Department of Psychiatry, Yale University, New Haven, CT 06519, USA.
Drug Alcohol Depend. 2011 Dec 15;119(3):e51-7. doi: 10.1016/j.drugalcdep.2011.05.026. Epub 2011 Jun 23.
Cocaine dependence is associated with cognitive deficits and altered task-related cerebral activation in cognitive performance (see Li and Sinha, 2008, for a review). Relatively little is known whether these individuals are also impaired in regional brain activation of the default mode network (DMN). We demonstrated previously that greater activation of the default brain regions precedes errors in a stop signal task performed by healthy controls (SST, Li et al., 2007). We seek to determine whether individuals with cocaine dependence are impaired in DMN activity, specifically activity preceding error, as compared to the healthy people. We also examine the relation to years of cocaine use.
Individuals with cocaine dependence (CD, n=23) and demographics-matched healthy controls (HC, n=27) performed a SST that employed a tracking procedure to adjust the difficulty of stop trials and elicit errors approximately half of the time. Blood oxygenation level dependent (BOLD) signals of go trials preceding stop error as compared to those preceding stop success trials were extracted with generalized linear models using statistical parametric mapping.
HC showed activation of bilateral precuneus and posterior cingulate cortices and ventromedial prefrontal cortex (vmPFC) preceding errors during the SST. In contrast, despite indistinguishable stop signal performance, CD did not show these error predicting activations. Furthermore, the effect size of error-preceding vmPFC activation was inversely correlated with years of cocaine use.
These findings indicate DMN deficits and could potentially add to our understanding of the effects of chronic cocaine use on cerebral functions in cocaine dependence. Work to further clarify potential changes in functional connectivity and gray matter volume is warranted to understand the relevance of DMN to the pathology of cocaine misuse.
可卡因依赖与认知功能障碍和认知表现相关的任务相关大脑激活改变有关(Li 和 Sinha,2008 年综述)。相对较少的是这些个体在默认模式网络(DMN)的区域大脑激活中是否也受到损害。我们之前已经证明,在健康对照组执行的停止信号任务(SST,Li 等人,2007 年)中,默认大脑区域的更大激活先于错误。我们试图确定与健康人相比,可卡因依赖个体是否在 DMN 活动中受损,特别是在错误之前的活动。我们还检查了与可卡因使用年限的关系。
可卡因依赖个体(CD,n=23)和人口统计学匹配的健康对照组(HC,n=27)进行 SST,该 SST 使用跟踪程序来调整停止试验的难度,并以大约一半的时间引出错误。使用统计参数映射的广义线性模型提取停止错误前的 GO 试验的血氧水平依赖性(BOLD)信号与停止成功试验前的 BOLD 信号进行比较。
HC 在 SST 期间显示出双侧楔前叶和后扣带回皮质以及腹内侧前额叶(vmPFC)的激活,而在错误之前。相比之下,尽管停止信号性能没有差异,但 CD 并没有显示这些错误预测激活。此外,错误预测 vmPFC 激活的效应大小与可卡因使用年限呈负相关。
这些发现表明 DMN 缺陷,可能有助于我们理解慢性可卡因使用对可卡因依赖者大脑功能的影响。进一步阐明功能连接和灰质体积潜在变化的工作是必要的,以了解 DMN 与可卡因滥用病理学的相关性。