CCSVI and CCVBP

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

Re: CCSVI and CCVBP

Postby NZer1 » Wed Oct 23, 2013 5:08 pm

Dr F is inflammation the main problem in the structural problems and injury problems of your hypothesis?

I have noticed that most if not all of the mimic diseases for MS also involve inflammation and in these cases it is often caused by infections, that to me seems interesting that the same symptom group can be from the Flanagan hypothesis and infection from pathogens?

If steroids are used for speeding up the symptom recovery in acute attacks of MS in the RRMS form isn't that also dampening the immune system which is 'out of control' so to say?

The calcitriol treatment if I understand it correctly is not about curing MS as such but about removing the immune cells that are not designed to be in the CNS. The CNS has it's own immune system and the system used outside the CNS does not come in contact with myelin in everyday terms so when it does when it 'breaches' the BBB then it removes it, sees it as foreign, which is destructive.

Dr F many of the situations and also the references in your book refer to injury as the primary event or trigger for MS to occur, including the court case you helped with. This method of MS occurring is also related to the rapid damage to the spine and skull which involves BBB breach and an inflammation cascade. The reflux back jet situations in CCSVI also cause breaches in the BBB and inflammation occurs at the same time and the bodies immune system rather than the CNS immune system has access to the CNS.

The recent grey matter damage and the atrophy findings are showing how little is know about MS damage over time imo, and that is also showing that the entry points or a breach of the BBB can be in many places in the skull. That is interesting because MS damage in the cord has more logical explanation than the lesions of the brain when looking for reasons for specific disabilities. So does that possibly mean that the lesions are not the key 'cause' of disability and that there is another form of damage that is the culprit, such as inflammation/infection types of reasoning?

So there seems to be a learning curve continuing in MS causation that I hope we can all keep up with and not be stuck on past or historic thoughts about the disease features.

:)
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Oct 24, 2013 2:22 am

Squeakycat wrote:... would like to explore how your theory of structurally induced neurodegeneration at least in MS is explained or not explained in light of the birth month and latitude effects which it seems to me are pretty well documented leaving out China for the moment and whether you see any relationship to vitamin D deficiency which is the conventional explanation for these factors.

I would also like to understand the theory itself in terms of whether you are saying that structure is what causes injury to blood vessels and that is what MS is? Or in your view, is MS something else that is caused by structural issues, not just damage to the plumbing?...


I have never heard of, considered or looked into the birth month effect. It is my contention, that the increase in the prevalence of MS in norther lattitudes has a lot to do with winter related trauma and its impact on different skull designs which affect the layout of the brain, blood and CSF circulatory systems.

My view of MS is the same as most professionals. It is a neurodegenerative disease. Neurodegenerative processes can be initiated by different causes. One well known cause is stroke and ischemia. Another cause is increased intracranial pressure. Toxins are a known cause of neurodegenerative diseases as are pathogens such as bacteria, viruses, fungi etc. Metabolic disorders can likewise initiate neurodegenerative processes.

It is my opinion that structural problems in the spine, especially the craniocervical junction, can interfere with blood and CSF pathways and flow between the cranial vault and spinal canal. The can lead to conditions of chronic ischemia, edema and normal pressure hydrocephalus. Chronic ischemia can lead to ischemic (glutamate) type degenerative cascades. Chroinic edema and NPH cause accumulation of metabolic and other wastes and potential pathogens. Edema and NPH also cause abnormal tension and shear stresses, as well as compression forces inside the cranial vault and spinal canal. The destructive effects of abnormal hydraulics in the brain is well known in hydrocephalus. It is likewise understood regarding the neurodegenerative effects of glaucoma on the optic nerve.
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Oct 24, 2013 3:04 am

Your points are all on target Nigel. Inflammation plays a big part in neurodegenerative processes. Infections are a known cause of acute disseminated encephalomyelitis. There is good reason to suspect that immunizations can cause encephalitis and are most likely the culprit behind the rapid rise in autism. Parents often describe their children exhibiting signs of brain inflammation.
Steroids are good an controlling acute inflammation but dangerous when over prescribed. They definitely throw the autoimmune system out of balance. They also adversely affect the endocrinological, circulatory, neurological, musculoskeletal etc., systems.

Although they lack a lymphatic system, the brain and cord don't have a unqiue immune system. They use they same white blood cell system as the rest of the body. I am sure there is a good explanation but I would have to read more to understand how calcitriol removes immune cells. It makes more sense that it restores calcium balance. The BBB is easily breached in traumatic brain injuries such as occur in severe whiplash cases. The BBB isn't the only thing breached. Other tissues can tear as well and broken blood vessels can bleed into the brain and cause clots in CSF pathways not designed tot transport blood. Given time, the breaches and bleeds heal, they don't continue to weep. More often, blockages to blood and CSF flow occur following traumatic brain injuries.

Grey matter damage isn't recent. I wrote about it in my book. Researchers continue to argue over which degenerates first the white or gray matter. The problem is we don't have the imaging technology yet to make a clear determination but it keeps getting better each year. It's incredible what engineers and radiologists are doing with imaging. Finding lesions in the cord is technically much more difficult but again, eggheads are improving the technology rapidly. It's mind boggeling and hard to keep up with.

Inflammation is a key culprit and many things from injuries to infections can cause inflammation. But there is much more to neurodegenerative diseases, much of it involves basic physics, nothing more. It's the impact of physics on physiology that sets up the neurodegenerative process.
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Re: CCSVI and CCVBP

Postby NZer1 » Thu Oct 24, 2013 11:41 am

uprightdoc wrote:
Although they lack a lymphatic system, the brain and cord don't have a unqiue immune system. They use they same white blood cell system as the rest of the body.

Inflammation is a key culprit and many things from injuries to infections can cause inflammation. But there is much more to neurodegenerative diseases, much of it involves basic physics, nothing more. It's the impact of physics on physiology that sets up the neurodegenerative process.


Dr F are you sure that is what you think?

The CNS definitely has a lymphatic system and you have spoken about it before. The lymph system is spoken about in Angelique Corthals, "Multiple Sclerosis (MS) is not a disease of the immune system," The Quarterly Review of Biology 86:4 (December 2011).
http://www.jstor.org/discover/10.1086/6 ... 2826242283
and;
http://www.eurekalert.org/pub_releases/ ... um=twitter

The issues of a dysfunctional immune system inside and outside the BBB are likely to go hand in glove with the Flanagan Hypothesis of physics and physiology in neuro-de-generative disease BUT cannot happen without each other!!

;)
Nigel

What prompted my comment above was the tireless work of a friend who spent time looking into the immune system or lymph system of the brain;

""Upright Doc
Although they lack a lymphatic system, the brain and cord don't have a unqiue immune system."


I've just pulled together some basic descriptions of glial cells, particularly the microglial cells that shows that this is a very different immune system than on the other side of BBB. Interestingly, with all the research on the role of vitamin D in the non-CNS side of the BBB, I can find little on what it does in the CNS, though I would expect it to be similar.

The discussion here seems to be about where discussions of its role in immunity was about 10-15 years ago in the rest of the body. It was simply not recognized that vitamin D as a regulatory hormone was what was directing all of this. Could be different. There may be some other hormone in the CNS, but I think that is not likely to be the case.

Regulation of innate immune responses in the brain
Serge Rivest
Abstract
Microglial cells are the main innate immune cells of the complex cellular structure of the brain. These cells respond quickly to pathogens and injury, accumulate in regions of degeneration and produce a wide variety of pro-inflammatory molecules. These observations have resulted in active debate regarding the exact role of microglial cells in the brain and whether they have beneficial or detrimental functions. Careful targeting of these cells could have therapeutic benefits for several types of trauma and disease specific to the central nervous system. This Review discusses the molecular details underlying the innate immune response in the brain during infection, injury and disease.

Wiki (I've highlighted things that are parallel to what vitamin D does in the body. Again, I suspect that this is all under the control of VitD, but there seems to be little research on that and all the immunological functions that are attributed here to microglial cells are likely to be directed by calcitriol within them, rather than the cells themselves, at least at the molecular level.)

Glial cells, sometimes called neuroglia or simply glia (Greek γλία, γλοία "glue"; pronounced in English as either /ˈɡliːə/ or /ˈɡlaɪə/), are non-neuronal cells that maintain homeostasis, form myelin, and provide support and protection for neurons in the brain and peripheral nervous system.[1]

As the Greek name implies, glia are commonly known as the glue of the nervous system; however, this is not fully accurate. Neuroscience currently identifies four main functions of glial cells:


To surround neurons and hold them in place,
To supply nutrients and oxygen to neurons,
To insulate one neuron from another,
To destroy pathogens and remove dead neurons.

During early embryogenesis glial cells direct the migration of neurons and produce molecules that modify the growth of axons and dendrites.

Glia have a role in the regulation of repair of neurons after injury. In the CNS (Central Nervous System), glia suppress repair. Glial cells known as astrocytes enlarge and proliferate to form a scar and produce inhibitory molecules that inhibit regrowth of a damaged or severed axon. In the PNS (Peripheral Nervous System), glial cells known as Schwann cells promote repair.

Microglia are a type of glial cell that are the resident macrophages of the brain and spinal cord, and thus act as the first and main form of active immune defense in the central nervous system (CNS).

The brain and spinal cord are considered "immune privileged" organs in that they are separated from the rest of the body by a series of endothelial cells known as the blood–brain barrier, which prevents most infections from reaching the vulnerable nervous tissue. In the case where infectious agents are directly introduced to the brain or cross the blood–brain barrier, microglial cells must react quickly to decrease inflammation and destroy the infectious agents before they damage the sensitive neural tissue. Due to the unavailability of antibodies from the rest of the body (few antibodies are small enough to cross the blood brain barrier), microglia must be able to recognize foreign bodies, swallow them, and act as antigen-presenting cells activating T-cells. Since this process must be done quickly to prevent potentially fatal damage, microglia are extremely sensitive to even small pathological changes in the CNS.[5]

Functions

Microglial cells fulfill a variety of different tasks within the CNS mainly related to both immune response and maintaining homeostasis. The following are some of the major known functions carried out by these cells.

Scavenging
In addition to being very sensitive to small changes in their environment, each microglial cell also physically surveys its domain on a regular basis. This action is carried out in the ameboid and resting states. While moving through its set region, if the microglial cell finds any foreign material, damaged cells, apoptotic cells, neural tangles, DNA fragments, or plaques it will activate and phagocytose the material or cell. In this manner microglial cells also act as "housekeepers" cleaning up random cellular debris.[7] During developmental wiring of the brain, microglial cells play a large role removing unwanted excess cellular matter. Post development, the majority of dead or apoptotic cells are found in the cerebral cortex and the subcortical white matter. This may explain why the majority of ameboid microglial cells are found within the "fountains of microglia" in the cerebral cortex.[12]

Phagocytosis
The main role of microglia, phagocytosis, involves the engulfing of various materials. Engulfed materials generally consist of cellular debris, lipids, and apoptotic cells in the non-inflamed state, and invading virus, bacteria, or other foreign materials in the inflamed state. Once the microglial cell is "full" it stops phagocytic activity and changes into a relatively non-reactive gitter cell.

Cytotoxicity
In addition to being able to destroy infectious organisms through cell to cell contact via phagocytosis, microglia can also release a variety of cytotoxic substances. Microglia in culture secrete large amounts of H2O2 and NO in a process known as ‘respiratory burst'. Both of these chemicals can directly damage cells and lead to neuronal cell death. Proteases secreted by microglia catabolise specific proteins causing direct cellular damage, while cytokines like IL-1 promote demyelination of neuronal axons. Finally, microglia can injure neurons through NMDA receptor-mediated processes by secreting glutamate and aspartate. Cytotoxic secretion is aimed at destroying infected neurons, virus, and bacteria, but can also cause large amounts of collateral neural damage. As a result, chronic inflammatory response can result in large scale neural damage as the microglia ravage the brain in an attempt to destroy the invading infection.[4]

Antigen presentation
As mentioned above, resident non-activated microglia act as poor antigen presenting cells due to their lack of MHC class I/II proteins. Upon activation they rapidly uptake MHC class I/II proteins and quickly become efficient antigen presenters. In some cases, microglia can also be activated by IFN-γ to present antigens, but do not function as effectively as if they had undergone uptake of MHC class I/II proteins. During inflammation, T-cells cross the blood–brain barrier thanks to specialized surface markers and then directly bind to microglia in order to receive antigens. Once they have been presented with antigens, T-cells go on to fulfill a variety of roles including pro-inflammatory recruitment, formation of immunomemories, secretion of cytotoxic materials, and direct attacks on the plasma membranes of foreign cells.[4][7]

Synaptic stripping
In a phenomenon first noticed in spinal lesions by Blinzinger and Kreutzberg in 1968, post-inflammation microglia remove the branches from nerves near damaged tissue. This helps promote regrowth and remapping of damaged neural circuitry.[4]

Promotion of repair
Post-inflammation, microglia undergo several steps to promote regrowth of neural tissue. These include synaptic stripping, secretion of anti-inflammatory cytokines, recruitment of neurons and astrocytes to the damaged area, and formation of gitter cells. Without microglial cells regrowth and remapping would be considerably slower in the resident areas of the CNS and almost impossible in many of the vascular systems surrounding the brain and eyes.[4][6]

Extracellular signaling
A large part of microglial cell's role in the brain is maintaining homeostasis in non-infected regions and promoting inflammation in infected or damaged tissue. Microglia accomplish this through an extremely complicated series of extracellular signaling molecules which allow them to communicate with other microglia, astrocytes, nerves, T-cells, and myeloid progenitor cells. As mentioned above the cytokine IFN-γ can be used to activate microglial cells. In addition, after becoming activated with IFN-γ, microglia also release more IFN-γ into the extracellular space. This activates more microglia and starts a cytokine induced activation cascade rapidly activating all nearby microglia. Microglia-produced TNF-α causes neural tissue to undergo apoptosis and increases inflammation. IL-8 promotes B-cell growth and differentiation, allowing it to assist microglia in fighting infection. Another cytokine, IL-1, inhibits the cytokines IL-10 and TGF-β, which downregulate antigen presentation and pro-inflammatory signaling. Additional dendritic cells and T-cells are recruited to the site of injury through the microglial production of the chemotactic molecules like MDC, IL-8, and MIP-3β. Finally, PGE2 and other prostanoids help prevent chronic inflammation by inhibiting microglial pro-inflammatory response and downregulating Th1 (T-helper cell) response.[7]

Role in chronic neuroinflammation

The word neuroinflammation has come to stand for chronic, central nervous system (CNS) specific, inflammation-like glial responses that may produce neurodegenerative symptoms such as plaque formation, dystrophic neurite growth, and excessive tau phosphorylation.[16] It is important to distinguish between acute and chronic neuroinflammation. Acute neuroinflammation is generally caused by some neuronal injury after which microglia migrate to the injured site engulfing dead cells and debris.[16] The term neuroinflammation generally refers to more chronic, sustained injury when the responses of microglial cells contribute to and expand the neurodestructive effects, worsening the disease process.[16]

When microglia are activated they take on an amoeboid shape and they alter their gene expression. Altered gene expression leads to the production of numerous potentially neurotoxic mediators. These mediators are important in the normal functions of microglia and their production is usually decreased once their task is complete.[17] In chronic neuroinflammation, microglia remain activated for an extended period during which the production of mediators is sustained longer than usual.[17] This increase in mediators contributes to neuronal death.[17]

Neuroinflammation is distinct from inflammation in other organs, but does include some similar mechanisms such as the localized production of chemoattractant molecules to the site of inflammation.[17] The following list contains a few of the numerous substances that are secreted when microglia are activated:

Cytokines
Microglia activate the proinflammatory cytokines IL-1α, IL-1β and TNF-α in the CNS.[17] Cytokines play a potential role in neurodegeneration when microglia remain in a sustained activated state.[17] Direct injection of the cytokines IL-1α, IL-1β and TNF-α into the CNS result in local inflammatory responses and neuronal degradation.[17] This is in contrast with the potential neurotrophic (inducing growth of neurons) actions of these cytokines during acute neuroinflammation.[17]

Chemokines
Chemokines are cytokines that stimulate directional migration of inflammatory cells in vitro and in vivo.[17] Chemokines are divided into four main subfamilies: C, CC, CXC, and CX3C. Microglial cells are sources of some chemokines and express the monocyte chemoattractant protein-1 (MCP-1) chemokine in particular.[17] Other inflammatory cytokines like IL-1β and TNF-α, as well as bacterial-derived lipopolysaccharide (LPS) may stimulate microglia to produce MCP-1, MIP-1α, and MIP-1β.[17] Microglia can express CCR3, CCR5, CXCR4, and CX3CR1 in vitro.[17] Chemokines are proinflammatory and therefore contribute to the neuroinflammation process.[17]"
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Re: CCSVI and CCVBP

Postby NZer1 » Thu Oct 24, 2013 4:07 pm

Hi everyone,
I was sent a link from David Hubbard's wife to alert me to the way the Hubbard Foundation is now looking at MS and CCSVI which I thought was very timely considering the talk here;

http://findmedicalsolutions.com/blog/wa ... ose_button

Great clarity of thought and with research to back it up, way to go David!! Thanks Arlene Pellar Hubbard and Hubbard Foundation

:)
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Oct 24, 2013 11:29 pm

Nigel,
What's your point regarding the glial cells? I said that the brain doesn't have a lymphatic system and that there is nothing unique about the immune system in the brain. You posted comments regarding physiology of the glial cells but nothing about particularly unique immunological processes used by the brain. The immune and complement immune system elsewhere in the body perform similar functions.
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Re: CCSVI and CCVBP

Postby uprightdoc » Thu Oct 24, 2013 11:48 pm

Excellent presentation by Dr. Hubbarb. I couldn't agree more. However, he left out stagnation due to obstruction of blood and CSF flow caused by malformations and misalignments of the craniocervical junction that affect the occipital marginal sinus and vertebral venous systems that are preferentially used to drain the brain during upright posture as proposed by Flanagan. Craniocervical syndroms are far more common and more likely to cause sluggish blood and CSF flow in the brain compared to insufficiency of the jugular veins.
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Re: CCSVI and CCVBP

Postby NZer1 » Fri Oct 25, 2013 12:33 am

Hi Dr F the reference was to show how there are different cells that perform on each side of the BBB and yes the body side do 'briefly' enter the BBB/CSF 'but' apoptosis is the method of depleting them quickly. If apoptosis is not happening due to the lack of the triggering hormone calcitriol then there are cells within the BBB that cause damage because of their programming such as the cells implicated in the myelin removal or clean up.

Glymphatic system
From Wikipedia, the free encyclopedia

The glymphatic system (or glymphatic clearance pathway) is a functional waste clearance pathway for the mammalian central nervous system (CNS). Although the lymphatic system is responsible for removing extracellular proteins, excess fluid, and metabolic waste products from the systemic tissues, curiously, the brain and spinal cord lack a lymphatic vasculature. Glymphatic flow answers the long standing question of how the sensitive neural tissue of the CNS functions in the absence of a conventional lymphatic circulation. The pathway consists of a para-arterial influx route for cerebrospinal fluid (CSF) to enter the brain parenchyma, along with a clearance mechanism for the removal of interstitial fluid (ISF) and extracellular solutes from the interstitial compartments of the brain and spinal cord. Clearance of soluble proteins, waste products, and excess extracellular fluid is accomplished through convective bulk flow of the ISF, facilitated by astrocytic aquaporin 4 (AQP4) water channels. The rate of waste clearance is much higher during sleep, which may partly explain its restorative function. This system was termed the ‘glymphatic’ pathway due to its dependence upon glial cells and its performance of peripheral ‘lymphatic’ functions in the CNS.
http://en.wikipedia.org/wiki/Glymphatic_system

:)
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Re: CCSVI and CCVBP

Postby uprightdoc » Fri Oct 25, 2013 2:51 am

Nigel,
The same thing happens in the body when white blood cells enter the interstitial spaces due to an injury or a leak. They can do a lot of damage if they are not controlled and cleared out in a timely fashion.

I discuss CSF pathways as the lymphatic system of brain thoroughly and throughout my book, website and blog. It is central to my thesis. Among other things, staganation of CSF causes metabolic wastes, such as iron and calcium, as well as pathogens to accumulate. The "Glymphatic System" is simply a new witty name that someone just recently decided to call it. The fact of the matter is that the brain has no lymph vessels or lymph glands. While the rate of clearance of ISF and CSF may be somewhat faster during sleep the bulk flow of CSF is determined by a pressure gradient between the high side in the ventricles and the low side in the superior sagittal sinus. The venous pressure gradient is the difference between pressure in the superior sagittal sinus and the vertebral veins and the internal jugular veins, which is decreased in the recumbent position. Thus the decrease in venous pressure gradient in the recumbent position decreases the CSF pressure gradient and its bulk flow which means more possibility of stagnation during sleep, not less. All systems in the body are restored and refreshed during sleep except respiration which is less efficient and can cause oxygen debt and lactic acid to accumulate during sleep. It is my opinion that the recumbent position used for sleep in humans helps restore CSF volume to support the brain during upright posture.
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Re: CCSVI and CCVBP

Postby NZer1 » Fri Oct 25, 2013 11:28 am

Thanks Dr F, I have also recently seen some posts by Joan about the sleep cycle being vital for PwMS.

** Dr if the problem was myelin eating cells, how are they stopped or removed? What does that? **

I think that the damage is agreed and the discussion seems to be changing to the timing of the immune cells arriving and what they are there doing. The discussion also seems to be about how the cells arrive, is it CCSVI causing the breaches or some other method for the infection/inflammation to occur.

** Do we need to also focus on how to stop and remove the problem cells and debri? **

The slow flow in the CSF that you are describing will be, 'I assume', the compounding or cascading or de-generative factor?

So does that mean that the 'overall' flow and coverage of the flow of CSF is the focus that is needed?

:)
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Re: CCSVI and CCVBP

Postby uprightdoc » Fri Oct 25, 2013 12:12 pm

The sleep cycle is vital to life. It gives the body a break and chance to replinish energy stores. It also decreases compression loads on the spine and the weight of the brain on the base of the skull and foramen magnum.

Immune cells can be called for or they can be forced into interstitial and CSF spaces and pathways. Red blood cells can also be forced into ISF and CSF in traumatic brain injuries. Chronic levels of increased immune cells is always irritating, as in allergies. It can also be destructive as in rheumatoid arthritis in body. The damaging effects of infections and encephalitis is well known and clinically demonstrated. Autoimmune-inflammatory immunological destruction of the brain is less understood and not clear as a cause of neurodegenerative conditions.

Removing damaged cells and debris may be the solution is some but not all cases. Improving blood (arterial and venous) and CSF flow, removing pressure and decreasing inflammation are likewise important, as are other therapies. It depends on the patient. Most patients with neurodegenerative conditions don't have autoimmune-inflammatory conditions. Blossom, Dania and Robert are good examples. Most patients with Alzheimer's could benefit from improved blood and CSF flow as well as cleaning-up damaged cells and debris, as well as pathogens caused by sluggish blood and CSF flow.
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Re: CCSVI and CCVBP

Postby NZer1 » Fri Oct 25, 2013 12:28 pm

uprightdoc wrote:The sleep cycle is vital to life. It gives the body a break and chance to replinish energy stores. It also decreases compression loads on the spine and the weight of the brain on the base of the skull and foramen magnum.

Immune cells can be called for or they can be forced into interstitial and CSF spaces and pathways. Red blood cells can also be forced into ISF and CSF in traumatic brain injuries. Chronic levels of increased immune cells is always irritating, as in allergies. It can also be destructive as in rheumatoid arthritis in body. The damaging effects of infections and encephalitis is well known and clinically demonstrated. Autoimmune-inflammatory immunological destruction of the brain is less understood and not clear as a cause of neurodegenerative conditions.

Removing damaged cells and debris may be the solution is some but not all cases. Improving blood (arterial and venous) and CSF flow, removing pressure and decreasing inflammation are likewise important, as are other therapies. It depends on the patient. Most patients with neurodegenerative conditions don't have autoimmune-inflammatory conditions. Blossom, Dania and Robert are good examples. Most patients with Alzheimer's could benefit from improved blood and CSF flow as well as cleaning-up damaged cells and debris, as well as pathogens caused by sluggish blood and CSF flow.


Does this mean that most people are structural caused MS and some later develop inflammation and infection issues?

Or could it be the other way round with inflammation and infection first with an incident of structural cause or de-generation and the inflammation/infection is overcome and leaves the structural issues needing attention?

It seems to my trouble shooting way of thinking that there would be a common theme such as CCSVI type of flow problem and then added differences that we are seeing such as mine, Pam, CN, Blossom, Diana and Robert?

Or am I off track and the combination isn't really a factor?

:)
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Re: CCSVI and CCVBP

Postby uprightdoc » Fri Oct 25, 2013 2:29 pm

From my experience, about two-thirds of the cases of MS are related to structural causes. Inflammation is a common finding in acute and chronic structural strains. The other third of the cases have been related to migraine autoimmune-inflammatory type conditions. I haven't seen any cases related to frank infections yet. Sluggish blood, lymph and CSF circulation, however, leads to the accumulation of metabolic wastes and pathogens that can cause inflammation and immunological reactions. By the time MS signs and symptoms show up it's typically a combination of problems, including orthopedic problems that tend to get overlooked. Everyone is different I like to fix what I find rather than trying to find something to fix that isn't broken. Blossom and Robert's weaknesses are mostly due to compression stress but also tension and shear stresses. Both have significant weakness in their extremities and both have significant cervical spondylosis. Happet Poet has spondylosis from stem to stern causing some compression issues but mostly severe arthritis type inflammation due to multiple structural problems in the spine. She has very little weakness but the pain and inflammation provoke severe muscle spasms, including the dreaded hug. Dania has similar problems to Blossom causing compression strains on the cord with severe pain and inflammation more like Happy Poet but without the spasms. She also has significant muscle weakness in her legs like Robert and like Robert and Blossom, she has significant spondylosis in her cervical as well as the rest of her spine. Although the degeneration in your spine doesn't seem as bad compared to Happy Poet, Dania and Blossom, because of your signs and symptoms I suspect the spine is the major culprit in your case as well.
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Re: CCSVI and CCVBP

Postby Robnl » Tue Oct 29, 2013 12:43 pm

Hi doc,

My Chiro wants to speak to you, can he call you, is that possible ?

Rgds,

Robert
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Re: CCSVI and CCVBP

Postby uprightdoc » Tue Oct 29, 2013 1:59 pm

Hello Robert,
I will PM you with my contact information.
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