Journal of neurotrauma
-
Journal of neurotrauma · Oct 2022
Trajectories of Visual and Vestibular Markers of Youth Concussion.
Visual and vestibular deficits, as measured by a visio-vestibular examination (VVE), are markers of concussion in youth. Little is known about VVE evolution post-injury, nor influence of age or sex on trajectory. The objective was to describe the time trend of abnormal VVE elements after concussion. ⋯ Females and those <14 years demonstrated slower resolution of VVE abnormalities. VVE deficits are common in adolescents after concussion, and the trajectory of resolution varies by age, sex, and concussion history. These data provide insight to clinicians managing concussions on the timing of deficit resolution after injury.
-
Journal of neurotrauma · Oct 2022
Chronic Cognitive and Cerebrovascular Function Following Mild Traumatic Brain Injury in Rats.
Severe traumatic brain injury (TBI) results in cognitive dysfunction in part due to vascular perturbations. In contrast, the long-term vasculo-cognitive pathophysiology of mild TBI (mTBI) remains unknown. We evaluated mTBI effects on chronic cognitive and cerebrovascular function and assessed their interrelationships. ⋯ NOR correlated with CBF in lateral hippocampus, medial hippocampus, and primary somatosensory barrel cortex, whereas it inversely correlated with arterial smooth muscle-dependent dilation. Six-month baseline endothelial and smooth muscle-dependent arterial function were similar among mTBI and sham, but post-angiotensin 2 stimulation, mTBI showed no change in smooth muscle-dependent dilation from baseline response, unlike the reduction in sham. mTBI led to chronic cognitive dysfunction and altered angiotensin 2-stimulated smooth muscle-dependent vasoreactivity. The findings of persistent pathophysiological consequences of mTBI in this animal model add to the broader understanding of chronic pathophysiological sequelae in human mild TBI.
-
Journal of neurotrauma · Oct 2022
Combined traumatic brain injury and hemorrhagic shock in ferrets leads to structural, neurochemical, and functional impairments.
Aeromedical evacuation-relevant hypobaria after traumatic brain injury (TBI) leads to increased neurological injury and death in rats relative to those maintained under normobaria. Applicability of rodent brain injury research to humans may be limited, however, by differences in neuroanatomy. Therefore, we developed a model in which ferrets are exposed to polytrauma consisting of controlled cortical impact TBI and hemorrhagic shock subjected 24 h later to 6 h of hypobaria or normobaria. ⋯ Finally, cortical lesion volume was not exacerbated by hypobaria exposure on day 7 post-injury. Results suggest that air travel 24 h after polytrauma is associated with structural changes in the ferret brain. Future studies should investigate secondary injury from hypobaria after polytrauma in greater detail including alternative outcome measures, time points, and exposure to multiple flights.