The Solt Laboratory studies 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. We 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.

Ken Solt currently directs a translational research program that studies the role of dopamine pathways in restoring consciousness and cognition after general anesthesia. In the laboratory, he combines intracranial stimulation, neurophysiological recordings, and cognitive testing in rodents to elucidate the neural circuits that govern reanimation, while his clinical research program tests novel methods to accelerate recovery of consciousness and cognition in surgical patients. His 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.

Principal Investigator

Ken Solt

Ken Solt is an Associate Professor of Anesthesia at Harvard Medical School, and a practicing anesthesiologist at the Massachusetts General Hospital. He is also a Research Affiliate at the MIT Brain and Cognitive Sciences Department. [Read More]

Reanimation from Anesthesia

Power spectral density

General anesthesia is a reversible coma. In contrast, emergence from general anesthesia has been treated as a passive process whereby anesthetic drugs are discontinued at the end of surgery and no drugs are administered to actively reverse their effects on the brain and central nervous system. [Read More]

Burst-Suppression

NSRL

Burst suppression is an EEG pattern characterized by alternating periods of high-amplitude activity (bursts) and relatively low amplitude activity (suppressions). Burst suppression can arise from several different pathological conditions, as well as from general anesthesia. [Read More]