Dopamine dysfunction in borderline personality disorder: A hypothesis
Dopamine dysfunction in borderline personality disorder: A hypothesis
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DOI：
10.1038/sj.npp.1300424
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发表时间：
2004-06-01
影响因子：
7.6
通讯作者：
Friedel, RO
中科院分区：
文献类型：
--
作者：
Friedel, RO
关于边缘型人格障碍（BPD）的生物学基础的研究主要集中在冲动性攻击的血清素模型上。然而，有证据表明多巴胺（DA）功能障碍也可能与BPD有关。相关的研究和评论文章，确定了Medline检索相关的主题，书籍，参考书目，并从1975年至2003年的会议记录，进行了审查。BPD中DA功能障碍的证据来自传统和非典型抗精神病药物在BED中的疗效，以及患有该疾病的受试者的安非他明和哌甲酯的挑衅性挑战。此外，人类和动物研究表明，DA活动在情绪信息处理，冲动控制和认知中起着重要作用。本综述的结果表明，DA功能障碍与BPD的三个维度，即情绪失调，冲动和认知知觉障碍。这一假设的主要局限性是，所审查的证据是间接的。没有研究直接证明BED中的DA功能障碍。此外，在BPD中观察到的抗精神病药物的治疗作用可能由非DA作用机制介导。如果上述假设是正确的，那么BED中的DA功能障碍可能是由遗传、发育或环境因素直接影响特定的DA通路引起的。或者，BED中的DA功能障碍可能是对控制情绪、冲动控制和认知的初级神经系统的改变的补偿性反应，这些神经系统由大脑的主要神经递质谷氨酸和GABA或一种或多种其他神经调节途径（如血清素、乙酰胆碱和去甲肾上腺素）介导。
Research on the biological basis of borderline personality disorder (BPD) has focused primarily on the serotonin model of impulsive aggression. However, there is evidence that dopamine (DA) dysfunction may also be associated with BPD. Pertinent research and review articles, identified by Medline searches of relevant topics, books, references from bibliographies, and conference proceedings from 1975 to 2003, were reviewed. Evidence of DA dysfunction in BPD derives from the efficacy of traditional and atypical antipsychotic agents in BED, and from provocative challenges with amphetamine and methylphenidate of subjects with the disorder. In addition, human and animal studies indicate that DA activity plays an important role in emotion information processing, impulse control, and cognition. The results of this review suggest that DA dysfunction is associated with three dimensions of BPD, that is, emotional dysregulation, impulsivity, and cognitive-perceptual impairment. The main limitation of this hypothesis is that the evidence reviewed is circumstantial. There is no study that directly demonstrates DA dysfunction in BED. In addition, the therapeutic effects of antipsychotic agents observed in BPD may be mediated by non-DA mechanisms of action. If the stated hypothesis is correct, DA dysfunction in BED may result from genetic, developmental, or environmental factors directly affecting specific DA pathways. Alternatively, DA dysfunction in BED may be a compensatory response to alterations in the primary neural systems that control emotion, impulse control, and cognition, and that are mediated by the brain's main neurotransmitters, glutamate, and GABA, or in one or more other neuromodulatory pathways such as serotonin, acetylcholine, and norepinephrine.