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  • 1.
    af Edholm, Karolina
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Lidman, Christer
    Karolinska University Hospital, Solna, Sweden.
    Andersson, Sören
    Örebro University, School of Medical Sciences.
    Solders, Göran
    Karolinska Institutet, Stockholm, Sweden.
    Paucar, Martin
    Karolinska University Hospital, Solna, Sweden.
    Clinical Reasoning: Leg weakness and stiffness at the emergency room2019In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 92, no 6, p. E622-E625Article in journal (Other academic)
    Abstract [en]

    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.

  • 2. Bahmanyar, S.
    et al.
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    Hillert, J.
    Ekbom, A.
    Olsson, T.
    Cancer risk among patients with multiple sclerosis and their parents2009In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 72, no 13, p. 1170-1177Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: We investigated cancer risk among patients with multiple sclerosis (MS) and whether variation by age at MS diagnosis helps to elucidate mechanisms underlying the previously reported reduced cancer risk. We also studied cancer risk among parents to ascertain if MS susceptibility genes may confer protection against cancer in relatives. METHODS: Cox proportional hazards regression, adjusted for age, sex, area, and socioeconomic index, estimated cancer risk among 20,276 patients with MS and 203,951 individuals without MS, using Swedish general population register data. Similar analyses were conducted among 11,284 fathers and 12,006 mothers of patients with MS, compared with 123,158 fathers and 129,409 mothers of controls. RESULTS: With an average of 35 years of follow-up, there was a decreased overall cancer risk among patients with MS (hazard ratio = 0.91, 0.87-0.95). Increased risks were observed for brain tumors (1.44, 1.21-1.72) and urinary organ cancer (1.27, 1.05-1.53). Parents of patients with MS did not have a notably increased or decreased overall cancer risk. CONCLUSIONS: The reduction in cancer risk in patients with multiple sclerosis (MS) may result from behavioral change, treatment, or we speculate that some immunologic characteristics of MS disease activity improve antitumor surveillance. The lack of association among parents indicates that a simple inherited characteristic is unlikely to explain the reduced cancer risk among patients with MS. MS is associated with increased risk for some cancers, such as of urinary organs and brain tumors (although surveillance bias may be responsible).

  • 3.
    Burkill, Sarah
    et al.
    Clinical Epidemiology Unit, Centre for Pharmacoepidemiology, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Clinical Epidemiology Unit, Centre for Pharmacoepidemiology, Department of Medicine Solna, Karolinska Institute, Sweden.
    Hajiebrahimi, Mohammad Hossein
    Clinical Epidemiology Unit, Centre for Pharmacoepidemiology, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden; Biostatistics and Epidemiology Unit, Health Faculty, Golestan University of Medical Sciences, Golestan, Iran.
    Hillert, Jan
    Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Olsson, Tomas
    Division of Neurology and Neuroimmunology Unit, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Bahmanyar, Shahram
    Clinical Epidemiology Unit, Centre for Pharmacoepidemiology, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.
    Mortality trends for multiple sclerosis patients in Sweden from 1968 to 20122017In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 89, no 6, p. 555-562Article in journal (Refereed)
    Abstract [en]

    Objective: To assess trends in mortality and causes of death for patients with multiple sclerosis (MS) relative to those without MS in Sweden.

    Methods: Patients with an MS diagnosis in Sweden between 1964 and 2012 were identified with the Patient Register and the Multiple Sclerosis Register. For this cohort study, each patient with MS (n = 29,617) was matched with 10 individuals without MS (n = 296,164) on sex, year of birth, vital status, and region of residence at the time of MS diagnosis with the Total Population Register. The Causes of Death Register was used to identify causes of death. Cox proportional hazard models were constructed to assess whether risk of mortality was increased for patients with MS.

    Results: The hazard ratio (HR) for patients with MS was 2.92 (95% confidence interval [CI] 2.86-2.99) for all-cause mortality over the entire study period. The largest differences between the cohorts were death resulting from respiratory (HR 5.07, 95% CI 4.87-5.26) and infectious (HR 4.07, 95% CI 3.70-4.47) diseases. Overall and for each specific cause, there have been improvements for the MS group and a subsequent reduction in the HR. The HR decreased from 6.52 (95% CI 5.79-7.34) for the period of 1968 to 1980 to 2.08 (95% CI 1.95-2.22) for the time period of 2001 to 2012. An interaction between time period and MS exposure showed that the decrease in mortality over time was statistically significant, with a larger decrease for patients with MS than their matched comparators.

    Conclusions: There has been a substantial improvement in mortality overall and for each specified cause of death for patients with MS compared with individuals without MS; however, large differences still remain.

  • 4.
    de Flon, Pierre
    et al.
    Department of Pharmacology and Clinical Neuroscience, Unit of Neurology, Östersund, Umeå University, Umeå, Sweden.
    Gunnarsson, Martin
    Örebro University, School of Medical Sciences. Department of Neurology.
    Laurell, Katarina
    Department of Pharmacology and Clinical Neuroscience, Unit of Neurology, Östersund, Umeå University, Umeå, Sweden.
    Söderström, Lars
    Unit of Research, Education and Development, Region Jämtland Härjedalen, Sweden.
    Birgander, Richard
    Department of Radiation Sciences, Diagnostic Radiology, Umeå University, Umeå, Sweden.
    Lindqvist, Thomas
    Department of Radiation Sciences, Diagnostic Radiology, Umeå University, Umeå, Sweden.
    Krauss, Wolfgang
    Örebro University, School of Medical Sciences. Department of Radiology.
    Dring, Ann
    Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.
    Bergman, Joakim
    Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.
    Sundström, Peter
    Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.
    Svenningsson, Anders
    Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden; Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Reduced inflammation in relapsing-remitting multiple sclerosis after therapy switch to rituximab2016In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 87, no 2, p. 141-147Article in journal (Refereed)
    Abstract [en]

    Objective: To describe the effects of switching treatment from ongoing first-line injectable therapies to rituximab on inflammatory activity measured by MRI and levels of CSF neurofilament light chain (CSF-NFL) in a cohort of patients with clinically stable relapsing-remitting multiple sclerosis (RRMS).

    Method: Seventy-five patients with clinically stable RRMS treated with the first-line injectables interferon-β (IFN-β) and glatiramer acetate (GA) at 3 Swedish centers were switched to rituximab in this open-label phase II multicenter study. After a run-in period of 3 months, 2 IV doses of 1,000 mg rituximab were given 2 weeks apart followed by repeated clinical assessment, MRI, and CSF-NFL for 24 months.

    Results: The mean cumulated number of gadolinium-enhancing lesions per patient at months 3 and 6 after treatment shift to rituximab was reduced compared to the run-in period (0.028 vs 0.36, p = 0.029). During the first year after treatment shift, the mean number of new or enlarged T2 lesions per patient was reduced (0.01 vs 0.28, p = 0.004) and mean CSF-NFL levels were reduced by 21% (p = 0.01).

    Conclusions: For patients with RRMS, a treatment switch from IFN or GA to rituximab is associated with reduced inflammatory activity measured by MRI and CSF-NFL.

    Classification of evidence: This study provides Class IV evidence that rituximab has an equal or superior effect in reducing inflammatory activity in RRMS measured by MRI and CSF-NFL compared to first-line injectables during the first year after treatment shift.

  • 5.
    Iacobaeus, Ellen
    et al.
    Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Burkill, Sarah
    Center for Pharmacoepidemiolog, Karolinska Institutet, Stockholm, Sweden.
    Bahmanyar, Shahram
    Center for Pharmacoepidemiolog, Karolinska Institutet, Stockholm, Sweden.
    Hakim, Ramil
    Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Byström, Camilla
    Center for Pharmacoepidemiolog, Karolinska Institutet, Stockholm, Sweden.
    Fored, Michael
    Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden.
    Olsson, Tomas
    Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm, Sweden; Neuroimmunology Unit, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Brundin, Lou
    Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm, Sweden; Neuroimmunology Unit, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health , University College London, London, UK.
    The national incidence of PML in Sweden, 1988-20132018In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 90, no 6, p. E498-E506Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate the incidence of progressive multifocal leukoencephalopathy (PML) and patient characteristics in Sweden between 1988 and 2013.

    Methods: All PML diagnoses in Sweden between 1988 and 2013 were identified in the National Patient Register. Information to validate the diagnosis and patient characteristics was obtained from medical records.

    Results: Medical record review classified 108 out of 250 patients (43%) as definite (n = 84), probable (n = 4), or possible (n = 20) PML according to diagnostic criteria. Accurate diagnoses were more common in records obtained from neurology departments (82% of patients seen in neurology departments) compared with other departments (31%) (p < 0.001). The incidence of PML increased from a largely stable level at 0.026 (95% confidence interval [CI] 0.021-0.031) per 100,000 individuals per year during 1988-2010 to 0.11 (95% CI 083-0.137) during 2011-2013, during which time there was a notable increase (p < 0.001). Hematologic malignancies (n = 34), HIV/AIDS (n = 33), and autoimmune disease (n = 23) were the most common underlying diseases. Treatment with a monoclonal antibody prior to PML diagnosis was identified in 26 patients.

    Conclusion: An increased incidence of PML in Sweden was observed and coincided with the prior use of monoclonal antibody treatment. The high level of misdiagnosis emphasizes the importance of immediate contact with a neurology center upon suspicion of PML.

  • 6.
    Liu, Bojing
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Pedersen, Nancy L.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychology, University of Southern California, Los Angeles, USA.
    Tillander, Annika
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden.
    Ekbom, Anders
    Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Svenningsson, Per
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Chen, Honglei
    Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing, USA.
    Wirdefeldt, Karin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Vagotomy and Parkinson disease: A Swedish register-based matched-cohort study2017In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 88, no 21, p. 1996-2002Article in journal (Refereed)
    Abstract [en]

    Objective: To examine whether vagotomy decreases the risk of Parkinson disease (PD).

    Methods: Using data from nationwide Swedish registers, we conducted a matched-cohort study of 9,430 vagotomized patients (3,445 truncal and 5,978 selective) identified between 1970 and 2010 and 377,200 reference individuals from the general population individually matched to vagotomized patients by sex and year of birth with a 40: 1 ratio. Participants were followed up from the date of vagotomy until PD diagnosis, death, emigration out of Sweden, or December 31, 2010, whichever occurred first. Vagotomy and PD were identified from the Swedish Patient Register. We estimated hazard ratios (HRs) with 95% confidence intervals (CIs) using Cox models stratified by matching variables, adjusting for country of birth, chronic obstructive pulmonary disease, diabetes mellitus, vascular diseases, rheumatologic disease, osteoarthritis, and comorbidity index.

    Results: A total of 4,930 cases of incident PD were identified during 7.3 million person-years of follow-up. PD incidence (per 100,000 person-years) was 61.8 among vagotomized patients (80.4 for truncal and 55.1 for selective) and 67.5 among reference individuals. Overall, vagotomy was not associated with PD risk (HR 0.96, 95% CI 0.78-1.17). However, there was a suggestion of lower risk among patients with truncal vagotomy (HR 0.78, 95% CI 0.55-1.09), which may be driven by truncal vagotomy at least 5 years before PD diagnosis (HR 0.59, 95% CI 0.37-0.93). Selective vagotomy was not related to PD risk in any analyses.

    Conclusions: Although overall vagotomy was not associated the risk of PD, we found suggestive evidence for a potential protective effect of truncal, but not selective, vagotomy against PD development.

  • 7.
    Longinetti, Elisa
    et al.
    Departments of Medical Epidemiology and Biostatistics, Department of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Mariosa, Daniela
    Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Ye, Weimin
    Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Ingre, Caroline
    Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Almqvist, Catarina
    Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Lichtenstein, Paul
    Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Piehl, Fredrik
    Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Fang, Fang
    Departments of Medical Epidemiology and Biostatistics, Departments of Clinical Neuroscience, Karolinska Institutet, Solna, Sweden.
    Neurodegenerative and psychiatric diseases among families with amyotrophic lateral sclerosis2017In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 89, no 6, p. 578-585Article in journal (Refereed)
    Abstract [en]

    Objective: To estimate risks of neurodegenerative and psychiatric diseases among patients with amyotrophic lateral sclerosis (ALS) and their families.

    Methods: We conducted a register-based nested case-control study during 1990-2013 in Sweden to assess whether patients with ALS had higher risks of other neurodegenerative and psychiatric diseases before diagnosis. We included 3,648 patients with ALS and 36,480 age-, sex-, and county of birth-matched population controls. We further conducted a follow-up study of the cases and controls to assess the risks of other neurodegenerative and psychiatric diseases after ALS diagnosis. To assess the potential contribution of familial factors, we conducted similar studies for the relatives of patients with ALS and their controls.

    Results: Individuals with previous neurodegenerative or psychiatric diseases had a 49% increased risk of ALS (odds ratio 1.49, 95% confidence interval 1.35-1.66) compared to individuals without these diseases. After diagnosis, patients with ALS had increased risks of other neurodegenerative or psychiatric diseases (hazard ratio 2.90, 95% confidence interval 2.463.43) compared to individuals without ALS. The strongest associations were noted for frontotemporal dementia, Parkinson disease, other dementia, Alzheimer disease, neurotic disorders, depression, stress-related disorders, and drug abuse/dependence. First-degree relatives of patients with ALS had higher risk of neurodegenerative diseases, whereas only children of patients with ALS had higher risk of psychiatric disorders, compared to relatives of the controls.

    Conclusions: Familial aggregation of ALS and other neurodegenerative diseases implies a shared etiopathogenesis among all neurodegenerative diseases. The increased risk of psychiatric disorders among patients with ALS and their children might be attributable to nonmotor symptoms of ALS and severe stress response toward the diagnosis.

  • 8.
    Ludvigsson, Jonas F.
    et al.
    Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Zingone, F.
    Department of Clinical and Experimental Medicine, Federico II University of Naples, Naples, Italy.
    Tomson, T.
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Ekbom, A.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ciacci, C.
    Department of Gastroenterology, University of Salerno, Salerno, Italy.
    Increased risk of epilepsy in biopsy-verified celiac disease: A population-based cohort study2012In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 78, no 18, p. 1401-1407Article in journal (Refereed)
    Abstract [en]

    Objectives: Celiac disease (CD) is associated with several neurologic disorders but it is unclear whether CD is associated with epilepsy. We therefore investigated whether biopsy-verified CD is associated with epilepsy.

    Methods: Cohort study. Using biopsy report data from all Swedish pathology departments (n = 28), we identified individuals with CD who were diagnosed from 1969 to 2008 (Marsh 3: villous atrophy). Through Cox regression, we calculated hazard ratios (HRs) for epilepsy (defined as a diagnosis of epilepsy in the Swedish National Patient Register) in 28,885 individuals with CD and 143,166 controls matched for age, sex, calendar period, and county.

    Results: Individuals with CD were at an increased risk of future epilepsy (HR = 1.42; 95% confidence interval [CI] = 1.24-1.62) (272 individuals with CD had a diagnosis of epilepsy vs an expected 192). The absolute risk of future epilepsy in patients with CD was 92/100,000 person-years (excess risk = 27/100,000 person-years). This risk increase was seen in all ages, including children with CD. The HR for having at least 2 interactions with health care due to epilepsy was 1.41 (95% CI = 1.19-1.66). When we restricted epilepsy to those with both a diagnosis of epilepsy and an independent record of antiepileptic drug prescriptions, CD was associated with a 1.43-fold increased risk of epilepsy (95% CI = 1.10-1.86).

    Conclusion: Individuals with CD seem to be at a moderately increased risk of epilepsy. Neurology (R) 2012;78:1401-1407

  • 9. Morita, M.
    et al.
    Al-Chalabi, A.
    Andersen, P. M.
    Hosler, B.
    Sapp, P.
    Englund, E.
    Mitchell, J. E.
    Habgood, J. J.
    de Belleroche, J.
    Xi, J.
    Jongjaroenprasert, W.
    Horvitz, H. R.
    Gunnarsson, Lars-Gunnar
    Örebro University, Department of Clinical Medicine.
    Brown, R. H.
    A locus on chromosome 9p confers susceptibility to ALS and frontotemporal dementia2006In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 66, no 6, p. 839-844Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To perform genetic linkage analysis in a family affected with ALS and frontotemporal dementia (FTD). METHODS: The authors performed a genome-wide linkage analysis of a four-generation, 50-member Scandinavian family in which five individuals were diagnosed with ALS and nine with FTD. Linkage calculations assuming autosomal dominant inheritance of a single neurodegenerative disease manifesting as either ALS or FTD with age-dependent penetrance were performed. Further analyses for ALS alone and FTD alone were performed. A parametric logarithm of odds (lod) score of 2.0 or greater was required for further study of a potential locus and crossover (haplotype) analysis. RESULTS: A new ALS-FTD locus was identified between markers D9s1870 and D9s1791 on human chromosome 9p21.3-p13.3. A maximum multipoint lod score of 3.00 was obtained between markers D9s1121 and D9s2154. Crossover analysis indicates this region covers approximately 21.8 cM, or 14Mb. CONCLUSIONS: A locus on chromosome 9p21.3-p13.3 is linked to ALS-FTD.

  • 10.
    Novakova, Lenka
    et al.
    Department of Clinical Neuroscience Institute of Neuroscience and Physiology,t Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Zetterberg, Henrik
    Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
    Sundström, Peter
    Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.
    Axelsson, Markus
    Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Khademi, Mohsen
    Department of Clinical Neuroscience, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Gunnarsson, Martin
    Örebro University, School of Medical Sciences. Department of Neurology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Malmeström, Clas
    Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Svenningsson, Anders
    Neuroimmunology Unit, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Olsson, Tomas
    Department of Clinical Neuroscience, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Piehl, Fredrik
    Department of Clinical Neuroscience, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Blennow, Kaj
    Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
    Lycke, Jan
    Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Monitoring disease activity in multiple sclerosis using serum neurofilament light protein2017In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 89, no 22, p. 2230-2237, article id 10.1212/WNL.0000000000004683Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To examine the effects of disease activity, disability, and disease-modifying therapies (DMTs) on serum neurofilament light (NFL) and the correlation between NFL concentrations in serum and CSF in multiple sclerosis (MS).

    METHODS: NFL concentrations were measured in paired serum and CSF samples (n = 521) from 373 participants: 286 had MS, 45 had other neurologic conditions, and 42 were healthy controls (HCs). In 138 patients with MS, the serum and CSF samples were obtained before and after DMT treatment with a median interval of 12 months. The CSF NFL concentration was measured with the UmanDiagnostics NF-light enzyme-linked immunosorbent assay. The serum NFL concentration was measured with an in-house ultrasensitive single-molecule array assay.

    RESULTS: In MS, the correlation between serum and CSF NFL was r = 0.62 (p < 0.001). Serum concentrations were significantly higher in patients with relapsing-remitting MS (16.9 ng/L) and in patients with progressive MS (23 ng/L) than in HCs (10.5 ng/L, p < 0.001 and p < 0.001, respectively). Treatment with DMT reduced median serum NFL levels from 18.6 (interquartile range [IQR] 12.6-32.7) ng/L to 15.7 (IQR 9.6-22.7) ng/L (p < 0.001). Patients with relapse or with radiologic activity had significantly higher serum NFL levels than those in remission (p < 0.001) or those without new lesions on MRI (p < 0.001).

    CONCLUSIONS: Serum and CSF NFL levels were highly correlated, indicating that blood sampling can replace CSF taps for this particular marker. Disease activity and DMT had similar effects on serum and CSF NFL concentrations. Repeated NFL determinations in peripheral blood for detecting axonal damage may represent new possibilities in MS monitoring.

  • 11.
    Sundelin, Helene E. K.
    et al.
    Department of Pediatrics, Linköping University Hospital, Linköping, Sweden.
    Chang, Zheng
    Departments of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Departments of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Departments of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almqvist, Catarina
    Departments of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Tomson, Torbjörn
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Departments of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham,UK; Department of Medicine, Columbia University, New York NY, USA.
    Epilepsy, antiepileptic drugs, and serious transport accidents: A nationwide cohort study2018In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 90, no 13, p. E1111-+Article in journal (Refereed)
    Abstract [en]

    Objectives: To investigate the association between epilepsy and antiepileptic drugs and serious transport accidents requiring emergency care or resulting in death.

    Methods: We identified 29,220 individuals 18 years or older with epilepsy without cerebral palsy or intellectual disability and 267,637 matched controls using Swedish registers. This nationwide cohort was followed from 2006 to 2013 for serious transport accidents. We used Cox regression to analyze the risk of serious transport accidents between individuals with epilepsy and matched controls, and then stratified Cox regression to compare the risk during periods of medication with the risk during nonmedication period within the same individual with epilepsy. We adjusted for civil status, employment, education, living area, psychiatric disorders prior to the start of follow-up, and psychotropic medication.

    Results: Compared to matched controls, individuals with epilepsy were at increased risk of serious transport accidents (hazard ratio [HR] 1.37; 95% confidence interval [CI] 1.29-1.46). There were increased risks of pedestrian accidents (HR 2.24, 95% CI 1.69-2.97), bicycle accidents (HR 1.68, 95% CI 1.49-1.89) and car accidents (HR 1.31, 95% CI 1.19-1.44). However, among patients with a diagnosis of epilepsy, use of antiepileptic drugs did not influence the risk of serious transport accidents in population-level comparisons (HR 0.97; 95% CI 0.85-1.11) or within-individual comparisons (HR 0.99; 95% CI 0.69-1.42).

    Conclusion: Serious transportation accidents were more common in individuals with epilepsy, but this risk was independent of use of antiepileptic drugs.

  • 12.
    Sundelin, Heléne E. K.
    et al.
    Department of Pediatrics, University Hospital, Linköping, Sweden .
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Hultman, Christina M.
    Departments of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Tomson, Torbjörn
    Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
    Autism and epilepsy: A population-based nationwide cohort study2016In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 87, no 2, p. 192-197Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate the risk of autism spectrum disorder (ASD) in individuals with epilepsy and in their first-degree relatives to determine shared etiology.

    Methods: Through the Swedish Patient Register, we identified 85,201 individuals with epilepsy, as well as all their siblings (n = 80,511) and offspring (n = 98,534). Each individual with epilepsy was compared with 5 controls, matched for age, sex, calendar period, and county, while siblings and offspring were compared with siblings and offspring of controls. We excluded siblings and offspring with epilepsy. Using Cox regression, we calculated hazard ratios (HRs) for future diagnosis of ASD. Logistic regression was applied to calculate odds ratios (ORs) for prior diagnosis of ASD.

    Results: During follow-up, 1,381 (1.6%) individuals with epilepsy and 700 (0.2%) controls were diagnosed with ASD. Individuals with epilepsy were therefore at increased risk of future ASD (HR 10.49, 95% confidence interval [CI] 9.55-11.53), with the highest risk seen in individuals diagnosed with epilepsy in childhood. Both siblings (HR 1.62, 95% CI 1.43-1.83) and offspring (HR 1.64, 95% CI 1.46-1.84) of epilepsy patients were at increased risk of ASD. The risk in the offspring was particularly high in mothers with epilepsy (HR 1.91; 95% CI 1.63-2.23). Epilepsy was also associated with a prior diagnosis of ASD (OR 4.56, 95% CI 4.02-5.18).

    Conclusions: Individuals with epilepsy are at increased risk of ASD, especially if epilepsy appears in childhood. Further, ASD is more common in the siblings and offspring of individuals with epilepsy, suggesting shared etiology.

  • 13.
    Wiggs, Kelsey K.
    et al.
    Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Chang, Zheng
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center for Health Statistics, University of Chicago, Chicago, USA.
    Quinn, Patrick D.
    Psychological and Brain Sciences, Indiana University, Bloomington, USA; Center for Health Statistics, University of Chicago, Chicago, USA.
    Hur, Kwan
    Center for Health Statistics, University of Chicago, Chicago, USA.
    Gibbons, Robert
    University of Chicago, Chicago, USA.
    Dunn, David
    Indiana University School of Medicine, Indianapolis IN, USA.
    Brikell, Isabell
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Attention-deficit/hyperactivity disorder medication and seizures2018In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 90, no 13, p. e1104-e1110Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Individuals with attention-deficit/hyperactivity disorder (ADHD) are at increased risk of seizures, but there is uncertainty about whether ADHD medication treatment increases risk among patients with and without preexisting seizures.

    METHODS: We followed a sample of 801,838 patients with ADHD who had prescribed drug claims from the Truven Health MarketScan Commercial Claims and Encounters databases to examine whether ADHD medication increases the likelihood of seizures among ADHD patients with and without a history of seizures. First, we assessed overall risk of seizures among patients with ADHD. Second, within-individual concurrent analyses assessed odds of seizure events during months when a patient with ADHD received ADHD medication compared with when the same individual did not, while adjusting for antiepileptic medications. Third, within-individual long-term analyses examined odds of seizure events in relation to the duration of months over the previous 2 years patients received medication.

    RESULTS: Patients with ADHD were at higher odds for any seizure compared with non-ADHD controls (odds ratio [OR] = 2.33, 95% confidence interval [CI] = 2.24-2.42 males; OR = 2.31, 95% CI = 2.22-2.42 females). In adjusted within-individual comparisons, ADHD medication was associated with lower odds of seizures among patients with (OR = 0.71, 95% CI = 0.60-0.85) and without (OR = 0.71, 95% CI = 0.62-0.82) prior seizures. Long-term within-individual comparisons suggested no evidence of an association between medication use and seizures among individuals with (OR = 0.87, 95% CI = 0.59-1.30) and without (OR = 1.01, 95% CI = 0.80-1.28) a seizure history.

    CONCLUSIONS: Results reaffirm that patients with ADHD are at higher risk of seizures. However, ADHD medication was associated with lower risk of seizures within individuals while they were dispensed medication, which is not consistent with the hypothesis that ADHD medication increases risk of seizures.

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