CCSVI and CCVBP
- blossom
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Re: CCSVI and CCVBP
nzer1, how are doing? i know it had been rough for you with the antibiotic treatment. are you seeing anything for the positive yet?---------i hope for a yes.
Re: CCSVI and CCVBP
I Bloss, Thanks for checking in 
I am making my way through the treatment slowly. There probably won't be any positives as such for a while yet. The bacterial or infection load takes time to gradually be removed. If it is done too fast the endo-toxin load can kill. So the Protocol is designed to be gradual and safe.
There are side effects from both the ABx and the secondary effect on body systems.
The Abx is quite minor things like very acute sun sensitivity and some rashes.
The secondary stuff is from the endo-toxins produced by the bacteria when they die. It's quite an interesting science lesson to understand and it is this that causes the more severe symptoms.
Sadly there is no magic pills and you have to go with flow.
We have 6 NZers on the Protocol now and we have our own online private support group and direct link to Paul Thibault as well. So there is a warm feeling amongst the group.
I am very positive that something good will come of all this there are many research papers to explain the process which is a relief to know that the method is working, who I will be in a year or two is an unknown of course, the Goal for me is to stop the progression.
Hope you are doing ok too Blossom, I often think about the Family here when I hear of News around the World
Regards,
Nigel
Not sure if I put this link on this thread, and it helps to connect the article about ALs, MS etc and CPn. Keeping in mind that Medical Science understands the processes of 0.04% of Bacteria and we have well over many Trillion that make up our 'body'.
When you think about it there are more bacteria than our 'own' cells, if they all talked we would be in the shit!
"Endothelial cells in CCSVI are stressed by the Vascular dysfunctions in MS and other de-generative diseases, when you add an infective bacteria there will be complications and symptoms.
Monocyte Stickiness and heart disease
Monocytes are large immune cells that eventually turn into
macrophages, the garbage collectors of the immune system. Before
they turn into macrophages, monocytes drift along in the
bloodstream, eating a germ here, a dead cell there, and generally
behaving themselves. In the course of their travels they brush
against the endothelial cells in our arteries, bounce off, and continue
to drift. Occasionally, however, a monocyte will stick to an
endothelial cell, then creep into the wall of the artery where it turns
into a macrophage and where, sometimes, it becomes a foam cell.
When millions of macrophages have become foam cells in one area,
we have an atherosclerotic plaque.
Researchers from the University of Wisconsin designed a study
to find out why some monocytes, but not others, stick to endothelial
cells. They found that monocytes infected with CPN were stickier
than uninfected monocytes.
1
Furthermore, the more heavily infected
the monocytes were, and the longer they had been infected, the
stickier they became. The CPN didn't have to be alive--monocytes
that ate dead CPN organisms also became sticky.
http://www.potbellysyndrome.com/attach/CPN.pdf"

I am making my way through the treatment slowly. There probably won't be any positives as such for a while yet. The bacterial or infection load takes time to gradually be removed. If it is done too fast the endo-toxin load can kill. So the Protocol is designed to be gradual and safe.
There are side effects from both the ABx and the secondary effect on body systems.
The Abx is quite minor things like very acute sun sensitivity and some rashes.
The secondary stuff is from the endo-toxins produced by the bacteria when they die. It's quite an interesting science lesson to understand and it is this that causes the more severe symptoms.
Sadly there is no magic pills and you have to go with flow.
We have 6 NZers on the Protocol now and we have our own online private support group and direct link to Paul Thibault as well. So there is a warm feeling amongst the group.
I am very positive that something good will come of all this there are many research papers to explain the process which is a relief to know that the method is working, who I will be in a year or two is an unknown of course, the Goal for me is to stop the progression.
Hope you are doing ok too Blossom, I often think about the Family here when I hear of News around the World

Regards,
Nigel
Not sure if I put this link on this thread, and it helps to connect the article about ALs, MS etc and CPn. Keeping in mind that Medical Science understands the processes of 0.04% of Bacteria and we have well over many Trillion that make up our 'body'.
When you think about it there are more bacteria than our 'own' cells, if they all talked we would be in the shit!
"Endothelial cells in CCSVI are stressed by the Vascular dysfunctions in MS and other de-generative diseases, when you add an infective bacteria there will be complications and symptoms.
Monocyte Stickiness and heart disease
Monocytes are large immune cells that eventually turn into
macrophages, the garbage collectors of the immune system. Before
they turn into macrophages, monocytes drift along in the
bloodstream, eating a germ here, a dead cell there, and generally
behaving themselves. In the course of their travels they brush
against the endothelial cells in our arteries, bounce off, and continue
to drift. Occasionally, however, a monocyte will stick to an
endothelial cell, then creep into the wall of the artery where it turns
into a macrophage and where, sometimes, it becomes a foam cell.
When millions of macrophages have become foam cells in one area,
we have an atherosclerotic plaque.
Researchers from the University of Wisconsin designed a study
to find out why some monocytes, but not others, stick to endothelial
cells. They found that monocytes infected with CPN were stickier
than uninfected monocytes.
1
Furthermore, the more heavily infected
the monocytes were, and the longer they had been infected, the
stickier they became. The CPN didn't have to be alive--monocytes
that ate dead CPN organisms also became sticky.
http://www.potbellysyndrome.com/attach/CPN.pdf"
- uprightdoc
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Re: CCSVI and CCVBP
The link between AD and pathogens such as viruses and bacteria, including PC, goes way back to when I first started my research. Viral and bacterial causes are relatively minor compared to the plethora of other known causes of dementia such as alcohol, anticholinergic medications including antihistamines, antidepressants, anticovulsants, antidepressants etc. Heart bypass surgery significantly increases the risk. Vascular dementia, which is closely related to AD is caused by typical vascular vactors such as heart disease, vascular degeneration, hypertension, diabetes etc. AD is also closely connected to NPH which is likewise connected to hypertension on the arterial supply side, as well as venous blood and CSF flow obstruction on the drainage side. AD is also connected to PD and secondary PD is connected to neurotoxins, such as pesticides. Glutamate toxicity such as from artificial sweetners has also been implicated. Glutamate toxicity is also a sequal to strokes which increased the risk of dementia. I further suspect that chronic ischemia and oxidative stress are associated with glutamate toxicity. Heavy metal toxins such as aluminum and iron have been implicated as well.
Inflammation is a common process to all degenerative conditions from cardiology, to endocrinology, orthopedics, neurology and immunology including infections. Inflammation is a destructive process used to kill and clean up pathogens and debris. Inflammation can be caused by many internal and external agents in the body both foreign and domestic. No matter what the source or trigger of the inflammation is, or which tissues it involves, chronic inflammation is always distructive. Chronic inflammation of muscles and fascia is called myofascitis. One of the key causes of myofascitis is ischemia. Sluggish blood and lymph or CSF flow is associated with the decreased wash-out and accumulation of metabolic and other wastes, including bacteria and viruses. One of the key metabolic wastes is lactic acid, which causes muscle cramps and spasms. Among other things, inflammation causes sluggish blood flow due to local alterations in viscosity as white blood cells and fluids leak into interstitial spaces, which results in edema. Chronic edema cause back pressure against lymphatic drainage. Chronic edema in the brain causes wastes, pathogens, toxins, metabolites, and break-down byproducts such as Beta amyloids to accumulate.
Inflammation is a common process to all degenerative conditions from cardiology, to endocrinology, orthopedics, neurology and immunology including infections. Inflammation is a destructive process used to kill and clean up pathogens and debris. Inflammation can be caused by many internal and external agents in the body both foreign and domestic. No matter what the source or trigger of the inflammation is, or which tissues it involves, chronic inflammation is always distructive. Chronic inflammation of muscles and fascia is called myofascitis. One of the key causes of myofascitis is ischemia. Sluggish blood and lymph or CSF flow is associated with the decreased wash-out and accumulation of metabolic and other wastes, including bacteria and viruses. One of the key metabolic wastes is lactic acid, which causes muscle cramps and spasms. Among other things, inflammation causes sluggish blood flow due to local alterations in viscosity as white blood cells and fluids leak into interstitial spaces, which results in edema. Chronic edema cause back pressure against lymphatic drainage. Chronic edema in the brain causes wastes, pathogens, toxins, metabolites, and break-down byproducts such as Beta amyloids to accumulate.
- uprightdoc
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Re: CCSVI and CCVBP
Brain - A Journal of Neurology (2004)
Normal pressure hydrocephalus (NPH): ischaemia, CSF stagnation or both
In NPH and in normal ageing, there is evidence for both a decrease in CSF production and an increase in the resistance to CSF absorption (May et al., 1990; Czosnyka et al., 1996; Albeck et al., 1998; Silverberg et al., 2002) Both events lead to a decrease in CSF turnover and, in turn, a decreased clearance of macromolecules. In NPH, the decrease in clearance of Aβ and Ô is suggested by the higher than expected coincidence of Alzheimer’s disease pathology in cortical biopsies taken from NPH patients at the time of shunt implantation. From 30 to 50% of NPH patients will exhibit plaques and tangles consistent with Alzheimer’s disease, and, in the severely demented NPH patients, 75% will show Alzheimer’s disease (Silverberg et al., 2003). It therefore seems likely that an inability to clear potentially toxic molecules, such as Aβ and Ô and probably other toxic products of brain metabolism, contributes primarily to the dementia of NPH, as well as secondarily by vasoconstriction, as suggested by the authors.
Normal pressure hydrocephalus (NPH): ischaemia, CSF stagnation or both
In NPH and in normal ageing, there is evidence for both a decrease in CSF production and an increase in the resistance to CSF absorption (May et al., 1990; Czosnyka et al., 1996; Albeck et al., 1998; Silverberg et al., 2002) Both events lead to a decrease in CSF turnover and, in turn, a decreased clearance of macromolecules. In NPH, the decrease in clearance of Aβ and Ô is suggested by the higher than expected coincidence of Alzheimer’s disease pathology in cortical biopsies taken from NPH patients at the time of shunt implantation. From 30 to 50% of NPH patients will exhibit plaques and tangles consistent with Alzheimer’s disease, and, in the severely demented NPH patients, 75% will show Alzheimer’s disease (Silverberg et al., 2003). It therefore seems likely that an inability to clear potentially toxic molecules, such as Aβ and Ô and probably other toxic products of brain metabolism, contributes primarily to the dementia of NPH, as well as secondarily by vasoconstriction, as suggested by the authors.
Re: CCSVI and CCVBP
Dr F I am beginning to see evidence that the articles about CSF flow and Vascular flow are secondary to the issues of Bacterial and Viral influence on the structure of tissues not only in veins and sinuses but also the influence in the Vit D VDR dyregulation.
It appears we have a chicken and egg situation that has occurred because of the technology available to support theories as time moves on.
The Vit D influence across many critical systems answers more questions that the basic flows and alignments because it confronts the cause of flows and alignments rather than saying that problems begin at any point, it indicates the multi factual findings of symptom outcomes from the spectrum of treatments we are trying, eg CCSVI PTA, AO adjusting, Diet, Stress minimising, hereditary links, geographical links, endothelial involvement, immune system activation, exercise and many more.
The bacteria and virus involvement is effecting many tissues and systems to support life continuum for itself, it is almost driving us rather than being simply a parasite on us.
The growing awareness that Inflammation is major problem in all diseases and health issues is now redirecting Medical Science's focus to understanding primary Health at a new and deeper level and that the primary causes a cascade leading to secondary diseases.
I don't think there will be a simple one stop fix, I do think that we have to remain open minded and flexible with our reading and thinking so that the pieces are free to fall into place.
It will take 'specialists' to push their barrows so that all points are brought to the table for consideration, respect of others inputs is vital imo.
Nigel
Check in with this thread for more thoughts on Vit D and the VDR dsyregulation.
http://www.thisisms.com/forum/post203165.html#p203165
It appears we have a chicken and egg situation that has occurred because of the technology available to support theories as time moves on.
The Vit D influence across many critical systems answers more questions that the basic flows and alignments because it confronts the cause of flows and alignments rather than saying that problems begin at any point, it indicates the multi factual findings of symptom outcomes from the spectrum of treatments we are trying, eg CCSVI PTA, AO adjusting, Diet, Stress minimising, hereditary links, geographical links, endothelial involvement, immune system activation, exercise and many more.
The bacteria and virus involvement is effecting many tissues and systems to support life continuum for itself, it is almost driving us rather than being simply a parasite on us.
The growing awareness that Inflammation is major problem in all diseases and health issues is now redirecting Medical Science's focus to understanding primary Health at a new and deeper level and that the primary causes a cascade leading to secondary diseases.
I don't think there will be a simple one stop fix, I do think that we have to remain open minded and flexible with our reading and thinking so that the pieces are free to fall into place.
It will take 'specialists' to push their barrows so that all points are brought to the table for consideration, respect of others inputs is vital imo.

Nigel
Check in with this thread for more thoughts on Vit D and the VDR dsyregulation.
http://www.thisisms.com/forum/post203165.html#p203165
- uprightdoc
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Re: CCSVI and CCVBP
Nigel,NZer1 wrote:...I am beginning to see evidence that the articles about CSF flow and Vascular flow are secondary to the issues of Bacterial and Viral influence on the structure of tissues not only in veins and sinuses but also the influence in the Vit D VDR dyregulation...
I don't think there will be a simple one stop fix, I do think that we have to remain open minded and flexible with our reading and thinking so that the pieces are free to fall into place...
Except for cases of frank meningitis, for the most part hydrocephalus, craniosynostosis, Chiari malformations, craniocervical junction malformations, Klippel-Feil, Dandy-Walker syndromes, tethered cords, spondylosis, scoliosis, stenosis etc, acromegaly, Morquio's, Pagets disease., and a multitude of other acquired and inherited structural problems that effect blood and CSF flow in the brain aren't caused by bacterial and viral infections. Neither is traumatic brain injury. They are due to structural issues.
There is no single cause or solution to fixing faulty cranial hydrodynamics. There are many causes and many solutions depending on the cause. Structural problems require structural correction. Dietary problems require dietary correction. Physiological, immunological, inflammatory and pathological problems require neutraceutical or pharmacogical intervention. Toxins and infections should likewise be treated accordingly with antidotes, antivirals and antibacterial agents.
Re: CCSVI and CCVBP
Believe it or not, I do agree with you Dr F.uprightdoc wrote:Nigel,NZer1 wrote:...I am beginning to see evidence that the articles about CSF flow and Vascular flow are secondary to the issues of Bacterial and Viral influence on the structure of tissues not only in veins and sinuses but also the influence in the Vit D VDR dyregulation...
I don't think there will be a simple one stop fix, I do think that we have to remain open minded and flexible with our reading and thinking so that the pieces are free to fall into place...
Except for cases of frank meningitis, for the most part hydrocephalus, craniosynostosis, Chiari malformations, craniocervical junction malformations, Klippel-Feil, Dandy-Walker syndromes, tethered cords, spondylosis, scoliosis, stenosis etc, acromegaly, Morquio's, Pagets disease., and a multitude of other acquired and inherited structural problems that effect blood and CSF flow in the brain aren't caused by bacterial and viral infections. Neither is traumatic brain injury. They are due to structural issues.
There is no single cause or solution to fixing faulty cranial hydrodynamics. There are many causes and many solutions depending on the cause. Structural problems require structural correction. Dietary problems require dietary correction. Physiological, immunological, inflammatory and pathological problems require neutraceutical or pharmacogical intervention. Toxins and infections should likewise be treated accordingly with antidotes, antivirals and antibacterial agents.
The point I am trying to make is that there are common links, Vit D and its regulation could possibly be one and not everyone has the diseases you list and not everyone with trauma has the outcomes that lead to disease, so what I hope for is open mindedness to see a bigger picture. There are links and they can't be discounted, yet!
In a generation or two people will be saying things about our discussions, I wonder why?
Nigel
Re: CCSVI and CCVBP
Hello Dr Flanagan,
Due to MS, I guess, I have lost a some sensitivity in the left side of my hip, although not to the point of being numb.
But during the night, if I sleep in the fetal position (that is, on one of the sides) I notice, when I wake up, that the left side of my hip is numb. This feeling dissapear quickly if I change from the fetal position to looking to the ceiling (on my back). If when I wake up, my position is the looking-to-the-ceiling one, then it doesn't feel numb.
When I was diagnosed MS, I had myself analysed for CCSVI following the Haacke CCSVI protocol, but the doctors said everything was OK in my veins.
But I recently read something in internet about how different positions of the body (supine, upright) could affect the flow of the CSF and may affect in the symptoms and evolution of MS.
When I was screened for CCSVI (MRI) I was scanned only in the looking-to-the-ceiling position. In which positions were you screened for CCSVI?
(They also studied my neck while I was sitting on a chair with a device that is like the one used for screening pregnant women).
Lately, I'm trying to sleep in the looking-to-the-ceiling position, but it is difficult because when I get asleep I change to the fetal position, and it is also not very comfortable. And I have not noticed any improvement since I'm trying to modify my sleeping position.
Do you think that my MS could have something to do with problems with CSF? Should I also try to sleep without pillow? (in fact I already tried, but could not sleep very well)
Sorry for my scant vocabulary of english and thank you.
Due to MS, I guess, I have lost a some sensitivity in the left side of my hip, although not to the point of being numb.
But during the night, if I sleep in the fetal position (that is, on one of the sides) I notice, when I wake up, that the left side of my hip is numb. This feeling dissapear quickly if I change from the fetal position to looking to the ceiling (on my back). If when I wake up, my position is the looking-to-the-ceiling one, then it doesn't feel numb.
When I was diagnosed MS, I had myself analysed for CCSVI following the Haacke CCSVI protocol, but the doctors said everything was OK in my veins.
But I recently read something in internet about how different positions of the body (supine, upright) could affect the flow of the CSF and may affect in the symptoms and evolution of MS.
When I was screened for CCSVI (MRI) I was scanned only in the looking-to-the-ceiling position. In which positions were you screened for CCSVI?
(They also studied my neck while I was sitting on a chair with a device that is like the one used for screening pregnant women).
Lately, I'm trying to sleep in the looking-to-the-ceiling position, but it is difficult because when I get asleep I change to the fetal position, and it is also not very comfortable. And I have not noticed any improvement since I'm trying to modify my sleeping position.
Do you think that my MS could have something to do with problems with CSF? Should I also try to sleep without pillow? (in fact I already tried, but could not sleep very well)
Sorry for my scant vocabulary of english and thank you.
- lyndacarol
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Re: CCSVI and CCVBP
On April 16, 2012, JackD posted the following information on cancer/pomegranates in the Introductions forum:uprightdoc wrote: Pomegranates have similar chemical agents and action to Diamox. Ask your pharmacist about supplements. You could also try the juice but it will be less concentrated and probably adulterated.
http://www.thisisms.com/forum/post19022 ... es#p190223
" Recent research has shown that pomegranate extracts selectively inhibit the growth of breast, prostate, colon and lung cancer cells in culture."
To keep information on pomegranates together in one place, I wish to add this article on punicalagin (potent antioxidant in pomegranate). With its keywords of shear stress, endothelial nitric oxide synthase, and nitric oxide, I place it in this forum since it may be of special interest to some here:
http://cardiovascre.oxfordjournals.org/ ... 4.full.pdf
On page 415, I found a couple interesting ideas: "We have previously shown that intervention with antioxidants and L-arginine reverses perturbed shear stress-related redox gene activation and increases eNOS expression both in cultured endothelial cells and in hypercholesterolemic mice."
And later: "Regular pomegranate juice administered to hypertensive patients caused a significant drop in blood pressure, a reduction in carotid plaque development, and an improvement of stress-induced myocardial ischemia in patients who have coronary heart disease."
It sounds like we all should have pomegranate juice for breakfast!
My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"
- uprightdoc
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Re: CCSVI and CCVBP
Hello Am65,am65 wrote:... Due to MS, I guess, I have lost a some sensitivity in the left side of my hip, although not to the point of being numb...
Your English is good and your explanation makes sense.
The numbness in your left leg may be due to a condition called meralgia paraesthetica. Meralgia paraesthetica is fairly common. It is caused by compression of the lateral femoral cutaneous nerves as it passes through a connective tissue tunnel between the pelvis and thigh. Lying on your left side compresses the tunnel. Lying on your right side stretches and deforms the tunnel.
Tunnel syndromes are treated by relieving the inflammation with antiinflammatory agents and physiotherapy such as ultrasound or electrical muscles stimulation etc., and eliminating or correcting the cause of the compression. I often use counter-strain positions to correct pelvic misalignments and decompress neurovascular tunnels.
http://en.wikipedia.org/wiki/Meralgia_paraesthetica
- uprightdoc
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Re: CCSVI and CCVBP
Hello Lyndacarrol,
There is nothing particularly magical about Pomegranates. Many plants have useful pharmacological properties. Tannins, antioxidants and flavonoids are key antiinflammatory agents and circulatory tonics that are common to many fruits and berries. Traditional Chinese Medicine uses a wide variety of different parts of fruit and berry plants including hawthorne, goji, orange, lemon, tangerine, mulberry, plums, cherries, peach etc. They all have slightly different qualities and characteristics. The best results are obtained by matching the medicine to the patient's antatomy, physiology and pathology. I like to use the TCM term "conformation" to describe the combination.
There is nothing particularly magical about Pomegranates. Many plants have useful pharmacological properties. Tannins, antioxidants and flavonoids are key antiinflammatory agents and circulatory tonics that are common to many fruits and berries. Traditional Chinese Medicine uses a wide variety of different parts of fruit and berry plants including hawthorne, goji, orange, lemon, tangerine, mulberry, plums, cherries, peach etc. They all have slightly different qualities and characteristics. The best results are obtained by matching the medicine to the patient's antatomy, physiology and pathology. I like to use the TCM term "conformation" to describe the combination.
Last edited by uprightdoc on Sat Jan 12, 2013 1:38 pm, edited 1 time in total.
- uprightdoc
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Re: CCSVI and CCVBP
I am very open minded. I like to think "outside the box." I was introduced to the black box theory many years ago in one of my brother's undergraduate engineering books. I have applied the principle ever since to most things I do. I was also a fan of Tom Peter's "In Search of Excellence." Peter's has graduate degrees in civil engineering and business. He is likewise and advocate for open ended thinking. I am not constrained by boxes. It's my lack of knowledge and talent that holds me back. If I was a carpenter my wife would be living under constant construction.NZer1 wrote:...The point I am trying to make is that there are common links, Vit D and its regulation could possibly be one and not everyone has the diseases you list and not everyone with trauma has the outcomes that lead to disease, so what I hope for is open mindedness to see a bigger picture. There are links and they can't be discounted, yet!...
I have tried to find studies on coal miners and neurodegenerative diseases such as MS due to their exposure to trauma, coal dust and heavy metal and other toxins. They also have decreased exposure to sunlight and many have poor diets. They should have a higher incidence of musculoskeletal and neurodegenerative diseases in general for many reasons. Unfortunately, as a population, coal miners have been intentionally overlooked and under studied. Many of their illnesses such as black lung diseases were swept under the rug and kept out of sight to protect profits and reduce medical and disability expenses. Miner's have always been expendable. It's easy and inexpensive to find replacements.
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Re: CCSVI and CCVBP
Causal criteria and counterfactuals; nothing more (or less) than scientific common sense
Carl V Phillips1* and Karen J Goodman1,2
Emerging Themes in Epidemiology 2006, 3:5
Two persistent myths in epidemiology are that we can use a list of "causal criteria" to provide an algorithmic approach to inferring causation and that a modern "counterfactual model" can assist in the same endeavor. We argue that these are neither criteria nor a model, but that lists of causal considerations and formalizations of the counterfactual definition of causation are nevertheless useful tools for promoting scientific thinking. They set us on the path to the common sense of scientific inquiry, including testing hypotheses (really putting them to a test, not just calculating simplistic statistics), responding to the Duhem-Quine problem, and avoiding many common errors. Austin Bradford Hill's famous considerations are thus both over-interpreted by those who would use them as criteria and under-appreciated by those who dismiss them as flawed. Similarly, formalizations of counterfactuals are under-appreciated as lessons in basic scientific thinking. The need for lessons in scientific common sense is great in epidemiology, which is taught largely as an engineering discipline and practiced largely as technical tasks, making attention to core principles of scientific inquiry woefully rare.
Carl V Phillips1* and Karen J Goodman1,2
Emerging Themes in Epidemiology 2006, 3:5
Two persistent myths in epidemiology are that we can use a list of "causal criteria" to provide an algorithmic approach to inferring causation and that a modern "counterfactual model" can assist in the same endeavor. We argue that these are neither criteria nor a model, but that lists of causal considerations and formalizations of the counterfactual definition of causation are nevertheless useful tools for promoting scientific thinking. They set us on the path to the common sense of scientific inquiry, including testing hypotheses (really putting them to a test, not just calculating simplistic statistics), responding to the Duhem-Quine problem, and avoiding many common errors. Austin Bradford Hill's famous considerations are thus both over-interpreted by those who would use them as criteria and under-appreciated by those who dismiss them as flawed. Similarly, formalizations of counterfactuals are under-appreciated as lessons in basic scientific thinking. The need for lessons in scientific common sense is great in epidemiology, which is taught largely as an engineering discipline and practiced largely as technical tasks, making attention to core principles of scientific inquiry woefully rare.
Re: CCSVI and CCVBP
Thanks for you answer, it could be that my probem is meralgia paraesthetica[/i} but I'm not sure, because it appeared in parallel to other symptoms of MS. And it is not in the tigh, only in the belt area, and once centimeter up and down. There is no pain, no reaction to hot water, only sometimes a bit on tingling in the area and in the buttocks. I can feel the warm as well as in the other side of the hip, but I do not feel mild coldness and something very cold (from the freezer) I can feel it after some seconds of touching it.uprightdoc wrote:Hello Am65,am65 wrote:... Due to MS, I guess, I have lost a some sensitivity in the left side of my hip, although not to the point of being numb...
Your English is good and your explanation makes sense.
The numbness in your left leg may be due to a condition called meralgia paraesthetica. Meralgia paraesthetica is fairly common. It is caused by compression of the lateral femoral cutaneous nerves as it passes through a connective tissue tunnel between the pelvis and thigh. Lying on your left side compresses the tunnel. Lying on your right side stretches and deforms the tunnel.
Tunnel syndromes are treated by relieving the inflammation with antiinflammatory agents and physiotherapy such as ultrasound or electrical muscles stimulation etc., and eliminating or correcting the cause of the compression. I often use counter-strain positions to correct pelvic misalignments and decompress neurovascular tunnels.
http://en.wikipedia.org/wiki/Meralgia_paraesthetica
When I sleep lying on my back it also happens to me that both hands go numb (specially the little finger), but this has happened to me since I was in my teens. Although now it happens to me almost every night. Then, it didn't happen to me very often and I thought it was because at some point I had slept over any of my arms and blocked blood circulation.
Thank you again because here at least I fell somebody paying attention to me. When I speaks to my neurologist about it he doesn't pay much attention and attributes almost every health problem I have to my MS diagnosis.
- uprightdoc
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Re: CCSVI and CCVBP
The fact that you symptoms are aggravated or relieved by certain positions of your spine make me suspect that you have structural problems. Degenerated nerves don't get better when you change positions.
Many types of structural problems in the spine can effect neurovascular tunnels and compress nerves and blood vessels in certain positions. Doctors use various types strain position tests to find the problem. For example, leaning to the right compresses the tunnels in the lower spine which contain the nerves to the right leg. If the tunnels are narrow due to degeneration (spondylosis) or a disc herniation, then leaning to the right will irritate the nerve. The test is called a Kemp's test. Consequently, patients often develop an "antalgic" lean to the left. Antalgia means away from pain. Leaning left decreases compression and pain.
The thoracic outlet between the neck, shoulders and rib cage likewise contains neurovascular tunnels that supply the arms and hand. The neurovascular tunnels of the thoracic outlet can be distorted and compressed by structural problems in the neck (spondylosis and stenosis), the collar bone (clavicle), the chest muscles (pectoralis minor), and alignment of the lower spine and leg lengths. My guess is that you have degeneration (spondylosis) and abnormal curvatures in your spine such as scoliosis and kyphosis. My theory is that spondylosis, scoliosis and stenosis (narrow nerve outlets in the spine) play a role in the cause of neurodegenerative conditions such as multiple sclerosis. Your problems may be due inherited (genetic) design issues or they could have been acquired through trauma, aging or a combination of both.
Many types of structural problems in the spine can effect neurovascular tunnels and compress nerves and blood vessels in certain positions. Doctors use various types strain position tests to find the problem. For example, leaning to the right compresses the tunnels in the lower spine which contain the nerves to the right leg. If the tunnels are narrow due to degeneration (spondylosis) or a disc herniation, then leaning to the right will irritate the nerve. The test is called a Kemp's test. Consequently, patients often develop an "antalgic" lean to the left. Antalgia means away from pain. Leaning left decreases compression and pain.
The thoracic outlet between the neck, shoulders and rib cage likewise contains neurovascular tunnels that supply the arms and hand. The neurovascular tunnels of the thoracic outlet can be distorted and compressed by structural problems in the neck (spondylosis and stenosis), the collar bone (clavicle), the chest muscles (pectoralis minor), and alignment of the lower spine and leg lengths. My guess is that you have degeneration (spondylosis) and abnormal curvatures in your spine such as scoliosis and kyphosis. My theory is that spondylosis, scoliosis and stenosis (narrow nerve outlets in the spine) play a role in the cause of neurodegenerative conditions such as multiple sclerosis. Your problems may be due inherited (genetic) design issues or they could have been acquired through trauma, aging or a combination of both.