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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 2014,29 Sep 2015

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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 pathogenesis of chronic post-traumatic headache however, this role is not well defined. This research investigates the contribution of acute and chronic inflammation to the development of headache after closed head injury. The specific aim 1 was to determine the pattern of inflammation-induced sensitization of the central trigeminal pain neurons, and if sensitization is detectable by quantitative EEG. Sprague Dawley rats underwent mild closed head injury CHI or served as an incision control group to determine the effects of graded inflammatory on central trigeminal pain neurons. CHI groups were subdivided intosingle CHIx1 or repeated two CHIx2 and three CHIx3 injury groups to determine the graded effects of inflammation. Acute endpoints were at 1 day and 1 week, and the chronic endpoints were at 4 weeks. Quantitative electroencephalography shows group differences in several frequency and cortices that persist over time and respond to light stimuli. Headache behavioral testing as well as immunohistochemical and molecular studies were used to uncover the underlying inflammatory contributions to post-traumatic headache. Outcomes from injury are dependent on the number of injuries and injury force parameters.

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