Oxidative mechanisms and tardive dyskinesia

被引:184
作者
Lohr, JB [1 ]
Kuczenski, R [1 ]
Niculescu, AB [1 ]
机构
[1] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA
关键词
D O I
10.2165/00023210-200317010-00004
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Tardive dyskinesia has been and continues to be a significant problem associated with long-term antipsychotic use, but its pathophysiology remains unclear. In the last 10 years, preclinical studies of the administration of antipsychotics to animals, as well as clinical studies of oxidative processes in patients given antipsychotic medications, with and without tardive dyskinesia, have continued to support the possibility that neurotoxic free radical production may be an important consequence of antipsychotic treatment, and that such production may relate to the development of dyskinetic phenomena. In line with this hypothesis, evidence has accumulated for the efficacy of antioxidants, primarily vitamin E (alpha-tocopherol), in the treatment and prevention of tardive dyskinesia. Early studies suggested a modest effect of vitamin E treatment on existing tardive dyskinesia, but later studies did not demonstrate a significant effect. Because evidence has continued to accumulate for increased oxidative damage from antipsychotic medications, but less so for the effectiveness of vitamin E, especially in cases of long-standing tardive dyskinesia, alternative antioxidant approaches to the condition may be warranted. These approaches may include the use of antioxidants as a preventive measure for tardive dyskinesia or the use of other antioxidant,, or neuroprotective drugs. such as melatonin, for established tardive dyskinesia.
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页码:47 / 62
页数:16
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