Circulatory effects of IJV compression study

[Cece]

http://www.ncbi.nlm.nih.gov/pubmed/12227629

Med Biol Eng Comput. 2002 Jul;40(4):423-31.

Circulatory effects of internal jugular vein compression: a computer simulation study.

Bosnjak R, Kordas M.
Source
Department of Neurosurgery, University Hospital Center, Ljubljana, Slovenia.

Abstract
The effects of compression of the internal jugular veins and the inferior vena cava are simulated using an equivalent electronic circuit, which included simulation of cardiocirculatory phenomena and special features of the cerebral circulation. Compression of the inferior vena cava resulted in a profound decrease in cardiac output (from 4.5 to 1.51min(-1)) and arterial pressure (from 140/85 to 50/35 mmHg). Compression of the internal jugular veins resulted in a negligible decrease in cardiac output and arterial pressure, with a cerebral blood flow that was slightly decreased. Cerebral capillary and internal jugular pressures were considerably increased, leading to obstruction of cerebral veins and increased pressure (from 9 to 22 mmHg) and volume (from 120 to 145 ml) of the cerebrospinal fluid (CSF). Increased cerebral capsule compliance resulted in decreased CSF pressure (from 9 to 8.5 mmHg), but CSF volume increased (from 120 to 190 ml). A small increase in brain volume (from 1,000 ml to 1,060 ml, 6% volume increase) was compensated for by an equal decrease in the volume of CSF. When brain volume was above 1,080 ml, the absorption of CSF was reduced, and its pressure increased.

[munchkin]

This is very interesting, thank you for finding and posting this. This information, the csf imaging from BNAC, and the symptoms for nph seem to fit together pretty well.

[Anonymoose]

How neat! It would be even better if it accounted for differences in individuals rather than assuming a standard response. I bet that could be programmed in there too though. They should make an app for that.

[Cece]

Compression of the internal jugular veins resulted in a negligible decrease in cardiac output and arterial pressure, with a cerebral blood flow that was slightly decreased. Cerebral capillary and internal jugular pressures were considerably increased, leading to obstruction of cerebral veins and increased pressure (from 9 to 22 mmHg) and volume (from 120 to 145 ml) of the cerebrospinal fluid (CSF).

I think this suggests that it may be more accurate to look at CCSVI as a hypertension disorder rather than an insufficiency? There was a decrease in cardiac output and arterial pressure and a reduction in cerebral blood flow but these were described as slight or negligible. The increase in pressure in the cerebral capillaries is considerable. This increase in pressure leads to the obstruction of cerebral veins. I agree with munchkin that this fits well with Dr. Zivadinov's findings of reduced parenchyma (reduced quantity of brain veins) in people with MS. An obstructed cerebral vein can be resorbed by the body. Also the cerebrospinal fluid is affected: increased pressure of CSF, increased volume of CSF.

I think individual differences comes into play as we develop collateral routes to compensate for some of these effects. This was looking at a computer simulation of compression of the IJV, not a simulation of long-term obstructions of the IJVs. A lot of research is done in an attempt to see past individual variation; get enough patients and you can see patterns emerge despite individual variation.

We need to see data on the opening levels of CSF pressure when lumbar punctures are done on MS patients. Is it normal?

[Anonymoose]

I agree that hypertension likely plays a big role in "CCSVI" (you did say that, didn't you?). In some, the hypertension may be caused or exacerbated by ijv compression causing the cerebral vessels to increase contact with the vagus nerve and/or rostral ventrolateral medulla resulting in autonomic dysregulation. To me, the safer thing to do is try the antihypertensive meds (especially those that target hpa axis dysregulation since that is a known problem with MS) and see if that manages the flow and endothelial issues adequately. If that's not good enough, then bring out the balloons for our veins and teflon cushions for our nerves. That said, I wish someone who was qualified (a doctor?!) to critique these assumptions would chime in and share thoughts on these ideas. Maybe they've already looked at these possibilities and thrown them out.

[Cece]

the hypertension at least as discussed in this article was from the compression (outflow obstruction) of the IJVs
compression of the IJVs led to increased pressure in the cerebral capillaries (hypertension of the cerebral capillaries?)
no word yet on if antihypertensives could help the situation
logically I would think it's a possibility!!

[Anonymoose]

the hypertension at least as discussed in this article was from the compression (outflow obstruction) of the IJVs
compression of the IJVs led to increased pressure in the cerebral capillaries (hypertension of the cerebral capillaries?)
no word yet on if antihypertensives could help the situation
logically I would think it's a possibility!!

But then we run back into that old question. How does CCSVI angioplasty sometimes cause such immediate and noticeable improvements? I don't see release of cerebral capillary hypertension on it's own having such a dramatic, instant effect. Some sort of major brain function has to be improved almost instantly with the release of the pressure. Doesn't it?

I wonder how much they compressed the jugulars and if it is similar to 'compression' in ms ccsvi. Also, if obstruction of cerebral veins leads to their death and resorption, then how would angioplasty undo their demise within minutes? If it only affects veins before they die but while they are sickly, instant noticeable improvements aren't likely either. Angioplasty has to do something bigger. Doesn't it?

Are there studies going on trying to figure out *why* and not *if* angioplasty works?

Do anti-hypertensives dilate stenosed areas too?

So many questions...

[Cece]

far more questions than answers

the release of cerebral capillary hypertension would, I believe, allow easier transport of glucose and oxygen across the blood brain barrier. but there may be several effects all in place that contribute to the amazing immediate improvements some people (me included) experience. I would like to understand it

I'd have to review Dr. Zivadinov's work about reduced parenchyma in MS to know if it is a significant reduction even in early MS or if it is mostly present in long term / advanced MS. Agree that relief of obstruction of cerebral capillaries would not lead to spontaneous immediate regeneration of any that are dead and gone.

No, antihypertensives cannot dilate annular stenoses with valve obstructions such as seen in many. But they would dilate other collateral blood vessels? Also would dilate hypoplastic jugulars, if that does any good, I think. Would antihypertensives reduce the amount of blood flow coming in arterially to the brain? Can't say that would be a good thing.

I think the physics studies such as Dr. Tucker has discussed are looking at the 'why'. Equations to see what effect the obstructions have on the closed loop with the CSF a factor too. He has described a situation in which incoming blood flow meets retrograde blood flow and the pressure of both is combined. But I do not know if there is research specifically saying what effect these surges of pressure have on the blood brain integrity and the neurons.

Lots to think about. You've got some good thoughts