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.

可卡因依赖 (CD) 与人格障碍高度共病，对较差的治疗反应有影响。这种合并症的神经生物学机制尚不清楚。我们旨在测试共病人格障碍在 CD 神经解剖学中的作用。我们使用高分辨率结构神经影像、心理问卷和认知测试检查了 4 组：CD ( n  = 19)、CD 和 B 型人格障碍 (CD + B, n  = 21)、CD 和 C 型人格障碍 (CD + C, n = 13) 和 21 个控件。我们比较了神经解剖学组，并假设（i）CD 将显示归因于奖励处理的纹状体区域（即伏隔核、尾状核和壳核）的改变，（ii）CD + B 和 CD + C 将显示支持情绪调节/社交的区域改变估值和焦虑/回避（即OFC和杏仁核）。CD + B 组的尾状核体积大于 CD ( p  =  . 01 , d  =  0 .94) 并且横向 OFC 厚度比 CD + C ( p  = .056, d = 0.71)。探索性相关性表明，这些组中 OFC 和尾状核的神经完整性改变会随着人格障碍的严重程度和冲动评分的恶化而加剧。伴有或不伴有人格障碍的 CD 可能具有部分不同的潜在机制和治疗目标。