Pregnancy, MS and changes to the veins

March 9, 2012 at 3:53pm

Naturally, there is lot of discussion on how the immune system is modulated while carrying a fetus...something the body sees as "other" and how this might affect MS.  And many people have mentioned hormones, especially estrogen.

But I wanted to discuss the vascular changes that happen while a woman is pregnant, because I never see this discussed, and I hope to encourage the ISNVD and other MS researchers to look into this correlation.

During pregnancy, a woman's blood volume increases by 50%.   This is to nourish the placenta and growing fetus, and also to compensate for blood loss during delivery.  If the blood vessels remained the same, with more blood volume, blood pressure would become dangerously high....so, the veins become more pliant, open and relaxed.  This is why many women develop varicose veins or hemorrhoids during preganancy.  

Venous Distension increases approximately to 150% during the course of gestation and the venous ends of capillaries become dilated.  Hormonal factors cause the veins to become more compliant. Together with the increased venous pressure that occurs later in pregnancy, these factors cause significant venous distension. Venous distendibility follows the rise in the hormones progesterone and relaxin.   Relaxin works by softening collagen and elastin in the tissues. It loosens the strong, cord-like fibers until they are super-pliable.

The hormone Relaxin is now being studied in cardiovascular disease, for its affects on the endothelium, via nitric oxide mechanisms.

The ovarian peptide hormone, relaxin, circulates during pregnancy, contributing to profound maternal vasodilation through endothelial and nitric oxide (NO)–dependent mechanisms. To conclude, relaxin is a novel regulator of BMDECs number and function, which has implications for angiogenesis and vascular remodeling in pregnancy, as well as therapeutic potential in vascular disease.

http://bloodjournal.hematologylibrary.org/content/119/2/629.abstract

Cerebral bloodflow increases during pregnancy:

Internal carotid artery blood flow volume increased during pregnancy from 318 mL/min ± 40.6 mL/min in the first trimester to 382.1 mL/min ± 50.0 mL/min during the third trimester, corresponding to CBF values of 44.4 and 51.8 mL/min(-1)/100 g(-1), respectively (P < .0001). CBF changes were associated with progressive decrease in cerebral vascular resistance and moderate increase in ICA diameter.

CONCLUSION:

Maternal CBF is gradually increasing during normal pregnancy. Vasorelaxing impact of estrogens and other factors on cerebral vessels may explain the changes in CBF during pregnancy.

http://www.ncbi.nlm.nih.gov/pubmed/20599183

 Could the hormonal relaxation of the jugular and azygos veins and increased blood volume during pregnancy account for better cerebral/spinal bloodflow?  Could this be why MS symptoms are less during pregnancy,  why pregnancy appears to "protect" women from MS?

more questions to ask, and to be answered--

Joan

Phlebology

June 26, 2011 at 3:08pm

Let's face it.  Phlebology, the diagnosis and treatment of venous disease, is just not as appealing as Neurology.  The word phlebology is hard to spell, hard to pronounce.  Reminiscent of phelgm, phlegmatic, other unsexy words that start with phl. 

The root of this word, phleb, is from the Latin fluere, meaning "to flow"

Truth is, phlebology is turning out to be a very, very important medical practice.  Veins, once thought to be uninvolved in disease, are turning out to be equally important as their brother arteries.  Maybe more so.

Veins take deoxygenated blood back to the heart.  If they are blocked, blood flow and hemodynamics are altered.  The influx of blood from the heart via the arteries is changed.   In the liver, in the kidneys, in the brain.  Any organ can be affected.  We think of varicose veins when we hear venous disease...again,  not sexy.  But veins run throughout the body, and if they are malformed, it can ruin our organs.

I got to meet and listen to a premiere phlebologist in Bologna in 2009.  Dr. Byung B. Lee was at the first symposium organized by Dr. Zamboni.  Dr. Lee talked about his introduction to venous disease as a liver transplant surgeon.    

Here are my notes from the conference.  Dr. Lee on venous malformations, in his own words.

Byung B. Lee- Georgetown University School of Medicine, Washington-Embryology of the venous system and origin of truncular venous malformations

Dr. Lee began as a transplant surgeon and admitted that his first liver transplant was a disaster. He learned the hard way that the vena cava is not just a single trunk, and a venous malformation was a most fearful thing, and a nightmare to a transplant surgeon. 

"We doctors have a tendency to specialize in our narrow fields, but I want to appeal to all of us to take a bird’s eye view. We need to look at the whole picture. We now understand the lower venous system, but it has taken us much too long to bring this knowledge all the way up to the neck and all the way to the junction of the superior vena cava.

Hypoperfusion (decreased blood flow) in MS

December 31, 2009 at 10:53am

Before 2009 comes to a close, I'd like to share more research on the decrease of blood flow in the MS brain. There are many researchers around the globe using new MRI technology to study slowed perfusion in MS brains.

I would like to break down this one medical research paper for you, to show you how these researchers' findings can be linked what Dr. Zamboni has discovered.  I will quote sections from the paper- and then we will discuss.

Hypoperfusion of the cerebral white matter in multiple sclerosis: possible mechanisms and pathophysiological significance

This work was supported by MS Anders (Amsterdam, The Netherlands).

Jacques De Keyser1,2, Christel Steen2, Jop P Mostert2 and Marcus W Koch2

1Department of Neurology, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel,Brussels, Belgium

2Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands

http://www.nature.com/jcbfm/journal/v28/n10/full/jcbfm200872a.html

from the abstract:

"A number of recent studies using perfusion magnetic resonance imaging in both relapsing and progressive forms of MS have shown a decreased perfusion of the NAWM, which does not appear to be secondary to axonal loss."

This means that in normal appearing white matter (NAWM) in MS brains, there is a slowing of blood flow which does not appear to be caused by axonal death. Something else is causing the slowed blood flow FIRST-because it shows up before we see lesions.

"The classic teaching is that MS is a T-cell-mediated autoimmune disorder of the central nervous system. However, a number of pathophysiological observations cannot be simply explained on the basis of autoimmune mechanisms. First, the progressive (neurodegenerative) component of the disease continues despite intense immunosuppressive interventions that effectively stop inflammatory disease activity (Coles et al, 1999; Metz et al, 2007; Roccatagliata et al, 2007; Samijn et al, 2006). Second, pathologic studies have shown that some demyelinating lesions develop without a preceding inflammatory reaction (Barnett and Prineas, 2004; Gay, 2007, 2006; Guseo and Jellinger, 1975; Lucchinetti et al, 2000). Third, another intriguing finding difficult to explain by autoimmune phenomena is the finding of a diffuse cerebral white matter hypoperfusion, which is the subject of this review."

The prior thought has been that MS is a t-cell mediated disease, autoimmune..we've all heard this. HOWEVER, the researchers wonder, how can the autoimmune hypothesis explain what we (many other researchers) are observing?

1. Even when suppressing the immune system, damage continues in the MS brain

2. Demyelinating lesions appear BEFORE inflammation

3, There is a slowing down of blood flow in cerebral white matter in MS brains