EEG Pattern Reflects Brain's Shift into Protective Mode

Burst suppression is a characteristic of an inactivated brain and is commonly observed at deep levels of general anesthesia (GA), hypothermia, and in pathological conditions such as coma and early infantile encephalopathy.

Using a biophysical computational model the researchers elucidated a unifying mechanism that showed how the prevailing features of burst suppression might arise through the interaction between neuronal dynamics and brain metabolism. In each condition, the model suggests that a decrease in cerebral metabolic rate, coupled with the stabilizing properties of adenosine triphosphate (ATP)-gated potassium channels, leads to the characteristic epochs of suppression. The model suggests that when brain energy supplies drop too low and cause a deficiency in ATP, potassium leaks from the nerve cells and signal transmission halts. The study was published early online on February 7, 2012, in the Proceeding of the National Academy of Sciences (PNAS).

“It looks like burst suppression shifts the brain into an altered physiologic state to allow for the regeneration of ATP, which is the essential metabolic substrate; during suppression, the brain is trying to recover enough ATP to restart,” said lead author postdoctoral fellow ShiNung Ching, PhD, of the MGH department of anesthesia, critical care, and pain medicine. “If the substrate doesn't regenerate quickly enough, the system will have these brief bursts of activity, stop and then need to recover again. The length of suppression is governed by how quickly ATP regenerates, which matches the observation that the deeper someone is anesthetized, the longer the periods of suppression.”

Burst suppression is characterized by periods of normal, high brain activity (the bursts) that are interrupted by stretches of greatly reduced activity that can last 10 seconds or longer. Previous investigations of burst suppression focused on characterizing the structure of the EEG patterns and understanding the brain's responsiveness to external stimuli while in this state, but not on understanding the underlying mechanism.

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