Evoked EEG patterns during burst suppression with propofol.

BACKGROUND: During EEG suppression with isoflurane or sevoflurane anaesthesia, median nerve stimulation causes cortical responses of two kinds: an N20 wave with a latency of 20 ms and an EEG burst with a latency of 200 ms. We tested the possibility that median nerve stimulation during EEG suppression with propofol would cause an EEG response that was consistent enough to be of use for neuromonitoring. METHODS: Eight patients were anaesthetized with propofol to allow burst suppression. Electrical stimulation of the median nerve was applied during general anaesthesia and the EEG was measured. RESULTS: The EEG response to a painful stimulus had four successive components: (i) N20 and P22 potentials, reflecting activation of fast somatosensory pathways; (ii) a high-amplitude negative wave, possibly reflecting activation of the somatosensory cortex SII bilaterally; (iii) a burst (i.e. a negative slow wave with superimposed 10 Hz activity, probably reflecting an arousal mechanism); and (iv) a 13-15 Hz spindle, probably originating from the thalamus, similar to sleep spindles. These could be seen separately and in different combinations. Bursts and spindles during burst suppression were also seen without stimulation. In deepening propofol anaesthesia, spindles were seen in the continuous EEG before burst suppression was achieved. In deep anaesthesia, spindles were seen when bursts had ceased, and painful stimuli evoked sharp waves without subsequent bursts. CONCLUSION: In addition to SSEP (somatosensory evoked potentials), three different evoked responses are noted that could be useful for clinical monitoring.

Utility of clinical criteria in differentiating frontotemporal lobar degeneration (FTLD) from AD.

OBJECTIVE: To assess the ability of the current diagnostic criteria for frontotemporal lobar degeneration (FTLD) to differentiate FTLD from AD. METHODS: Thirty cases with autopsy-proven FTLD and 30 cases of AD, matched for Mini-Mental State Examination score, were identified from the clinical databases of three dementia subspecialty centers, and their charts were reviewed for the presence of clinical features described in the current criteria for FTLD. The proportion of patients with each clinical feature at the first clinical presentation was compared across groups. RESULTS: A significantly larger proportion of patients with FTLD showed behavioral abnormalities, particularly social and personal conduct disorders and emotional blunting, than patients with AD. Few differences in language features were seen between the groups, and many of the language features detailed in the criteria were found in only a small proportion of patients. In both groups, many patients showed neuropsychological abnormalities, except for perceptual difficulties, which were present in many patients with AD but only in a few patients with FTLD. Extrapyramidal motor symptoms were more likely to be present in FTLD. Logistic regression revealed that five features-social conduct disorders, hyperorality, akinesia, absence of amnesia, and the absence of a perceptual disorder-correctly classified 93% of patients with FTLD and 97% of patients with AD. CONCLUSION: A combination of behavioral, neuropsychological, and physical findings is most useful in distinguishing FTLD from AD. Future studies should be directed at establishing more objective methods of identifying these clinical features.

Transient interference of right hemispheric function due to automatic emotional processing.

We examined the effects of emotional stimuli on right and left hemisphere detection performance in a hemifield visual discrimination task. A group of 18 healthy subjects were asked to discriminate between upright and inverted triangles (target). Targets were randomly presented in the left or right visual hemifield (150 ms target duration). A brief emotional picture (pleasant or unpleasant; 150 ms stimulus duration) or neutral picture selected from the International Affective Picture System was randomly presented either in the same (47%) or the opposite (47%) spatial location to the subsequent target. Emotional or neutral stimuli offset 150 ms prior to the subsequent target. Subjects were instructed to ignore the pictures and respond to the targets as quickly and accurately as possible. Independent of field of presentation, emotional stimuli prolonged reaction times (P < 0.01) to LVF targets, with unpleasant stimuli showing a greater effect than pleasant stimuli. The current study shows that brief emotional stimuli selectively impair right hemispheric visual discrimination capacity. The findings suggest automatic processing of emotional stimuli captures right hemispheric processing resources and transiently interferes with other right hemispheric functions.

Monitoring the integrity of somatosensory pathways with evoked electroencephalographic bursts.

During isoflurane-induced electroencephalographic (EEG) suppression, external stimuli evoke high-amplitude cortical responses (bursts). We tested whether bursts evoked by somatosensory stimuli would reliably distinguish intact somatosensory pathways from pathways in which peripheral nerve conduction had been blocked by local anesthetic. Ten subjects were anesthetized with isoflurane until burst suppression was achieved. During EEG suppression, they were given somatosensory stimulation, consisting of 3-s episodes of 60 electric pulses (20 mA, 0.2 ms), to the tips of the left and right fifth fingers alternately for 10 min. One finger was then anesthetized at the base of the proximal phalanx with prilocaine and the other finger was injected with saline in a double-blind manner. The stimulation was continued for 20 min. In nine patients, the disappearance of bursts in response to stimuli applied to the anesthetized finger clearly indicated the side of the conduction block. After the injection of local anesthetic, there was a predominance of offset bursts over onset bursts in response to stimuli applied to the anesthetized finger (P < 0.05) before the responses disappeared. We conclude that evoked bursts merit further investigation for potential use in monitoring the integrity of neural pathways.

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)