Saxena S, Gorbis E, O'Neill J, Baker S K, Mandelkern M A, Maidment K M, Chang S, Salamon N, Brody A L, Schwartz J M, London E D
Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla, CA 92161, USA.
Mol Psychiatry. 2009 Feb;14(2):197-205. doi: 10.1038/sj.mp.4002134. Epub 2008 Jan 8.
Brief intensive cognitive-behavioral therapy (CBT) using exposure and response prevention significantly improves obsessive-compulsive disorder (OCD) symptoms in as little as 4 weeks. However, it has been thought that much longer treatment was needed to produce the changes in brain function seen in neuroimaging studies of OCD. We sought to elucidate the brain mediation of response to brief intensive CBT for OCD and determine whether this treatment could induce functional brain changes previously seen after longer trials of pharmacotherapy or standard CBT. [(18)F]-fluorodeoxyglucose positron emission tomography brain scans were obtained on 10 OCD patients before and after 4 weeks of intensive individual CBT. Twelve normal controls were scanned twice, several weeks apart, without treatment. Regional glucose metabolic changes were compared between groups. OCD symptoms, depression, anxiety and overall functioning improved robustly with treatment. Significant changes in normalized regional glucose metabolism were seen after brief intensive CBT (P=0.04). Compared to controls, OCD patients showed significant bilateral decreases in normalized thalamic metabolism with intensive CBT but had a significant increase in right dorsal anterior cingulate cortex activity that correlated strongly with the degree of improvement in OCD symptoms (P=0.02). The rapid response of OCD to intensive CBT is mediated by a distinct pattern of changes in regional brain function. Reduction of thalamic activity may be a final common pathway for improvement in OCD, but response to intensive CBT may require activation of dorsal anterior cingulate cortex, a region involved in reappraisal and suppression of negative emotions.
使用暴露与反应阻止法的简短强化认知行为疗法（CBT）在短短4周内就能显著改善强迫症（OCD）症状。然而，人们一直认为需要更长时间的治疗才能产生在强迫症神经影像学研究中所见的脑功能变化。我们试图阐明针对强迫症的简短强化CBT反应的脑中介作用，并确定这种治疗是否能诱发先前在更长时间的药物治疗或标准CBT试验后所见的脑功能变化。在10名强迫症患者接受4周强化个体CBT治疗前后，进行了[（18）F] - 氟脱氧葡萄糖正电子发射断层扫描脑部扫描。12名正常对照者在相隔数周的时间里接受了两次扫描，未接受治疗。比较了各组之间的局部葡萄糖代谢变化。治疗后，强迫症症状、抑郁、焦虑和整体功能均有显著改善。简短强化CBT后，标准化局部葡萄糖代谢出现显著变化（P = 0.04）。与对照组相比，强迫症患者在接受强化CBT后，双侧丘脑标准化代谢显著降低，但右侧背侧前扣带回皮质活动显著增加，且与强迫症症状改善程度密切相关（P = 0.02）。强迫症对强化CBT的快速反应是由区域脑功能的独特变化模式介导的。丘脑活动的减少可能是强迫症改善的最终共同途径，但对强化CBT的反应可能需要激活背侧前扣带回皮质，该区域参与对负面情绪的重新评估和抑制。
