scholarly journals Microstructural MRI Correlates of Cognitive Impairment in Multiple Sclerosis: The Role of Deep Gray Matter

Diagnostics ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1103
Author(s):  
Marco Pitteri ◽  
Ilaria Boscolo Galazzo ◽  
Lorenza Brusini ◽  
Federica Cruciani ◽  
Caterina Dapor ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cognitive Impairment ◽  
Gray Matter ◽  
Diffusion Mri ◽  
Cognitively Normal ◽  
Superior Frontal Gyrus ◽  
Microstructural Damage ◽  
Deep Gray Matter ◽  
Cortical Regions

Although cognitive impairment (CI) is frequently observed in people with multiple sclerosis (pwMS), its pathogenesis is still controversial. Conflicting results emerged concerning the role of microstructural gray matter (GM) damage especially when involving the deep GM structures. In this study, we aimed at evaluating whether differences in cortical and deep GM structures between apparently cognitively normal (ACN) and CI pwMS (36 subjects in total) are present, using an extensive set of diffusion MRI (dMRI) indices and conventional morphometry measures. The results revealed increased anisotropy and restriction over several deep GM structures in CI compared with ACN pwMS, while no changes in volume were present in the same areas. Conversely, reduced anisotropy/restriction values were detected in cortical regions, mostly the pericalcarine cortex and precuneus, combined with reduced thickness of the superior frontal gyrus and insula. Most of the dMRI metrics but none of the morphometric indices correlated with the Symbol Digit Modality Test. These results suggest that deep GM microstructural damage can be a strong anatomical substrate of CI in pwMS and might allow identifying pwMS at higher risk of developing CI.

scholarly journals Intrathecal Inflammation in Progressive Multiple Sclerosis

2020 ◽  
Vol 21 (21) ◽  
pp. 8217
Author(s):  
Salvatore Monaco ◽  
Richard Nicholas ◽  
Richard Reynolds ◽  
Roberta Magliozzi
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Gray Matter ◽  
Molecular Mechanisms ◽  
Progressive Multiple Sclerosis ◽  
Brain Parenchyma ◽  
Inflammatory Factors ◽  
Deep Gray Matter ◽  
Bidirectional Exchange

Progressive forms of multiple sclerosis (MS) are associated with chronic demyelination, axonal loss, neurodegeneration, cortical and deep gray matter damage, and atrophy. These changes are strictly associated with compartmentalized sustained inflammation within the brain parenchyma, the leptomeninges, and the cerebrospinal fluid. In progressive MS, molecular mechanisms underlying active demyelination differ from processes that drive neurodegeneration at cortical and subcortical locations. The widespread pattern of neurodegeneration is consistent with mechanisms associated with the inflammatory molecular load of the cerebrospinal fluid. This is at variance with gray matter demyelination that typically occurs at focal subpial sites, in the proximity of ectopic meningeal lymphoid follicles. Accordingly, it is possible that variations in the extent and location of neurodegeneration may be accounted for by individual differences in CSF flow, and by the composition of soluble inflammatory factors and their clearance. In addition, “double hit” damage may occur at sites allowing a bidirectional exchange between interstitial fluid and CSF, such as the Virchow–Robin spaces and the periventricular ependymal barrier. An important aspect of CSF inflammation and deep gray matter damage in MS involves dysfunction of the blood–cerebrospinal fluid barrier and inflammation in the choroid plexus. Here, we provide a comprehensive review on the role of intrathecal inflammation compartmentalized to CNS and non-neural tissues in progressive MS.

scholarly journals Iron and Volume in the Deep Gray Matter: Association with Cognitive Impairment in Multiple Sclerosis

2014 ◽  
Vol 36 (1) ◽  
pp. 57-62 ◽  
Author(s):  
C. M. Modica ◽  
R. Zivadinov ◽  
M. G. Dwyer ◽  
N. Bergsland ◽  
A. R. Weeks ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cognitive Impairment ◽  
Gray Matter ◽  
Deep Gray Matter

Detection of Cortical and Deep Gray Matter Lesions in Multiple Sclerosis Using DIR and FLAIR at 3T

2020 ◽  
Author(s):  
Charlie C. Park ◽  
Dean W. Thongkham ◽  
Gelareh Sadigh ◽  
Amit M. Saindane ◽  
Renxin Chu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Gray Matter ◽  
Deep Gray Matter

NODDI microstructural abnormalities in normal-appearing gray matter and white matter contribute to cognitive impairment in multiple sclerosis

2021 ◽  
Vol 429 ◽  
pp. 118088
Author(s):  
Paolo Preziosa ◽  
Lorenzo Conti ◽  
Elisabetta Pagani ◽  
Olga Marchesi ◽  
Maria Rocca ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cognitive Impairment ◽  
White Matter ◽  
Gray Matter

scholarly journals Cerebral Arterial Bolus Arrival Time is Prolonged in Multiple Sclerosis and Associated with Disability

2013 ◽  
Vol 34 (1) ◽  
pp. 34-42 ◽  
Author(s):  
David Paling ◽  
Esben Thade Petersen ◽  
Daniel J Tozer ◽  
Daniel R Altmann ◽  
Claudia AM Wheeler-Kingshott ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Gray Matter ◽  
Arrival Time ◽  
Arterial Hemodynamics ◽  
Normal Appearing White Matter ◽  
Imaging Sequence ◽  
Disability Status ◽  
Relapsing Remitting ◽  
Bolus Arrival Time ◽  
Deep Gray Matter

Alterations in the overall cerebral hemodynamics have been reported in multiple sclerosis (MS); however, their cause and significance is unknown. While potential venous causes have been examined, arterial causes have not. In this study, a multiple delay time arterial spin labeling magnetic resonance imaging sequence at 3T was used to quantify the arterial hemodynamic parameter bolus arrival time (BAT) and cerebral blood flow (CBF) in normal-appearing white matter (NAWM) and deep gray matter in 33 controls and 35 patients with relapsing–remitting MS. Bolus arrival time was prolonged in MS in NAWM (1.0±0.2 versus 0.9±0.2 seconds, P=0.031) and deep gray matter (0.90±0.18 versus 0.80±0.14 seconds, P=0.001) and CBF was increased in NAWM (14±4 versus 10±2 mL/100 g/min, P=0.001). Prolonged BAT in NAWM ( P=0.042) and deep gray matter ( P=0.01) were associated with higher expanded disability status score. This study demonstrates alteration in cerebral arterial hemodynamics in MS. One possible cause may be widespread inflammation. Bolus arrival time was longer in patients with greater disability independent of atrophy and T2 lesion load, suggesting alterations in cerebral arterial hemodynamics may be a marker of clinically relevant pathology.

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