Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2003
Clinical TrialChanges in consciousness, conceptual memory, and quantitative electroencephalographical measures during recovery from sevoflurane- and remifentanil-based anesthesia.
It is unclear whether opioid-induced changes in electroencephalogram (EEG) or auditory evoked potentials (AEPs) reliably correspond with consciousness. We examined the correlation between 1) the clinically assessed state of consciousness, 2) implicit and explicit memory (by use of word pairs), and 3) various measures of EEG and AEP-bispectral index (BIS), A-Line ARX AEP index, spectral entropy, and entropy of the singular value decomposition (SVDEN; a measure of the complexity of the EEG). We studied 21 women during a two-stage awakening (sevoflurane washout followed by remifentanil washout) after anesthesia for gynecological surgery. All were amnesic, and 19 were unresponsive to verbal command with remifentanil alone. In six patients, BIS decreased paradoxically as the remifentanil concentration decreased; this was caused by a low-amplitude EEG, which was misinterpreted by the Aspect algorithm as burst suppression. Most of the EEG/AEP variables were sensitive to the decrease in sevoflurane and the recovery of consciousness, but not to the effects of decreasing remifentanil concentrations. SVDEN was the only variable that demonstrated significant increases for both the sevoflurane and remifentanil washout phases. With the prediction probability statistic during remifentanil washout, SVDEN = 0.79, spectral entropy = 0.81, A-Line ARX AEP index = 0.63, and BIS = 0.58. Entropy measures appear to be worthy of further clinical evaluation in a larger series of patients. SVDEN may be a useful variable for assessing anesthetic and analgesic effects on the central nervous system. ⋯ During the recovery phase from a remifentanil-based anesthetic, the bispectral index is not reliably predictive of the depth of consciousness, because of suppression ratio artifacts. Entropy measures of the electroencephalogram show promise, but there is still no gold standard to estimate anesthetic depth.
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Anesthesia and analgesia · Mar 2003
GABA(A) receptor blockade antagonizes the immobilizing action of propofol but not ketamine or isoflurane in a dose-related manner.
The enhancing action of propofol on gamma-amino-n-butyric acid subtype A (GABA(A)) receptors purportedly underlies its anesthetic effects. However, a recent study found that a GABA(A) antagonist did not alter the capacity of propofol to depress the righting reflex. We examined whether the noncompetitive GABA(A) antagonist picrotoxin and the competitive GABA(A) antagonist gabazine affected a different anesthetic response, immobility in response to a noxious stimulus (a tail clamp in rats), produced by propofol. This effect was compared with that seen with ketamine and isoflurane. Picrotoxin increased the 50% effective dose (ED(50)) for propofol by approximately 379%; gabazine increased it by 362%, and both antagonists acted in a dose-related manner with no apparent ceiling effect (i.e., no limit). Picrotoxin maximally increased the ED(50) for ketamine by approximately 40%-50%, whereas gabazine increased it by 50%-60%. The isoflurane minimum alveolar anesthetic concentration increased by approximately 60% with the picrotoxin and 70% with the gabazine infusion. The ED(50) for propofol was also antagonized by strychnine, a non-GABAergic glycine receptor antagonist and convulsant, to determine whether excitation of the central nervous system by a non-GABAergic mechanism could account for the increases in propofol ED(50) observed. Because strychnine only increased the immobilizing ED(50) of propofol by approximately 50%, GABA(A) receptor antagonism accounted for the results seen with picrotoxin and gabazine. We conclude that GABA(A) antagonism can influence the ED(50) for immobility of propofol and the non-GABAergic anesthetic ketamine, although to a different degree, reflecting physiologic antagonism for ketamine (i.e., an indirect effect via a modulatory effect on the neural circuitry underlying immobility) versus physiologic and pharmacologic antagonism for propofol (i.e., a direct effect by antagonism of propofol's mechanism of action). This study also suggests that the immobilizing action of isoflurane probably does not involve the GABA(A) receptor because antagonism of GABA(A) receptors for animals anesthetized with isoflurane produces results quantitatively and qualitatively similar to ketamine and markedly different from propofol. ⋯ IV picrotoxin and gabazine antagonized the immobilizing action of propofol in a dose-related manner, whereas antagonism of the immobilizing action of ketamine and isoflurane was similar, smaller than for propofol, and not dose-related. These results are consistent with a role for gamma-amino-n-butyric acid subtype A receptors in mediating propofol anesthesia but not ketamine or isoflurane anesthesia.
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Anesthesia and analgesia · Mar 2003
Case ReportsCase series: IV regional anesthesia with ketorolac and lidocaine: is it effective for the management of complex regional pain syndrome 1 in children and adolescents?
We report our experience with ketorolac/lidocaine IV regional anesthesia (Bier block) (IVRA) in two adolescents with complex regional pain syndrome 1. IVRA resulted in complete resolution of symptoms.
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Anesthesia and analgesia · Mar 2003
The effects of intrathecal tramadol on spinal somatosensory-evoked potentials and motor-evoked responses in rats.
Tramadol has been proven to exert a local anesthetic-type effect on peripheral nerves in both clinical and laboratory studies. In this study, we evaluated the effects of tramadol on sensory and motor neural conduction when administered intrathecally in the rat. Tramadol (0, 1, or 2 mg) was administered through an intrathecal catheter. Spinal somatosensory-evoked potentials (SSEPs) were recorded at the thoracolumbar junction after stimulation of the sciatic nerve. An evoked compound muscle action potential (CMAP) was recorded in the intrinsic muscles of the foot in response to electric stimulation of the lower thoracic (T1213) interspinous space. Both SSEP and CMAP were obtained before drug application as the pretreatment baseline and at 5, 15, and 30 min after treatment, and at 30- or 60-min intervals thereafter for another 4.5 h. SSEP was averaged from 20 responses, whereas CMAP was obtained from a single stimulation. Reproducible SSEPs and CMAP were consistently recorded in all rats. Intrathecal tramadol dose-dependently reduced the amplitude and delayed the latency in both SSEPs and CMAP. Generally, the suppressive effects occurred immediately after injection and recovered over 2 h. Combined administration with 20 micro g of intrathecal naloxone did not attenuate the inhibition of spinal SSEPs. We conclude that intrathecal tramadol causes a dose-related suppressive effect on both sensory and motor neural conduction in the spinal cord. ⋯ Spinal somatosensory-evoked potentials and evoked compound muscle action potential were used to evaluate the effects of intrathecal tramadol on sensory and motor neural conduction. Intrathecal tramadol dose-dependently reduced the amplitude and delayed the latency of both spinal somatosensory-evoked potentials and compound muscle action potential. These results indicate that tramadol exerts a dose-related central neural blockade.