在功能性磁振造影以情緒性及顏色史楚普作業 探討憂鬱症的神經異常活動

Abstract

憂鬱是老年人常見的健康議題之一，老年憂鬱症已證實與輕度認知功能障礙以及在一些執行功能上有異常的大腦神經活動。本功能性磁振造影研究探討老年憂鬱症患者在認知及情緒兩個層面上，對於抑制控制能力的神經機制。本研究使用顏色字及情緒性史楚普作業評估老年憂鬱症及正常老年人在干擾效應過濾抑制不相關干擾訊息的認知能力。在本研究中分為兩部分的實驗，實驗一主要為探討老年憂鬱症在認知及情緒控制執行功能上神經活動的影響，實驗二為探討在藥物治療後不同恢復程度的控制執行功能神經機制差異。 實驗結果顯示老年憂鬱症患者在顏色及情緒性史楚普作業的反應時間較長，且準確率較正常人低。在大腦神經活動方面，老年憂鬱症患者在處理認知及情感/情緒兩者的衝突訊息上前額葉皮質的神經活動都有減少，可能反映出在老年憂鬱症上的認知神經功能障礙。進一步發現，老年憂鬱症患者對於處理正向情緒字詞刺激在左腦額中葉皮質的神經活動有增加，而對於負向情緒字詞刺激的處理則在左腦額下葉皮質的神經活動有減少，這些結果可能反映出老年憂鬱症患者對於情緒性訊息的調控功能受損。此外，在恢復程度較好的老年憂鬱症病患發現在處理認知及情緒方面，皆有額外的前額葉神經網絡參與，這可能是在恢復過程中的補償機制。本研究成果將提供未來臨床上輔助診斷及治療老年憂鬱症的影像標記因子參考。

Depression is one of major geriatric health issues. The late life depression (LLD) patients have been identified to be associated with mild cognitive impairment and abnormal neural activity in executive functions. This functional magnetic resonance imaging (fMRI) study was designed to examine the neural responses of inhibitory­control processing in LLD with focusing on both cognitive and emotional factors. The modified color­word Stroop and emotional Stroop paradigms were used to assess interference effects that are known to involve filtering out distracting irrelevant information in geriatric major depression and healthy older adults. In this thesis, the first study is to examine the effects of depressive disorder on neural activation during executive control function in both cognitive and affective domains; the second study is to explore the difference between remitted LLD (rLLD) and non-remitted LLD (LLD) groups in neural mechanisms during executive controls. Behaviorally, the LLD patients showed slower responses and less accuracy on the color­word Stroop task as well as emotional Stroop task. In the neural level, the LLD patients showed decreased activation in prefrontal cortex in both cognitive and affective/emotional conflict, reflecting neurocognitive impairment in geriatric depression. Moreover, the LLD patients showed increased left middle frontal cortex activation for positive emotional words and decreased left inferior frontal cortex activation for negative emotional words, these results suggest an impaired modulation of emotional information. Finally, additional frontal networks were recruited during both cognitive and affective/emotional dimension which suggests a compensatory neural mechanism in LLD remission. Our neuroimaging findings provide a potential neuroimaging marker for early detection for the patients with depressive disorder.