强迫症学术论文(3)
可见，OCD的脑功能障碍明显涉及额叶皮层-皮层下的多个神经网络的信息加工，任何一个加工阶段出现的故障都可能导致OCD相关症状的出现。OFC和ACC是前额皮层的重要网络作用节点，它们都参与了错误信号的识别加工，并通过向尾状核的大量投射强化行为计划。纹状体，尤其尾状核是皮层下的关键网络作用节点，它在奖赏驱动行为的情绪性和动机性加工中发挥重要作用，因而可以选择和产生新的活动模式，以便对环境中有意义的信息作出反应。反复的强迫性行为也许就是来自对这些加工的过多的表达，以兑现奖赏来缓解内部紧张。另外，来自脑干的多巴胺和5-羟色胺能神经递质都作用于以上主要的网络节点，多巴胺功能增强与5-羟色胺功能减弱，以及两者间的相互作用也会调节OCD强迫症状的产生。
显然，来自神经解剖、神经生理、神经心理和神经功能成像的研究资料在一定程度上支持了OCD症状的现象学解释，但有关OCD症状与脑功能障碍之间的联系仍有一定的推测性，其中有些重要问题尚未解决。首先，由神经功能成像技术观察到的OCD病人前额叶脑区和皮层下相关结构的功能改变是强迫症状的原因还是结果，还需进一步确认;其次，既然这些功能改变所涉及的几个关键脑区，如OFC、ACC和DLPC在人类的动机、情绪、高级认知和目的行为的调节中起着关键作用，那么，为什么多数OCD病人除了表现出特定的强迫症状之外，一般均有正常的自知力、智能水平?近期的一些研究资料[3,13]也提示，OCD病人在多数执行功能相关的任务的加工中并没有缺陷;再次，OCD是由这些神经网络回路内特定脑区之间特殊神经联系的机能障碍所致，还是由多巴胺系统与5-羟色胺系统之间不平衡造成的;最后，导致这种脑功能障碍的原因是什么?是发生在大脑特定区域的某些结构缺陷，还是受精神因素影响所出现的病理性突触改变。这些问题的解答将有助于最终揭示OCD的发病机制，为临床上对OCD的有效诊断与治疗奠定基础。
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