CCSVI-10
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zeiler
Ik word toch zo moe van dat continue geleuter van die Marsei en haar grote lappen nietszeggend geblaat. Dat hele csvii kost nog steeds emmers vol euri's en enig positief effect heb ik na al die jaren nog steeds niet gezien. Sterker nog; zelfs in Belgie zijn vrijwel alle centra gestopt met 'dotteren' en steeds meer prima mensen kunnen de ms-beperkingen niet meer aan en stoppen ermee! En die Marsei blijft maar stug volhouden dat die neurologen lekker bezig zijn en MS eigenlijk tot het verleden behoort. Bah!
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Robbie
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Marsei
De link werkt niet, [URL="http://www.veithsymposium.org/index.php?pg=program-2017"][U]deze[/U][/URL] hopelijk wel.
Van de Alliance:
[QUOTE]Dr. Paolo Zamboni to speak at the VEITH 2017 Symposium.....Update On The Endovascular Treatment Of Chronic Cerebrospinal Venous Insufficiency (CCSVI) To Improve Multiple Sclerosis Symptoms: Status And Results Of The BRAVE DREAMS Randomized Sham Controlled Trial[/QUOTE]
De presentatie duurt 5 minuten, dus er zal waarschijnlijk niet veel nieuws zijn.
Van de Alliance:
[QUOTE]Dr. Paolo Zamboni to speak at the VEITH 2017 Symposium.....Update On The Endovascular Treatment Of Chronic Cerebrospinal Venous Insufficiency (CCSVI) To Improve Multiple Sclerosis Symptoms: Status And Results Of The BRAVE DREAMS Randomized Sham Controlled Trial[/QUOTE]
De presentatie duurt 5 minuten, dus er zal waarschijnlijk niet veel nieuws zijn.
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Marsei
[QUOTE=zeiler;1088467]En die Marsei blijft maar stug volhouden dat die neurologen lekker bezig zijn en MS eigenlijk tot het verleden behoort. Bah![/QUOTE]
Omdat je wat moeite hebt met lezen zal ik het even voor je samenvatten:
- Afgezien van een kleine groep neurologen zijn het niet de neurologen die lekker bezig zijn, maar de vaatspecialisten en interventie radiologen.
- Al hoewel vrijwel alle MS-ers problemen met bepaalde vaten hebben, heeft niet iedereen baat bij de behandeling. Bij sommige mensen ziet het er naar uit dat het de ziekte activiteit stopt, bij anderen verbeteren sommige symptomen maar stopt de ziekte niet en bij nog weer anderen verandert de behandeling niets.
De grootste kans op succes is bij RR en bij mensen die nog niet lang de diagnose hebben. Maar het is geen wet van Meden en Perzen, er zijn ook PP-ers die al lang MS hebben die veel baat bij de behandeling hebben.
Het hoe en waarom is nog onbekend, het onderzoek staat nog steeds in de kinderschoenen.
- Mochten de resultaten van Brave Dreams positief zijn, dan gaat het zeker nog 5 a 10 jaar duren voor de behandeling ingevoerd is.
Omdat je wat moeite hebt met lezen zal ik het even voor je samenvatten:
- Afgezien van een kleine groep neurologen zijn het niet de neurologen die lekker bezig zijn, maar de vaatspecialisten en interventie radiologen.
- Al hoewel vrijwel alle MS-ers problemen met bepaalde vaten hebben, heeft niet iedereen baat bij de behandeling. Bij sommige mensen ziet het er naar uit dat het de ziekte activiteit stopt, bij anderen verbeteren sommige symptomen maar stopt de ziekte niet en bij nog weer anderen verandert de behandeling niets.
De grootste kans op succes is bij RR en bij mensen die nog niet lang de diagnose hebben. Maar het is geen wet van Meden en Perzen, er zijn ook PP-ers die al lang MS hebben die veel baat bij de behandeling hebben.
Het hoe en waarom is nog onbekend, het onderzoek staat nog steeds in de kinderschoenen.
- Mochten de resultaten van Brave Dreams positief zijn, dan gaat het zeker nog 5 a 10 jaar duren voor de behandeling ingevoerd is.
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Marsei
Magnetic resonance imaging perfusion is associated with disease severity and activity
Magnetic resonance imaging perfusion is associated with disease severity and activity
Tweet Zamboni:
[QUOTE]Reduced Brain Perfusion=Bad prognosis of #MultipleSclerosis #ccsvi treatment better perfusion of the Brain
[/QUOTE]
[URL="https://www.ncbi.nlm.nih.gov/pubmed/28585082"][U]Magnetic resonance imaging perfusion[/U][/URL] is associated with disease severity and activity in multiple sclerosis - oa Nygaard
[QUOTE][B]Abstract[/B]
[B]PURPOSE:[/B]
The utility of perfusion-weighted imaging in multiple sclerosis (MS) is not well investigated. The purpose of this study was to compare baseline normalized perfusion measures in subgroups of newly diagnosed MS patients. We wanted to test the hypothesis that this method can differentiate between groups defined according to disease severity and disease activity at 1 year follow-up.
[B]METHODS:[/B]
Baseline magnetic resonance imaging (MRI) including a dynamic susceptibility contrast perfusion sequence was performed on a 1.5-T scanner in 66 patients newly diagnosed with relapsing-remitting MS. From the baseline MRI, cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) maps were generated. Normalized (n) perfusion values were calculated by dividing each perfusion parameter obtained in white matter lesions by the same parameter obtained in normal-appearing white matter. Neurological examination was performed at baseline and at follow-up approximately 1 year later to establish the multiple sclerosis severity score (MSSS) and evidence of disease activity (EDA).
[B]RESULTS:[/B]
Baseline normalized mean transit time (nMTT) was lower in patients with MSSS >3.79 (p = 0.016), in patients with EDA (p = 0.041), and in patients with both MSSS >3.79 and EDA (p = 0.032) at 1-year follow-up. Baseline normalized cerebral blood flow and normalized cerebral blood volume did not differ between these groups.
[B]CONCLUSION:[/B]
Lower baseline nMTT was associated with higher disease severity and with presence of disease activity 1 year later in newly diagnosed MS patients. Further longitudinal studies are needed to confirm whether baseline-normalized perfusion measures can differentiate between disease severity and disease activity subgroups over time.[/QUOTE]
Tweet Zamboni:
[QUOTE]Reduced Brain Perfusion=Bad prognosis of #MultipleSclerosis #ccsvi treatment better perfusion of the Brain
[/QUOTE]
[URL="https://www.ncbi.nlm.nih.gov/pubmed/28585082"][U]Magnetic resonance imaging perfusion[/U][/URL] is associated with disease severity and activity in multiple sclerosis - oa Nygaard
[QUOTE][B]Abstract[/B]
[B]PURPOSE:[/B]
The utility of perfusion-weighted imaging in multiple sclerosis (MS) is not well investigated. The purpose of this study was to compare baseline normalized perfusion measures in subgroups of newly diagnosed MS patients. We wanted to test the hypothesis that this method can differentiate between groups defined according to disease severity and disease activity at 1 year follow-up.
[B]METHODS:[/B]
Baseline magnetic resonance imaging (MRI) including a dynamic susceptibility contrast perfusion sequence was performed on a 1.5-T scanner in 66 patients newly diagnosed with relapsing-remitting MS. From the baseline MRI, cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) maps were generated. Normalized (n) perfusion values were calculated by dividing each perfusion parameter obtained in white matter lesions by the same parameter obtained in normal-appearing white matter. Neurological examination was performed at baseline and at follow-up approximately 1 year later to establish the multiple sclerosis severity score (MSSS) and evidence of disease activity (EDA).
[B]RESULTS:[/B]
Baseline normalized mean transit time (nMTT) was lower in patients with MSSS >3.79 (p = 0.016), in patients with EDA (p = 0.041), and in patients with both MSSS >3.79 and EDA (p = 0.032) at 1-year follow-up. Baseline normalized cerebral blood flow and normalized cerebral blood volume did not differ between these groups.
[B]CONCLUSION:[/B]
Lower baseline nMTT was associated with higher disease severity and with presence of disease activity 1 year later in newly diagnosed MS patients. Further longitudinal studies are needed to confirm whether baseline-normalized perfusion measures can differentiate between disease severity and disease activity subgroups over time.[/QUOTE]
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Marsei
Fibrin(ogen) and neurodegeneration in the progressive multiple sclerosis cortex
Fibrin(ogen) and neurodegeneration in the progressive multiple sclerosis cortex
Van Joan:
[QUOTE][URL="https://www.ncbi.nlm.nih.gov/pubmed/28719020"][U]A new study from Oxford[/U][/URL] corroborates what Gladstone Institute researchers have published: Fibrinogen, a blood clotting protein, is "extensively deposited" in progressive MS brain tissue, and linked to neurodegeneration.
[URL="http://ccsviinms.blogspot.nl/2014/03/blood-matters.html"][U]Here[/U][/URL] is some background on WHY this matters--[/QUOTE]
[QUOTE][B]Fibrin(ogen) and neurodegeneration in the progressive multiple sclerosis cortex[/B]
[B]
Abstract[/B]
[B]OBJECTIVE[/B]:
Neuronal loss, a key substrate of irreversible disability in multiple sclerosis (MS), is a recognised feature of MS cortical pathology of which the cause remains unknown. Fibrin(ogen) deposition is neurotoxic in animal models of MS, but has not been evaluated in human progressive MS cortex. The aim of this study was to investigate the extent and distribution of fibrin(ogen) in progressive MS cortex and elucidate its relationship with neurodegeneration.
[B]METHODS:[/B]
A post-mortem cohort of pathologically confirmed MS (n=47) and control (n=10) cases was used. The extent and distribution of fibrin(ogen) was assessed and related to measures of demyelination, inflammation, and neuronal density. In a subset of cases (MS, n=20; control, n=10), the expression of plasminogen activator inhibitor (PAI-1), a key enzyme in the fibrinolytic cascade, was assessed and related to the extent of fibrin(ogen).
[B]RESULTS:[/B]
Motor cortical fibrin(ogen) deposition was significantly overrepresented in MS compared to control cases in all compartments studied (i.e. extracellular (p=0.001), cell body (p=0.003) and neuritic/glial-processes (p=0.004)). MS cases with high levels of extracellular fibrin(ogen) had significantly up-regulated PAI-1 expression in all cortical layers assessed (p<0.05) and reduced neuronal density (p=0.017), including in the functionally-relevant layer 5 (p=0.001).
[B]INTERPRETATION[/B]:
For the first time, we provide unequivocal evidence that fibrin(ogen) is extensively deposited in progressive MS motor cortex, where regulation of fibrinolysis appears perturbed. Progressive MS cases with severe fibrin(ogen) deposition have significantly reduced neuronal density. Future studies are needed to elucidate the provenance and putative neurotoxicity of fibrin(ogen), and its potential impact on clinical disability. This article is protected by copyright. All rights reserved.[/QUOTE]
Van Joan:
[QUOTE][URL="https://www.ncbi.nlm.nih.gov/pubmed/28719020"][U]A new study from Oxford[/U][/URL] corroborates what Gladstone Institute researchers have published: Fibrinogen, a blood clotting protein, is "extensively deposited" in progressive MS brain tissue, and linked to neurodegeneration.
[URL="http://ccsviinms.blogspot.nl/2014/03/blood-matters.html"][U]Here[/U][/URL] is some background on WHY this matters--[/QUOTE]
[QUOTE][B]Fibrin(ogen) and neurodegeneration in the progressive multiple sclerosis cortex[/B]
[B]
Abstract[/B]
[B]OBJECTIVE[/B]:
Neuronal loss, a key substrate of irreversible disability in multiple sclerosis (MS), is a recognised feature of MS cortical pathology of which the cause remains unknown. Fibrin(ogen) deposition is neurotoxic in animal models of MS, but has not been evaluated in human progressive MS cortex. The aim of this study was to investigate the extent and distribution of fibrin(ogen) in progressive MS cortex and elucidate its relationship with neurodegeneration.
[B]METHODS:[/B]
A post-mortem cohort of pathologically confirmed MS (n=47) and control (n=10) cases was used. The extent and distribution of fibrin(ogen) was assessed and related to measures of demyelination, inflammation, and neuronal density. In a subset of cases (MS, n=20; control, n=10), the expression of plasminogen activator inhibitor (PAI-1), a key enzyme in the fibrinolytic cascade, was assessed and related to the extent of fibrin(ogen).
[B]RESULTS:[/B]
Motor cortical fibrin(ogen) deposition was significantly overrepresented in MS compared to control cases in all compartments studied (i.e. extracellular (p=0.001), cell body (p=0.003) and neuritic/glial-processes (p=0.004)). MS cases with high levels of extracellular fibrin(ogen) had significantly up-regulated PAI-1 expression in all cortical layers assessed (p<0.05) and reduced neuronal density (p=0.017), including in the functionally-relevant layer 5 (p=0.001).
[B]INTERPRETATION[/B]:
For the first time, we provide unequivocal evidence that fibrin(ogen) is extensively deposited in progressive MS motor cortex, where regulation of fibrinolysis appears perturbed. Progressive MS cases with severe fibrin(ogen) deposition have significantly reduced neuronal density. Future studies are needed to elucidate the provenance and putative neurotoxicity of fibrin(ogen), and its potential impact on clinical disability. This article is protected by copyright. All rights reserved.[/QUOTE]
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Marsei
Trailer film Living Proof
Trailer film Living Proof
[URL="http://www.tiff.net/tiff/living-proof/?v=living-proof"][U]Trailer[/U][/URL] film Living Proof
[URL="https://www.youtube.com/watch?v=fjwSz2xsD1s"][U]YouTube[/U][/URL]
[QUOTE]Diagnosed with multiple sclerosis, documentarian Matt Embry takes viewers on a transnational journey — from Italy to Canada, and from the lab to the home — in order to examine the politics of the condition.[/QUOTE]
Met o.a. Jeff Beal
[URL="http://www.tiff.net/tiff/living-proof/?v=living-proof"][U]Trailer[/U][/URL] film Living Proof
[URL="https://www.youtube.com/watch?v=fjwSz2xsD1s"][U]YouTube[/U][/URL]
[QUOTE]Diagnosed with multiple sclerosis, documentarian Matt Embry takes viewers on a transnational journey — from Italy to Canada, and from the lab to the home — in order to examine the politics of the condition.[/QUOTE]
Met o.a. Jeff Beal
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Marsei
Breakthrough device heals organs with a single touch
Breakthrough device heals organs with a single touch
Breakthrough device [URL="https://medicalxpress.com/news/2017-08- ... evice.html"][U]heals organs[/U][/URL] with a single touch
[QUOTE]Researchers at The Ohio State University Wexner Medical Center and Ohio State's College of Engineering have developed a new technology, Tissue Nanotransfection (TNT), that can generate any cell type of interest for treatment within the patient's own body. This technology may be used to repair injured tissue or restore function of aging tissue, including organs, blood vessels and nerve cells.[/QUOTE]
[QUOTE]"By using our novel nanochip technology, injured or compromised organs can be replaced. We have shown that skin is a fertile land where we can grow the elements of any organ that is declining," said Dr. Chandan Sen, director of Ohio State's Center for Regenerative Medicine & Cell Based Therapies, who co-led the study with L. James Lee, professor of chemical and biomolecular engineering with Ohio State's College of Engineering in collaboration with Ohio State's Nanoscale Science and Engineering Center.
Researchers studied mice and pigs in these experiments. In the study, researchers were able to reprogram skin cells to become vascular cells in badly injured legs that lacked blood flow. Within one week, active blood vessels appeared in the injured leg, and by the second week, the leg was saved. In lab tests, this technology was also shown to reprogram skin cells in the live body into nerve cells that were injected into brain-injured mice to help them recover from stroke.
"This is difficult to imagine, but it is achievable, successfully working about 98 percent of the time. With this technology, we can convert skin cells into elements of any organ with just one touch. This process only takes less than a second and is non-invasive, and then you're off. The chip does not stay with you, and the reprogramming of the cell starts. Our technology keeps the cells in the body under immune surveillance, so immune suppression is not necessary," said Sen, who also is executive director of Ohio State's Comprehensive Wound Center.[/QUOTE]
Breakthrough device [URL="https://medicalxpress.com/news/2017-08- ... evice.html"][U]heals organs[/U][/URL] with a single touch
[QUOTE]Researchers at The Ohio State University Wexner Medical Center and Ohio State's College of Engineering have developed a new technology, Tissue Nanotransfection (TNT), that can generate any cell type of interest for treatment within the patient's own body. This technology may be used to repair injured tissue or restore function of aging tissue, including organs, blood vessels and nerve cells.[/QUOTE]
[QUOTE]"By using our novel nanochip technology, injured or compromised organs can be replaced. We have shown that skin is a fertile land where we can grow the elements of any organ that is declining," said Dr. Chandan Sen, director of Ohio State's Center for Regenerative Medicine & Cell Based Therapies, who co-led the study with L. James Lee, professor of chemical and biomolecular engineering with Ohio State's College of Engineering in collaboration with Ohio State's Nanoscale Science and Engineering Center.
Researchers studied mice and pigs in these experiments. In the study, researchers were able to reprogram skin cells to become vascular cells in badly injured legs that lacked blood flow. Within one week, active blood vessels appeared in the injured leg, and by the second week, the leg was saved. In lab tests, this technology was also shown to reprogram skin cells in the live body into nerve cells that were injected into brain-injured mice to help them recover from stroke.
"This is difficult to imagine, but it is achievable, successfully working about 98 percent of the time. With this technology, we can convert skin cells into elements of any organ with just one touch. This process only takes less than a second and is non-invasive, and then you're off. The chip does not stay with you, and the reprogramming of the cell starts. Our technology keeps the cells in the body under immune surveillance, so immune suppression is not necessary," said Sen, who also is executive director of Ohio State's Comprehensive Wound Center.[/QUOTE]
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Marsei
Factors influencing the hemodynamic response to balloon angioplasty in the treatment
Factors influencing the hemodynamic response to balloon angioplasty in the treatment
[URL="http://www.jvsvenous.org/article/S2213- ... 0/fulltext"][U]Factors[/U][/URL] influencing the hemodynamic response to balloon angioplasty in the treatment of outflow anomalies of internal jugular veins - oa Beggs en Veroux
[QUOTE][B]Abstract[/B]
[B]Objective[/B]
Percutaneous transluminal angioplasty (PTA) of the internal jugular veins (IJVs) has been proposed in recent years to treat chronic cerebrovascular venous insufficiency, with discordant results. Moreover, very little is known about the efficacy of PTA in restoring a normal cerebral venous outflow. The aim of this study was to investigate the anatomic factors and patient characteristics that might influence the efficacy of PTA of the IJV.
[B]Methods[/B]
There were 797 consecutive patients with venous outflow anomalies who underwent standardized, operator-independent catheter venography and PTA of the IJVs. Before and after PTA, morphologic and hemodynamic anomalies of the IJVs were documented. The primary end point of the study was to evaluate the morphologic factors influencing the efficacy of angioplasty in improving IJV outflow.
[B]Results[/B]
PTA resulted in an increased outflow through the IJVs in most patients. However, younger individuals with transverse endoluminal defects and higher pre-PTA flows are more likely to respond well to PTA compared with those who exhibit hypoplasia, stenosis, or longitudinal endoluminal defects.
[B]Conclusions[/B]
This study identified the factors that influence and could predict the efficacy of PTA in the treatment of IJV anomalies.[/QUOTE]
[URL="http://www.jvsvenous.org/article/S2213- ... 0/fulltext"][U]Factors[/U][/URL] influencing the hemodynamic response to balloon angioplasty in the treatment of outflow anomalies of internal jugular veins - oa Beggs en Veroux
[QUOTE][B]Abstract[/B]
[B]Objective[/B]
Percutaneous transluminal angioplasty (PTA) of the internal jugular veins (IJVs) has been proposed in recent years to treat chronic cerebrovascular venous insufficiency, with discordant results. Moreover, very little is known about the efficacy of PTA in restoring a normal cerebral venous outflow. The aim of this study was to investigate the anatomic factors and patient characteristics that might influence the efficacy of PTA of the IJV.
[B]Methods[/B]
There were 797 consecutive patients with venous outflow anomalies who underwent standardized, operator-independent catheter venography and PTA of the IJVs. Before and after PTA, morphologic and hemodynamic anomalies of the IJVs were documented. The primary end point of the study was to evaluate the morphologic factors influencing the efficacy of angioplasty in improving IJV outflow.
[B]Results[/B]
PTA resulted in an increased outflow through the IJVs in most patients. However, younger individuals with transverse endoluminal defects and higher pre-PTA flows are more likely to respond well to PTA compared with those who exhibit hypoplasia, stenosis, or longitudinal endoluminal defects.
[B]Conclusions[/B]
This study identified the factors that influence and could predict the efficacy of PTA in the treatment of IJV anomalies.[/QUOTE]
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Marsei
Diagnostic performance of central vein sign for multiple sclerosis
Diagnostic performance of central vein sign for multiple sclerosis
Diagnostic performance of [URL="https://www.ncbi.nlm.nih.gov/pubmed/28820013"][U]central vein sign[/U][/URL] for multiple sclerosis with a simplified three-lesion algorithm.
[QUOTE][B]Abstract[/B]
[B]BACKGROUND:[/B]
Detection of a "central vein sign" (CVS) on FLAIR* magnetic resonance imaging (MRI) is highly specific and sensitive for multiple sclerosis (MS). We evaluated the specificity and sensitivity of simplified CVS algorithms for MS diagnosis.
[B]METHODS:[/B]
MRIs from 10 participants with MS without additional comorbidities for MRI white matter abnormalities; 10 with MS and additional comorbidities for white matter abnormalities; 10 with migraine, white matter abnormalities, and no additional comorbidities; and 10 who had previously been erroneously diagnosed with MS were evaluated. 3T MRI T2-FLAIR and T2*-weighted sequences were acquired to create FLAIR* images. Three MS physician reviewers, blinded to diagnosis, evaluated two different algorithms: (1) three lesions pre-selected on FLAIR were subsequently evaluated for CVS on FLAIR*( select3). (2) FLAIR* was evaluated for up to three lesions with CVS ( select3*).
[B]RESULTS:[/B]
For select3, average specificity across reviewers for MS was 0.98 and sensitivity 0.52 and a correct prediction of diagnosis demonstrated kappa = 0.29. For select3*, specificity was 0.81, sensitivity was 0.83, and kappa was 0.31.
[B]CONCLUSION:[/B]
A simplified determination of CVS in three white matter lesions on 3T FLAIR* MRI demonstrated good specificity and sensitivity and fair inter-rater reliability for a diagnosis of MS and with further study, may be a candidate for clinical application.
[/QUOTE]
Tweet Zamboni:
[QUOTE]The central vein at MRI biomarker of #MultipleSclerosis[/QUOTE]
Diagnostic performance of [URL="https://www.ncbi.nlm.nih.gov/pubmed/28820013"][U]central vein sign[/U][/URL] for multiple sclerosis with a simplified three-lesion algorithm.
[QUOTE][B]Abstract[/B]
[B]BACKGROUND:[/B]
Detection of a "central vein sign" (CVS) on FLAIR* magnetic resonance imaging (MRI) is highly specific and sensitive for multiple sclerosis (MS). We evaluated the specificity and sensitivity of simplified CVS algorithms for MS diagnosis.
[B]METHODS:[/B]
MRIs from 10 participants with MS without additional comorbidities for MRI white matter abnormalities; 10 with MS and additional comorbidities for white matter abnormalities; 10 with migraine, white matter abnormalities, and no additional comorbidities; and 10 who had previously been erroneously diagnosed with MS were evaluated. 3T MRI T2-FLAIR and T2*-weighted sequences were acquired to create FLAIR* images. Three MS physician reviewers, blinded to diagnosis, evaluated two different algorithms: (1) three lesions pre-selected on FLAIR were subsequently evaluated for CVS on FLAIR*( select3). (2) FLAIR* was evaluated for up to three lesions with CVS ( select3*).
[B]RESULTS:[/B]
For select3, average specificity across reviewers for MS was 0.98 and sensitivity 0.52 and a correct prediction of diagnosis demonstrated kappa = 0.29. For select3*, specificity was 0.81, sensitivity was 0.83, and kappa was 0.31.
[B]CONCLUSION:[/B]
A simplified determination of CVS in three white matter lesions on 3T FLAIR* MRI demonstrated good specificity and sensitivity and fair inter-rater reliability for a diagnosis of MS and with further study, may be a candidate for clinical application.
[/QUOTE]
Tweet Zamboni:
[QUOTE]The central vein at MRI biomarker of #MultipleSclerosis[/QUOTE]