scholarly journals RORγt Expression and Lymphoid Neogenesis in the Brain of Patients with Secondary Progressive Multiple Sclerosis

2016 ◽  
Vol 75 (9) ◽  
pp. 877-888 ◽  
Author(s):  
Barbara Serafini ◽  
Barbara Rosicarelli ◽  
Caterina Veroni ◽  
Ling Zhou ◽  
Camilla Reali ◽  
...  
2010 ◽  
Vol 17 (3) ◽  
pp. 289-296 ◽  
Author(s):  
I-Y Choi ◽  
S-P Lee ◽  
DR Denney ◽  
SG Lynch

Background: Disability levels for patients with secondary progressive multiple sclerosis (SPMS) often worsen despite a stable MRI T2 lesion burden. The presence of oxidative stress in the absence of measurable inflammation could help explain this phenomenon. In this study, the assessment of an in vivo marker of oxidative stress, cerebral glutathione (GSH), using magnetic resonance chemical shift imaging (CSI) is described, and GSH levels were compared in patients with SPMS and healthy controls. Objective: To assess whether GSH, a key antioxidant in the brain, is lower in the SPMS patients compared to matched controls. Methods: Seventeen patients with SPMS (Expanded Disability Status Scale = 4.0–7.0; length of MS diagnosis = 19.4 ± 7 years) and 17 age- and gender-matched healthy controls were studied. GSH levels were measured in the fronto-parietal regions of the brain using a specially designed magnetic resonance spectroscopy technique, CSI of GSH, at 3T. Results: The levels of GSH were lower for SPMS patients than for controls, the largest reduction (18.5%) being in the frontal region ( p = 0.001). Conclusion: The lower GSH levels in these patients indicate the presence of oxidative stress in SPMS. This process could be at least partially responsible for ongoing functional decline in SPMS.


2019 ◽  
Vol 22 (3) ◽  
pp. 123-128
Author(s):  
Ishu Arpan ◽  
Brett Fling ◽  
Katherine Powers ◽  
Fay B. Horak ◽  
Rebecca I. Spain

Abstract Background: Secondary progressive multiple sclerosis (SPMS) is characterized by worsening of postural control and brain atrophy. However, little is known about postural deficits and their neuroanatomical correlates in this population. We aimed to determine the neuroanatomical correlates of postural deficits in people with SPMS and whether posture control deteriorates concomitantly with the brain and spinal cord atrophy in 2 years in SPMS. Methods: This study is a post hoc analysis of data from 27 people with SPMS (mean ± SE age, 58.6 ± 1.1 years). Participants had magnetic resonance imaging (MRI) of the brain and cervical spinal cord followed by sway testing using inertial sensors during standing with eyes open (EO) and eyes closed without (EC) and with (ECC) a cognitive task. Partial correlations investigated relationships between postural control and MRI measures at baseline and 2 years. Results: At baseline, sway measures were inversely related to cortical thickness and cord cross-sectional area (CSA) during the EO task but only to cord CSA with EC (P < .05). After 2 years, the percentage change in sway amplitude and dispersion during EO tasks significantly related to the percentage decline in cord CSA (P < .01). Conclusions: Cortical and spinal cord inputs are essential for regulation of postural control during standing with EO in SPMS. Without visual input, people with SPMS preferentially rely on somatosensory inputs from the spinal cord for maintaining postural control. Postural deficits related to cord atrophy over 2 years, suggesting that postural control may be a surrogate marker of disease progression in people with SPMS.


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