The burst suppression (BS) pattern on electroencephalogram (EEG) was first demonstrated in 1936 by Derbshire et al. in response to anesthetics. The term "burst suppression" was introduced by Swank and Watson in 1948 in experiments studying the effects of barbiturates on EEG patterns in various areas of the brain.
BS is a periodic pattern of high-voltage, slow, sharp, spiking complexes that are interspersed by low-voltage (<10 mV) complexes or isoelectric periods.
At present, BS is usually induced with barbiturates or other anesthetics in order to decrease cerebral metabolic activity in the setting of focal ischemia or status epilepticus.
Physiology Principles
Neuronal electrical activity accounts for 5060% of the brain's oxygen consumption. Thus, suppression of electrical activity with anesthetic and sedative medications can help restore a favorable balance between oxygen delivery and consumption.
Technique: EEG can be monitored with as little as 1 lead in the OR or a full EEG in the ICU. In the ICU, it can be performed by an anesthesiologist or neuromonitoring team. An amplitude-integrated EEG (aEEG) is used to simplify long-term monitoring of brain function. It filters the EEG and displays it on a compressed time scale, providing a simplified method to monitor brain activity.
BS is defined as a burst of slow, sharp, and spiking activity followed by reduced or suppressed electrical activity. There is no universal standard; however, most clinicians aim for an interburst interval of about 10 s.
Anatomy
Barbiturates bind to the GABAA receptor (a chloride ion channel) and potentiate the effect of GABAA neurotransmitter. This results in chloride ion entry into the cell and hyperpolarization; the action potential of postsynaptic neurons is increased and neuronal signaling activity is decreased.
Inhaled anesthetic agents inhibit excitatory neurotransmission and potentiate inhibitory receptors and ion channels. This leads to decreased oxygen requirements and ATP production associated with signaling activity.
It has been proposed that the thalamus generates a "fundamental brain-rhythm," which is relatively resistant to the effects of anesthetics. Modern agents act primarily on the cerebral cortex; thus, the characteristic BS pattern emerges at this site before thalamic suppression.
Physiology/Pathophysiology
Hypothermia: Therapeutic hypothermia (TH) following adult cardiac arrest alters prognostic accuracy. Monitoring the EEG for BS can aid with predicting outcome and titrating temperature; the presence of BS is associated with unfavorable outcomes.
Encephalopathy: Burst suppression is characteristic of early myoclonic encephalopathy (EME) and Ohtahara syndrome2 rare and devastating CNS disorders of infancy.
EME is characterized by erratic myoclonic activity. Simple partial seizures, general myoclonus, and tonic spasms can also occur. Severe developmental delay, marked hypotonia, and altered level of consciousness are consistent findings. Some patients deteriorate into a vegetative state.
Ohtahara syndrome is a precursor to West Syndrome and LennoxGastaut syndrome. Frequent tonic spasms appear in the 1st month of life and partial motor seizures may occur. Marked developmental delay and intractable epilepsy are common in patients who survive beyond infancy.
Premature infants
Intracranial hemorrhage: BS with low voltage has a 100% positive predictive value although a lower negative predictive value.
Hypoxia/asphyxia: The presence of BS suggests a poor prognosis.
Perioperative Relevance
Induced BS: The BS pattern on EEG can be used clinically to titrate general anesthetics to their maximally effective dose, as well as for any procedure where there is a chance of focal brain ischemia (e.g., aneurysm clipping, carotid endarterectomy, large intracranial masses, etc.). However, a growing body of evidence suggests that BS doses of anesthetics, especially barbiturates, are not necessary for optimal brain protection.
Barbiturates: Drug metabolism is slowed at levels required to achieve BS and it may take several hours for the patient to emerge. This typically requires postoperative intubation/continued ventilatory support and delays neurologic examination. Consequently, this technique has fallen out of favor in modern neurosurgical anesthesia.
Can be induced with any inhaled or intravenous induction agent; however, evidence of brain protection is only available with isoflurane and barbiturates.
Seizure treatment: Seizure activity is characterized by an abnormal increase in electrical activity that increases the demand for oxygen. This can quickly lead to ischemia. Decreasing oxygen consumption can effectively protect neurons from injury.
Incomplete cerebral ischemia: In this setting, areas of the brain adjacent to the ischemic region (penumbra) may be subject to low oxygen concentrations. Since neurons in the penumbra remain intact immediately after an infarct, decreasing their oxygen demand can limit the extent of neurologic injury
Global ischemia: Anesthetic-induced BS following global ischemia, such as in cardiac arrest, has not been shown to improve neurologic outcome since brain autoregulation remains intact and the oxygen requirements to maintain electrical activity do not increase.
BIS: Only the EEG pattern on the BIS may be correlated; BS does not correlate with any particular BIS number.
Graphs/Figures
FIGURE 1. Burst suppression is characterized by a periodic pattern of high-voltage, slow, sharp, spiking complexes that are interspersed by low-voltage complexes or isoelectric periods.
References⬆⬇
ChalakLF, SikesNC, MasonMJ, et al.Low-voltage aEEG as predictor of intracranial hemorrhage in preterm infants. Pedtiatr Neurol. 2011;44(5):364369.
DerbyshireAJ, RempelB, forbesA, et al.The effects of anesthetics on action potentials in the cerebral cortex of the cat. Am J Physiol. 1936;116:577596.
DrummondJ.Brain protection during anesthesia: A reader's guide. Anesthesiology. 1993;79:877880.
HenryCE, ScovilleWB.Suppression-burst activity from isolated cerebral cortex in man. EEG Clin Neurophysiol. 1952;1:122.
Judy-FrayF, KroegerD, OanaC, et al.Cortical inhibition during burst suppression induced with isoflurane anesthesia. J Neurosci. 2009;29:98509860.
NiedermeyerE.The burst-suppression electroencephalogram. Am J Electroneuro-diagnostic Technol. 2009;49:333334.
The burst suppression pattern on EEG can be used to determine maximal effector site concentration of various anesthetics used in general anesthesia.
Pharmacologic suppression of cortical electrical activity may be beneficial in protecting the brain after focal ischemia but has no neuroprotective effects following global ischemia.
Intravenous anesthetic agents, such as barbiturates, propofol, and etomidate, may be used to decrease ICP secondary to traumatic brain injury, but they have not been shown to decrease the extent of neurologic injury.