:Introduction:Choreaform movements provoked by opiates is an infrequent adverse event. Buprenorphine induction of chorea has not heretofore been described. Such a case is presented.METHOD:Case Study: A 38-year-old female presented with a decade long history of alcohol, cocaine, benzodiazepine, and heroin abuse. The patient was insufflating 1.5 grams of heroin daily. On presentation, she was actively withdrawing, scoring 17 on the Clinical Opioid Withdrawal Scale. Urine toxicology screening was positive for opiates, cocaine, and cannabinoids. Buprenorphine 4 mg sublingual was initiated. Within one hour, she observed, “My legs were moving uncontrollably as if I was a marionette.” These dance-like movements were isolated to both legs and gradually resolved after discontinuation of buprenorphine: most of the movements manifested in the first 8 hours, and dissipated over the next 2 days. She did have similar movements after treatment with quetiapine during a previous hospitalization, years earlier.RESULTS:Abnormalities in physical examination: General: goiter, bilateral palmar erythema. Neurological examination: Cranial Nerve (CN) Examination: CN I: Alcohol Sniff Test: 2 (anosmia). Motor Examination: Drift testing: mild right pronator drift. Reflexes: 3+ bilateral lower extremities. Neuropsychiatric Examination: Clock Drawing Test: 3 (abnormal). Animal Fluency Test: 18 (normal). Go-No-Go Test 6/6 (normal).DISCUSSION:Buprenorphine induced chorea could be a result of partial mu-opioid agonism, or kappa and delta receptor antagonism (Burke, 2018; Cowan, 1977). Mu-opioid receptor activation causes increased dopamine turnover in the nigrostriatum, which is responsible for locomotor sensitization (Campos-Jurado, 2017). With the addition of mu-opioid receptor modulation of dopamine release, kappa-opioid receptor alters various neurotransmitters in the basal ganglia, potentiating hyperkinetic movements. Buprenorphine’s choreiformogenic action may be due to kappa-opioid receptors ability to augment neurotransmission in the striatum (Escobar, 2017; Bonnet, 1998). The combination of simultaneous activity of these three opioid receptors may cause chorea, since they act to modulate dopamine, glutamate, and GABA in the direct and indirect pathways within the basal ganglia (Abin, 1989; Cui, 2013; Allouche, 2014; Trifilieff, 2013). This patient’s history of heroin and cocaine use may have caused supersensitization of dopamine receptors (Memo, 1981), provoking hyperkinesia. Involvement of substance-induced sensitization with concurrent kappa-opioid receptor neurotransmitter augmentation in direct and indirect pathways in the basal ganglia may have primed our patient to the development of chorea after buprenorphine administration. Further investigation for the presence of extrapyramidal movements in those undergoing buprenorphine treatment is warranted.

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131 牵线的木偶师：丁丙诺啡引起的舞蹈病一例

:Introduction:阿片类药物引起的舞蹈形式运动是一种罕见的不良事件。迄今为止，尚未描述丁丙诺啡对舞蹈症的诱导。提出了这样一个案例。方法：案例研究：一名 38 岁的女性出现了长达十年的酗酒、可卡因、苯二氮卓类药物和海洛因滥用史。患者每天吹入 1.5 克海洛因。就诊时，她正在积极戒断，在临床阿片类药物戒断量表上得分 17。尿液毒理学筛查对鸦片制剂、可卡因和大麻素呈阳性。开始舌下含丁丙诺啡 4 mg。不到一小时，她就观察到，“我的腿不受控制地移动，就像我是一个木偶一样。” 这些类似舞蹈的动作孤立于双腿，并在丁丙诺啡停药后逐渐消退：大部分动作在前 8 小时内表现出来，并在接下来的 2 天内消散。在几年前的一次住院期间，她在接受喹硫平治疗后确实有类似的运动。结果：体格检查异常：一般：甲状腺肿，双侧手掌红斑。神经系统检查：颅神经 (CN) 检查：CN I：酒精嗅探测试：2（嗅觉丧失）。运动检查：漂移测试：轻微的右旋前肌漂移。反射：3+双下肢。神经精神检查：时钟绘图测试：3（异常）。动物流利度测试：18（正常）。Go-No-Go 测试 6/6（正常）。讨论：丁丙诺啡诱发的舞蹈症可能是部分 mu-阿片样物质激动或 kappa 和 delta 受体拮抗作用的结果（Burke，2018；Cowan，1977）。Mu-阿片受体激活导致黑质纹状体中的多巴胺转换增加，它负责运动致敏（Campos-Jurado，2017）。随着 mu-阿片受体对多巴胺释放的调节作用，κ-阿片受体改变了基底神经节中的各种神经递质，增强了多动运动。丁丙诺啡的舞蹈形成作用可能是由于 kappa-阿片受体能够增强纹状体中的神经传递（Escobar，2017；Bonnet，1998）。这三种阿片受体同时活动的组合可能导致舞蹈病，因为它们在基底神经节内的直接和间接途径中调节多巴胺、谷氨酸和 GABA（Abin，1989；Cui，2013；Allouche，2014；Trifilieff， 2013）。该患者的海洛因和可卡因使用史可能导致多巴胺受体超敏化（Memo，1981），引发运动机能亢进。在基底神经节的直接和间接途径中，物质诱导的致敏与同时增加的 kappa-阿片受体神经递质增加可能使我们的患者在丁丙诺啡给药后发展为舞蹈病。有必要进一步调查接受丁丙诺啡治疗的患者是否存在锥体外系运动。