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  • 學位論文

巴金森氏病病人的腦血流循環動態的研究

Cerebral hemodynamics in patients with Parkinson’s disease

指導教授 : 林則彬

摘要


背景與目的:腦血管的自動調節機能(cerebrovascular autoregulation,CAR)能夠使腦組織維持恆定的血流量。它主要是經由下列三個機轉來控制:血管肌肉性因素,化學代謝因素,和神經因素-特別是自主神經。關於巴金森氏病病人的腦血流循環動態的研究迄今不多。巴金森氏病病人,即便是在疾病早期,常會有自主神經系統障礙。關於巴金森氏病病人其經由神經系統管控的腦血流(neurogenic control of cerebral circulation),特別是腦血管的自動調適機能(autoregulation),是否會受到影響,這一方面的研究到目前為止還很少。另外,巴金森氏病病人是否有合併腦血管的自動調節機能障礙影響到腦血流的灌流,以致於加速其神經退化和智能減退則一直仍有爭議。本研究利用快速換氣和冰水加壓測試來觀察巴金森氏病病人的身體血流循環與腦血流循環動態進而評估其腦血管反應度是否有受損。 方法:本研究共收集49原發性位巴金森氏病病人和49位性別與年齡相對應的正常人。本研究包含兩部分:第一部分是快速換氣,先使受測者安靜休息取得基礎值1,然後讓其做三分鐘的快速換氣;第二部分是再使受測者安靜休息取得基礎值2,然後讓其做一分鐘的冰水加壓測試。使用彩色顱內超音波(transcranial color-coded Doppler ultrasonography,TCCS)測量中大腦動脈的血流速度(cerebral blood flow velocity,CBFV)和血流波形脈動指數(pulsatility index,PI)。也同時測量平均動脈壓(mean arterial blood pressure,MAP),心跳次數(heart rate),和潮氣末二氧化碳分壓(end-tidal CO2,Et-CO2)。以平均動脈壓除於平均腦血流速度(mean cerebral blood flow velocity,Vm)算出腦血管阻力(cerebrovascular resistance,CVR)。同時評估Vm,PI,和CVR在快速換氣和冰水加壓時變化量的百分比。 結果:在休息狀態下的基礎值兩組之間並無統計學上的差異。在快速換氣時,兩組受測者皆呈現輕微的血壓下降和心跳次數加快,但和基礎值比較並無統計學上的意義;中大腦動脈血流速度和基礎值比較兩組都呈現有意義的下降,但兩組之間並無明顯的差異;PI以及CVR和基礎值比較兩組都呈現有意義的上升,但兩組之間並無明顯的差異;Vm,PI,和CVR變化量的百分比在兩組之間也無統計學上的差異。在冰水加壓測試時,MAP,HR,和Vm和基礎值比較皆呈現統計學上有意義地增加;而PI和CVR則呈現統計學上有意義地下降;兩組間相比,Vm和MAP增加量的百分比以及PI和CVR下降量的百分比則呈現正常對照組明顯大於巴金森氏病病人。 結論:本研究間接證明巴金森氏病病人經由二氧化碳調控的腦血管反應是正常的,而經由交感神經調控的腦血管反應則有障礙。是否可以利用冰水加壓測試評估腦血管反應度來早期診斷巴金森氏病病人是否有自主神經調控的腦血管自動調節障礙,則需要以後更進一步的研究來證實我們的假說。

並列摘要


Background and purpose: Cerebrovascular autoregulation (CAR) regulates the cerebral blood flow (CBF) through neurogenic, myogenic, and metabolic mechanism. The studies of cerebral hemodynamics in patients with Parkinson’s disease are rare. Disturbance of the autonomic nervous system (ANS) is frequently encountered in Parkinson’s disease (PD), even in early stage. The studies concerning the function of ANS-controlled CAR in PD are also scarce. It has been debated whether an additional impairment of CAR may influence the brain perfusion to exacerbate the neuronal degeneration or to promote the mental decline in PD patients. In this study, we examined changes in systemic and cerebral hemodynamics during hyperventilation induced hypocapnia state and during the cold pressor test (CPT) to determine whether cerebrovascular reactivity is intact or impaired in patients with PD. Methods: Forty-nine patients with PD and 49 sex- and age-matched non-PD subjects were evaluated. Two protocols were conducted in this study. In protocol I, measurements were performed in the resting state and over a period of three minutes of hyperventilation. After 20 minutes rest, protocol II was performed with measurement of resting state and a period of one minute of CPT. The cerebral blood flow velocity (CBFV) and pulsatility index (PI) of the middle cerebral artery (MCA) were recorded by transcranial color-coded Doppler ultrasonography (TCCS). Mean arterial blood pressure (MAP), heart rate (HR), and end-tidal CO2 (Et-CO2) were investigated simultaneously. The resistance of the cerebrovascular bed (CVR) was calculated as the ratio of mean arterial blood pressure to mean cerebral blood flow velocity (Vm). Percent changes of Vm, PI and CVR in response to the hyperventilation and cold pressor test were evaluated. Results: Baseline values for control and PD subjects showed no statistical difference. Hyperventilation induced a mild decrease of MAP and mild increased of HR in both groups. The Vm was significantly decreased, and the pulsatility index (PI) and CVR were significantly increased in both groups during hyperventilation. However, the percent change of Vm, PI, and CVR did not have statistic difference between two groups during hyperventilation. CPT induced a significant increase in MAP, HR, and Vm in both groups. PI and CVR were decreased in both groups during CPT. Percent increases of Vm (P < 0.001) and MAP (P = 0.011) were significantly higher while the percent decreases of PI (P = 0.002) and CVR (P = 0.007) were significantly decreased more in the non-PD group. Conclusions: This study indirectly shows that the CO2-mediated cerebrovascular reactivity is intact, nevertheless, the ANS-mediated cerebrovascular reactivity is impaired in patients with PD. Further investigations are needed to confirm the hypothesis that using the cold pressor test to evaluate cerebrovascular reactivity might be beneficial in early diagnosis of impairment of ANS-mediated cerebrovascular autoregulation in patients with PD.

參考文獻


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