The French Neurologist Jean-Martin Charcot, practicing at the Parisian la Pitié-Salpetrière hospital, first described Multiple Sclerosis (Sclérose en Plaques) in 1868. Among other things, he defined MS as a “rigidity disorder”. Unfortunately, he thus set the tone in the Neurology profession of cruel arrogance towards MS patients by claiming their “rigidity” symptoms were psychological in origin - signs of neurotic (usually female) hysteria.
I now believe it is just this rigidity which is at the root of MS progression, but its origin is physiological, NOT psychological. Damaged nerves send “misfired” signals to the muscles which cramp and/or go into spasms. As the nervous system degenerates, the body becomes increasingly rigid, compressed as it is by muscles in spasm. And it is just this rigidity which triggers the process damaging to the central nervous system.
Let’s backtrack a bit.
As early as 1863 the Swiss pathologist George Edward Rindfleisch observed that MS lesions clustered around the brain’s draining veins. Disparate testimonies of this phenomena continued to surface thereafter, but it was only in 2008 that the Italian Professor Paolo Zamboni published a paper on the Internet offering an explanation. He described a condition he has named CCSVI in which venous blood “refluxes” into the Central Nervous System (CNS) owing to stenosed or damaged veins. As a variation on the same idea, Dr. Owiesy of Los Angeles has suggested that a disregulated Autonomic Nervous System (ANS) triggers spasms in the smooth muscles of these same veins. The ensuing blood back jets injure the tissue which leads to inflammation of the myelin sheath and an immune system response. These early “attacks” describe relapse/remission MS (RRMS). Dr. Zamboni has thus discovered the origin of the “wound” which triggers the immune response. (He recommends angioplasty to enlarge the stenosed veins. Dr. Owiesy suggests the administration of a mixture of dexmethasone/lidocaine/thiamine in the perivenous space to release the spasms.)
Progressive MS presents the exception. My brief synopsis derived from MS UK’s site reads
“Primary Progressive MS (PPMS) concerns about 10 to 15% of MS cases. In contrast to RRMS (Relapse Remission) cases, the disease progresses continually without respite after striking an older population (age 40’ and 50’s). Unlike RRMS, there is little to no inflammation, there are fewer brain lesions, the lesions which do exist present fewer inflammatory cells, and more are found on the spinal cord than in the brain which leads to mobility problems. While PPMS cases exhibit less inflammation, there appears to be greater damage to the axons.”
Eventually RRMS may evolve into Secondary Progressive MS which resembles the primary form.
What does this imply to me? The driving factor in progressive MS is no longer centered in obstructed venous blood flow but obstructed cerebro-spinal fluid circulation and a damaged spine which impedes communication between the autonomic nervous system and the brain.
And here we can understand the MS positive feedback loop.
MS venous blood circulation is deficient for any number of reasons. A stress attack can trigger the blood “reflux” into the central nervous system (brain/spine) which inevitably damages the nerves. When the nerves are damaged, muscles cramp up, perhaps go into spasms. As the body freezes up, fluid circulation (blood/cerebrospinal fluid) slows setting the stage for the slightest stress event to trigger another “attack”. Thus each “attack” triggers muscle cramps and body rigidity which in turn sets the stage for more attacks. (I include ANY illness and/or toxicity as stress events. Also, poor blood circulation in the brain persists apart from occasional relapses so constant effort must be made to release body tension and blood/cerebrospinal fluid circulation.)
Diet? Inflammatory foods such as glutens, milk, sugar as well as toxicity and the Epstein Barr herpes virus (EBV) cause cellular inflammation which releases stores of calcium leading to cramps/spasms in skeletal muscles as well as smooth muscles of the Autonomic Nervous System (ANS). Dr Owiesy has expanded on Dr. Zamboni’s theory by suggesting that spasms in these smooth muscles of the brain’s draining veins trigger the blood back jets which injure the brain.
Eventually the body rigidity/muscle spasms damage the spine by literally pulling the vertebrae out of alignment to obstruct the free flow of CSF cerebro-spinal fluid. Worse, communication is disrupted between the brain and the ANS Autonomic Nervous System (involuntary control of internal organs, heart rate, digestion, bladder and bowel function, respiratory rate, papillary response, vasomotor action on the blood vessels) which operates through the spine. At this point while the blood reflux inflammation continues to “wound” the CNS, the trauma to the myelin sheath in the spinal cord triggers anarchy in signalization of the ANS to the brain. We now have SPMS and increasing issues with mobility as well as loss of general body function.
Obviously this implies that at the onset of RRMS one should make every effort to enhance blood/cerebrospinal fluid circulation through the brain/spinal cord in order to stop the blood “reflux” and the attendant muscle spasms/rigidity. One must also limit cellular inflammation (eliminate glutens, other inflammatory foods while enhancing the immune system through diet/supplements/oxygen). “Liberation therapy” (angioplasty) works best in the early RRMS phase when stenosed veins are the primary problem and treatment “liberates” the blood flow. (This is probably true also for Dr. Owiesy’s treatment.) One has thus prevented the wound. Once Progression sets in, there is little to no inflammation which implies that the veins are no longer the primary issue. In that case attention should focus on treating lesions on the spine. And since drug therapy focuses on the inflammation, none is proposed for Progressive MS. At this point therapies which enhance mobility in the spine (Pilates, Yoga, massage) may help maintain communication between the ANS and brain.
I will continue the following treatments with increasing attention to maintaining flexibility in the spine, overcoming body rigidity as well as nourishing the grey matter of the brain.
THE SIX STEPS TO MULTIPLE SCLEROSIS HEALTH
“Dr. Hyman explains his 10 day detox diet.
want2bike (From Thisisms.com)
I had the advice/assistance of a kinesiologist/nutritionist and won’t myself suggest a detox protocol. Dr. Hyman maintains that a simple diet change over 10 days will do the trick (or at least be a beginning) which is something anyone can try. So why not?
2. OPTIMAL NUTRITION AND SUPPLEMENTS
3. ENHANCE BLOOD/CEREBROSPINAL FLUID CIRCULATION - CCSVI -
Simple blood/cerebrospinal fluid circulation thérapies such massage, acupuncture, neuro-muscular electrical stimulation, osteopathy, or swimming may suffice. I do daily Tens self acupressure treatments to stay afloat and try to get an acupuncture or osteopathic treatment once a month. Dr. Owiesy’s idea of administration of dexmethasone/lidocaine/thiamine to the perivenous space may suffice. A serious venous blockage may require ANGIOPLASTY whose effectiveness, unfortunately, is limited without stents to prevent re-stenosis. Prior to taking that decision, one might consult a specialist in skeletal disorders (e.g. Chiropractors or Osteopaths) to be certain a bone or muscle is not obstructing the vein. (FONAR MRI).
4. SUNLIGHT OR UV RAYS on the skin at least 15 minutes daily to release Nitric Oxide essential to vascular health and blood circulation.
5. The homeopathic remedy OSCILLOCOCCINUM by Boiron works wonders to stop (or attenuate the effects of) viruses. I could have avoided so much grief over a lifetime had this been available to me.
6. EXERCISE BUILD UP PROGRESSIVELY (Consulting a Physical Therapist can help) Scott1 recommends Pilates and Yoga.
Previously published on my site MSCureEnigmas.net www.mscureenigmas.net/
Greetings:SeanReynolds wrote:How about the MAP or CPn theses of MS causation? Causing perforation of blood vessels, damage to the eye, and so on.
Sorry for my delayed response. Could you please send me links of articles which explain your comment, or perhaps explain it yourself? I would include CPn and MAP as illnesses or stress events which cause cellular inflammation leading to dysfunction in the Autonomic Nervous Sustem and poor venous blood circulation. And I always keep in mind the fact that studies have revealed it takes twice as long for blood to circulate from the heart through the brain in MSers than normals. For me it is the blood "back jets" (poor vascular circulation) which injure the nervous system, not an infecting agent. Do challenge this idea, your comments are welcome.
Best regards, Vesta
If you factor in the fact that CPn in its invasion of the body perforates blood vessels, and I guess the immune system does its best to fix up the damage without being able to properly identify or kill the invader (for possibly genetic weakness reasons in susceptible individuals as recently discussed elsewhere in this forum) then it could certainly cause problems with circulatory slowdowns and so on -- it's a little like the road system is continually and permanently under roadworks with inflammation and attempted repairs going on everywhere all the time with inevitable traffic holdups! Causing a decreased flow of blood and so on.
Everything I've seen so far fits in biologically plausibly with the Cpn thesis as an explanatory tool, nothing has yet contradicted it.
I'll include a few triangulating articles in a fresh response below which help to make the case, in case the forum software blocks them or something.
It's possible that the CPn is just opportunistic, but you have to ask how CPn travelled through your BBB and got to your eye, when it's meant to be a pneumonia bug which your immune system normally defeats. Also, Dr David Wheldon has pointed out it fits the profile of the primary culprit in a number of measurable ways around the way it attacks blood vessels and weak cells like oligodendrocytes.
Immunology and Microbiology | July 2001
Chlamydial Antibodies in Patients with Previous Acute Anterior Uveitis
Conclusions. The high frequency of IgA antibodies to Cpn Hsp60 in patients with past AAU indicates that such patients may have persisting or recurrent infections due to C. pneumoniae. This finding suggests that C. pneumoniae may play a role in the pathogenesis of AAU.
http://iovs.arvojournals.org/article.as ... id=2199996
New Research: Uveitis, an Inflammatory Eye Disease, May Signal the Onset of Multiple Sclerosis
The British Journal of Ophthalmology
And last month, at the 2014 American Academy of Ophthalmology Annual Meeting, American and European researchers presented results from Characterization of Uveitis in Patients with Multiple Sclerosis, a large retrospective study which revealed that nearly 60 percent of persons with both uveitis, an inflammatory eye disease, and multiple sclerosis (MS) are diagnosed with each within a five-year span. In other words, uveitis may be a warning sign that could help doctors detect MS earlier in the course of the disease.
http://www.visionaware.org/blog/visiona ... lerosis/12
I see these isolated pieces of research when drawn together as an absolute smoking gun. Further, many MS patients are getting better on a PID type combined antibiotic protocol (CAP). RHB-104 which is more designed to kill MAP is also reporting success with treating MS, however I suspect that's because CPn is also susceptible to the same antibiotic classes as occur in RHB-104, which are fairly vicious and poorly tolerated abx compared to Wheldon's choices.
There are still more research papers in isolation on these topics when you go looking.