[Increase in somatosensory evoked potentials during anesthesia induction with etomidate].
E. Kochs, Rolf‐Detlef Treede, J Schulte am Esch
Abstract
E. Kochs, Rolf‐Detlef Treede, J Schulte am Esch
Abstract
In 43 patients the time-dependent behaviour of somatosensory evoked potentials (SSEP) before and during induction of anesthesia with 0.3 mg/kg etomidate was studied. The SSEP components could be reliably recorded in one-minute intervals and the modulations of SSEP (early and middle latencies) following bolus injection with its pharmacokinetically non-stationary states could be quantified. The central conduction time (CCT) between the cervical N13- and the cortical N20-component was less prolonged (from 5.6 ms to 6.4 ms) than known from other anesthetics. Middle latency SSEP exhibited a more marked increase and were reduced in amplitude. All patients showed a 2- to 12-fold increase of the primary complex N20/P25 2-3 min after bolus injection. This amplification cannot be explained either by muscle artifacts nor exclusively by activation of muscle afferents. Myoclonia as a side effect of etomidate coincide with the increase of SSEP-components. The combination of myoclonia and SSEP-enhancement is known to be associated with the familial progressive myoclonus epilepsy. This observation therefore may indicate a cortical excitatory or disinhibitory effect, although no spike-wave complexes have been reported in the EEG after etomidate.
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In 43 patients the time-dependent behaviour of somatosensory evoked potentials (SSEP) before and during induction of anesthesia with 0.3 mg/kg etomidate was studied. The SSEP components could be reliably recorded in one-minute intervals and the modulations of SSEP (early and middle latencies) following bolus injection with its pharmacokinetically non-stationary states could be quantified. The central conduction time (CCT) between the cervical N13- and the cortical N20-component was less prolonged (from 5.6 ms to 6.4 ms) than known from other anesthetics. Middle latency SSEP exhibited a more marked increase and were reduced in amplitude. All patients showed a 2- to 12-fold increase of the primary complex N20/P25 2-3 min after bolus injection. This amplification cannot be explained either by muscle artifacts nor exclusively by activation of muscle afferents. Myoclonia as a side effect of etomidate coincide with the increase of SSEP-components. The combination of myoclonia and SSEP-enhancement is known to be associated with the familial progressive myoclonus epilepsy. This observation therefore may indicate a cortical excitatory or disinhibitory effect, although no spike-wave complexes have been reported in the EEG after etomidate.
Key concepts: Etomidate, Somatosensory evoked potential, Medicine, Anesthesia, Somatosensory system, Electroencephalography, Bolus (digestion), Internal medicine