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Correspondence  |   October 1995
Carbon Dioxide Reactivity and Cerebral Ischemia: Is the Cortical Somatosensory Evoked Potential a Sensitive Detector of Cerebral Ischemia?
Author Notes
  • Michael E. Mahla, M.D., Associate Professor of Anesthesiology and Neurosurgery, Chief, Division of Neuroanesthesia Assistant Chairman for Education.
  • Cheri A. Sulek, M.D., Assistant Professor of Anesthesiology and Neurosurgery, Departments of Anesthesiology and Neurosurgery University of Florida College of Medicine P.O. Box 100254 Gainesville, Florida 32610-0254.
Article Information
Correspondence
Correspondence   |   October 1995
Carbon Dioxide Reactivity and Cerebral Ischemia: Is the Cortical Somatosensory Evoked Potential a Sensitive Detector of Cerebral Ischemia?
Anesthesiology 10 1995, Vol.83, 889-890.. doi:
Anesthesiology 10 1995, Vol.83, 889-890.. doi:
To the Editor:--Thiel et al. [1] attempted to establish a relationship between preoperative changes in cerebrovascular reactivity to carbon dioxide as determined by transcranial Doppler sonography and intraoperative changes in the cortical somatosensory evoked potential (SEP) waveforms. The authors concluded that, in patients with impaired carbon dioxide reactivity, the risk of cerebral ischemia, as assessed by intraoperative SEP recordings during carotid endarterectomy, was not increased. We are not sure, however, that the monitor used to detect cerebral ischemia is sensitive enough to warrant that conclusion. The investigators used cortical SEPs to monitor for cerebral ischemia based on the rationale that there is consensus that SEP monitoring is both highly sensitive and specific in detecting ischemia during carotid surgery. [2-4] In our opinion, that statement contains a bias according to the results of two other studies, [5,6] a laboratory study examining the threshold at which SEP changes during ischemia and a clinical study comparing SEP monitoring with electroencephalography (EEG) during carotid vascular surgery. The data from these studies suggest that SEP is less sensitive than EEG in detecting cortical cerebral ischemia. Nevertheless, data from humans do not show that one monitor is superior to the other in predicting clinically detectable postoperative neurologic deficit. Answering that question would require a very large study. In the absence of such a study, EEG monitoring is considered by many clinicians involved in neurologic monitoring, including us, to be more sensitive in detecting cerebral ischemia during carotid surgery. SEP monitoring likely misses mild ischemia, which might be reflected by EEG changes. Using continuous EEG as a monitor of ischemia would better test the primary hypothesis that preoperative loss of carbon dioxide reactivity predicts an increased risk of intraoperative cerebral ischemia. In our opinion, the authors can conclude only that, in patients with impaired carbon dioxide reactivity, the risk of severe cerebral ischemia is not increased during carotid crossclamping.
Michael E. Mahla, M.D., Associate Professor of Anesthesiology and Neurosurgery, Chief, Division of Neuroanesthesia Assistant Chairman for Education.
Cheri A. Sulek, M.D., Assistant Professor of Anesthesiology and Neurosurgery, Departments of Anesthesiology and Neurosurgery University of Florida College of Medicine P.O. Box 100254 Gainesville, Florida 32610-0254.
(Accepted for publication July 27, 1995.)
REFERENCES
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