Propofol and sevoflurane in subanesthetic concentrations act preferentially on the spinal cord: evidence from multimodal electrophysiological assessment.
BACKGROUND
Animal experiments in recent years have shown that attenuation of motor responses by general anesthetics is mediated at least partly by spinal mechanisms. Less is known about the relative potency of anesthetic drugs in suppressing cortical and spinal electrophysiological responses in vivo in humans, particularly those, but not only those, connected with motor responses. Therefore, we studied the effects of sevoflurane and propofol in humans using multimodal electrophysiological assessment.


METHODS
We studied nine healthy volunteers in two sessions during steady state sedation with 0.5, 1.0, and 1.5 microg/l (targeted plasma concentration) propofol or 0.2 and 0.4 vol% (end-tidal) sevoflurane. Following a 15-min equilibration period, motor responses to transcranial magnetic stimulation and peripheral (H-reflex, F-wave) stimulation were recorded, while electroencephalography and auditory evoked responses were recorded in parallel.


RESULTS
At concentrations corresponding to two thirds of C(50 awake), motor responses to transcranial magnetic stimulation were reduced by approximately 50%, H-reflex amplitude was reduced by 22%, F-wave amplitude was reduced by 40%, and F-wave persistence was reduced by 25%. No significant differences between sevoflurane and propofol were found. At this concentration, the Bispectral Index was reduced by 7%, and the middle-latency auditory evoked responses were attenuated only mildly (N(b) latency increased by 11%, amplitude P(a)N(b) did not change). In contrast, the postauricular reflex was suppressed by 77%.


CONCLUSIONS
The large effect of both anesthetics on all spinal motor responses, compared with the small effect on electroencephalography and middle-latency auditory evoked responses, assuming that they represent cortical modulation, may suggest that the suppression of motor responses to transcranial magnetic stimulation is largely due to submesencephalic effects.
Kammer
Thomas
T
Department of Neurobiology, Max Planck Institute for Biological Cybernetics, Spemannstrasse 38, D-72076 Tuebingen, Germany. thomas.kammer@tuebingen.mpg.de
Rehberg
Benno
B
Menne
Dieter
D
Wartenberg
Hans-Christian
HC
Wenningmann
Ingobert
I
Urban
Bernd W
BW
D000328:Adult; D018685:Anesthetics, Inhalation / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004569:Electroencephalography / Q000187:drug effects*; D004594:Electrophysiology; D005072:Evoked Potentials, Auditory / Q000187:drug effects; D005260:Female; D006181:H-Reflex / Q000187:drug effects*; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008738:Methyl Ethers / Q000008:administration & dosage / Q000494:pharmacology*; D015742:Propofol / Q000008:administration & dosage / Q000494:pharmacology*; D000077149:Sevoflurane; D013116:Spinal Cord / Q000187:drug effects* / Q000502:physiology
D018685:Anesthetics, Inhalation; D008738:Methyl Ethers; D000077149:Sevoflurane; D015742:Propofol