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1
Littleton, Edward Theodore. "Autoantibodies in Multiple Sclerosis". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491344.
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rvIultiple sclerosis (MS) is an inflammatory disease of the central nervous system, characterised by axonal demyelination and degeneration. Hypothesised as autoimmune, antibodies to neuronal and myelin proteins have been reported, but there is little evidence of pathogenic antibodies against cell membrane targets. The aim of this thesis was to investigate whether MS patient sera contain antibodies against neuronal or oligodendroglial cells, and to develop techniques by which protein antigenic targets on cell membranes could be identified. Forty-one MS sera were tested for IgG binding to rat brain. Antibody binding to whlte matter was more frequent amongst relapsing-remitting MS patients compared to healthy controls, but western immunoblotting of myelin and rat brain extracts failed to demonstrate any specific reactivity of MS sera. One hundred MS sera were tested by immunofluorescence for IgG or IgM binding to the cell surface of neuroblastoma and oligodendroglioma cells. The number of sera containing cell-binding antibodies was not significantly greater amongst MS patients than amongst healthy controls. Using muscle specific tyrosine kinase (MuSK) seropositive myasthenia gravis as an experimental paradigm, an immunoprecipitation technique to isolate cell surface antigenic targets of serum antibodies, employing cell surface biotin labelling, was developed. Immunoprecipitated proteins were visualised with great sensitivity after gel electrophoresis and blotting. Two MS sera were found 'which specifically immunoprecipitated certain proteins, but development of an unbiased mass spectrometry technique for identifying immunoprecipitated proteins proved difficult due to immunoprecipitate impurity. Eventually, a new protocol for immunoprecipitate digestion and purification prior to mass spectrometry allowed reliable identification of MuSK exclusively in immunoprecipitates derived from MuSK seropositive patients. Thus, a clinically relevant cell membrane antigen has been identi?ed using a novel, non-candidate, unbiased proteomic approach. The same versatile techruque could be applied to identify proteins in immunoprecipitates derived from patients with MS or other putative antibody-mediated diseases. II Supplied by The British Library - 'The world's knowledge' I II. 11 has been observed on carbon nanotubes than graphite. The adsorption isotherms follow Langmuir isotherm except cytosine. Mathematical adsorption models devised here reveal that adenine binding onto graphite could be explained by the interaction between neutral base molecules and neutral surfaces. The adsorption is suggested to be goyemed by three factors: solubility, basestacking and the 1t-1t electron interactions. The adsorption onto quartz, gibbsite and feldspar show little or no adsorption but adsorption onto 'halloysite' is strong with the molecules containing cytosine or adenine groups, especially cytosine groups. Nucleotides adsorb the most followed by bases and nucleosides in this case. pH dependence of cytosine adsorption onto halloysite has been analysed by mathematical adsorption models as well, which shows that the whole adsorption constituents two types of adsorption. Type I can be ascribed to the binding between =SiO- and protonated cytosine, or the binding between =SiOH and neutral cytosine independently. Type 2 can be designated to the binding between =SiO- and neutral cytosine. Mathematical model analysis of literature data illustrates that the adsorption ofbases/nucleosides onto montmorillonite could be described by two types of bindings independently: =AIOH groups bind protonated bases/nucleosides, and =AIOH2+ groups bind neutral bases/nucleosides.- Graphite could prefer to concentrate nucleosides while halloysite could favour nucleotides accumulation. Carbon nanotubes and halloysite, which are both tubular, could have facilitated biomolecules adsorption from diluted primitive oceans. Although no new ideas have been discovered in the process of origins of life, the adsorption difference onto different minerals have shown the importance of minerals in concentrating, selecdng and possible protecting and storing prebiotic biomolecules.
2
Bloem, Liezl. "Iron and multiple sclerosis". Thesis, Link to the online version, 2007. http://hdl.handle.net/10019/340.
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Kaiser, Cora. "Autoantibodies in Multiple Sclerosis". Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-171441.
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Rigby, Sally. "Coping with multiple sclerosis". Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288858.
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Claffey, Austin M. "Metamemory in multiple sclerosis". Thesis, Brunel University, 2010. http://bura.brunel.ac.uk/handle/2438/4513.
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The concept of metamemory proposes that supplementary to typically measured memory abilities, memory monitoring and control processes are used to optimise learning. Accurate memory monitoring appears to be underpinned by a range of cognitive, and possibly affective, contributions. In populations with these deficits, metamemory has been shown to be impaired. In Multiple Sclerosis (MS), only a limited metamemory literature exists, surprising given that MS is a leading cause of disability among people of working age, and cognitive and mood disorder is common. Using structural equation modelling, this study of 100 people with MS explored factors contributing to performance on episodic Judgment of Learning, Retrospective Confidence and Feeling of Knowing. Given its negative influence on cognitive domains in MS, the impact of information processing deficits on metamemory was also investigated. Finally, memory self-report, a frequently used clinical indicator of memory functioning, was assessed. Findings suggest that memory complaint is associated with mood, and is unrelated to tested memory. Second, Retrospective Confidence Judgments were predictive of memory performance, even in the presence of memory impairment. Third, an unusual finding of maintained underconfidence at delay was observed in the Judgment of Learning task. Finally, Feeling of Knowing judgments related to executive, but not to memory ability. A novel finding in respect of this judgment was of processing speed relating negatively to accuracy, in the context of executive dysfunction. This suggests that some top-down direction of processing resources may be a factor in supporting accuracy, rather than the speed at which information is processed. Of all the task-based judgments, accuracy in this judgment was the only one with a reliable association with mood. Faster processing speed, executive dysfunction and least depression symptomatology related to low accuracy, perhaps typifying a profile of disinhibition seen in MS, characterised by poorly constrained processing and apparently elevated mood.
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Connolly, Gayle Wood. "Pain in multiple sclerosis". Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/5115/.
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Multiple Sclerosis (MS) is a chronic, progressive disease which presents as a variety of cognitive, motor and sensory deficits (Compston and Coles, 2008). Pain is one of the most common and often severe symptoms of the disease. It is associated with poorer general health, and its management is therefore an important therapeutic target. People with MS can suffer from neuropathic pain as a direct result of damage to the central nervous system, or nociceptive pain, as a result of changes to the musculoskeletal system, secondary to disease progression. This was the first epidemiological study to measure the prevalence, characteristics, and impact of MS-related pain, using validated, IMMPACT-recommended measures. Neuropathic pain, common in MS, is a challenge to manage and is shown to impact on a person health-related quality of life (HR-QOL). Subsequently, the second part of this study explored the impact of Transcutaneous Electrical Nerve Stimulation (TENS) on neuropathic pain in MS, in a randomised controlled trial. A postal survey design was used to target the MS population of the NHS Ayrshire and Arran health board area, who completed a questionnaire on their pain experience (n=302). Clinically significant pain, defined as ongoing bothersome pain, was experienced by over two-thirds (71.5%), whilst chronic pain, defined as pain present for at least six months, was experienced by over half (59.2%) of the MS population. Neuropathic pain, assessed using the PainDETECT screening tool, was experienced by almost one third (32.7%) of the sample, with a further 14.7% identified as potentially having neuropathic pain. Thus 47.4% of the sample could potentially have neuropathic pain, which is higher than previous estimates, and that experienced by the general population. Approximately half the population experienced painful tonic spasms (44.5%) and dysaesthetic pain (56.2%). Burning pain, unpleasant paraesthetic sensations (i.e. crawling, tingling), and sharp pain were commonly experienced in the population with neuropathic pain. Multiple logistic regression analysis revealed Type of MS (p=0.001) and disability level (Guys Neurological Disability Scale (GNDS) (p<0.001) as independent predictors of neuropathic pain, possibly related to the pathophysiology of the disease. Neuropathic pain was shown as statistically more severe (using the 11-point Numerical Rating Scale of pain intensity (NRS-11) (p<0.001), more emotionally unpleasant (using the SF-MPQ) (p<0.001), with greater sleep disturbance (p<0.001), than nociceptive pain. Despite over two-thirds (68.5%) of those with neuropathic pain currently using prescribed, pain-relieving medication, over half (53.7%) still experienced severe (7-10 on NRS-11) pain. The presence of neuropathic also had a significantly negative impact on HR-QOL (EQ-5D) (p<0.001). The results of the epidemiological study increase understanding of the extent and demanding nature of pain in MS. Clinically, it will also facilitate timely screening for the neuropathic pain subtype, to minimise its impact on HR-QOL. Following the epidemiological findings, a randomised, double-blind, placebo-controlled trial, explored the efficacy of Transcutaneous Electrical Nerve Stimulation (TENS) in the treatment of chronic, neuropathic pain in MS (n=46). Participants were recruited from the MS Service, NHS Ayrshire and Arran, with a diagnosis of lower limb neuropathic pain (score of ≥19 on the PainDETECT Screening tool for neuropathic pain), experienced for a minimum of six months. For the active TENS group, standard ‘Conventional’ TENS settings were applied, whilst a low frequency, low intensity, long pulse duration electrical current was used for the placebo application, which has no known analgesic effect, but still provides a sensory stimulus. Both groups used the TENS machine for a minimum of four hours/day, for a two-week period. Two long self-adhesive, hypo-allergenic electrodes were placed paravertebrally over the lumbar spine to stimulate the spinal nerve roots. The primary outcome measure was the (NRS-11), whilst secondary outcome measures included the Neuropathic Pain Scale (NPS), and the Patients Global Impression of Change (PGIC). Level of pain related interference on function was measured using the Brief Pain Inventory (BPI). Compared to the control group, the group receiving active TENS demonstrated a statistically (p<0.001) and clinically significant reduction in the intensity of neuropathic pain over the two-week intervention period. It was particularly effective for the burning, and sharp neuropathic pain qualities, that were commonly associated with neuropathic pain in the epidemiological study. TENS was also shown to reduce the emotional unpleasantness of pain (the affective component), which was high in those with neuropathic pain in the epidemiological study. This may have implications for the role of TENS in managing the psychological aspect of chronic neuropathic pain. TENS has no effect on pain–related interference on function, possibly due to the relatively short TENS intervention period. Future studies should explore longer intervention periods to explore the longer-term effects of TENS for pain in MS. The pharmacological management of neuropathic pain is not without its challenges. TENS as an inexpensive, non-invasive modality, with no side-effects, could be considered for the management of neuropathic pain, a common phenomenon in the MS population.
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O'Gorman, Cullen. "Epidemiology of Multiple Sclerosis". Thesis, Griffith University, 2018. http://hdl.handle.net/10072/374775.
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Multiple sclerosis (MS) is a chronic disabling disease of the central nervous
system commonly affecting young adults. Pathologically, there are patches
of inflammation (plaques) with demyelination of axons and associated loss
of oligodendrocytes. Genome-wide association studies have identified over
105 loci of susceptibility, but the total number of possible contributory loci
may be considerably higher.
Family recurrence risks are available for several northern hemisphere
countries, but there are few data for the southern hemisphere and regions
at lower latitude such as Australia. The published family data could provide
useful recurrence risks if appropriately analysed. Segregation analysis can
be used to model the genetic architecture of MS.
There is a global latitude gradient in MS prevalence, and the incidence
of MS is increasing (particularly in females). These changes suggest a major
role for environmental factors in the causation of disease.
In the last 20 years there has been increasing evidence for the role of smoking in the aetiology of multiple sclerosis. Cigarette smoking is also
associated with increased risk of developing the progressive form of MS.
This risk factor has not previously been analysed in Queensland. Furthermore,
cigarette smoking represents a possible cause of the changing prevalence of
MS over time.
Methods
The family risks in Australia were measured in three regions at different
latitudes. Immediate and extended family pedigrees were collected for three
cohorts of MS patients in Queensland, Victoria and Tasmania. Age of onset
data from Queensland were utilised to estimate age-adjusted recurrence
rates.
Meta-analysis of all available family recurrence risk data was performed
to define risks to relatives. Standard methods of meta-analysis were combined
with novel approaches to age adjustment to provide directly comparable
estimates of lifetime risk. Segregation analysis was used to estimate the
proportion of the overall genetic risk that can be attributed to identified
susceptibility genes.
To evaluate risks from smoking in Queensland, a large case-control study
was performed, comparing risk of MS (by smoking habit) using regression
modelling.
The risk of developing progressive disease was measured in a cohort
from an MS clinic in Queensland, followed from first clinic attendance until
the onset of clinically determined progressive disease. Risk of progression was analysed with gender, age, age of onset, exposure to disease modifying
therapy, and smoking status as covariates in a Cox proportional hazards
analysis.
Finally, a comprehensive meta-analysis was performed of eligible casecontrol
and cohort studies that evaluated the risk of MS in smokers and exsmokers.
The influence of study design, gender, latitude and year of study
were explored with regression modelling.
Results
Recurrence risks in Australia were significantly lower than in studies from
northern hemisphere populations. The age-adjusted risk for siblings across
Australia was 2.1% compared with 3.5% for the northern hemisphere. A
similar pattern was seen for other relatives. The risks to relatives were
proportional to the population risks for each site, and hence the relative
risk for siblings (lS) was similar across all sites.
From the meta-analysis of family recurrence risks, the overall recurrence
risk for monozygotic twins was 18.2% and for siblings 2.7%. The recurrence
risk for dizygotic twins was significantly higher than for siblings. The overall
estimate of sibling relative risk (lS) was 16.8. Risks for older relatives
(parents, siblings, aunts, uncles and cousins) show a latitudinal gradient, in
line with population risk. No latitudinal gradient for lS was seen. Segregation
analysis supports a multiplicative model of one locus of moderate effect with
many loci of small effect. The estimated contribution of the known MS loci is 18–24% of lS.
The case-control study in Queensland confirmed an association between
increased risk of MS and smoking. The overall adjusted odds ratio was
1.9 (95% confidence interval, CI 1.5–2.5) for ever smokers. There was no
statistically significant difference in the risks for males and females.
In the progression study, there were significantly higher risks of secondary
progressive disease in males (Hazard Ratio, HR 1.83, 95% CI 1.3–2.7) and
in ever smokers (HR 1.4, 95% CI 1.0–2.0). Progressive disease occurred
approximately 4 years earlier in ever smokers. Smoking did not affect age
of onset of primary progressive disease.
The meta-analysis of smoking risk included 26 studies representing 8615
cases and 392,352 controls and an additional 792 cases included from a
total cohort population of 601,492 individuals, representing more than 9
million person-years. There was a consistent association between smoking
and MS with an odds ratio of approximately 1.5, with males at higher risk.
This finding was independent of study design. However, latitude and year
of study may have unexpected influence. Smoking appeared to confer a
greater risk to females living closer to the equator than to females at higher
latitudes. Additionally, the effect of cigarette smoke exposure on MS risk
may not be fixed over time, but could be increasing.
Discussion
The familial recurrence risk of MS in Australia is lower than in previously
reported studies. This is directly related to the lower population prevalence
of MS. The overall genetic susceptibility in Australia as measured by the lS is similar to that seen in the northern hemisphere, suggesting that the
difference in population risk is explained largely by environmental factors
rather than by genetic admixture.
The meta-analysis of family data supports the notion of MS risk being
derived from multiple susceptibility genes and environmental factors. Genetic
susceptibility appears to be independent of latitude, and the latitudinal
gradient of MS prevalence is likely due to environmental factors.
The results of the case-control study in Queensland replicate existing
work that has shown cigarette smoking increases the risk of MS. Cigarette
smoking represents an important modifiable risk factor for the development
of MS.
Cigarette smoking was also associated with earlier onset of progressive
disease in the large clinical cohort studied in Queensland. For patients with
relapsing-remitting disease, smoking cessation should be encouraged.
The results of the meta-analysis of smoking studies suggest a threshold
model of MS risk that includes a fairly constant genetic risk (for Caucasian
populations) together with variable environmental risks which are dominated
by vitamin D deficiency at higher latitudes and are more significant in women who have an intrinsically lower threshold for development of disease.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medicine
Griffith Health
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Foley, Peter Leonard. "Pain in multiple sclerosis". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28949.
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Background: Pain is frequently reported by people with multiple sclerosis (MS). It has been associated with decreased quality of life, psychiatric morbidity, interference with day to day activities, and frequent healthcare attendance. It has been reported by people with multiple sclerosis to be one of their most important symptoms, and available treatments are limited in their effectiveness. Despite this, our understanding of the epidemiology and mechanisms of pain in people with MS are limited. Our understanding of the interactions of central nervous system mechanisms and pain states overall is growing. However, the application of this knowledge to MS is incomplete. Previous studies have shown that the descending pain modulatory system (DPMS) is an endogenous network of cortical and subcortical brain structures which act to limit, or accentuate, an individual’s perception of pain, via descending brainstem pathways. Associated clinical measures include depression, anxiety, and cognitive flexibility. Our understanding of the function or dysfunction of this system in MS is limited. We do not know if the MS disease process may adversely affect the structure or function of the DPMS. Hypothesis: In people with neuropathic limb pain in relapsing remitting MS (RRMS), compared to people with RRMS who do not have pain, there will be disruption of the endogenous descending pain modulatory system. This will manifest as impaired descending inhibition of pain. Aims and Methods Establishing the background using systematic reviews: The first aim of this thesis was to establish the prevalence, natural history and associations of pain (and pain syndromes) occurring in people with MS. The second aim was to explore existing knowledge of how the MS disease process may contribute to pain states, using a systematic review of neuroimaging studies. Prospective clinical study: A case-control study of 47 people with RRMS was then carried out. 31 of these had neuropathic pain in the limbs, and 16 did not have pain. Using targeted assessments, function of the descending pain modulatory system was assessed in the following ways: First: Detailed clinical, behavioural and neuropsychological assessment, focussing on cognitive, behavioural and affective features known to be closely related to the DPMS. Second: MRI imaging of brain structure, focussing on the volume and location of MS lesions, as well as the volume of key grey-matter structures involved in the DPMS. Third: Resting state functional MRI imaging of the brain, focussing on functional connectivity between the rostral anterior cingulate cortex and two other key DPMS structures (dorsolateral prefrontal cortex, and periaqueductal gray). Results: Systematic reviews: Meta-analysis of existing prospective studies confirmed that pain is very common in MS, affecting about 63% of people with MS on average (95%CI between 55 and 70%). Many different types of pain contribute to this overall estimate. No significant associations with disease course or stage emerged. Several neuroimaging studies have assessed people with MS-associated pain using MRI. These studies were often small, and with associated methodological issues. It is likely that location of MS lesions is implicated in aetiology of pain syndromes in some cases, though our overall knowledge is limited. Prospective study: In a prospective study, people with and without pain were matched for age and gender. Furthermore, groups were balanced for a range of other variables. The pain group more frequently received gabapentinoid medications. The presence of pain was significantly associated with increased scores for depression, fatigue and catastrophising, as well as with specific impairments at neuropsychological assessment, including cognitive flexibility. Many of these impairments are directly relevant to existing models of the DPMS. Overall volume of MS lesions was not different in people with pain, though lesions were more likely to occur in the brainstem. Some alterations of grey-matter volumes in people with pain which mirrored studies of pain disorders outside MS were found, but these did not involve structures key to the DPMS. Affected structures included trigeminothalamic nucleus (relative volume increase in pain group), posterior cingulate cortex and parahippocampal gyrus (volume decrease in pain group). Functional connectivity of the rostral anterior cingulate cortex to the periaqueductal grey matter, a key structure in the descending modulation of pain, was stronger in the group without pain. Conversely, functional connectivity to the dorsolateral prefrontal cortex, repeatedly implicated in the DPMS and thought to be involved in cognitive evaluation and flexibility, was stronger in the pain group. MS lesion volume appeared to account for some of this difference in a multivariate analysis. Limitations: Key limitations of this work include cross-sectional design, small sample size, and number of statistical comparisons carried out. Conclusions: Systematic reviews examined the prevalence, natural history and associations of pain in MS, as well as examining existing neuroimaging studies which investigated how the MS disease process could contribute to pain states. A prospective study found evidence of both emotional/affective and cognitive dysfunctions relevant to the hypothesis of dysfunction in the DPMS. Higher likelihood of MS lesions in the brainstem could be relevant to DPMS function. Separately, there were structural grey-matter volume alterations reflecting those found in many pain studies outside MS. Importantly, however, these did not affect key DPMS structures. Resting state functional MRI however demonstrated altered connectivity of core DPMS structures, which may be partly mediated by MS lesion volume. Functional connectivity findings could be consistent with the hypothesis of impaired descending pain inhibition, in people with relapsing remitting MS affected by neuropathic limb pain.
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Ligers, Arturs. "Immunogenetic studies of multiple sclerosis /". Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-019-9/.
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Lu, Ellen Meng-I. "Perinatal outcomes in multiple sclerosis". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44199.
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Lee, Martin A. "Imaging pathology in multiple sclerosis". Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312191.
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Chataway, Simon Jeremy Stovold. "Genetic analysis of multiple sclerosis". Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621942.
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Camp, Sophie Jane. "Memory function in multiple sclerosis". Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327043.
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Davies, Jessica Lesley. "Functional immunogenomics in multiple sclerosis". Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709188.
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Yeo, Tai Wai. "Genetic analysis of multiple sclerosis". Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612481.
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Hughes, S. E. "Epidemiological perspectives on multiple sclerosis". Thesis, Queen's University Belfast, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.676616.
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Multiple sclerosis (MS) is the most common cause of neurological disability in young adults in the developed world. Given the clinical heterogeneity in MS, it is difficult to predict the rate at which an individual will accumulate disability. Natural history studies in MS have provided insight but many questions remain unanswered. MS registries fulfil an important role in providing longitudinal data from multi-centric MS cohorts. The analyses described in this thesis were performed using an international MS database, the MSBase Registry, which currently contains records of over 21,000 people with MS from clinics in 64 countries. Expanded Disability Status Scale (EDSS) scores recorded in the MSBase Registry were used to examine disability progression, by ranking scores at specific disease durations, as used to devise the MS Severity Score (MSSS). I demonstrated strong correlation in EDSS rank over five-year periods, from four years after MS onset, suggesting that the concept of EDSS ranking could be useful in predicting later disease severity. I then sought to determine which clinical features influenced EDSS rank change, observing that factors such as gender, relapse rate, treatment exposure and brain imaging findings predicted this outcome, using quantile regression models. These results may prove useful for clinicians in the design of treatment algorithms and clinical trial endpoints in MS. Using the MSBase Registry, the relationship between pregnancy and MS was examined. I confirmed that pregnancy has a favourable effect on relapses but that relapse rate increases in the. postpartum period, as shown in previous studies. A novel association between pre-conception treatment exposure and postpartum relapses was observed. This could allow neurologists to employ a strategy to minimise risk of postpartum relapses in women with MS who are planning conception. Identifying those people with MS who are at high risk of developing disability is becoming increasingly important given the advent of new MS therapies. It is also vital to improve our understanding of the effect of pregnancy on MS, given that onset is common during childbearing years. With these issues in mind, I performed analyses of longitudinal data from the MSBase Registry, producing findings of clinical interest to neurologists worldwide.
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Souberbielle, Bernard. "Immunological investigation in multiple sclerosis". Thesis, University of St Andrews, 1993. http://hdl.handle.net/10023/13440.
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In this thesis, immunological parameters in multiple sclerosis patients (MS) have been examined and techniques contributing to the study of these aspects have been developed. The epidemiology of MS suggests that both environmental and genetic factors contribute to the disease process. According to a widespread theory, an autoimmune reaction leading to demyelination could be induced, in genetically determined individuals, by an infectious agent (s) e.g a paramyxovirus or a retrovirus. In the first part of the thesis, the oligoclonal immunoglobulin (Igs) in the CSF of MS patients in relation to the paramyxovirus SV5 were studied. This was to complement an initial observation made in the department that a significant proportion of cerebrospinal fluids (CSF) could have oligoclonal bands directly acting against antigens (Ags) of this virus. In the second part of the thesis, techniques were developed for the analysis of proliferative capacity of peripheral lymphocytes of MS and control patients using possible MS autoantigens viz myelin and brain vessels. The humoral response against these Ags was also assessed by immunoblotting using MS, neurological and normal control patients. In parallel and in the view to obtaining antigens for the immunological studies, techniques for the purification and characterisation of human brain vessels from post mortem brains were assessed and attempts to culture human brain endothelial cell lines were made.
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Gardiner, Fiona. "Articulatory dysfunction in multiple sclerosis /". [St. Lucia, Qld.], 2000. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16324.pdf.
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Turcotte, Dana. "Multiple sclerosis-induced neuropathic pain". The Consultant Pharmacist, 2004. http://hdl.handle.net/1993/23316.
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Neuropathic pain (NPP) is a chronic syndrome suffered by patients with multiple sclerosis (MS), for which there is no cure. Underlying cellular mechanisms involved in its pathogenesis are multifaceted, resulting in significant challenges in its management. In addition to its complex pathophysiology, the clinical management of MS-induced NPP is further complicated by the lack of clinical therapeutics trials specific to this population. The primary aim of the work underlying this thesis was to contribute to the evidence-based management of individuals with MS-induced NPP through the completion of two clinical therapeutics trials in this population. A secondary aim was to describe pain variability in this patient population through the development and validation of a pain variability algorithm tool. Resulting from this work, we demonstrated that nabilone – a synthetic oral cannabinoid – represents an effective, well-tolerated and novel treatment for MS-induced NPP. Additionally, we show that the SSRI paroxetine was poorly tolerated in our patient population, with a correspondingly high attrition rate. As a result, we were unable to determine any treatment effect in this trial due to insufficient recruitment due to drop-out. Lastly, we were able to define and describe pain instability in this cohort, noting that approximately 30% of individuals with MS-induced NPP experiencing highly variable daily pain. The results of these projects provide novel information for this patient population. Patients currently living with the daily burden of MS-induced NPP would benefit from additional trials ensuing from this, and other, research in order to initiate a momentum for much-needed clinical research in this complicated patient cohort.
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Shaw, Sally. "Trying to take control while attempting to adapt perspectives of people with multiple sclerosis on the twelve months following diagnosis /". Swinburne Research Bank, 2007. http://hdl.handle.net.
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Thesis (DPsych) -- Faculty of Life and Social Sciences, Swinburne University of Technology, 2007.Submitted in fulfillment of the requirements of the degree of the Professional Doctorate of Psychology, Faculty of Life and Social Sciences, Swinburne University of Technology, 2007. Includes bibliographical references (p. 300-346).
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Parikh, Khyati. "Investigating the role of auto-immune responses to transient axonal glycoprotein-1 (TAG-1) in experimental autoimmune encephalomyelitis (EAE)". Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25214.
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Shacklady, Justine. "Perceptions of prosody in multiple sclerosis /". [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19221.pdf.
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O'Doherty, Catherine. "Genetics and pharmacogenomics of Multiple Sclerosis". Thesis, Queen's University Belfast, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486179.
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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system which is th9ught to be triggered by environmental factors in a genetically predisposed individual. The genetic component is probably attributable to the collective effects of a number of genes each conferring a minor risk. One aspect of this project was to identify variations in candidate genes beyond the MHC Class II region which may influence susceptibility to MS. The genes investigated included PACAP, ITGA-I. MHC2TA, IURA and a group of cytokine genes. PACAP and IL7RA were not major MS susceptibility loci. A SNP in ITGA4 showed evidence of a susceptibility effect in two populations, and MHC2TA may influence risk of chronic inflammatory diseases including MS, RA, and JIA. In the screen of cytokine genes an IL23R SNP showed a similar trend in allele frequency between MS patients and controls in two populations. IFN-P is the most prominent disease modifying drug used in the treatment of MS, decreasing relapse rates and delaying progression of the disease. However an estimated 30-50% of patients fail to respond to treatment. The second aim of this project was to detemline polymorphisms which may modify IFN responsiveness. We screened 61 SNPs in 34 candidate response genes, selected on the basis of their function and the literature. We primarily chose SNPs in the promoter region, hypothesizing that polymorphisms may modify 1FN inducibility. Polymorphisms were typed in samples from 255 Irish patients classified as responders or non-responders. A cohort of 120 healthy controls was also included in the study to determine whether these SNPs' influenced susceptibility to MS. We explored allelic combinations which may influence susceptibility to disease and also response to treatment. A JAK2-IL-IOC4SP3 combination most significantly affected'treatment response and a JAK2-ILI O-CASP I0 combination was the most influential in terms of risk modification.
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Bowman, Marjorie June. "Quality of Life in Multiple Sclerosis". Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34448.
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Objective: To explore quality of life in patients with multiple sclerosis.
Concept Analysis: A concept analysis of quality of life in multiple sclerosis was conducted using Rodgers’ evolutionary concept analysis method. Eighty-three studies were reviewed.
Study Proposal for Secondary Analysis: The proposal was for a secondary analysis using a quantitative, longitudinal, repeated measures design to determine if stem cell transplant has an impact on the quality of life of multiple sclerosis patients with aggressive disease.
Summary of Findings: A concept analysis provided valuable insight into the use and understanding of the concept of quality of life in the multiple sclerosis literature. The subjective and multidimensional attributes of quality of life in multiple sclerosis were similar to findings in previous concept analyses of quality of life in general and in other diseases. The other attributes of the concept being measureable, modifiable and predictable revealed the uniqueness of quality of life in multiple sclerosis and provided a foundation for the development of future research. The results of the secondary analysis will provide new knowledge of a novel treatment for multiple sclerosis and its impact on quality of life. This advancement of knowledge in nursing and across health care disciplines will aid in the delivery of collaborative and comprehensive patient-centred care to ultimately improve the lives of multiple sclerosis patients.
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He, Bing. "Susceptibility gene mapping in multiple sclerosis /". Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980608he.
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Salzer, Jonatan. "Environmental risk factors for multiple sclerosis". Doctoral thesis, Umeå universitet, Klinisk neurovetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-64212.
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Background Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. It usually strikes during young adulthood, and 2.5 million individuals are estimated to have the disease worldwide. The causes of MS are not known, but several factors have been shown to be associated with the risk of the disease, including certain genes, vitamin D, smoking and Epstein- Barr virus infection. Little is known about how/if these factors interact. Methods Study I: The risk of MS by month of birth was investigated using MS cases from the Swedish MS registry and using general population controls. Studies II–V: We identified MS cases who had donated blood prior to disease onset, and MS cases whose mothers had donated blood during pregnancy, by cross-linking a database of MS cases, and a database of mothers of MS cases, to two local biobank cohorts. One of them consisted of blood samples collected during early pregnancy, and one with samples collected during health controls. Levels of 25(OH)D (25-hydroxyvitamin D), RBP (retinol binding protein, a surrogate marker for vitamin A), CRP (C- reactive protein), cotinine (a nicotine metabolite) and anti Epstein-Barr virus nuclear antigen-1 (EBNA-1) antibodies were measured in cases and matched controls. The risk of MS by categories of these exposures was estimated in bi- and multivariable matched logistic regression models. Results Subjects born in spring had a higher risk of MS, but no influence of early gestational levels of the measured risk factors on the risk of MS in the offspring was observed. In prospective samples from MS cases and controls, 25(OH)D levels ≥75 nmol/l, intermediate RBP levels, and elevated CRP levels in young were associated with a decreased risk of MS. Elevated cotinine levels (suggestive of smoking) and high antibody reactivity against EBNA-1 were associated with an increased risk of MS. All factors but RBP were more clearly associated with MS in young subjects. Conclusion All factors analyzed in prospectively collected samples were associated with the risk of MS, and taken together, the data indicate that the key etiopathological events that lead to MS occur before the age of 20–30. Study II provides support for trials exploring the primary preventive potential of oral vitamin D supplementation.
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Levesque, Ives. "Magnetization transfer imaging of multiple sclerosis". Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79030.
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Magnetization transfer (MT) imaging is a magnetic resonance imaging techniqu ewhich permits indirect observation of the macromolecular component of biological tissue. Semi-quantitative implementations such as magnetization transfer ratio (MTR) imaging are very useful in the study of neuro-degenerative diseases, despite the relatively limited information provided by such single measurement methods. Quantitative techniques provide estimated measures of model parameters that more accurately describe the MT process. This thesis presents the application of quantitative MT imaging in a cross-sectional study of multiple sclerosis (MS) patients and healthy controls, exploring the on-going changes that occur in MS. Quantitative results are investigated to determine which model parameters play a role in the MTR. The findings demonstrate regional variations in white matter structures, and significant differences between healthy and normal-appearing MS tissue. The results also indicate the dominant role of macromolecular content in MTR, and confirm the destructive nature of T 1-hypointense lesions.
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Wood, Nicholas William. "The immunogenetic basis of multiple sclerosis". Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338015.
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Wegner, Christiane. "Analysing cortical changes in multiple sclerosis". Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427613.
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Parratt, J. D. E. "Multiple sclerosis and Chlamydia pneumoniae infection". Thesis, University of Aberdeen, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590948.
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Coles, A. "Monoclonal antibody therapy of multiple sclerosis". Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597844.
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T cells mediate the inflammatory activity of multiple sclerosis, which is directed against an unknown autoantigen. A non-antigen specific treatment strategy was tested, drawing on the experimental demonstration of long term allograft acceptance following short term therapy with monoclonal antibodies against T cells. The treatment of 27 patients with multiple sclerosis using a single pulse of humanised anti-lymphocyte (CD52) antibody, Campath-1H, was investigated. With the first dose of monoclonal antibody, patients experienced a rehearsal of previous relapses that fully resolved and was associated with a transient rise in serum TNF-α and IFN-γ. This suggested that inflammatory mediators may impede axonal conduction at previously demyelinated sites. After five consecutive daily doses of Campath-1H, the circulating T lymphocyte count was suppressed for at least 18 months, without any serious infective complications. The in vitro mitogen induced proliferation, and IFN-γ secretion, of patients' peripheral blood mononuclear cells was reduced after treatment and there was also a signficant rise in the peripheral B cell count above pre-treatment levels. This deviation of immune responses away from the Th1 phenotype would, under the hypothesis that multiple sclerosis is a "Th1 disease", be expected to abrogate cerebal inflammation. Unexpectedly, one third of patients developed Graves' disease, an adverse effect not induced by any other therapies nor by Campath-1H treatment of other diseases. By analogy with experimental models of autoimmunity following prolonged lymphocyte depletion, Campath-1H may have selectively depleted T cell clones which suppress autoreactive T cells, although why Graves' disease specifically was induced remains unexplained. Radiological markers of cerebral inflammation were suppressed for at least 18 months in all patients, who experienced no new relapses. However half the patients continued to accumulate disability from deficits acquired prior to monoclonal antibody treatment. In these patients there was both a higher inflammatory load at baseline and progressive cerebral atrophy, which may represent axonal degeneration. It is concluded that inflammation is a necessary prerequisite for new lesion formation and that the secondary progressive phase of multiple sclerosis is initiated by demyelination but proceeds by non-inflammatory mechanisms.
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Manson, Stephanie C. "The invisible pathology of multiple sclerosis". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509990.
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Hewitt, Peter. "Experiences of multiple sclerosis in families". Thesis, University of Oxford, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599906.
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Multiple Sclerosis (MS) is a progressive demyelinating disease of the central nervous system that affects not only those with MS, but also those who are close to them. The present papers aim to explore the experiences of MS in families. The first paper presents a review and synthesis of the qualitative literature exploring first-hand accounts of family members of people with MS. The twenty studies that met the inclusion criteria captured the perspectives of individuals with MS, partners, children, siblings and parents. The studies were generally of a reasonable quality, with findings identifying a range of factors salient to the experiences of family members. Methodological limitations indicated areas for future research that would strengthen the evidence base. The second paper used a modified grounded theory methodology and semi-structured interviews to explore couples' joint narratives of their experiences of MS. The findings demonstrated that MS can have a significant impact on the couple relationship, often affecting areas of great importance and meaning for the couple. MS can lead to emotional and social changes for each partner, as well as shifts in their attitudes, values and philosophies and hopes, fears and expectations. Dynamic changes in couples shared understanding were identified, as was an on-going process of sense making. Couples' responses to the challenges posed were in many cases broad and flexible. The balance for both partners between expressing and asserting their own needs and positions whilst recognising and appreciating those of their partner was a characteristic to emerge from the data. An explanatory model grounded in the data is presented. Areas for future research and the clinical implications are explored. The target journal for both Paper A and Paper B is Psychology and Health, a journal that promotes the study and application of psychological approaches to health and illness.
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Lim, Ee Tuan. "Neurodegenerative markers : insights into multiple sclerosis". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444993/.
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Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) characterised pathologically by inflammation, demyelination and variable degrees of axonal loss and gliosis. Remyelination, axonal and synaptic plasticity have been identified as mechanisms underlying functional recovery. MS typically follows a chronic course, in the sense that new episodes or steady progression are the rule. Currently radiological surrogates of inflammation, demyelination and axonal loss are available, but these correlate only modestly with the development of cumulative disability. In this thesis, potential brain specific protein (BSP) markers for these pathological processes are identified and compared to existing magnetic resonance (MR) markers. OBJECTIVES: Levels of the nervous system proteins S100B (astrocytic activation), glial fibrillary acidic protein (GFAP astrogliosis), neurofilaments (axonal marker) and ferritin (microglial activation) and other inflammatory markers (i.e. anti-myelin antibodies) were measured. These values were correlated with both histopathological measurements in post-mortem specimens and MR imaging measures in patients with MS. Histology and immunochemistry of tissue sections characterised normal and pathological CNS and localized the extent of demyelinating plaques.
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Lee, Wing-ming Mary. "Psychosocial adjustment of multiple sclerosis patients". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1987. http://hub.hku.hk/bib/B29653058.
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Petzhold, Axel. "Brain-specific proteins in multiple sclerosis". Thesis, University College London (University of London), 2003. http://discovery.ucl.ac.uk/19072/.
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Brain–specific proteins (BSP) are each relatively specific for particular cell–types within the nervous system. The BSP studied were glial fibrillary acidic protein (GFAP) and S100B for the astrocyte, ferritin for microglia and neurofilaments (Nf) for the axon. BSP are released into the extracellular fluid (ECF) following cellular destruction and during phases of high cellular activity such as astrocytic or microglial activation. ECF BSP equilibrate with those in the cerebrospinal fluid (CSF). This allows us to quantify BSP from the CSF and estimate the overall average of axonal damage (CSF Nf), astrocytic and microglia activation (respectively CSF S100B, CSF ferritin) and astrogliosis (CSF GFAP). New enzyme linked immunoabsorbant assays (ELISA) have been developed for measuring Nf and GFAP in the CSF. Previously established ELISAs have been used to measure S100B and ferritin. It has been shown that spinal cord atrophy in a mouse model of autoimmune encephalomyelitis (EAE) was paralleled by a decrease of Nf indicating loss of axons, and an increase in GFAP indicating astrogliosis. These findings have been confirmed and extended in a human post–mortem study where BSP levels were quantified in multiple sclerosis (MS) lesions of different age and activity. S100B and Nf were associated with acute lesions, ferritin was elevated in all lesion types, while GFAP was increased in both acute and chronic lesions. CSF BSP levels were then quantified in a cross–sectional study of MS patients with the aim of distinguishing clinical subgroups, such as relapsing remitting (RR), primary progressive (PP) and secondary progressive (SP) disease. In addition an attempt was made to relate CSF BSP levels to grades of disability using clinical scales including Kurtzke’s EDSS, an ambulation index (AI) and the 9–hole PEG test (9HPT). It was shown that CSF S100B was higher in RR MS while CSF ferritin was elevated in PP MS patients. The S100B:ferritin ratio emphasised the distinction between the MS subtypes. CSF GFAP was higher in poorly ambulating (AI) and severely disabled (EDSS) patients. CSF GFAP correlated with the EDSS in SP MS patients. This suggests that gliosis is an important feature in SP MS. CSF Nf levels were quantified in a longitudinal study at baseline and at 3–year follow–up. It was shown that more SP/PP than RR MS patients experienced an increase in CSF Nf levels over this time, suggesting cumulative axonal damage in this subgroup. RR MS patients who had elevated CSF Nf levels at baseline had a worse clinical course, suggesting that initial high CSF Nf levels in RR MS patients are a poor prognostic sign. CSF Nf levels at follow–up correlated with the EDSS, AI and 9HPT suggesting that axonal pathology in MS is a dynamic process possibly balancing features of de- and regenerative activities.
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Sharrack, Basil. "Assessment of disability in multiple sclerosis". Thesis, King's College London (University of London), 1999. https://kclpure.kcl.ac.uk/portal/en/theses/assessment-of-disability-in-multiple-sclerosis(52778e49-f801-4fc8-b81b-aea8ac20d2a2).html.
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Craig, Charles J. "Studies of immunoregulation in Multiple Sclerosis". Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328088.
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Gay, Frederick William. "On the cause of multiple sclerosis". Thesis, Queen's University Belfast, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317532.
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Young, Colin D. "Aspects of coping with multiple sclerosis". Thesis, Cardiff University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244851.
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Vora, Abhilash Jaysukhlal. "Leucocyte-endothelial interactions in multiple sclerosis". Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309293.
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Kellar-Wood, Helen Fiona. "Candidate susceptibility genes in multiple sclerosis". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361751.
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Dobson, Ruth. "Towards an endophenotype in multiple sclerosis". Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8779.
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An endophenotype is a concept that allows the description of complex diseases with genetic and environmental contributions,enabling the identification of an at risk population. I aim to describe an endophenotypic gradient between healthy controls, siblings of people with MS and people with MS. Siblings of people with MS are at increased risk of developing MS; this is thought to be a result of genetic and environmental contributions. Epidemiological studies have identified a number of factors contributing to MS risk including smoking,vitamin D,infection with Epstein Barr virus and HLAZDRB1*1501. A genome wide association study in 2011 gave information regarding the contribution of HLAZtype and nonZHLA"SNPs to MS risk. I set out to integrate these into an endophenotypic risk score for MS. When the genetic contribution from HLAZDRB1*1501 alone was used,the mean MS risk score was significantly higher for people with MS than siblings or controls. Siblings had a higher MS risk score than controls. The differences between the three groups become more apparent when all genetic information was used in the MS risk score. I used MRI and biomarker studies to validate the MS risk score generated. Preliminary studies enabled an evaluation of the potential association between selected biomarkers and CSF oligoclonal bands. The analyses performed demonstrate the potential clinical utility of such a score in describing MS risk. Siblings have a risk score intermediate to people with MS and controls, confirming their “at"risk” position in the endophenotype construct. Much of the MS risk in siblings can be attributed to genetics, with environmental factors potentially providing the trigger for clinically apparent disease. The findings of this research have the potential to enrich future prevention studies with individuals at high risk of developing MS,enabling such studies to be performed within a realistic timeframe.
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Roxburgh, Richard Hugh Stephen Richards. "The genetic epidemiology of multiple sclerosis". Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614977.
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Wilkinson, Hannah R. "Living with unpredictability in Multiple Sclerosis". Thesis, University of Lincoln, 2014. http://eprints.lincoln.ac.uk/18979/.
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Background: Unpredictability is identified as a major factor in Multiple Sclerosis (MS) and reported to be a “constant companion” for individuals living with MS. It is reported to be a factor of uncertainty, which is indicated to have a biopsychosocial impact on these individuals. However the impact of uncertainty is argued to diminish over time. Whereas, the lived experience of unpredictability is reported to be continual. Furthermore, unpredictability is argued to have a continual psychological effect on individuals with MS. However, unpredictability is an aspect that remains relatively unaddressed in the research. Qualitative research has been highlighted to be fundamental in exploring the individual experience of illness, providing rich detailed descriptions. In addition it has been instrumental in the development of services to meet the needs of these individuals. The significance of unpredictability in MS highlights the need for further exploration of lived experience of this aspect of the illness to support healthcare professionals and the development of services to meet the needs of these individuals. Aim: This study aimed to address the limited research examining unpredictability in MS, to develop a comprehensive understanding of how this aspect affects the lives of individuals with MS. Method: This study employed a qualitative design. Twelve participants were recruited through the MS Society, local advertisements and by a ‘snowballing’ sampling technique. All participants lived in England, had a diagnosis of MS, and were able to provide consent to participate. Individual interviews were conducted (7 face-to-face and 5 telephone interviews) using a semi-structured interview. Interviews were transcribed verbatim and analysed by the researcher using a thematic analysis (TA) approach. Results: Three main themes were derived from the analysis: 1) Challenges to meaning-making; 2) A wide picture of unpredictability; and 3) Surviving unpredictability. Each of the themes generated between two or three sub-themes. The themes told the participant’s story for living with unpredictability. Conclusion and recommendations: Unpredictability was reported to be a key factor of living with MS, yet it was challenging and difficult to understand. Participants described the wide reaching impact of unpredictability influencing them personally and socially. Pragmatic and psychological approaches were employed by participants to deal with unpredictability. The findings offer insight into the individual’s experience of living with unpredictability. It is argued the findings represent individuals who have reached a stage of acceptance with their illness and therefore may offer health professionals guidance around how to support individuals who have not been able to come to terms with the unpredictability of their illness. Furthermore, the findings highlight the wide reaching impact of unpredictability emphasising the importance of the family team. These findings may offer health professionals guidance around providing family education and support to help develop a cohesive network of support for the individual and the family experiencing the effects of unpredictability in MS.
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Pashkovskyy, V. M. "Depression and anxiety with multiple sclerosis". Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18746.
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Kharel, Prakash. "RNA OXIDATION IN MULTIPLE SCLEROSIS NEURODEGENERATION". Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1540822739224289.
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Langer-Gould, Annette. "T cells, pregnancy and multiple sclerosis /". May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
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Alali, Dalal. "Dysphagia in Adults with Multiple Sclerosis". Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20807.
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Dysphagia, or swallowing impairment, may affect adults diagnosed with Multiple Sclerosis (MS) but prevalence estimates vary greatly. Unreliable estimates may be contributing to the lack of established protocols for diagnosing and treating dysphagia in MS and, therefore, a heightened risk of adverse outcomes. This thesis addresses these issues in four studies. First, a self-report questionnaire was given to 103 adults with MS in a metropolitan outpatient clinic. Responses revealed that 38% of cases had swallowing problems, with both physical and social consequences. These findings suggest that dysphagia in MS is relatively common and routine screening should be done to establish optimal care. The second study aimed to validate an existing diagnostic tool, the 10-item Dysphagia in Multiple Sclerosis (DYMUS) questionnaire. Analyses revealed that a 5-item DYMUS had high internal consistency, satisfactory reproducibility, and adequate correlation with the commonly used 10-item Eating Assessment Tool (EAT-10). The 5-item DYMUS is a valid tool that is quick to administer and score. Once diagnosed with dysphagia, preventive or compensatory treatment can reduce symptoms of dysphagia, such as weight loss and aspiration pneumonia. A systematic review was conducted to identify the best available treatment options for MS-related dysphagia. Five studies were identified, with two showing positive therapeutic effects but limited internal validity. Therefore, a randomized controlled trial was conducted to compare one of these interventions, neuromuscular electrical stimulation plus exercise (n = 6), to sham stimulation plus exercise (n = 6). Symptoms of dysphagia were significantly more reduced in those receiving the active condition, providing the strongest evidence to date for dysphagia treatment in MS. Finally, findings across the studies are summarised. In addition, evidence-based recommendations for clinical practice, thesis limitations and future directions are discussed.
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Spear, Estelle Trego. "Altered Gastrointestinal Motility in Multiple Sclerosis". ScholarWorks @ UVM, 2018. https://scholarworks.uvm.edu/graddis/837.
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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system that causes motor, visual, and sensory symptoms. Patients also experience constipation, which is not yet understood, but could involve dysfunction of the enteric nervous system (ENS). Autoimmune targeting of the ENS occurs in other autoimmune diseases that exhibit gastrointestinal (GI) symptoms, and similar mechanisms could lead to GI dysfunction in MS. Here, we characterize GI dysmotility in the experimental autoimmune encephalomyelitis (EAE) model of MS and test whether autoantibodies targeting the ENS are present in the serum of MS patients.
Male SJL or B6 mice were induced with EAE by immunization against PLP139-151, MOG35-55, or mouse spinal cord homogenate, and monitored daily for somatic motor symptoms. EAE mice developed GI symptoms consistent with those observed in MS. In vivo motility analysis demonstrated slower whole GI transit, and decreased colonic propulsive motility. EAE mice had faster rates of gastric emptying, with no changes in small intestinal motility. Consistent with these results, ex vivo evaluation of isolated colons demonstrated that EAE mice have slower colonic migrating myoelectric complexes and slow wave contractions. Immunohistochemistry of EAE colons exhibited a significant reduction in GFAP area of ENS ganglia, with no changes in HuD, S100, or neuron numbers.
To test whether antibodies in MS bind to ENS structures, we collected serum samples from MS patients with constipation and without constipation, and healthy control patients without constipation. Immunoreactivity was tested using indirect immunofluorescence by applying serum samples to guinea pig ENS tissue. MS serum exhibited significantly higher immunoreactivity against guinea pig ENS than control patients, which was particularly evident in MS patients who did not experience constipation. There was no significant difference in immunoreactivity between MS patients with and without constipation. Targets of human MS and mouse EAE serum include enteric glia and neurons.
Taken together, these data validate EAE as a model for constipation in MS, and support the concept that this symptom involves changes within the neuromuscular system of the colon. EAE mice develop symptoms consistent with constipation that affects functional ENS networks and may result in structural or phenotypic changes at the cellular level. Serum immunoreactivity suggests that autoantibodies could play a role in the development of constipation in MS by targeting the ENS itself.