Yale Child Study Center, PO Box 207900, New Haven, CT 06520-7900.
Yale Child Study Center, New Haven, Connecticut, USA.
J Clin Psychiatry. 2020 May 26;81(4):19r12798. doi: 10.4088/JCP.19r12798.
To examine the efficacy of pharmacologic treatments for tardive dyskinesia (TD).
PubMed was searched on December 12, 2017, for randomized, placebo-controlled trials examining the treatment of TD using the search terms (drug-induced dyskinesia OR tardive dyskinesia) AND (psychotic disorders OR schizophrenia).
Studies were included if they examined tardive dyskinesia treatment as the primary outcome and were randomized and placebo-controlled trials.
The effect size (standard mean difference) of improvement (compared to placebo) stratified by medication class is reported for each of the trials included in this systematic review. A meta-analysis was conducted utilizing a fixed-effects model.
Vitamin E was associated with significantly greater reduction in TD symptoms compared to placebo (standardized mean difference [SMD] = 0.31 ± 0.08; 95% CI, 0.16 to 0.46; z = 4.1; P < .001). There was significant evidence of publication bias in vitamin E studies (Egger test: P = .02). Shorter duration of treatment and lower dose of vitamin E were significantly associated with greater measured treatment benefit. Vitamin B₆ was associated with significantly greater reduction in TD symptoms compared to placebo (SMD = 1.41 ± 0.22; 95% CI, 0.98 to 1.85; z = 6.4; P < .001) in 2 trials conducted by the same research group. Vesicular monoamine transporter 2 (VMAT2) inhibitors demonstrated significant benefit on tardive dyskinesia symptoms compared to placebo (SMD = 0.63 ± 0.11; 95% CI, 0.41 to 0.85; z = 5.58; P < .005). Amantadine was associated with significantly greater score reduction compared to placebo (SMD = 0.46 ± 0.21; 95% CI, 0.05 to 0.87; z = 2.20; P < .05). Calcium channel blockers were not associated with significantly greater score reduction compared to placebo (SMD = 0.31 ± 0.33; 95% CI, -0.34 to 0.96; z = 0.93; P = .35).
Data from multiple trials suggests that VMAT2 inhibitors, vitamin E, vitamin B₆, and amantadine may be effective for the treatment of TD. Evidence of publication bias and a significant negative association of dose and duration of treatment with measured efficacy suggest that the benefits of vitamin E in TD may be overstated. Head-to-head trials are needed to compare the efficacy and cost-effectiveness of pharmacologic agents for TD.
研究药物治疗迟发性运动障碍（TD）的疗效。
2017 年 12 月 12 日，在 PubMed 上以“药物诱导性运动障碍”或“迟发性运动障碍”和“精神障碍”或“精神分裂症”为检索词，检索了随机、安慰剂对照试验，以评估使用这些药物治疗 TD 的效果。
如果研究将迟发性运动障碍的治疗作为主要结果，并进行了随机和安慰剂对照试验，则将其纳入研究。
对纳入本系统评价的每一项试验，按照药物类别报告改善（与安慰剂相比）的效应大小（标准化均数差）。采用固定效应模型进行荟萃分析。
与安慰剂相比，维生素 E 显著降低 TD 症状（标准化均数差[SMD] = 0.31 ± 0.08；95%置信区间，0.16 至 0.46；z = 4.1；P <.001）。维生素 E 研究存在显著的发表偏倚证据（Egger 检验：P =.02）。较短的治疗持续时间和较低的维生素 E 剂量与更大的治疗获益显著相关。与安慰剂相比，维生素 B₆（SMD = 1.41 ± 0.22；95%置信区间，0.98 至 1.85；z = 6.4；P <.001）在两项由同一研究组进行的试验中显著降低了 TD 症状。囊泡单胺转运体 2（VMAT2）抑制剂与安慰剂相比，显著改善迟发性运动障碍症状（SMD = 0.63 ± 0.11；95%置信区间，0.41 至 0.85；z = 5.58；P <.005）。金刚烷胺与安慰剂相比，评分降低更显著（SMD = 0.46 ± 0.21；95%置信区间，0.05 至 0.87；z = 2.20；P <.05）。与安慰剂相比，钙通道阻滞剂对评分的降低无显著影响（SMD = 0.31 ± 0.33；95%置信区间，-0.34 至 0.96；z = 0.93；P =.35）。
多项试验的数据表明，VMAT2 抑制剂、维生素 E、维生素 B₆ 和金刚烷胺可能对 TD 的治疗有效。发表偏倚的证据以及治疗剂量和持续时间与疗效测量之间的显著负相关表明，维生素 E 在 TD 中的益处可能被夸大了。需要进行头对头试验来比较治疗 TD 的药物的疗效和成本效益。
