdon, J. H. Lecithin can suppress tardive dyskinesia. New England Journal of Medicine. 298(18):1029-1030, 1978.
[no abstract available].
·Zeisel, S. H., et al. Use of choline and lecithin in the treatment of tardive dyskinesia. Adv Biochem Psychopharmacol. 24:463-70, 1980.
[no abstract available].
poster:nolvas
thread:825125
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