Abstract
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°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.
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Hayes, K., Hsieh, J., Potter, P. et al. Effects of induced hypothermia on somatosensory evoked potentials in patients with chronic spinal cord injury. Spinal Cord 31, 730–741 (1993). https://doi.org/10.1038/sc.1993.115
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DOI: https://doi.org/10.1038/sc.1993.115
