Burst Suppression Pattern Research Articles

Uncommon EEG burst-suppression in severe postanoxic encephalopathy

In patients suffering from severe hypoxia, the EEG may show a burst-suppression pattern, characterized by low-voltage activity and the occurrence of high amplitude burst-like events. We describe the two-timescale burst phenomenology of this postanoxic condition. We present EEG recordings showing remarkable burst phenomenology in two postanoxic patients and consider potential mechanisms responsible for the generation of the burst-suppression patterns. We quantify the postanoxic condition in terms of the dimension (number of degrees of freedom) of its dynamics by comparing our data with a system of three ordinary differential equations with two timescales subject to varying degrees of noise. EEGs displayed extreme similarity of the bursts, separated by interburst intervals up to more than 300s. This pattern reflects a significant reduction in the number of functional brain states. This post-anoxic condition is found to have dimension 3, consisting of fast dynamics responsible for the bifurcation to bursting behavior, and a long time-scale responsible for burst termination and the interburst intervals. Low-dimensional postanoxic brain states, as manifested by burst-similarity, appears to indicate an irreversible loss of brain function and consciousness. Evidence of brain functionality in a persistent low dimensional state due to severe hypoxia is indicative of permanent loss of consciousness with essentially no chance for recovery. Quantitative evidence for such degenerate states is important for clinical decision making.

NEW-ONSET REFRACTORY STATUS EPILEPTICUS WITH RESTRICTED DWI AND NEURONOPHAGIA IN THE PULVINAR

New-onset refractory status epilepticus (NORSE) is a recently defined clinical entity which describes patients who present with severe generalized seizures of unclear etiology that occur in the context of a preceding febrile illness.1–3 These seizures are typically unresponsive to antiepileptic medications. ### Case report. A 26-year-old otherwise healthy right-handed man presented with generalized tonic-clonic seizures after a 1-week history of headache, fever, and myalgias. He was admitted to our intensive care unit for treatment and underwent continuous EEG monitoring for 77 days. On admission to our intensive care unit, the CSF contained 92 × 106 white blood cells (96% lymphocytes). Consistent with previous reports of NORSE, an exhaustive structural, infectious, toxic/metabolic, autoimmune, neoplastic, and paraneoplastic workup did not identify a clear underlying etiology (figure, A). IV infusions of propofol or thiopental were used to maintain the patient in either an electrographic burst suppression pattern or electrographic silence, while enteral antiepileptic medications were titrated to therapeutic doses (e.g., phenytoin, valproic acid, clobazam, topiramate, vigabatrin, phenobarbital, and levetiracetam) (figure, B). Attempts to wean IV antiepileptic drugs were met with recurrence of electrographic multifocal sharp transients, originating from either temporal lobe, which evolved into clinical and electrographic seizures. Figure Laboratory investigations, imaging, and pathologic findings in a case of new-onset refractory status epilepticus (A) Table of investigations performed to identify the underlying etiology of the …

The prognostic value of early aEEG in asphyxiated infants undergoing systemic hypothermia treatment

Induced moderate hypothermia (HT) for 72 h has been shown to reduce the combined outcome of death or severe neurodevelopmental disabilities in asphyxiated full-term infants. A pathological amplitude integrated EEG background as early as 3-6 h after birth, has been shown to correlate to poor prognosis. The aim of this study was to investigate the correlation between amplitude integrated EEG during HT treatment and short-term outcome in asphyxiated full-term infants with moderate/severe hypoxic-ischaemic encephalopathy. Between December 2006 and December 2007, 24 infants were treated with moderate HT (33.5 degrees C for 72 h) using a cooling mattress. Motor functions were assessed at 4 and 12 months of age. Of the total birth cohort of 28,837 infants, 26 infants fulfilled the criteria for HT treatment (0.9/1000) of whom 23 was treated with HT and all of these infants had available amplitude integrated EEG data. Normal 1-year outcome was found in 10/15 infants with severely abnormal burst-suppression pattern or worse at 6 h of age. Severe abnormalities were found to be significantly predictive for abnormal outcome after 36 h. Among asphyxiated infants treated with HT, only those who had aEEG abnormalities persisting at and beyond 24 h after birth showed poor neurological outcome at 1 year.

EFNS guideline on the management of status epilepticus in adults

The objective of the current article was to review the literature and discuss the degree of evidence for various treatment strategies for status epilepticus (SE) in adults. We searched MEDLINE and EMBASE for relevant literature from 1966 to January 2005 and in the current updated version all pertinent publications from January 2005 to January 2009. Furthermore, the Cochrane Central Register of Controlled Trials (CENTRAL) was sought. Recommendations are based on this literature and on our judgement of the relevance of the references to the subject. Recommendations were reached by informative consensus approach. Where there was a lack of evidence but consensus was clear, we have stated our opinion as good practice points. The preferred treatment pathway for generalised convulsive status epilepticus (GCSE) is intravenous (i.v.) administration of 4-8 mg lorazepam or 10 mg diazepam directly followed by 18 mg/kg phenytoin. If seizures continue more than 10 min after first injection, another 4 mg lorazepam or 10 mg diazepam is recommended. Refractory GCSE is treated by anaesthetic doses of barbiturates, midazolam or propofol; the anaesthetics are titrated against an electroencephalogram burst suppression pattern for at least 24 h. The initial therapy of non-convulsive SE depends on type and cause. Complex partial SE is initially treated in the same manner as GCSE. However, if it turns out to be refractory, further non-anaesthetising i.v. substances such levetiracetam, phenobarbital or valproic acid should be given instead of anaesthetics. In subtle SE, in most patients, i.v. anaesthesia is required.

Desflurane Versus Sevoflurane to Reduce Blood Loss in Maxillofacial Surgery

In our study, desflurane was hypothesized to reduce blood loss more than sevoflurane, both used with targeted mild controlled hypotension. A total of 20 American Society of Anesthesiologists Class I patients undergoing maxillofacial elective surgery for maxillary and mandibular osteotomies were randomized to a desflurane group or a sevoflurane group. Anesthesia was performed with an end tidal value of the inhaled agent to obtain a bispectral index value <30 but without burst-suppression patterns (minimal alveolar concentration age-corrected between 0.7 and 0.9). Remifentanil was administered at a dose of 0.5 microg x kg(-1) x min(-1) to obtain analgesia and a <2 surgical field level in Fromme's modified scale. Sodium-nitroprusside was administered on demand to have a surgical field level of <2 when the anesthesia plan was not sufficient to achieve this target. The minimal value of the mean arterial pressure achievable was 60 mm Hg. In the desflurane group, blood loss was more restricted. The hypotensive drug was used in 8 patients in the sevoflurane group and 2 patients in the desflurane group. Anesthesia with desflurane can reduce blood loss and could give an acceptable surgical field with mild controlled hypotension and with a substantial reduction in the vasoactive drug requirement. These data need to be assessed with an enlargement of the statistical sample.

The effects of EEG suppression and anesthetics on stimulus thresholds in functional cortical motor mapping

To investigate the effects of EEG suppression and anesthetics on variability of electrical stimulus thresholds during functional cortical motor mapping, and the possible influences of age, lesion location and pathology. Multivariate regression analysis was performed to study these relationships in 60 cases of successful mapping using the monopolar multipulse train technique. An increase in the length of EEG "flats" by 1s produced an increase in stimulus threshold by 1.08 mA (p=0.0004). Administration of TIVA (total intravenous anesthesia) or inhalational agents produced an additional increase in threshold by 1.27 mA (p=0.38) or 4.84 mA (p=0.04) respectively, when compared to awake patients. Depth of cortical suppression impacts the stimulus thresholds. The effect of TIVA on thresholds is mediated by its effect on cortical excitability. The effects of inhalational agents on thresholds involve their influence on excitability at other levels of the neuraxis. The study represents an important step towards building a predictive model for stimulus thresholds. It also improves our understanding of the relationships of anesthetics, EEG burst suppression pattern and age with cortical excitability.

A novel ARX phenotype: rapid neurodegeneration with Ohtahara syndrome and a dyskinetic movement disorder

ARX mutations are associated with variable clinical phenotypes. We report a new neurodegenerative phenotype associated with a known ARX mutation and causing early abnormal neurodevelopment, a complex movement disorder, and early infantile epileptic encephalopathy with a suppression-burst pattern (Ohtahara syndrome). A male infant presented at age 5 months with a dyskinetic movement disorder, which was initially diagnosed as infantile spasms. Clinical deterioration was accompanied by progressive cortical atrophy with a reduction in white matter volume and resulting in death in the first year of life; such a rapidly progressive and severe phenotype has not previously been described. ARX mutation testing should be undertaken in children aged less than 1 year with Ohtahara syndrome and a movement disorder, and in infants with unexplained neurodegeneration, progressive white matter loss, and cortical atrophy.

Automatic classification of background EEG activity in healthy and sick neonates

The overall aim of our research is to develop methods for a monitoring system to be used at neonatal intensive care units. When monitoring a baby, a range of different types of background activity needs to be considered. In this work, we have developed a scheme for automatic classification of background EEG activity in newborn babies. EEG from six full-term babies who were displaying a burst suppression pattern while suffering from the after-effects of asphyxia during birth was included along with EEG from 20 full-term healthy newborn babies. The signals from the healthy babies were divided into four behavioural states: active awake, quiet awake, active sleep and quiet sleep. By using a number of features extracted from the EEG together with Fisher's linear discriminant classifier we have managed to achieve 100% correct classification when separating burst suppression EEG from all four healthy EEG types and 93% true positive classification when separating quiet sleep from the other types. The other three sleep stages could not be classified. When the pathological burst suppression pattern was detected, the analysis was taken one step further and the signal was segmented into burst and suppression, allowing clinically relevant parameters such as suppression length and burst suppression ratio to be calculated. The segmentation of the burst suppression EEG works well, with a probability of error around 4%.

Assessing the depth of hypnosis of xenon anaesthesia with the EEG / Bestimmung der Hypnosetiefe bei Xenon-Narkosen mit dem EEG

Xenon was approved as an inhaled anaesthetic in Germany in 2005 and in other countries of the European Union in 2007. Owing to its low blood/gas partition coefficient, xenons effects on the central nervous system show a fast onset and offset and, even after long xenon anaesthetics, the wake-up times are very short. The aim of this study was to examine which electroencephalogram (EEG) stages are reached during xenon application and whether these stages can be identified by an automatic EEG classification. Therefore, EEG recordings were performed during xenon anaesthetics (EEG monitor: Narcotrend®). A total of 300 EEG epochs were assessed visually with regard to the EEG stages. These epochs were also classified automatically by the EEG monitor Narcotrend® using multivariate algorithms. There was a high correlation between visual and automatic classification (Spearman's rank correlation coefficient r=0.957, prediction probability Pk=0.949). Furthermore, it was observed that very deep stages of hypnosis were reached which are characterised by EEG activity in the low frequency range (delta waves). The burst suppression pattern was not seen. In deep hypnosis, in contrast to the xenon EEG, the propofol EEG was characterised by a marked superimposed higher frequency activity. To ensure an optimised dosage for the single patient, anaesthetic machines for xenon should be combined with EEG monitoring. To date, only a few anaesthetic machines for xenon are available. Because of the high price of xenon, new and further developments of machines focus on optimizing xenon consumption.

The Burst-Suppression Electroencephalogram

The burst suppression (BS) pattern of the EEG was originally described as a response to large dosages of anesthetics and sedatives. It was subsequently found over/in isolated cortex due to surgical procedures or lesions underlying the cortex. Around 1960 with the introduction of modern intensive care treatment (intubation, artificial respiration) the BS pattern has become a typical EEG correlate of cerebral anoxia. These obvious consequences of this therapeutic approach with their impact on the EEG picture are more or less inexplicable.The BS pattern is also typical in two rare and severe central nervous system (CNS) disorders in infants: early infantile myoclonic encephalopathy (EIME) and Ohtahara syndrome.

Electroencephalographic changes in pyridoxine‐dependant epilepsy: new observations

Pyridoxine-dependent epilepsy (PDE) is a rare disease, of which the EEG manifestations are only partially characterised. We report our observations of EEG recordings in four patients with PDE. EEG tracings from four patients fulfilling the clinical criteria for PDE were reviewed. Relative to the time of treatment with pyridoxine, EEG recordings were available before treatment in two patients (at ages four and 10 months), immediately after treatment in two patients and during long-term follow-up with treatment in all four patients. Pre-pyridoxine interictal EEG findings included: diffuse slowing, bilateral independent multifocal epileptiform discharges, generalized bursts of polyspike slow waves and focal or generalized sharp waves. In addition, the EEG was often asymmetrical and included: generalized semi-rhythmic sharp and slow waves, a burst suppression pattern and continuous generalized spike and slow waves. In one patient, who was followed subsequently, a decrease in multifocal spikes and sharp waves and permanent cessation of clinical seizures, within 10 minutes of concurrent reduction of spikes in the pre-existing generalized spike slow wave pattern, was observed immediately after pyridoxine treatment. However, despite the clinical response in this patient we observed persistent generalized burst suppression for four days, and fluctuation of the EEG with diffuse slowing on day four and transient exacerbation of discharges with continuous spike slow waves on day 22. This was followed by intermittent sharp waves at eight and 20 months, mild slowing at 31 months and normal EEG at 43 months. Long-term EEG findings in the other three patients receiving pyridoxine ranged between normal and intermittent multifocal sharp waves. Our data confirm previous observations and provide the following new findings: (1) the presence of burst suppression pattern after cessation of seizures can occur for up to five days after initiation of pyridoxine and should not exclude the diagnosis of PDE, (2) possible fluctuation and even transient worsening of electrographic discharges were observed for up to three weeks after initiation of pyridoxine and (3) the abnormal EEG can persist for up to 43 months before normalizing (range 1-43 months) and in other cases in which it continues to be abnormal it may still improve after increasing the dose of pyridoxine.

How useful is EEG and EEG monitoring in the acutely ill and how to interpret it?

How useful is EEG and EEG monitoring in the acutely ill and how to interpret it?

Functional cortical deafferentation from the subcortical structures in a patient with early myoclonic encephalopathy: A functional neuroimaging study

We, for the first time, used functional neuroimaging analyses for a girl with early myoclonic encephalopathy (EME). The interictal single photon emission computed tomography (SPECT) and [18F]-fluoro-D-deoxyglucose positron emission tomography (FDG-PET) at 1 month of age showed hypoperfusion and hypometabolism of bilateral basal ganglia, thalami, and the right parietooccipital cerebral cortices, showing that there is profound dysfunction of the basal ganglia and thalamus as well as cerebral cortex. On the other hand, subtraction ictal SPECT of tonic spasms clearly showed hyperperfusion of the bilateral basal ganglia, thalami, brainstem, and deep cortical layer of bilateral frontoparietal cortices. The present study suggests that functional deafferentation of the cortex from subcortical structures exists in EME, and that these imaging abnormalities may provide insight into the pathophysiology of suppression-burst pattern in EME.

Early Myoclonic Encephalopathy and Nonketotic Hyperglycinemia

Early myoclonic encephalopathy is an epileptic syndrome with different etiologies. Nonketotic hyperglycinemia is one cause. We describe two cases of early myoclonic encephalopathy, secondary to nonketotic hyperglycinemia, with fatal evolution in the neonatal period. These two cases may better clarify clinical findings that can be associated with impairment of glycine metabolism. Distinguishing features include agenesis of the corpus callosum in patient 1, and weight loss exceeding 10%, associated with metabolic acidosis, in patient 2. The burst-suppression electroencephalography pattern is relatively common in neonatal encephalopathies, and is frequently associated with seizures. Nonketotic hyperglycinemia is an inborn error of metabolism caused by mutations in genes encoding protein in the mitochondrial glycine cleavage system. The neonatal form is a severe, frequently lethal neurologic disease. When associated with electro-clinical features, progressive lethargy and hypotonia occur in the first days of life, progressing to apnea and often death. Prospective treatment with oral sodium benzoate, the N-methyl-d-aspartate receptor antagonist ketamine, and dextromethorphan can favorably modify the early neonatal course of severe nonketotic hyperglycinemia, but does not prevent poor long-term outcomes.

Basal Forebrain Histaminergic Transmission Modulates Electroencephalographic Activity and Emergence from Isoflurane Anesthesia

The tuberomammillary histaminergic neurons are involved in the sedative component of anesthetic action. The nucleus basalis magnocellularis (NBM) in the basal forebrain receives dense excitatory innervation from the tuberomammillary nucleus and is recognized as an important site of sleep-wake regulation. This study investigated whether NBM administration of histaminergic drugs may modulate arousal/emergence from isoflurane anesthesia. Microinjections of histaminergic agonists and antagonists were made into the NBM of rats anesthetized with isoflurane. The changes in electroencephalographic activity, including electroencephalographic burst suppression ratio and power spectra, as well as respiratory rate, were recorded under basal conditions and after NBM injection. Time to resumption of righting reflex was recorded as a measure of emergence from anesthesia. The rats displayed a burst suppression electroencephalographic pattern at inhaled isoflurane concentrations of 1.4-2.1%. Application of histamine (1 microg/0.5 microl) to the NBM reversed the electroencephalographic depressant effect of isoflurane; i.e., electroencephalographic activity shifted from the burst suppression pattern toward delta activity at 1.4% isoflurane, and the burst suppression ratio decreased at 2.1% isoflurane. Histamine-evoked activation of electroencephalography was blocked by NBM pretreatment with a H1 receptor antagonist, triprolidine (5 microg/1 microl), but not by a H2 receptor antagonist, cimetidine (25 microg/1 microl). The respiratory rate was significantly increased after histamine injection. NBM application of histamine facilitated, while triprolidine delayed, emergence from isoflurane anesthesia. Histamine activation of H1 receptors in the NBM induces electroencephalographic arousal and facilitates emergence from isoflurane anesthesia. The basal forebrain histaminergic pathway appears to play a role in modulating arousal/emergence from anesthesia.

V11 Poster location 011 Seizures in infants with pyridoxine-dependent epilepsy and pyridoxine phosphate oxidase deficiency

Introduction: We report on seizure symptoms and EEGfindings in 4 infants with pyridoxine-dependent epilepsy (PDE) and in one with pyridoxine phosphate oxidase deficiency (PNPO). Methods: Seizure videos and EEG were analysed and compared with seizure videos from our neonatal archive. PDE and PNPO was proven by response to pyridoxine or pyridoxal 5′-phosphate and by relapse after withdrawal. Mutations in the antiquitin gene were found in 3 patients and in the PNPO gene in 1 child. Results: Prolonged erratic multifocal or generalised myoclonic jerks were observed in all infants as well as abnormal eye movements, grimacing, focal or generalised tonic symptoms, crying and irritability. Symptoms often occurred intermixed and with variable intensity. None of >100 archived neonatal seizures of different aetiologies showed a comparable mix of seizure symptoms. In 2 older infants irritability, inconsolable crying and frightful facial expression was the prominent symptom during withdrawal. Divers visual symptoms occurred in a 4 year old child with PNPO (probably because of underdosing) and were suspected in a 14 month old child with PDE during withdrawal. Ictal EEG was very variable. Beside continuous spike wave discharges or suppression burst pattern we registered multifocal sharp waves, intermittent prolonged periods of suppression or even normal EEG activity during the seizures. Conclusion: PDE or PNPO should be considered in infants with prolonged seizures with mixed multifocal myoclonic tonic symptoms, often associated with grimacing and abnormal eye movements.

Effects of Remifentanil on the Spectrum and Quantitative Parameters of Electroencephalogram in Propofol Anesthesia

A high dose of opioids associated with a low dose of propofol has become a popular anesthetic technique. However, the influence of opioids on the electroencephalographic phenomenon related to induction of anesthesia and, thereby, on the quantitative parameters used in the depth-of-anesthesia estimation is not well known. Twenty-seven patients were divided into three groups to receive saline, low-dose remifentanil (7.5 microg x kg x h) or high-dose remifentanil (30 microg x kg x h) during induction of anesthesia with propofol (30 mg . kg . h). Electroencephalogram was recorded from Fz electrode, and its time-frequency properties in the patient groups were analyzed from the induction of anesthesia to the occurrence of burst suppression pattern. The group differences in 14 quantitative spectral parameters used in the depth-of-anesthesia estimation were examined as well. The time-frequency properties of electroencephalogram were different between groups. The high-frequency (greater than 14 Hz) activity during light anesthesia was decreased in remifentanil groups; whereas, increased activity in extended alpha band (7-14 Hz) and decreased activity in delta band (0.5-4 Hz) was observed during deep anesthesia. This resulted in statistically significant changes in all 14 quantitative parameters. The effect of remifentanil on the spectrum and quantitative parameters of electroencephalogram is significant and strongly dependent on the level of anesthesia. Coadministration of opioids therefore challenges the reliability of the spectral properties of electroencephalogram in the depth-of-anesthesia estimation by using a frontal montage. Furthermore, the finding has implications for design of opioid coadministration studies.

Good outcome in a patient with prolonged comatose state, critically elevated serum neuron-specific enolase and electroencephalic burst-suppression pattern

Introduction: The neurological outcome after cardiopulmonary resuscitation (CPR) is limited by the susceptibility of neurons to the lack of oxygen. Up to 70% of patients with successful restoration of spontaneous circulation (ROSC) later reach a state with severe neurological impairment. Several parameters have been identified in order to predict the neurological outcome after CPR. Prolonged or late-onset CPR, serum neuron-specific enolase (sNSE) values beyond time-related thresholds (33µg/l within 24 hours, 24–33µg/l within 48 hours, 35–40µg/l within 72 hours after ROSC), neurophysiological investigation revealing electroencephalic burst-suppression or generally suppressed patterns or bilateral loss of somatosensory evoked potentials (SEPs) are considered to be associated with a poor neurological outcome.

Using the nonlinear control of anaesthesia-induced hypersensitivity of EEG at burst suppression level to test the effects of radiofrequency radiation on brain function.

BackgroundIn this study, investigating the effects of mobile phone radiation on test animals, eleven pigs were anaesthetised to the level where burst-suppression pattern appears in the electroencephalogram (EEG). At this level of anaesthesia both human subjects and animals show high sensitivity to external stimuli which produce EEG bursts during suppression. The burst-suppression phenomenon represents a nonlinear control system, where low-amplitude EEG abruptly switches to very high amplitude bursts. This switching can be triggered by very minor stimuli and the phenomenon has been described as hypersensitivity. To test if also radio frequency (RF) stimulation can trigger this nonlinear control, the animals were exposed to pulse modulated signal of a GSM mobile phone at 890 MHz. In the first phase of the experiment electromagnetic field (EMF) stimulation was randomly switched on and off and the relation between EEG bursts and EMF stimulation onsets and endpoints were studied. In the second phase a continuous RF stimulation at 31 W/kg was applied for 10 minutes. The ECG, the EEG, and the subcutaneous temperature were recorded.ResultsNo correlation between the exposure and the EEG burst occurrences was observed in phase I measurements. No significant changes were observed in the EEG activity of the pigs during phase II measurements although several EEG signal analysis methods were applied. The temperature measured subcutaneously from the pigs' head increased by 1.6°C and the heart rate by 14.2 bpm on the average during the 10 min exposure periods.ConclusionThe hypothesis that RF radiation would produce sensory stimulation of somatosensory, auditory or visual system or directly affect the brain so as to produce EEG bursts during suppression was not confirmed.

Low bispectral index values in hydranencephaly

Editor, We read with great interest the article by Prabhakar et al. [1] regarding the use of bispectral index (BIS) monitoring for an elective frontal craniotomy and fenestration in a 2-year-old boy with bilateral frontal lobe porencephalic cysts. During the procedure, the patient presented low preanaesthetic BIS values (39) that showed no significant change (between 30 and 40), despite a reduction in the inspired concentration of sevoflurane from 1 to 0.2%. No burst suppression pattern was observed, and BIS values remained low after anaesthetic recovery. In the discussion, the authors suggest that intracranial pressure increments could be responsible for the low BIS values.