2015
DOI: 10.1016/j.pediatrneurol.2014.10.013
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Part I—Evaluation of Pediatric Post-traumatic Headaches

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Cited by 22 publications
(23 citation statements)
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References 66 publications
(81 reference statements)
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“…The presumed mechanism of mTBI involves stretching or shearing of axons, followed by an early metabolic cascade leading to disturbance and alteration of cerebral blood flow and a mismatch in available vs required cerebral metabolic energy 15,16 . There may also be an abnormal release of neuroinflammatory peptides and excitatory neurotransmitters leading to cortical hyperexcitability that contributes to the development of PTH 7,17 . Injury to the neuroanatomic pathways involved in head pain, specifically the trigeminovascular system, may lead to headaches.…”
Section: Pathophysiology Of Concussion and Post‐traumatic Headachementioning
confidence: 99%
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“…The presumed mechanism of mTBI involves stretching or shearing of axons, followed by an early metabolic cascade leading to disturbance and alteration of cerebral blood flow and a mismatch in available vs required cerebral metabolic energy 15,16 . There may also be an abnormal release of neuroinflammatory peptides and excitatory neurotransmitters leading to cortical hyperexcitability that contributes to the development of PTH 7,17 . Injury to the neuroanatomic pathways involved in head pain, specifically the trigeminovascular system, may lead to headaches.…”
Section: Pathophysiology Of Concussion and Post‐traumatic Headachementioning
confidence: 99%
“…Persistent peripheral activation of the trigeminal or cervical pain systems may lead to central sensitization of these systems causing persistent headaches and allodynia. Trauma causing muscle strain, vertebral misalignment, or ligamentous injuries may compress, irritate, or activate the occipital or trigeminal nerves, resulting in neuralgic pain in the distribution of the nerve and/or activation of central pain systems involved in headache 17 . In a study of children with PTH, a high rate of cutaneous allodynia was observed in those with PTH (53.8%), leading to the hypothesis that central sensitization might be a shared pathophysiological mechanism with migraine 18 .…”
Section: Pathophysiology Of Concussion and Post‐traumatic Headachementioning
confidence: 99%
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“…Mild TBI is defined as a head injury associated with loss of consciousness of <30 minutes, Glasgow Coma Scale of 13 or higher, post-traumatic amnesia <24 hours, altered level of awareness of <24 hours and normal neuroimaging. 3 The most recent consensus statement on concussion in sport defines a concussion as a TBI induced by biomechanical forces and caused by either a direct blow to the head, face, neck or elsewhere on the body with an impulsive force transmitted to the head, which typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously, but in some cases, the signs and symptoms evolve over a number of minutes to hours. The acute clinical signs and symptoms reflect a functional disturbance rather than a structural injury and may or may not include loss of consciousness.…”
mentioning
confidence: 99%