From blast to bench: A translational mini‐review of posttraumatic headache
Mild TBI (mTBI), which is synonymous with concussion, is the most prevalent form of head trauma, and posttraumatic headache (PTH) is the most common symptom of mTBI. The incidence of PTH is highest following mTBI and is less frequently observed following moderate or severe TBI (Nampiaparampil, 2008; Hoffman et al., 2011; Lucas et al., 2012; Theeler et al., 2013). Up to 90% of patients with mTBI have been reported to suffer from PTH, which can persist in a subset of patients for over a year post injury (Couch and Bearss, 2001; Okie, 2005; Nampiaparampil, 2008; Hoffman et al., 2011; Lieba‐Samal et al., 2011; Lucas et al., 2012). Chronic PTH is defined by the International Classification of Headache Disorder (ICHD‐3 beta version) as a secondary headache disorder, one that develops within 7 days of TBI or within 7 days after regaining consciousness from a TBI (ICHD, 2013). While acute PTH is resolved within 3 months, persistent PTH is observed beyond this time frame. The persistence of PTH long after tissue healing suggests that some form of central sensitization and neuroadaptation has occurred. Often, the most severe and long‐lasting PTHs have a migraine phenotype (Hoffman et al., 2011; Theeler et al., 2013), and migraine‐like PTH is associated with greater cognitive impairment and increased recovery time. There is a large number of civilians, veterans, and active duty military personnel suffering from PTH, and this has important implications for long‐term health outcomes and quality of life. In this review we provide an overview of the epidemiology of PTH, current research models, and molecular mechanisms underlying this disorder.