Development Of Post-traumatic Headache Research Articles

Identification of brain areas in mice with peak neural activity across the acute and persistent phases of post-traumatic headache.

Post-traumatic headache is very common after a mild traumatic brain injury. Post-traumatic headache may persist for months to years after an injury in a substantial proportion of people. The pathophysiology underlying post-traumatic headache remains unknown but is likely distinct from other headache disorders. Identification of brain areas activated in acute and persistent phases of post-traumatic headache can provide insights into the underlying circuits mediating headache pain. We used an animal model of mild traumatic brain injury-induced post-traumatic headache and c-fos immunohistochemistry to identify brain regions with peak activity levels across the acute and persistent phases of post-traumatic headache. Male and female C57BL/6 J mice were briefly anesthetized and subjected to a sham procedure or a weight drop closed-head mild traumatic brain injury . Cutaneous allodynia was assessed in the periorbital and hindpaw regions using von Frey filaments. Immunohistochemical c-fos based neural activity mapping was then performed on sections from whole brain across the development of post-traumatic headache (i.e. peak of the acute phase at 2 days post- mild traumatic brain injury), start of the persistent phase (i.e. >14 days post-mild traumatic brain injury) or after provocation with stress (bright light). Brain areas with consistent and peak levels of c-fos expression across mild traumatic brain injury induced post-traumatic headache were identified and included for further analysis. Following mild traumatic brain injury, periorbital and hindpaw allodynia was observed in both male and female mice. This allodynia was transient and subsided within the first 14 days post-mild traumatic brain injury and is representative of acute post-traumatic headache. After this acute post-traumatic headache phase, exposure of mild traumatic brain injury mice to a bright light stress reinstated periorbital and hindpaw allodynia for several hours - indicative of the development of persistent post-traumatic headache. Acute post-traumatic headache was coincident with an increase in neuronal c-fos labeling in the spinal nucleus of the trigeminal caudalis, primary somatosensory cortex, and the nucleus accumbens. Neuronal activation returned to baseline levels by the persistent post-traumatic headache phase in the spinal nucleus of the trigeminal caudalis and primary somatosensory cortex but remained elevated in the nucleus accumbens. In the persistent post-traumatic headache phase, coincident with allodynia observed following bright light stress, we observed bright light stress-induced c-fos neural activation in the spinal nucleus of the trigeminal caudalis, primary somatosensory cortex, and nucleus accumbens. Examination of mild traumatic brain injury-induced changes in peak c-fos expression revealed brain regions with significantly increased neural activity across the acute and persistent phases of post-traumatic headache. Our findings suggest mild traumatic brain injury-induced post-traumatic headache produces neural activation along pain relevant pathways at time-points matching post-traumatic headache-like pain behaviors. These observations suggest that the spinal nucleus of the trigeminal caudalis, primary somatosensory cortex, and nucleus accumbens may contribute to both the induction and maintenance of post-traumatic headache.

Associations between Zygoma Fracture and Post-Traumatic Headache: A Study among Taiwanese Population.

Few studies have discussed the development of post-traumatic headache (PTH) after zygoma fracture. This research aimed to examine the association between zygoma fracture and PTH and its other associated factors. A total of 3043 patients with zygoma fracture and 3043 patients with non-fracture were included in this analysis. They were matched to a non-fracture cohort from the National Health Insurance database according to age, sex, and index year. The incidence of PTH and its association with zygoma fracture were assessed. The zygoma fracture cohort had a significantly higher cumulative incidence of PTH than the non-fracture cohort in a 10-year follow-up. The confounding risk factors of PTH included zygoma fracture, female sex, and comorbidities, including obesity and depression. Female patients under 40 years old who had zygoma fractures had a higher incidence of PTH than the non-fracture group. Moreover, patients with zygoma fractures commonly developed PTH within three months after injury. Female patients under 40 years old with precedent zygoma fractures had a higher incidence rate of PTH than those without fractures. Moreover, patients with zygoma fractures commonly developed PTH within three months after injury. Nevertheless, before widely applying our results, a prospective study must be conducted to verify the risk factors found in this study.

Risk Factors for Development of Post-Concussive Headaches in a Pediatric TBI Subspecialty Clinic Population (P01.179)

Objective: This study was conducted to further understand the factors that contribute to development of post-traumatic headache in a pediatric subspecialty population. Background Traumatic brain injury is a major pediatric public health problem, with as many as 500,000 children under the age of 15 presenting to the emergency department annually. Approximately 80% of these can be classified as mild. Even in this population, children can suffer from acute and persistent post-concussive symptoms, including headache. Design/Methods: Data was collected from children ages 6 months-21 years, presenting to our pediatric neurology clinic with mild traumatic brain injury (TBI). The data was prospectively collected. 61 patients had follow-up within 6 months after injury. Of these patients, 32 suffered a sports-related injury, and were between the ages of 7-21 years. Results: Approximately half of all mild TBI patients suffered from post-traumatic headache. Those that were injured due to a sports-related mechanism were 2.7 times more likely to have post-traumatic headache than those whose mild TBI was not sports-related (95% CI 1.0-7.8). Additionally, patients who had a premorbid diagnosis of headache were 5.3 times more likely to suffer from post-traumatic headache, than those without premorbid headaches (95% CI 0.8-147.1). Statistical analysis was performed using odds ratio estimations and confidence intervals using EpiTools: R Package for Epidemiologic Data and Graphics (version 0.5-6). Conclusions: Understanding the risk factors for the development of headaches following mild TBI may provide an indication for those patients who may benefit from a referral to a pediatric neurology TBI clinic. Supported by: UCLA BIRC, NS05720, NS027544, Child Neurology Foundation, TTCF, Thrasher Research Fund, UCLA FGP. Disclosure: Dr. Choe has nothing to disclose. Dr. Valino has nothing to disclose. Dr. McArthur has nothing to disclose. Dr. Giza has nothing to disclose.

Sequelae of craniocerebral injuries in a neurologic patient sample--an attempt at interpreting post-traumatic headache

The sequelae of a head injury that had occurred at least six months previously, were examined in 457 patients. Neurological deficiencies, psychoorganic disturbances and disability caused by the injury correlated positively with its severity. Posttraumatic epilepsies were diagnosed approximately equally often in patients with minor head injuries and in those with more severe ones. It is probable that epilepsies have been diagnosed too often in patients with minor head injuries. Headache occurs significantly more often in patients with minor head injuries. This cannot be explained by the selection of patients alone. A hypothesis explaining the development of posttraumatic headache is presented and discussed.