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Dr. Arata talked about the vagus nerve as a potential contributor to dysregulation of the autonomic nervous system here, if I am remembering correctly:

and Dr. Driscoll talked about it at ISNVD:

Abnormal Venous Flow and Neurodegenerative Disease: Part IV
Dr. Timothy Q. Duong talked on investigating the vasculature of the eye. MRI offers depth resolved, layerspecific
anatomical layers, quantitative retinal and choroid blood flow, BOLD fMRI responses in the human
retina. Dr. Simka talked about retinal abnormalities in multiple sclerosis patients with associated chronic
cerebrospinal venous insufficiency. The asymmetric outflow from the brain to the asymmetric stenosis of the
IJV was associated with higher risk of retinal neurodegeneration. High prevalence of ocular pathology was
also observed in MS patients without CCSVI. Dr. Diana Driscoll discussed the CCSVI and eyes. She gave an
introduction of vagus nerve suppression when IJV and/or ICA (internal carotid artery) expand due to
insufficient venous blood flow or stenosis in the jugular veins. On the basis of her interpretation of the
symptoms presented, it might be important to study vagus nerve compression as a likely cause (secondary to
CCSVI) of the symptoms for MS. She explained vagus nerve compression and CCSVI angioplasty (after
controlling the mast cells/ inflammatory cytokines) helps with some of the symptoms immediately.

http://www.isnvd.org/files/ISNVD_Newsletter.pdf

Could reduction of compression of the vagus nerve by the distended jugular or distended carotid artery after ccsvi venoplasty explain some of our immediate improvements?

Cece wrote:Dr. Arata talked about the vagus nerve as a potential contributor to dysregulation of the autonomic nervous system here, if I am remembering correctly:

and Dr. Driscoll talked about it at ISNVD:

Abnormal Venous Flow and Neurodegenerative Disease: Part IV
Dr. Timothy Q. Duong talked on investigating the vasculature of the eye. MRI offers depth resolved, layerspecific
anatomical layers, quantitative retinal and choroid blood flow, BOLD fMRI responses in the human
retina. Dr. Simka talked about retinal abnormalities in multiple sclerosis patients with associated chronic
cerebrospinal venous insufficiency. The asymmetric outflow from the brain to the asymmetric stenosis of the
IJV was associated with higher risk of retinal neurodegeneration. High prevalence of ocular pathology was
also observed in MS patients without CCSVI. Dr. Diana Driscoll discussed the CCSVI and eyes. She gave an
introduction of vagus nerve suppression when IJV and/or ICA (internal carotid artery) expand due to
insufficient venous blood flow or stenosis in the jugular veins. On the basis of her interpretation of the
symptoms presented, it might be important to study vagus nerve compression as a likely cause (secondary to
CCSVI) of the symptoms for MS. She explained vagus nerve compression and CCSVI angioplasty (after
controlling the mast cells/ inflammatory cytokines) helps with some of the symptoms immediately.

http://www.isnvd.org/files/ISNVD_Newsletter.pdf

Could reduction of compression of the vagus nerve by the distended jugular or distended carotid artery after ccsvi venoplasty explain some of our immediate improvements?

I had the same question in regards to this report, as it may be speaking to cases similar to mine. Thanks for posting all the summaries Cece!

tilt

Cases like mine too. Immediate improvements on the table both times. The improvements were weird things like my hearing improving, fentanyl-related wooziness clearing instantly, color vision improving dramatically, and during my second procedure, everything getting whiter/brighter in a flick, as if the lights had been turned up. I don't think any of that is autonomic nervous system though?

Dr. Zamboni's plethysmography shows that there is a greater volume of blood in the necks of MS patients, and that greater volume could result in compression of the vagus nerve, but doesn't that volume return to normal (it just takes longer to do so than the controls)? I am trying to figure out where the dilatation is that would be compressing the vagus nerve. Above the stenoses there can be dilatation, or at the top of the vein. If dilatation is something that worsens as patients age, then vagus nerve compression could worsen along with it, and that could explain the onset of symptoms or the worsening of some symptoms? Not sure.

If the vagus and other autonomic nerves are contained in a sheath with veins that are trying to expand to accommodate increased pressure, wouldn't that tend to compress the nerves? Can that happen anywhere else where nerves travel in parallel with veins or arteries inside a non-compliant casing? Will it happen more with venous pressure than arterial pressure due to the relatively compliant vein walls?

I don't know, but good questions.
Here's an image of dilatation of the jugular vein in jugular phlebectasia. This is considered a benign condition. If jugular phlebectasia does not compress the vagus nerve, I do not think CCSVI dilatation would. Or am I missing something?

http://www.ijoonline.com/viewimage.asp? ... 324_f2.jpg

Cece wrote:I don't know, but good questions.
Here's an image of dilatation of the jugular vein in jugular phlebectasia. This is considered a benign condition. If jugular phlebectasia does not compress the vagus nerve, I do not think CCSVI dilatation would. Or am I missing something?

http://www.ijoonline.com/viewimage.asp? ... 324_f2.jpg

i strongly doubt this hypothesis. The pressure in the jugular vein is so low, that it is unlikely to have an affect on the vagus nerve function.

Also the vocal cords are controlled by the vagus nerve and i do not think that patients with ccsvi or m s have hoarse voices very commonly. and that would be affected by vagal nerve in the neck being dysfunctional.

it is far more likely that the cranial nerves are affected by the demyelination intracranially in the brain stem

Dysautonomia is very common in MS but i think its cause is inside the skull

That’s an interesting paper regarding the topic - “out of control” pulsatile pressure (artery) on the brain stem perhaps caused by a crazy blood flow (wrong volume, wrong speed, wrong directions etc.) started somewhere in a renal, cava, azygous, jugular whatever vein further down? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1250685/

muse wrote:That’s an interesting paper regarding the topic - “out of control” pulsatile pressure (artery) on the brain stem perhaps caused by a crazy blood flow (wrong volume, wrong speed, wrong directions etc.) started somewhere in a renal, cava, azygous, jugular whatever vein further down? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1250685/

I do not think it is a direct effect on the brain stem. I would suggest that perhaps better csf drainage may reduce pressure on the brainstem. I highly doubt that renal, cava, azygous veins have direct efffect on brain stem

Sorry for slight hijack...I had significant head and neck trauma through falls and vehicle accidents before my M.S. appeared. I still have after 40 years, neck issues that cause a jolt occasionally. I had 2 stenosis ballooned by Dr Sisken 18 months ago with no improvements. My question is what/how would I have my Vagus nerve looked at? P.M. is fine.

I do not think it is a direct effect on the brain stem. I would suggest that perhaps better csf drainage may reduce pressure on the brainstem. I highly doubt that renal, cava, azygous veins have direct efffect on brain stem

I don't think it is a direct effect on the brain stem either. I just wanted to say (I’m not a native speaker, sorry) that perhaps the main culprit is an arterial insufficiency, a pulsatile aterial compression of the medulla oblongata if it comes to cranial nerve dysfunctions/autonomic nerve dysfunctions rather then a venous insufficiency.
E.g mechanical forces acting upon the neck at any age can cause Vertebrobasilar insufficiency and all that gets worse with aging. I had an angioplasty (both jugulars) done twice with great improvements of all my vascular symptoms! but nevertheless my autonomic dysfunctions (no lesions at the brain stem!) stayed absolutely unimpressed of it. At the end the intake of very high dosages of Magnesium chloride is helping me a lot more to control my out of control autonomic nervous system as any angioplasty of the jugulars ever did.

Here's another twist on this: the last time my wife had the procedure done, she was treated with a 20 mm balloon in her jugulars. After the procedure she was hoarse, and had difficulty swallowing for about 24 hours. Could the ballooning have irritated the vagus nerve?

Autonomic dysfunction: A unifying multiple sclerosis theory, linking chronic cerebrospinal venous insufficiency, vitamin D3, and Epstein-Barr virus
Zohara Sternberg, Department of Neurology, Baird MS center, Jacobs Neurological Institute, 100 High St. Buffalo, NY 14203, USA, 28 April 2012.
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.
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.
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. 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. 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.
Abbreviations
• ANS, autonomic nervous system;
• BBB, blood brain barrier;
• BP, blood pressure;
• CCSVI, chronic cerebrospinal venous insufficiency;
• CIS, clinically isolated syndrome;
• CP, chronic progressive;
• CrCP, critical closure pressure;
• EBV, Epstein-Barr virus;
• EDSS, expanded disability status scale;
• HR, heart rate;
• IJV, internal jugular vein;
• MBP, myelin basic protein;
• PTA, percutaneous transluminal angioplasty;
• RR, relapsing remitting;
• SLE, systemic lupus erythematosus;
• Vit D, 1,25-dihydroxyvitamin D

read more at: http://www.sciencedirect.com/science/ar ... 7212000845

....Vitamin D deficiency= Magnesium deficiency in the first place, isn't it???

tzootsi wrote:Here's another twist on this: the last time my wife had the procedure done, she was treated with a 20 mm balloon in her jugulars. After the procedure she was hoarse, and had difficulty swallowing for about 24 hours. Could the ballooning have irritated the vagus nerve?

That is likely to be the result of stretch of the vagus nerve or its recurrent laryngeal branch

Anybody who has had or known someone with "MS" long enough, will know the hoarse, shallow breath, where being heard is a problem because you cannot breathe well enough, and your vocal cords are under far less control. It happens also when people get old. If you listen to the later singing voice of somebody like Pete Seeger it also causes a large tremolo that is due to it being so much more difficult to control pitch.

From "Dr. Arata Responds to Question Regarding New York Times Magazine Article on CCSVI " - http://blog.synergyhealthconcepts.com/d ... -magazine/

Fortunately we followed all our patients symptoms. A trend became evident after hundreds of patients. Despite the myriad presentations of MS, the same constellation of symptoms were present in our patients. This consistent group of symptoms were those of autonomic dysfunction. Autonomic dysfunction as the underlying entity satisfied some of the discontinuities we encountered. For example, autonomic dysfunction is associated with all neurodegenerative diseases not just MS. This explained how a patient with Parkinson’s could benefit from CCSVI. The vagus nerve is the conduit for autonomic signals and it travels alongside the jugular vein. Renal denervation therapy has shown us that autonomic fibers can be manipulated via a transvascular approach. If the balloon mechanically stimulated the vagus nerve and it was what lead to the response to treatment it would solve the mystery of how a patient with a normal jugular vein could respond to jugular ballooning.
The implications were so compelling that we changed our protocol and now focus on autonomic dysfunction. Treatment rests on definitive testing for it with HRV analysis rather than venous studies. Interestingly enough we are now able to objectively document response to therapy. Conjecture of a placebo effect has been nullified. I firmly believe that jugular ballooning treats autonomic dysfunction. Any impact on MS is mediated by alteration of the autonomic system not by changes in blood flow. Future investigations need to include a means of measuring autonomic function for patient screening and assessment of treatment response.