Journal of neurotrauma
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Journal of neurotrauma · Oct 2006
Impact of additional extracranial injuries on outcome after mild traumatic brain injury.
Many patients with mild traumatic brain injury (MTBI) concurrently sustain extracranial injuries; however, little is known about the impact of these additional injuries on outcome. We assessed the impact of additional injuries on the severity of postconcussional symptoms (PCS) and functional outcome 6 months post-injury. A questionnaire (including the Rivermead Post-Concussion Questionnaire and SF-36) was sent to consecutive MTBI patients (hospital admission Glasgow Coma Score 13-15; age range 18-60 years) admitted to the emergency department of a level-I trauma center, and, to serve as a baseline for PCS, a control group of minor-injury patients (ankle or wrist distortion). ⋯ Regardless of the presence of additional injuries, patients that were still in treatment reported significantly more severe PCS, with highest rates in patients with isolated MTBI. In conclusion, many patients with additional extracranial injuries are still in the process of recovery at 6 months after injury. However, despite more severe impact to the head and inferior functional outcomes, these patients do not report more severe PCS.
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Journal of neurotrauma · Oct 2006
Nicotinamide treatment reduces behavioral impairments and provides cortical protection after fluid percussion injury in the rat.
This study examined the ability of nicotinamide (vitamin B3) to improve functional outcome in a dose-dependent manner following fluid percussion injury (FPI). Injured (duration of unconsciousness mean = 85.8 sec; apnea = 9.9 sec), rats were administered nicotinamide (500 or 50 mg/kg; ip) or saline at 15 min and 24 h. Serum analysis of nicotinamide concentrations were conducted 1 h following the last injection. ⋯ Both doses significantly reduced tissue loss and glial fibrillary acid protein (GFAP) expression in the cortex. The 500 mg/kg dose reduced GFAP expression in the hippocampus. This data suggests that nicotinamide has substantial preclinical efficacy for TBI, and there appears to be some differences in the ability of the doses to improve performance in the MWM.
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Journal of neurotrauma · Oct 2006
Recovery of function after vagus nerve stimulation initiated 24 hours after fluid percussion brain injury.
Recent evidence from our laboratory demonstrated in laboratory rats that stimulation of the vagus nerve (VNS) initiated 2 h after lateral fluid percussion brain injury (FPI) accelerates the rate of recovery on a variety of behavioral and cognitive tests. VNS animals exhibited a level of performance comparable to that of sham-operated uninjured animals by the end of a 2-week testing period. The effectiveness of VNS was further evaluated in the present study in which initiation of stimulation was delayed until 24 h post-injury. ⋯ On day 14, the FPI-VNS animals did not differ in the latency to find the platform from sham controls, whereas the injured controls did; however, the FPI-VNS animals and injured controls were not significantly different. Despite the lack of significant histological differences between the FPI groups, VNS, when initiated 24 h following injury, clearly attenuated the ensuing behavioral deficits and enhanced acquisition of the cognitive task. The results are discussed with respect to the norepinephrine hypothesis.
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Journal of neurotrauma · Oct 2006
Traumatic brain injury produces delay-dependent memory impairment in rats.
Memory impairment following traumatic brain injury (TBI) is common in both humans and animals. A noteworthy feature of memory dysfunction in human TBI is impaired memory performance that is dependent on the delay between initial learning and recall of information. However, previous studies of TBI-induced memory impairment in animals have failed to control for the initial amount of learning between sham and injured animals. ⋯ However, as the delay increased to 30 and 120 sec, the performance of the injured animals deteriorated (p < 0.05). These results indicate that LFP injury produces delay-dependent memory impairments in rats. This is therefore a valid model of an important feature of memory impairment in human TBI, and should be a useful addition to the available methods for assessing memory impairment and the effect of therapeutic interventions after TBI.