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可卡因依赖中的共病性人格障碍会加剧神经解剖学改变吗?一项结构神经影像学研究。

Do comorbid personality disorders in cocaine dependence exacerbate neuroanatomical alterations? A structural neuroimaging study.

作者信息

Roberts Carl A, Lorenzetti Valentina, Albein-Urios Natalia, Kowalczyk Magdalena A, Martinez-Gonzalez Jose M, Verdejo-Garcia Antonio

机构信息

Department of Psychological Sciences, University of Liverpool, UK.

Department of Psychological Sciences, University of Liverpool, UK; Neuroscience of Addiction and Mental Health Program, Healthy Brain and Mind Research Centre, School of Behavioural and Health Sciences, Faculty of Health Sciences, Australian Catholic University, Fitzroy, VIC 3065, Australia.

出版信息

Prog Neuropsychopharmacol Biol Psychiatry. 2021 Aug 30;110:110298. doi: 10.1016/j.pnpbp.2021.110298. Epub 2021 Mar 11.

DOI:10.1016/j.pnpbp.2021.110298
PMID:33716043
Abstract

Cocaine dependence (CD) is highly comorbid with personality disorders, with implications for poorer treatment response. The neurobiological mechanisms of this comorbidity are unclear. We aimed to test the role of comorbid personality disorders in the neuroanatomy of CD. We examined 4 groups using high-resolution structural neuroimaging, psychological questionnaires and cognitive tests: CD (n = 19), CD and personality disorder type B (CD + B, n = 21), CD and personality disorder C (CD + C, n = 13) and 21 controls. We compared groups in neuroanatomy and hypothesised that (i) CD would show altered striatal areas ascribed to reward processing (i.e., accumbens, caudate and putamen), (ii) CD + B and CD + C would show altered areas supporting emotional regulation/social valuation and anxiety/avoidance (i.e., OFC and amygdala). The CD + B group had larger caudate volumes than CD (p = .01, d = 0.94) and reduced lateral OFC thickness than CD + C (p = .056, d = 0.71). Exploratory correlations showed that altered neural integrity of the OFC and of the caudate nucleus in these groups exacerbated with worse personality disorder severity and impulsivity scores. CD with and without comorbid personality disorders may have partially distinct underlying mechanisms and targets for treatment.

摘要

可卡因成瘾(CD)与人格障碍高度共病,这对较差的治疗反应有影响。这种共病的神经生物学机制尚不清楚。我们旨在测试共病的人格障碍在CD神经解剖学中的作用。我们使用高分辨率结构神经成像、心理问卷和认知测试对4组进行了检查:CD组(n = 19)、CD合并B型人格障碍组(CD + B,n = 21)、CD合并C型人格障碍组(CD + C,n = 13)和21名对照组。我们比较了各组的神经解剖结构,并假设:(i)CD组在归因于奖励处理的纹状体区域(即伏隔核、尾状核和壳核)会出现改变;(ii)CD + B组和CD + C组在支持情绪调节/社会评估以及焦虑/回避的区域(即眶额皮质和杏仁核)会出现改变。CD + B组的尾状核体积大于CD组(p = 0.01,d = 0.94),其外侧眶额皮质厚度小于CD + C组(p = 0.056,d = 0.71)。探索性相关性分析表明,这些组中眶额皮质和尾状核神经完整性的改变随着人格障碍严重程度和冲动性得分的增加而加剧。伴有和不伴有共病性人格障碍的CD可能具有部分不同的潜在机制和治疗靶点。

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