Restor Neurol Neuros
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Restor Neurol Neuros · Jan 2004
ReviewModulation of motor function and cortical plasticity in health and disease.
Basic science studies demonstrated mechanisms of plasticity and metaplasticity. More recent human studies identified some of these mechanisms as operating in multiple areas of human cognition, such as learning and memory, and in functional recovery from lesions in the CNS, as in stroke. ⋯ Understanding the mechanisms and functional role of human plasticity could lead to the development of therapeutic options in situations in which there is virtually no treatment alternative, as in chronic stroke. We review some of the work performed to better understand the substrates and mechanisms underlying cortical plasticity and discuss some experimental approaches to enhance cortical plasticity and recovery of function, like cortical stimulation.
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Restor Neurol Neuros · Jan 2004
Comparative StudyBridging short nerve defects by direct repair under tension, nerve grafts or longitudinal sutures.
To compare the longitudinal suture model for bridging nerve defects with direct approximation under tension or with autologuos nerve grafting. ⋯ Longitudinal sutures can be used to bridge short nerve defects and could be an alternative to nerve grafting.
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Restor Neurol Neuros · Jan 2004
Inhibition of vascular endothelial growth factor receptor (VEGFR) signaling by BSF476921 attenuates regional cerebral edema following traumatic brain injury in rats.
In the present study we assessed the ability of BSF476921, an inhibitor of vascular endothelial growth factor receptor (VEGFR) kinase signal transduction, to reduce edema formation and neurologic motor dysfunction following lateral fluid percussion (FP) brain injury in rats. ⋯ To our knowledge, this is the first report of a small molecule VEGFR kinase inhibitor reducing cerebral edema in a widely accepted model of brain injury.
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Restor Neurol Neuros · Jan 2003
ReviewSerum S-100B protein as a molecular marker in severe traumatic brain injury.
There is growing evidence that S-100B protein may be used as a novel biochemical marker of brain cell damage, measured by a simple blood test. In this paper, we summarize the current knowledge about S-100B serum measurements in severe head injury and address actual controversies. ⋯ S-100B belongs to a new generation of molecular serum markers of brain damage. These markers will have potential as a surrogate outcome marker or monitoring parameters for both clinical and experimental settings.
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Restor Neurol Neuros · Jan 2003
ReviewMolecular markers of brain damage--clinical and ethical implications with particular focus on cardiac arrest.
Although 25-50% of patients suffering from cardiac arrest can be stabilised haemodynamically, the hospital discharge rate is only 2-14%. One of the major causes of this discrepancy is persistent brain damage. Studies to assess the prognostic value of early prediction of neurologic and overall outcome in patients with cardiac arrest have not yet produced precise and generally accepted diagnostic rules. ⋯ Although it cannot be absolutely determined whether cerebral or cardiac release of S100 is predominant in this clinical setting, recent studies have revealed that S100 serum levels are a useful diagnostic tool for outcome prediction. In contrast, after cardiac arrest serum levels of protein S100 did not reach a 100% specificity and sensitivity in clinical studies, and, therefore, elevated S100 in these patients has to be interpreted with caution. Nonetheless, low S100 serum levels have been correlated with good outcome and, therefore, even if all other diagnostic tests indicate poor outcome, all therapeutic efforts must be undertaken, as no single study has shown that normal S100 serum levels were associated with poor prognosis.