臺灣博碩士論文加值系統

根據神經傳導和運動單元作用的基本生理機轉，「傳導阻斷」是造成週邊神經病變病患肌力下降的原因。而造成傳導阻斷的原因，可能是蘭氏結處的細胞膜閾值太高或充電電流不足。目前臨床上用來評估週邊神經功能的傳統電生理檢查，只給予神經單一電刺激，與真實的生理機制並不同。實際上神經的訊息傳遞是藉由動作電位反覆活化的「頻率」來控制強弱。而應用在偵測閾值的閾值追蹤電生理方法，只能偵測施予電刺激該處的軸突細胞膜閾值變化，不能偵測動作電位沿著軸突傳遞下來的最後結果。本研究提出反覆電刺激的方法，模擬最接近生理狀態的神經訊號傳遞，在人體身上定量施予軸突壓力(stress)，藉由分析刺激神經近端與遠端所造成的結果差異，證明當給予人類神經超過15Hz以上的反覆刺激，將會造成傳導阻斷現象，阻斷的程度隨著電刺激頻率的增快而遞增。這種現象在正常人就會出現，顯示人類軸突在承受高頻刺激時，會出現傳導阻斷現象。這個現象與此新的檢查方法將可應用於其他週邊神經病變的檢查，以及對週邊神經病變病態生理機轉的探討。

Frequency-dependent conduction block could not be detected by routine nerve conduction studies, in which stimuli are usually administered at a very low rate and produce little stress on the tested axons. Therefore, the repetitive nerve stimulation test (RNST) would be an adequate tool to demonstrate the frequency-dependent conduction block at a higher stimulation frequency. We enrolled 20 healthy subjects and performed RNST by delivering a repetitive supramaximal current with 1, 5, 10, 15, 20 and 30 Hz at the distal and proximal parts of the median and tibial nerves, respectively. Pseudofacilitation could be seen at higher stimulation frequencies, which was more prominent when giving stimulation at the distal nerve. A decrease in amplitude instead of pseudofacilitation was found while administering stimulation frequencies beyond 20 Hz at the proximal nerve in most subjects. Conduction block between these two stimulation sites is our favorable interpretation. Results also show that the higher stimulation frequencies the more chances of conduction block appear. Using this method, we directly show the frequency-dependent conduction block in human nerves.

目錄

中文摘要 2
英文摘要 3
背景與目的 5
研究方法 21
研究結果與分析 29
討論 59
參考文獻 66
附件一(人體試驗委員會同意書) 68

Boe SG, Stashuk DW, Doherty TJ. Within-subject reliability of motor unit number estimates and quantitative motor unit analysis in a distal and proximal upper limb muscles. Clin Neurophysiol 2006; 117: 596-603
Bostock H and Grafe P. Activity-dependent excitability changes in normal and demyelinated rat spinal root axons. J Physiol 1985; 365: 239-57
Burke D, Kiernan MC, Bostock H. Excitability of human axons. Clin Neurophysiol 2001; 112: 1575-85
Cappelen-Smith C, Kuwabara S, Lin C S-Y, Mogyoros I, Burke D. Activity-dependent hyperpolarization and conduction block in chronic inflammatory demyelinating polyneuropathy. Ann Neurol 2000; 48: 826-32
Cappelen-Smith C, Lin C S-Y, Burke D. Activity-dependent hyperpolarization and impulse conduction in motor axons in patients with carpal tunnel syndrome. Brain 2003; 126: 1001-8
Galea V, McComas A. Effects of ischemia on M-wave potentiation in human biceps brachii muscles. J Physiol 1991; 438: 212
Hicks A, Fenton J, Garner S, McComas AJ. M wave potentiation during and after muscle activity. J Appl Physiol 1989; 66: 2606-10
Kimura J. Electrodiagnosis in diseases of nerve and muscle. 3rd edition 2001; pp81-2.
McComas AJ, Galea V, Einhorn RW. Muscle Nerve 1994; 17: 599-607
Nodera H and Kaji R. Nerve excitability testing and its clinical application to neuromuscular diseases. Clin Neuriphysiol 2006; 117: 1902-16
Poliak S and Peles E. The local differentiation of myelinated axons at node of Ranvier. Nature Rev Neurosci 2003; 4: 968-80
Rubinstein S, Kamen G. Decreases in motor unit firing rate during sustained maximal-effort contractions in young and older adults. J Electromyography Kinesiol 2005; 15: 536-43
Rutkove SB. Pseudofacilitation: a temperature-sensitive phenomenon. Muscle Nerve 2000; 23: 115-8
Tasaki I. Conduction of the nerve impulse. In Handbook of physiology,section I, Neurophysiology, ed. FIELD, J. 1959; 75-121. Washington DC: American Physiology Society.
Vagg R, Mogyoros I, Kiernan MC, Burke D. Activity-dependent hyperpolarization of human motor axons produced by natural activity. J Physiol 1998; 507: 919-25
van Dijk JG, van der Hoeven BJ, van der Hoeven H. Repetitive nerve stimulation: effects of recording site and the nature of ‘pseudofacilitaion’. Clin Neurophysiol 2000; 111: 1411-9