神經病變痛之機制與治療

Mechanism and Treatment of Neuropathic Pain

疼痛是一種因為真正存在，或潛在的身體組織損傷，所引起的不舒服知覺和心理變化，所以疼痛不僅是一種感覺，也伴隨情緒反應。疼痛的生理目的，是要告知大腦身體內外環境中，有潛在的傷害性刺激存在，是一個用來保護人體的警告系統，避免人體進一步受到傷害。反之神經病變痛，是由於體感覺神經系統疾病直接導致的疼痛，是涉及小纖維溫度疼痛，神經傳導路徑病變常見的症狀，它是一種病態性的疼痛，即便沒有其他任何組織受傷或外來的傷害性刺激，它也會持續或間歇地、自發地或被誘發性地產生疼痛感覺，這種疼痛就失去了其生理上提供身體保護的功能，相反地它只會干擾病人生活品質及功能。目前我們對於神經病變痛發生的機制仍有諸多不了解，而且因為神經病變痛的表現多為病人主觀的症狀，臨床上缺乏客觀的檢查工具及診斷標準，因此神經性痛的診斷及治療，是臨床醫師須面臨的重大挑戰。本章節將介紹：（1）疼痛是如何產生：包括周邊神經及大腦路徑和機制；（2）神經病變痛與正常疼痛之相異處，及其表現特點、分類、診斷條件與工具方法；（3）神經病變痛的病理機制：包括體感覺神經路徑異常電氣活動，所引起之自發性疼痛，及周邊與中樞神經異常敏感化所導致的誘發性疼痛，這其中可能涉及適應不良的結構變化，如離子通道和突觸活性的改變等機轉。我也將以腦中風後神經病變痛為例，介紹利用「經顱磁刺激」這種非侵入性腦刺激工具，闡明運動皮層的適應不良性變化與神經病變痛的相關性；及（4）神經病變痛的治療進展及機制導引的治療策略。

Pain is an unpleasant and emotional experience associated with actual or potential tissue damage, and is a warning system to protect the human body from the potential harmful stimuli in the internal and external environment of the body. Neuropathic pain, resulting from neurological disorders affecting the somatosensory system, is a pathological pain which occurs spontaneously or is evoked by non-painful stimuli without tissue injury. Neuropathic pain is devastating to patients experiencing it, and its diagnosis and treatment of neuropathic pain is a substantial challenge for physician. Clinically neuropathic pain is usually diagnosed by subjective painful symptoms reported by patients. There is a lack of objective evaluating tools for neuropathic pain and the mechanism of neuropathic pain is not well elucidated. In the present chapter, we will introduce: (1) where and how the pain originates: from nociceptors, peripheral nerves, brain network to mechanism; (2) Differences between physiological pain and neuropathic pain, and features, classification, diagnostic criteria and tools of neuropathic pain; (3) patholophysiological mechanisms of pain, including spontaneous pain caused by abnormal electrical activity of somatosensory pathways and evoked pain caused by abnormal sensitization of peripheral and central nervous system, which may involve maladaptive changes in ion channels and synaptic activity, like the disinhibition of primary motor cortex in post-stroke neuropathic pain demonstrated by transcranial magnetic stimulation; and (4) the treatment of neuropathic pain, especially the mechanism-guided therapeutic strategies.