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深部脑刺激可诱导强迫症患者纹状体多巴胺释放。

Deep brain stimulation induces striatal dopamine release in obsessive-compulsive disorder.

机构信息

Department of Psychiatry, Academic Medical Center, Amsterdam; Brain Imaging Center, Academic Medical Center, Amsterdam.

Department of Psychiatry, Academic Medical Center, Amsterdam.

出版信息

Biol Psychiatry. 2014 Apr 15;75(8):647-52. doi: 10.1016/j.biopsych.2013.06.021. Epub 2013 Aug 12.

DOI:10.1016/j.biopsych.2013.06.021
PMID:23938318
Abstract

BACKGROUND

Obsessive-compulsive disorder is a chronic psychiatric disorder related to dysfunctional dopaminergic neurotransmission. Deep brain stimulation (DBS) targeted at the nucleus accumbens (NAc) has recently become an effective treatment for therapy-refractory obsessive-compulsive disorder, but its effect on dopaminergic transmission is unknown.

METHODS

We measured the effects of NAc DBS in 15 patients on the dopamine D2/3 receptor availability in the striatum with [(123)I]iodobenzamide ([(123)I]IBZM) single photon emission computed tomography. We correlated changes in [(123)I]IBZM binding potential (BP) with plasma levels of homovanillic acid (HVA) and clinical symptoms.

RESULTS

Acute (1-hour) and chronic (1-year) DBS decreased striatal [(123)I]IBZM BP compared with the nonstimulated condition in the putamen. BP decreases were observed after 1 hour of stimulation, and chronic stimulation was related to concurrent HVA plasma elevations, implying DBS-induced dopamine release. BP decreases in the area directly surrounding the electrodes were significantly correlated with changes in clinical symptoms (45% symptom decrease).

CONCLUSIONS

NAc DBS induced striatal dopamine release, which was associated with increased HVA plasma levels and improved clinical symptoms, suggesting that DBS may compensate for a defective dopaminergic system.

摘要

背景

强迫症是一种与多巴胺能神经传递功能障碍相关的慢性精神疾病。针对伏隔核(NAc)的深部脑刺激(DBS)最近已成为治疗难治性强迫症的有效方法,但它对多巴胺能传递的影响尚不清楚。

方法

我们使用[(123)I]碘苯甲酰胺([(123)I]IBZM)单光子发射计算机断层扫描,测量了 15 例强迫症患者 NAc-DBS 对纹状体中多巴胺 D2/3 受体可及性的影响。我们将[(123)I]IBZM 结合潜能 (BP) 的变化与血浆高香草酸 (HVA) 和临床症状相关联。

结果

与非刺激状态相比,急性(1 小时)和慢性(1 年)DBS 降低了壳核中的[(123)I]IBZM BP。刺激 1 小时后观察到 BP 下降,慢性刺激与同时升高的 HVA 血浆水平相关,表明 DBS 诱导多巴胺释放。电极直接周围区域的 BP 下降与临床症状的变化显著相关(症状减轻 45%)。

结论

NAc-DBS 诱导纹状体多巴胺释放,与 HVA 血浆水平升高和临床症状改善相关,表明 DBS 可能补偿多巴胺能系统的缺陷。

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