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G Plourde

Publications and source records attributed to G Plourde.

At least 19 recordsLinked to original sources

Auditory evoked potentials.

This chapter will focus on the two auditory evoked potentials (AEP) most commonly used to assess the effects of general anesthetics on the brain, the auditory middle latency response (AMLR) and the 40 Hz auditory steady-state response (40 Hz-ASSR). We will review their physiological basis, the recording methodology, the effects of general anesthetics, their ability to track changes in level of consciousness and their clinical applications. Because of space constraints, this review will be limited to human studies.

Anesthesia, General↗

Antagonism of sevoflurane anaesthesia by physostigmine: effects on the auditory steady-state response and bispectral index.

BACKGROUND: Physostigmine, a centrally acting anticholinesterase, antagonizes the hypnotic effect of propofol, as shown by the return of consciousness (response to commands) or wakefulness (spontaneous eye-opening without response to commands) and by recovery of auditory evoked potentials (40 Hz auditory steady-state response (ASSR)) and the bispectral index (BIS). We measured the effects of physostigmine on the hypnotic effect of inhaled volatile anaesthetics, using sevoflurane as the representative agent. METHODS: Eight healthy volunteers received sevoflurane adjusted to produce loss of consciousness. Physostigmine (plus glycopyrrolate) was given while the end-tidal concentration of sevoflurane was kept constant. RESULTS: Loss of consciousness was accompanied by a significant (P<0.02) decrease in ASSR amplitude (to 21% of awake value) and BIS (to 70% of awake value). Five subjects had return of consciousness or wakefulness after physostigmine. The others showed no behavioural change. Physostigmine caused a significant increase of the mean ASSR amplitude from 0.11 (SD 0.04) to 0.17 (0.06) microV (P<0.05). The BIS also increased, from 66 (12) to 74 (12), but the difference was not significant. CONCLUSIONS: Physostigmine can antagonize, at least partially, the hypnotic effect of sevoflurane and changes in arousal after physostigmine are shown by ASSR measurements. However, the antagonism is not as clear or reliable as with propofol.

Adolescent↗

Propofol anesthesia and cerebral blood flow changes elicited by vibrotactile stimulation: a positron emission tomography study.

We investigated the effects of the general anesthetic agent propofol on cerebral structures involved in the processing of vibrotactile information. Using positron emission tomography (PET) and the H(2)(15)O bolus technique, we measured regional distribution of cerebral blood flow (CBF) in eight healthy human volunteers. They were scanned under five different levels of propofol anesthesia. Using a computer-controlled infusion, the following plasma levels of propofol were targeted: Level W (Waking, 0 microg/ml), Level 1 (0.5 microg/ml), Level 2 (1.5 microg/ml), Level 3 (3.5 microg/ml), and Level R (Recovery). At each level of anesthesia, two 3-min scans were acquired with vibrotactile stimulation of the right forearm either on or off. The level of consciousness was evaluated before each scan by the response of the subject to a verbal command. At Level W, all volunteers were fully awake. They reported being slightly drowsy at Level 1, they had a slurred speech and slow response at Level 2, and they were not responding at all at Level 3. The following variations in regional CBF (rCBF) were observed. During the waking state (Level W), vibrotactile stimulation induced a significant rCBF increase in the left thalamus and in several cortical regions, including the left primary somatosensory cortex and the left and right secondary somatosensory cortex. During anesthesia, propofol reduced in a dose-dependent manner rCBF in the thalamus as well as in a number of visual, parietal, and prefrontal cortical regions. At Level 1 through 3, propofol also suppressed vibration-induced increases in rCBF in the primary and secondary somatosensory cortex, whereas the thalamic rCBF response was abolished only at Level 3, when volunteers lost consciousness. We conclude that propofol interferes with the processing of vibrotactile information first at the level of the cortex before attenuating its transfer through the thalamus.

Adolescent↗

Auditory steady-state response and bispectral index for assessing level of consciousness during propofol sedation and hypnosis.

UNLABELLED: We assessed the effect of propofol on the auditory steady-state response (ASSR), bispectral (BIS) index, and level of consciousness in two experiments. In Experiment 1, propofol was infused in 11 subjects to obtain effect-site concentrations of 1, 2, 3, and 4 microg/mL. The ASSR and BIS index were recorded during baseline and at each concentration. The ASSR was evoked by monaural stimuli. Propofol caused a concentration-dependent decrease of the ASSR and BIS index values (r(2) = 0.76 and 0.93, respectively; P<0.0001). The prediction probability for loss of consciousness was 0.89, 0.96, and 0.94 for ASSR, BIS, and arterial blood concentration of propofol, respectively. In Experiment 2, we compared the effects of binaural versus monaural stimulus delivery on the ASSR in six subjects during awake baseline and propofol-induced unconsciousness. During baseline, the ASSR amplitude with binaural stimulation (0.47+/-0.13 microV, mean +/- SD) was significantly (P<0.002) larger than with monaural stimulation (0.35+/-0.11 microV). During unconsciousness, the amplitude was 0.09+/-0.09 microV with monaural and 0.06+/-0.04 microV with binaural stimulation (NS). The prediction probability for loss of consciousness was 0.97 (0.04 SE) for monaural and 1.00 (0.00 SE) for binaural delivery. We conclude that the ASSR and BIS index are attenuated in a concentration-dependent manner by propofol and provide a useful measure of its sedative and hypnotic effect. BIS was easier to use and slightly more sensitive. The ASSR should be recorded with binaural stimulation. The ASSR and BIS index are both useful for assessing the level of consciousness during sedation and hypnosis with propofol. However, the BIS index was simpler to use and provided a more sensitive measure of sedation. IMPLICATIONS: We have compared two methods for predicting whether the amount of propofol given to a human subject is sufficient to cause unconsciousness, defined as failure to respond to a simple verbal command. The two methods studied are the auditory steady-state response, which measures the electrical response of the brain to sound, and the bispectral index, which is a number derived from the electroencephalogram. The results showed that both methods are very good predictors of the level of consciousness; however, bispectral was easier to use.

Adolescent↗

Physostigmine reverses propofol-induced unconsciousness and attenuation of the auditory steady state response and bispectral index in human volunteers.

BACKGROUND: It is postulated that alteration of central cholinergic transmission plays an important role in the mechanism by which anesthetics produce unconsciousness. The authors investigated the effect of altering central cholinergic transmission, by physostigmine and scopolamine, on unconsciousness produced by propofol. METHODS: Propofol was administered to American Society of Anesthesiologists physical status 1 (n = 17) volunteers with use of a computer-controlled infusion pump at increasing concentrations until unconsciousness resulted (inability to respond to verbal commands, abolition of spontaneous movement). Central nervous system function was assessed by use of the Auditory Steady State Response (ASSR) and Bispectral Index (BIS) analysis of electrooculogram. During continuous administration of propofol, reversal of unconsciousness produced by physostigmine (28 microgram/kg) and block of this reversal by scopolamine (8.6 microgram/kg) were evaluated. RESULTS: Propofol produced unconsciousness at a plasma concentration of 3.2 +/- 0.8 (+/- SD) microgram/ml (n = 17). Unconsciousness was associated with reductions in ASSR (0.10 +/- 0.08 microV [awake baseline 0.32 +/- 0.18 microV], P < 0.001) and BIS (55.7 +/- 8.8 [awake baseline 92.4 +/- 3.9], P < 0.001). Physostigmine restored consciousness in 9 of 11 subjects, with concomitant increases in ASSR (0.38 +/- 0.17 microV, P < 0.01) and BIS (75.3 +/- 8.3, P < 0.001). In all subjects (n = 6) scopolamine blocked the physostigmine-induced reversal of unconsciousness and the increase of the ASSR and BIS (ASSR and BIS during propofol-induced unconsciousness: 0.09 +/- 0.09 microV and 58.2 +/- 7.5, respectively; ASSR and BIS after physostigmine administration: 0.08 +/- 0.06 microV and 56.8 +/- 6.7, respectively, NS). CONCLUSIONS: These findings suggest that the unconsciousness produced by propofol is mediated at least in part via interruption of central cholinergic muscarinic transmission.

Adolescent↗

Treating obesity. Lost cause or new opportunity?

OBJECTIVE: To review therapies for treating obese patients. QUALITY OF EVIDENCE: Advice in this paper is based mainly on the results of randomized controlled trials. Some data from smaller, more physiologic studies are included. When appropriate, advice is based on consensus. MAIN MESSAGE: Recent medical evidence indicates that a modest weight loss (5% to 10%) can alleviate symptoms of obesity-related comorbidity. Treatment of obesity should be comprehensive and integrated into a multi-component approach and should involve both patients and their families. The main challenge of obesity is maintaining a reduced weight. CONCLUSION: A multi-component approach to treating obesity can help make treatment less frustrating and more rewarding for patients and physicians.

Anti-Obesity Agents↗

Brain mechanisms of propofol-induced loss of consciousness in humans: a positron emission tomographic study.

In the present study, we used positron emission tomography to investigate changes in regional cerebral blood flow (rCBF) during a general anesthetic infusion set to produce a gradual transition from the awake state to unconsciousness. Five right-handed human volunteers participated in the study. They were given propofol with a computer-controlled infusion pump to achieve three stable levels of plasma concentrations corresponding to mild sedation, deep sedation, and unconsciousness, the latter defined as unresponsiveness to verbal commands. During awake baseline and each of the three levels of sedation, two scans were acquired after injection of an H215O bolus. Global as well as regional CBF were determined and correlated with propofol concentrations. In addition, blood flow changes in the thalamus were correlated with those of the entire scanned volume to determine areas of coordinated changes. In addition to a generalized decrease in global CBF, large regional decreases in CBF occurred bilaterally in the medial thalamus, the cuneus and precuneus, and the posterior cingulate, orbitofrontal, and right angular gyri. Furthermore, a significant covariation between the thalamic and midbrain blood flow changes was observed, suggesting a close functional relationship between the two structures. We suggest that, at the concentrations attained, propofol preferentially decreases rCBF in brain regions previously implicated in the regulation of arousal, performance of associative functions, and autonomic control. Our data support the hypothesis that anesthetics induce behavioral changes via a preferential, concentration-dependent effect on specific neuronal networks rather than through a nonspecific, generalized effect on the brain.

Adult↗

40 Hz auditory steady-state response and EEG spectral edge frequency during sufentanil anaesthesia.

PURPOSE: The auditory steady-state evoked response (ASSR) is an evoked potential which provides a sensitive measure of the effects of general anaesthetics on the brain. We used pharmacokinetic-pharmacodynamic (PK-PD) modelling to compare the effects of sufentanil on the amplitude of the ASSR with its effect on spectral edge frequency (SEF) of the electroencephalogram. METHODS: Nine patients scheduled for elective cardiac surgery participated. Midazolam (70 micrograms.kg-1 i.m.) was given 60 min before entering the operating room. Anaesthesia was induced with 5 micrograms.kg-1 sufentanil at a rate of 0.83 microgram.kg-1.min-1. The ASSR, SEF and plasma sufentanil concentrations were measured for 30 min after induction of anaesthesia before surgery. The half-life between the central and effect site compartments (t1/2Keo), the 50% inhibitory concentration (IC50) and the slope factor (gamma) were computed. RESULTS: The amplitude of the ASSR increased during the first three minutes of infusion of sufentanil by up to 40%. This was followed by a rapid decrease between the fourth and fifth minutes to 16% of baseline. The SEF decreased progressively during the first five minutes of infusion to 18% of baseline. Both measures subsequently showed modest recovery. The parameters gamma, IC50 and t1/2Keo for ASSR were (mean +/- SD) 6.0 +/- 3.7, 2.1 +/- 1.2 ng.ml-1 and 7.3 +/- 2.4 min. For SEF the values were 5.9 +/- 5.2, 1.4 +/- 0.7 ng.ml-1 (P < 0.05 compared with ASSR) and 6.8 +/- 2.4 min. CONCLUSION: The sensitivity of ASSR to sufentanil is less than that of the SEF.

Acoustic Stimulation↗

Effect of isoflurane on the auditory steady-state response and on consciousness in human volunteers.

BACKGROUND: The auditory steady state response (ASSR) is a sustained electrical response of the brain to auditory stimuli delivered at fast rates (30-50 responses/s). The aim of this study was to evaluate the effect of 0.26-0.50% isoflurane on the ASSR and on consciousness, defined as responsiveness to verbal commands. METHODS: Ten volunteers (21-31 yr) participated. Isoflurane was administered at three stable, end-tidal concentrations: 0.26%, 0.38%, and 0.50%. The ASSR in response to 18,000 stimuli (500-Hz tonebursts, 10 ms, 82-dB, the right ear, 35-45 bursts/s) was recorded from the vertex with reference to the right mastoid. Recordings were made during baseline, at each isoflurane concentration, and during recovery. RESULTS: The mean (SD) ASSR amplitudes were 0.32 (0.23) microV during baseline, 0.24 (0.17) microV during 0.26% isoflurane, 0.09 (0.05) microV during 0.38% isoflurane, 0.04 (0.03) microV during 0.50% isoflurane, and 0.29 (0.33) microV during recovery. The amplitude during baseline and recovery was larger than during 0.38% and 0.50% isoflurane (P < 0.001). The amplitude at 0.26% was larger than at the other concentrations (P < 0.025). The logarithm of the ASSR amplitude was related linearly to the concentration of isoflurane (r = 0.85; P < 0.0001). The prediction probability (Pk) for loss of consciousness was 0.95 for both ASSR and measured isoflurane concentration. An ASSR amplitude < 0.07 microV was always associated with unconsciousness. CONCLUSIONS: The ASSR is attenuated in a concentration-dependent manner by isoflurane. Suppression of consciousness and maximal attenuation of ASSR occur in the same isoflurane concentration range. Profound attenuation of ASSR appears to reflect unconsciousness, defined as unresponsiveness to verbal commands.

Acoustic Stimulation↗

Temperature during cardiopulmonary bypass for coronary artery operations does not influence postoperative cognitive function: a prospective, randomized trial.

OBJECTIVE: The objective was to examine the effect of temperature (28 degrees vs 36 degrees C) during cardiopulmonary bypass on postoperative cognitive functions in a prospective, double-blind, and randomized manner. METHODS: Sixty-two patients scheduled for coronary operations were randomized to warm or cold cardiopulmonary bypass. Preoperative and postoperative (7 days) neuropsychologic evaluations were performed by an observer unaware of cardiopulmonary bypass temperature. RESULTS: Fifty-four patients completed the study (cold bypass, n = 24; warm bypass, n = 30). Significant (p < 0.01) postoperative deterioration for tests of psychomotor coordination and verbal memory was noted in both warm and cold groups, but no differences were observed between groups. CONCLUSION: Temperature during cardiopulmonary bypass for coronary operations does not influence postoperative cognitive function.

Adult↗

Ketamine increases the amplitude of the 40-Hz auditory steady-state response in humans.

The auditory middle latency response (AMLR) and the 40-Hz auditory steady-state response (40-Hz ASSR) are evoked potentials which possibly arise from the same generators in the primary auditory cortex. Both responses are attenuated by most general anaesthetics. Ketamine, however, has been reported to have no effect on the AMLR. Our aim was to evaluate the effects of ketamine on the 40-Hz ASSR. Spectral analysis of the electroencephalogram (EEG) was also conducted to independently examine the effects of ketamine. Ketamine 1.5 mg kg-1 was given to 12 patients for induction of general anaesthesia. Recordings of the 40-Hz ASSR and EEG were obtained every minute from 3 min before administration of ketamine to 5 min after injection, when the study was terminated. Similar recordings were obtained in three control subjects under identical conditions except that no medication was administered. Consciousness, defined as responsiveness to verbal commands, was assessed before each recording. Ketamine caused an increase in the amplitude of the 40-Hz ASSR (P < 0.01). Using published AMLR data, we conducted a simulation experiment that suggested that the effect of ketamine on the AMLR can explain its effects on the amplitude of the 40-Hz ASSR. There was a pronounced increase in relative theta (3.9-7.9 Hz) EEG power and a decrease in relative alpha (8.0-12.8 Hz) power (P < 0.001). These changes were not observed in the control group. Ketamine produced unconsciousness until the end of the study in five patients and transient unconsciousness in five patients. Two patients did not lose consciousness after administration of ketamine. The 40-Hz ASSR and EEG revealed no consistent differences between conscious and unconscious patients. No relationship could be demonstrated between the increase in amplitude of the 40-Hz ASSR or of relative theta power (the hallmark of ketamine effect) and loss of responsiveness to commands. We conclude that ketamine, unlike other anaesthetics, increases the amplitude of the 40-Hz ASSR.

Acoustic Stimulation↗

The role of radiologic methods in assessing body composition and related metabolic parameters.

The measurement of body composition and related metabolic parameters has become an important issue in clinical nutrition. Numerous techniques to assess visceral fat, which is strongly associated with metabolic disorders, have been developed. Other techniques focus mainly on the measurement of specific body components related to metabolic disturbances. This paper reviews methods that directly assess body composition and associated metabolic parameters. The principles of these methods and their accuracy, reproducibility and safety, as well as the clinical implications of their use, are discussed. Recent studies have documented the safety and efficacy of radiologic methods of assessing visceral fat, muscle mass, and morphology to obtain body composition data related to metabolic disturbances. Because these techniques have been documented to be safe and effective, clinicians should consider using them in the evaluation and follow-up of patients with various conditions.

Absorptiometry, Photon↗

Unintentional intraoperative awareness during sufentanil anaesthesia for cardiac surgery.

PURPOSE: The aim of this clinical report is to describe a case of unintentional intraoperative awareness during sufentanil anaesthesia in a patient undergoing elective aortocoronary bypass grafting. CLINICAL FINDINGS: After premedication with morphine (5 mg) and scopolamine (0.2 mg), this 51-yr-old woman received sufentanil (10 micrograms.kg-1), midazolam (4 mg) and isoflurane (0.3-0.4% end-tidal). The patient recalled specific events and discussions which took place in the operating room during surgery. This patient's report was clear and corroborated by operating room personnel. The patient denied having felt pain, anxiety or emotional distress. CONCLUSION: Although awareness during opioid anaesthesia has been previously described with morphine and fentanyl, as far as we know this is the first clinical report of awareness with sufentanil. Given that recent efforts of early extubation in cardiac surgery patients may involve a reduction in the amount of opioid administered, this report serves as a reminder of the ever present potential for this disturbing complication.

Anesthesia, General↗

Comparison of the effects of enflurane/N2O on the 40-Hz auditory steady-state response versus the auditory middle-latency response.

The auditory middle-latency response (AMLR) is a sequence of negative-positive waves occurring 12-50 ms after the onset of an auditory stimulus presented at rates of 10/s or less. When the rate of stimulus presentation is increased to approximately 40/s, overlapping of the AM-LRs results in a sustained, nearly sinusoidal wave, called the "40-Hz auditory steady-state response" (40-Hz ASSR). The AMLR and 40-Hz ASSR have been used to study the effects of general anesthetics on the brain. The primary aim of this investigation was to determine whether the effects of a general anesthetic, namely enflurane, on the 40-Hz ASSR can be predicted from its effects on the AMLR. A secondary aim was to examine the relationship between the level of consciousness and the 40-Hz ASSR during emergence from anesthesia. Twelve ASA class I-II women undergoing reduction mammoplasty were tested. Anesthesia was induced with fentanyl (3 micrograms/kg) and thiopental (3-5 mg/kg) intravenously and was maintained with enflurane (0.5%, 0.8%, or 1.1% end-tidal; four patients per concentration; random assignment) in N2O (66% end-tidal), along with fentanyl (1 microgram/kg as needed). The 40-Hz ASSR and AMLR were recorded before induction and during anesthesia and surgery. The 40-Hz ASSR was also recorded during emergence. The amplitude of the 40-Hz ASSR was reduced profoundly during anesthesia and surgery (P < 0.001). The attenuation was not dose-dependent, and was much more pronounced than predicted by the effects of enflurane on the AMLR. The 40-Hz ASSR during anesthesia was surprisingly large (0.09 and 0.11 microV) in two patients, both of the 1.1% enflurane group. The regaining of the ability to follow verbal commands was associated with a significant (P < 0.001) increase in the amplitude of the 40-Hz ASSR. We conclude that, although auditory neurons remain capable of responding at a slow stimulus rate during enflurane-N2O anesthesia, their ability to be driven at a faster stimulus rate is markedly curtailed. The 40-Hz ASSR may be useful for detecting unintentional intraoperative awareness because the return of consciousness is associated with a clear increase in amplitude.

Adjuvants, Anesthesia↗