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    Chronic Sensory and Affective Craniofacial Pain After Blast-Induced Traumatic Brain Injury and Peripheral Nerve Injury in Rats

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    Author
    Studlack, Paige Elizabeth
    0000-0002-3626-1865
    Advisor
    Keller, Asaf
    Simard, J. Marc
    Date
    2017
    Type
    dissertation
    
    Metadata
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    Abstract
    Thousands of military members suffer long-term consequences of blast-induced traumatic brain injury (Blast-TBI), including chronic head and face pain. Pain after blast-TBI usually manifests as post-traumatic headaches with a high degree of comorbid mood disorders, suggesting that the affective dimension of pain may burden survivors of blast-TBI. Here, we tested the hypothesis that an innovative model of the unique aspect of blast-TBI over blunt-force TBI, the primary blast injury, directed over the cranium sufficiently modeled long-term conditions of human blast exposure in rats. Rats exposed to cranium-directed primary blast-TBI demonstrated behavioral manifestations of ongoing pain, mechanical hyperalgesia, and cold allodynia three weeks after injury, recapitulating chronic facial pain in patients after blast-TBI. We predicted that maladaptive changes to pain-signaling and -processing nuclei in CNS would induce and maintain pain behavior after blast-TBI. We recorded single units in sensory pain-associated nuclei, the posterior nucleus of the thalamus (PO) and spinal trigeminal nucleus caudalis (SpVc), which have previously been causally associated with pain after spinal cord injury. We observed hyperexcitability at baseline of PO neurons after blast injury in absence of changes to evoked response to cutaneous noxious stimuli. Neuronal hyperexcitability in PO is not associated with persistent gliosis. Affective pain processing through the parabrachial complex (PB) occurs in parallel to information coding the sensory dimension of pain through PO. We assessed central changes to PB neuronal activity in a robust model of post-traumatic pain using the chronic constriction injury of the infraorbital nerve (CCI-ION). PB neurons, weeks to months after injury, are hyper-excitable in chronic pain, as shown by prolonged response after presentation of noxious cutaneous stimulation ("after-discharges"), previously observed to be causally-related to pain due to CCI-ION in SpVc. Further study of PB hyperexcitability in blast-TBI rodent models may elucidate the mechanism underlying blast-TBI-associated affective pain.
    Description
    University of Maryland, Baltimore. Neuroscience. Ph.D. 2017
    Keyword
    chronic constriction injury
    posterior thalamus
    rat model
    Brain Injuries, Traumatic
    Pain
    Parabrachial Nucleus
    Posterior Thalamic Nuclei
    Rats
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/7365
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    Theses and Dissertations School of Medicine
    Theses and Dissertations All Schools

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