• Dan Levy, Shahaf Edut, Renana Baraz-Goldstein, Vardit Rubovitch, Ruth Defrin, Dara Bree, Helaine Gariepy, Jun Zhao, and Chaim G Pick.
• Department of Anesthesia Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, USA Harvard Medical School, USA dlevy1@bidmc.harvard.edu.
• Cephalalgia. 2016 Sep 1; 36 (10): 915-23.

BackgroundChronic post-traumatic headache (PTH) is one of the most common symptoms of mild traumatic brain injury (mTBI) but its underlying mechanisms remain unknown. Inflammatory degranulation of dural mast cells (MCs) is thought to promote headache, and may play a role in PTH. Whether mTBI is associated with persistent degranulation of dural MCs is yet to be determined.MethodsHistochemistry was used to evaluate time course changes in dural MC density and degranulation level in concussive head trauma and blast mouse models of mTBI. The effects of sumatriptan and the MC stabilizer cromolyn sodium on concussion-evoked dural MC degranulation were also investigated.ResultsConcussive head injury evoked persistent MC degranulation for at least 30 days. Blast trauma gave rise to a delayed MC degranulation response commencing at seven days that also persisted for at least 30 days. Neither sumatriptan nor cromolyn treatment reduced concussion-evoked persistent MC degranulation.ConclusionsmTBI evoked by closed head injury or blast exposure is associated with persistent dural MC degranulation. Such a response in mTBI patients may contribute to PTH. Amelioration of PTH by sumatriptan may not involve inhibition of dural MC degranulation. If persistent dural MC degranulation contributes to PTH, then cromolyn treatment may not be effective.© International Headache Society 2015.

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