scholarly journals Correction to: Detecting neurodegenerative pathology in multiple sclerosis before irreversible brain tissue loss sets in

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Jeroen Van Schependom ◽  
Kaat Guldolf ◽  
Marie Béatrice D’hooghe ◽  
Guy Nagels ◽  
Miguel D’haeseleer
Keyword(s):  
Multiple Sclerosis ◽  
Brain Tissue ◽  
Tissue Loss ◽  
Original Publication ◽  
Neurodegenerative Pathology

In the original publication of this article [1], the following statement should be added in the Acknowledgement section.

Interferon beta-1a for brain tissue loss in patients at presentation with syndromes suggestive of multiple sclerosis: a randomised, double-blind, placebo-controlled trial

The Lancet ◽  
2004 ◽  
Vol 364 (9444) ◽  
pp. 1489-1496 ◽  
Author(s):  
Massimo Filippi ◽  
Marco Rovaris ◽  
Matilde Inglese ◽  
Frederik Barkhof ◽  
Nicola De Stefano ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Brain Tissue ◽  
Interferon Beta ◽  
Controlled Trial ◽  
Tissue Loss ◽  
Double Blind ◽  
Double Blind Placebo

Brain atrophy in multiple sclerosis: impact of lesions and of damage of whole brain tissue

2002 ◽  
Vol 8 (5) ◽  
pp. 410-414 ◽  
Author(s):  
N F Kalkers ◽  
H Vrenken ◽  
B MJ Uitdehaag ◽  
C H Polman ◽  
F Barkhof
Keyword(s):  
Multiple Sclerosis ◽  
Brain Tissue ◽  
Brain Atrophy ◽  
Brain Volume ◽  
Peak Height ◽  
Tissue Loss ◽  
Magnetization Transfer Ratio ◽  
Lesion Volume ◽  
Intracranial Volume ◽  
Whole Brain

Introduction: In multiple sclerosis (MS), brain atrophy measurement on magnetic resonance imaging (MRI) reflects overall tissue loss, especially demyelination and axonal loss. We studied which factor contributes most to the development of brain atrophy: extent and severity of lesions or damage of whole brain tissue (WBT). Methods: Eighty-six patients with MS [32 primary progressive (PP), 32 secondary progressive (SP)] and 22 relapsing-remitting (RR) were studied. MRI included T1- and T2-weighted imaging to obtain hypointense T1 lesion volume (T1LV) and two brain volume measurements: 1) the parenchymal fraction (PF; whole brain parenchymal volume/intracranial volume) as a marker of overall brain volume, and 2) the ventricular fraction (VF; ventricular volume/intracranial volume) as a marker of central atrophy. From magnetization transfer ratio (MTR) histograms, the relative peak height (rHp) was derived as an index of damage of WBT (a lower peak height reflects damage of WBT). Results: Multiple linear regression analysis revealed that damage of WBT explains most of the variance of PF (standardized coefficient b=0.59, p <0.001 for WBT and b= −0.19, p <0.05 for T1LV). These findings are independent of disease phase; even in RR patients, damage of WBT plays a dominant role in explaining the variance in overall brain volume. By contrast, the variance in VF is explained by both T1LV and damage of WBT (standardized coefficient b =0.43, p<0.001 for T1LV and b = −0.38, p <0.001 for WBT). Conclusion: This study shows that overall brain volume (PF) is best explained by damage of WBT, supporting the significance of nonfocal pathology in MS in producing tissue loss. Central atrophy (VF) is determined by both lesion volume and damage of WBT. Our results underline the importance of nonfocal pathology even in the early (RR) phase of the disease.

Acute and chronic synaptic pathology in multiple sclerosis gray matter

2021 ◽  
pp. 135245852110221
Author(s):  
Marco Vercellino ◽  
Stella Marasciulo ◽  
Silvia Grifoni ◽  
Elena Vallino-Costassa ◽  
Chiara Bosa ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Brain Tissue ◽  
Gray Matter ◽  
Axonal Loss ◽  
Strong Indication ◽  
Synaptic Loss ◽  
Synaptic Density ◽  
Synaptic Pathology ◽  
Gabaergic Synapses ◽  
And Control

Objectives: To investigate the extent of synaptic loss, and the contribution of gray matter (GM) inflammation and demyelination to synaptic loss, in multiple sclerosis (MS) brain tissue. Methods: This study was performed on two different post-mortem series of MS and control brains, including deep GM and cortical GM. MS brain samples had been specifically selected for the presence of active demyelinating GM lesions. Over 1,000,000 individual synapses were identified and counted using confocal microscopy, and further characterized as glutamatergic/GABAergic. Synaptic counts were also correlated with neuronal/axonal loss. Results: Important synaptic loss was observed in active demyelinating GM lesions (−58.9%), while in chronic inactive GM lesions, synaptic density was only mildly reduced compared to adjacent non-lesional gray matter (NLGM) (−12.6%). Synaptic loss equally affected glutamatergic and GABAergic synapses. Diffuse synaptic loss was observed in MS NLGM compared to control GM (−21.2% overall). Conclusion: This study provides evidence, in MS brain tissue, of acute synaptic damage/loss during active GM inflammatory demyelination and of synaptic reorganization in chronically demyelinated GM, affecting equally glutamatergic and GABAergic synapses. Furthermore, this study provides a strong indication of widespread synaptic loss in MS NLGM also independently from focal GM demyelination.

Detection of Herpesviridae in postmortem multiple sclerosis brain tissue and controls by polymerase chain reaction

1996 ◽  
Vol 2 (4) ◽  
pp. 249-258 ◽  
Author(s):  
Virginia J Sanders ◽  
Stephen Felisan ◽  
Aimee Waddell ◽  
Wallace W Tourtellotte
Keyword(s):  
Multiple Sclerosis ◽  
Polymerase Chain Reaction ◽  
Brain Tissue ◽  
Chain Reaction ◽  
Polymerase Chain

Progressive brain tissue loss in schizophrenia

2016 ◽  
Vol 173 (3) ◽  
pp. 121-123 ◽  
Author(s):  
Neeltje E.M. van Haren ◽  
René S. Kahn
Keyword(s):  
Brain Tissue ◽  
Tissue Loss

Detection of lithocholic acid in multiple sclerosis brain tissue

Lipids ◽  
1970 ◽  
Vol 5 (6) ◽  
pp. 578-580 ◽  
Author(s):  
S. H. Mujtaba Naqvi ◽  
Robert B. Ramsey ◽  
H. J. Nicholas
Keyword(s):  
Multiple Sclerosis ◽  
Brain Tissue ◽  
Lithocholic Acid

Abstract T P234: Multiparametric Assessment of Longitudinal Changes in Tissue Microstructure in Normal and Abnormal Brain Tissue in Patients with Small Vessel Disease

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Maria D Valdes-Hernandez ◽  
Paul A Armitage ◽  
Eleni Sakka ◽  
Susana Munoz Maniega ◽  
Natalie A Royle ◽  
...  
Keyword(s):  
White Matter ◽  
Brain Tissue ◽  
Small Vessel Disease ◽  
Brain Mri ◽  
Mean Diffusivity ◽  
Tissue Loss ◽  
Minor Stroke ◽  
Normal Brain ◽  
Limited Information ◽  
Time Points

Background: Volume measures of normal brain tissue and white matter hyperintensities (WMH) between two time points gives limited information about the complex dynamics of tissue change. We evaluated two quantitative parameters that characterise the microstructure of normal-appearing white matter (NAWM), deep grey matter (DGM) and WMH on brain images obtained at presentation with minor stroke and at 1 year to investigate the microstructural changes. Methods: From 182 brain MRI datasets of patients with minor stroke obtained at baseline and 1 year, we extracted the WMH, DGM and NAWM, and separated WMH into less-intense and intense WMH, using validated semi-automatic methods and validated criteria. We registered the binary structural masks to diffusion space and performed a voxel-wise subtraction of the combined masks at both time points. Then we measured fractional anisotropy (FA) and mean diffusivity (MD)(valuex10 -9 m 2 /s) in each tissue mask at baseline and 1 year. Results: WMH volume median increase was 1.4ml (IQR 6.98) mainly due to changes in less-intense WMH: 0.94ml (7.13). WMH that were visible at both time points, ie damage that remained after a year, had the lowest FA= 0.21(0.06) and highest MD=1.05(0.12) at baseline, and were mainly intense WMH at baseline (FA=0.12(0.03), MD=1.55(0.27)). WMH seen only at follow-up, ie that were NAWM at baseline, had the highest FA=0.30(0.06) and lowest MD=0.85 (0.06) at baseline. WMH that were observed only at baseline had intermediate FA=0.26(0.08) and MD=0.90(0.10). NAWM FA=0.26(0.03), MD=0.78(0.04) and DGM FA=0.23(0.03), MD=0.79(0.06) did not change between time points. Conclusions: WMH at baseline can partially evolve to normal-appearing tissues, remain or precede tissue loss. Differentiation between severe and subtle damage and spatial analysis are necessary to characterise the dynamic of WMH evolution.

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