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CCSVI symptoms, aging

Posted: Fri Oct 15, 2010 1:13 pm
by dunkempt
Interesting. And aren't many of the symptoms which seem to respond to treating CCSVI: cold extremities, weak voice, fatigue, etc., frequently associated with aging? In my case, for example, my voice had aged a lot faster than the rest of me: I sounded like my dad. This changed at once following procedure.

-d

Posted: Wed Oct 20, 2010 11:56 am
by gibbledygook
Cheereo, please keep posting research like this. Always interesting.

Re: CCSVI symptoms, aging

Posted: Wed Oct 20, 2010 12:50 pm
by cheerleader
dunkempt wrote:Interesting. And aren't many of the symptoms which seem to respond to treating CCSVI: cold extremities, weak voice, fatigue, etc., frequently associated with aging? In my case, for example, my voice had aged a lot faster than the rest of me: I sounded like my dad. This changed at once following procedure.

-d
That was the first thing we noticed with my Dad, D...he lost his voice, it became a whisper. He'd fall asleep sitting on the couch, exhausted. And his hands and feet were cold. He was 77 when he died, so it's seen as "aging." But in you, a younger person...it's just not a good thing. His carotid arteries were checked, they were clear, his heart was checked, it was strong. No one looked at venous return. This seems to be a big question mark in medical studies. What about the jugular veins?

Yeah, Gibbs. I can't quit this research....like a bad boyfriend :) I've seen some more stuff on hypotension and venous return, and always think of you. Hope the baby is keeping you focused on all that is good and sweet and life-affirming. Babies rule.

I got a hold of the two complete Chung papers from my doctor buddy.
Here's more on the changing venous hemodynamics of aging.
Our results mainly reveal the effect of age on the hemodynamics of the IJVs. We found an increase in the lumen area and a decrease in bilateral IJV flow velocity with aging. Furthermore, although the total IJV blood flow volume did not change, the distribution of venous drainage changed as the age of subjects increased (Fig. 2). The prevalence of left JVR also significantly increased with increasing age. When impaired venous outflow results in venous pressure elevation, the upstream vein will dilate its lumen and its flow velocity will be reduced (Attubato et al. 1994; Bousser et al. 1985; Donahue et al. 2009; Schaller and Graf 2004; Schaller 2004). If the extent of venous hypertension exceeds the ability of venous dilatation to compensate for it and compromises the competence of the jugular venous valve, the direction of venous flow will be reversed[(Bousser et al. 1985; Schaller and Graf 2004; Schaller
2004). Therefore, a dilated lumen, reduced flow velocity and increased prevalence of JVR in the left IJV, added to the fact that the proportion of blood flow volume in the left IJV decreases with aging, suggests that left IJV venous outflow impedance may be associated with increasing age.
So, it's the combo platter of a stretched out lumen, slower flow from the brain, reflux of blood and decreased blood flow volume that appears to be the problem in an aging patient. Dr. Chung later postulates that this is what created the ischemic white matter lesions in the elderly with LA.

This is very, very, very different than CCSVI in young people, where it is an occlusion in the jugular/azygos veins that is creating the slowed drainage and reflux. But the result of venous reflux is like the aging process....happening decades too soon.

Man, I wish the venous doctors would get together and do more research on the jugular veins in normal young people. What does "normal" jugular return look like? That's what we need to know.
cheer

Re: CCSVI symptoms, aging

Posted: Wed Oct 20, 2010 2:22 pm
by 1eye
cheerleader wrote: This is very, very, very different than CCSVI in young people, where it is an occlusion in the jugular/azygos veins that is creating the slowed drainage and reflux. But the result of venous reflux is like the aging process....happening decades too soon.

Man, I wish the venous doctors would get together and do more research on the jugular veins in normal young people. What does "normal" jugular return look like? That's what we need to know.
cheer
A friend said that 'MS' was making us both 'prematurely old'. I did have the reversal of my vocal strength after Liberation. I think it has mostly lasted. The azygous drains the ribcage, and thus may have some effect on vocal power, IMO. When my other friend was near his death at the age of 30 from CCSVI he sounded very very old.

I think there is abundant ageism in the treatment of people generally, but also that it is a big part of the 'adios' that seems to happen when 'MS'/CCSVI becomes 'progressive'. Coincidentally, their voices often start to crack.

Posted: Wed Oct 20, 2010 4:20 pm
by dunkempt
Yes, as I said the other day on a different thread, my voice had got old (and recovered - at once - following liberation). With the other troubles I had, I had never been conscious of this one, but other people noticed the rejuvenation right away.
However in my case the azygous wasn't treated.
-d

Hippocampus

Posted: Fri Oct 22, 2010 11:36 am
by Gordon

There is also NAWM in Leukoaraiosis, and it is similar to MS

Posted: Sat Jun 01, 2013 1:25 pm
by frodo
I have raised this old thread because I have got more information. In particular, an article showing more similarities betwee Leukoaraiosis and MS. In this case it is shown that they are similar even in the chemistry of NAWM areas. I think this was not reported previously.

I quote from the enclosed article:

The ratios of NAA/Cho and NAA/Cr in normal appearing white matter (NAWM) were higher than lesioned white matter and lower than controls, but this difference was not significant (P>0.05). There was a positive relationship between Mini-Mental State Examination (MMSE) and NAA/Cho in NAWM (r = 0.417, P = 0.048),

http://www.ncbi.nlm.nih.gov/pubmed/23146302


Other important article says that a proteine named Klotho could be involved.

http://www.medicalnewstoday.com/articles/255715.php

A team of researchers at Boston University School of Medicine have identified a new drug target for Alzheimer's disease and multiple sclerosis. They discovered the importance of a protein called Klotho which helps maintain healthy myelin - an insulating material allowing communication between nerve cells.

As people begin to age the levels of Klotho in the brain also begin to decrease. They published their findings online in Journal of Neuroscience.

New article about Leukoaraiosis

Posted: Wed Jun 05, 2013 2:02 pm
by frodo
New article just published, fresh from the press, it reports more striking similarities between MS and Leukoaraiosis, and it is fully available for free.

http://www.biomedcentral.com/1741-7015/11/142

Re: Jugular Venous reflux in Leukoaraiosis

Posted: Wed Jun 05, 2013 2:20 pm
by Cece
Thanks for the heads up on this one. It's Dr. Beggs.
Venous abnormalities contribute to the pathophysiology of several neurological conditions. This paper reviews the literature regarding venous abnormalities in multiple sclerosis (MS), leukoaraiosis, and normal-pressure hydrocephalus (NPH). The review is supplemented with hydrodynamic analysis to assess the effects on cerebrospinal fluid (CSF) dynamics and cerebral blood flow (CBF) of venous hypertension in general, and chronic cerebrospinal venous insufficiency (CCSVI) in particular.

CCSVI-like venous anomalies seem unlikely to account for reduced CBF in patients with MS, thus other mechanisms must be at work, which increase the hydraulic resistance of the cerebral vascular bed in MS. Similarly, hydrodynamic changes appear to be responsible for reduced CBF in leukoaraiosis. The hydrodynamic properties of the periventricular veins make these vessels particularly vulnerable to ischemia and plaque formation.

Venous hypertension in the dural sinuses can alter intracranial compliance.
Consequently, venous hypertension may change the CSF dynamics, affecting the intracranial windkessel mechanism. MS and NPH appear to share some similar characteristics, with both conditions exhibiting increased CSF pulsatility in the aqueduct of Sylvius.

CCSVI appears to be a real phenomenon associated with MS, which causes venous hypertension in the dural sinuses. However, the role of CCSVI in the pathophysiology of MS remains unclear.
I am going to have to read it again tomorrow, as some of it was heavy going. Really good article.

Re: Jugular Venous reflux in Leukoaraiosis

Posted: Thu Jun 06, 2013 12:26 pm
by 1eye
Just wanted to highlight that we have not heard the claim of 100% specificity in a long time... Thank you, Dr. Beggs.

From one of the references in the above paper:
Sensitivity and specificity of SWI venography for detection of cerebral venous alterations in multiple sclerosis

Authors: Beggs, Clive B1; Shepherd, Simon J1; Dwyer, Michael G2; Polak, Paul2; Magnano, Christopher2; Carl, Ellen2; Poloni, Guy U2; Weinstock-Guttman, Bianca2; Zivadinov, Robert2

Source: Neurological Research, Volume 34, Number 8, October 2012 , pp. 793-801(9)

Publisher: Maney Publishing


Abstract:
Objectives: To determine the sensitivity and specificity of decreased venous vasculature visibility (VVV) on susceptibility-weighted imaging (SWI) venography in multiple sclerosis (MS) patients versus controls, and to compare this with assessment of whole brain atrophy.

Methods: Forty MS patients and 22 controls without known central nervous system (CNS) disease who had non-specific white-matter (WM) lesions were imaged on a 3T GE scanner using SWI venography. Apparent total venous volume (ATVV) and increased average distance from vein (DFV) were calculated for various vein mean diameter categories: <0·3, 0·3‐0·6, 0·6‐0·9, and >0·9 mm. Principal component analysis (PCA) was used to identify potential discriminatory metrics. Receiver operating characteristics (ROC) of these metrics, along with normalized brain volume (NBV), were calculated to determine sensitivity and specificity values between the groups. The efficacy of the metrics was validated against blinded data from 14 MS patients and 8 controls who had non-specific WM lesions.

Results: PCA identified 0·3‐0·6 mm venous relative fraction (VRF) and DFV as useful metrics. ROC analysis results in initial sample of 40 MS patients and 22 controls were (sensitivity, specificity): 0·3‐0·6 mm VRF (95·0%, 100·0%); DFV (100·0%, 100·0%); and NBV (82·5%, 68·2%). The results in validation sample were: 0·3‐0·6 mm VRF (92·9%, 75·0%); DFV (100·0%, 100·0%); and NBV (78·6%, 75·0%).

Discussion: Altered VVV indices on SWI venography showed high sensitivity and specificity for MS. The value of SWI venography for diagnosis of MS has to be further tested at early disease stages and against patients with other neurologic diseases.

Re: Jugular Venous reflux in Leukoaraiosis

Posted: Mon Jun 24, 2013 1:44 am
by frodo
1eye wrote:Just wanted to highlight that we have not heard the claim of 100% specificity in a long time... Thank you, Dr. Beggs.
I have just realized that this nearly 100% specificity is respect the "McDonalds-CDMS status" because people in the trial was recruited with this criteria, and McDonalds is not 100% reliable. Maybe a study comparing SWI with postmortem autopsies would be even better.

Re: Jugular Venous reflux in Leukoaraiosis

Posted: Mon Jun 24, 2013 8:45 am
by 1eye
I don't know if I met the McDonald/CDMS criteria, but the time/space thing is only because they didn't have anything better, and it's unusually cruel for a sick person. Makes the work of diagnosis less stressful for the doctor.

From the first event I was not diagnosed for 15 years. OHIP (Ontario universal health insurance) paid for all the tests for all those years. A lot of space-time went by, and so did a lot of money.

Re: Jugular Venous reflux in Leukoaraiosis

Posted: Tue Jun 25, 2013 12:39 pm
by frodo
1eye wrote:I don't know if I met the McDonald/CDMS criteria, but the time/space thing is only because they didn't have anything better, and it's unusually cruel for a sick person. Makes the work of diagnosis less stressful for the doctor.

From the first event I was not diagnosed for 15 years. OHIP (Ontario universal health insurance) paid for all the tests for all those years. A lot of space-time went by, and so did a lot of money.
I am afraid they still don't have anything better, except a biopsy. McDonalds criteria sucks but for other reasons, like to diagnose MS only when no other explanation can be found for the symptoms.