Titlebook: Mechanisms of Secondary Brain Damage from Trauma and Ischemia; Recent Advances of o A. Baethmann,J. Eriskat,N. Plesnila Conference proceedi

correspondent

The natural course of lesion development in brain ischemiactacidosis, microcirculatory disturbances, and flow-metabolism uncoupling among others. Problems involved in the subject under focus are related to maturation phenomena of injury and the different imaging modalities (metabolic imaging, NMR imaging, positron emission tomography) that require a subtly

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Glial scar and axonal regeneration in the CNS: lessons from GFAP and vimentin transgenic miceaxonal regeneration. In experimental animals, a hemisection of the spinal cord was performed utilizing the above mentioned double-mutant mice. The knock-out mice were generated by gene targeting. Double-mutants were obtained by crossing single null mice.

Cacophonous

Recovery from spinal cord injury — underlying mechanisms and efficacy of rehabilitation of a step cycle with a daily locomotor training, coincident with a significant decrease of body unloading. In contrast to this, neither clinical nor electrophysiological examination scores improve. The locomotor pattern depends on the level of lesion: the higher the level of spinal cord lesion the

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The MRC CRASH trial — a large, simple randomised trial of steroids in head injurycompatible with there being no real benefit, but it is also compatible with there being a small benefit of a few percent. An improvement in mortality of 2% would theoretically save 10,000 lives per 500,000 patients treated. The global impact of such a treatment effect would be significant as the num

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https://doi.org/10.1007/978-3-7091-0603-7brain; brain injury; cerebral ischemia; electroencephalography (EEG); head; head injury; pathophysiology; r

allude

978-3-7091-7206-3Springer-Verlag Wien 2004

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Mechanisms of Secondary Brain Damage from Trauma and Ischemia978-3-7091-0603-7Series ISSN 0065-1419 Series E-ISSN 2197-8395

動(dòng)作謎

0065-1419 Overview: Top level clinical and laboratory scientists present updates and exchanges of their most recent clinical and experimental findings and concepts.Includes supplementary material: 978-3-7091-7206-3978-3-7091-0603-7Series ISSN 0065-1419 Series E-ISSN 2197-8395

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L-type calcium channel antagonist nifedipine reduces neurofilament restitution following traumatic o.. The aim of the present study was to observe if the use of the L-type calcium channel antagonist nifedipine would offer advantages for the retinal ganglion cells and the restitution of the axonal cytoskeleton after optic nerve crush.

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