EFFECTS OF INDUCED HYPOTHERMIA ON SOMATOSENSORY-EVOKED POTENTIALS IN PATIENTS WITH CHRONIC SPINAL-CORD INJURY

被引:19
作者
HAYES, KC
HSIEH, JTC
POTTER, PJ
WOLFE, DL
DELANEY, GA
BLIGHT, AR
机构
[1] Department of Physical Medicine & Rehabilitation, Parkwood Hospital, The University of Western Ontario, London, ON
来源
PARAPLEGIA | 1993年 / 31卷 / 11期
关键词
SEPS; SPINAL CORD INJURY; DEMYELINATION; HYPOTHERMIA;
D O I
10.1038/sc.1993.115
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
We have investigated the effects of mild whole body hypothermia on the amplitude and latency of somatosensory evoked potentials (SEPs) in control subjects (n = 12) and patients (n = 15) with chronic compressive or contusive spinal cord injury (SCI). Mild hypothermia (-1 degrees C) was induced by controlled circulation of propylene glycol through a `microclimate' head and vest garment while reductions in oral and limb temperatures were monitored. Cooling induced a delayed onset and reduced amplitude of tibial nerve SEPs in control subjects. All SCI patients with recordable SEPs (n = 11) showed similarly delayed onset of the cortical response. In contrast to the controls, nine of the 11 SCI patients showed an increase in amplitude of cortical SEPs. In three of these patients the increase in amplitude exceeded 100% of the precooling values. The cooling-induced changes in SEP amplitude and latency reversed on rewarming for both groups. The cooling-induced increases in cortical SEP amplitude support the a priori hypothesis that cooling would enhance central conduction in some SCI patients with conduction deficits due to focal demyelination.
引用
收藏
页码:730 / 741
页数:12
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共 56 条
[1]  
McDonald W.I., Mechanisms of functional loss and recovery in spinal cord damage: In: Ciba Foundation Symposium 34 (new series), Symposium on the Outcome of Severe Damage to the Central Nervous Sysiem, pp. 23-34, (1975)
[2]  
Wakefield C.L., Eidelberg E., Electron microscopic observations of the delayed effects of spinal cord compression, Exp Neusvl, 48, pp. 634-646, (1975)
[3]  
Yeo J.D., A review of experimental research in spinal cord injiiry, Parapleuea, 14, pp. 1-11, (1976)
[4]  
Young W., Yen V., Blight A., Extracellular calcium ionic activity in experimental spinal cord contusion, Brvin Rerearvh, 253, pp. 105-113, (1982)
[5]  
Dimitrijevic M.R., Residual motor functions in spinal cord injury, Advances in Neasolofy 47. Functional Recovery in Neusoloficap Diseure, (1988)
[6]  
Blight A.R., Cellular morphology of chronic spinal cord injury in the cat: Analysis of myelinated axons by line-sampling, Neusoseieach, 10, 2, pp. 521-646, (1973)
[7]  
Blight A.R., Axonal physiology of chronic spinal cord injury in the cat: Intracellular recording in vitro, Neusoseieach, 10, pp. 1961-1963, (1983)
[8]  
Blight A.R., Delayed demyelination and macrophage invasion: A candidate for secondary cell damage in spinal cord injury, Ceat Nervsysi Trouma, 1, pp. 299-314, (1973)
[9]  
Blight A.R., Young W., Central axons in injured cat spinal cord recover electrophysiological function following remyelination by Schwann cells, J Nut Sei, 91, pp. 19-64, (1973)
[10]  
Gledhill R.F., Harrison B.M., McDonald W.I., Demyelination and remyelination after acute spinal cord compression, Exp Neat, 38, pp. 465-663, (1975)