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研究生:陳韋達
研究生(外文):Wei-Ta Chen
論文名稱:偏頭痛疾患之視覺皮質興奮性異常
論文名稱(外文):Alteration of visual cortical excitabilities in migraine
指導教授:林慶波林慶波引用關係林永煬林永煬引用關係王署君王署君引用關係
指導教授(外文):Ching-Po LinYung-Yang LinShuu-Jiun Wang
學位類別:博士
校院名稱:國立陽明大學
系所名稱:神經科學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2009
畢業學年度:97
語文別:中文
論文頁數:81
中文關鍵詞:腦磁圖視覺誘發磁場偏頭痛無預兆偏頭痛慢性偏頭痛刺激空間頻率
外文關鍵詞:Magnetoencephalography (MEG)Visual evoked magnetic field (VEF)MigraineMigraine without aura (MoA)Chronic migraine (CM)Stimulus spatial frequency
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偏頭痛的致病機轉目前並不清楚,但有研究顯示,患者大腦皮質的興奮性異常。部分視覺、聽覺與體感覺刺激的誘發電位研究顯示,患者大腦的初級感覺皮質興奮性偏低,隨著外在刺激的持續給與,感覺皮質的誘發反應並未因正常的「習慣化 (habituation)」現象而變小,反而是持平甚至變大。其中,有關視覺皮質的研究最為重要,因為偏頭痛發作時會畏光 (photophobia),而視覺刺激也可以誘發偏頭痛。部分偏頭痛患者在頭痛前會出現預兆 (aura),也幾乎都是視覺症狀。
儘管如此,偏頭痛疾患的視覺皮質興奮性研究,至今並未獲得一致的結論。究其原因,刺激方法、記錄方式、臨床診斷、頭痛發作與否等條件差異均有可能。傳統的視覺誘發電位,還有「異側化 (paradoxical lateralization)」與「體積傳導效應 (conduction volume effect)」等缺點,限制了視覺皮質興奮性研究的精確性。
腦磁圖 (magnetoencephalography) 的空間解析度比傳統腦波好,也沒有上述視覺誘發電位的缺點,因此,本研究嘗試利用腦磁圖來探討偏頭痛疾患的視覺皮質興奮性異常。研究的假設是:習慣化缺陷,是偏頭痛疾患最重要的皮質興奮性異常,此一行為表現,同時受到內在 (如:血清張力素等神經傳導活性) 與外在因素 (如:不同的刺激方式或次數) 的影響而不斷變動,反映出偏頭痛患者失衡的神經調控。
本研究包含三個實驗,均是以棋盤方格刺激 (checkerboard reversal) 受試者的左半視野,再以腦磁圖記錄右側視覺皮質的「視覺誘發磁場反應 (visual evoked magnetic field,VEF)」,分析刺激後100毫秒左右的P100m反應。實驗一,以健康人為受試者,改變棋盤方格刺激的空間 (方格大小) 與時間 (閃動頻率) 頻率,發現棋盤方格大小,會明顯改變P100m振幅,且120分 (弧度) 的方格大小,能誘發最強的磁場反應。實驗二選用四種不同方格大小 (15,30,60,120分) 的棋盤方格,受試者包括無預兆偏頭痛患者 (另分為發作期與發作間期兩組) 與正常對照組。結果顯示,無預兆偏頭痛患者的習慣化程度較正常人差,且此種興奮性改變,只出現於120分的方格刺激。另外,偏頭痛急性發作前後兩天,此一改變恢復正常。實驗三,受試者為慢性偏頭痛患者,並與陣發性偏頭痛 (無預兆型)及正常人對照。結果顯示,在發作間期,慢性偏頭痛患者的視覺皮質呈現敏感化現象 (P100m振幅增強),且習慣化正常,沒有陣發性患者的習慣化缺陷。
偏頭痛疾患的視覺皮質興奮性異常,以習慣化缺陷為主要表現。此現象與外在視覺刺激的空間、時間頻率有關,且受內在偏頭痛發作週期的影響。當陣發性偏頭痛演變為慢性偏頭痛時,反覆的急性偏頭痛發作,使習慣化恢復正常,並因長期刺激視覺皮質而導致其敏感化。總之,偏頭痛患者對重覆不斷的感覺刺激有異常的中樞反應性,而此種神經調控異常,可能源自於神經傳導物質,尤其是血清張力素之傳遞障礙。本研究對內外在多種因素影響視覺皮質興奮性之探討,可解釋過去誘發電位研究之間的結論差異。
The pathophysiology of migraine has been proposed as “dysexcitability” of the brain. A constellation of evoked potential studies using visual, auditory, or somatosensory stimulation methods indicate that baseline (pre-excitation) excitability of primary sensory cortices in migraine tend to be lower compared to healthy controls. However, in contrast to normal habituation pattern, evoked cerebral responses in migraine patients are not attenuated as the stimulation continues.
Acute migraine is associated with the symptoms of photophobia. Light stimuli may trigger migraine attacks. Aura symptoms of migraine are mostly of the visual type. Thus, the visual cortex seems pivotal in the pathophysiology of migraine. However, findings of visual evoked potential (VEP) studies in migraine remain contradictory. In addition to methodology differences, the phenomenon of “paradoxical lateralization” and conduction volume effect inherent to traditional electroencephalography (EEG) hinder the use of VEP in investigating the visual cortical excitability.
Magnetoencephalography (MEG) is free of the above limitations and is better in spatial resolution when compared to EEG. It is hypothesized that habituation deficit is the pivotal alteration of visual cortical excitability in migraine. The abnormality is continuously affected by various internal (e.g. serotonin transmission) and external (e.g. stimulus characteristics) factors, and reflects neural dysmodulation of the brain.
The present study aimed to investigate the visual cortical dysexcitability in migraine disorders using MEG. It was composed of three experiments, all using left hemifield checkerboard reversals to elicit visual evoked magnetic field (VEF). The magnetic activation ~100 ms (P100m) was analyzed by single dipole modeling. Experiment 1 identified the modulating effect of P100m by spatial (check size) and temporal (reversal rate) frequencies of the visual stimuli in healthy subjects. There was a substantial effect of check size on P100m activations and the 120' (minutes of arc) checks were optimum. In experiment 2 four check sizes (15', 30', 60', and 120') were used to investigate excitability changes of the visual cortex in migraine without aura (MoA). Patients with MoA showed potentiation of VEF responses compared to healthy controls selectively at 120', which was normalized during peri-ictal periods. Patients with chronic migraine (CM) were further enrolled in Experiment 3, which showed sensitization of the visual cortex in the interictal period. Habituation behavior of the visual cortex in CM was otherwise normal, in contrast to the deficient habituation of MoA.
Alteration of visual cortical excitability in migraine is mainly characterized by habituation deficit, which is dependent on temporal and spatial frequencies of visual stimuli, and the ictal-interictal cycle of migraine. In the chronicity of migraine, repetitive activations by headache render the visual cortex sensitized with ensuing normalized habituation. Thus, the brain with migraine shows abnormal reactivity to repetitive external stimulations. The underpinning neural dysmodulation may reflect dysfunction of neurotransmission, especially of serotonin. The present findings also help explain the contradictory findings of pertinent VEP studies.
Abstract--------------------------------------------p1
Keywords and Abbreviations -------------------------p6
Introduction and Literature Review------------------p7
General Methodology --------------------------------p15
Experiment 1 ---------------------------------------p21
Experiment 2 ---------------------------------------p33
Experiment 3 ---------------------------------------p46
Conclusion -----------------------------------------p57
References -----------------------------------------p58
Tables ---------------------------------------------p66
Figures --------------------------------------------p75
Publication list -----------------------------------p80
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