在單側腦缺血再灌流(ischemia-reperfusion)的中風模型實驗中，以體感覺誘發電位(Somatosensory evoked potential, SSEP)評估中風後周邊神經傳遞至中樞神經的狀態發現，在中風後不僅患側神經傳遞速率與反應大小皆有降低，連健側也出現降低幅度大小的神經官能聯繫不良(diaschisis)反應，顯示單側腦部損傷可造成遠處訊號傳遞受阻。本研究所用的電生理檢測方法為體感覺誘發電位，測量雄性大白鼠(Sprague-Dawley, SD)在中大腦動脈局部缺血前後電生理反應的差異，暫時性局部腦缺血是藉著近端右中大腦動脈(MCA)的內動脈縫合線閉塞來達成，分別在阻塞30分鍾、90分鐘和150分鐘後取出塞線，達到腦部再灌流現象。永久性腦缺血分為兩大類，其一為藉由內動脈縫合線持續阻塞中大腦動脈，另一類以電燒中大腦動脈遠端分枝造成。實驗數據主要由單因子變異數分析(ANOVA)比較各組之間的差異，並以最小顯著差異法(LSD)做事後檢定，以相依樣本t檢定比較梗塞前後電生理學上的變化，皆以p<0.05視其達到統計上的顯著差異。結果顯示儘管腦部組織學上梗塞區域相似，持續性梗塞在官能聯繫不良現象上明顯大於暫時性腦梗塞，且由Fluoro-Jade標定的神經元退化現象也顯著大於暫時性缺血的組別。在臨床上局部大腦損傷伴隨有造成對側大腦、小腦等遠端區域傷害的現象，在本研究中藉由組織學與電生理學觀察，大鼠大腦皮質損傷程度與官能聯繫不良現象有較高度的相關，對臨床上中風患者感覺喪失、功能受損、以致於患者昏迷等大腦訊息傳遞功能降低現象提供其探討，顯示再灌流有助於降低患者官能聯繫不良症狀。

Ischemia stroke is the most common type of stroke. The remote changes in blood flow, metabolism and electric activity resulted from focal cerebral injury were called diaschisis. Ischemic models were evaluated electrophysiological diaschisis and benefits of reperfusion in this research. Diaschisis is often seen clinically after brain injury. We designed several different models to evaluate the phenomena of electrophysiological diaschisis. This study included three transient models (occlusion of the MCA for 30, 90 and 150 min) and two permanent models (occluded proximal MCA without reperfusion and electrocoagulation of the distal MCA). SSEP was recorded prior to MCAo and 24 hours, 7 days after reperfusion. Brain infarction was assessed by Nissle staining and quantified by MCID program. We measured the Fluoro-Jade positive cells which quantification of degenerate neuron. SSEP stimuli were recorded in the somatosensory cortex after stimulating the fore- and hind-limb with 3.0 mA DC potential. The amplitude between the first positive (P1) and the first negative (N1) peaks and the P1 latency were analyzed. The suppressed SSEP amplitude was significantly different between permanent and transient groups. The suppressed amplitude was recorded not only from ischemic but also non-ischemic hemispheres. Interestingly, diaschisis is a common consequence after brain damages especially those with cortical infarction. Reperfusion ameliorated neuron degeneration, electrophysiological function and diaschisis. In conclusion, our results suggest that cortical lesion leads to diaschisis, which can be reversed by reperfusion.

1. Andrews, R.J., Transhemispheric diaschisis. A review and comment. Stroke. 22(7): p.943-9, 1991.
2. Astrup, J., Siesjo, B.K., and Symon, L., Thresholds in cerebral ischemia - the ischemic penumbra. Stroke. 12(6): p.723-5, 1981.
3. Bamford, J., Sandercock, P., Dennis, M., Burn, J., and Warlow, C., A prospective study of acute cerebrovascular disease in the community: the Oxfordshire Community Stroke Project--1981-86. 2. Incidence, case fatality rates and overall outcome at one year of cerebral infarction, primary intracerebral and subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. 53(1): p.16-22, 1990.
4. Baron, J., Bousser, M., Comar, D., and Castaigne, P., `Crossed cerebellar diaschisis' in human supratentorial brain infarction. Trans Am Neurol Assoc. 105: p.459-461, 1980.
5. Belayev, L., Alonso, O.F., Busto, R., Zhao, W., and Ginsberg, M.D., Middle cerebral artery occlusion in the rat by intraluminal suture. Neurological and pathological evaluation of an improved model. Stroke. 27(9): p.1616-22; discussion 1623, 1996.
6. Block, F., Dihne, M., and Loos, M., Inflammation in areas of remote changes following focal brain lesion. Prog Neurobiol. 75(5): p.342-65, 2005.
7. Bodis-Wollner, I., Evoked poentials. 1982, New York: The New York Academy of Sciences.
8. Bordi, F., Pietra, C., Ziviani, L., and Reggiani, A., The glycine antagonist GV150526 protects somatosensory evoked potentials and reduces the infarct area in the MCAo model of focal ischemia in the rat. Exp Neurol. 145(2 Pt 1): p.425-33, 1997.
9. Brint, S., Jacewicz, M., Kiessling, M., Tanabe, J., and Pulsinelli, W., Focal brain ischemia in the rat: methods for reproducible neocortical infarction using tandem occlusion of the distal middle cerebral and ipsilateral common carotid arteries. J Cereb Blood Flow Metab. 8(4): p.474-85, 1988.
10. Buchkremer-Ratzmann, I., August, M., Hagemann, G., and Witte, O.W., Electrophysiological transcortical diaschisis after cortical photothrombosis in rat brain. Stroke. 27(6): p.1105-9; discussion 1109-11, 1996.
11. Buchkremer-Ratzmann, I. and Witte, O.W., Pharmacological reduction of electrophysiological diaschisis after photothrombotic ischemia in rat neocortex. Eur J Pharmacol. 320(2-3): p.103-9, 1997.
12. Carmichael, S.T., Tatsukawa, K., Katsman, D., Tsuyuguchi, N., and Kornblum, H.I., Evolution of diaschisis in a focal stroke model. Stroke. 35(3): p.758-63, 2004.
13. Chen, T.Y., Lee, M.Y., Chen, H.Y., Kuo, Y.L., Lin, S.C., Wu, T.S., and Lee, E.J., Melatonin attenuates the postischemic increase in blood-brain barrier permeability and decreases hemorrhagic transformation of tissue-plasminogen activator therapy following ischemic stroke in mice. J Pineal Res. 40(3): p.242-50, 2006.
14. Clark, W.M., Rinker, L.G., Lessov, N.S., Hazel, K., Hill, J.K., Stenzel-Poore, M., and Eckenstein, F., Lack of interleukin-6 expression is not protective against focal central nervous system ischemia. Stroke. 31(7): p.1715-20, 2000.
15. Coull, B.M., Williams, L.S., Goldstein, L.B., Meschia, J.F., Heitzman, D., Chaturvedi, S., Johnston, K.C., Starkman, S., Morgenstern, L.B., Wilterdink, J.L., Levine, S.R., and Saver, J.L., Anticoagulants and antiplatelet agents in acute ischemic stroke: report of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the American Stroke Association (a division of the American Heart Association). Stroke. 33(7): p.1934-42, 2002.
16. Enager, P., Gold, L., and Lauritzen, M., Impaired neurovascular coupling by transhemispheric diaschisis in rat cerebral cortex. J Cereb Blood Flow Metab. 24(7): p.713-9, 2004.
17. Feeney, D.M. and Baron, J.C., Diaschisis. Stroke. 17(5): p.817-30, 1986.
18. Gharbawie, O.A., Gonzalez, C.L., and Whishaw, I.Q., Skilled reaching impairments from the lateral frontal cortex component of middle cerebral artery stroke: a qualitative and quantitative comparison to focal motor cortex lesions in rats. Behav Brain Res. 156(1): p.125-37, 2005.
19. Ginsberg, M.D., Reivich, M., Giandomenico, A., and Greenberg, J.H., Local glucose utilization in acute focal cerebral ischemia: local dysmetabolism and diaschisis. Neurology. 27(11): p.1042-8, 1977.
20. Gott, P.S., Karnaze, D.S., and Fisher, M., Assessment of median nerve somatosensory evoked potentials in cerebral ischemia. Stroke. 21(8): p.1167-71, 1990.
21. Hacke, W., Hennerici, M., Gelmers, H.J., and Kramer, G., Cerebral Ischemia. 1989, New Tork: Springer-Verlag. 5-9.
22. Jellema, T., Brunia, C.H., and Wadman, W.J., Sequential activation of microcircuits underlying somatosensory-evoked potentials in rat neocortex. Neuroscience. 129(2): p.283-95, 2004.
23. Juhasz, C., Kamondi, A., and Szirmai, I., Spectral EEG analysis following hemispheric stroke: evidences of transhemispheric diaschisis. Acta Neurol Scand. 96(6): p.397-400, 1997.
24. Kempinsky, W.H., Steady potential gradients in experimental cerebral vascular occlusion. Electroencephalogr Clin Neurophysiol. 6(3): p.375-88, 1954.
25. Kety, S.S. and Schmidt, C.F., The nitrous oxide method for the quantitative determination of cerebral blood flow in man; theory, procedure and normal values. J Clin Invest. 27(4): p.476-83, 1948.
26. Lee, E.J., Lee, M.Y., Chang, G.L., Chen, L.H., Hu, Y.L., Chen, T.Y., and Wu, T.S., Delayed treatment with magnesium: reduction of brain infarction and improvement of electrophysiological recovery following transient focal cerebral ischemia in rats. J Neurosurg. 102(6): p.1085-93, 2005.
27. Lee, E.J., Lee, M.Y., Chen, H.Y., Hsu, Y.S., Wu, T.S., Chen, S.T., and Chang, G.L., Melatonin attenuates gray and white matter damage in a mouse model of transient focal cerebral ischemia. J Pineal Res. 38(1): p.42-52, 2005.
28. Lee, E.J., Wu, T.S., Lee, M.Y., Chen, T.Y., Tsai, Y.Y., Chuang, J.I., and Chang, G.L., Delayed treatment with melatonin enhances electrophysiological recovery following transient focal cerebral ischemia in rats. J Pineal Res. 36(1): p.33-42, 2004.
29. Liu, F., Schafer, D.P., and McCullough, L.D., TTC, fluoro-Jade B and NeuN staining confirm evolving phases of infarction induced by middle cerebral artery occlusion. J Neurosci Methods. 179(1): p.1-8, 2009.
30. Macdonell, R.A., Donnan, G.A., and Bladin, P.F., Serial changes in somatosensory evoked potentials following cerebral infarction. Electroencephalogr Clin Neurophysiol. 80(4): p.276-83, 1991.
31. Memezawa, H., Smith, M.L., and Siesjo, B.K., Penumbral tissues salvaged by reperfusion following middle cerebral artery occlusion in rats. Stroke. 23(4): p.552-9, 1992.
32. Mountz, J.M., Nuclear medicine in the rehabilitative treatment evaluation in stroke recovery. Role of diaschisis resolution and cerebral reorganization. Eura Medicophys. 43(2): p.221-39, 2007.
33. Muller, C., Achermann, P., Bischof, M., Nirkko, A.C., Roth, C., and Bassetti, C.L., Visual and spectral analysis of sleep EEG in acute hemispheric stroke. Eur Neurol. 48(3): p.164-71, 2002.
34. Mun-Bryce, S., Roberts, L., Bartolo, A., and Okada, Y., Transhemispheric depolarizations persist in the intracerebral hemorrhage swine brain following corpus callosal transection. Brain Res. 1073-1074: p.481-90, 2006.
35. Paxinos, G. and Watson, C., The Rat Brain in Stereotaxic Coordinates. 1997, Academic, San Diego.
36. Reinecke, S., Lutzenburg, M., Hagemann, G., Bruehl, C., Neumann-Haefelin, T., and Witte, O.W., Electrophysiological transcortical diaschisis after middle cerebral artery occlusion (MCAO) in rats. Neurosci Lett. 261(1-2): p.85-8, 1999.
37. Rubin, G., Levy, E.I., Scarrow, A.M., Firlik, A.D., Karakus, A., Wechsler, L., Jungreis, C.A., and Yonas, H., Remote effects of acute ischemic stroke: A xenon CT cerebral blood flow study. Cerebrovasc Dis. 10(3): p.221-8, 2000.
38. Sakatani, K., Iizuka, H., and Young, W., Somatosensory evoked potentials in rat cerebral cortex before and after middle cerebral artery occlusion. Stroke. 21(1): p.124-32, 1990.
39. Seitz, R.J., Azari, N.P., Knorr, U., Binkofski, F., Herzog, H., and Freund, H.J., The role of diaschisis in stroke recovery. Stroke. 30(9): p.1844-50, 1999.
40. van der Staay, F.J., Augstein, K.H., and Horvath, E., Sensorimotor impairments in rats with cerebral infarction, induced by unilateral occlusion of the left middle cerebral artery: strain differences and effects of the occlusion site. Brain Res. 735(2): p.271-84, 1996.
41. Von Monakow, C., Diaschisis [1914 article translated by G. Harris]. In: Brain and Behavior I: Mood States and Mind. 1969, KH, ed.: Baltimore: Penguin. 27-36.
42. Yatsu, F.M., Grotta, J.C., and Pettigrew, L.C., Stroke. 1995, Houston, USA: Mosby. 3-14.
43. 朱復禮, 臨床神經醫學. 民81, 台北: 合記.
44. 行政院衛生署編印, -台灣地區死因統計結果. 2008.
45. 吳進安, 基礎神經學. 民85, 台北: 合記.
46. 張楊全, 簡明臨床神經生理學. 2003, 台北: 力大圖書有限公司.
47. 楊明杰, 余政展, 吳佳穎, 吳承學, 吳孟儒, 李威廷, 林均一, 周昆達, 張曜任, 莊暘安, 黃嘉文, 詹東霖, 趙又麟, and 趙勇全, Ganong醫學生理學(1). 民 87, 台北: 合記.
48. 顱榮昌, 臨床神經解剖與神經生理學手冊. 2000, 台北市: 合記. 279-284.