MS lesions and edema

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

MS lesions and edema

Postby dignan » Sat Nov 07, 2009 11:55 am

This is interesting...


Acute Multiple Sclerosis Lesion: Conversion of Restricted Diffusion Due to Vasogenic Edema.

J Neuroimaging. 2009 Nov 3.
Balashov KE, Aung LL, Dhib-Jalbut S, Keller IA.
From the Departments of Neurology (KB, LLA, SD-J); Department of Radiology (IAK), UMDNJ - Robert Wood Johnson Medical School, New Brunswick, New Jersey.

It is widely accepted that acute demyelinating plaques in patients with multiple sclerosis (MS) demonstrate increased apparent diffusion coefficient (ADC) and increased diffusion weighted imaging (DWI) signals on MRI. These imaging characteristics in acute MS lesions have been postulated to be due to peripheral vasogenic edema that typically increases the ADC. This assumption is commonly used to differentiate stroke from MS lesions since acute and subacute stroke lesions demonstrate increased DWI signal with reduced ADC due to acute cytotoxic edema.

We report a case of active relapsing-remitting MS with two new symptomatic contrast-enhancing lesions. The lesions had reduced diffusion on the ADC map in the early acute phase of MS exacerbation. The reduced ADC signal was subsequently "converted" to increased ADC signal that coincided with the development of profound peripheral vasogenic edema seen on T2-weighted images.

To our knowledge, this is the first serial MRI study describing decreased ADC signal in the early acute phase of contrast-enhancing MS lesion. The implications of decreased diffusion in the acute phase of MS lesions for the disease pathogenesis are discussed.

http://www.ncbi.nlm.nih.gov/pubmed/19888931
User avatar
dignan
Family Elder
 
Posts: 1610
Joined: Wed Aug 11, 2004 3:00 pm

Advertisement

Postby ozarkcanoer » Sat Nov 07, 2009 12:06 pm

Very very interesting, especially the : "profound peripheral vasogenic edema" part. Good for you to discover this !!!!
User avatar
ozarkcanoer
Family Elder
 
Posts: 1273
Joined: Thu Oct 15, 2009 3:00 pm
Location: St. Louis, Missouri

Postby cheerleader » Sat Nov 07, 2009 12:48 pm

Thanks, dig! Very interesting.
To break this abstract down into plain English for myself and others...

It's always been accepted that early MS lesions have increased apparent diffusion coefficient (ADC)...this means an increase of water molecules are seen in the demyelinated lesion. Also assumed has been increased diffusion weighted imaging (DWI)- showing more mobility of water in the brain.

This has been used to differentiate MS lesions from stroke lesions...since stoke lesions show up with decreased ADC and decreased DWI, due to acute cytotoxic edema (a swelling of brain tissue stops the water molecules from swimming around.)

What this study found was that in the very beginning of lesion formation in an MS patient, in the early acute phase of an exacerbation- the lesion had a reduced DWI (like a stroke lesion, the water in the area wasn't mobile) AND decreased ADC...just like a stroke lesion. They looked at these lesions again, and the ADC increased in the new MS lesions as profound peripheral edema happened over time...it was the vasogenic edema that converted the ADC (Vasogenic edema is characterized by an increase in extracellular fluid volume due to increased permeability of brain capillary endothelial cells) Those extra water molecules came from the edema. The lesion began its life with decreased ADC first...just like a stroke.

Would like to read the whole paper to see what their conclusions were-

We've been discussing how CCSVI can create stroke like/hypoxic injury, and this study confirms that in the beginning of the life of an MS lesion, it looks alot like a stroke hyperintensity on MRI.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
User avatar
cheerleader
Family Elder
 
Posts: 4939
Joined: Mon Sep 10, 2007 3:00 pm
Location: southern California

Postby mrhodes40 » Sat Nov 07, 2009 2:55 pm

Dignan I am glad you posted that, I was reading a related paper yesterday that I was debating making a post on, I'll go ahead and add it here..

FULL TEXT HERE

New MRI techniques such as the analysis of magnetization transfer or diffusion have provided evidence for subtle progressive alterations in tissue integrity prior to focal leakage of the blood–brain barrier (BBB) as part of plaque formation in multiple sclerosis. Since inflammation is capable of modulating the microcirculation, we investigated the hypothesis that changes in the local perfusion might be one of the earliest signs of lesion development. 20 patients with definite relapsing–remitting multiple sclerosis were analysed with regard to cerebral blood volume, cerebral blood flow, mean transit time and apparent diffusion coefficient (ADC), as well as conventional MRI parameters, on monthly follow-up scans. Among 89 gadolinium-enhancing lesions, we selected 18 that developed during the study and met strict inclusion criteria. In these, changes of perfusion parameters were detectable not only prior to the BBB breakdown, but also prior to increases in the ADC. Our data indicate that inflammation is accompanied by altered local perfusion, which can be detected prior to permeability of the BBB.


It is interesting how much of this study had to do with blood flow, yet they were primarily interested in inflammation and how that changed microcirculation.

Microcirculation is also changed by increased pressure from venous reflux.

CLICK HERE TO SEE SOURCE
Local Microcirculation in Chronic Venous Incompetence and Leg Ulcers
Bengt Fagrell
Department of Medicine , Karolinska Institute at St. Erik's Hospital, Stockholm, Sweden

Most chronic leg ulcers (90 to 95%) are caused by incompetence of the deep venous system and/or the perforators of the lower leg. Superficial venous incompetence does not give rise to necrotic skin ulcers. The primary cause of venous leg ulcers is the marked increase in pressure that builds up in the deep veins of the lower leg during walking. This pressure is transformed to the skin vessels through the ankle perforators, out to the nutritional vascular bed of the skin. The intracapillary pressure increases tremendously and this causes the capillaries to dilate and become tortuous. The blood elements leak out through the capillary wall into the surrounding tissue and form a specific microedema, which gives rise to an effective nutritional block between the capillaries and the skin cells. This microedema is most probably the main cause of the development of venous leg ulcers.



Vascular and Endovascular Surgery, Vol. 13, No. 4, 217-225 (1979)



They know that in the case of venous reflux restoring normal circulation usually allows healing of the venous lesions, which in the case of the leg, are skin ulcers.

SOURCE HERE

Monitoring for 94% of patients lasted a mean 22 months (range, 1 to 107 months). Stenting was performed with no mortality (<30 days) and low morbidity. Thrombotic events were rare (1.5%) during the postoperative period (<30 days) and during later follow-up (3%). At 72 months, primary, assisted-primary, and secondary cumulative patency rates were 79%, 100%, and 100% in nonthrombotic disease and 57%, 80%, and 86% in thrombotic disease, respectively. Cumulative rate of severe in-stent restenosis (>50%) occurred in 5% of limbs at 72 months (10% in thrombotic limbs, 1% in nonthrombotic limbs). The main risk factors associated with stent occlusion were the presence and severity of thrombotic disease; thrombophilia by itself was not a risk factor. The median pain score and degree of swelling decreased significantly poststent. Severe leg pain (visual analogue scale >5) and leg swelling (grade 3) decreased from 54% and 44% prestent to 11% and 18% poststent, respectively. At 5 years, cumulative rates of complete relief of pain and swelling were 62% and 32%, respectively, and ulcer healing was 58%. The mean CIVIQ scores of QOL improved significantly in all categories. Mean hand-foot pressure differential decreased and mean ambulatory venous pressure improved in stented limbs with no concomitant reflux. The hemodynamic response was modified, depending on the presence of deep and superficial reflux in subsets of patients with adjunct saphenous procedures. No increase in venous reflux was observed.

Conclusions
Venous stenting can be performed with low morbidity and mortality, long-term high patency rate, and a low rate of in-stent restenosis. It resulted in major symptom relief in patients with chronic venous disease, which was not consistently reflected in any substantial hemodynamic improvement by conventional measurements. The beneficial clinical outcome occurred regardless of presence of remaining reflux, adjunct saphenous procedures, or etiology of obstruction.



Basically if they opened up the veins people did very well...
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
http://www.ccsvibook.com Read my book published by McFarland Health topics
User avatar
mrhodes40
Family Elder
 
Posts: 2066
Joined: Thu Sep 23, 2004 3:00 pm
Location: USA


Return to Chronic Cerebrospinal Venous Insufficiency (CCSVI)

 


  • Related topics
    Replies
    Views
    Last post

Who is online

Users browsing this forum: No registered users