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Results for “Burst-suppression”

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At least 19 recordsLinked to original sources

PubMed1978

[Transitory burst-suppression pattern in endogenous-exogenous encephalopathy (author's transl)].

A status epilepticus was observed in a 22 year old female patient during endotoxinshock. The status epilepticus was treated with a high dosage of diazepame. The EEG showed a burst suppression pattern, in our case mixed by anoxia and diazepame. The burst-suppression pattern and the clinical suspicion of delayed degradation of diazepame caused by toxic hepatic failure suggested the therapy of forced diuresis. This therapy was followed by decreasing suppression periods, indicating the dominante influence of the hypnotic drug. This result shows the diagnostic as well as the therapeutic value of forced diuresis in this case.

Adult↗

PubMed1991

Variance of interburst intervals in burst suppression.

Each EEG performed over a 3 year period at the University of Michigan with a diagnosis of generalized burst-suppression (BS) was reviewed. Ten EEGs from 10 patients with hypoxic-ischemic encephalopathy (HIE-BS) and 21 records from 8 patients with pentobarbital induced burst-suppression for treatment of status epilepticus (SE-BS) were reviewed. For each EEG, the mean duration of 40 interburst intervals (IBIs) as well as their coefficient of variability were calculated. We found that in the SE-BS group the coefficient of variability of IBI duration was highly correlated with the logarithm of mean IBI duration while in the HIE-BS group, there was no significant correlation between these 2 variables. This suggests that the underlying mechanism causing BS is different in the 2 groups and might be related to a uniform and progressive affection of similar brain structures in the SE-BS group and a more patchy and variable pathology in the HIE-BS group.

Adolescent↗

PubMed1979

Heart rate variability in full-term normal and abnormal newborn infants during sleep.

Heart rate variability was studied in normal and abnormal newborn infants during sleep in relation to the EEG background. The background EEGs of the full-term newborn infants were classified into normal, minimal depression, mild depression, moderate depression, burst-suppression and flat patterns in order of increasing severity. Nonsequential and sequential histograms were produced with the aid of a computer from some 500 consecutive RR intervals of the ECG recorded on a magnetic tape during polygraphic recordings. The seuential curves mainly showed fast oscillation during quiet sleep and slow oscillation during active sleep in normal infants. The infants who had moderately depresed EEGs presented pronounced oscillation. In those whose EEGs displayed burst-suppression and flat patterns, the sequential curves showed very little heart rate variability. They were often flat (fixed heart rate). Thus, heart rate variability was found to be one of the valuable parameters in evaluating abnormality of the CNS in newborn infants.

Asphyxia Neonatorum↗

PubMed2026

Early infantile developmental and epileptic encephalopathy: clinical spectrum, diagnosis, outcomes, and evolving treatment strategies.

Early infantile developmental and epileptic encephalopathy (EIDEE) is among the most severe epilepsy syndromes, with onset before three months of age and an estimated incidence of approximately 10 per 100,000 live births. The 2022 International League Against Epilepsy classification unified the historically distinct Ohtahara syndrome and early myoclonic encephalopathy under a single diagnostic framework defined by frequent drug-resistant tonic and/or myoclonic seizures, an abnormal neurological examination, and an abnormal interictal electroencephalogram-most characteristically a burst-suppression pattern. This narrative review synthesizes the clinical, electrophysiological, neuroimaging, genetic, and therapeutic literature within the EIDEE framework. The clinical phenotype is characterized by central hypotonia, postnatal microcephaly, cortical visual impairment, and age-dependent syndromic evolution toward infantile epileptic spasms syndrome or Lennox-Gastaut syndrome in the majority of patients. Electroencephalography remains essential for syndromic classification, while systematic metabolic screening and early trio whole-exome or whole-genome sequencing are central to the etiologic workup, achieving diagnostic yields of 60-65%. The most commonly identified genetic causes include STXBP1, KCNQ2, and SCN2A variants. Outcomes are poor overall and strongly etiology-dependent: vitamin-responsive disorders carry a substantially more favorable prognosis, whereas mortality reaches 25% in genetic cohorts. Genotype-guided pharmacotherapy is now applicable to a clinically meaningful subset of patients, with sodium channel blockers, potassium channel openers, and emerging antisense oligonucleotide therapies representing important therapeutic advances. Gene therapy trials are underway but have encountered early safety signals, underscoring the vulnerability of this population. Critical unmet needs include earlier molecular diagnosis, precision therapies targeting developmental outcomes beyond seizure control, and prospective international registries to characterize the long-term natural history of EIDEE.

Humans↗

PubMed1977

EEG recognition of Aicardi's syndrome.

Thirty-two EEGs from six cases of Aicardi's syndrome were reviewed. A characteristic EEG pattern was found in all cases. This consists of multifocal epileptiform abnormalities occurring on a burst-suppression pattern showing complete asynchrony between the two hemispheres. This pattern has been described so far only in Aicardi's syndrome. These characteristic EEG features are more readily found early in the course of the disease and occur less frequently six months after from the onset of symptoms, at which time they are often replaced by multiple epileptic foci on a severely disorganized background. The EEG sleep pattern was profoundly altered in all stages of the disease. The EEG is considered a helpful tool in the diagnosis of Aicardi's syndrome.

Bone and Bones↗

PubMed1991

Electroencephalographic mapping during isoflurane anesthesia for treatment of mental depression.

Seven patients undergoing isoflurane anesthesia were studied using electroencephalographic (EEG) mapping, a computer-assisted technique of EEG processing that permits the analysis of the spatial distribution of frequency components of the human EEG. After induction with thiopental, the patients were hyperventilated (carbon dioxide tension, 25 to 28 mm Hg) with 4% isoflurane in oxygen until a burst-suppression EEG appeared. Brain electrical activity was compared before anesthesia, at 0.5 to 0.8% and 1.8 to 2.1% isoflurane, during bursts, and after anesthesia. Starting from an alpha EEG with occipital predominance, a distinct alpha activation appeared over the whole cortex during 0.5 to 0.8% isoflurane. Decreased alpha amplitude with a maximum over the frontotemporal regions was observed during 1.8 to 2.1% isoflurane. Bursts consisted of high amplitude in all frequency bands. In the delta and the theta bands, voltage was very low before isoflurane administration, and increased in relation to depth of anesthesia. A minimum in delta and theta amplitudes occurred over both central regions. The dominant frequency, defined as the frequency component with the highest amplitude in the frequency spectrum, decreased from 8 to 4 and finally to 1 Hz, while its amplitude increased from 3 to 13 microV. As anesthesia deepened, the dominant frequency shifted from the occiput to the frontal cortex. Brain mapping transfers an immense amount of electroencephalographic (EEG) data into a comprehensive, easily readable image of brain function during anesthesia for therapy of mental depression. To make use of this technique in the operating room, further investigation and development toward on-line mapping are necessary.

Adult↗

PubMed1991

EEG changes during recovery from acute severe neonatal citrullinemia.

We report our observations of serial clinical and EEG examinations in 3 neonates during recovery from acute severe encephalopathy due to citrullinemia. Their electroclinical picture closely resembles the clinical stages of experimental models of hyperammonemia in monkeys. The length of the EEG interburst interval, a quantitative measure of EEG background abnormality, correlated with elevated serum levels of ammonia and suggests that hyperammonemia itself is a key figure in the genesis of encephalopathy in this condition. Finally, the manner in which the EEG normalizes during recovery from hyperammonemia in this setting suggests that burst-suppression resembles an exaggerated regression to the discontinuity of the very premature infant.

Ammonia↗

PubMed1992

Correlations between verbal memory performance and electrocorticographically determined suppression of electrical brain activity in intracarotid amobarbital tests.

As a part of presurgical evaluation, bilateral intracarotid amobarbital procedures (IAPs) were performed in 42 patients (84 tests) with long-standing, medically intractable complex-partial seizures. During the IAPs, electrocorticographic (ECoG) recording was carried out via bilaterally implanted subdural electrodes. Five distinct patterns of suppression of electrical brain activity were observed: (1) an isoelectric line; (2) a burst-suppression pattern; (3) polyphasic waves; (4) high-voltage beta; and (5) low-voltage beta activity. Further, two types of specific reactions of the epileptic focus were detectable: (1) spike-burst-suppression patterns (SBS; 11 left; 7 right; 6 in both IAPs) and amobarbital-induced spikes (7 left; 4 right). ECoG suppression patterns as well as SBS and spike induction showed great variability in duration and overall occurrence. To determine the influence of these amobarbital-induced ECoG changes on results of IAP memory testing, performance in a verbal learning task was analyzed according to the ECoG patterns predominant during encoding. In left IAPs, it was found that SBS at the beginning of or during encoding had a significant negative effect on verbal memory. In right IAPs, verbal memory performance improved significantly with the decline of ECoG suppression. Hence, verbal memory performance in IAPs is significantly affected by specific ECoG suppression patterns and activation of the epileptic focus.

Adolescent↗

PubMed1991

Intractable seizures from infancy can be associated with dentato-olivary dysplasia.

Five children with severe developmental delay had intractable fits of various types but tonic, often extensor, seizures were prominent from an early stage. Onset was in the neonatal period in 4 cases. EEGs were severely abnormal and showed a "burst-suppression" pattern in the first months of life. There were no metabolic or consistent neuroradiological abnormalities. A distinctive form of dentato-olivary dysplasia was found in all cases. Inferior olives were hook-shaped, coarse and lacking undulations, while dentate nuclei showed a compact arrangement of interconnected islands. The clinico-pathological findings form a novel nosological entity.

Apgar Score↗

PubMed1990

Vasoparalysis associated with brain damage in asphyxiated term infants.

The relationship of cerebral blood flow to acute changes in arterial carbon dioxide and mean arterial blood pressure (MABP) was determined during the first day of life in 19 severely asphyxiated term infants supported by mechanical ventilation. For comparison, 12 infants without perinatal asphyxia were also investigated. Global cerebral blood flow (CBF infinity) was determined by xenon 133 clearance two or three times within approximately 2 hours. During the cerebral blood flow measurement, the amplitude-integrated electroencephalogram and visual-evoked potential were recorded. Changes in arterial carbon dioxide pressure followed adjustments of the ventilator settings, whereas MABP fluctuated spontaneously. Arterial oxygen pressure and blood glucose concentration were in the normal range. Five of the asphyxiated infants had isoelectric electroencephalograms and died subsequently with severe brain damage. They had a high CBF infinity (mean 30.6 ml/100 gm/min) and abolished carbon dioxide and MABP reactivity. Lower CBF infinity (mean 14.7 ml/100 gm/min) and abolished MABP reactivity were found in another five asphyxiated infants with burst-suppression electroencephalograms in whom computed tomographic or clinical signs of brain lesions developed. The carbon dioxide reactivity was preserved in these infants. In the remaining nine asphyxiated infants without signs of central nervous system abnormality, carbon dioxide and MABP reactivity were preserved, as was also the case in the control group. We conclude that abolished autoregulation is associated with cerebral damage in asphyxiated infants and that the combination of isoelectric electroencephalograms and cerebral hyperperfusion is an early indicator of very severe brain damage.

Asphyxia Neonatorum↗

PubMed1992

Effects of midazolam on electroencephalograms of seriously ill patients.

Midazolam hydrochloride, a water-soluble benzodiazepine for intravenous injection, is frequently used to provide sedation to mechanically ventilated patients in the critical-care unit. Although the effects of midazolam on the electroencephalograms (EEGs) of healthy volunteers have been reported previously, to our knowledge such effects in ill patients have not been documented. Herein we describe the effects of intravenously administered midazolam on the EEGs of eight seriously ill patients (age range, 49 to 80 years; mean, 69 years). The EEGs showed drug-induced relatively fast (alpha or beta) frequency activity superimposed on delta slowing in six patients and mild to moderate voltage attenuation in three patients. An alpha frequency coma pattern, a transient burst-suppression pattern, and a spindle coma pattern were also seen. Thus, the effects of intravenously administered midazolam on the EEGs of seriously ill patients are similar to those noted after the administration of other benzodiazepines. These potential effects should be considered when their EEG tracings are interpreted.

Aged↗

PubMed1991

[Cerebral anoxia in near-drowning of children. The prognostic value of EEG].

The retrospective electroclinical evaluation of anoxia by near-drowning in 23 children observed between 1985 and 1989 revealed 2 groups, each with a distinct evolution: the first group, with good prognosis of 17 children, which recovered consciousness without neurological complications between 2 d and 1 wk after the accident. The second group of 6 children with a poor outcome--either i), death; or ii), state of permanent injury; or iii), a high level of clinical deficits. The gravity of the early clinical state, the estimated duration of cardiorespiratory arrest, the severity of the hypothermia, the seizures and the paroxysmic activity, do not determine the severity of near-drowning encephalopathy. The EEG patterns described in correlation with the group and the clinical outcome permitted determination of prognostic criteria. A good prognostic consisted of the following: moderate background activity, sleep patterns, response to auditory and painful stimulations, and numerous beta rhythms. A bad outcome was defined by: high voltage, rhythmic delta waves; biphasic sharp waves; monotonous EEG, "burst-suppression" pattern, absence of beta rhythms. The importance of EEG recordings is emphasized performed as early as possible and until 3 or 7 d after the near-drowning. Any modification in the EEG, with attenuation or disappearance of fast frequencies and painful reactivity, appearance or enhancement of slow and biphasic sharp waves, are ominous signs and may be accompanied by the appearance of cerebral oedema and decerebration.

Child↗

PubMed1992

Repeated negative DC deflections in rat cortex following middle cerebral artery occlusion are abolished by MK-801: effect on volume of ischemic injury.

Following permanent occlusion of the left middle cerebral artery (MCA) in rats, electrophysiological and hemodynamic characteristics of the periinfarct border zone were investigated in sham-operated (n = 6), untreated (n = 6), and MK-801-treated (3.0 mg/kg; n = 6) animals. For this purpose, direct current potential (DC), EEG, and blood flow (laser-Doppler flowmetry) were recorded from the cortex in the periphery of the MCA territory. In sham-operated rats, a single negative cortical DC deflection was observed after electrocoagulation of the cortex, whereas in untreated MCA-occluded animals, three to eight transient DC deflections were monitored during the initial 3 h of ischemia. The duration of these cortical DC shifts gradually increased from 1.2 +/- 0.3 to 3.7 +/- 2.7 min (mean +/- SD; p less than 0.05) during this time. In animals treated intraperitoneally with MK-801 (3.0 mg/kg) immediately after MCA occlusion, the number of cortical DC shifts significantly declined to one to three deflections (p less than 0.005). The EEG of the treated animals revealed low-amplitude burst-suppression activity. In the untreated and treated experimental group, the reduction of cortical blood flow amounted to 69 +/- 25 and 49 +/- 13% of control, respectively. Despite the more pronounced cortical oligemia, MK-801 treatment resulted in a significant decrease of the volume of the ischemically injured tissue from 108 +/- 38.5 (untreated group) to 58 +/- 11.5 (p less than 0.05) mm3. Our results suggest that repetitive cortical DC deflections in the periinfarct border zone contribute to the expansion of ischemic brain infarcts.

Action Potentials↗

PubMed1978

Sympathetic nervous system response to lidocaine induced seizures in cats.

The effect on arterial pressure, EEG, preganglionic sympathetic nervous activity and pulse rate of repeated intravenous administrations of lidocaine (3 mg/kg) was investigated in cats anaesthetized with nitrous oxide. A continuous high voltage, burst-suppression EEG indicating constant seizure activity was found, whereas arterial pressure and sympathetic nervous activity did not change significantly. Although the onset of EEG seizure activity did not change the mean sympathetic activity level, the pattern of firing changed dramatically as every EEG seizure triggered a burst of sympathetic impulses. Barostatic reflexes were active after lidocaine administration unless seizure activity occurred. Thiopental 5 mg/kg given intravenously to cats during continuous lidocaine-induced EEG seizures always abolished the seizure activity without excessive depression of arterial pressure.

Animals↗

PubMed1991

Status epilepticus: clinical experience with two special devices for continuous cerebral monitoring.

Continuous cerebral monitoring (CCM) was performed on 34 patients in status epilepticus (SE), using changes in amplitude detected by the cerebral function monitor (CFM) and changes in frequency detected by compressed spectral array (CSA). The EEG was used intermittently to help identify seizure patterns obtained with these methods. Seventeen patients in clinically manifest SE also had non-convulsive seizures. In 17 patients, SE was refractory to conventional anticonvulsants, requiring treatment with pentobarbital or paraldehyde. In these patients, CCM provided dynamic electroencephalographic monitoring of burst-suppression and prompt detection of breakthrough seizures. Patients in SE should undergo CCM to differentiate between non-convulsive seizures and post-ictal state both of which may produce prolonged unresponsiveness following clinical seizures. CCM after data reduction with the two special devices used is a viable and practical alternative to continuous conventional EEG monitoring during SE. However, in order to evaluate the sensitivity and specificity of these methods, it will be necessary to design a study in which both the EEG and the devices using data reduction be used continuously and concurrently.

Adolescent↗

PubMed1979

Patterns resembling tracé alternant in quiet sleep of an adult.

An 18-year-old man with lymphoma and Listeria meningitis developed a pattern similar to tracé alternant during quiet sleep. This is a pattern normally seen in the neonate during quiet sleep and probably represents diffuse brain disturbance of both cortical and deep gray matter if occurring in the adult, as with other discontinuous or burst-suppression patterns.

Adolescent↗

PubMed1990

The significance of myoclonic status epilepticus in postanoxic coma.

We report 11 adults who exhibited myoclonic status epilepticus (MSE) after cardiac arrest. Based on pathologic, electroencephalographic, and clinical evidence, we conclude that our patients died from the initial anoxic-ischemic insult rather than as a result of MSE. We suggest that the seizures in these nonsurvivors were self-limited events arising from lethal damage to neurons. Thus, in patients with bilaterally synchronous facial myoclonus, bilateral loss of pupillary or oculovestibular reflexes, and suppression and burst-suppression on EEG, it is not warranted to use anesthetic barbiturates to treat MSE.

Adult↗

PubMed1990

Myoclonic status epilepticus: a clinical and electroencephalographic study.

We reviewed the clinical features and ictal EEGs in 23 adults with myoclonic status epilepticus (MSE). Anoxic encephalopathy was the most common cause of MSE, occurring in 15 patients; 8 developed MSE within 14 hours following the anoxic insult. Metabolic encephalopathies were present in 4 patients, while 2 had degenerative CNS disorders. In 2 patients with generalized epilepsy, MSE developed during a medication change. Five types of EEG patterns were associated with MSE. Generalized periodic complexes (usually spikes, polyspikes, or sharp waves), often with attenuation of background activity between complexes (11 patients) or a burst-suppression pattern (4 patients), were the most common types. Outcome was poor: 20 patients died without regaining consciousness, while 1 remains in a vegetative state. The 2 patients with generalized epilepsy, both of whom were conscious during MSE, survived without sequelae.

Adult↗