Anesthesia and analgesia
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Anesthesia and analgesia · May 2003
Low baseline Bispectral Index of the electroencephalogram in patients with dementia.
The baseline value of the Bispectral Index (BIS) is 96-99 in the awake state. Patients with Alzheimer's disease or vascular dementia may show an increase in slow wave and a decrease in fast wave activity of the electroencephalogram (EEG). BIS is presumed to decrease with EEG slowing. We hypothesized that the baseline "awake" BIS is lower in dementia than in normal elderly patients. We studied 36 patients with Alzheimer's disease or multiinfarct dementia and 36 control patients aged >75 yr. Both groups were assessed with a Mini-Mental State Test. BIS (version 3.4) was recorded from a frontal derivation using an Aspect A-2000 EEG monitor. Off-line data analysis was also performed with the newer version 4.0 of the BIS algorithm. Fourteen of 36 (38%) dementia patients and 4 of 36 (11%) controls had mean baseline BIS 3.4 <93 (P = 0.006). Eighteen of 36 (50%) dementia patients and 8 of 36 (22%) controls had mean BIS 4.0 <93 (P = 0.026). Mean (95% confidence interval) BIS 3.4 was 92.9 (91-95) in the dementia and 96.1 (95-97) in the control group (P = 0.02). Values with BIS 4.0 were, respectively, 89.1 (86-92) and 94.7 (93-96) (P = 0.002). No significant difference was found in age, sex, activity from the electromyogram, and signal quality index. As expected, the difference in Mini-Mental State Test scores was significant (P < 0.0001). A significant proportion of patients with dementia shows a low baseline BIS. The utility of the BIS monitor in detecting dementia warrants further investigation. ⋯ This prospective, controlled, observational study demonstrates that electroencephalogram slowing associated with dementia affects the Bispectral Index of the electroencephalogram. A significant proportion of patients with dementia have a lower than normal "awake" Bispectral Index.
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Anesthesia and analgesia · May 2003
Mutation of KCNK5 or Kir3.2 potassium channels in mice does not change minimum alveolar anesthetic concentration.
Several reports suggest that clinically used concentrations of inhaled anesthetics can increase conductance through noninactivating potassium channels and that the resulting hyperpolarization might decrease excitability, thereby leading to the anesthetic state. We speculated that animals deficient in such potassium channels might be resistant to the effects of anesthetics. Thus, in the present study, we measured the minimum alveolar anesthetic concentration (MAC) needed to prevent movement in response to a noxious stimulus in 50% of adult mice lacking functional KCNK5 potassium channel subunits and compared these results with those for heterozygous and wild-type mice. We also measured MAC in weaver mice that had a mutation in the potassium channel Kir3.2 and compared the resulting values with those for wild-type mice. MAC values for desflurane, halothane, and isoflurane for KCNK5-deficient mice and isoflurane MAC values for weaver mice did not differ from MAC values found in control mice. Our results do not support the notion that these potassium channels mediate the capacity of inhaled anesthetics to produce immobility. In addition, we found that the weaver mice did not differ from control mice in their susceptibility to convulsions from the nonimmobilizers flurothyl [di-(2,2,2,-trifluoroethyl)ether] or 2N (1,2-dichlorohexafluorocyclobutane). ⋯ Mice harboring mutations in either of two different potassium channels have minimum alveolar anesthetic concentration (MAC) values that do not differ from MAC values found in control mice. Such findings do not support the notion that these potassium channels mediate the capacity of inhaled anesthetics to produce immobility in the face of noxious stimulation.
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Anesthesia and analgesia · May 2003
Halothane and isoflurane have additive minimum alveolar concentration (MAC) effects in rats.
Studies suggest that at concentrations surrounding MAC (the minimum alveolar concentration suppressing movement in 50% of subjects in response to noxious stimulation), halothane depresses dorsal horn neurons more than does isoflurane. Similarly, these anesthetics may differ in their effects on various receptors and ion channels that might be anesthetic targets. Both findings suggest that these anesthetics may have effects on movement in response to noxious stimulation that would differ from additivity, possibly producing synergism or even antagonism. We tested this possibility in 20 rats. MAC values for halothane and (separately) for isoflurane were determined in duplicate before and after testing the combination (also in duplicate; six determinations of MAC for each rat). The sum of the isoflurane and halothane MAC fractions for individual rats that produced immobility equaled 1.037 +/- 0.082 and did not differ significantly from a value of 1.00. That is, the combination of halothane and isoflurane produced immobility in response to tail clamp at concentrations consistent with simple additivity of the effects of the anesthetics. These results suggest that the immobility produced by inhaled anesthetics need not result from their capacity to suppress transmission through dorsal horn neurons. ⋯ Despite differences in their capacities to inhibit spinal dorsal horn cells, isoflurane and halothane are additive in their ability to suppress movement in response to a noxious stimulus.