Could it be that CCSVI just makes MS worse?

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Could it be that CCSVI just makes MS worse?

Postby frodo » Mon Oct 23, 2017 1:39 am

Could it be that CCSVI just makes MS worse?

This is an idea that came to me after reading an article named "The topograpy of demyelination and neurodegeneration in the multiple sclerosis brain" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4766379/). I enclose here some quotes:

"Their location (of the lesions), shape and patterns of active demyelination are compatible with the view that they are driven by a soluble factor, produced in the inflammatory infiltrates of the meninges, which diffuses into the cortex and triggers demyelination either directly or indirectly through microglia activation"

"There is a flow of CSF within the arachnoid compartment of the meninges at the outer surface of the brain hemispheres (Abbott, 2004), which is likely to be dynamically restricted [...]. This may explain the preferential accumulation of inflammation and subpial cortical demyelination at these sites"

"Recent data suggest that oxidative injury at least in part mediates demyelination and neurodegeneration in the multiple sclerosis brain. Oxidative injury can trigger mitochondrial dysfunction and subsequent energy failure, a process termed histotoxic or ‘virtual’ hypoxia"

"Thus, low blood perfusion and oxygen tension may amplify tissue damage more severely in lesions formed in the progressive stage than in those arising at earlier phases of the disease".
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Re: Could it be that CCSVI just makes MS worse?

Postby violin » Wed Oct 25, 2017 4:35 pm

When I first read your post I got concerned, because I just now wrote Dr. Sclafani again about scheduling my 2nd ccsvi treatment. So what you mean by CCSVI is the condition of having jugular veins stenosis, not the CCSVI treatment, right? That brain lesions already exist due to oxidative stress, and the jugular veinous insufficiency "just makes [already existing] MS worse?"
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Re: Could it be that CCSVI just makes MS worse?

Postby NHE » Thu Oct 26, 2017 1:43 am

violin wrote:When I first read your post I got concerned, because I just now wrote Dr. Sclafani again about scheduling my 2nd ccsvi treatment. So what you mean by CCSVI is the condition of having jugular veins stenosis, not the CCSVI treatment, right? That brain lesions already exist due to oxidative stress, and the jugular veinous insufficiency "just makes [already existing] MS worse?"

That would be my take on it.
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Re: Could it be that CCSVI just makes MS worse?

Postby jimmylegs » Thu Oct 26, 2017 4:58 am

same. ccsvi does not equal ccsvi treatment.
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
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Re: Could it be that CCSVI just makes MS worse?

Postby frodo » Sun Oct 29, 2017 1:24 am

violin wrote:When I first read your post I got concerned, because I just now wrote Dr. Sclafani again about scheduling my 2nd ccsvi treatment. So what you mean by CCSVI is the condition of having jugular veins stenosis, not the CCSVI treatment, right? That brain lesions already exist due to oxidative stress, and the jugular veinous insufficiency "just makes [already existing] MS worse?"


Yes. I meant CCSVI condition, not CCSVI procedure.
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Re: Could it be that CCSVI just makes MS worse?

Postby Cece » Thu Nov 02, 2017 1:50 pm

From the introduction:
We and others recently proposed that microglia activation, production of reactive oxygen species and oxidative damage are key mechanisms driving demyelination and neurodegeneration, particularly in the progressive disease stage (Haider et al., 2011; Fischer et al., 2013). In addition, mitochondrial injury (Mahad et al., 2008; Campbell et al., 2011) may further propagate oxygen radical production (Murphy, 2009) and amplify demyelination and neurodegeneration by energy deficiency through histotoxic hypoxia (Trapp and Stys, 2009; Witte et al., 2010). With disease progression, the intensity of the inflammatory response declines, but oxidative injury and mitochondrial damage are aggravated by additional factors related to ageing of the patients and to the accumulation of disease and lesion burden (Mahad et al., 2015).

If this concept is valid, besides density of veins and meningeal inflammatory infiltrates also arterial anatomy of the brain should influence the topographical distribution of demyelinated lesions and neurodegeneration within the CNS due to varying basic levels of oxygen tension (Desai et al., 2014). In our study we analysed predilection sites of demyelination and neurodegeneration and how these relate to arterial and venous anatomy and inflammation or demyelination in multiple sclerosis.

Really interesting and on point. Also this is an explanation for the progressive part of the disease, where there is total need for any effective treatments.
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Re: Could it be that CCSVI just makes MS worse?

Postby frodo » Mon Dec 11, 2017 3:31 am

More about the same:

Vascular comorbidities in the onset and progression of multiple sclerosis

Source: http://www.jns-journal.com/article/S002 ... X/fulltext

Abstract

Vascular comorbidities are common in the general population and are associated with adverse health outcomes. In people with multiple sclerosis (MS), an increasing amount of evidence suggests that vascular comorbidities are also common, but an association with MS risk and disability has not been conclusively established.

This review aims to critically examine published data on the relationship between vascular comorbidities (including vascular risk factors) and MS. The evidence suggests an increased risk of MS in people with a high BMI during childhood or adolescence but not adulthood. People with established MS appear to have a slightly increased risk of cardiovascular disease and a greater proportion of people with MS die from cardiovascular disease, which has important implications for clinicians trying to identify risk factors for cardiovascular disease and reviewing treatment options.

In relation to whether vascular comorbidities influence MS clinical disability or other aspects of the disease course, the key finding was that having type-2-diabetes, hypertension, dyslipidaemia or peripheral vascular disease at any point in the disease course may be associated with a greater progression in disability. Additionally, a negative effect of high cholesterol and triglycerides and a positive effect of higher HDL (high density lipoprotein) levels on acute inflammatory activity were observed on magnetic resonance imaging.

The results of the published clinical trials of statins as an intervention in MS were however conflicting and care needs to be taken when treating people with MS with statins. Taken together, the literature seems to indicate a potential association of vascular comorbidities with MS risk and disability, but the number of prospective studies was sparse, thus precluding ascription of causality.

We therefore recommend that future studies of the frequency and effects of vascular comorbidities on MS risk and disability should be prospective and objective where relevant.
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