University of Kentucky
Diffuse Traumatic Brain Injury Exacerbates Inflammatory Pain
Institution
University of Kentucky
Faculty Advisor/ Mentor
Jonathan Lifshitz
Abstract
The prevalence of traumatic brain injury (TBI) in the United States exceeds 1.5 million annually. The majority of TBIs involve diffuse mild to moderate brain injuries resulting from falls, motor vehicle accidents, and contact sports. TBI reduces quality of life as cognitive, emotional and sensory deficits manifest. Similar abnormal or adverse behavioral responses can be elicited in a rat model of diffuse mild to moderate TBI (McNamara, 2010).The purpose of the present study was to test whether experimental brain injury increases behavioral signs of pain associated with cutaneous inflammation. Moderate fluid percussion injury (FPI) (1.9 atm), mild FPI (1.0 atm) or sham brain injured rats were evaluated bi-weekly for thermal hypersensitivity using cool and warm stimuli over a 10-week time course. At the 10th week, 0.5% carrageenan was injected intraplantar into the left hind paw to produce inflammatory pain. Withdrawal responses to cool and heat were tested one-three hours post-injection. To assess spontaneous pain at 2-3 hours post-injection, we recorded the duration of paw withdrawal in the absence of stimulation over 3 min. The results indicate that neither mild nor moderate brain injury changed thermal responses over the 10 week period. After the induction of inflammation, sham and TBI increased heat hypersensitivity to the same extent. Furthermore, both mild and moderate TBI dramatically increased behavioral signs of spontaneous pain at 1, 2 and 3 hours post-carrageenan. These results indicated that TBI does not change the sensitivity of tactile and thermal somatosensory pathways, but does increase the spontaneous pain.
Diffuse Traumatic Brain Injury Exacerbates Inflammatory Pain
The prevalence of traumatic brain injury (TBI) in the United States exceeds 1.5 million annually. The majority of TBIs involve diffuse mild to moderate brain injuries resulting from falls, motor vehicle accidents, and contact sports. TBI reduces quality of life as cognitive, emotional and sensory deficits manifest. Similar abnormal or adverse behavioral responses can be elicited in a rat model of diffuse mild to moderate TBI (McNamara, 2010).The purpose of the present study was to test whether experimental brain injury increases behavioral signs of pain associated with cutaneous inflammation. Moderate fluid percussion injury (FPI) (1.9 atm), mild FPI (1.0 atm) or sham brain injured rats were evaluated bi-weekly for thermal hypersensitivity using cool and warm stimuli over a 10-week time course. At the 10th week, 0.5% carrageenan was injected intraplantar into the left hind paw to produce inflammatory pain. Withdrawal responses to cool and heat were tested one-three hours post-injection. To assess spontaneous pain at 2-3 hours post-injection, we recorded the duration of paw withdrawal in the absence of stimulation over 3 min. The results indicate that neither mild nor moderate brain injury changed thermal responses over the 10 week period. After the induction of inflammation, sham and TBI increased heat hypersensitivity to the same extent. Furthermore, both mild and moderate TBI dramatically increased behavioral signs of spontaneous pain at 1, 2 and 3 hours post-carrageenan. These results indicated that TBI does not change the sensitivity of tactile and thermal somatosensory pathways, but does increase the spontaneous pain.