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No / Fatigue is common in people with multiple sclerosis (MS) and symptoms of fatigue are often reported as the most debilitating symptoms of the disease. However, there are few reports of interventions for fatigue in MS. A systematic review of published literature examining pharmacological and psychosocial/psychological interventions for fatigue in MS was conducted. The search and review strategy undertaken used the Centre for Reviews and Dissemination guidelines. Papers were reviewed by two independent reviewers. Of 81 studies short-listed for inclusion, 15 studies were included, of which 10 were studies of pharmacological therapy and five were studies of psychosocial/psychological interventions. Of the pharmacological studies, two were rated as of moderate-to-high quality, three of moderate quality, two of moderate-to-low quality and three of low quality. Of the psychosocial/psychological studies, three were rated as of moderate quality and two of moderate-to-low quality. None of the studies reviewed reached the highest level of quality according to pre-agreed criteria. Regardless of level of quality, effectiveness of both pharmacological and psychosocial/psychological interventions was modest at best and often absent. Accordingly, there is little evidence-based advice that can be offered to people with MS to help manage their fatigue.

Multiple sclerosis (MS) is a prevalent and progressive autoimmune inflammatory disease affecting both white and gray matter and resulting in lesions and atrophy within the central nervous system (CNS) (Bermel & Bakshi, 2006; Confavreux & Vukusic, 2006; Cree, 2012; Friese, Schattling, & Fugger, 2014). Fine motor impairment, including manual motor speed and fine motor dexterity deficits, is common in MS patients (e.g., Benedict et al., 2011; Chipchase, Lincoln, & Radford, 2003). However, impairment does not progress uniformly across patients (Confavreux, Vukusic, Moreau, & Adeleine, 2000; Filippi & Rocca, 2011; Scalfari, Neuhaus, Daumer, DeLuca, & Muraro, 2013) and the association between disease burden and physical disability is moderate at best (Bermel & Bakshi, 2006; Filippi et al., 2013). Though the brain reserve hypothesis has helped to explain the clinico-pathologic dissociation between cognitive functioning and disease burden in MS patients (Sumowski et al., 2013; Sumowski et al., 2014a), there is no published literature on brain reserve and motor functioning in MS. Instead, only preliminary data have been presented on brain reserve and general physical disability (Sumowski et al., 2014b). As such, the purpose of this dissertation was to examine the protective effect of brain reserve, estimated via intracranial volume (ICV), on fine motor functioning in relapse-onset MS patients. A sample of 178 relapse-onset, right-handed MS patients underwent neuropsychological testing along with neurological examination, including magnetic resonance imaging (MRI). As part of the evaluation, patients were administered the Nine Hole Peg Test (NHPT; a measure of fine motor speed and dexterity) and the Finger Tapping Test (FTT; a measure of manual motor speed), which served as this study’s outcomes (i.e., dependent variables). Predictors (i.e., independent variables) included demographic variables (age, sex), disease variables (disease duration and disease phenotype, including relapsing-remitting MS (RRMS) or secondary-progressive MS (SPMS)), MRI estimates of disease burden (T2 lesion volume [T2LV], normalized brain volumes as measures of cerebral atrophy), and MRI-derived measures of ICV as an estimate of brain reserve. Results revealed that phenotype (r = .56, p < .001) significantly predicted performance on the NHPT, such that patients with SPMS did worse than patients with RRMS. Regarding disease burden, T2LV (r = .24, p = .001) and normalized gray matter volume (r = -.18, p = .019) predicted NHPT, with less disease burden associated with better performance. Greater ICV (r = -.21, p =.006) was also significantly associated with better performance on the NHPT. Next, phenotype (r = -.45, p < .001) predicted FTT with SPMS patients again performing worse than RRMS patients. Sex (r = .40, p < .001) was a significant predictor of FTT with men outperforming women, on average. For FTT, normalized gray matter volume (r = .36, p < .001) was the only measure of disease burden that predicted performance, with greater volume (i.e., less atrophy) associated with better performance. Similarly, greater ICV (r = .31, p < .001) significantly predicted better performance on the FTT. For both NHPT and FTT, interactions between measures of disease burden and ICV were not significant. As such, some evidence from this study was not consistent with the reserve hypothesis; however, this finding may be due to differences in the way brain reserve impacts motor outcomes (relative to cognitive outcomes). Nonetheless, as ICV was associated with better performance for both outcome measures, these findings provide partial support for the brain reserve hypothesis in fine motor functioning in MS. Therefore, findings from this study have real-life applications with regard to improved understanding of fine motor disability in MS and identification of patients at risk for upper extremity dysfunction, leading to the possibility of early intervention. Findings also have implications for informing clinical research in MS. Future research should examine the protective effect of brain reserve on fine motor functioning within larger cross-sectional samples (i.e., RRMS vs. SPMS), within primary-progressive MS (PPMS) patients, and when using additional measures of upper extremity disability (e.g., Grip Strength Test). Longitudinal research would also help to determine whether there is a moderating effect of brain reserve on fine motor disability progression as well as allow patients to serve as their own baseline, which would control for individual differences in motor functioning. Next, examining reserve in patients experiencing lesions and atrophy in specific brain regions underlying motor function (e.g., cerebellum and precentral gyrus) may help explain why interactions between disease burden and ICV were not significant within the present study. Finally, by testing the brain reserve hypothesis as it relates to fine motor functioning in non-clinical, healthy controls, it would be possible to determine whether the protective effect of reserve is present premorbidly.

Multiple Sclerosis (MS) is a chronic neurological condition, which affects around 2.5 million people worldwide. At a time when there is yet no recognised cure, it is imperative that MS patients learn to cope and adjust well to living with the illness. However, research has found high rates of psychological distress associated with MS (Minden &amp; Schiffer, 1991). This highlights the need for research to investigate the psychological factors, which make MS patients vulnerable to psychological distress. One popular social cognition model called the Self-Regulation Model (Leventhal et al., 1980) has been found to successfully predict adjustment in a range of chronic illnesses. However, previous research applying the SRM to understand adjustment to MS has been limited. The current research therefore represented the first attempt to successfully apply the full SRM to an MS population prospectively. The present thesis is comprised of three studies and employed a mixed quantitative and qualitative research design method. Studies 1 (N=103) and 3 (N=150) were both quantitative studies, which applied an extended SRM model to clinical samples of MS patients and assessed indices of psychological distress over time. Study 2 (N=15) however was a qualitative study, designed to investigate MS patients experiences of living with the condition. By combining both quantitative and qualitative methods, the findings provided a fuller understanding of the psychological factors underlying successful adjustment to MS. Overall the findings provided some support for the utility of the extended SRM in predicting adjustment to MS and highlighted the importance of positive mind states and acceptance for successful adjustment to the condition. The findings also had a number of clinical implications, which are also discussed.

Multiple sclerosis is a progressive autoimmune disease where myelin is gradually stripped from axons. Axon degeneration inevitably follows protracted myelin loss ultimately leading to irreversible neurological decline. To better understand the cellular mechanisms associated with the axon loss phase of the disease, spinal cord axons from the experimental autoimmune encephalomyelitis (EAE) animal model of multiple sclerosis were examined using correlated in vivo time-lapse microscopy and serial section transmission electron microscopic (ssTEM) reconstruction. A novel technique, termed near infrared burning (NIRB), was developed that took advantage of a femtosecond-pulsed mode locked laser’s ability to create photoconvertable fiducial markers for routine identification of previously imaged axons for ssTEM reconstruction. This combination of imaging techniques revealed the subcellular milieu that underlies axon degeneration at both the light and electron microscopic level. In particular, paranodal regions of axons in EAE animals contained a significantly higher population of mitochondria with large rounded, electron lucid, vesiculated mitochondria with unorganized cristae compared to controls. This effect was largely restricted to the paranodal region and was not always associated with direct immune cell interaction or myelin loss. Together, these results suggest a novel mechanism for axon degeneration that is not only focal in nature, but decoupled with myelin loss in the EAE animal model of multiple sclerosis. / Department of Biology

The purpose of this investigation was to examine the effects of Multiple Sclerosis (MS) on the structural and functional characteristics of skeletal muscle. More specifically, we analyzed the myosin heavy chain (MHC) and fiber type distribution of the vastus lateralis, measured single fiber cross sectional area (CSA), and determined the isokinetic and isotonic strength of the knee extensor muscles. Six sedentary subjects with MS (age: 44 ± 2 yrs) and six sedentary gender-matched controls (age: 46 ± 4) were evaluated. EachMS subject was rated on the Kurtzke's Expanded Disability Status Scale (EDSS) and performed an 8-meter walk test to determine gait speed. Furthermore, the spasticity of the knee extensors was evaluated in each MS subject and weekly energy expenditure was estimated using the Yale Physical Activity Survey. Concentric and eccentric isokinetic strength of the right knee extensors (left in one MS subject) was determined at 60 and 180°/sec and a bilateral isotonic one-repetition maximum (1-RM) was evaluated in eachsubject. Muscle biopsies were taken from the right vastus lateralis (left in one MS subject) and individual fibers were dissected from these samples. Fibers were submitted to SDSPAGE with silver staining to determine MHC expression. Densitometry was performed on MHC hybrid fibers to determine the degree of co-expression. An additional section ofthe biopsy was stained for mATPase activity and further analyzed for single fiber CSA and fiber type. The mean EDSS score for the MS subjects was 5.4 ± 0.6 (range 3.5-6.5) and MS patients were slower than controls (p < 0.05) on the walk-test. AshworthSpasticity Scores ranged from 0 - 2. No differences were noted in weekly energy expenditure. The controls were 45 and 56% stronger than the MS group at isokinetic concentric velocities of 60 and 180°/sec (p < 0.05), respectively. The isotonic 1-RM andthe eccentric isokinetic contractions were not different between the two groups. There were no differences noted in any of the MHC isoforms or percentage of hybrid fibers. Furthermore, mATPase fiber type distribution and single fiber CSA were not different between the groups. There was a greater proportion of MHC IIx dominant MHC IIa/IIx fibers in the MS groups (p < 0.05). Multiple Sclerosis appears to result in large strengthdeficits, when compared to healthy individuals. Based on our findings, these strength differences cannot be explained by alterations in MHC/fiber type expression or decreases in fiber CSA. / School of Physical Education

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Thesis (MSc (Genetics))--University of Stellenbosch, 2007. / Multiple sclerosis (MS) is a disease that causes neurological dysfunction. Studies attempting to elucidate the role of genes in MS development may aid efforts to control the damage caused by the disease that affects two million people worldwide, e.g. improved diagnosis and treatment. Although the association of MS and genes has not been fully characterized the proposed genetic etiology has been supported by the observed association of MS with the Major Histocompatibility Complex (MHC), haplotype HLA-DRB1*1501, DRB5*0101, DQA1*0102, DQB1*0602. Iron, or rather the dysregulation thereof, has also been implicated as a precipitating factor in MS development. Considering the factors of iron dysregulation and the genes involved in iron regulation, this study aims to identify variation within genes involved in iron metabolism namely the high iron gene (HFE), solute-carrier family 40 (iron regulated transporter) member 1 gene (SLC40A1), hepcidin anti-microbial peptide (HAMP), cytochrome b reductase 1 (CYBRD1) and hemojuvelin (HJV). Screening of 40 patients (33 female, seven male; 33 Caucasian, seven Coloured) for each of the five genes was achieved by the Heteroduplex Single-Stranded Conformation Polymorphism (HEX-SSCP) technique. Semi-automated DNA sequencing allowed for verification and characterization of the variants detected. Results included identification of four novel variants present in only the Caucasian patient group, characterized as IVS4-53G→A (HFE) (one of 33 patients; 3%), IVS2-65delA (CYBRD1) (two of 32 patients; 6.3%), 3’UTR+26delACGTCACGTTTCAAAACTA (CYBRD1) (one of 31 patients; 3.2%) and 219delG (HJV) (two of 33 patients; 6%). In addition, a total of 15 previously described variants were identified (seven intronic and eight exonic) of which three were also prevalent in only the Caucasian patient group. This study aimed to investigate the differences ...

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Bakgrund I Sverige får varje år cirka 1 000 personer diagnosen multipel skleros (MS) och ungefär 28 000 har sjukdomen. 80 procent av de som insjuknar får symtom som yttrar sig som energilöshet, svårigheter att koncentrera sig, försvagad mental styrka och sänkt livskvalitet, återhämtningstiden är också längre än vid annan trötthet. Det finns mycket som personen med MS kan göra i form av egenvård både fysiskt och psykiskt, Ökad fysisk aktivitet och även mental träning, har visat sig effektivt mot fatigue, ju mer en person tränar desto piggare blir denne. Syfte  Beskriva personer med MS erfarenheter av sin livskvalitet efter att ha utövat olika former av träning regelbundet. Regelbunden fysisk aktivitet innebär att, alla vuxna bör vara fysiskt aktiva under veckan, både vardagar och helger. Bäst effekt har träningsformer som innehåller både fysisk och mental träning (Folkhälsomyndigheten.se. 2021-10-04). Metod  En beskrivande litteraturstudie av 12 vetenskapliga artiklar med kvantitativ ansats granskades och analyserades. Huvudresultat Deltagarnas erfarenhet av fysiska aktiviteter var att dessa förbättrade livskvalitén och fysiska funktioner hos de som deltog i studien. Vilken träningsform och vilken intensitet den utövades med påverkade resultaten.  Slutsatser Deltagarna i studiernas erfarenhet av träningen var att livskvaliteten förbättrades, både fysiskt och mentalt. Olika träningsformer påverkade resultaten beroende på tyngden på träningen och sjuksköterskan kan ha en stor roll gällande motivering, utbildning och guidning till ett sunt och hälsobringande levnadsätt. Nyckelord Multiple sclerosis, wellbeing och quality of life.