Advances in understanding gray matter pathology in multiple sclerosis
Advances in understanding [URL="http://www.biomedcentral.com/content/pd ... 7-12-9.pdf"][U]gray matter[/U][/URL] pathology in multiple sclerosis: Are we ready to redefine disease pathogenesis?
[QUOTE]The purpose of this special issue in BMC Neurology is to summarize advances in our understanding of the pathological, immunological, imaging and clinical concepts of gray matter (GM) pathology in patients with multiple sclerosis (MS).
Review articles by Lucchinetti and Popescu, Walker and colleagues, Hulst and colleagues and Horakova and colleagues summarize important recent advances in understanding GM damage and its implications to MS pathogenesis. They also raise a number of important new questions and outline comprehensive approaches to addressing those questions in years to come.
In the last decade, the use of immunohistochemistry staining methods and more advanced imaging techniques to detect GM lesions, like double inversion recovery, contributed to a surge of studies related to cortical and subcortical GM pathology in MS. It is becoming more apparent from recent biopsy studies that subpial cortical lesions in early MS are highly inflammatory.
The mechanisms responsible for triggering meningeal inflammation in MS patients are not yet elucidated, and they should be further investigated in relation to their role in initiating and perpetuating the disease process. Determining the role of antigens, environmental and genetic factors in the pathogenesis of GM involvement in MS is critical.
The early involvement of cortical and subcortical GM damage in MS is very intriguing and needs to be further studied. As established in numerous cross-sectional and longitudinal studies, GM damage is a better predictor of physical disability and cognitive impairment than WM damage. Monitoring the evolution of GM damage is becoming an important marker in predicting future disease course and response to therapy in MS patients.[/QUOTE]
Reactie van Marie Rhodes hierop op [URL="https://www.facebook.com/pages/CCSVI-in ... 297?ref=ts"][U]FB[/U][/URL]:
[QUOTE]this has been a long time coming for the focus of MS to shift from white matter to grey matter disease because there has been research for years suggesting that grey matter changes are far more associated with progression that white matter lesions.
The reason this matters to us is that ALL of the current drug therapies are shown to impact white matter inflammation: but we only have evidence of impact on white matter lesions and inflammation; we don't actually know what they do to grey matter inflammation or degeneration. Many MS experts assume that this reduction in white matter inflammation will necessarily result in less degeneration and grey matter damage over time, but this is an assumption based on the idea that the WM inflammation is the beginning step that leads to GM damage. SUch a theory is just an unproven hypothesis.[/QUOTE]
[QUOTE]of course I think current therapies are not very effective because they do leave the main problem unaddressed--and GM damage and how it relates to CCSVI is an area that is un-investigated at this time, but to me the possibility that the venous changes impact the meninges and GM is obvious. I'd be very interested in what they know about all this some 20 years from now... ;-) research and more research![/QUOTE]
Witte stof / grijze stof
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Sara
Prijs
Prijs
Een prijs voor Jeroen Geurts voor zijn onderzoek naar de betrokkenheid van grijze stof bij MS:
[url]https://www.hersenstichting.nl/actueel/ ... etail.html[/url]
Een prijs voor Jeroen Geurts voor zijn onderzoek naar de betrokkenheid van grijze stof bij MS:
[url]https://www.hersenstichting.nl/actueel/ ... etail.html[/url]
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Marsei
Mapping regional grey and white matter atrophy in relapsing–remitting MS
Mapping regional grey and white matter atrophy in relapsing–remitting MS
Mapping regional [URL="http://msj.sagepub.com/content/early/20 ... 9.abstract"][U]grey and white matter atrophy[/U][/URL] in relapsing–remitting multiple sclerosis
[QUOTE][B]Results[/B]: Patients with RRMS experienced atrophy of the deep GM nuclei, and several cortical regions mainly located in the fronto-parietal lobes. WM atrophy involved posterior regions of the brain, including the cerebellum and brainstem.
Compared with men, affected women showed atrophy of several WM tracts, while gender did not impact GM atrophy. Disease duration > 5 years was associated with atrophy of the thalami and inferior frontal gyrus, while WM atrophy was already prominent in patients with disease duration ≤ 5 years. Expanded Disability Status Scale score > 3.0 was associated with diffuse WM atrophy and basal ganglia and precentral gyrus atrophy. T2 lesions were marginally associated to focal atrophy.
[B]Discussion[/B]: In RRMS, GM and WM atrophy have distinct patterns of regional distribution, with a sparing of GM infratentorial regions. Gender, disease duration and disability affect differently the topography of GM/WM atrophy, while T2 lesions play a modest role.[/QUOTE]
Mapping regional [URL="http://msj.sagepub.com/content/early/20 ... 9.abstract"][U]grey and white matter atrophy[/U][/URL] in relapsing–remitting multiple sclerosis
[QUOTE][B]Results[/B]: Patients with RRMS experienced atrophy of the deep GM nuclei, and several cortical regions mainly located in the fronto-parietal lobes. WM atrophy involved posterior regions of the brain, including the cerebellum and brainstem.
Compared with men, affected women showed atrophy of several WM tracts, while gender did not impact GM atrophy. Disease duration > 5 years was associated with atrophy of the thalami and inferior frontal gyrus, while WM atrophy was already prominent in patients with disease duration ≤ 5 years. Expanded Disability Status Scale score > 3.0 was associated with diffuse WM atrophy and basal ganglia and precentral gyrus atrophy. T2 lesions were marginally associated to focal atrophy.
[B]Discussion[/B]: In RRMS, GM and WM atrophy have distinct patterns of regional distribution, with a sparing of GM infratentorial regions. Gender, disease duration and disability affect differently the topography of GM/WM atrophy, while T2 lesions play a modest role.[/QUOTE]
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Marsei
Grijze stof atrofie al bij begin van MS
Grijze stof atrofie al bij begin van MS
Subcortical and Cortical [URL="http://www.ncbi.nlm.nih.gov/pubmed/22499842"][U]Gray Matter Atrophy[/U][/URL] in a Large Sample of Patients with Clinically Isolated Syndrome and Early Relapsing-Remitting Multiple Sclerosis.
[QUOTE][B]CONCLUSION[/B]: Significant SDGM (Subcortical Deep Gray Matter), but not cortical, atrophy develops during the first 4 years of the RRMS. GM atrophy is relevant for disease progression from the earliest clinical stages.[/QUOTE]
[B]Subcorticale atrofie (SDGM)[/B]: een toename van het volume van de ventrikels is een teken van subcorticale atrofie (atrofie van het binnenste gedeelte van de hersenen).
[B]Corticale atrofie[/B] : een afname in het volume van de grijze stof aan de buitenkant van de hersenen
Subcortical and Cortical [URL="http://www.ncbi.nlm.nih.gov/pubmed/22499842"][U]Gray Matter Atrophy[/U][/URL] in a Large Sample of Patients with Clinically Isolated Syndrome and Early Relapsing-Remitting Multiple Sclerosis.
[QUOTE][B]CONCLUSION[/B]: Significant SDGM (Subcortical Deep Gray Matter), but not cortical, atrophy develops during the first 4 years of the RRMS. GM atrophy is relevant for disease progression from the earliest clinical stages.[/QUOTE]
[B]Subcorticale atrofie (SDGM)[/B]: een toename van het volume van de ventrikels is een teken van subcorticale atrofie (atrofie van het binnenste gedeelte van de hersenen).
[B]Corticale atrofie[/B] : een afname in het volume van de grijze stof aan de buitenkant van de hersenen
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Marsei
IJzerdepots voorafgaand aan atrofie
IJzerdepots voorafgaand aan atrofie
[URL="http://www.ajnr.org/content/early/2012/ ... 0.abstract"][U]Iron Deposition[/U][/URL] on SWI-Filtered Phase in the Subcortical Deep Gray Matter of Patients with Clinically Isolated Syndrome May Precede Structure-Specific Atrophy
[QUOTE][B]CONCLUSION[/B]: Patients with CIS showed significantly increased content and volume of iron, as determined by abnormal SWI-phase measurement, in the various SDGM structures, suggesting that iron deposition may precede structure-specific atrophy.[/QUOTE]
[URL="http://www.ajnr.org/content/early/2012/ ... 0.abstract"][U]Iron Deposition[/U][/URL] on SWI-Filtered Phase in the Subcortical Deep Gray Matter of Patients with Clinically Isolated Syndrome May Precede Structure-Specific Atrophy
[QUOTE][B]CONCLUSION[/B]: Patients with CIS showed significantly increased content and volume of iron, as determined by abnormal SWI-phase measurement, in the various SDGM structures, suggesting that iron deposition may precede structure-specific atrophy.[/QUOTE]
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Marsei
Gray matters!!
Gray matters!!
Van Joan op [URL="https://www.facebook.com/notes/ccsvi-in ... 1434857211"][U]FB[/U][/URL]: Gray matters!!
Van Joan op [URL="https://www.facebook.com/notes/ccsvi-in ... 1434857211"][U]FB[/U][/URL]: Gray matters!!
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Marsei
Nederlands onderzoek
Nederlands onderzoek
[URL="http://www.ncbi.nlm.nih.gov/pubmed/23042930"][U]Multicontrast MR Imaging at 7T[/U][/URL] in Multiple Sclerosis: Highest Lesion Detection in Cortical Gray Matter with 3D-FLAIR.
[QUOTE][B]BACKGROUND AND PURPOSE[/B]:7T MR imaging has led to improved detection and classification of cortical MS lesions, mainly based on T2*-weighted gradient-echo sequences. Depiction of cortical GM by using the recommended MS imaging protocol has not yet been investigated at 7T. We aimed to investigate prospectively which recommended sequence for clinical use has the highest value at 7T, in terms of GM and WM lesion detection.
[B]MATERIALS AND METHODS[/B]:Thirty-seven patients with MS (mean age, 43.8 years; 25 women) and 7 healthy controls (mean age, 40.4 years; 5 women) underwent multicontrast 7T MR imaging including the recommended clinical 2D-T2WI, 3D-T1WI, 3D-FLAIR, and GMspecific 3D-DIR. Lesions were scored and categorized anatomically by 3 raters, in consensus. The value of sequences was evaluated lesion-wise and patient-wise (Wilcoxon signed-rank test).
[B]RESULTS[/B]:At 7T, 3D-FLAIR detected the highest number of total cortical GM lesions (217), 89% more than 3D-DIR and 87% and 224% more than 2D-T2WI and 3D-T1WI. Patient-wise analysis showed that this difference between 3D-FLAIR and 3D-DIR was statistically significant (P<.04), and most pronounced for the number of mixed lesions (P<.03). 3D-FLAIR also detected the highest number of total WM lesions (2605), but the difference with 3D-DIR and 3D-T1WI was not significant.
[B]CONCLUSIONS[/B]:When using recommended clinical sequences at 7T, the best way to detect corticalGMlesions is with 3D-FLAIR and not by GM-specific 3D-DIR or by conventional 2D-T2WI and 3D-T1WI sequences.[/QUOTE]
[URL="http://www.ncbi.nlm.nih.gov/pubmed/23042930"][U]Multicontrast MR Imaging at 7T[/U][/URL] in Multiple Sclerosis: Highest Lesion Detection in Cortical Gray Matter with 3D-FLAIR.
[QUOTE][B]BACKGROUND AND PURPOSE[/B]:7T MR imaging has led to improved detection and classification of cortical MS lesions, mainly based on T2*-weighted gradient-echo sequences. Depiction of cortical GM by using the recommended MS imaging protocol has not yet been investigated at 7T. We aimed to investigate prospectively which recommended sequence for clinical use has the highest value at 7T, in terms of GM and WM lesion detection.
[B]MATERIALS AND METHODS[/B]:Thirty-seven patients with MS (mean age, 43.8 years; 25 women) and 7 healthy controls (mean age, 40.4 years; 5 women) underwent multicontrast 7T MR imaging including the recommended clinical 2D-T2WI, 3D-T1WI, 3D-FLAIR, and GMspecific 3D-DIR. Lesions were scored and categorized anatomically by 3 raters, in consensus. The value of sequences was evaluated lesion-wise and patient-wise (Wilcoxon signed-rank test).
[B]RESULTS[/B]:At 7T, 3D-FLAIR detected the highest number of total cortical GM lesions (217), 89% more than 3D-DIR and 87% and 224% more than 2D-T2WI and 3D-T1WI. Patient-wise analysis showed that this difference between 3D-FLAIR and 3D-DIR was statistically significant (P<.04), and most pronounced for the number of mixed lesions (P<.03). 3D-FLAIR also detected the highest number of total WM lesions (2605), but the difference with 3D-DIR and 3D-T1WI was not significant.
[B]CONCLUSIONS[/B]:When using recommended clinical sequences at 7T, the best way to detect corticalGMlesions is with 3D-FLAIR and not by GM-specific 3D-DIR or by conventional 2D-T2WI and 3D-T1WI sequences.[/QUOTE]
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Marsei
Iron deposition in the precentral grey matter in patients with multiple sclerosis
Iron deposition in the precentral grey matter in patients with multiple sclerosis
Iron deposition in the [URL="http://www.ejradiology.com/article/S072 ... 2/abstract"][U]precentral grey matter[/U][/URL] in patients with multiple sclerosis: A quantitative study using susceptibility-weighted imaging
[QUOTE][B]Purpose[/B]
Several studies suggest that iron deposition may play a role in multiple sclerosis (MS) pathology. Three-dimensional (3D) enhanced T2*-weighted angiography (ESWAN) at 3T was used to quantify iron deposition in the precentral grey matter in MS and its relationship with disease duration, atrophy and Expanded Disability Status Scale (EDSS) scores.
[B]Methods[/B]
We recruited 33 patients with diagnosis of clinically definite MS and 31 age- and sex-matched healthy controls who underwent conventional brain MRI, 3D-ESWAN and 3D T1sequences. We obtained the mean phase values (MPVs) of the precentral grey matter on ESWAN-filtered phase images and volume of the precentral gyrus on 3D T1 images. We investigated the correlation between precentral grey matter MPVs, precentral gyrus volume, disease duration and EDSS scores of MS patients and healthy controls.
[B]Results[/B]
The precentral grey matter MPVs in MS patients and controls were 1870.83±56.61 and 1899.22±51.73 respectively and had significant difference in the MS group vs. the control group (t=−2.09, P=0.04).
There was significant negative correlation between precentral grey matter MPVs and disease duration (r=−0.365, P=0.03). No correlation was found between MPVs and EDSS scores.
Mean precentral gyrus volume in MS patients was 4368.55±867.78 whereas in controls was 5701.00±1184.03 with significant difference between volume of the precentral gyrus in MS patients compared to healthy controls (t=−5.167, P<0.001). There was a positive correlation between MPVs and precentral gyrus volume (r=0.291, P=0.020).
[B]Conclusions[/B]
Our study demonstrated that quantitative assessment of abnormal iron deposition in the precentral grey matter in MS patients can be measured using 3D-ESWAN.[/QUOTE]
Iron deposition in the [URL="http://www.ejradiology.com/article/S072 ... 2/abstract"][U]precentral grey matter[/U][/URL] in patients with multiple sclerosis: A quantitative study using susceptibility-weighted imaging
[QUOTE][B]Purpose[/B]
Several studies suggest that iron deposition may play a role in multiple sclerosis (MS) pathology. Three-dimensional (3D) enhanced T2*-weighted angiography (ESWAN) at 3T was used to quantify iron deposition in the precentral grey matter in MS and its relationship with disease duration, atrophy and Expanded Disability Status Scale (EDSS) scores.
[B]Methods[/B]
We recruited 33 patients with diagnosis of clinically definite MS and 31 age- and sex-matched healthy controls who underwent conventional brain MRI, 3D-ESWAN and 3D T1sequences. We obtained the mean phase values (MPVs) of the precentral grey matter on ESWAN-filtered phase images and volume of the precentral gyrus on 3D T1 images. We investigated the correlation between precentral grey matter MPVs, precentral gyrus volume, disease duration and EDSS scores of MS patients and healthy controls.
[B]Results[/B]
The precentral grey matter MPVs in MS patients and controls were 1870.83±56.61 and 1899.22±51.73 respectively and had significant difference in the MS group vs. the control group (t=−2.09, P=0.04).
There was significant negative correlation between precentral grey matter MPVs and disease duration (r=−0.365, P=0.03). No correlation was found between MPVs and EDSS scores.
Mean precentral gyrus volume in MS patients was 4368.55±867.78 whereas in controls was 5701.00±1184.03 with significant difference between volume of the precentral gyrus in MS patients compared to healthy controls (t=−5.167, P<0.001). There was a positive correlation between MPVs and precentral gyrus volume (r=0.291, P=0.020).
[B]Conclusions[/B]
Our study demonstrated that quantitative assessment of abnormal iron deposition in the precentral grey matter in MS patients can be measured using 3D-ESWAN.[/QUOTE]
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Marsei
White matter and deep gray matter hemodynamic changes
White matter and deep gray matter hemodynamic changes
White matter and deep gray matter [URL="http://www.ncbi.nlm.nih.gov/pubmed/22367604"][U]hemodynamic changes[/U][/URL] in multiple sclerosis patients with clinically isolated syndrome.
[QUOTE]The dynamic susceptibility contrast magnetic resonance imaging perfusion technique was used to investigate possible hemodynamic changes in normal appearing white matter and deep gray matter (DGM) of 30 patients with clinically isolated syndrome (CIS) and 30 patients with relapsing-remitting multiple sclerosis. Thirty normal volunteers were studied as controls.
Cerebral blood volume, cerebral blood flow (CBF), and mean transit time values were estimated. Normalization was achieved for each subject with respect to average values of CBF and mean transit time of the hippocampi's dentate gyrus. Measurements concerned three regions of normal white matter of normal volunteers, normal appearing white matter of CIS and patients with relapsing-remitting multiple sclerosis, and DGM regions, bilaterally.
All measured normal appearing white matter and DGM regions of the patients with CIS had significantly higher cerebral blood volume and mean transit time values, while averaged DGM regions had significantly lower CBF values, compared to those of normal volunteers (P < 0.001).
Regarding patients with relapsing-remitting multiple sclerosis, all measured normal appearing white matter and DGM regions showed lower CBF values than those of normal volunteers and lower cerebral blood volume and CBF values compared to patients with CIS (P < 0.001).
These data provide strong evidence that hemodynamic changes-affecting both white and DGM-may occur even at the earliest stage of multiple sclerosis, with CIS patients being significantly different than relapsing-remitting multiple sclerosis patients.[/QUOTE]
White matter and deep gray matter [URL="http://www.ncbi.nlm.nih.gov/pubmed/22367604"][U]hemodynamic changes[/U][/URL] in multiple sclerosis patients with clinically isolated syndrome.
[QUOTE]The dynamic susceptibility contrast magnetic resonance imaging perfusion technique was used to investigate possible hemodynamic changes in normal appearing white matter and deep gray matter (DGM) of 30 patients with clinically isolated syndrome (CIS) and 30 patients with relapsing-remitting multiple sclerosis. Thirty normal volunteers were studied as controls.
Cerebral blood volume, cerebral blood flow (CBF), and mean transit time values were estimated. Normalization was achieved for each subject with respect to average values of CBF and mean transit time of the hippocampi's dentate gyrus. Measurements concerned three regions of normal white matter of normal volunteers, normal appearing white matter of CIS and patients with relapsing-remitting multiple sclerosis, and DGM regions, bilaterally.
All measured normal appearing white matter and DGM regions of the patients with CIS had significantly higher cerebral blood volume and mean transit time values, while averaged DGM regions had significantly lower CBF values, compared to those of normal volunteers (P < 0.001).
Regarding patients with relapsing-remitting multiple sclerosis, all measured normal appearing white matter and DGM regions showed lower CBF values than those of normal volunteers and lower cerebral blood volume and CBF values compared to patients with CIS (P < 0.001).
These data provide strong evidence that hemodynamic changes-affecting both white and DGM-may occur even at the earliest stage of multiple sclerosis, with CIS patients being significantly different than relapsing-remitting multiple sclerosis patients.[/QUOTE]
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Marsei
Cortical Lesions in Multiple Sclerosis
Cortical Lesions in Multiple Sclerosis
[URL="http://www.medscape.com/viewarticle/773247?src=nl_topic"][U]Cortical Lesions[/U][/URL] in Multiple Sclerosis
[QUOTE]In conclusion, the two studies published in this issue of Brain add interesting new information to the enigma of cortical lesion pathogenesis in multiple sclerosis. The data support the view that meningeal inflammation plays an important role in the induction and propagation of cortical pathology in multiple sclerosis, but they also indicate that additional and, thus far, unknown mechanisms are necessary to trigger widespread demyelination and neurodegeneration in the cortex.[/QUOTE]
[URL="http://www.medscape.com/viewarticle/773247?src=nl_topic"][U]Cortical Lesions[/U][/URL] in Multiple Sclerosis
[QUOTE]In conclusion, the two studies published in this issue of Brain add interesting new information to the enigma of cortical lesion pathogenesis in multiple sclerosis. The data support the view that meningeal inflammation plays an important role in the induction and propagation of cortical pathology in multiple sclerosis, but they also indicate that additional and, thus far, unknown mechanisms are necessary to trigger widespread demyelination and neurodegeneration in the cortex.[/QUOTE]