Abstract
The electroencephalogram (EEG) reflects brain electrical activity. A flat (isoelectric) EEG, which is usually recorded during very deep coma, is considered to be a turning point between a living brain and a deceased brain. Therefore the isoelectric EEG constitutes, together with evidence of irreversible structural brain damage, one of the criteria for the assessment of brain death. In this study we use EEG recordings for humans on the one hand, and on the other hand double simultaneous intracellular recordings in the cortex and hippocampus, combined with EEG, in cats. They serve to demonstrate that a novel brain phenomenon is observable in both humans and animals during coma that is deeper than the one reflected by the isoelectric EEG, and that this state is characterized by brain activity generated within the hippocampal formation. This new state was induced either by medication applied to postanoxic coma (in human) or by application of high doses of anesthesia (isoflurane in animals) leading to an EEG activity of quasi-rhythmic sharp waves which henceforth we propose to call ν-complexes (Nu-complexes). Using simultaneous intracellular recordings in vivo in the cortex and hippocampus (especially in the CA3 region) we demonstrate that ν-complexes arise in the hippocampus and are subsequently transmitted to the cortex. The genesis of a hippocampal ν-complex depends upon another hippocampal activity, known as ripple activity, which is not overtly detectable at the cortical level. Based on our observations, we propose a scenario of how self-oscillations in hippocampal neurons can lead to a whole brain phenomenon during coma.
Highlights
Regardless of the underlying causes, coma is a state during which the brain reaches a low level of neuronal activity and metabolism
We have shown that coma induced by a variety of anesthetics presents a time-frame during which the cortex is in a hyperexcitable state that is responsible for the genesis of the burstsuppression (BS) pattern [1]
It was dominated by bursts of rhythmic spike-like discharges, somewhat akin in shape and frequency to hippocampal ripple events (Rs), with each burst lasting for several seconds
Summary
Regardless of the underlying causes, coma is a state during which the brain reaches a low level of neuronal activity and metabolism. Possible etiologies range from safe and fully reversible pharmacological interventions (such as general anesthesia) to severe, irreversible brain damage. There is virtually no systematic investigation of the cerebral cellular mechanisms at work during coma and attempts to compare pathological and pharmacological etiologies are scarce. It is no surprise that the outcome from coma is often predicted on a statistical basis. We have shown that coma induced by a variety of anesthetics presents a time-frame during which the cortex is in a hyperexcitable state that is responsible for the genesis of the burstsuppression (BS) pattern [1]. We reported evidence that isoflurane-induced BS opens the blood-brain barrier [2]
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