Can electromyographic arousal be detected visually on the Datex-Ohmeda S/5™ anesthesia monitor?

BACKGROUND: Electroencephalogram (EEG)-based depth of anaesthesia monitoring is susceptible to contaminating electromyographic (EMG) activity. Many authorities have suggested that anaesthesiologists using these monitors should interpret the raw EEG waveform seen on the anaesthesia monitor. METHODS: In 34 patients anaesthetized with propofol using two doses of rocuronium (0.6 and 1.2 mg/kg), we studied whether the EMG arousal can be detected visually on the anaesthesia monitor. The Bispectral Index (BIS) and Entropy biosignals on the monitor were recorded with a video camera, and the one-channel EEG recorded by the Entropy strip was collected on a laptop computer. The recordings and the one-channel EEG were analyzed offline by two experts (anaesthesiologist and neurophysiologist), both with a long experience on anaesthesia-related EEG. RESULTS: EMG arousal existed in 14/34 and 13/33 patients in the BIS and Entropy biosignals, respectively. The anaesthesiologist detected EMG on the monitor in 7/14 patients with BIS (sensitivity 50%) and in 4/13 patients with Entropy (31%). The clinical neurophysiologist detected EMG in 6/14 (43%) patients with BIS and in 5/13 (38%) with Entropy. The specificity of the EMG analyses was 55 and 65% with BIS, and 85 and 90% with Entropy. EMG arousal was detected in BIS biosignal in 10/17 and 4/17 patients with 0.6 and 1.2 mg/kg doses of rocuronium (P = 0.04). CONCLUSIONS: In contrast to many EEG phenomena, EMG activity cannot be accurately detected visually from the raw EEG on the anaesthesia monitor. Further development in the quality of the anaesthesia monitors is warranted.

Explaining Entropy responses after a noxious stimulus, with or without neuromuscular blocking agents, by means of the raw electroencephalographic and electromyographic characteristics.

BACKGROUND: Entropy™, an anaesthetic EEG monitoring method, yields two parameters: State Entropy (SE) and Response Entropy (RE). SE reflects the hypnotic level of the patient. RE covers also the EMG-dominant part of the frequency spectrum, reflecting the upper facial EMG response to noxious stimulation. We studied the EEG, EMG, and Entropy values before and after skin incision, and the effect of rocuronium on Entropy and EMG at skin incision during sevoflurane-nitrous oxide (N2O) anaesthesia. METHODS: Thirty-eight patients were anaesthetized with sevoflurane-N2O or sevoflurane-N2O-rocuronium. The biosignal was stored and analysed off-line to detect EEG patterns, EMG, and artifacts. The signal, its power spectrum, SE, RE, and RE-SE values were analysed before and after skin incision. The EEG arousal was classified as ß (increase in over 8 Hz activity and decrease in under 4 Hz activity with a typical ß pattern) or δ (increase in under 4 Hz activity with the characteristic rhythmic δ pattern and a decrease in over 8 Hz activity). RESULTS: The EEG arousal appeared in 17 of 19 and 15 of 19 patients (NS), and the EMG arousal in 0 of 19 and 13 of 19 patients (P<0.01) with and without rocuronium, respectively. Both ß (n=30) and EMG arousals increased SE and RE. The δ arousal (n=2) decreased both SE and RE. A significant increase in RE-SE values was only seen in patients without rocuronium. CONCLUSIONS: During sevoflurane-N2O anaesthesia, both EEG and EMG arousals were seen. ß and δ arousals had opposite effects on the Entropy values. The EMG arousal was abolished by rocuronium at the train of four level 0/4.

Facial muscle activity, Response Entropy, and State Entropy indices during noxious stimuli in propofol-nitrous oxide or propofol-nitrous oxide-remifentanil anaesthesia without neuromuscular block.

BACKGROUND: Entropy is an anaesthetic EEG monitoring method, calculating two numerical parameters: State Entropy (SE, range 0-91) and Response Entropy (RE, range 0-100). Low Entropy numbers indicate unconsciousness. SE uses the frequency range 0.8-32 Hz, representing predominantly the EEG activity. RE is calculated at 0.8-47 Hz, consisting of both EEG and facial EMG. RE-SE difference (RE-SE) can indicate EMG, reflecting nociception. We studied RE-SE and EMG in patients anaesthetized without neuromuscular blockers. METHODS: Thirty-one women were studied in propofol-nitrous oxide (P) or propofol-nitrous oxide-remifentanil (PR) anaesthesia. Target SE value was 40-60. RE-SE was measured before and after endotracheal intubation, and before and after the commencement of surgery. The spectral content of the signal was analysed off-line. Appearance of EMG on EEG was verified visually. RESULTS: RE, SE, and RE-SE increased during intubation in both groups. Elevated RE was followed by increased SE values in most cases. In these patients, spectral analysis of the signal revealed increased activity starting from low (<20 Hz) frequency area up to the highest measured frequencies. This was associated with appearance of EMG in raw signal. No spectral alterations or EMG were seen in patients with stable Entropy values. CONCLUSIONS: Increased RE is followed by increased SE at nociceptive stimuli in patients not receiving neuromuscular blockers. Owing to their overlapping power spectra, the contribution of EMG and EEG cannot be accurately separated with frequency analysis in the range of 10-40 Hz.

The N-methyl-D-aspartate antagonist memantine has no neuroprotective effect during hypothermic circulatory arrest: a study in the chronic porcine model.

BACKGROUND: Glutamate excitotoxicity has an important role in the development of brain injury after prolonged hypothermic circulatory arrest. The goal of the present study was to determine the potential efficacy of memantine, an N -methyl-D -aspartate receptor antagonist, to mitigate cerebral injury after hypothermic circulatory arrest. METHODS: Twenty pigs (23-33 kg) were randomly assigned to receive memantine (5 mg/kg) or placebo in a blinded fashion before a 75-minute period of hypothermic circulatory arrest at 20 degrees C. Hemodynamic, electroencephalographic, and metabolic monitoring were carried out. The intracerebral concentrations of glucose, lactate, glutamate, and glycerol were measured by means of enzymatic methods on a microdialysis analyzer. Daily behavioral assessment was performed until the animals died or were put to death on day 7. Histologic analysis of the brain was carried out in all animals. RESULTS: In the memantine group, 5 of 10 animals survived 7 days compared with 9 of 10 in the placebo group. The median behavioral score at day 7 was 3.5 in the memantine group and 7.5 in the placebo group (P >.2). Among the surviving animals, medians were 9.0 and 8.0 on day 7 (P >.2), respectively. The medians of recovered electroencephalographic bursts were equal in both groups. The median of total histopathologic score was 16 in the memantine group and 14 in the placebo group (P >.2). There was a negative correlation between glutamate levels and electroencephalographic burst recovery (tau = -0.377, P =.043). A positive correlation was found between the highest individual glutamate value and histopathologic score (tau = 0.336, P =.045). CONCLUSIONS: The present study demonstrates that memantine has no neuroprotective effect after hypothermic circulatory arrest in the pig. In addition, we have shown the accuracy of cerebral glutamate measurements to predict histopathologic injury after hypothermic ischemia.

Lamotrigine improves cerebral outcome after hypothermic circulatory arrest: a study in a chronic porcine model.

BACKGROUND: Glutamate excitotoxicity has an important role in the development of brain injury after prolonged hypothermic circulatory arrest. The goal of the present studies was to determine the potential efficacy of lamotrigine, an Na(+) channel blocker, to mitigate cerebral injury after hypothermic circulatory arrest. METHODS: Sixteen pigs (21-27 kg) were randomly assigned to receive lamotrigine (20 mg/kg) or placebo in a blinded fashion before a 75-minute period of hypothermic circulatory arrest (20 degrees C). Hemodynamic, electroencephalographic, and metabolic monitoring were carried out. S-100beta protein was determined up to the first postoperative morning. Daily behavioral assessment was performed until the animal died or was put to death on day 7. Histologic analysis of the brain was carried out in all animals. RESULTS: Complete behavioral recovery was seen in 5 of 8 (63%) animals after lamotrigine administration, compared with 1 of 8 (13%) in the placebo group (P =.02). Among the animals that survived for 7 days, the median behavioral score was higher in the lamotrigine group (8 vs 7, P =.02). The medians of recovered electroencephalographic bursts in the lamotrigine group were higher than those in the placebo group 4 1/2 hours after the start of rewarming (P =.01). The median S-100beta level was lower in the lamotrigine group (0.01 microg/L) than in placebo controls (0.1 microg/L) 20 hours after the start of rewarming (P =.01). The median of total histopathologic score was 5.5 in the lamotrigine group and 7.5 in the placebo group (P =.06). CONCLUSIONS: The present data suggest that lamotrigine improves neurologic outcome after a prolonged period of hypothermic circulatory arrest.

Lowered yields of virus-induced interferon production in leukocyte cultures and risk of recurrent respiratory infections in children.

OBJECTIVE: To study the correlation between the yield of virus-induced interferon (IFN) production in leukocyte cultures and the risk of recurrent respiratory infections. METHODS: A sample of 71 consecutive children enrolled in the Finnish Otitis Media Cohort Study were selected. Children suffering from frequently recurring respiratory infections (FRRIs) were defined as the highest quintile of the entire cohort of 329 children, as regards the number of upper respiratory infections (URIs) and/or episodes of acute otitis media (AOM) during the follow-up period from 2 to 24 months. RESULTS: In the sample of 71 children, there were 18 children with FRRI (> or = 9 URI and/or > or = 4 AOM). Leukocyte cultures, prepared from blood drawn from these 18 children at 6 months of age, produced lower yields of IFN than those of the remaining 53 children, when stimulated with adenovirus (P <0.001), coronavirus (P<0.001) or rhinovirus (P=0.002). The difference in IFN yields was even greater (P<0.001 with all three viruses) if the comparison was made between children with FRRI and those with no or maximally one URI during the follow-up period. When the IFN production capacity induced by rhinovirus was measured at the age of 24 months, a statistically significant difference between the children with FRRI and the others was also seen (P=0.002). Influenza A virus-induced IFN production capacity did not differ between the groups at either age (P=0.209). CONCLUSIONS: Lowered IFN responses in children suffering from recurrent URIs and/or AOM may, in a subgroup of the children, be due to a genetic property of the child. However, because of the great interindividual variations, we cannot use the IFN production capacity as such for prediction of forthcoming respiratory infections and/or otitis media.

Cold retrograde cerebral perfusion improves cerebral protection during moderate hypothermic circulatory arrest: A long-term study in a porcine model.

BACKGROUND: Deep hypothermic circulatory arrest is an effective method of cerebral protection, but it is associated with long cardiopulmonary bypass times and coagulation disturbances. Previous studies have shown that retrograde cerebral perfusion can improve neurologic outcomes after prolonged hypothermic circulatory arrest. We tested the hypothesis that deep hypothermic retrograde cerebral perfusion could improve cerebral outcome during moderate hypothermic circulatory arrest. METHODS: Twelve pigs (23-29 kg) were randomly assigned to undergo either retrograde cerebral perfusion (15 degrees C) at 25 degrees C or hypothermic circulatory arrest with the head packed in ice at 25 degrees C for 45 minutes. Flow was adjusted to maintain superior vena cava pressure at 20 mm Hg throughout retrograde cerebral perfusion. Hemodynamic, electrophysiologic, metabolic, and temperature monitoring were carried out until 4 hours after the start of rewarming. Daily behavioral assessment was performed until elective death on day 7. A postmortem histologic analysis of the brain was carried out on all animals. RESULTS: In the retrograde cerebral perfusion group, 5 (83%) of 6 animals survived 7 days compared with 2 (33%) of 6 in the hypothermic circulatory arrest group. Complete behavioral recovery was seen in 4 (67%) animals after retrograde cerebral perfusion but only in 1 (17%) animal after hypothermic circulatory arrest. Postoperative levels of serum lactate were higher, and blood pH was lower in the hypothermic circulatory arrest group. There were no significant hemodynamic differences between the study groups. CONCLUSIONS: Cold hypothermic retrograde cerebral perfusion during moderate hypothermic circulatory arrest seems to improve neurologic outcome compared with moderate hypothermic circulatory arrest with the head packed in ice.

Clonidine does not attenuate median nerve somatosensory evoked potentials during isoflurane anesthesia.

BACKGROUND: Clonidine, an alpha2 agonist, reduces the requirements of several anesthetics. However, the effects of clonidine on somatosensory evoked potentials (SEPs) are unclear. These effects on cortical SEPs during isoflurane anesthesia were studied in 20 ASA I-II patients scheduled for elective surgery. Furthermore, the isoflurane concentration required to induce electroencephalogram (EEG) burst-suppression with and without clonidine was studied. METHODS. Anesthesia was maintained with isoflurane at a FiO2 of 0.4. At 1 MAC isoflurane the patients were randomly given either intravenous clonidine 2 microg kg(-1) (ten patients) or saline (ten patients). Finally, the isoflurane concentration was increased to a point at which a burst-suppression pattern appeared in the EEG. SEPs upon median nerve stimulation were recorded (1) before induction of anesthesia, (2) at 1 MAC before clonidine/saline, (3) at 1 MAC after clonidine/saline, (4) at EEG burst-suppression. RESULTS: The cortical SEP amplitude was attenuated from 3.7 (2.0) microV to 2.1 (1.3) microV (p < 0.001) and the peak latency increased from 19.3 (1.1) ms to 22.0 (1.3) ms (p < 0.0001) during 1 MAC isoflurane anesthesia, but the addition of clonidine did not further increase these changes. The isoflurane end-tidal concentration needed to induce burst-suppression EEG was not significantly different in the clonidine group compared with the placebo group (2.0% vs. 2.1%, p = 0.07). CONCLUSIONS: The effect of clonidine in reducing the requirements of anesthetics during general anesthesia is not seen in the cortical SEPs. The isoflurane-induced burst-suppression in the EEG was not affected by clonidine, suggesting that the EEG effects of clonidine and isoflurane were not additive. If SEPs are monitored intraoperatively, clonidine can be used as an adjuvant during isoflurane anesthesia without harmful effects on SEP monitoring.

Effects of hypothermia and sternal retractors on median nerve somatosensory evoked potentials.

BACKGROUND: Somatosensory evoked potentials (SEPs) are altered by hypothermia, which is often used during cardiopulmonary bypass (CPB). However, the effect of hypothermia on SHP amplitudes is unclear. Also, the sternal retractors used during open heart surgery are reported to cause brachial plexus distension and SEP changes. METHODS: Median nerve SEPs under hypothermic CPB were studied in 29 elective patients scheduled for open heart surgery. In 23 patients who underwent left internal mammary artery (IMA) dissection, the effects of sternal retractors on cortical SEP before the initiation of CPB were investigated. RESULTS: A latency shift of all SEP components was detected when nasopharyngeal temperature decreased from 35.7(SD 0.4) degrees C to 27.8(SD 0.25) degrees C. The mean cortical N20 latency was increased by 39% (P < 0.0001), cervical N13 by 33% (P < 0.0001), and peripheral N9 by 27% (P < 0.0001). The latency changes were reversible when normothermia was restored. The effect of hypothermia on SEP amplitudes was more complex. The mean amplitude of N20 decreased from 2.7 microV to 2.2 microV (P < 0.05) and the amplitude of N13 from 2.5 microV to 2.0 microV (P < 0.0001). In contrast, the N9 component showed an increase from 1.4 microV to 2.1 microV (P < 0.0001) during hypothermia. The sternal retractors did not cause significant cortical SEP amplitude changes during IMA dissection or sternotomy. Also, the latency changes were small, although significant (P < 0.05). CONCLUSION: Despite the moderate amplitude changes produced by hypothermia, SEPs can be successfully monitored during hypothermia. Theoretically, the different behaviour of amplitude in peripheral and cranial components of SEP during hypothermia is interesting. Hypothermia has a more profound effect on synaptic transmission, represented by the cortical N20 latency, than on the peripheral nerve conduction velocity. Intraoperative monitoring of temperature is essential whenever SEPs are recorded. The sternal retractors were not responsible for the intraoperative SEP changes.

Nitrous oxide has different effects on the EEG and somatosensory evoked potentials during isoflurane anaesthesia in patients.

BACKGROUND: Electroencephalogram (EEG) and somatosensory evoked potentials (SEPs) are altered by inhalation anaesthesia. Nitrous oxide is commonly used in combination with volatile anaesthetics. We have studied the effects of nitrous oxide on both EEG and SEPs simultaneously during isoflurane burst-suppression anaesthesia. METHODS: Twelve ASA I-II patients undergoing abdominal or orthopaedic surgery were anaesthetized with isoflurane by mask. After intubation and relaxation the isoflurane concentration was increased to a level at which an EEG burst-suppression pattern occurred (mean isoflurane end-tidal concentration 1.9 (SD 0.2) %. With a stable isoflurane concentration, the patients received isoflurane-air-oxygen and isoflurane-nitrous oxide-oxygen (FiO2 0.4) in a randomized cross-over manner. EEG and SEPs were simultaneously recorded before, and after wash-out or wash-in periods for nitrous oxide. The proportion of EEG suppressions as well as SEP amplitudes for cortical N20 were calculated. RESULTS: The proportion of EEG suppressions decreased from 53.5% to 34% (P < 0.05) when air was replaced by nitrous oxide. At the same time, the cortical N20 amplitude was reduced by 69% (P < 0.01). CONCLUSION: The results suggest that during isoflurane anaesthesia, nitrous oxide has a different effect on EEG and cortical SEP at the same time. The effects of nitrous oxide may be mediated by cortical and subcortical generators.

Cortical reactivity during isoflurane burst-suppression anesthesia.

We studied cortical reactivity to auditory, visual, and somatosensory stimuli during moderate and deep levels of isoflurane anesthesia at which the electroencephalogram (EEG) showed burst suppression patterns, defined as alternating high amplitude bursts and periods of suppressed background activity. Fifteen patients scheduled for gynecologic surgery were anesthetized with isoflurane until burst suppression appeared in the EEG. During steady state burst suppression at 1.5 end-tidal isoflurane concentration (ETisof), each patient was given a 5-min interval each of episodes of visual, auditory, and somatosensory stimulation. During the 5-min interval of visual stimulation the patient was given 3-s episodes of 60 flashes, 4 ms duration each, at a 20-Hz frequency via redlight-emitting diode goggles. Corresponding auditory and somatosensory stimulation consisted of 60 clicks (80 dB, 0.1 ms, 20 Hz) via earphones and 60 pulses to the median nerve at the wrist (20 mA, 0.2 ms, 20 Hz). The 3-s episodes of stimulation were given at irregular intervals ranging from 5 to 20 s. End-tidal isoflurane was then increased by 0.3 vol% and 15 min later the stimulation sequence was repeated. During anesthesia at 1.5 +/- 0.1 ETisof all stimulus modalities readily evoked bursts. One hundred percent of visual stimuli, 98% +/- 4% of somatosensory stimuli, and 94% +/- 9% of auditory stimuli, given during EEG suppression, evoked bursts. Somatosensory and visual stimulation evoked bursts at both onset and offset of the 3-s episodes of stimuli. The responses to auditory stimuli were related mainly to the ending of the 3-s episode of clicks.(ABSTRACT TRUNCATED AT 250 WORDS)

Somatosensory evoked potentials during isoflurane anaesthesia.

Short latency somatosensory evoked potentials (SEPs) to median nerve stimulation during isoflurane anaesthesia were recorded in 12 elective-surgery patients. The effect of isoflurane on the shape, amplitude and latency of SEPs was evaluated. SEPs were recorded at awake, 1 MAC, 1.5 MAC, at electroencephalogram (EEG) burst suppression and at continuous suppression levels. Finally, SEPs were recorded when anaesthesia was lightened back to 1 MAC. The peak latency and amplitude of the first cortical N20 wave were measured. The latencies increased with increasing isoflurane concentrations. At high concentrations only an almost monophasic N20 wave was recorded, reduced in shape and amplitude. No specific changes could be correlated with the burst suppression or suppression patterns. This suggests that EEG and SEP generators are differently affected with increasing isoflurane concentration. The results indicate that SEPs can also be recorded in drug-induced EEG suppression.

Changes in the T-wave amplitude of ECG during isoflurane anaesthesia.

R/T-wave amplitude ratio of electrocardiogram (ECG), heart rate (HR) and systolic arterial pressure (SAP) were recorded in 15 patients awake, at 1 minimal alveolar concentration of isoflurane before and during surgery, and in deep anaesthesia (electroencephalogram burst suppression) during surgery. R/T-wave amplitude ratio and HR were sensitive to both surgery and changes in the level of isoflurane anaesthesia; induction of anaesthesia, skin incision and the rapid increase in the concentration of isoflurane all significantly decreased the T-wave amplitude, without influence on the R-wave. Changes in the T-wave amplitude correlated directly to HR. SAP increased at skin incision and decreased when the anaesthesia was deepened. The authors conclude that the R/T-wave amplitude ratio of ECG provides a reliable method for monitoring the sympathetic tone during isoflurane anaesthesia.

Nitrous oxide-mediated activation of the EEG during isoflurane anaesthesia in patients.

We have studied the effects of nitrous oxide on EEG burst suppression patterns during stable isoflurane anaesthesia in 13 ASA I patients. After induction of anaesthesia with propofol, the concentration of isoflurane was increased with continuous EEG monitoring to burst suppression level (mean end-tidal concentration of isoflurane, 1.7 (SD 0.2)%), and kept constant during the study. During surgery, isoflurane in air and oxygen (FIO2 0.35), or isoflurane in 65% nitrous oxide in oxygen were given to each patient for 30 min, in random order. EEG was recorded and digitized off-line. The proportion of EEG suppression time was measured after a washin or washout period of at least 15 min for nitrous oxide. There was a significant decrease in the proportion of EEG suppression time (from 69.5 to 43.7%) when air was replaced by nitrous oxide. We conclude that the EEG effects of isoflurane and nitrous oxide are not additive and that nitrous oxide opposes the depression of isoflurane on the central nervous system.

Carpal tunnel syndrome in vibration disease.

The presence of carpal tunnel syndrome (CTS) in 125 forestry workers with exposure to vibration was examined clinically by electromyography and by determining vibration detection thresholds. Numbness of the hands was present in 43%, history of diminished hand muscle force in 15%, and Raynaud's phenomenon in 27%. The muscle weakness correlated significantly with motor nerve conduction velocity in the median nerve in both hands. In 25 forestry workers CTS was diagnosed. The condition was bilateral in 48%; otherwise it was more common on the right side. Fifteen patients were referred for surgery but because of spontaneous recovery or refusal by the patients only five underwent surgery; of these four improved. The motor conduction velocity of the ulnar nerve was decreased among patients with CTS supporting the idea that entrapment neuropathies in the hands may be due to tissue swelling caused by vibration at work. Total exposure time to vibration correlated with the decrease in motor conduction velocity in the ulnar nerve.

Correlation between EEG and heart rate variation in deep enflurane anaesthesia.

Variations in heart rate during deep enflurane anaesthesia were studied in 11 women admitted for elective surgery. Correlation was found between heart rate variations and bursts and suppressions in the EEG patterns. The onset of bursts coincided with accelerating heart rate, and the onset of suppressions was combined with a fall in heart rate in all patients. The correlation is not explained by ventilation arrhythmia. Both the cortical electrical activity and heart rate fluctuation are probably controlled by the same subcortical factor.