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1.
Mult Scler ; 23(7): 1008-1017, 2017 Jun.
Article in English | MEDLINE | ID: mdl-27600114

ABSTRACT

BACKGROUND: The aim was to investigate predictive values of coping styles, clinical and demographic factors on time to unemployment in patients diagnosed with multiple sclerosis (MS) during 1998-2002 in Norway. METHOD: All patients ( N = 108) diagnosed with MS 1998-2002 in Hordaland and Rogaland counties, Western Norway, were invited to participate in the long-term follow-up study in 2002. Baseline recordings included disability scoring (Expanded Disability Status Scale (EDSS)), fatigue (Fatigue Severity Scale (FSS)), depression (Beck Depression Inventory (BDI)), and questionnaire assessing coping (the Dispositional Coping Styles Scale (COPE)). Logistic regression analysis was used to identify factors associated with unemployed at baseline, and Cox regression analysis to identify factors at baseline associated with time to unemployment during follow-up. RESULTS: In all, 41 (44%) were employed at baseline. After 13 years follow-up in 2015, mean disease duration of 22 years, 16 (17%) were still employed. Median time from baseline to unemployment was 6 years (±5). Older age at diagnosis, female gender, and depression were associated with patients being unemployed at baseline. Female gender, long disease duration, and denial as avoidant coping strategy at baseline predicted shorter time to unemployment. CONCLUSION: Avoidant coping style, female gender, and longer disease duration were associated with shorter time to unemployment. These factors should be considered when advising patients on MS and future employment.


Subject(s)
Adaptation, Psychological , Multiple Sclerosis, Chronic Progressive/psychology , Multiple Sclerosis, Relapsing-Remitting/psychology , Unemployment , Adult , Age Factors , Cost of Illness , Depression/psychology , Disability Evaluation , Female , Humans , Insurance, Disability , Logistic Models , Male , Middle Aged , Multiple Sclerosis, Chronic Progressive/diagnosis , Multiple Sclerosis, Chronic Progressive/physiopathology , Multiple Sclerosis, Relapsing-Remitting/diagnosis , Multiple Sclerosis, Relapsing-Remitting/physiopathology , Multivariate Analysis , Norway , Odds Ratio , Pensions , Proportional Hazards Models , Prospective Studies , Risk Factors , Sex Factors , Surveys and Questionnaires , Time Factors
2.
BMC Gastroenterol ; 12: 13, 2012 Feb 08.
Article in English | MEDLINE | ID: mdl-22316329

ABSTRACT

BACKGROUND: A waterborne outbreak of Giardia lamblia gastroenteritis led to a high prevalance of long-lasting fatigue and abdominal symptoms. The aim was to describe the clinical characteristics, disability and employmentloss in a case series of patients with Chronic Fatigue Syndrome (CFS) after the infection. METHODS: Patients who reported persistent fatigue, lowered functional capacity and sickness leave or delayed education after a large community outbreak of giardiasis enteritis in the city of Bergen, Norway were evaluated with the established Centers for Disease Control and Prevention criteria for CFS. Fatigue was self-rated by the Fatigue Severity Scale (FSS). Physical and mental health status and functional impairment was measured by the Medical Outcome Severity Scale-short Form-36 (SF-36). The Hospital Anxiety and Depression Scale (HADS) was used to measure co-morbid anxiety and depression. Inability to work or study because of fatigue was determined by sickness absence certified by a doctor. RESULTS: A total of 58 (60%) out of 96 patients with long-lasting post-infectious fatigue after laboratory confirmed giardiasis were diagnosed with CFS. In all, 1262 patients had laboratory confirmed giardiasis. At the time of referral (mean illness duration 2.7 years) 16% reported improvement, 28% reported no change, and 57% reported progressive course with gradual worsening. Mean FSS score was 6.6. A distinctive pattern of impairment was documented with the SF-36. The physical functioning, vitality (energy/fatigue) and social functioning were especially reduced. Long-term sickness absence from studies and work was noted in all patients. CONCLUSION: After giardiasis enteritis at least 5% developed clinical characteristics and functional impairment comparable to previously described post-infectious fatigue syndrome.


Subject(s)
Absenteeism , Disability Evaluation , Enteritis/complications , Enteritis/parasitology , Fatigue Syndrome, Chronic/epidemiology , Giardia/isolation & purification , Giardiasis/complications , Adult , Anxiety/epidemiology , Anxiety/psychology , Depression/epidemiology , Depression/psychology , Fatigue Syndrome, Chronic/psychology , Female , Humans , Incidence , Male , Norway , Retrospective Studies , Severity of Illness Index , Time Factors
4.
Arch Neurol ; 65(6): 809-11, 2008 Jun.
Article in English | MEDLINE | ID: mdl-18541802

ABSTRACT

BACKGROUND: Vitamin D-dependent rickets type I (VDDR I) (OMIM 264700) is a rare hereditary condition caused by a mutation in CYP27B1. Vitamin D is emerging as an important risk factor for susceptibility to multiple sclerosis (MS), but there have been no studies on the possible association between hereditary rickets and this disease. OBJECTIVE: To investigate the association between VDDR I and MS. DESIGN: Case studies. SETTING: Haukeland University Hospital, Bergen, Norway. PATIENTS: Three patients in 2 families with a co-occurrence of VDDR I and MS. RESULTS: All 3 patients had VDDR I verified by genetic testing and fulfilled the Poser criteria for MS. Two of the patients have undergone magnetic resonance imaging, which confirmed the diagnosis of long-lasting MS. CONCLUSIONS: Vitamin D-dependent rickets type I is a very uncommon genetic subtype of rickets. We have identified 3 patients with this disease who later developed MS. We propose that VDDR I and possibly other hereditary rickets mutations that influence vitamin D metabolism could be risk factors for this disease.


Subject(s)
Familial Hypophosphatemic Rickets/complications , Familial Hypophosphatemic Rickets/genetics , Multiple Sclerosis/etiology , Vitamin D/genetics , Vitamin D/metabolism , Familial Hypophosphatemic Rickets/pathology , Female , Humans , Middle Aged , Multiple Sclerosis/genetics , Multiple Sclerosis/pathology , Risk Factors , Vitamin D/physiology
5.
PLoS One ; 3(2): e1530, 2008 Feb 13.
Article in English | MEDLINE | ID: mdl-18270557

ABSTRACT

BACKGROUND: Mitochondrial DNA (mtDNA) polymorphism is a possible factor contributing to the maternal parent-of-origin effect in multiple sclerosis (MS) susceptibility. METHODS AND FINDINGS: In order to investigate the role of mtDNA variations in MS, we investigated six European MS case-control cohorts comprising >5,000 individuals. Three well matched cohorts were genotyped with seven common, potentially functional mtDNA single nucleotide polymorphisms (SNPs). A SNP, nt13708 G/A, was significantly associated with MS susceptibility in all three cohorts. The nt13708A allele was associated with an increased risk of MS (OR = 1.71, 95% CI 1.28-2.26, P = 0.0002). Subsequent sequencing of the mtDNA of 50 individuals revealed that the nt13708 itself, rather than SNPs linked to it, was responsible for the association. However, the association of nt13708 G/A with MS was not significant in MS cohorts which were not well case-control matched, indicating that the significance of association was affected by the population structure of controls. CONCLUSIONS: Taken together, our finding identified the nt13708A variant as a susceptibility allele to MS, which could contribute to defining the role of the mitochondrial genome in MS pathogenesis.


Subject(s)
DNA, Mitochondrial/genetics , Electron Transport Complex I/genetics , Genetic Predisposition to Disease , Mitochondrial Proteins/genetics , Multiple Sclerosis/genetics , Polymorphism, Single Nucleotide/physiology , Alleles , Case-Control Studies , Europe/epidemiology , Gene Frequency , Humans , Molecular Epidemiology , Multiple Sclerosis/epidemiology , Multiple Sclerosis/etiology , Odds Ratio , Sequence Analysis, DNA
6.
Cerebrovasc Dis ; 20(4): 245-50, 2005.
Article in English | MEDLINE | ID: mdl-16123544

ABSTRACT

BACKGROUND: To study the impact of fatigue in young ischaemic stroke patients. METHODS: The Fatigue Severity Scale score was obtained in 192 patients (mean time 6.0 years after the stroke) and 212 controls. RESULTS: Fatigue was associated with cerebral infarction in a multivariate analysis of patients and controls (p = 0.002). Fatigue was independently associated with unfavourable functional outcome (p = 0.001), depression (p < 0.001), and basilar artery infarction through interaction with the modified Rankin Scale score (p = 0.047) in patients. CONCLUSION: Fatigue is frequent in young adults with cerebral infarction. Stroke-related factors independently associated with fatigue include functional outcome. Stroke location may influence fatigue.


Subject(s)
Cerebral Infarction/complications , Disability Evaluation , Fatigue/etiology , Activities of Daily Living , Adolescent , Adult , Cerebral Infarction/psychology , Depression/etiology , Depression/psychology , Fatigue/psychology , Female , Follow-Up Studies , Humans , Male , Middle Aged , Multivariate Analysis , Psychology , Vertebrobasilar Insufficiency/complications , Vertebrobasilar Insufficiency/psychology
7.
J Neuropathol Exp Neurol ; 62(7): 723-32, 2003 Jul.
Article in English | MEDLINE | ID: mdl-12901699

ABSTRACT

The extent and pattern of demyelination in the cerebral cortex was determined in 78 tissue blocks from the brains of 20 multiple sclerosis (MS) patients and 28 tissue blocks from 7 patients without neurological disease. Tissue blocks from 4 predetermined areas (cingulate gyrus, frontal, parietal, and temporal lobe) were studied, irrespective of macroscopically evident MS plaques. All tissue blocks contained cerebral cortex and periventricular and/or subcortical white matter. One hundred and nine demyelinating lesions were detected in the cerebral cortex, of which 92 (84.4%) were purely intracortical and 17 (15.6%) were lesions extending through both white and gray matter areas. In 5 of the 20 MS brains, subpial demyelination was extensive in the 4 widely spaced cortical areas studied, thus considered to represent a general cortical subpial demyelination. The percentage of demyelinated area was significantly higher in the cerebral cortex (mean 26.5%, median 14.1%) than in white matter (mean 6.5%, median 0%) (p = 0.001). Both gray and white matter demyelination was more prominent in the cingulate gyrus than in the other areas examined (p < 0.05). These results indicate that the cerebral cortex is likely to be a predilection site for MS lesions and identify general cortical subpial demyelination as a distinct pattern occurring in a significant subpopulation of MS patients.


Subject(s)
Axons/pathology , Cerebral Cortex/pathology , Multiple Sclerosis/pathology , Nerve Fibers, Myelinated/pathology , Pia Mater/pathology , Adult , Aged , Cerebral Cortex/physiopathology , Female , Frontal Lobe/pathology , Frontal Lobe/physiopathology , Gyrus Cinguli/pathology , Gyrus Cinguli/physiopathology , Humans , Immunohistochemistry , Male , Middle Aged , Multiple Sclerosis/physiopathology , Myelin Basic Protein/metabolism , Myelin Proteolipid Protein/metabolism , Parietal Lobe/pathology , Parietal Lobe/physiopathology , Temporal Lobe/pathology , Temporal Lobe/physiopathology
8.
J Neurol Sci ; 202(1-2): 93-7, 2002 Oct 15.
Article in English | MEDLINE | ID: mdl-12220699

ABSTRACT

The expression level of interleukin-10 (IL-10) is related to polymorphisms -1082 (G/A), -819 (T/C) and -592 (A/C) in the promoter region of the IL-10 gene. The distribution of these polymorphisms was analyzed to determine whether they could influence disease susceptibility or clinical course in multiple sclerosis (MS). The -1082 (G/A), -819 (T/C) and -592 (A/C) genotypes were similarly distributed between MS patients and the controls. The primary progressive MS patients with the low IL-10 expression haplotype showed a trend towards a worse clinical outcome than did patients with medium- or high-expression haplotypes (P = 0.056). The polymorphisms did not influence the clinical course in patients with relapsing-remitting MS.


Subject(s)
Interleukin-10/genetics , Multiple Sclerosis, Chronic Progressive/genetics , Multiple Sclerosis, Relapsing-Remitting/genetics , Polymorphism, Genetic , Promoter Regions, Genetic , Adult , Female , Genetic Predisposition to Disease , Haplotypes , Humans , Male , Multiple Sclerosis, Chronic Progressive/immunology , Multiple Sclerosis, Relapsing-Remitting/immunology
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