Journal of neurotrauma
-
Journal of neurotrauma · Jun 2015
Characterizing the temporal development of cardiovascular dysfunction in response to spinal cord injury.
Spinal cord injury (SCI) is associated with rapid and sustained impairments in cardiovascular function that ultimately cause an early onset of cardiovascular disease. We know remarkably little about the temporal progression of cardiovascular disturbances, but such an understanding is critical to inform clinical management and develop appropriate intervention strategies. To characterize the cardiovascular response to SCI, six male Wistar rats were instrumented with telemetry and assessed for continuous arterial blood pressure (BP), core body temperature, and heart rate (HR) 7 days before and up to 28 days after T3 SCI. ⋯ The pressor response to colorectal distension was greater at 14, 21, and 28 days post-SCI compared with at 7 days post-SCI (all p<0.004). In conclusion, SCI induces rapid and profound alterations in basal hemodynamics and diurnal rhythms that partially recover by 14 days post-SCI. AD, on the other hand, is acutely present post-SCI, but the frequency and severity of AD events increase substantially from 14 days post-SCI on.
-
Journal of neurotrauma · Jun 2015
Endogenous neural stem/progenitor cells stabilize the cortical microenvironment following traumatic brain injury.
Although a myriad of pathological responses contribute to traumatic brain injury (TBI), cerebral dysfunction has been closely linked to cell death mechanisms. A number of therapeutic strategies have been studied in an attempt to minimize or ameliorate tissue damage; however, few studies have evaluated the inherent protective capacity of the brain. Endogenous neural stem/progenitor cells (NSPCs) reside in distinct brain regions and have been shown to respond to tissue damage by migrating to regions of injury. ⋯ Two weeks after CCI injury, mice deficient in NSPCs had reduced neuronal survival in the perilesional cortex and fewer Iba-1-positive and glial fibrillary acidic protein-positive glial cells but increased glial hypertrophy at the injury site. These findings suggest that the presence of NSPCs play a supportive role in the cortex to promote neuronal survival and glial cell expansion after TBI injury, which corresponds with improvements in motor function. We conclude that enhancing this endogenous response may have acute protective roles after TBI.
-
Journal of neurotrauma · Jun 2015
Decompressive craniectomy reduces white matter injury following controlled cortical impact in mice.
Reduction and avoidance of increases in intracranial pressure (ICP) after severe traumatic brain injury (TBI) continue to be the mainstays of treatment. Traumatic axonal injury is a major contributor to morbidity after TBI, but it remains unclear whether elevations in ICP influence axonal injury. Here we tested the hypothesis that reduction in elevations in ICP after experimental TBI would result in decreased axonal injury and white matter atrophy in mice. ⋯ At 4 weeks post-injury, Open animals had an 18% reduction in white matter volume compared with 34% in Closed animals (p<0.01). Thus, our results indicate that CCI with decompressive craniectomy was associated with reductions in ICP and reduced pericontusional axonal injury and white matter atrophy. If similar in humans, therapeutic interventions that ameliorate intracranial hypertension may positively influence white matter injury severity.