Journal of neurotrauma
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Journal of neurotrauma · Sep 2011
Multicenter StudyNatural history of headache after traumatic brain injury.
Headache is one of the most common persisting symptoms after traumatic brain injury (TBI). Yet there is a paucity of prospective longitudinal studies of the incidence and prevalence of headache in a sample with a range of injury severity. We sought to describe the natural history of headache in the first year after TBI, and to determine the roles of prior history of headache, sex, and severity of TBI as risk factors for post-traumatic headache. ⋯ Overall, headache is common in the first year after TBI, independent of the severity of injury range examined in this study. Use of the International Classification of Headache Disorders criteria requiring onset of headache within 1 week of injury underestimates rates of post-traumatic headache. Better understanding of the natural history of headache including timing, type, and risk factors should aid in the design of treatment studies to prevent or reduce the chronicity of headache and its disruptive effects on quality of life.
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Journal of neurotrauma · Sep 2011
Ethanol intoxication is associated with a lower incidence of admission coagulopathy in severe traumatic brain injury patients.
The aim of this study was to determine the impact of ethanol (ETOH) on the incidence of severe traumatic brain injury (sTBI)-associated coagulopathy and to examine the effect of ETOH on in-hospital outcomes in patients sustaining sTBI. Patients admitted to the surgical intensive care unit from June 2005 through December 2008 following sTBI, defined as a head Abbreviated Injury Scale (AIS) score ≥3, were retrospectively identified. Patients with a chest, abdomen, or extremity AIS score >3 were excluded to minimize the impact of extracranial injuries. ⋯ ETOH (+) patients had a significantly lower in-hospital mortality rate than ETOH (-) patients [9.8% versus 16.6%; adjusted p=0.011; adjusted OR (95% CI)=0.39 (0.19,0.81)]. For brain-injured patients arriving alive to the hospital, ETOH intoxication is associated with a significantly lower incidence of early coagulopathy and in-hospital mortality. Further research to establish the pathophysiologic mechanisms underlying any potential beneficial effect of ETOH on the coagulation system following sTBI is warranted.
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Journal of neurotrauma · Sep 2011
Post-injury administration of the mitochondrial permeability transition pore inhibitor, NIM811, is neuroprotective and improves cognition after traumatic brain injury in rats.
Mitochondrial dysfunction is known to play a pivotal role in cell death mechanisms following traumatic brain injury (TBI). N-methyl-4-isoleucine-cyclosporin (NIM811), a non-immunosuppressive cyclosporin A (CsA) analog, inhibits the mitochondrial permeability transition pore (mPTP) and has been shown to be neuroprotective following TBI in mice. However, the translation of the neuroprotective effects of mPTP inhibitors, including CsA and NIM811, into improved cognitive end points has yet to be fully investigated. ⋯ For behavioral studies, rats were administered NIM811 at 15 min and 24 h post-injury, with cognitive testing beginning 10 days post-injury. Mitochondrial studies involved a single injection of NIM811 at 15 min post-injury followed by mitochondrial isolation at 6 h post-injury. The results revealed that the optimal dose of NIM811 improves cognition, improves mitochondrial functioning, and reduces oxidative damage following TBI.
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Journal of neurotrauma · Sep 2011
MTHFR C677T genotype as a risk factor for epilepsy including post-traumatic epilepsy in a representative military cohort.
The well-studied C677T variant in the methylenetetrahydrofolate reductase (MTHFR) enzyme is a biologically plausible genetic risk factor for seizures or epilepsy. First, plasma/serum levels of homocysteine, a pro-convulsant, are moderately elevated in individuals with the homozygote TT genotype. Furthermore, the TT genotype has been previously linked with migraine with aura-a comorbid condition-and with alcohol withdrawal seizures. ⋯ In our sensitivity analysis, risk was most evident for patients with repeated rather than single medical encounters for epilepsy (crude OR=1.85 [1.14-2.97], p=0.011, adjusted OR=1.95 [1.19-3.19], p=0.008), and particularly for PTE (crude OR=3.14 [1.41-6.99], p=0.005; adjusted OR=2.55 [1.12-5.80], p=0.026). Our early results suggest a role for the common MTHFR C677T variant as a predisposing factors for epilepsy including PTE. Further exploration of baseline homocysteine and folate levels as predictors of seizure risk following traumatic brain injury is warranted.
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Journal of neurotrauma · Sep 2011
Acetylcholinesterase inhibition and locomotor function after motor-sensory cortex impact injury.
Traumatic brain injury (TBI) induces transient or persistent dysfunction of gait and balance. Enhancement of cholinergic transmission has been reported to accelerate recovery of cognitive function after TBI, but the effects of this intervention on locomotor activity remain largely unexplored. The hypothesis that enhancement of cholinergic function by inhibition of acetylcholinesterase (AChE) improves locomotion following TBI was tested in Sprague-Dawley male rats after a unilateral controlled cortical impact (CCI) injury of the motor-sensory cortex. ⋯ PHY improved performance in the accelerating Rotarod at 1.6 and 3.2 μmol/kg/day (AChE activity 95 and 78% of control, respectively), however, higher doses induced progressive deterioration. No effect or worsening of outcomes was observed at all PHY doses for home cage activity, rearing, and horizontal ladder walking. Potential benefits of cholinesterase inhibition on locomotor function have to be weighed against the evidence of the narrow range of useful doses.