Emery Brown
Department of Medical Engineering and Neuroscience
Massachusetts Institute of Technology
(October 17, 2016)
The Dynamics of the Unconscious Brain Under General Anesthesia
The experience of being under anesthesia is a strange one. How do these medications block consciousness, pain and movement, leaving us unable to recall what has been happening around us? Dr. Emory Brown discussed his work measuring brain activity in patients under general anesthesia. He has found that the altered states of consciousness are associated with oscillations, or regular bursts of brain activity. These oscillations make it more difficult for brain areas to communicate with one another. Dr. Brown also discussed results showing that the response to anesthesia changes with the type of medication used and among different age groups.
General anesthesia is a man-made, drug-induced process that has enabled the safe and human provision of invasive diagnostic and surgical care for 170 years. During the last 10 years, our laboratory has helped define the neurophysiological mechanisms through which anesthetics induce altered arousal states. We discuss the implications of these new insights for creating translational opportunities in anesthesiology, in other fields of clinical neuroscience, and for gaining a new, fundamental understanding of how the brain’s arousal systems work.
General anesthesia is comprised of five behavioral states: unconsciousness, amnesia (loss of memory), analgesia (loss of pain sensation), akinesia (immobility), and hemodynamic stability with control of the stress response. Our work shows that a primary mechanism through which anesthetics create these altered states of arousal is by initiating and maintaining highly structured oscillations. These oscillations impair communication among brain regions. We illustrate this effect by presenting findings from our human studies of general anesthesia using high-density EEG recordings and intracranial recordings. These studies have allowed us to give a detailed characterization of the neurophysiology of loss and recovery of consciousness due to propofol. We show how these dynamics change systematically with different anesthetic classes and with age. We present a neuro-metabolic model of burst suppression, the profound state of brain inactivation seen in deep states of general anesthesia. We use our characterization of burst suppression, to implement a closed-loop anesthesia delivery system for control of a medically induced coma. Finally, we demonstrate that the state of general anesthesia can be rapidly reversed, by activating specific brain circuits. The success of our research has depended critically on tight coupling of experiments, signal processing research and mathematical modeling.