Journal of neurotrauma
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Journal of neurotrauma · Jan 2011
ReviewAnemia in the setting of traumatic brain injury: the arguments for and against liberal transfusion.
Anemia is recognized as a possible cause of secondary injury following traumatic brain injury (TBI). Cogent arguments can be made for both liberal and restrictive blood transfusion practices in this setting. In this narrative review, we summarize available knowledge regarding the risks of anemia and transfusion in patients with TBI. ⋯ Alternatively, studies that have analyzed transfusion as a predictor of worse outcome have consistently identified such an association, but these studies may involve residual confounding. What little information exists from randomized trials that have included patients with TBI and evaluated liberal versus restrictive transfusion strategies is inconclusive. Since anemia in the setting of TBI is relatively common and there is considerable variation in transfusion preferences, greater study of this topic - preferably with one or more rigorous, adequately powered, non-inferiority randomized trials - is desirable.
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Journal of neurotrauma · Jan 2011
Post-traumatic seizures exacerbate histopathological damage after fluid-percussion brain injury.
The purpose of this study was to investigate the effects of an induced period of post-traumatic epilepsy (PTE) on the histopathological damage caused by traumatic brain injury (TBI). Male Sprague Dawley rats were given a moderate parasagittal fluid-percussion brain injury (1.9-2.1 atm) or sham surgery. At 2 weeks after surgery, seizures were induced by administration of a GABA(A) receptor antagonist, pentylenetetrazole (PTZ, 30 mg/kg). ⋯ In addition, the TBI-PTZ rats showed less NeuN-immunoreactive cells within the ipsilateral parietal cerebral cortex (p < 0.05) and there was a trend for decreased hippocampal CA3 neurons in TBI-PTZ rats compared with TBI-saline or sham-operated rats. These results demonstrate that an induced period of post-traumatic seizures significantly exacerbates the structural damage caused by TBI. These findings emphasize the need to control seizures after TBI to limit even further damage to the injured brain.
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Journal of neurotrauma · Jan 2011
Case ReportsDecompressive craniectomy for severe head injury: does an outcome prediction model influence clinical decision-making?
The use of a prognostic model to aid clinician decision-making with regard to decompressive craniectomy for patients with severe neurotrauma has not been examined. Thus in this study we assessed whether an internationally validated prediction model would influence clinician decision-making about craniectomy. A two-part structured interview, given before and after knowing the predicted risks of unfavorable neurological outcomes at 6 months, was used to assess the participants' recommendations about performing decompressive craniectomy in three patients with severe traumatic brain injury. ⋯ The participants were significantly more likely to recommend decompressive craniectomy for their patients than for themselves, especially when the next of kin of the patient demanded the procedure, and were more similar in their own preferences to patients who had advance directives. Clinicians' preferences to perform the procedure for both themselves and their patients was significantly reduced after knowing the predicted risks of unfavorable outcomes, and these changes in attitude were consistent across those with different specialties, regardless of the amount of experience caring for similar patients, or religious background. In conclusion, the predicted risks of unfavorable outcomes influenced clinician decision-making about recommending decompressive craniectomy for patients with very severe neurotrauma.
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Journal of neurotrauma · Jan 2011
Phenylephrine infusion prevents impairment of ATP- and calcium-sensitive potassium channel-mediated cerebrovasodilation after brain injury in female, but aggravates impairment in male, piglets through modulation of ERK MAPK upregulation.
Traumatic brain injury (TBI) contributes to morbidity in children and boys, and hypotension worsens outcome. Extracellular signal-related kinase (ERK) mitogen-activated protein kinase (MAPK) is upregulated more in males and reduces cerebral blood flow (CBF) after fluid percussion injury (FPI). Increased cerebral perfusion pressure (CPP) via phenylephrine (Phe) sex-dependently improves impairment of the cerebral autoregulation seen after FPI through modulation of ERK MAPK upregulation, which is aggravated in males, but is blocked in females. ⋯ Co-administration of U 0126, an ERK antagonist, and Phe fully restored dilation to cromakalim, calcitonin gene-related peptide (CGRP), and NS 1619, in males after FPI. These data indicate that Phe sex-dependently prevents impairment of Katp and Kca channel-mediated cerebrovasodilation after FPI in females, but aggravates impairment in males, through modulation of ERK MAPK upregulation. Since autoregulation of CBF is dependent on intact functioning of potassium channels, these data suggest a role for sex-dependent mechanisms in the treatment of cerebral autoregulation impairment after pediatric TBI.
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Journal of neurotrauma · Jan 2011
A longitudinal proton magnetic resonance spectroscopy study of mild traumatic brain injury.
Despite the prevalence and impact of mild traumatic brain injury (mTBI), common clinical assessment methods for mTBI have insufficient sensitivity and specificity. Moreover, few researchers have attempted to document underlying changes in physiology as a function of recovery from mTBI. Proton magnetic resonance spectroscopy (¹H-MRS) was used to assess neurometabolite concentrations in a supraventricular tissue slab in 30 individuals with semi-acute mTBI, and 30 sex-, age-, and education-matched controls. ⋯ In addition, 17 mTBI patients (57%) returned for a follow-up evaluation (mean = 120 days post-injury). A significant group × time interaction indicated recovery in the mTBI group for gray matter Glx, and trends toward recovery in white matter Cre and Glx. An estimate of premorbid intelligence predicted the magnitude of neurometabolite normalization over the follow-up interval for the mTBI group, indicating that biological factors underlying intelligence may also be associated with more rapid recovery.