Presyncope caused by central hypovolaemia is not preceded by evoked potential alterations

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Abstract
The mechanism(s) responsible for the onset of presyncope during a central hypovolaemic challenge have gone undefined for many years. It has been speculated that a decrease in cerebral blood flow initiates presyncopal responses, which in turn lead to greater decreases in cerebral oxygen delivery and unconsciousness. Somatosensory evoked potentials (SEP) were monitored as a measure of cerebral functioning in ten subjects during presyncopal symptom limiting lower body negative pressure (a central hypovolaemic challenge). SEP latency and amplitudes have been correlated with cerebral oxygen uptake, so SEP activity can serve as an indirect indicator of cerebral homeostasis. SEPs were generated by electrically stimulating the median nerve and recoding the resulting potentials over the contralateral cerebral cortex. While heart rate and mean blood pressure both fell at presyncope, there were no changes noted in either SEP latency or amplitude at any point before (latency = 22.9 +/- 9 ms; amplitude = 2.86 +/- 0.24 microV), during (22.6 +/- 0.9 ms; 2.68 +/- 0.2 microV), or after (22.7 +/- 0.9 ms; 2.37 +/- 0.23 microV) the occurrence of presyncope. We conclude that the onset of presyncope is not associated with a decrease in cerebral function.