Clive Begg's model of cerebral venous return

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

Clive Begg's model of cerebral venous return

Postby cheerleader » Thu Mar 17, 2011 3:39 pm

The abstract from the ISNVD presentation:
http://ccsvism.xoom.it/ISNVD/Other/Abst ... l%20of.pdf

Dr. Beggs explains his view of the Doepp results--

Model of the cerebral venous return
Authors & Affiliation: Clive Beggs - Centre for Infection Control & Biophysics,
University of Bradford, Bradford, UK

Introduction: Within the multiple sclerosis (MS) research community the concept of chronic cerebrospinal venous insufficiency (CCSVI) has caused much controversy, and this has led some researchers to challenge the findings of Zamboni et al [1]. In particular, Doepp et al found no evidence of CCSVI in MS patients [2]. However, no hydrodynamic analysis was performed on the blood flow data collected during this study. Independent analysis of Doepp et al’s data by Beggs [3] suggested that contrary
to Doepp et al’s assertions, the study actually revealed severe venous abnormalities in MS patients. In this paper, Beggs’ initial hydrodynamic analysis is expanded using a simple model of the extracranial venous system.

Materials & Methods: This paper uses a simple hydrodynamic model of the
extracranial venous system to interpret Doepp et al’s blood flow data. In particular, analysis is undertaken of the impact that extracranial venous stenosis has on cerebral blood flow (CBF) in the upright position.
Results: Hydrodynamic analysis of the data indicates that, when upright, the MS patients in Doepp et al’s study exhibited considerable rerouting of the extracranial venous blood flows compared with health controls. This suggests that in these patients venous stenosis was present, resulting in extensive collateral rerouting of the blood flow back to the heart. The results also indicate that there is a strong postural component to be abnormalities observed.

Discussion & Conclusion: Extensive collateral rerouting to the venous blood flow from the brain is something that has been observed by Zamboni et al [4]. Although this rerouting will help to relieve intracranial venous hypertension, stenosis of the extracranial venous pathways will inevitably increase the overall hydraulic resistance of the cerebral vascular circuit. Increasing the system resistance will have a dual effect; firstly, it will tend to reduce cerebral blood flow (CBF), and secondly, it will raise the pressure in the venous sinuses [1]. Evidence supporting the former conclusion comes from several studies [5-7], all of which observed lower CBF in the normally appearing white matter of MS patients compared with healthy controls, particularly in the periventricular region. While no published data exists regarding blood pressure in the venous sinuses of MS patients, indirect evidence of hypertension in these vessels comes
from two studies [8, 9]. In the first of these, Zamboni et al observed that following angioplasty to open up stenotic vessels, the venous pressure in MS patients dropped by approx. 2.2 mm Hg [8]. In the second study [9], Zamboni et al found that the bulk flow of the CSF in MS patients was greatly reduced compared with healthy controls; something that is indicative of raised blood pressure in the SSS.

Doepp et al’s data appear to confirm that there may be a postural element in the pathophysiology of MS. Previous researchers have observed abnormal heart rate and blood pressure responses in MS patients during tilt table tests and have attributed this to cardiovascular autonomic regulation failure [10, 11]. Flachenecker et al [12] found that
fatigue in MS patients correlated with autonomic dysfunction and postulated that that this was possibly due to lesions impacting on the a sympathetic vasomotor. However, while these investigators performed standard autonomic control tests on MS patients, none measured the changes in the extracranial venous flow rate that occur when subjects move from the supine to upright position.
When supine, the IJVs generally act as the principle route by which blood drains from the brain, whereas when upright, their role becomes minimal, with the vast majority of the blood traveling either down the VVs or through other venous pathways [13, 14]. In Doepp et al’s study both cohorts conformed to this norm when supine, whereas only the healthy controls did when upright – a situation that is highly unusual. Doepp et al’s results therefore suggest that, rather than any autonomic cause, the rerouting of blood in MS patients occurs as a result of stenosis which primarily affects the venous pathways that are normally used to transport blood back to the heart when upright.
References: (1) Zamboni et al. J Neurol Neurosurg Psychiatry 80:392, 2209. (2) Doepp et al. Ann
Neurol 68:173, 2010. (3) Beggs. Ann Neurol 68:560, 2010. (4) Zamboni et al. Curr Neurovasc Res 6:204,
2009. (5) Law et al. Radiology 231:645, 2004. (6) Varga et al. J Neurol Sci 282:28, 2009. (7) Adhya et al.
Neuroimage 33:1029, 2006. (8) Zamboni et al. J Vasc Surg 50:1348, 2009. (9) Zamboni et al. Funct
Neurol 24:133, 2009. (10) Saari et al. Clin Neurophysiol 115:1473, 2004. (11) Kanjwal et al. Int J Med
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby Cece » Thu Mar 17, 2011 4:05 pm

Results: Hydrodynamic analysis of the data indicates that, when upright, the MS patients in Doepp et al’s study exhibited considerable rerouting of the extracranial venous blood flows compared with health controls. This suggests that in these patients venous stenosis was present, resulting in extensive collateral rerouting of the blood flow back to the heart. The results also indicate that there is a strong postural component to be abnormalities observed.

I am so confused by why it's abnormal when we are upright. I have been thinking the worst is when we are lying down, as that's when the jugulars are primarily used.
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Postby CuriousRobot » Thu Mar 17, 2011 4:12 pm

Cece wrote:
Results: Hydrodynamic analysis of the data indicates that, when upright, the MS patients in Doepp et al’s study exhibited considerable rerouting of the extracranial venous blood flows compared with health controls. This suggests that in these patients venous stenosis was present, resulting in extensive collateral rerouting of the blood flow back to the heart. The results also indicate that there is a strong postural component to be abnormalities observed.

I am so confused by why it's abnormal when we are upright. I have been thinking the worst is when we are lying down, as that's when the jugulars are primarily used.


I think the jugulars aren't used when lying down but the vertebral veins. The jugulars are used when upright.

I may be wrong, though, but this is what an endovascular surgeon told me not too long ago. Anyone can make a mistake, really.
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Postby cheerleader » Thu Mar 17, 2011 4:16 pm

Cece wrote:I am so confused by why it's abnormal when we are upright. I have been thinking the worst is when we are lying down, as that's when the jugulars are primarily used.


I'm with you, Cece. This is all way above my ken. I'm just glad we have biophysicists looking at the slowed bloodflow thru MS brains and trying to figure out what is going on. I know it relates to lack of cerebral spinal fluid, pressure changes, collateral circulation and stenosis...but I am not even going to try and explain it. No hose analogies :)

The jugulars are the main exit route when lying down, the vertebrals and other veins when upright. That much I remember....
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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby 1eye » Thu Mar 17, 2011 5:23 pm

Please correct me if I'm wrong:

Doepp et al’s results therefore suggest that, rather than any autonomic cause, the rerouting of blood in MS patients occurs as a result of stenosis which primarily affects the venous pathways that are normally used to transport blood back to the heart when upright.


So, because we can't take the jugular route when prone because of stenosis, we do our best to build up a decent set of alternate paths for that time. This will be vertebrals, other veins, collateral veins. They take up what we should be able to have flowing, and would, when prone, except that stenosis is stopping it. The drainage must happen by other routes when we are lying down. So we build up more than normal capacity by expanding the veins, growing collaterals, etc.

When we sit back up, the normal thing is for jugulars to collapse. They do, but only part way. The stenosis may help or hinder the collapse. But the jugular path becomes less useable. The resistance to blood flow becomes higher than it was when we were prone. So now, to get the same amount of blood back down to the heart, as we did before sitting up, more extra-jugular capacity is needed than when we were prone, and there is more pressure, due to gravity.

The stenosis is the problem both when partially collapsed and not. Lying down is bad, but sitting up is worse.

Does that fit with the facts?

We respond over time if we can by building collateral paths. Is the difference between phenotypes partly due to whether the stenosis helps or hinders the normal jugular vein collapse when we are upright? I am still unclear about the how of that, except that it might have something to do with the short bend from front to back of the head that the vein takes at the brain end.

Anybody still with me? Have I got this all wrong?
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Postby Cece » Thu Mar 17, 2011 6:12 pm

cheerleader wrote:
Cece wrote:I am so confused by why it's abnormal when we are upright. I have been thinking the worst is when we are lying down, as that's when the jugulars are primarily used.


I'm with you, Cece. This is all way above my ken. I'm just glad we have biophysicists looking at the slowed bloodflow thru MS brains and trying to figure out what is going on. I know it relates to lack of cerebral spinal fluid, pressure changes, collateral circulation and stenosis...but I am not even going to try and explain it. No hose analogies :)

A lot has changed in the last two years. We didn't use to have biophysicists at work on this. It is good to see the momentum building.

MrSuccess, you are a valued member of the community here, as is Cheer....
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Postby MrSuccess » Thu Mar 17, 2011 9:52 pm

I think you mean '' kin'' ..... as in kinfolk ..... not Ken .... as in Barbie & Ken .... :wink:

Nice reply from Clive Begg ....... any and all new discoveries or ideas are certainly met with open arms .....







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Re: Clive Begg's model of cerebral venous return

Postby 1eye » Sun Jul 14, 2013 7:01 pm

Dr. Beggs explains the Doepp result with:
Doepp et al’s results therefore suggest that, rather than any autonomic cause, the rerouting of blood in MS patients occurs as a result of stenosis which primarily affects the venous pathways that are normally used to transport blood back to the heart when upright.

This is of prime importance. In contrast with research I found at CCSVI-Locator this morning, it seems very certain that "MS" patients have problems with venous blood-flow. The excessive sodium that has been found in nerves: is it from the vein stenosis?
That aside, maybe one difference between progression and not, is in additions to the network of veins we use when upright. I continue to believe that collaterals being added are the reason for the (often only partial) remissions which happen in only some "MS". I think these are not new spare jugular-type veins with similar large capacity, but additions to the spinal venous pathways (described above as "normally used ... when upright").

These are not the same veins that Zamboni et al had venoplasty done on (jugulars). They are normally used when upright, instead of the jugulars, which normally are a low-resistance path for venous return when we are lying down, not when we are upright. Because the stenosis in jugulars does not affect us when standing (jugulars not used), why do we have any problems at all?

I would suggest that the new collateral pathways are never quite enough to do the job of the IJVs. If stenosis gets worse, exacerbations happen. The limit to recovery from exacerbations is our limited ability to replace jugular capacity with new collateral veins. As we age, and progress, we lose more and more of that ability.

Generally, exacerbations happen when we go from prone to standing, in my experience. After worsening, the collapse of the jugulars that happens when standing up means the other venous pathways of the neck do not adequately replace the jugular flow that was there when lying down. That must mean the jugular had worsening of its stenosis during sleep. The extreme of this is 100% blocking of both jugulars.

The veins that are used when we are upright don't collapse when we lie down. While normals (no "MS") are lying down sleeping they have more brain drainage capacity than when upright. That may be why they dream, but we don't. I think there is also a difference due to reorientation in the gravity field, making circulation slower when a normal person is lying down. The autonomic and conscious control of things that affect our heart rate are trained during childhood to expect the posture to change for sleep, once we have learned to walk.

But when stenosis happens, the blood flow can't slow down as much when we lie down. This is why I can sit up with a computer on my lap till all hours, but as soon as I lie down, problems begin. I can't even get to sleep with my eyes closed, sometimes for the whole night. My father was like this later in his life, too. He didn't have "MS" but had late-onset diabetes, and peripheral neuropathy.

Another thing that happens when I have recently been asleep, is that I can play better piano (it's all bad, really :smile: ) for a variable, but always short, length of time. That does not last, lately, for longer than about an hour. If I nap during the day, i can sometimes get it back, but it won't last as long.
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Re:

Postby euphoniaa » Tue Jul 16, 2013 1:35 pm

MrSuccess wrote:I think you mean '' kin'' ..... as in kinfolk ..... not Ken .... as in Barbie & Ken .... :wink:

Nice reply from Clive Begg ....... any and all new discoveries or ideas are certainly met with open arms .....

Mr. Success

Actually, Mr. S, cheerleader was entirely correct using the term "ken" as in understanding and not "kin" as in her kinfolk. :wink:

Cheer's quote was, "This is all way above my ken," as in above her understanding rather than above her relatives. :smile:
Dx'd with MS & HNPP (hereditary peripheral neuropathy) 7/03 but must have had MS for 30 yrs before that. I've never taken meds for MS except 1 yr experiment on LDN. (I found diet, exercise, sleep, humor, music help me the most.)
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Re: Clive Begg's model of cerebral venous return

Postby blossom » Tue Jul 16, 2013 4:54 pm

i'll bet upright doc. flanagan could answer and explain these questions.
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Re: Clive Begg's model of cerebral venous return

Postby 1eye » Wed Jul 17, 2013 8:44 am

Does anybody but me think the two of them should get in touch? Or is that too much to ask of them?
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Re: Clive Begg's model of cerebral venous return

Postby AndrewKFletcher » Tue Aug 06, 2013 12:56 am

A postural connection with ms? Now where have we heard this before?
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