Articles: brain-injuries.
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J Head Trauma Rehabil · Apr 2001
ReviewQuantitative magnetic resonance imaging in traumatic brain injury.
Quantitative neuroimaging has now become a well-established method for analyzing magnetic resonance imaging in traumatic brain injury (TBI). A general review of studies that have examined quantitative changes following TBI is presented. ⋯ Various clinical caveats are provided including how quantitative neuroimaging findings can be used clinically and in predicting rehabilitation outcome. The future of quantitative neuroimaging also is discussed.
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Traumatic brain injury poses a serious public health challenge. Treatment paradigms have dramatically shifted with the introduction of the American Association of Neurologic Surgeons (AANS) Guidelines for the Management of Severe Head Injury. Implementation of the AANS guidelines positively affects patient outcomes and can be successfully introduced in a community hospital setting. ⋯ Implementation of a traumatic brain injury protocol in a community hospital setting is practical and efficacious. Appropriate invasive monitoring of systemic and cerebral parameters guides care decisions. The protocol results in an increase in resource usage, but it also results in statistically improved outcomes justifying the increase in expenditures.
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J. Cereb. Blood Flow Metab. · Apr 2001
The maxi-K channel opener BMS-204352 attenuates regional cerebral edema and neurologic motor impairment after experimental brain injury.
Large-conductance, calcium-activated potassium (maxi-K) channels regulate neurotransmitter release and neuronal excitability, and openers of these channels have been shown to be neuroprotective in models of cerebral ischemia. The authors evaluated the effects of postinjury systemic administration of the maxi-K channel opener, BMS-204352, on behavioral and histologic outcome after lateral fluid percussion (FP) traumatic brain injury (TBI) in the rat. Anesthetized Sprague-Dawley rats (n = 142) were subjected to moderate FP brain injury (n = 88) or surgery without injury (n = 54) and were randomized to receive a bolus of 0.1 mg/kg BMS-204352 (n = 26, injured; n = 18, sham), 0.03 mg/kg BMS-204352 (n = 25, injured; n = 18, sham), or 2% dimethyl sulfoxide (DMSO) in polyethylene glycol (vehicle, n = 27, injured; n = 18, sham) at 10 minutes postinjury. ⋯ Administration of 0.03 mg/kg BMS-204352 significantly reduced cerebral edema in the ipsilateral thalamus (P < 0.05). No effects on cognitive function or cortical tissue loss were observed with either dose. These results suggest that the novel maxi-K channel opener BMS-204352 may be selectively beneficial in the treatment of experimental TBI.
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Comparative Study
The effects of litigation on symptom expression: a prospective study following mild traumatic brain injury.
To prospectively assess the association between litigation and neurobehavioural symptoms following mild Traumatic Brain Injury (TBI). ⋯ the data demonstrate an association between litigation and increased psychological distress at the outset of the litigation process. While association is not synonymous with causality, the absence of demographic, premorbid and TBI related differences between litigants and non-litigants suggests that the pursuit of compensation may influence the subjective expression of symptoms following mild traumatic brain injury.
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Experimental neurology · Apr 2001
Therapeutic effects of environmental enrichment on cognitive function and tissue integrity following severe traumatic brain injury in rats.
Postinjury environmental enrichment (EE) has been shown to alter functional and anatomical outcomes in a number of injury paradigms, including traumatic brain injury (TBI). The question of whether EE alters functional outcome following TBI in a model which produces overt histopathological consequences has not been addressed. We investigated this question using the severe, parasagittal fluid percussion injury (FPI) model. ⋯ At 14 days post-TBI, enriched animals had approximately twofold smaller lesion areas in regions of the cerebral cortex posterior to the injury epicenter (-4.5, -5.8, -6.8 mm relative to bregma; P < 0.05) compared to injured/standard animals. In addition, overall lesion volume for the entire injured cortical hemisphere was significantly smaller in animals recovering in the enriched environment. These results indicate that noninvasive environmental stimulation is beneficial in attenuating cognitive deficits and preserving tissue integrity in a TBI model which causes cerebral contusion and cell death.