うつ病の認知に関する神経基盤(シンポジウム : 情動形成とその異常の脳内機構-情動と心身相関のBlack Boxに迫る-,2006年,第47回日本心身医学会総会(東京))  [in Japanese] Neural Basis of Cognition in Depression(Symposium : Brain Mechanism of Normal and Abnormal Emotional Processing : Exploring Black Box of Emotion and Mind-Body Interaction)  [in Japanese]

われわれは,うつ病の認知的側面に着目し,病態解明に向けたfunctional magnetic resonance imaging (fMRl)を用いた研究を行っている.本稿では,Beck(1967)の提案したABC図式のB(Belief)に関連した脳機能局在(Kurosaki, et al. 2005),推論の誤りに関連した脳内機構(Ueda, et al. 2003), Teasdale (1988)の提唱したdifferential activation hypothesisに類似した脳内機構(Tanaka, et al. 2004)などについて紹介する.次に,現在行っているうつ病に対する集団認知行動療法(CBHT)前後の脳機能の変化について報告する.治療前のうつ病では,健常者で課題遂行中に賦活される脳領域において活動性低下が認められた.うつ病のCBGT前後の変化では,個別の検討でBDIの改善度が高い症例では,CBGT後の脳活動が健常者に近いレベルまで改善していた.

In this article, we present our neuroimaging studies by functional Magnetic Resonance Imaging (fMRI) about the brain mechanism of cognition toward elucidation of pathophysiology in depression. The first and second data show the brain mechanism (Kurosaki et al. 2005 ; Ueda et al. 2003) related to dysfunctional beliefs and systematic cognitive errors identified by Beck (1967), and the third is that (Tanaka et al. 2004) related to differential activation hypothesis proposed by Teasdale (1988). Lastly, we also show the change of brain function before and after cognitive behavioral group therapy (CBGT). Depressed patients before the CBGT showed attenuated activation in the dorsolateral prefrontal cortex, parietal cortex, and striatum were activated during the task. After the CBGT, the brain activation in good responders was restored as same as that in healthy control. However, in poor responder, there was no change on brain activation between before and after CBGT.