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Träfflista för sökning "WFRF:(Lindgren Arne) srt2:(2005-2009)"

Sökning: WFRF:(Lindgren Arne) > (2005-2009)

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  • Jönsson, Ann-Cathrin, et al. (författare)
  • Prevalence and intensity of pain after stroke: a population based study focusing on patients' perspectives.
  • 2005
  • Ingår i: Journal of Neurology, Neurosurgery and Psychiatry. - 1468-330X. ; , s. 590-595
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To determine prevalence and intensity of pain after stroke, focusing on patients' perspectives. METHODS: During a one year period, 416 first-ever stroke patients were included in the population based Lund Stroke Register. After 4 and 16 months (median), 297 patients (98% of survivors) were followed up. Worst pain intensity during the previous 48 hours was assessed on a visual analogue scale (VAS), range 0 to 100: a score of 0 to 30 was defined as no or mild pain; 40 to 100 as moderate to severe pain. NIH stroke scale (NIHSS) score and HbA1c were assessed at baseline. At 16 months, screening for depression was done using the geriatric depression scale (GDS-20), and cognition with the mini-mental state examination (MMSE). Predictors of pain were determined by multivariate analyses. RESULTS: Moderate to severe pain was reported by 96 patients (32%) after four months (VAS median=60). Predictors of pain were younger age (p=0.01), female sex (p=0.006), higher NIHSS score (p<0.001), and raised HbA1c (p=0.001) at stroke onset. At 16 months, only 62 patients (21%) had moderate to severe pain, but pain intensity was more severe (median VAS score=70; p<0.016). Higher pain intensity correlated with female sex, worse GDS-20 score, better MMSE score, and raised HbA1c. Pain was persistent in 47%, disturbed sleep in 58%, and required rest for relief in 40% of patients. CONCLUSIONS: Although prevalence of pain after stroke decreased with time, after 16 months 21% had moderate to severe pain. Late pain after stroke was on average more severe, and profoundly affected the patients' wellbeing.
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  • Jönsson, Ann-Cathrin, et al. (författare)
  • Weight loss after stroke: a population-based study from the Lund Stroke Register.
  • 2008
  • Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 39:3, s. 918-923
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND PURPOSE: Data on the prevalence and indicators of weight loss in population-based groups of stroke survivors are scarce. We aimed to find the predictors and indicators of weight loss >3 kg as a possible marker of malnutrition after stroke. METHODS: We registered weight at baseline, after 4 months, and 1 year later in 305 survivors from a population-based cohort of first-ever stroke patients. Characteristics of the patients were registered at baseline and follow-ups, including glycosylated hemoglobin at baseline and follow-up II, eating difficulties at both follow-ups, and screening for depression at follow-up II. We used univariate and multivariate analyses to find baseline predictors and follow-up indicators related to weight loss >3 kg from baseline. RESULTS: Among the 305 patients, 60% were male, the mean age was 72.5 years, and mean body mass index was 25.8 kg/m(2). The main stroke types were cerebral infarction (89%), intracerebral hemorrhage (7%), and subarachnoid hemorrhage (4%). Weight loss >3 kg was found in 74 (24%) patients (mean, -6.6 kg) after 4 months and in 79 patients (26%; mean, -8.3 kg) 1 year later. Severe stroke and elevated glycosylated hemoglobin levels were baseline predictors of weight loss >3 kg. Indicators associated with short-term weight loss (at follow-up I) were eating difficulties, low prealbumin value, and dependence (Barthel Index), whereas indicators associated with long-term weight loss (follow-up II) were eating difficulties, hemorrhagic stroke, and low prealbumin value. CONCLUSIONS: Weight loss >3 kg after stroke indicates the need for closer observation regarding nutritional status. Monitoring of body weight may be useful, particularly among patients with severe stroke, eating difficulties, low prealbumin values, and impaired glucose metabolism
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  • Lindgren, Ingrid, et al. (författare)
  • Shoulder Pain After Stroke. A Prospective Population-Based Study.
  • 2007
  • Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 38, s. 343-348
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND PURPOSE: Shoulder pain is a well-known complication after stroke, but data on prevalence, predictors, and outcome in unselected stroke populations are limited.METHODS: During a 1-year period, 416 first-ever stroke patients were included in the population-based Lund Stroke Register. After 4 months, 327 patients were followed up and 1 year later, the surviving 305 patients were followed up again. General status (National Institutes of Health Stroke Scale score) was registered at stroke onset. Shoulder pain intensity (visual analog scale, score 0 to 30=no-mild and 40 to 100=moderate-severe pain); arm motor function; restricted dressing and/or ambulating; and functional status (Barthel Index) were registered at both follow ups.RESULTS: Shoulder pain onset within 4 months after stroke was reported by 71 patients (22%). Among the 61 patients able to score the visual analog scale, 79% had moderate-severe pain. One year later, 8 of these 71 patients had died, 17 had no remaining pain, and 28 additional patients had developed shoulder pain since the first follow up. Lost or impaired arm motor function and high National Institutes of Health Stroke Scale score were predictors of shoulder pain. Shoulder pain restricted daily life often or constantly when dressing for 51%/31% and when ambulating for 29%/13% of the patients at 4 and 16 months, respectively.CONCLUSIONS: Almost one third of the 327 patients developed shoulder pain after stroke onset, a majority with moderate- severe pain. Shoulder pain restricts patients' daily life after stroke. The increased risk of shoulder pain for patients with impaired arm motor function and/or low general status needs close attention in poststroke care.
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  • Lindgren, Stefan, et al. (författare)
  • Intravenous iron sucrose is superior to oral iron sulphate for correcting anaemia and restoring iron stores in IBD patients : A randomized, controlled, evaluator-blind, multicentre study
  • 2009
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 44:7, s. 838-845
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. Patients with inflammatory bowel disease (IBD) often have low iron stores or anaemia. There is controversy about whether iron should be supplemented orally or intravenously (i.v.). The purpose of this study was to investigate whether treatment with intravenous iron is superior to treatment with oral iron. The primary end-points were response and remaining anaemia at the end of treatment (EOT).Material and methods. Ninety-one patients with IBD and anaemia (B-Hb <115 g/L) were randomized to oral iron sulphate (n=46) or intravenous iron sucrose (n=45) treatment for 20 weeks.Results. Forty-three patients in the intravenous iron group completed the study compared to 35 patients in the oral iron group (p=0.0009). Only 22 patients (48%) tolerated the prescribed oral dose, and 52% reduced the dose or withdrew from treatment because of poor tolerance. At EOT, 47% patients in the oral iron group increased their B-Hb by ≥20 g/L, compared with 66% in the intravenous iron group (p=0.07). In the oral iron group, 41% still had anaemia versus 16% of the patients in the intravenous iron group (p=0.007), and 22% versus 42% reached their reference B-Hb level (p=0.04). Treatment with intravenous iron sucrose improved iron stores faster and more effectively than oral iron (p=0.002). Under treatment with intravenous iron, 74% of the patients had no anaemia and normal S-ferritin levels (>25 µg/L) at EOT compared with 48% of patients receiving oral iron (p=0.013).Conclusions. Treatment with intravenous iron sucrose is effective, safe, well tolerated and superior to oral iron in correcting haemoglobin and iron stores in patients with IBD.
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  • Bollmann, Andreas, et al. (författare)
  • Atrial fibrillatory rate and risk of stroke in atrial fibrillation.
  • 2009
  • Ingår i: Europace. - : Oxford University Press (OUP). - 1532-2092 .- 1099-5129. ; 11, s. 582-586
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims In atrial fibrillation (AF), a relation between electrocardiogram (ECG) parameters such as fibrillatory wave amplitude and stroke has been sought with conflicting results. In this study, we tested the hypothesis that the atrial fibrillatory rate of surface ECG lead V1 is related to stroke risk and may consequently be helpful for identifying high-risk patients. Methods and results Atrial fibrillatory rate of 79 consecutive patients with AF and embolic stroke (age 83 +/- 7 years, 41% male) was compared with those of a matched AF population without stroke (n = 79). Atrial fibrillatory rate was determined from the surface ECG using spatiotemporal QRST cancellation and time-frequency analysis of lead V1. There was no significant difference in any clinical or echocardiographic variable in patients with stroke compared with AF controls without stroke. Atrial fibrillatory rate measured 373 +/- 55 fibrillations per minute (fpm; range 235-505 fpm) in the entire population. There was no fibrillatory rate difference between stroke patients (369 +/- 54 fpm, range 256-505 fpm) and AF controls without stroke (378 +/- 56 fpm, range 235-488 fpm). There was an inverse correlation between fibrillatory rate and age (R = -0.219, P = 0.006). Individuals aged >/=85 years had a significantly lower fibrillatory rate (356 +/- 44 fpm) than individuals aged 65-74 years (384 +/- 56 fpm, P = 0.033) and individuals aged 75-84 years (384 +/- 60 fpm, P = 0.016). In those subgroups, fibrillatory rates were, however, also similar in stroke patients and AF controls. Conclusion Atrial fibrillatory rate obtained from surface ECG lead V1 is not a risk marker for stroke in AF.
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  • Brådvik, Louise, et al. (författare)
  • Number of addictive substances used related to increased risk of unnatural death: a combined medico-legal and case-record study.
  • 2009
  • Ingår i: BMC Psychiatry. - 1471-244X. ; 9:Aug 4
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Substance use disorders have repeatedly been found to lead to premature death, i.e. drug-related death by disease, fatal intoxications, or trauma (accidents, suicide, undetermined suicide, and homicide). The present study examined the relationship between multi-drug substance use and natural and unnatural death. METHODS: All consecutive, autopsied patients who had been in contact with the Addiction Centre in Malmö University Hospital from 1993 to 1997 inclusive were investigated. Drug abuse was investigated blindly in the case records and related to the cause of death in 387 subjects. RESULTS: Every substance apart from alcohol used previously in life added to the risk of unnatural death in a linear way. There were independent increased risks of fatal heroin overdoses or undetermined suicide. Death by suicide and violent death were unrelated to additional abuse. CONCLUSION: The number of drugs used was related to an increased risk of unnatural death by undetermined suicide (mainly fatal intoxications) and heroin overdose.
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10.
  • Canhao, P C, et al. (författare)
  • Causes and predictors of death in cerebral venous thrombosis
  • 2005
  • Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 36:8, s. 1720-1725
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Purpose - The causes of death of patients with cerebral venous thrombosis (CVT) have not been systematically addressed in previous studies. We aimed to analyze the causes and predictors of death during the acute phase of CVT in the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) to identify preventable or treatable causes. Methods - ISCVT is a multinational, prospective, observational study including 624 patients with CVT occurring between May 1998 and May 2001, in which 27 patients (4.3%) died during the acute phase, 21 (3.4%) within 30 days from symptom onset. Inclusion forms and a questionnaire assessing the causes of death were analyzed. A logistic regression analysis was performed to identify the predictors of death within 30 days from symptom onset of CVT. Results - Median time between onset of symptoms and death was 13 days and between diagnosis and death, 5 days. Causes of death were mainly transtentorial herniation due to a unilateral focal mass effect (10 patients) or to diffuse edema and multiple parenchymal lesions (10 patients). Independent predictors of death were coma (odds ratio [OR], 8.8; 95% confidence interval [CI], 2.8 to 27.7), mental disturbance (OR, 2.5; 95% CI 0.9 to 7.3), deep CVT thrombosis (OR, 8.5; 95% CI, 2.6 to 27.8), right intracerebral hemorrhage (OR, 3.4; 95% CI, 1.1 to 10.6), and posterior fossa lesion (OR, 6.5; 95% CI, 1.3 to 31.7). Worsening of previous focal or de novo focal deficits increased the risk of death. Conclusions - The main causes of acute death were neurologic, the most frequent mechanism being transtentorial herniation.
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