Simpson G M, Pi E H, Sramek J J
Drugs. 1982 May;23(5):381-93. doi: 10.2165/00003495-198223050-00003.
Tardive dyskinesia is now widely recognised as a neurological side effect produced in susceptible individuals by ingestion of neuroleptics. In general, the disorder tends to be late in onset, but has also been reported in a small number of individuals who have received neuroleptics for only brief periods. Much effort has been spent searching for predisposing factors, but the only consistent findings are that subjects are usually elderly (and elderly females in particular), in addition to having been exposed to neuroleptic agents. More recently, the increased finding of the presence of buccolingual facial movements in elderly populations never exposed to neuroleptics may bring out a re-evaluation of the role of these agents in the aetiology of tardive dyskinesia. Although much information on tardive dyskinesia has accrued in recent years, the precise definition, subtypes and pathophysiology remain unclear. With the development and availability of standardised rating scales, the clinical description of tardive dyskinesia has expanded from the initial buccolingual masticatory syndrome to include various abnormal movements of the fingers, arms, legs etc. Efforts have been made to distinguish withdrawal tardive dyskinesia from persistent tardive dyskinesia, but, irrespective of the classification, the disorder is in many instances reversible. However, it is impossible at present to predict the reversibility of each patient: therefore early detection of tardive dyskinesia remains an important clinical goal. Pharmacological treatments are based on the currently accepted hypothesis of dopamine receptor hypersensitivity. Selective dopamine blockers (D2) which suppress tardive dyskinesia without causing an increase in Parkinsonian symptoms are at various stages of development. Acetylcholine and gamma-aminobutyric acid (GABA) also appear to play a reciprocal role with dopamine as seen by moderate success using cholinergics and 'GABAergics'. However, there is no completely satisfactory treatment at present, indicating that prevention must be the primary aim. Above all, clinicians should carefully evaluate the indication for neuroleptic drugs, and avoid their use in conditions which may be treated with more benign drugs. A strategy for management of tardive dyskinesia is presented, and indications for withdrawing or continuing neuroleptics, the treatment of withdrawal dyskinesias and the role of experimental therapies are discussed.
迟发性运动障碍目前被广泛认为是易感个体因摄入抗精神病药物而产生的一种神经副作用。一般来说，这种疾病往往起病较晚，但也有报道称，少数仅短期接受过抗精神病药物治疗的个体也会出现。人们花费了大量精力寻找诱发因素，但唯一一致的发现是，除了接触过抗精神病药物外，患者通常为老年人（尤其是老年女性）。最近，在从未接触过抗精神病药物的老年人群中，越来越多地发现存在颊舌面部运动，这可能会促使人们重新评估这些药物在迟发性运动障碍病因学中的作用。尽管近年来积累了许多关于迟发性运动障碍的信息，但确切的定义、亚型和病理生理学仍不清楚。随着标准化评定量表的发展和应用，迟发性运动障碍的临床描述已从最初的颊舌咀嚼综合征扩展到包括手指、手臂、腿部等各种异常运动。人们已努力区分撤药后迟发性运动障碍和持续性迟发性运动障碍，但无论分类如何，这种疾病在许多情况下是可逆的。然而，目前还无法预测每个患者的可逆性：因此，早期发现迟发性运动障碍仍然是一个重要的临床目标。药物治疗基于目前被广泛接受的多巴胺受体超敏假说。能抑制迟发性运动障碍而不导致帕金森症状加重的选择性多巴胺阻滞剂（D2）正处于不同的研发阶段。乙酰胆碱和γ-氨基丁酸（GABA）似乎也与多巴胺相互作用，使用胆碱能药物和“GABA能药物”已取得一定成效。然而，目前尚无完全令人满意的治疗方法，这表明预防必须是首要目标。最重要的是，临床医生应仔细评估使用抗精神病药物的指征，避免在可用更温和药物治疗的情况下使用它们。本文提出了一种迟发性运动障碍的管理策略，并讨论了停用或继续使用抗精神病药物的指征、撤药后运动障碍的治疗以及实验性治疗的作用。
