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Sökning: WFRF:(Lindén Thomas 1962)

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31.
  • Cumming, T. B., et al. (författare)
  • The AVERT MoCA Data: Scoring Reliability in a Large Multicenter Trial
  • 2020
  • Ingår i: Assessment. - : SAGE Publications. - 1073-1911 .- 1552-3489. ; 27:5, s. 976-981
  • Tidskriftsartikel (refereegranskat)abstract
    • The Montreal Cognitive Assessment (MoCA) is a widely used cognitive screening tool in stroke. As scoring the visuospatial/executive MoCA items involves subjective judgement, reliability is important. Analyzing data on these items from A Very Early Rehabilitation Trial (AVERT), we compared the original scoring of assessors (n= 102) to blind scoring by a single, independent rater. In a sample of scoresheets from 1,119 participants, we found variable interrater reliability. The match between original assessors and the independent rater was the following: trail-making 97% (kappa = 0.94), cube copy 90% (kappa = 0.80), clock contour 92% (kappa = 0.49), clock numbers 89% (kappa = 0.67), and clock hands 72% (kappa = 0.46). For all items except clock contour, the independent rater was "stricter" than the original assessors. Discrepancies were typically errors in original scoring, rather than borderline differences in subjective judgement. In trials that include the MoCA, researchers should emphasize scoring rules to assessors and implement independent data checking, especially for clock hands, to maximize accuracy.
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32.
  • Cumming, Toby B, et al. (författare)
  • The High Prevalence of Anxiety Disorders After Stroke.
  • 2016
  • Ingår i: The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. - : Elsevier BV. - 1545-7214. ; 24:2, s. 154-60
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous studies indicate that post-stroke anxiety is common and persistent. We aimed to determine whether point prevalence of anxiety after stroke is higher than in the population at large, and whether the profile of anxiety symptoms is different.This case-control study was conducted in Göteborg, Sweden, with stroke patients recruited from the Sahlgrenska University Hospital and a comparison group selected from local population health studies. We included 149 stroke survivors (assessed at 20 months post-stroke) and 745 participants from the general population matched for age and sex. A comprehensive psychiatric interview was conducted, with anxiety and depressive disorders diagnosed according to DSM-III-R criteria.Those in the stroke group were significantly more likely than those in the comparison group to have generalized anxiety disorder (GAD) (27% versus 8%), phobic disorder (24% versus 8%) and obsessive-compulsive disorder (9% versus 2%). Multivariate regression indicated that being in the stroke group, female sex, and having depression were all significant independent associates of having an anxiety disorder. In terms of symptom profile, stroke survivors with GAD were significantly more likely to report vegetative disturbance than those in the comparison group with GAD but less likely to have observable muscle tension or reduced sleep.Point prevalence of anxiety disorders is markedly higher after stroke than in the general population, and this cannot be attributed to higher rates of comorbid depression.
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35.
  • Deshpande, J, et al. (författare)
  • Ultrastructural changes in the hippocampal CA1 region following transient cerebral ischemia: evidence against programmed cell death.
  • 1992
  • Ingår i: Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. - 0014-4819. ; 88:1, s. 91-105
  • Tidskriftsartikel (refereegranskat)abstract
    • The ultrastructural changes in the pyramidal neurons of the CA1 region of the hippocampus were studied 6 h, 24 h, 48 h, and 72 h following a transient 10 min period of cerebral ischemia induced by common carotid occlusion combined with hypotension. The pyramidal neurons showed delayed neuronal death (DND), i.e. at 24 h and 48 h postischemia few structural alterations were noted in the light microscope, while at 72 h extensive neuronal degeneration was apparent. The most prominent early ultrastructural changes were polysome disaggregation, and the appearance of electron-dense fluffy dark material associated with tubular saccules. Mitochondria and nuclear elements appeared intact until frank neuronal degeneration. The dark material accumulated with extended periods of recirculation in soma and in the main trunks of proximal dendrites, often beneath the plasma membrane, less frequently in the distal dendrites and seldom in spines. Protein synthesis inhibitors (anisomycin, cycloheximide) and an RNA synthesis inhibitor (actinomycin D), administered by intrahippocampal injections or subcutaneously, did not mitigate neuronal damage. Therefore, DND is probably not apoptosis or a form of programmed cell death. We propose that the dark material accumulating in the postischemic period represents protein complexes, possibly aggregates of proteins or internalized plasma membrane fragments, which may disrupt vital cellular structure and functions, leading to cell death.
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37.
  • Forsberg, Kalle, et al. (författare)
  • A Systematic Review Of Erythropoietin In Experimental Stroke
  • 2009
  • Ingår i: Stroke. - 0039-2499. ; 40:4
  • Konferensbidrag (refereegranskat)abstract
    • Introduction: Erythropoietin (EPO), a hematopoietic growth factor, has promise as a neuroprotectant in animal models of ischemic stroke. EPO is thought not only to protect neurons from cell death, but also is hypothesized to promote regeneration post stroke. Here we report a systematic review and meta-analysis of the published animal data characterizing the efficacy of EPO. Methods We conducted a systematic review and random effects weighted mean difference meta-analysis only including studies describing the efficacy of EPO in models of focal cerebral ischemia. Primary outcomes were infarct size and neurobehavioral score. A stratified analysis to identify the impact of elements of study quality and design was also conducted. Results Only 11 of 943 studies met our inclusion criteria. Infarct size was reported in 15 experiments using 191 animals. Neurobehavioral score was reported in 16 experiments using 287 animals. EPO improved infarct size by 30.5% (95%Cl 19.3%-41.7%) and neurobehavioral score by 37.4% (31.2– 43.7%). For infarct size, EPO was least effective in thrombotic models of ischemia, (16% versus to 44.8% and 24% in permanent and transient models of ischemia respectively, X2 =1.47 x 10–04). Using a scoring system derived from the STAIR criteria,study quality was modest with a median score of 4 out of 11 for both outcomes. Studies that randomized to treatment group reported smaller infarct sizes compared to those that did not (18.0% versus 44.8%, n=113 versus 78 animals, X2 = 3.4 x 10–05). Studies that blinded assessment of outcome also showed a smaller improvement in neurobehavioral score (31.1% versus 41.6%, n=107 versus 167, X2 = 8.9 x 10–4). Only 11.7% of the animals in the total dataset had a co-morbidity common to human stroke (hypertension) and this co-morbidity was only reported for neurobehavioral comparisons, not for infarct size. Blinded induction of ischemia was reported in 2 experiments (21.5% of animals) measuring infarct volume. Conclusions: Aggregation of the animal data for EPO in ischemic stroke indicates mean effect sizes of 30.5% and 37.4% for infarct volume and neurobehavioral score respectively. However, when the impact of common sources of bias are considered these effect sizes fall suggesting we are overestimating its potential benefit. As common human co-morbidities may reduce therapeutic efficacy, broader testing to delineate the range of circumstances in which EPO works would be beneficial before clinical trialing.
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38.
  • Ha, Jason, 1985, et al. (författare)
  • Bed rest or mobilization after rt-PA? A case-crossover study of factors influencing clinical decision making in stroke services
  • 2013
  • Ingår i: International journal of stroke. - : SAGE Publications. - 1747-4949 .- 1747-4930. ; 8:3, s. 172-179
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Acute stroke management is a dynamic field. Treatment with recombinant tissue plasminogen activator is standard care in Australia, but there are no evidence-based practice guidelines about first out of bed activity (mobilization) after recombinant tissue plasminogen activator. Aims To identify factors influencing clinicians' decisions to delay or allow mobilization. Methods Case-crossover design. Using hypothetical case vignettes, we explored the factors that clinicians consider when deciding to first mobilize a patient after recombinant tissue plasminogen activator. Acute stroke physicians and nurses from Australian hospitals known to treat with recombinant tissue plasminogen activator participated. Information about hospital recombinant tissue plasminogen activator protocols and perceived benefits and harms of mobilization after recombinant tissue plasminogen activator were also captured. Results Fifty-four clinicians, 52% senior nurses, and 48% senior physicians from all states of Australia participated. Of the factors influencing decisions about mobilization after recombinant tissue plasminogen activator, neurological decline (0·29; confidence interval 0·12, 0·46; P=0·001), neurological decline with symptomatic intracerebral hemorrhage (0·41; confidence interval 0·24, 0·59; P<0·0001), infection of uncertain cause (0·32; confidence interval 0·14, 0·50; P=0·0010), severe chest infection (0·35; confidence interval 0·16, 0·53; P=0·0004), severe stroke (0·29; confidence interval 0·12, 0·46; P=0·0010), drowsiness (0·47; confidence interval 0·29, 0·63; P<0·0001), and confusion (0·31; confidence interval 0·15, 0·47; P=0·0001) significantly influenced decisions. Falls risk was a common concern (85%). Conclusion Growing interest in development of clear protocols that guide first mobilization after recombinant tissue plasminogen activator prompted this study. We have identified factors that may influence decisions about when to allow patients to mobilize after recombinant tissue plasminogen activator. These, combined with emerging evidence of risks and benefits of early mobilization, should help protocol development in the future.
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40.
  • Helldén, Anders, et al. (författare)
  • Death delusion. : Cotard's syndrome as an adverse drug reaction to (val-)aciclovir
  • 2007
  • Ingår i: BMJ (Clinical research ed.). - 1468-5833. ; 335:7633
  • Tidskriftsartikel (refereegranskat)abstract
    • We report two cases of Cotard’s syndrome that occurred as an adverse drug reaction to aciclovir and its prodrug valaciclovir. In the 1880s Jules Cotard first described his eponymous syndrome, a rare psychiatric condition with strong delusions of being dead. Aciclovir or valaciclovir may cause neuropsychiatric side effects such as confusion, somnolence, and hallucinations, mainly in patients with impaired renal function. To our knowledge, Cotard’s syndrome has never been reported as a suspected adverse drug reaction but associated with severe somatic stress as well as general and localised cerebral pathologies. Our findings add adverse response to an antiviral drug as another cause and provide clues to the syndrome’s possible neuropsychiatric origin. Clinicians should be aware of the association between body scheme disturbances and (val)aciclovir. Affected patients with Cotard’s syndrome and renal failure should preferably be sent to the dialysis unit, not to the department of psychiatry.
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