強迫癥學術論文(3)
強迫癥學術論文
可見，OCD的腦功能障礙明顯涉及額葉皮層-皮層下的多個神經網絡的信息加工，任何一個加工階段出現的故障都可能導致OCD相關癥狀的出現。OFC和ACC是前額皮層的重要網絡作用節點，它們都參與了錯誤信號的識別加工，并通過向尾狀核的大量投射強化行為計劃。紋狀體，尤其尾狀核是皮層下的關鍵網絡作用節點，它在獎賞驅動行為的情緒性和動機性加工中發揮重要作用，因而可以選擇和產生新的活動模式，以便對環境中有意義的信息作出反應。反復的強迫性行為也許就是來自對這些加工的過多的表達，以兌現獎賞來緩解內部緊張。另外，來自腦干的多巴胺和5-羥色胺能神經遞質都作用于以上主要的網絡節點，多巴胺功能增強與5-羥色胺功能減弱，以及兩者間的相互作用也會調節OCD強迫癥狀的產生。
顯然，來自神經解剖、神經生理、神經心理和神經功能成像的研究資料在一定程度上支持了OCD癥狀的現象學解釋，但有關OCD癥狀與腦功能障礙之間的聯系仍有一定的推測性，其中有些重要問題尚未解決。首先，由神經功能成像技術觀察到的OCD病人前額葉腦區和皮層下相關結構的功能改變是強迫癥狀的原因還是結果，還需進一步確認;其次，既然這些功能改變所涉及的幾個關鍵腦區，如OFC、ACC和DLPC在人類的動機、情緒、高級認知和目的行為的調節中起著關鍵作用，那么，為什么多數OCD病人除了表現出特定的強迫癥狀之外，一般均有正常的自知力、智能水平?近期的一些研究資料[3,13]也提示，OCD病人在多數執行功能相關的任務的加工中并沒有缺陷;再次，OCD是由這些神經網絡回路內特定腦區之間特殊神經聯系的機能障礙所致，還是由多巴胺系統與5-羥色胺系統之間不平衡造成的;最后，導致這種腦功能障礙的原因是什么?是發生在大腦特定區域的某些結構缺陷，還是受精神因素影響所出現的病理性突觸改變。這些問題的解答將有助于最終揭示OCD的發病機制，為臨床上對OCD的有效診斷與治療奠定基礎。
參考文獻
[1] Schwartz J M. Neuroanatomical aspects of cognitive behavioural therapy response in obsessive compulsive disorder. An evolving perspective on brain and behaviour. British Journal of Psychiatry, 1998, (Suppl.):38~44
[2] Schwartz J M. A role of volition and attention in the generation of new brain circuitry: Toward a neurobiology of mental force. Journal of Consciousness Study, 1999, 6: 115~142
[3] Aouizerate B, Guehl D, Cuny E, et al. Pathophysiology of obsessivecompulsive disorder: A necessary link between phenomenology, neuropsychology, imagery and physiology. Progress in Neurobiology, 2004 , 72: 195~221
[4] Krawczyk D C. Contributions of the prefrontal cortex to the neural basis of human decision making. Neuroscience of Biobehavioral Review, 2002, 26: 631~664
[5] Passingham R E. The frontal lobes and voluntary action. Oxford: Oxford University Press, 1993
[6] Tremblay L, Schultz W. Modifications of reward expectation-related neuronal activity during learning in primate orbitofrontal cortex. Journal of Neurophysiology, 2000, 83: 1877~1885
[7] Alptekin K, Degirmenci B, Kivircik B, et al. Tc-99m HMPAO brain perfusion SPECT in drug-free obsessive compulsive patients without depression. Psychiatry Research, 2001, 107: 51~56
[8] Swedo S E, Schapiro M B, Grady C L, et al. Cerebral glucose metabolism in childhood-onset obsessivecompulsive disorder. Archives of General Psychiatry, 1989, 46: 518~523
[9] Lacerda A L, Dalgalarrondo P, Caetano D, et al. Elevated thalamic and prefrontal regional cerebral blood flow in obsessivecompulsive disorder: A SPECT study. Psychiatry Research, 2003, 123: 125~134
[10] Bannon S, Gonsalves C J, Croft R J. Response inhibition deficits in obsessive compulsive disorders. Psychiatry Research, 2002, 110: 165~174
[11] Bokura H, Yamaguchi S, Kobayashi S. Electrophysiological correlates for response inhibition in a Go/No-Go task. Clinical Neurophysiology, 2001,112: 2224~2232
[12] Casey B J, Trainor R J, Orendi J L, et al. A developmental functional MRI study of prefrontal activation during performance of a Go-No-Go task. Journal of Cognitive Neuroscience, 1997, 9: 835~847
[13] Evans DW, Lewis M D, Iobst E. The role of the orbitofrontal cortex in normally developing compulsive-like behaviors and obsessive-compulsive disorder. Brain and Cognition, 2004, 55: 220~234
[14] Ochsner K N, Bunge S A, Gross J J, et al. Rethinking feelings: An fMRI study of the cognitive regulation of emotion. Journal of Cognitive Neuroscience, 2002, 14: 1215~1229
[15] Depue R A, Collins P F. Neurobiology of the structure of personality: dopamine, facilitation of incentive motivation, and extraversion. Behavioral and Brain Science, 1999, 22: 491~569
[16] Molina V, Montz R, Martin-Loeches M, et al. Drug therapy and cerebral perfusion in obsessivecompulsive disorder. Journal of Nuclear Medicine, 1995, 36: 2234~2238
[17] Perani D, Colombo C, Bressi S, et al. [18F]FDG PET study in obsessivecompulsive disorder: A clinical/metabolic correlation study after treatment. British Journal of Psychiatry, 1995, 166: 244 ~ 250
[18] 蔡厚德, 劉昌. 大腦前扣帶回皮層與執行功能. 心理科學進展, 2004, 12(5): 643~650
[19] Bush G, Luu P, Posner M I. Cognitive and emotional influences in anterior cingulate cortex. Trends in Cognitive Science, 2000,4: 215~222
強迫癥學術論文相關文章：