My clinical and research interests are grounded in my longstanding expertise in both traumatic brain injury, pain, and the endocannabinoid system. I have worked extensively with models of mild-moderate traumatic brain injury including concussion to study the underlying mechanisms driving post-concussion headache, and related behaviors (sleep disruption, anxiety, and memory and learning). My previous work focuses on the pathophysiological mechanisms associated with the trigeminal pain pathway that contribute to post-traumatic headache and related neurological effects of traumatic brain injury. In a series of studies my laboratory showed increases in key pain signaling molecules are amenable to alleviate pain behaviors.  

My interest in the endocannabinoid system for its therapeutic potential in treating pain and neurological effects associated with traumatic brain injury continues to grow. The endogenous cannabinoid system or endocannabinoid system is essential to central nervous system homeostasis and plays a significant role in the regulation of inflammation and pain. I am fascinated by the many ways to manipulate the endocannabinoid system through its ligands, receptors, and enzymes. Equally intriguing is that some variations of cannabinoid targets can be therapeutic without the unwanted extremes of psychotropic effects. Studies of this system may have originated from those involving THC (tetrahydrocannabinol), the exogenous constituent and psychoactive cannabinoid of marijuana and hemp. However, the endocannabinoid system is much more extensive and comprised of endogenously produced cannabinoids, their receptors, and the proteins contributing to their synthesis and degradation. The two cannabinoid receptors that have been most extensively studied are the cannabinoid 1 (CB1) receptor and the cannabinoid 2 (CB2) receptor. My past work specifially studied the anti-inflammatory and analgesic effects of the cannabinoid receptor type-2 in the traumatized brain.