Peer-review means that other scientists look at the evidence and consider if the new theory should be published in a journal. It doesn't mean the theory is 100% accurate, or the science is bullet-proof. It just means that other researchers have looked at the evidence of their professional peers and found something of value in the science.
All of Dr. Zamboni's research was peer-reviewed and published. But it was more than just a theory. He had a diagnostic procedure and medical treatment in 65 patients, with documented changes in venous blood flow before and after treatment. He had discovered a new medical condition he called CCSVI, but it was based on long-recognized venous insufficiency and vascular malformations found in other veins.
That's why the researchers at Stanford gave me the time of day when I sent them Zamboni's papers back in 2008. They saw that other vascular researchers had read his CCSVI research, found something of merit in his science and published it in journals. Jeff was diagnosed and treated for venous malformations seen on MRV and venography.Not for MS, not for CCSVI. His was a real, quantifiable problem. We saw on MRV how his jugular veins looked before and after treatment, and his venous return was measured and had improved after stent placement. Dr. Dake published the results he saw as part of a retrospective study in a peer-reviewed vascular journal.
http://www.ncbi.nlm.nih.gov/pubmed/22496109
Here's a great resource for those who want to read the peer-reviewed papers on CCSVI and MS, from CCSVI Alliance
http://www.ccsvi.org/index.php/componen ... ask=search
And here's Marie Rhode's wonderful book, which used over 400 peer-reviewed and published papers to explain the connection of MS and the venous system:
http://ccsvibook.com
This is very, very different than having a theory which you twitter, or a blog, or a Facebook page. That's why I'm not a scientist, just a patient advocate. It's really easy for me to write on Facebook, not so easy to get published
Marie knows how much work it takes to get published! When researchers publish, they build on the knowledge base, and are actually able to help more people around the world. It's a virtuous cycle.
Let's get our terms and history straight.
What is autonomic dysfunction, also known as dysautonomia?
This is a broad medical term which relates to the malfunctioning of any body system related to the autonomic nervous system. It means a malfunctioning of the systems we don't have to think about, that our body takes care of on it's own, literally "self-controlled"--like breathing, heart rate, blood pressure, and the digestive tract. Pretty broad system, right? Right.
The autonomic nervous system is broken down into 2 sections: the sympathetic and the parasympathetic (see the pic below.)
Here's a great video with info on the differences in these two systems, for those who want to learn more.
http://wps.aw.com/bc_goodenough_boh_3/1 ... index.html
A common form of autonomic dysfunction we may know about is orthostatic hypotension...this is dizziness when we stand up quickly, and the blood doesn't get to our brains in a timely manner, and we feel faint. It's about changes in posture. I have a mild case of this, and sometimes I wobble a bit when I get up. My Dad had it, and we both have low blood pressure. I've had the tilt table test, and got the diagnosis. What works best for me is regular exercise, great nutrition, hydration and good sleep. I'm not medicated for this, and neither was my Dad. It happens a lot in the elderly, and is what causes them to fall. People who have severe cases have neurologic disease, and they can receive medication, but it's a multi-system approach which works best. Here are the A, B, Cs of treating orthostatic hypotension.
http://www.ccjm.org/content/77/5/298.full
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I first heard about this connection of dysautonomia and CCSVI from Dr. Diana Driscoll, who was putting together her theory of CCSVI, based on her personal experience with Ehler Danlos disease, POTs and MS. I met her on This is MS. Dr. Driscoll has spoken at length about her theory, written about it, and made YouTube videos. She has not published anything in a peer-reviewed journal. That doesn't mean she's wrong, it simply means it hasn't been published or peer-reviewed. She has always suggested a multi-disciplinary approach. Here is her website, where she has been discussing her theories for over a decade.
http://prettyill.com
Sadly, Dr. Driscoll did not publish her theory in a peer-reviewed journal, and because of this, it has not been easy for her. The great thing about publishing in a respected journal is that other scientists read your theory, and can expound on it. They can credit you--by using a citation--and build on your work. Publishing really is the key to gaining acceptance and further knowledge.
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Here is a paper on the theory of treating rheumatoid arthritis with vagal nerve stimulators (VNS) to treat the underlying autonomic system imbalances.
VNS is currently an approved treatment for epilepsy and depression. It is an FDA approved implanted device which delivers charges to the vagus nerve. These researchers believe this treatment may be helpful for those with RA.
Please note that this is not a one-time bump into the vagus nerve with a balloon---this is treatment using ongoing, electrical impulses. Because autonomic dysfunction is an ongoing problem. Venous malformations can be corrected with ballooning and stenting, but there is not evidence that ballooning does anything for autonomic dysfunction.
Vagus nerve stimulation already is used in patients with drug-resistant epilepsy and depression. The left vagus nerve is stimulated via an implantable electrode. Vagus nerve stimulation had beneficial effects in both disorders without major side effects (99). A recent study investigating in more detail the effect of VNS on the immune system in 11 patients with refractory epilepsy demonstrated that VNS causes a rebalancing of the immune system compared with a control group (102).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3188868/
VNS devices may well be a viable treatment option for those with CCSVI/MS due to autonomic dysfunction.
It is an FDA-approved device, covered by insurance. But there needs to be more published research before it can be approved.
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Dr. Zohara Sternberg, from BNAC, has published her THEORY of the connection between Autonomic Dysfunction, CCSVI, D3 levels and Epstein Barr virus. Again, this is just a THEORY, meaning that it's not right or wrong, it's just looking at connections and hypothesizing. Dr. Sternberg is not suggesting any treatment or way to deal with this. She's just putting some puzzle pieces together.
Let's break down her abstract together. The abstract will be in italics, my thoughts will be in regular text.
Abstract
Multiple sclerosis (MS) is a disease with multiple etiologies. The most recent theory of the vascular etiology of MS, Chronic Cerebrospinal Venous Insufficiency (CCSVI), suggests that cerebral venous obstruction could lead to cerebral venous reflux, promoting local inflammatory processes.
--Well, this isn't really a complete review of Dr. Zamboni's research, but it will suffice for the abstract. Abstracts are not complete papers. If we want to read all of the science, we can purchase the full paper through the online website.
This review article offers strong evidence that the route of the observed narrowing of cerebral veins arises from autonomic nervous system dysfunction, particularly cardiovascular autonomic dysfunction.
--Please note that she is talking about CEREBRAL VEINS....this is not the same as CCSVI, which is narrowing of the veins outside the brain, or extracranial veins--the jugular and azygous. She is looking at how the veins inside the brain might be narrowing, due to a malfunctioning of the cardiovascular system.
The dysfunction of this system has two major effects: 1) the reduction of mean arterial blood pressure, which has the potential to reduce the cerebral perfusion pressure and the transmural pressure, and 2) the failure of cerebral autoregulation to maintain constant cerebral blood flow in the face of fluctuations in cerebral perfusion pressure. Alterations in cerebral autoregulation could in turn raise the critical closure pressure, indicated to be the cerebral perfusion pressure at which the transmural pressure will be sub-sufficient to overcome the active tension imparted by the smooth muscle layer of the vessel.
--OK, this is actually a lot more easy to understand then it appears at first glance
If the cardiovascular system's auto-pilot feature is malfunctioning, this could slow down blood going into the brain, and reduce the pressure inside the brain. If the autonomic system isn't working between the heart and the head, constant cerebral blood flow can be altered, and the system of blood flow between the head and heart can be changed. This will change the lining of the blood vessels, and make them tighter. Just like what we were talking about in orthostatic hypotension above. The cerebral blood vessels are compensating for the slowed blood flow.
These two effects of autonomic nervous system dysfunction (reduction in arterial blood pressure and alterations in cerebral autoregulation), when combined with inflammation-induced high levels of nitric oxide in the brain, will lower transmural pressure sufficiently to the point where the threshold for critical closure pressure is reached, leading to venous closure.
In addition, cerebral vessels fail to overcome the closure as a result of low central venous pressure, which is also regulated by autonomic nervous system function.
--So, what she is describing is a cascade effect. Less blood pressure in the brain means less blood flow, means more inflammation, and will make the blood move even more slowly, causing the veins to constrict even more.
Furthermore, through their neuroregulatory effects, infectious agents such as the Epstein-Barr virus and vitamin D3 are able to alter the functions of the autonomic nervous system, influencing the rate of CCSVI occurrence.
The absence of CCSVI specificity for MS, observed in recent clinical studies, may stem from a high prevalence of autonomic nervous system dysfunction in control groups which were recruited to these studies. Future studies should investigate CCSVI in relation to cardiovascular autonomic function.
--Now she's looking at a couple of things we know thru previously published scientific research are related to MS, and trying to connect the dots. We know pwMS have lower levels of the hormone D3, and we know that the EBV virus has been linked to MS. These factors have been discussed in other research. If we had the full paper, we could read more about her hypothesized connection between EBV, D3 and changes to the autonomic nervous system. WHat she's theorizing is that the fact that CCSVI is showing up in normals is because the control population might have autonomic function problems, which might be right. Again---this is all conjecture. Just a theory.