Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatosensory evoked potentials (SEPs) following median nerve stimulation were recorded over Erb's point (N10), neck (N13) and scalp (N20) of 17 neurologically normal patients during hypothermic cardiopulmonary bypass. Anesthesia was induced with fentanyl and 100% oxygen, and supplemented with isoflurane as necessary. All 3 SEPs were recorded at esophageal temperatures (Te) of down to 19.5 degrees C. The central conduction time (CCT, defined as N20-N13 interpeak interval) increased exponentially with decreasing temperature (CCTTe = 1.066(37)-Te X CCT37; r = -0.96). The spinal conduction time (SCT, defined as N13-N10 interpeak interval) also increased exponentially but less steeply than the CCT (SCTTe = 1.047(37)-Te X SCT37; r = -0.89), and the N10 peak latency increased exponentially and least steeply (N10Te = 1.033(37)-Te. N10(37); r = -0.87). Anesthetic doses of fentanyl (75 micrograms/kg) did not affect the SEPs. Isoflurane (inspired concentration, 0.25-2.0%) produced dose-dependent increases in CCT of up to 13% and decreased N20 amplitude. All patients had normal CTs after rewarming and none suffered postoperative neurological deficits. Differences in slopes of the latency-temperature functions indicate that cooling produces more conduction slowing in central than in peripheral segments of the pathway and can be accounted for by estimates of the effects of cooling on synaptic delay and axonal conduction between wrist and cortex. The consistency of SEPs between patients both during stable hypothermia and when temperature was changing suggests their potential as a sensitive monitor of cerebral status during hypothermic cardiopulmonary bypass.
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PMID:Central and spinal somatosensory conduction times during hypothermic cardiopulmonary bypass and some observations on the effects of fentanyl and isoflurane anesthesia. 241 46

Median nerve somatosensory evoked potentials were recorded in 21 patients undergoing cardiac surgical procedures utilizing cardiopulmonary bypass, in order to establish the effects of hypothermia, reductions in mean arterial pressure, and alterations in cardiopulmonary bypass flows on evoked potential latency. Induction and maintenance of anesthesia with fentanyl caused a significant prolongation of latency of the first cortical peak. Temperature changes were linearly correlated with changes in latency for peaks recorded from Erb's point (r = -0.843, p less than 0.01) and the contralateral cortex (r = 0.843, p less than 0.01). There was no significant effect of mean arterial pressure or cardiopulmonary bypass flow reductions on latencies under the conditions of this study. Our results emphasize the importance of monitoring peripheral and first cortical peak latencies in evaluating somatosensory evoked potentials. It is suggested that peak latency prolongations beyond those predicted by temperature alterations may be indicative of hypoperfusion.
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PMID:The effect of temperature, mean arterial pressure, and cardiopulmonary bypass flows on somatosensory evoked potential latency in man. 242 87

Subcortical somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded serially in 35 patients during the evolution towards brain death and in brain death. Neuropathological alterations of the central nervous system down to the C1/C2 spinal cord segment in brain death are well known. SEP components supposed to be generated above this level should be lost in brain death, while components generated below should not be altered. Erb's point, scalp and neck potentials were recorded at C3/4, or over the spinous process C7, using an Fz reference. In 10 patients additional montages, including spinous process C2-Fz, a non-cephalic reference (Fz-contralateral shoulder) and a posterior to anterior neck montage (spinous process C7-jugulum) were used. The cephalic referenced N9 and N11 peaks remained unchanged until brain death. N9 and N11 decreased in parallel in amplitude and increased in latency after systemic effects like hypoxia or hypothermia occurred. The cephalic referenced 'N14' decreased in amplitude and increased in latency after the clinical brain death syndrome was observed, while N13 in the posterior to anterior neck montage remained unchanged. The alteration of 'N14' went parallel to the decrease of the P14 amplitude. The subcortical SEPs in the cephalic referenced lead are supposed to be a peak composed by a horizontally orientated dorsal horn generated N13 and a rostrally orientated P14 arising at the level of the foramen magnum. The deterioration of the non-cephalic referenced P14 and of its cephalic referenced reflection 'N14' seems to provide an additional objective criterion for the diagnosis of brain death.
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PMID:Serial recording of median nerve stimulated subcortical somatosensory evoked potentials (SEPs) in developing brain death. 244 17

Somatosensory evoked potentials recorded over Erb's point and the cervical spine (at C2 and C7) were studied in a series of children undergoing cardiopulmonary bypass surgery with hypothermia alone (n = 15) or profound hypothermia and complete circulatory arrest (n = 15). A bifid response was recorded at normothermia or mild degrees of hypothermia at both C7 (N12a, N13a) and C2 (N12b, N13b). The differential responses of these components to profound hypothermia and ischaemia suggest that N12a and N12b represent components of the same dorsal root/dorsal column travelling wave, while N13a and N13b reflect postsynaptic activities which are thought to be generated at the dorsal horn and cuneate nucleus, respectively.
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PMID:The effects of profound hypothermia on the cervical SEP in humans: evidence of dual generators. 258 58

The surgical repair of ascending aorta aneurysms can only be carried out under total circulatory arrest, and is consequently to be performed under deep hypothermia, in order to adequately decrease the metabolic requirements of the brain. However, the optimal temperature to be reached is poorly known. SEPs to median nerve stimulation were recorded in 21 operations performed in 20 patients undergoing profound hypothermia. The latencies of all SEP components increase to 21 degrees C. Waves N20 and P14 disappear at mean naso-pharyngeal temperatures of 20 degrees C and 17 degrees C, respectively, although a wide inter-individual variability was observed. We suggest to use the P14 disappearance as the criterion to perform the circulatory arrest: in fact, all surviving patients in whom this criterion was fulfilled recovered without any detectable neurological sequellae, while three patients in whom brain activities disappeared independently on body temperature presented with neurological sequellae. Moreover, particularly if patients presenting with ischemia-induced disappearance of Erb's point activities were excluded, we found a significant correlation between the duration of the circulatory arrest and the delay of N20 and P14 reappearance on rewarming. This confirms the importance of sufficient hypothermia, on the one hand; and on the other hand, our findings imply that, even if SEP monitoring considerably decreases the risk of neurological sequellae associated with these operations, the duration of the circulatory arrest should be reduced as far as possible.
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PMID:[Somatosensory evoked potentials in patients undergoing circulatory arrest under profound hypothermia]. 832 30