Audiovestibular symptoms in patients with multiple sclerosis: A correlation between self-reported symptomatology and MRI findings to monitor disease progression

2020 ◽  
Vol 45 ◽  
pp. 102431 ◽  
Author(s):  
Arianna Di Stadio ◽  
Massimo Ralli ◽  
Marta Altieri ◽  
Antonio Greco ◽  
Daniela Messineo ◽  
...  
2009 ◽  
Vol 36 (S 02) ◽  
Author(s):  
A Hahn ◽  
T Schmidt-Wilcke ◽  
S Prügl ◽  
G Schuierer ◽  
U Bogdahn ◽  
...  

2020 ◽  
Vol 19 (6) ◽  
pp. 376-385
Author(s):  
Md. A. Islam ◽  
Shoumik Kundu ◽  
Rosline Hassan

Multiple Sclerosis (MS) is the most common autoimmune demyelinating disease of the Central Nervous System (CNS). It is a multifactorial disease which develops in an immune-mediated way under the influences of both genetic and environmental factors. Demyelination is observed in the brain and spinal cord leading to neuro-axonal damage in patients with MS. Due to the infiltration of different immune cells such as T-cells, B-cells, monocytes and macrophages, focal lesions are observed in MS. Currently available medications treating MS are mainly based on two strategies; i) to ease specific symptoms or ii) to reduce disease progression. However, these medications tend to induce different adverse effects with limited therapeutic efficacy due to the protective function of the blood-brain barrier. Therefore, researchers have been working for the last four decades to discover better solutions by introducing gene therapy approaches in treating MS generally by following three strategies, i) prevention of specific symptoms, ii) halt or reverse disease progression and iii) heal CNS damage by promoting remyelination and axonal repair. In last two decades, there have been some remarkable successes of gene therapy approaches on the experimental mice model of MS - experimental autoimmune encephalomyelitis (EAE) which suggests that it is not far that the gene therapy approaches would start in human subjects ensuring the highest levels of safety and efficacy. In this review, we summarised the gene therapy approaches attempted in different animal models towards treating MS.


Author(s):  
D.W. Paty

ABSTRACT:MS could well be a two stage disease. The first stage involves the sequential development of multiple small lesions, mostly inflammatory, that accumulate at a given rate. The second stage could be that of consolidation and confluence of lesions that involves not only demyelination but gliosis. MRI now gives us an opportunity to watch the evolution of these processes and also to monitor treatment effects. It is only after the evolution of this process is understood that we can design rational therapies directed toward the prevention of spasticity in MS.


2007 ◽  
Author(s):  
Alexis Wong ◽  
Arkadiusz Gertych ◽  
Chi-Shing Zee ◽  
Bing Guo ◽  
Brent J. Liu

2012 ◽  
Vol 18 (11) ◽  
pp. 1577-1584 ◽  
Author(s):  
Lukas Filli ◽  
Louis Hofstetter ◽  
Pascal Kuster ◽  
Stefan Traud ◽  
Nicole Mueller-Lenke ◽  
...  

Background: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. MS lesions show a typical distribution pattern and primarily affect the white matter (WM) in the periventricular zone and in the centrum semiovale. Objective: To track lesion development during disease progression, we compared the spatiotemporal distribution patterns of lesions in relapsing–remitting MS (RRMS) and secondary progressive MS (SPMS). Methods: We used T1 and T2 weighted MR images of 209 RRMS and 62 SPMS patients acquired on two different 1.5 Tesla MR scanners in two clinical centers followed up for 25 (± 1.7) months. Both cross-sectional and longitudinal differences in lesion distribution between RRMS and SPMS patients were analyzed with lesion probability maps (LPMs) and permutation-based inference. Results: MS lesions clustered around the lateral ventricles and in the centrum semiovale. Cross-sectionally, compared to RRMS patients, the SPMS patients showed a significantly higher regional probability of T1 hypointense lesions ( p≤0.03) in the callosal body, the corticospinal tract, and other tracts adjacent to the lateral ventricles, but not of T2 lesions (peak probabilities were RRMS: T1 9%, T2 18%; SPMS: T1 21%, T2 27%). No longitudinal changes of regional T1 and T2 lesion volumes between baseline and follow-up scan were found. Conclusion: The results suggest a particular vulnerability to neurodegeneration during disease progression in a number of WM tracts.


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