Burst suppression

Burst suppression is an electroencephalography (EEG) pattern that is characterized by periods of high-voltage electrical activity alternating with periods of no activity in the brain. The pattern is found in patients with inactivated brain states, such as from general anesthesia, coma, or hypothermia. This pattern can be physiological, as during early development, or pathological, as in diseases such as Ohtahara syndrome.

The burst suppression pattern was first observed by Derbyshire et al. while studying effects of anesthetics on feline cerebral cortices in 1936, where the researchers noticed mixed slow and fast electrical activity with decreasing amplitude as anesthesia deepened. In 1948, Swank and Watson coined the term "burst-suppression pattern" to describe the alternation of spikes and flatlines in electrical activity in deep anesthesia. It wasn't until after the early 1960s that the burst suppression pattern began being used in medical settings; it had been primarily observed in animal studies and psychosurgeries.

In 1952, Henry and Scoville recorded the electrical activity of patients during lobotomy and found the burst suppression pattern present in the recorded electrical activity. In 1963, Fischer-Williams and Cooper found the pattern present in patients suffering from cerebral anoxia, hypoxia, and various types of intracortical lesions. Treiman et al. observed the pattern in deep coma, various infantile encephalopathies, and the final stages of deteriorated status epilepticus. Both Schwartz et al. in 1989 and Akrawi et al. in 1996 observed the pattern when the brain was subject to hypothermia and high levels of many sedative and anesthetic agents.

The pseudo-rhythmic pattern of burst suppression is dictated by extracellular calcium depletion and the ability of neurons to restore the concentration. Bursts are accompanied by depletion of extracellular cortical calcium ions to levels that inhibit synaptic transmission, which leads to suppression periods. During suppression, neuronal pumps restore the calcium ion concentrations to normal levels, thus causing the cortex to be subject to the process again. As the brain becomes more inactive, burst periods become shorter and suppression periods become longer. The shortening of bursts and lengthening of suppression is caused by the central nervous system's inability to properly regulate calcium levels due to increased blood-brain permeability.

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