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개의 마미압박으로 생기는 전기진단검사 및 조직의 변화

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 Electrodiagnostic and histologic changes of graded caudal compression in dog 
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[한글] 종래 척수와 말초신경의 급성압박에 대한 실험적 보고는 많이 있어 왔으나(Perot 및 Vera,1982; Cheng등, 1984; Schiff등, 1984; Nacimento등, 1986; Nystrom등, 1988; Arbit등, 1989)지속적이고 만성적인 압박에 대해서는 1990년 Delamarter등이 처음으로 개에서 인 위적인 마미압박 증후군을 만들어 압박의 정도에 따른 감각유발전위와 미세혈관 조영술 및 조직병리 소견을 보고한 이외 별로 연구업적이 없다. 만성적인 마미압박은 정도와 예후를 예측하기 힘들기 때문에 정확한 신경압박의 정도를 예측하고 또한 시간경과에 따른 회복의 징후를 예견할 수 있는 지표를 찾기위해 본 연구에서는 개를 이용하여 압박의 정도를 달리하면서 인위적으로 만든 마미압박 증후군에 대하여 수술후 시기별로 신경검사와 감각유발전위, 그리고 구해면체반사를 측정하고, 수술후 3개월에 조직표본을 만들어 육안 및 광학현미경으로 조직의 변화를 관찰하여 다음과 같은 결과를 얻었다. 1. 경미한 마미의 압박으로 신경학적 소견이 발현되지 않더라도 감각유발전위와 구해면체반사는 초기부터 이상소견을 보였으며, 중증도 이상의 마미압박에서는 시간경과에 따라 감각유발전위와 구해면체반사가 회복되면서 신경학적 소견도 점진적으로 회복되는 결과를 보였다. 2. 마미의 50% 압박군에서 감각유발전위와 구해 면체반사의 소실, 신경 검사의 이상 그리고 조직학적 이상을 보였으나, 동시에 회복가능의 한계점(critical point)이었으며, 그 이상의 압박은 회복이 어려웠다. 3. 1개월 이내에 감각유발전위와 구해면체반사가 회복되는 소견을 보이면 신경증상도 시간이 경과함에 따라 회복되었다. 이상의 결과로 미루어 만성적인 마미압박의 예후를 알기 위해서는 신경학적 검사외에 감각유발전위와 구해면체반사 측정을 병행하는 것이 도움이 된다고 판단되었다.
[영문] Our understanding of the neuropathophysiological changes in the chronically compressed cauda equina is limited, and the precise etiology of neurological signs and symptoms associated with lumbar spinal stenosis is unknown. The signs and symptoms of chronic compression of the cauda equina have been related to changes in the intrinsic blood supply, changes in axoplasmic flow, and direct neural compression. The degree of narrowing of the spinal canal that causes electrophysiological, histological, and neurological changes is not known. Previous experimental studies have shown the effects of acute compression of the spinal cord and peripheral nerve roots. However, few animal model of chronic compression of the cauda equina has been described. The purpose of this study was to develop a reproducible animal model of lumbar spinal stenosis in order to increase understanding of the long-term histological and electrophysiological changes of chronic compression of the cauda equina. An animal model of lumbar spinal stenosis was developed in which the pathophysiology of this condition could be examined. Four experimental groups, each containing six dogs, were studied. One group had a laminectomy of the sixth and seventh lumbar vertebrae only; these animals served as controls. In the three othere groups, a laminectomy was performed and the cauda equina was constricted by 25, 50, or 75 per cent to produce chronic compression. Weekly neurological examinations were carried out, and the neurological deficits were graded using the Tarlov system. Somatosensory evoked potentials and bulbocavernosus reflexes were recorded preoperatively, immediately after constriction, and at two weeks, one, two, and three months postoperatively. After three months of constriction, the cauda equina of six dogs in each group was examined histologically. The animals in the control group showed no neurological abnormalities, no changes in cortical evoked potentials, normal latencies of bulbocavernosus relexes, and no histopathological changes in the nerve roots or the spinal cord. The dogs in which the cauda equina had been constricted 25 per cent had no neurological deficits, mild changes in cortical evoked potentials, normal latencies of bulbocavernosus reflexes, and no histological changes. The dogs in which the cauda equina had been constricted 50 per cent had mild initial motor weakness, maior changes in cortical evoked potentials, delayed bulbocavernosus reflexes, and edema and loss of myelin in the root of the seventh lumbar nerve. The does in which the cauda equina had been constricted 75 per cent had significant weakness, paralysis of the tail, and urinary incontinence: all doss partially recovered by the third month, but all had neurogenic changes in cortical evoked potentials and abscence or marked delayed bulbocavernosus reflexes, and had complete nerve-root atrophy at the level of the constriction. There was blockage of axoplasmic flow and Wallerian degeneration of the motor nerve roots distal to the constriction and of the sensory roots proximal to the constriction. Somatosensory evoked potentials and bulbocavernosus reflexes revealed neurological abnormalities before the appearance of neurological signs and symptoms. Constriction of more than 50 per cent was the critical point that resulted in complete loss of cortical evoked potentials and in neurological deficits and histological abnormalities. In cases recovered from somatosensory evoked potentials and bulbocavernosus reflexes within 1 month, neurological symptom and sign have also gradually been recovered. In conclusion, for the accurate forecasting of prognosis of chronic cauda equina compression, the combined diagnostic study of somatosensory evoked potential with bulbocavernosus reflex is recommanded.
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