CCSVI and CCVBP

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

Re: CCSVI and CCVBP

Postby uprightdoc » Thu Jul 18, 2013 5:24 am

Heat increases peripheral vasodilation and consequently blood flow the carotid arteries. The carotid canal passes through the petrous portion of temporal bone and is separated by a thin wall from the inner the ear which is why tinnitus is often associated with circulatory problems. I am not sure what the doctors mean by internal vasoconstriction. Heat doesn't cause vasoconstriction of the coronary or respiratory vessels. Instead, metabolic and cooling demands dilate vessels and divert blood and energy to systems where it is needed and away from less critical systems such as those for digestion and elimination.
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Jul 18, 2013 5:46 am

Nigel,

I don't know what system Dr. Arata is interested in but brain blood flow is an issue. I suspect that one of the key overlooked problems is related to the vertebral arteries which I discuss at length in my next book on migraines. The vertebral arteries, VVP and CSF pathways are affected by the health and alignment of the spine. Among other things, malformations and misalignments of the upper cervical spine and spondylosis, scoliosis and stenosis in the lower spine can cause chronic ischemia, edema and NPH.

Dysregulation can occur in chronic conditions. I suspect that chronic ischemia is a cause of ischemic (glutamate) cascade and neuroexcitotoxicity due to wearing out and eventual failure of the sodium pumps. Chronic inflammation can cause dysregulation of blood flow and metabolism.
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Re: CCSVI and CCVBP

Postby dania » Thu Jul 18, 2013 6:11 am

More discoveries! I believe my coccyx is broken, I can feel it moving and it is shifted to the left side. If one looks at me in my W/C my left shoulder is sloping severely downwards, left leg is pushed up into my abdomen. When I cup my coccyx with my hand pushing it to the right, I need only my abdomen muscles to lift/move my torso (a situp). Do not need my hands to push/keep me up.
If my pelvis is not supported in my W/C I can no longer remain seated, I fall forward or sideways if I do not use my hands to steady myself.
My problem? Definitely structural, mechanical!!!!!!!!!!!!!!!!!!
Now, how do I get a doctor to see this is real and I am not faking? Because that's what they think. Who would want to live like this?
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Jul 18, 2013 9:49 am

Tailbones misalign but they don't move much.

You would have to find a doctor who is skilled with lots of experience in orthodox clinical manual muscle testing. Very few doctors do specific manual muscle testing. But even if they did, the problem is what can be done about it if you do find differences in muscle strength.

In an ideal world, cases like you should be treated with spinal decompression and plenty of regular physiotherapy including active and passive exercises in professional offices, other outside facilities and at home.
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Re: CCSVI and CCVBP

Postby dania » Thu Jul 18, 2013 10:28 am

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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Jul 18, 2013 12:02 pm

Interesting. Great pictures and just what you need along with lumbopelvic x-rays. Slippage of segments is called listhesis and is a sign connective tissue tears and joint laxity.
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Jul 18, 2013 12:24 pm

Have you ever tried sitting on a "donut" for tailbone injuries?
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Re: CCSVI and CCVBP

Postby NZer1 » Thu Jul 18, 2013 12:27 pm

uprightdoc wrote:Nigel,

I don't know what system Dr. Arata is interested in but brain blood flow is an issue. I suspect that one of the key overlooked problems is related to the vertebral arteries which I discuss at length in my next book on migraines. The vertebral arteries, VVP and CSF pathways are affected by the health and alignment of the spine. Among other things, malformations and misalignments of the upper cervical spine and spondylosis, scoliosis and stenosis in the lower spine can cause chronic ischemia, edema and NPH.

Dysregulation can occur in chronic conditions. I suspect that chronic ischemia is a cause of ischemic (glutamate) cascade and neuroexcitotoxicity due to wearing out and eventual failure of the sodium pumps. Chronic inflammation can cause dysregulation of blood flow and metabolism.


Morning from NZ,
does this mean that the inflow is not as much a problem and the outflow is where the focus needs to be?
This is probably going back to the very beginning by asking such a question.
If the flow and pressure arriving is 'good' and the restrictions are from the outlet then most degenerative diseases have origin in outlet flow and pressures?
The testing for flow that Dr Zamboni is remaining focused on with his testing and papers is mostly about the differences in 'normals' to PwMS and he is not focusing on the Western Model of research approach where one theory of cause or one cause is where the answer lies. I like that!
When I look at the research papers on MS there is such a misleading method by using stats to implicate one factor in incidences of our disease.
I think that the global approach that you use Dr F is achieving more in the search for symptom management as the primary focus in 'unknown' diseases. If all the symptoms are dissected and treatments used then what is left over is the learning.
If for instance an answer to 'how does Vit D effect MS' is to be found the way forward is not to use people with low Vit D rather people with MS and good Vit D. If the question was how does diet effect MS then find someone with poor diet and MS. If the next question was how does trauma effect MS then find someone without a trauma history. Going through and eliminating all the statistical 'co-incidences' gives a more direct route to finding the basics of MS, imo (today).

To often assumptions are made because there is a common factor when it should be a screening tool to remove the red herrings. For instance the focus for decades has been RRMS and that has lead in reality, nowhere on the knowledge journey, BUT it has made allot of Money for the system!
If all the common factor (stats) people are removed for a study group the remaining people have a 'more pure' form of the disease.
If the group that remain are not collectively sharing the same factors them 'MS' as a dx or label is wrong and the PwMS need to be assessed in the Flanagan way! Find the separate factors that cause the disability and work individually on those factors, the snow flake effect of MS where no two PwMS are the same!

:)
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beautiful Sun rise in NZ this morning!
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Jul 18, 2013 3:01 pm

Good evening Nigel,
It's nice to hear you are having a terrific sunny day. I just got back from back stroking and have the grill stoked up and ready for dinner.

Arterial inflow problems play a major role in migraines and Alzheimer's. Outflow is also a problem in many neurodegenerative conditions. Some people have inflow and outflow problems. The problem is in the cranial hydrodynamics (fluid mechanics) inside the relatively closed container of the cranial vault.

Statistical double blinded type studies have done very little to add to knowledge or research of neurodegenerative diseases. In my opinion they have misled and held back research. Most of our knowledge has come from neurologists and neurosurgeons. MRI and radiologists have made the most recent and significant contributions. We need more physiological studies based on MRI, US, EMG, neurological and manual muscle testing etc, as well as a common sense approach based on biological plausibility.
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Re: CCSVI and CCVBP

Postby NZer1 » Thu Jul 18, 2013 10:39 pm

Beautiful day of amazing colours and warmer weather after so many weeks of Cold!

I received this link which gives more info on Dr Arata's insights with CCSVI/MS;

"ccsvi autonomic dysfunction
Chronic CerebroSpinal Venous Insufficiency (CCSVI) has been described as a hemodynamic disturbance of the CNS venous drainage. The theory being that CCSVI results from obstructing lesions of the extra-cranial veins in the CNS drainage pathway. Venous hypertension, as a result of the impaired venous drainage seen with CCSVI, is postulated to play a role in the pathogenesis of multiple sclerosis (MS). However, subsequent studies have been inconclusive in establishing a relationship between extra-cranial venous abnormalities and manifestations of MS.

Autonomic nervous system dysfunction has been described as a possible explanation for the occurrence of CCSVI by Z. Sternberg. This theory is supported by my clinical experience of autonomic symptoms commonly being present in patients presenting for evaluation of CCSVI. While autonomic symptoms may be variable and diverse in nature, our patients tend to experience fatigue, interrupted sleep, brain fog, thermal intolerance, awakening headache, bowel and bladder dysfunction. Signs of autonomic dysfunction such as low blood pressure (BP), low body temperature and abnormalities in heart rate variability (HRV) are also commonly present.

In my experience, when this constellation of symptoms is present, patients are likely to respond to venous angioplasty. Additionally, the patients showing deviation from normal in systolic and diastolic BP were often corrected in patients after BA. Therefore, normalization of BP and HRV may be used as surrogate markers to assess the utility of therapeutic intervention.

Decentralized venous drainage has been described following spinal cord injury, a common inciting factor for acute autonomic dysfunction. Abnormal cerebral venous drainage may therefore be one of the many manifestations of the autonomic dysfunction rather than a cause as Zamboni has suggested. Another test of autonomic function showing abnormalities in MS patients is HRV. HRV reflects the influence of autonomic system on the function of the heart.

The implications of autonomic dysfunction in the pathology of the cerebral venous system also necessitated a reappraisal of our treatment approach. The physiologic basis of renal denervation served as a theoretical model. Renal denervation therapy, with its transvascular augmentation of periadventitial autonomic fibers, offers an alternate route to modulate the ANS function. Therefore, we have modified Zamboni’s technique of angioplasty to extend beyond dilation of venous obstructing lesion, in an effort to effect autonomic stimulation. This modification involved delivery of mechanical energy to the periadventitial fibers associated with the internal jugular veins, as well as the renal vein. This modified technique can best be described by the term Transvascular Autonomic Modulation (TVAM).

Find out more about TVAM here."
http://www.synergyhealthconcepts.com/th ... ejPG9KBnoB

Dr F does this fit with your experiences and insights of injury leading to 'MS'?

Dr F did you try a 'ManCinki' when you were looking for swim wear? I have heard they are user friendly and not restrictive, the audience may or may not agree!

;)
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Re: CCSVI and CCVBP

Postby uprightdoc » Fri Jul 19, 2013 4:39 am

Nigel,

I think what Dr. Arata has stumbled upon is very interesting in light of cranial hydrodynamics but I don't think that autonomic dysfunction is the cause of CCSVI or MS. Instead, as I mentioned previously to Dr. Arata, I suspect that decreased blood and CSF flow in the hypothalamus is the cause of the dysautonomia. Rather than its affect on the vagus, i suspect that jugular venoplasty probably improves blood flow to the hypothalamus. Malformations and misalignments of the craniocervical junction are much more likely to cause MS due to their effect on blood and CSF flow and the impact of deficient flows on the ANS.

Decentralized venous drainage in spinal cord injuries are most likely due to associated injuries to the spine that effect blood flow in the VVP as well as CSF flow cord not autonomic dysfunction

Renal denervation therapy was successfully used to treat hypertension decades ago. It fell out of favor when effective medicines became available.

My insights and experiences are based on a vast amount of knowledge regarding hydrocephalus, traumatic brain injuries and strokes. My theory is that faulty cranial hydrodynamics can cause chronic ischemia, edema and hydrocephalus that lead to neurodegenerative conditions.

I haven't tried or heard of ManCinki swim wear but CinkiMan doesn't sound as user friendly as Speedos or the expensive second skins. CinkiMan swimwear must be a NZer thing.
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Re: CCSVI and CCVBP

Postby dania » Fri Jul 19, 2013 6:00 am

Dr Flanagan, what is the cause of the swelling in our legs? Mine are like tree trunks now. I know it is blood pooling in the legs and feet, not water.

Another thing I noticed is that my hot head comes and goes instantaneously when I change positions. Happens in a second.

I will try a donut, see what happens. TY
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Re: CCSVI and CCVBP

Postby uprightdoc » Fri Jul 19, 2013 9:14 am

The cause of the swelling in the legs is blood and lymph. I previously discussed pneumatic compression therapy in repsonse to a question by Blossom. The veins have valves but no muscles to move blood. They depend on pressure gradients and movement. The same is true for lymph. In contrast to the cranial vault, the legs are highly expandable compartments so its easy for fluids to accumulate if pressure and movement are insufficient.

In contrast to the ManSinki swim suits they use in NZ, competitive swim suits use compression technology. Compression streamlines the body and reduces drag. Many athletes say it also improve endurance which is currently attributed to maintaining heat in the muscle. So many records were broken with competitive swimsuit technology that full body second skins have now been banned from competition. Some speculate the full suits not only decrease drag but they also increase bouyancy. My theory is that compression improves circulatory efficiency and decreased metabolic wastes such a lactic acid that causes muscles to cramp.

I use jammers which are still allowed. Jammers extend only to the knee. Freestyle and backstrokes are notorius for causing leg cramps, especially foot cramps. I found the jammers have significantly reduced the fatigue and post exercise spasm in my bad right leg. I haven't had any foot cramps since using them while doing fairly long distance freestyle and backstroke.

Compression and decompression physiotherapies are helpful to many conditions, including circulation. So it aqua therapy.
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Re: CCSVI and CCVBP

Postby Music » Fri Jul 19, 2013 10:25 am

Hi Dr. Flanagan and Dania,

I use compression stockings and a recumbent bike and these seem to help for the most part. Not perfect but pretty helpful. I sit in my w/c and use the bike.

Dania, have had tail bone issues too. UGHH! When I was young and then last year. Had some good whacks in that area.
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Re: CCSVI and CCVBP

Postby uprightdoc » Fri Jul 19, 2013 10:49 am

Thanks music for the sound advice.
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