Journal of neurotrauma
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Journal of neurotrauma · Jul 2012
Multicenter StudyBrain-derived neurotrophic factor (Val66Met) polymorphism does not influence recovery from a post-traumatic vegetative state: a blinded retrospective multi-centric study.
Brain-derived neurotrophic factor (BDNF) is a neurotrophin that influences neuronal plasticity throughout life. Emergence from a vegetative state (VS) after a traumatic brain injury (TBI) implies that the brain undergoes plastic changes. A common polymorphism in the BDNF gene--BDNF Val66Met (referred to herein as BDNF(Met))--impairs cognitive function in healthy subjects. ⋯ The percentages of patients in the Val and Met groups who emerged from the VS were 36.4% and 30% at 3 months, 66.3% and 70% at 6 months, and 70% and 87.5% at 12 months (p>0.05), respectively. These findings provide evidence that the BDNF(Met) polymorphism is not involved in cognitive improvement in patients with a VS following TBI. Future studies should focus on the role of other BDNF polymorphisms in the recovery from a VS.
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Journal of neurotrauma · Jul 2012
ReviewManagement of cardiovascular disease risk factors in individuals with chronic spinal cord injury: an evidence-based review.
Clinical scenario: A 37-year-old man suffered a complete spinal cord injury (C8, American Spinal Injury Association Impairment Scale [ASIA] score A) 10 years ago in a car accident. Should primary prevention of cardiovascular disease be a priority in this patient? In order to answer this question, we performed a systematic review of the literature to inform an evidence-based clinical review. The objective was to provide a comprehensive and up-to-date review of the clinical management of cardiovascular disease (CVD) and risk factors for individuals with spinal cord injury (SCI). ⋯ These limitations notwithstanding, we present a series of contemporary practice suggestions with regard to CVD event risk modification in SCI patients. For optimal outcomes, health care providers should be cognizant of these heightened CVD risk factors and the resultant increased CVD morbidity and mortality in SCI patients. Despite the absence of high-quality evidence-based treatment strategies, clinicians should re-examine their own CVD risk factor treatment strategies to better reflect contemporary practice in similar high-CVD-event-risk patients and populations.
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Journal of neurotrauma · Jul 2012
Medical care costs associated with traumatic brain injury over the full spectrum of disease: a controlled population-based study.
Data on traumatic brain injury (TBI) economic outcomes are limited. We used Rochester Epidemiology Project (REP) resources to estimate long-term medical costs for clinically-confirmed incident TBI across the full range of severity after controlling for pre-existing conditions and co-occurring injuries. All Olmsted County, Minnesota, residents with diagnoses indicative of potential TBI from 1985-2000 (n=46,114) were identified, and a random sample (n=7175) was selected for medical record review to confirm case status, and to characterize as definite (moderate/severe), probable (mild), or possible (symptomatic) TBI. ⋯ By contrast, cost differences between possible TBI cases and controls were not as great within the first 6 months, but were substantial among 1-year survivors. Although mean incremental costs were highest for definite cases, probable and possible cases accounted for>90% of all TBI events and 66% of total incremental costs. Preventing probable and possible events might facilitate substantial reductions in TBI-associated medical care costs.
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Journal of neurotrauma · Jul 2012
Traumatic brain injury in young rats leads to progressive behavioral deficits coincident with altered tissue properties in adulthood.
Traumatic brain injury (TBI) affects many infants and children, and results in enduring motor and cognitive impairments with accompanying changes in white matter tracts, yet few experimental studies in rodent juvenile models of TBI (jTBI) have examined the timeline and nature of these deficits, histologically and functionally. We used a single controlled cortical impact (CCI) injury to the parietal cortex of rats at post-natal day (P) 17 to evaluate behavioral alterations, injury volume, and morphological and molecular changes in gray and white matter, with accompanying measures of electrophysiological function. At 60 days post-injury (dpi), we found that jTBI animals displayed behavioral deficits in foot-fault and rotarod tests, along with a left turn bias throughout their early developmental stages and into adulthood. ⋯ The final lesion constituted only ∼3% of brain volume, and morphological tissue changes were evaluated using MRI, as well as immunohistochemistry for neuronal nuclei (NeuN), myelin basic protein (MBP), neurofilament-200 (NF200), and oligodendrocytes (CNPase). White matter morphological changes were associated with a global increase in MBP immunostaining and reduced compound action potential amplitudes at 60 dpi. These results suggest that brain injury early in life can induce long-term white matter dysfunction, occurring in parallel with the delayed development and persistence of behavioral deficits, thus modeling clinical and longitudinal TBI observations.
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Journal of neurotrauma · Jul 2012
Traumatic brain injury increased IGF-1B mRNA and altered IGF-1 exon 5 and promoter region epigenetic characteristics in the rat pup hippocampus.
Traumatic brain injury (TBI) is a major cause of acquired cognitive disability in childhood. Such disability may be blunted by enhancing the brain's endogenous neuroprotective response. An important endogenous neuroprotective response is the insulin-like growth factor-1 (IGF-1) mRNA variant, IGF-1B. ⋯ We report for the first time that hippocampal IGF-1B mRNA increased after developmental TBI. We speculate that epigenetic modifications at the P2 and exon 5/ESE regions are important in the regulation of IGF-1B mRNA expression. The exon 5/ESE region may present a means for future therapies to target IGF-1B transcription after TBI.