Journal of neurotrauma
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Journal of neurotrauma · May 2012
Clinical TrialSafety of early warfarin resumption following burr hole drainage for warfarin-associated subacute or chronic subdural hemorrhage.
The primary objective of this study was to evaluate the safety of early warfarin resumption following burr hole drainage for warfarin-associated subdural hemorrhage (SDH). This prospective, single-arm, single-center trial was conducted from February 2008 to April 2010. Inclusion criteria were premorbid warfarin therapy, subacute or chronic SDH requiring burr hole drainage, and an International Normalized Ratio (INR) of >1.5 at presentation. ⋯ SDH recurrence was found to be associated with older age (≥ 75 years), and a thicker SDH (≥ 25 mm), but not with post-operative anticoagulation status. None of the study subjects experienced a thromboembolic event during the study period. Restarting warfarin therapy does not need to be withheld for more than 3 days after burr hole drainage, particularly in patients with a high thromboembolic risk.
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Journal of neurotrauma · May 2012
Trends in the incidence of physician-diagnosed mild traumatic brain injury among active duty U.S. military personnel between 1997 and 2007.
Mild traumatic brain injury (mTBI) has been described as the most common form of traumatic brain injury within military populations; however, few epidemiologic studies have examined incidence rates for mTBI in this population. The objective of this study was to examine trends in the incidence of mTBI among active-duty U. S. service members between 1997 and 2007. ⋯ Overall, for 2006-2007 versus 1997-2005, the rate ratio was 1.61 (95% CI 1.58,1.65). The greatest increase in the rate of mTBI was observed among those serving in Iraq, who experienced a 38.4% (95% CI 35.4%,41.1%) annual increase in new cases. The observed increase in the incidence of mTBI in this population has significant policy implications in terms of allocating appropriate health care resources.
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Journal of neurotrauma · May 2012
Paroxysmal sympathetic hyperactivity after traumatic brain injury: clinical and prognostic implications.
A proportion of patients surviving severe traumatic brain injury (TBI) have symptoms suggestive of excessive sympathetic discharge, here termed paroxysmal sympathetic hyperactivity (PSH). The goals of this study were: (1) to describe the clinical associations and radiological findings of PSH, its incidence, and features in subjects with severe TBI in the intensive care unit (ICU); (2) to investigate the potential role of increased intracranial pressure in the pathogenesis of PSH; and (3) to determine the prognostic influence of PSH during the ICU stay, on discharge from the ICU, and at 12 months post-injury. A prospective cohort study was undertaken of all ICU admissions with severe TBI older than 14 years over an 18-month period. ⋯ At 1 year post-injury, 20% of this group demonstrated ongoing PSH episodes. Over 18 months, 10.1% of admissions following severe TBI demonstrated PSH features in ICU. Subjects with PSH had a longer ICU stay and higher rate of complications, although this did not appear to compromise their long-term neurological recovery.
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Journal of neurotrauma · May 2012
Comparative StudyTBI sex dependently upregulates ET-1 to impair autoregulation, which is aggravated by phenylephrine in males but is abrogated in females.
Traumatic brain injury (TBI) contributes to morbidity in children, and boys are disproportionately represented. Endothelin-1 (ET-1) contributes to impaired autoregulation via oxygen (O₂⁻) after TBI in piglets, but its relative role in males compared with females has not been previously investigated. Increased cerebral perfusion pressure (CPP) via phenylephrine (Phe) sex dependently improves impairment of autoregulation after TBI through modulation of extracellular signal-related kinase (ERK) mitogen-activated protein kinase (MAPK) upregulation, aggravated in males, but blocked in females. ⋯ These data indicate that TBI upregulates ET-1 more in males than in females. Elevation of CPP with Phe sex dependently prevents impairment of cerebral autoregulation after TBI through modulation of ET-1, O₂⁻, and ERK mediated impairment of K channel vasodilation. These observations advocate for the consideration of development of sex-based therapies for the treatment of hemodynamic sequelae of pediatric TBI.
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Journal of neurotrauma · May 2012
Comparative StudyEffects of hypothermia on cerebral autoregulatory vascular responses in two rodent models of traumatic brain injury.
Traumatic brain injury (TBI) can trigger disturbances of cerebral pressure autoregulation that can translate into the generation of secondary insults and increased morbidity/mortality. Few therapies have been developed to attenuate the damaging consequences of disturbed autoregulatory control, although some suggest that hypothermia may exert such protection. Here we reexamine this issue of traumatically induced autoregulatory disturbances and their modulation by hypothermic intervention, examining these phenomena in two different models of TBI. ⋯ However, with LFPI, the use of 2 h of hypothermia provided partial vascular protection. These results clearly illustrate that TBI can alter the cerebral autoregulatory vascular response to sequentially induced hypotensive insult, whereas the use of post-traumatic hypothermia provides benefit. Collectively, these studies also demonstrate that different animal models of TBI can evoke different biological responses to injury.