TBI-induced nociceptive sensitization is regulated by histone acetylation
Traumatic brain injury (TBI) is a leading cause of death and disability worldwide, affecting all ages and demographics. In the United States alone, approximately 1.7 million new cases are reported annually. While the vast majority of these injuries are mild, even these have been associated with a number of adverse consequences. These include memory impairment, anxiety, depression and other changes with variable patterns of onset and persistence. One of the most common complaints of patients after TBI is, however, chronic pain; it has been estimated that more than 50% of TBI patients develop chronic pain at some point after their injuries. TBI was observed to confer an odds ratio of 5.0 for chronic pain in a recently described military cohort. Unlike some of the more severe motor and cognitive consequences, chronic pain after TBI appears to be at least as likely to be experienced by those with mild as opposed to severe injuries.
Although only limited experimentation has been conducted, researchers are beginning to define the interactions of TBI with pain signaling pathways using laboratory models.
Read the full article on IBRO Reports.
Posted: June 1, 2017