Journal of neurotrauma
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Journal of neurotrauma · Jul 2012
Multicenter StudyUtilization and costs of health care after geriatric traumatic brain injury.
Despite the growing number of older adults experiencing traumatic brain injury (TBI), little information exists regarding their utilization and cost of health care services. Identifying patterns in the type of care received and determining their costs is an important first step toward understanding the return on investment and potential areas for improvement. We performed a health care utilization and cost analysis using the National Study on the Costs and Outcomes of Trauma (NSCOT) dataset. ⋯ In the unadjusted model index hospitalization costs and inpatient rehabilitation costs were significantly lower in the oldest age category, while outpatient care costs and nursing home stays were lower in the younger age categories. In the adjusted model, in addition to these cost drivers, re-hospitalization costs were significantly higher among those 75-84 years of age, and receipt of informal care from friends and family was significantly different, being lowest among those aged 65-74 years, and highest among those aged 75-84 years. Identifying variations in care that these patients are receiving and determining the costs versus benefits is an important next step in understanding potential areas for improvement.
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Journal of neurotrauma · Jul 2012
MT5-MMP, ADAM-10, and N-cadherin act in concert to facilitate synapse reorganization after traumatic brain injury.
Matrix metalloproteinases (MMPs) influence synaptic recovery following traumatic brain injury (TBI). Membrane type 5-matrix metalloproteinase (MT5-MMP) and a distintegrin and metalloproteinase-10 (ADAM-10) are membrane-bound MMPs that cleave N-cadherin, a protein critical to synapse stabilization. This study examined protein and mRNA expression of MT5-MMP, ADAM-10, and N-cadherin after TBI, contrasting adaptive and maladaptive synaptogenesis. ⋯ Our results confirm time- and injury-dependent expression of MT5-MMP, ADAM-10, and N-cadherin during reactive synaptogenesis. Persistent ADAM-10 expression was correlated with attenuated N-cadherin level and reduced functional recovery. MMP inhibition shifted ADAM-10 and N-cadherin toward adaptive expression and improved synaptic function.
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Journal of neurotrauma · Jul 2012
Acute neuroimmune modulation attenuates the development of anxiety-like freezing behavior in an animal model of traumatic brain injury.
Chronic anxiety is a common and debilitating result of traumatic brain injury (TBI) in humans. While little is known about the neural mechanisms of this disorder, inflammation resulting from activation of the brain's immune response to insult has been implicated in both human post-traumatic anxiety and in recently developed animal models. ⋯ Acute peri-injury administration of ibudilast (MN166), a glial cell activation inhibitor, suppressed both reactive gliosis and freezing behavior, and continued neuroprotective effects were apparent several months post-injury. These results support the conclusion that inflammation produced by neuroimmune responses to TBI play a role in post-traumatic anxiety, and that acute suppression of injury-induced glial cell activation may have promise for the prevention of post-traumatic anxiety in humans.
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Journal of neurotrauma · Jul 2012
Delayed applications of L1 and chondroitinase ABC promote recovery after spinal cord injury.
The inhibitory environment of the injured spinal cord is an obstacle to functional recovery and axonal regeneration in adult mammals. We had previously shown that injection of adeno-associated virus (AAV) encoding the L1 cell adhesion molecule (AAV-L1) at the time of acute thoracic compression injury of adult mice promotes locomotor recovery, which is associated with ameliorated astrogliosis and improved axonal regeneration in the lumbar spinal cord. In the present study, we investigated whether delayed injection of AAV-L1, chondroitinase ABC (Chase), or the combination of the two agents into the mouse spinal cord 3 weeks after injury would also lead to improved recovery. ⋯ Mice with the combined application of AAV-L1 and Chase showed improvement in both parameters. Enhanced motor recovery after combined application correlated with increased densities of cholinergic and GABAergic terminals at motoneuronal cell bodies, and of lamina-specific glutamatergic sensory afferents 15 weeks after injury, indicating enhanced synaptic rearrangements in the lumbar spinal cord below the lesion site. These findings suggest that L1 overexpression combined with Chase application may contribute to the treatment of sub-chronic spinal cord injury.
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Journal of neurotrauma · Jul 2012
Review Comparative StudyPharmacologic venous thromboembolism prophylaxis after traumatic brain injury: a critical literature review.
Despite the frequency and morbidity of venous thromboembolism (VTE) development after traumatic brain injury (TBI), no national standard of care exists to guide TBI caregivers for the use of prophylactic anticoagulation. Fears of iatrogenic propagation of intracranial hemorrhage patterns have led to a dearth of research in this field, and it is only relatively recently that studies dedicated to this question have been performed. These have generally been limited to retrospective and/or observational studies in which patients are classified in a binary fashion as having the presence or absence of intracranial blood. ⋯ This review seeks to critically assess the literature on this question by examining the existing evidence on the safety and efficacy of pharmacologic VTE prophylaxis in the setting of elective craniotomy (as this is the closest model available from which to extrapolate) and after TBI. In doing so, we critique studies that approach TBI as a homogenous or a heterogenous study population. Finally, we propose our own theoretical protocol which stratifies patients into low, moderate, and high risk for the likelihood of natural progression of their hemorrhage pattern, and which allows one to tailor a unique VTE prophylaxis regimen to each individual arm.