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Sökning: L773:0967 5868 OR L773:1532 2653 > (2010-2014)

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  • Kremer, Christine, et al. (författare)
  • Dissociation of severity of stroke and aphasia recovery early after intravenous recombinant tissue plasminogen activator thrombolysis.
  • 2014
  • Ingår i: Journal of Clinical Neuroscience. - : Elsevier BV. - 1532-2653 .- 0967-5868. ; 21:10, s. 1828-1830
  • Tidskriftsartikel (refereegranskat)abstract
    • Clinical observation suggested to us that aphasia recovers relatively better than other deficits early after intravenous recombinant tissue plasminogen activator (IV-rtPA) treatment in stroke patients with minor deficits, while the reverse seemed the case in those with severe deficits. Retrospective analysis of acute ischemic stroke patients with aphasia admitted within 3hours from symptom onset and treated with IV-rtPA was carried out. Stroke severity, aphasia and global neurological impairment were assessed at admission and 24hours after thrombolysis. Improvement of aphasia (gain of ⩾1 point on the National Institutes of Health Stroke Scale [NIHSS] aphasia score) and global neurological improvement (gain of ⩾4 points on the NIHSS) were compared in minor strokes (NIHSS ⩽7), moderate strokes (NIHSS 8-15), and major strokes (NIH ⩾16). Sixty-nine of 243 stroke patients suffered from aphasia. Improvement of aphasia occurred in 7/16 minor strokes, 11/25 moderate strokes, and 7/28 severe strokes. Improvement of ⩾4 points on the NIHSS occurred in 3/16 minor strokes, 17/25 moderate strokes and 15/28 severe strokes. There is a significant (X(2)=4.073, p<0.05) dissociation of recovery of aphasia and that of other neurological deficits between minor versus severe strokes. This confirms the clinically suspected dissociation between a good early recovery from aphasia in minor strokes relative to recovery of other neurological deficits, as opposed to a better recovery from other neurological deficits than from aphasia in patients with severe strokes.
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  • Li, Xiaogai, et al. (författare)
  • Decompressive craniotomy causes significant strain increase in axonal fiber tracts
  • 2012
  • Ingår i: Journal of clinical neuroscience. - : Elsevier BV. - 0967-5868 .- 1532-2653. ; 20:4, s. 509-513
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundDecompressive craniotomy allows expansion of the swollen brain outside the skull, resulting in axonal stretch, which might lead to neural injury and consequently cause unfavorable outcome for the patients. The aim of this study was to assess and quantify the axonal deformation at both pre- and post-craniotomy period in order to provide more insight into the mechanical effects on the axonal fibers upon such a treatment.MethodsDisplacement fields representing the structural changes in whole brain were obtained by a nonlinear image registration method based on the three-dimensional CT imaging data sets of a patient both before and after decompressive craniotomy. Axonal fiber tracts together with their orientations were extracted from diffusion weighted (DW) images from a healthy brain and adapted to the patient’s brain by image registration. The deformation of the brain tissue in the form of Lagrangian finite strain tensor for the entire brain was then calculated from the displacement field. Based on the obtained brain tissue strain tensor and the axonal fiber tracts, 1st principal strain was extracted at axonal fibers. Furthermore, other axonal deformation measures, i.e., axonal strain, and axonal effective shear strain were also quantified.ResultsGreatest axonal fiber displacement (up to 12 mm) was found predominantly located in the treated part of the craniotomy, accompanied by a large axonal deformation, e.g., 1st principal strain up to 0.49. This indicated the extent of axonal fiber stretching due to the neurosurgical intervention. Other strain measures, such as axonal strain and axonal effective shear strain also showed an increased level at the treated part for post-craniotomy compared to that found in the pre-craniotomy period.ConclusionsThe distortion (stretching or shearing) of axonal fibers at the treated part of the craniotomy may influence the axonal fibers in such a way that the neurochemical events are jeopardized. It is suggested that such a quantitative model may clarify some of the potential problems with such a treatment. Also, by further development of the technology it is quite possible to judge the outcome of strain levels already before the decompressive craniotomy is performed. This may have the possibility to optimize the size as well as the area of craniotomy.
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  • Olivecrona, Magnus, et al. (författare)
  • Use of the CRASH study prognosis calculator in patients with severe traumatic brain injury treated with an intracranial pressure-targeted therapy
  • 2013
  • Ingår i: Journal of clinical neuroscience. - : Elsevier BV. - 0967-5868 .- 1532-2653. ; 20:7, s. 996-1001
  • Tidskriftsartikel (refereegranskat)abstract
    • Based on the Corticosteroid Randomisation after Significant Head Injury (CRASH) trial database, a prognosis calculator has been developed for the prediction of outcome in an individual patient with a head injury. In 47 patients with severe traumatic brain injury (sTBI) prospectively treated using an intracranial pressure (ICP) targeted therapy, the individual prognosis for mortality at 14 days and unfavourable outcome at 6 months was calculated and compared with the actual outcome. An overestimation of the risk of mortality and unfavourable outcome was found. The mean risk for mortality and unfavourable outcome were estimated to be 44.6 +/- 32.5% (95% confidence interval [CI], 35.1-54.2%) and 69.3 +/- 23.7% (95% CI, 62.3-76.2%). The actual outcome was 4.3% and 42.6% respectively. The absolute risk reduction (ARR) for mortality was 33.1% and for unfavourable outcome 29.8%. A logistic fit for outcome at 6 months shows a statistically significant difference (p < 0.01). A receiver operating characteristic (ROC) curve analysis shows an area under the curve (AUC) of 0.691. The CRASH prognosis calculator overestimates the risk of mortality and unfavourable outcome in patients with sTBI treated with an ICP-targeted therapy based on the Lund concept. We do not advocate the use of the calculator for treatment decisions in individual patients. We further conclude that patients with blunt sTBI admitted within 8 hours of trauma should be treated regardless of their clinical status as long as the initial cerebral perfusion pressure is > 10 mmHg.
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