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Central Pain Mechanisms and Novel Therapeutic Strategies in a Model of Closed Head Injury

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Technical Report,30 Sep 2015,29 Sep 2016

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Thomas Jefferson University Philadelphia United States

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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.

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  • Medicine and Medical Research

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