PNAS:注意力缺陷多动障碍药物可能用于治疗毒品成瘾

2010-07-27 00:00 · Elijah

一项研究说,治疗注意力缺陷多动障碍的药物--利他林的活性成分可能促进可卡因成瘾者的自我控制。Chiang-shan Ray Li及其同事让可卡因成瘾的志愿受试者服用了哌醋甲酯。这组科学家然后让这些志愿者接受评估冲动控制的计算机测试,同时利用功能磁共振成像(fMRI)扫描了他们大脑

一项研究说,治疗注意力缺陷多动障碍的药物--利他林的活性成分可能促进可卡因成瘾者的自我控制。Chiang-shan Ray Li及其同事让可卡因成瘾的志愿受试者服用了哌醋甲酯。这组科学家然后让这些志愿者接受评估冲动控制的计算机测试,同时利用功能磁共振成像(fMRI)扫描了他们大脑。在这项测试中,受试者被要求在屏幕上显示“开始”的提示的时候迅速按一个按钮。

然而,“开始”的提示之后会随机地迅速出现“停止”的提示,这表明受试者应该抗拒按按钮的冲动。这组作者说,这项任务可以被认为是大脑信号之间的竞赛:为了压制这种冲动,在开始信号引发运动之前,就必须把停止信号处理完。这组作者报告说,经过哌醋甲酯治疗的受试者比对照组能更好地抵抗按按钮的冲动,而且fMRI大脑扫描显示了中前额皮层的活动与兴奋抑制控制是正相关的。这组作者说,这些发现提示,应该对作为自我控制缺陷相关疾病疗法的哌醋甲酯进行进一步的研究。


推荐原文出处:

PNAS doi: 10.1073/pnas.1002467107

Biological markers of the effects of intravenous methylphenidate on improving inhibitory control in cocaine-dependent patients

Chiang-shan R. Lia,b,c,1, Peter T. Morgana, David Matuskeya, Osama Abdelghanyd, Xi Luoa,e, Jeremy L. K. Changa, Bruce J. Rounsavillea,f, Yu-shin Dingg,h, and Robert T. Malisona

Departments of aPsychiatry and gDiagnostic Radiology and hPositron Emission Tomography Center, Yale University, New Haven, CT 06519;

bDepartment of Neurobiology and cInterdepartmental Neuroscience Program, Yale University, New Haven, CT 06520; dInvestigational Drug Service, Yale New Haven Hospital, New Haven, CT 06519; eDepartment of Statistics, Wharton School, University of Pennsylvania, Philadelphia, PA 19104; and

f Veterans Administration Connecticut Healthcare System, West Haven, CT 06516

Prior research points to the importance of psychostimulants in improving self-control. However, the neural substrates underlying such improvement remain unclear. Here, in a pharmacological functional MRI study of the stop signal task, we show that methylphenidate (as compared with placebo) robustly decreased stop signal reaction time (SSRT), an index of improved control, in cocaine-dependent patients (a population in which inhibitory control is impaired). Methylphenidate-induced decreases in SSRT were positively correlated with inhibition-related activation of left middle frontal cortex (MFC) and negatively with activation of the ventromedial prefrontal cortex (vmPFC) in whole brain linear regressions. Inhibition-related MFC but not vmPFC activation distinguished individuals with short and long SSRT in 36 demographically matched healthy individuals, whereas vmPFC but not MFC activation, along with improvement in SSRT, was correlated with a previously implicated biomarker of methylphenidate response (systolic blood pressure). These results implicate a specific neural (i.e., vmPFC) mechanism whereby stimulants improve inhibitory control. Altered ventromedial prefrontal activation and increased blood pressure may represent useful CNS and peripheral biomarkers in individualized treatment with methylphenidate for patients with cocaine dependence.

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