The Electroencephalogram (EEG) records the electrical activity of the brain through electrodes placed on the scalp. Normally, this monitoring shows continuous, rhythmic wave patterns reflecting the subject’s state of consciousness. Burst suppression (BS) is an extremely abnormal EEG pattern signaling a profound state of diffuse cerebral depression or inactivation. This discontinuous pattern alternates between two drastically different states of electrical output, indicating that brain metabolism and oxygen consumption have been significantly reduced. It is a state just short of a completely flatline EEG, which denotes total electrocerebral inactivity.
Visualizing the Burst Suppression Pattern
The burst suppression pattern is visually distinct, defined by the systematic, quasi-periodic alternation between two phases on the EEG tracing. The first phase is the “burst,” which appears as a short period of high-voltage, high-frequency electrical activity. These bursts typically show a mix of slow waves, sharp waves, or spikes, with amplitudes often ranging between 75 and 250 microvolts (µV).
The second phase is the “suppression,” characterized by a period of near-total electrical silence or marked inactivity. This is seen as a flattened, low-amplitude line, often defined as activity below 5 µV lasting for at least half a second. This suppressed phase reflects a temporary, widespread cessation of synchronized synaptic activity, suggesting a deep reduction in neuronal function.
Clinicians use the Burst Suppression Ratio (BSR) to quantify the pattern and measure the intensity of cerebral depression. The BSR represents the percentage of time the brain tracing spends in the suppressed state within a given monitoring epoch. A BSR of zero means the brain is continuously active, while a BSR of one hundred indicates complete electrocerebral inactivity. Monitoring the BSR allows for objective tracking of the depth of brain inactivation, particularly in therapeutic settings where the pattern is intentionally induced.
Contexts Where Burst Suppression Occurs
Burst suppression arises from two broad categories: conditions intentionally induced for medical treatment and those resulting from severe underlying pathology. Differentiating these contexts is foundational to understanding the patient’s neurological state. Induced causes are generally temporary and reversible, while pathological causes reflect severe, spontaneous injury to the brain.
One common induced cause is deep general anesthesia, particularly with GABAergic agents like propofol or barbiturates. These medications are administered at high doses to achieve profound brain inactivation, reducing the brain’s metabolic rate and oxygen demand to protect neurons during certain surgeries. In these controlled settings, the anesthesiologist monitors and adjusts the drug infusion rate to maintain a targeted BSR.
Burst suppression is also intentionally induced to treat refractory status epilepticus, a life-threatening, continuous seizure state that resists initial medications. Clinicians induce a medically controlled coma, typically targeting a BSR between 50% and 95%, to halt seizure activity and prevent neuronal damage. Another induced context is controlled therapeutic hypothermia, where lowered body temperature slows brain metabolism and produces the burst suppression pattern to protect the brain following injury.
Pathological burst suppression occurs spontaneously due to severe injury or metabolic failure. The most common pathological cause is severe anoxic brain injury, widespread damage resulting from a lack of oxygen, often following cardiac arrest. This pattern can also appear in patients in a deep coma caused by massive trauma, profound metabolic disturbances, or drug intoxication. Furthermore, rare genetic conditions, such as Ohtahara syndrome, are characterized by a persistent burst suppression pattern.
Interpreting Clinical Significance and Prognosis
The clinical significance of burst suppression depends entirely on whether the pattern is induced or results from spontaneous pathology. In the induced setting, the pattern serves as a monitoring tool and electrophysiological endpoint. It assures the critical care team that the patient has reached the required depth of anesthesia or is receiving sufficient treatment to control continuous seizures.
Maintaining a controlled BSR under deep anesthesia indicates cerebral protection during procedures like cardiac surgery, where reducing metabolic demand is beneficial. Conversely, in critically ill patients not being treated for seizures, unintended burst suppression due to over-sedation is associated with increased mortality and longer hospital stays.
In the context of spontaneous pathological causes, the pattern carries significant prognostic value. Burst suppression that appears soon after severe anoxic brain injury and persists without sedating medications is traditionally associated with a very poor neurological outcome. A specific pathological pattern, “burst suppression with identical bursts,” has been linked to particularly poor outcomes in comatose patients following cardiac arrest.
Newer research suggests that the prognostic value is complex and depends on the pattern’s evolution and specific clinical context, especially following therapeutic hypothermia. While pathological burst suppression remains a serious finding, the decision regarding brain recovery is influenced by the pattern’s persistence, morphology, and presence before or after the patient was weaned off sedatives. These characteristics help guide the clinical team in making informed decisions about the likelihood of regaining consciousness.