Facial muscles: a window to unconsciousness.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H L Edmonds.
Explore the source record for details and available documents.
We evaluated computerized quantitative electroencephalography for the intraoperative detection of cerebral dysfunction. The quantitative electroencephalogram was recorded continuously during 96 myocardial revascularizations involving hypothermic cardiopulmonary bypass using Cerebrovascular Intraoperative MONitor (CIMON) software. CIMON relies on an adaptive statistical approach to detect subtle, but clinically relevant, changes in electroencephalographic activity indicative of cerebrocortical dysfunction. Relative (percent of total) low-frequency (1.5 to 3.5 Hz) power was chosen as the single quantitative electroencephalographic descriptor because it is an established hallmark of cortical dysfunction and is surprisingly insensitive to moderate changes in body temperature and level of opioid anesthesia. Reference values for this measure were established for each patient after anesthetic induction before sternotomy. The large sample variance often seen in low-frequency power was dramatically decreased by using log-transformed data and allowing each patient to serve as his own control. Quantitative electroencephalographic changes in standard deviation units or z-scores were determined from the individualized reference self-norm. Prolonged (greater than 5 minutes) and statistically significant (greater than 3 standard deviation) focal increases in relative low-frequency power were temperature-corrected to determine a standardized cerebrocortical dysfunction time at 37 degrees C. (CDT37). In phase I (n = 48), this objective quantitative electroencephalogram-based numeric descriptor was used to predict neuropsychologic outcome. These CDT37 greater than 5-minute episodes occurred 38 times in 19 patients. The quantitative electroencephalogram-based descriptor predicted the occurrence of such disorientation (n = 14 or 29%) with a 68% false positive rate but only an 8% false negative rate. Since these intraoperative quantitative electroencephalographic episodes were often (19/38) associated with low (less than 50 mm Hg) pump pressures, phase II (n = 48) sought to correct the quantitative electroencephalographic abnormality and prevent postoperative disorientation by appropriate increases in cerebral perfusion. Although the number of episodes of quantitative electroencephalographic abnormality was similar (n = 31) in phase II, these ischemic events disappeared after prompt elevation of perfusion pressure. The phase II disorientation rate fell significantly (p less than 0.002) to 4%. Thus statistically significant increases in low-frequency electroencephalographic relative power persisting for a temperature-corrected duration of 5 minutes or more are a reliable means of alerting the surgical/anesthesia team to the presence of cerebrocortical dysfunction and provide a rational and objective basis for corrective intervention. This form of electroencephalographic monitoring appears to offer an opportunity for the timely correction of perfusion abnormalities or the administration of cerebroprotectant compounds.
Determination of defibrillation thresholds (DFTs) and implantable cardioverter defibrillator (ICD) testing requires repeated inductions of ventricular fibrillation (VF) and defibrillation attempts using known energy outputs. Little is known about the individual and cumulative effects of repetitive brief episodes of VF and hypoperfusion on cerebral function. The potential clinical utility of quantitative electroencephalographic (QEEG) monitoring during intraoperative ICD testing, by using processed 19-channel EEG (0.5-35 Hz bandwidth), was examined in ten anesthetized patients, five males and five females (mean age 62 +/- 10 years), who underwent ICD implantation and testing. Ischemic QEEG patterns were defined as those with a 3 standard deviation increase (P less than 0.01) in absolute delta (1.5-3.5 Hz) power persisting for greater than or equal to 2.5 minutes. The majority (80%) of the VF episodes (70) were accompanied by QEEG "slowing" (doubling of the pre-VF low frequency delta waves amplitude). All the patients (5/5) experiencing greater than 6 VF episodes showed a statistically significant increase in the low frequency amplitude. In contrast, this EEG abnormality was apparent in only one of five patients experiencing less than 6 VF episodes. These results suggest a cumulative QEEG depression associated with ICD testing. QEEG may provide an objective means for establishing an individualized upper safe limit of DFT testing and the total number of induced VF episodes.
Transcranial magnetic motor evoked potentials (tcMMEP) were used to assess the functional integrity of the descending motor pathways. The tcMMEP, recorded bilaterally from anterior tibialis muscles, were evoked by an electric current induced in the motor cortex by a high-intensity transient magnetic field applied to the scalp surface. Potentials were recorded from ten of 12 volunteer subjects and preoperatively in 11 of 11 scoliotic patients. Group mean latency in the volunteers (32.0 +/- 2.1 msec) did not differ from that of the scoliotics (28.6 +/- 5.0 msec), but values in the latter group were more variable. During nitrous oxide-narcotic anesthesia, tcMMEP with reproducible latencies were obtained in 9 of 11 (82%) cases. A small, but statistically significant, increase in latency occurred during anesthesia. Compared with preoperative values (523 +/- 490 microV), individual tcMMEP amplitudes were significantly decreased intraoperatively (163 +/- 153 microV). Although the absolute amplitudes varied widely, the minimum recorded value was over 20 microV. Thus, intraoperative tcMMEP waveforms were readily discriminable from background electrical noise. These results demonstrate the technical feasibility of intraoperative tcMMEP monitoring. Combined somatosensory evoked potential and tcMMEP monitoring may provide a more complete picture of spinal cord function, intraoperatively.
We compared changes in biopotentials arising from upper facial (FEMG) and abdominal (AEMG) muscles associated with alterations in alveolar enflurane concentration and neuromuscular block. Induction of anaesthesia significantly reduced both FEMG and AEMG mean amplitudes (-60% and -43%, respectively). Neuromuscular blocker-induced abolition of the electrically evoked thenar EMG response did not prevent FEMG and/or AEMG activation during endotracheal intubation. Decreasing the alveolar enflurane concentration was associated with an increase in FEMG amplitude prior to visible signs of arousal in half of the patients. Movement and other signs of inadequate anaesthesia were associated with distinct increases in FEMG amplitude in 29 out of 30 patients. Recovery from neuromuscular block during unchanged alveolar enflurane concentration was associated with increasing amplitudes of both FEMG and AEMG. Finally, very low-amplitude FEMG recordings were always associated with relaxed abdominal muscles.
Facial and hand muscles are used frequently for monitoring neuromuscular blockade. Therefore, we compared changes in electrically evoked muscle potential magnitude in upper facial and hypothenar muscles after fixed doses of neuromuscular blockers (succinylcholine, 750 micrograms/kg; pancuronium, 70 micrograms/kg; vecuronium, 50 micrograms/kg; and atracurium, 300 micrograms/kg). Face-hand comparisons were made in both anesthetized (nitrous oxide/narcotic, n = 51) and comatose (closed-head injuries, n = 5) patients. In 24 anesthetized patients, complete blockade of the hypothenar muscles prevented quantitative comparison. In the remaining 27 patients, the relaxant effect (as determined by the percentage change from prerelaxant baseline muscle potentials) was significantly smaller (P less than 0.0001) in the upper facial muscles (65 +/- 24% versus 92 +/- 8%, mean +/- SD). All four evoked muscle responses to train-of-four stimulation were detectable in upper facial muscles of the 19 patients receiving non-depolarizing neuromuscular blocking drugs; this pattern was seen in hand muscles of only 7 patients (P less than 0.001). The neuromuscular blockade in both the hand (49 +/- 54%) and the upper facial area (68 +/- 28%, P greater than 0.05) of comatose patients was smaller and more variable than that seen during anesthesia. These results illustrate the value of quantitative monitoring of neuromuscular function, especially during highly variable and unpredictable drug-induced blockade in the comatose state. We conclude that during narcotic-based anesthesia the upper facial and hand muscles are differentially sensitive to commonly used neuromuscular blockers.
1. Activity of the mimetic muscles of the upper face were recorded from awake and anesthetized patients by surface electromyography (SEMG). 2. High amplitude SEMG accompanied ketamine anesthesia and/or the presentation of pain-provoking stimuli. 3. During periods of elevated facial muscle activity, fentanyl or butorphanol decreased SEMG amplitude. 4. The opioid-induced SEMG depression was not consistently associated with either lowered vigilance or analgesia but did provide an objective measure of drug effect.
In vitro brain slices are the preparation of choice for the detailed examination of local circuit properties in mammalian brain. However it is the investigator's responsibility to verify that the circuits under investigation are indeed confined within the boundaries of the functional region of the slice used. The medium in which the slice is maintained is under the full control of the investigator. This places the burden on the investigator to ensure that: (1) the properties of the medium are fully under control; (2) the effects of the medium on the slice are known; (3) the conditions under which the slice is being maintained bear some reasonable relation to those it enjoys (or endures) in vivo. Generalizations to in vivo conditions must be made with caution. If at all possible, similar studies (perhaps less extensive, due to the greater technical difficulties) should be done in vivo to provide a basis for comparison. Investigators using drugs should be aware of, and respect, the basic pharmacological principles cited in the text. In particular, the substantial freedom the investigator has in defining the extracellular medium should not be abused.
Explore the source record for details and available documents.
The interest in the possibility of cerebral resuscitation has been growing exponentially during the last decade. It became clear that pharmacotherapeutic interaction can possibly alter the outcome of cerebral hypoxia/ischemia. The present review is an attempt to provide an organizational framework for a systematic integration of studies specifically dealing with pharmacological treatment post-insult.
A dual linear-flow chamber for comparative studies using brain slices is described. Electrophysiological and ultrastructural analysis of rat hippocampal slices incubated in the chamber showed that its two compartments allows performance of reliable paired comparison studies in a highly efficient manner.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Studies were conducted on a colony of purebred beagle dogs. Animals with spontaneous seizures were classed as epileptic beagles (EB). Those without spontaneous seizures were termed nonepileptic beagles (NEB). The median convulsant current for maximal electroshock seizure (MES) threshold was 175(194-158)mA for EB and 390 (417-364) mA for NEB. Similarly the median convulsant dose of pentylenetetrazol (PTZ) was 7.9 (10.1-6.2) mg/kg for EB and 20.2 (24.2-17.6) mg/kg for NEB. Following pretreatment with graded doses of ropizine (SC 13504), the median protective dose against MES was 6.0(9.2-3.9) mg/kg in EB and 3.2(4.8-2.1) mg/kg in NEB. Based on the incidence of ataxia, EB had a median toxic dose (TD50) of 14.0(16.5-11.9) mg/kg, while in NEB it was 18.0(23.6-13.7)mg/kg. The TD50 doses were unable to protect against a convulsive dose of PTZ. It is concluded first that ropizine may have anti-grand mal activity but apparently lacks an anti-petit mal action. Secondly, EB are more sensitive than NEB to the convulsive effects of electric current and PTZ, yet less responsive to the anticonvulsant actions of ropizine.
Dose-response studies were performed on freely moving rats bearing chronically implanted electrodes. The effects of intracortical injections of penicillin, bicuculline, and conjugated estrogens (Premarin) were determined on EEG activity and motor performance. Bicuculline in doses of 0.025 and 0.05% regularly produced spike and afterdischarge (AD) patterns of rapid onset (less than 10 sec,) brief duration (less than 20 min), and marked intensity. Lower doses had little or no effect. Premarin 1% and penicillin 100 international units produced spike and AD patterns of slower onset (5 min), longer duration (up to 2 hr), and mild intensity. Smaller doses generally produced no AD activity, whereas larger doses produced epileptic patterns severe enough to preclude their use in operant studies. Penicillin and Premarin both produced a significant decrease in operant-response rate in animals trained to bar press on a FR 20 schedule. A marked variability was noted in the behavioral responses of individual rats to the disruptive effects of the epileptogens.
Explore the source record for details and available documents.
Explore the source record for details and available documents.