Neurological research
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Neurological research · Apr 2003
The long-term effect of recombinant tissue-plasminogen-activator (rt-PA) on edema formation in a large-animal model of intracerebral hemorrhage.
Hematoma puncture, fibrinolysis, and aspiration of the liquefied clot is a promising new treatment strategy for large intracerebral hemorrhages (ICH). Characteristics of the cellular injury and neuronal and glial cell death associated with ICH and the administration of fibrinolytic agents still need to be defined. We developed a porcine model to study the histopathological effects of recombinant tissue-Plasminogen-Activator (rt-PA) on perihematomatous cell integrity. ⋯ Although rt-PA significantly accelerated clot resolution compared to controls (p < 0.02), the increase of perihematomatous edema volume within 10 days was not significantly ameliorated in rt-PA-treated animals compared to controls on MRI. The extent of inflammatory infiltrates on histology was more pronounced in animals treated with rt-PA. In conclusion, despite significant reduction in the size of the hematoma clot liquefication with rt-PA and aspiration invokes a substantial inflammatory response when studied after 10 days and does not result in a reduction of the perihematomatous edema.
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Neurological research · Mar 2003
Noninvasive assessment of cerebral oxygenation during high altitude trekking in the Nepal Himalayas (2850-5600 m).
Mountain trekking is significantly increasing in popularity. Hypoxia seems to play a key role in the pathogenesis of acute mountain sickness (AMS). The purpose of this study was to investigate regional cerebral (rSO2) and peripheral (SaO2) oxygen saturation for the first time, during 22 days high altitude trekking (measurement points: 3450, 4450, 4750, 5050 and 2850 m) in the Khumbu region of Nepal with near infrared spectroscopy and pulse oximetry. ⋯ The decrease in cerebral oxygen saturation was more pronounced at higher altitudes than in the periphery (rSO2/SaO2 = 0.56 at 5050 m). At higher altitudes (> 4450 m), two subjects showed reversible symptoms of AMS. The present data indicates that acute reduction in rSO2 values might be a primary cause of AMS, however, further studies and analysis are necessary to correlate our findings with cerebral symptom scores.
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Neurological research · Dec 2002
Randomized Controlled Trial Clinical TrialRandomized evaluation of adverse events and length-of-stay with routine emergency department use of phenytoin or fosphenytoin.
Intravenous phenytoin has come under increased scrutiny with the introduction of the prodrug, fosphenytoin. We evaluated adverse events and length-of-stay using parenteral the two drugs in routine emergency department use. Open-label randomization of phenytoin or fosphenytoin in 256 Emergency Department patients prescribed 279 parenteral doses of a phenytoin-equivalent. ⋯ One patient developed hypotension (fosphenytoin); there were no other serious adverse events, including phlebitis. Median Emergency Department length-of-stay was 6.7 h for phenytoin and 5.7 h for fosphenytoin (p = 0.6). In routine Emergency Department use, our data do not support formulary conversion from phenytoin to fosphenytoin, based on the incidence of adverse events or Emergency Department length-of-stay.
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Neurological research · Dec 2002
Case ReportsAssessment of prognostic factors in severe traumatic brain injury patients treated by mild therapeutic cerebral hypothermia therapy.
This study analyzed the predictable factors of outcome such as neuro-parameters and systemic complications to elucidate the indications for therapeutic hypothermia. In our institute, 35 patients with severe head injury (Glasgow Coma Scale 3-7) were treated with mild hypothermia therapy (33 degrees-35 degrees C). Twenty-two of these 35 patients underwent complete neuromonitoring and outcome assessments by Glasgow Outcome Scale (GOS) at three months after injury. ⋯ All patients with thrombocytopenia had poor outcome. Hypothermia therapy can improve outcome in patients with traumatic brain injury who are younger than 50 years old, without severe brain damage, and if improvement of cerebral perfusion is expected. Systemic complications must be prevented as far as possible by combination with other therapies.
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Neurological research · Sep 2002
Comparative StudyInfluence of inspired oxygen on glucose-lactate dynamics after subdural hematoma in the rat.
The mechanisms causing brain damage after acute subdural hematoma (SDH) are poorly understood. A decrease in cerebral blood flow develops immediately after the hematoma forms, thus reducing cerebral oxygenation. This in turn may activate mitochondrial failure and tissue damage leading to ionic imbalance and possibly to cellular breakdown. ⋯ We hypothesize that increased neural tissue oxygen tension, in presence of reduced regional CBF, and possibly compromised mitochondrial function, after acute SDH results in upregulation of rate-limiting enzyme systems responsible for both glycolytic and aerobic metabolism. Similar changes have been seen in severe human head injury, and suggest that a simple therapeutic measure, such as early ventilation with 100% O2, may improve cerebral energy metabolism, early after SDH. Further studies to measure the generation of adenosine triphosphate (ATP) are needed to validate the hypothesis.