Associate Professor of Anaesthesia, Harvard Medical School
ResearchI study the mechanisms of emergence and cognitive recovery from general anesthesia using a systems neuroscience approach. In current clinical practice, emergence from general anesthesia is treated as a passive process dictated by the pharmacokinetics of anesthetic drug clearance. My group discovered that methylphenidate (Ritalin) and dopamine agonists induce active emergence from general anesthesia, a process that we term "reanimation." We subsequently discovered that electrical stimulation of the ventral tegmental area (VTA), a key dopamine nucleus in the midbrain, also induces reanimation.
I currently direct a translational research program that studies the role of dopamine pathways in restoring consciousness and cognition after general anesthesia. In my laboratory, we combine intracranial stimulation, neurophysiological recordings, and cognitive testing in rodents to elucidate the neural circuits that govern reanimation, while my clinical research program tests novel methods to accelerate recovery of consciousness and cognition in surgical patients. Our long-term goal is to make general anesthesia safer by developing new therapeutic options for common clinical problems such as post-operative delirium and cognitive dysfunction.
Administration of the commonly used stimulant drug methylphenidate was able to speed recovery from general anesthesia in an animal study conducted at MGH. The report is the first demonstration in mammals of what could be a safe and effective way to induce arousal from general anesthesia.
The ability of the commonly used stimulant methylphenidate (Ritalin) to speed recovery from general anesthesia appears to apply both to the inhaled gas isoflurane, as previously reported, and to the intravenous drug propofol.
Stimulating one of two dopamine-producing regions in the brain was able to arouse animals receiving general anesthesia with either isoflurane or propofol.