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1.
  • Aarnio, K., et al. (författare)
  • Cardiovascular events after ischemic stroke in young adults: A prospective follow-up study
  • 2016
  • Ingår i: Neurology. - 0028-3878. ; 86:20, s. 1872-1879
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives:To study the long-term risk of recurrent cardiac, arterial, and venous events in young stroke patients, and whether these risks differed between etiologic subgroups.Methods:The study population comprised 970 patients aged 15-49 years from the Helsinki Young Stroke Registry (HYSR) who had an ischemic stroke in 1994-2007. We obtained follow-up data until 2012 from the Finnish Care Register and Statistics Finland. Cumulative 15-year risks were analyzed with life tables, whereas relative risks and corresponding confidence intervals (CI) were based on hazard ratios (HR) from Cox regression analyses.Results:There were 283 (29.2%) patients with a cardiovascular event during the median follow-up of 10.1 years (range 0.1-18.0). Cumulative 15-year risk for venous events was 3.9%. Cumulative 15-year incidence rate for composite vascular events was 34.0 (95% CI 30.1-38.2) per 1,000 person-years. When adjusted for age and sex, patients with an index stroke caused by high-risk sources of cardioembolism had the highest HR for any subsequent cardiovascular events (3.7; 95% CI 2.6-5.4), whereas the large-artery atherosclerosis group had the highest HR (2.7; 95% CI 1.6-4.6) for recurrent stroke compared with patients with stroke of undetermined etiology.Conclusions:The risk for future cardiovascular events after ischemic stroke in young adults remains high for years after the index stroke, in particular when the index stroke is caused by high-risk sources of cardioembolism or large-artery atherosclerosis.
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  • af Edholm, Karolina, et al. (författare)
  • Clinical Reasoning : Leg weakness and stiffness at the emergency room
  • 2019
  • Ingår i: Neurology. - : Lippincott Williams & Wilkins. - 0028-3878 .- 1526-632X. ; 92:6, s. E622-E625
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • A 48-year-old woman from the Maghreb came to the emergency department with insidious gait difficulties, urgency, and constipation starting 6 months prior to the visit. The patient's complaints consisted of weakness, stiffness, and pain in her legs. Her medical history consisted of Hashimoto thyroiditis and breast cancer, with the latter having motivated surgery 4 months prior to admission. Histopathologic examination had demonstrated ductal cancer sensitive to estrogen and mapping with sentinel node biopsy ruled out metastasis. For that reason, the patient was treated with local radiation given weekly over 1 month and treatment with tamoxifen was started. Physical examination upon admission demonstrated weakness and spasticity in both legs. Reflexes were brisk; bilateral nonsustained foot clonus and Babinski sign were also present. Bilateral dorsal flexion was reduced, but vibration and sensation to touch and pinprick were normal. Sphincter tonus was reduced; systemic manifestations such as myalgias, fever, skin rashes, uveitis, sicca, and arthritic joints were absent.
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5.
  • Akram, Harith, et al. (författare)
  • Optimal deep brain stimulation site and target connectivity for chronic cluster headache
  • 2017
  • Ingår i: Neurology. - : LIPPINCOTT WILLIAMS & WILKINS. - 0028-3878 .- 1526-632X. ; 89:20, s. 2083-2091
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To investigate the mechanism of action of deep brain stimulation for refractory chronic cluster headache and the optimal target within the ventral tegmental area. Methods: Seven patients with refractory chronic cluster headache underwent high spatial and angular resolution diffusion MRI preoperatively. MRI-guided and MRI-verified electrode implantation was performed unilaterally in 5 patients and bilaterally in 2. Volumes of tissue activation were generated around active lead contacts with a finite-element model. Twelve months after surgery, voxel-based morphometry was used to identify voxels associated with higher reduction in headache load. Probabilistic tractography was used to identify the brain connectivity of the activation volumes in responders, defined as patients with a reduction of >= 30% in headache load. Results: There was no surgical morbidity. Average follow-up was 34 +/- 14 months. Patients showed reductions of 76 +/- 33% in headache load, 46 +/- 41% in attack severity, 58 +/- 41% in headache frequency, and 51 +/- 46% in attack duration at the last follow-up. Six patients responded to treatment. Greatest reduction in headache load was associated with activation in an area cantered at 6 mm lateral, 2 mm posterior, and 1 mm inferior to the midcommissural point of the third ventricle. Average responders' activation volume lay on the trigeminohypothalamic tract, connecting the trigeminal system and other brainstem nuclei associated with nociception and pain modulation with the hypothalamus, and the prefrontal and mesial temporal areas. Conclusions: We identify the optimal stimulation site and structural connectivity of the deep brain stimulation target for cluster headache, explicating possible mechanisms of action and disease pathophysiology.
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6.
  • Alping, Peter, et al. (författare)
  • Safety of Alemtuzumab and Autologous Hematopoietic Stem Cell Transplantation Compared to Noninduction Therapies for Multiple Sclerosis
  • 2021
  • Ingår i: Neurology. - : Ovid Technologies (Wolters Kluwer Health). - 0028-3878 .- 1526-632X. ; 96:11, s. E1574-E1584
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To assess safety outcomes for the induction therapies alemtuzumab and autologous hematopoietic stem cell transplantation (AHSCT) compared to noninduction disease-modifying therapies. Methods We performed a population-based cohort study linking the Swedish Multiple Sclerosis Register to national health care registers. Alemtuzumab, AHSCT, and a matched reference group of noninduction therapies (natalizumab, dimethyl fumarate, rituximab, fingolimod) were included if started between 2008 and 2017. Main outcomes were death, thyroid disease, nonthyroid autoimmune disease, and infection. Results We identified 132 alemtuzumab-treated and 139 AHSCT-treated (68% high-dose cyclo-phosphamide and anti-thymocyte globulin [ATG], 32% BCNU, etoposide, cytosine-arabinoside, and melphalan/ATG) patients, together with 2,486 matched patients treated with noninduction therapies. Four patients in the alemtuzumab group died (incidence rate [IR] per 1,000 person-years 8.6, 95% confidence interval [CI] 2.3-22.0) compared to 1 patient in the AHSCT group (IR 1.7, 95% CI 0.0-9.6), and the mortality rate in the reference group was 0.7 (95% CI 0.3-1.3). Thyroid disease was most frequent in the alemtuzumab group (IR 109, 95% CI 75-154) but also occurred more often for AHSCT (IR 34, 95% CI 18-56) compared to the reference (IR 5.3 95% CI 3.9-7.1). The incidence of nonthyroid autoimmune disease was similar in all groups. IR for infection diagnosed >= 6 months from therapy initiation was 53 (95% CI 30-87) for alemtuzumab, 108 (95% CI 75-150) for AHSCT, and 51 (95% CI 46-57) for the reference. Conclusion We confirmed a high incidence of thyroid disease in alemtuzumab- and, to a smaller extent, AHSCT-treated patients and found a higher incidence of infection for AHSCT compared to both alemtuzumab and noninduction therapies. The incidence of nonthyroid autoimmune disease was low for both therapies. Classification of evidence This study provides Class III evidence of an increased risk of thyroid disease with alemtuzumab and an increased risk of infection with AHSCT treatment.
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7.
  • Alves, G., et al. (författare)
  • CSF A beta(42) predicts early-onset dementia in Parkinson disease
  • 2014
  • Ingår i: Neurology. - 0028-3878. ; 82:20, s. 1784-1790
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective:To test in vivo the proposal from clinicopathologic studies that -amyloid (A) pathology shortens the time to dementia in Parkinson disease (PD), and to explore the utility of CSF A and related measures as early prognostic biomarkers of dementia in an incident PD cohort.Methods:We assessed a population-based incident cohort of 104 patients with PD who underwent lumbar puncture at diagnosis. We analyzed CSF concentrations of A42, A40, and A38 using a multiplexed immunoassay with electrochemiluminescence (ECL) detection and levels of A42, total tau, and phosphorylated tau using ELISA. Patients were followed prospectively for 5 years. Dementia was diagnosed according to published criteria.Results:CSF levels of A42 were significantly decreased in patients who developed dementia (n = 20, 19.2%) compared to those who did not (n = 84, 80.8%), as measured by ECL (-33%, p = 0.006) as well as ELISA (-36%, p < 0.001). No differences were observed for other markers. Low A42 values predicted a substantially increased risk for subsequent dementia at high sensitivity (85%), with hazard ratios of 9.9 (95% confidence interval 2.3-43.5, p = 0.002) for A42(ECL) <376 pg/mL and 7.6 (2.2-26.4, p = 0.001) for A42(ELISA) <443 pg/mL, after adjustment for baseline age and PD-mild cognitive impairment (MCI) status. A42 reductions tended to precede the onset of PD-MCI that progressed to dementia.Conclusions:These in vivo data support the role of A pathology in the etiology and highlight the potential utility of CSF A42 as an early prognostic biomarker of dementia associated with PD.
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8.
  • Andersen, Oluf, 1941, et al. (författare)
  • Predictive MS risk factors and axonal disintegration
  • 2020
  • Ingår i: Neurology. - 0028-3878. ; 94:18, s. 771-772
  • Tidskriftsartikel (refereegranskat)abstract
    • EDITORIAL. The important take-home message of the study by Cortese et al. is that the serum NfL seems to be useful not only for assessing the current status of patients but also as a long-term outcome. Related article; Cortese et al.: Vitamin D, smoking, EBV, and long-term cognitive performance in MS: 11-year follow-up of BENEFIT. Neurology 2020;94:781.
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9.
  • Andersen, Peter M. (författare)
  • Is all ALS genetic?
  • 2017
  • Ingår i: Neurology. - 0028-3878 .- 1526-632X. ; 89:3, s. 220-221
  • Tidskriftsartikel (övrigt vetenskapligt)
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10.
  • Andersson-Roswall, Lena, 1965, et al. (författare)
  • Cognitive outcome 10 years after temporal lobe epilepsy surgery: a prospective controlled study
  • 2010
  • Ingår i: Neurology. - 0028-3878. ; 74:24, s. 1977-1985
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To explore late effects of temporal lobe resection (TLR) for epilepsy on general cognitive level and memory. Methods: Fifty-one patients who had undergone TLR (23 in the speech-dominant temporal lobe [DTL] and 28 in the nondominant temporal lobe [NDTL]) were assessed preoperatively and 2 and 10 years postoperatively. Twenty-three healthy controls were assessed at baseline and at corresponding intervals. A battery of standardized tests for assessment of general cognitive level and memory was analyzed using a linear mixed model of between-subjects treatment effect and within-subject time effect. Results: The main result was cognitive stability from 2 to 10 years after TLR. The DTL group had declined in verbal memory at the 10-year follow-up compared to the NDTL group and to the controls. However, this decline was detected already 2 years postoperatively, with no further decline from 2 to 10 years. The memory decline was not related to seizure outcome or AED treatment. The NDTL group showed less improvement in performance IQ (PIQ) at the 10-year follow-up compared to the controls. The most important correlate to inferior PIQ scores was continuing seizures, which was more frequent in the NDTL group. Conclusions: In this study, the main finding was cognitive stability from 2 to 10 years after temporal lobe resection. There was no further decline in verbal memory from 2 to 10 years after surgery, lending no support to the notion of an ongoing progressive decline in verbal memory after temporal lobe resection. The verbal memory course was not dependent on seizure outcome or antiepileptic drug treatment.
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