This Is MS Multiple Sclerosis Knowledge & Support Community

Posted: **Sat Sep 21, 2013 5:54 pm**

http://www.ncbi.nlm.nih.gov/pubmed/24039024

J Neurol Neurosurg Psychiatry. 2013 Sep 13. doi: 10.1136/jnnp-2013-305612. [Epub ahead of print]
Reduced grey matter perfusion without volume loss in early relapsing-remitting multiple sclerosis.
Debernard L, Melzer TR, Van Stockum S, Graham C, Wheeler-Kingshott CA, Dalrymple-Alford JC, Miller DH, Mason DF.
Source
New Zealand Brain Research Institute, , Christchurch, New Zealand.
Abstract
BACKGROUND:
Grey matter (GM) pathology in multiple sclerosis (MS) is associated with progressive long-term disability. Detection of GM abnormalities in early MS may therefore be valuable in understanding and predicting the long-term course. However, structural MRI measures such as volume loss have shown only modest abnormalities in early relapsing-remitting MS (RRMS). We therefore investigated for evidence of abnormality in GM perfusion, consistent with metabolic dysfunction, in early RRMS.
METHODS:
25 RRMS patients with ≤5 years disease duration and 25 age-matched healthy controls underwent 3 Tesla MRI with a pseudo-continuous arterial spin labelling sequence to quantify GM perfusion and a volumetric T1-weighted sequence to measure GM volume. Neurological status was assessed in patients and neuropsychological evaluation undertaken in all subjects. Voxel-based analysis was used to compare regional GM perfusion and volume measures in patients and controls.
RESULTS:
There was reduced global GM perfusion in patients versus controls (50.6±5.8 mL/100 g/min vs 54.4±7.6 mL/100 g/min, p=0.04). Voxel-based analysis revealed extensive regions of decreased cortical and deep GM perfusion in MS subjects. Reduced perfusion was associated with impaired memory scores. There was no reduction in global or regional analysis of GM volume in patients versus controls.
CONCLUSIONS:
The decrease in GM perfusion in the absence of volume loss is consistent with neuronal metabolic dysfunction in early RRMS. Future studies in larger cohorts and longitudinal follow-up are needed to investigate the functional and prognostic significance of the early GM perfusion deficits observed.
KEYWORDS:
CEREBRAL BLOOD FL

When it says without volume loss, does that mean that atrophy cannot be the cause of the reduced perfusion? The conclusion is that the reduced perfusion is due to metabolic dysfunction but of course it seems plausible to me that jugular and azygous blockages are at the root of it all.

Posted: **Mon Sep 23, 2013 12:24 pm**

Cece wrote:http://www.ncbi.nlm.nih.gov/pubmed/24039024
When it says without volume loss, does that mean that atrophy cannot be the cause of the reduced perfusion? The conclusion is that the reduced perfusion is due to metabolic dysfunction but of course it seems plausible to me that jugular and azygous blockages are at the root of it all.

Interesting paper Cece, you could be correct. Instead of asking the complex question of what causes what, I suggest that we collect papers which show that perfusion is reduced in MS. Then get someone to show that venoplasty decreases the reduction in perfusion or even reverses it. Then there is a logical argument for pwMS having venoplasty.
We need an argument for performing venoplasty which has a measurable effect rather than explaining what causes MS. That was Prof Zamboni's error at the start of this saga. (I have probably committed an unpardonable sin).
Kind regards,
MarkW

Posted: **Mon Sep 23, 2013 1:38 pm**

Dr. Zivadinov and Dr. Zamboni showed how reduced perfusion in gray matter was related to CCSVI severity back in 2010, and the Hubbard Foundation fMRI BOLD technology showed how venoplasty corrected this hypoperfusion.

for papers and links:
http://ccsviinms.blogspot.com/2011/03/dr.html

http://ccsviinms.blogspot.com/search?q=fMRI

Posted: **Tue Sep 24, 2013 12:13 pm**

cheerleader wrote:Dr. Zivadinov and Dr. Zamboni showed how reduced perfusion in gray matter was related to CCSVI severity back in 2010, and the Hubbard Foundation fMRI BOLD technology showed how venoplasty corrected this hypoperfusion.
for papers and links:
http://ccsviinms.blogspot.com/2011/03/dr.html
http://ccsviinms.blogspot.com/search?q=fMRI

I agree that to a logical person there is sufficient evidence. However, we are dealing with Neuros. I have not seen any papers which go in sequence:
1-Reduced perfusion is seen in x percent of pwMS and other people with neurological syndromes.
2-Reduced perfusion is detected in these areas
3-Reduced perfusion is chronic in pwMS.
4-Performing balloon venoplasty on valves in named veins improves perfusion.
The key here is getting many IRs to repeat the tests. Also not to use the term CCSVI, its a red rag to neuros.
For me, the first step is showing that pwMS and others have reduced cerebral perfusion. Let's call the syndrome Cerebral Perfusion Insufficiency, adding Chronic when the evidence emerges. Syndrome would better named Chronic Cerebral Perfusion Insufficiency (CCPI). Note I avoid hypoperfusion as the general public gets hypo and hyper confused, quite often.

I would not talk about the causes of MS as they are not known, just the syndrome (CCPI) and how it could be treated.
I would also get a group of medical marketing experts to critique any paper not just IRs/Vascular experts.

Its wonderful not to have cog fog after my venoplasties and have time to think outside the box.
Kind regards,
MarkW

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reduced grey matter perfusion without volume loss

reduced grey matter perfusion without volume loss

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