Central Pain Mechanisms and Novel Therapeutic Strategies in a Model of Closed Head Injury
Abstract
Headache is the most common, persistent symptom of post-concussion syndrome and highly prevalent following traumatic brain injury of all severities. Inflammation is an early promoter of pain, and is proposed to play an important role in the pathogenesisof chronic post-traumatic headache; however, this role is not well defined. This research investigates the contribution of acuteand chronic inflammation to the development of headache after closed head injury. The specific aim (1) was to determine thepattern of inflammation-induced sensitization of the central trigeminal pain neurons, and if sensitization is detectable by quantitative EEG. Sprague Dawley rats were randomized to mild closed head injury (CHI), repetitive mild CHI (rCHI) with twoinjuries (rCHI2) and three injuries (rCHI3) groups or served as an incision control group to determine the effects of gradedinflammatory on central trigeminal pain neurons at acute 1 day and 1 week and chronic 4 week endpoints. Quantitative EEGheadache behavioral testing, as well as immunohistochemical and molecular studies uncover underlying inflammatorycontributors to post-traumatic headache. An in vitro slice assay was used to test anti-inflammatory and anti-nociceptivemechanisms using a cannabinoid receptor type-2 agonist in trigeminal pain pathway tissues.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2016
- Accession Number
- AD1033192
Entities
People
- Melanie Elliott
Organizations
- Thomas Jefferson University