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.

Treatment with thiamine hydrochloride and astaxanthine for the prevention of yolk-sac mortality in Baltic salmon fry (M74 syndrome).

Two practical methods are reported for treating feral Baltic salmon with thiamine hydrochloride against M74 syndrome (abnormally high yolk-sac fry mortality of the Baltic salmon). Both bathing of the yolk-sac fry in thiamine hydrochloride (1000 mg l-1, 1 h) and a single intraperitoneal injection given to the female brood fish (100 mg kg-1 fish) during the summer 3 mo before stripping were shown to elevate the whole body total thiamine concentration in the fry. Both treatments were also shown to be effective in preventing mortality due to M74 syndrome. The effect of bathing the yolk-sac fry was shown to be dose-dependent. The results support the view that there is a causal relationship between the thiamine status of the yolk-sac fry and M74 mortality. An intraperitoneal injection of astaxanthine suspension administered to the female brood fish (11 mg kg-1 fish) in the summer 3 mo before stripping elevated the astaxanthine concentration in the eggs but did not affect mortality due to M74 syndrome. An interaction between astaxanthine and thiamine may occur in the developing embryo or yolk-sac fry, however. No association could be demonstrated between the various thiamine hydrochloride treatment practices and hepatic cytochrome P450 dependent 7-ethoxyresorufin-O-deethylase (EROD) activity in the yolk-sac fry. An injection of thiamine hydrochloride into the peritoneal cavity of wild Baltic salmon females could be used to raise thiamine concentrations in their offspring in the rivers. The effect on smolt production in Finnish Baltic salmon rivers needs to be investigated further, however.

Cortical responses to auditory stimuli during isoflurane burst suppression anaesthesia.

The cortical responses to auditory stimuli were studied in 12 patients during isoflurane anaesthesia producing burst suppression (ETisof (SD) 1.4 (0.2) vol.%). Earphones were used to give 3-s trains of auditory click stimuli (60 clicks, 20 clicks per second, 80 dB, 0.1 ms) at irregular intervals. In 10 patients, the electroencephalography (EEG) showed a burst suppression pattern consisting of high-amplitude activity intermingled with suppressed background activity. In eight patients with burst suppression patterns, there was a strong cortical reactivity to the termination, not to the beginning, of auditory stimuli: 80 (20)% of all stimuli presented during EEG suppression evoked high amplitude cortical response, offset-burst. The latency of these auditory offset evoked bursts was 540 (60) ms. Auditory offset evoked bursts suggest that in spite of cortical suppression during deep anaesthesia the brain retains its ability to respond to changes in the acoustic environment.

Spontaneous and evoked cortical dynamics during deep anaesthesia.

In this paper we have studied cortical dynamics as assessed using graphical methods during deep anaesthesia. Graphical analysis was carried out by autocorrelation functions and return maps with different lags. During moderate and deep anaesthesia, the electroencephalogram (EEG) shows a burst suppression pattern, consisting of abruptly-occurring high amplitude bursts alternating with periods of relative silence. Deep anaesthesia with burst suppression pattern provides a simple model of brain activity when the noise that is usually present in a subject who is awake is suppressed. During anaesthesia-induced EEG suppression, the brain reacts to different external stimuli with bursts. In respect to sensory processing during anaesthesia, it is interesting to know whether these bursts have different dynamics depending on the stimuli used. We have used graphical analysis to reveal the possible differences in bursts evoked by different stimuli. Externally evoked bursts were induced by auditory, electric and visual stimuli. The EEG studied in this paper consists of 25 bursts from one subject. We have estimated the autocorrelation function for each burst and used the formation gained from such autocorrelation coefficients as the grounds for determining different lags for return maps. The graphical methods used revealed differences in dynamics and topology of bursts as evoked by different stimuli. Spontaneous bursts clearly had different dynamics from evoked burst; which could not be seen directly from the raw EEG data. This study suggests that graphical analysis is a useful tool to obtain information about the dynamics of neuronal processes behind cortical responses during deep anaesthesia.

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.

Suppression of F-VEP during isoflurane-induced EEG suppression.

We recorded visual evoked potentials (VEPs) to flash stimuli in moderately deep anaesthesia when EEG showed burst suppression pattern. Flash VEPs could consistently be recorded in all 8 test subjects during bursts but not during suppressions. We conclude that during isoflurane-induced EEG suppression VEPs to flash stimuli are also suppressed. This effect should be taken into account in evoked potential testing during anaesthesia.

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)

Propofol and isoflurane induced EEG burst suppression patterns in rabbits.

The aim of this study was to compare propofol produced EEG burst suppression with isoflurane produced burst suppression in rabbits and to see whether rabbits can serve as models in studying the effects of different anaesthetics on human EEG. We recorded EEG of eight rabbits anaesthetised with isoflurane and propofol. The isoflurane bursts had higher amplitude than propofol bursts (P < 0.005). Isoflurane bursts appeared on distinct DC-shifts while propofol bursts were on slow waves. The EEG patterns were, however, different from those seen in humans. Rabbits did not have the rhythms seen in humans. We conclude that rabbits can be used to study the EEG effects of anaesthetics, such as the timing properties and reactivity of burst suppression pattern. However, this model seems less promising in the study of rhythmic activity seen in human EEG during burst suppression.

Visually evoked bursts during isoflurane anaesthesia.

We studied EEG reactivity to visual stimuli during deep isoflurane (1.5-2.05 vol% end-tidal concentration) anaesthesia. Twelve patients were anaesthetized with isoflurane until burst suppression occurred in the EEG. Red LED goggles were used to give visual stimulation of 60 flashes, 4-ms duration each, at a frequency of 20 Hz. The stimuli, 3-strains of flashes, were given at random intervals. Both onset and offset of stimulation evoked bursts. The latency of visually evoked bursts was comparable with long latency evoked potentials, which are known to be related to cognitive processing. Our data showed that the central nervous system reacts strongly to photic stimulation during deep anaesthesia.

Adaptive segmentation of burst-suppression pattern in isoflurane and enflurane anesthesia.

In this paper a developed novel algorithm for adaptive segmentation of Burst-suppression EEG is presented. The algorithm can detect bursts, suppression and artifacts, dividing the signal into corresponding segments. A compact representation of burst-suppression EEG, useful in monitoring long-term recordings, is presented. In the second part of the paper the burst-suppression patterns of isoflurane and enflurane anesthesia are compared. It is found that bursts as well as suppression segments are shorter in enflurane anesthesia while the coefficient of variability of the segment lengths is similar for the two anesthetics.

A Finnish multicentre quality assurance project in bone scintigraphy and brain SPET: a phantom study.

We examined all routinely used bone scintigraphy and brain single photon emission tomographic (SPET) systems in 19 laboratories in Finland. Physical performance of bone scintigraphy systems was measured with a 57Co flood source and with a NEMA resolution phantom. Total performance of the systems was evaluated with a transmission phantom simulating bone imaging of the thorax. It was acquired both with the protocol used in a given laboratory and with a fixed protocol. The participant laboratories were asked to report all accumulations on a diagrammatic thorax drawing. Tomographic uniformity, contrast and resolution (i.e. physical performance) of the SPET systems were evaluated with a special phantom. In addition, a Hoffman brain phantom was measured with routinely used acquiring and reconstruction protocols (total performance). All measurements were performed with the same test objects supervised by the same physicist. Manufacturer, age or the collimator of the camera did not correlate with the physical performance of the imaging systems (r < 0.65). This is probably due to lack of regular quality control of the gamma cameras in some laboratories. Comparison of the physical and the total performance shows that the detector itself is not necessarily responsible for inaccurate findings from the test object. Use of dual intensity and digital images in both scintigraphy could certainly increase the sensitivity of the findings: sensitivity of single intensity images was 65% (33-89%), dual 73% (28-100%), analog 65% (28-100%) and digital 74% (50-94%). Standardization of acquisition and reconstruction protocols will improve quality of brain SPET images and comparability between laboratories. This study showed the need for objective audit tests of bone scintigraphy and brain SPET systems in Finland.

Epileptic EEG discharges during burst suppression.

Barbiturate anaesthesia is used in the treatment of status epilepticus and severe epilepsy of children. EEG is then used as a measure of the depth of anaesthesia, burst suppression being an easily identified EEG pattern. In this case report we describe epileptiform discharges during EEG suppression in two children undergoing barbiturate anaesthesia for treatment of intractable seizures. One of them had focal, rhythmic discharges of negative spikes on the positive suppression level. Bursts were readily produced by visual stimuli with flashes of red light but this did not increase the frequency of focal spike discharges after bursts. The other patient had generalised, high amplitude spike-wave complexes, which were easy to distinguish from the bursts. We emphasise that it is important to make a distinction between electrocerebral silence, or isoelectric EEG as it was previously called, from EEG suppression. It is also important to distinguish epileptiform discharges from bursts, if the intention is to keep the anaesthesia at EEG burst suppression level.

Age pigments in different populations of peripheral neurons in vivo and in vitro.

The distribution and ultrastructure of lipopigments in the rat sympathetic, vagus and spinal ganglion neurons were studied in vivo and in vitro using fluorescence and electron microscopy. Newborn, 3-6 mo and 24-30 mo-old male Wistar rats were used. In vivo, the age pigments in the sympathetic neurons showed a tendency to form unipolar or bipolar caps, whereas in the vagus and spinal ganglion neurons pigment granules were packed in the peripheral area of the perikarya during aging. Ultrastructurally, lipid-like vacuoles and a rather homogeneous matrix were the components shared by pigment bodies of all types of peripheral neurons. However, pigment granules in sympathetic neurons frequently had a third, osmiophilic component, which likely represents neuromelanin. In vitro, the cytoplasmic area occupied by autofluorescent pigments was increased in most of the neurons. Some neurons, however, showed the same amount of lipopigments as in vivo. In electron microscopy, age pigment granules typical of each type of neuron were found, and their number and intracellular distribution seemed to be comparable with those in vivo. In most of the neurons cultured from all ages and of all types of ganglion, there appeared to be accumulations of another, very homogeneous and large type of pigment body. In some cases, they were structurally connected with classical pigment bodies or they had a finger print-like substructure. Large homogeneous pigment bodies were also seen in surrounding satellite cells. All these changes were most frequently seen in cultures of spinal ganglia from old animals. It is concluded that although classical age pigments maintain their characteristics in cultured peripheral neurons, there is, in addition, a rapid accumulation of ceroid-like pigments, which may be caused by the inability of the cultured neurons to cope with increased peroxidative damage.