CCSVI and CCVBP

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

Re: CCSVI and CCVBP

Postby uprightdoc » Sat Oct 06, 2012 5:39 am

NZer1 wrote:...there has to be an entrance to the BBB for the issues to be symptomatic once there is infection load and immune system reaction/inflammation and that process enables the pathogen to spread by stealth means of replicating the DNA of the immune system and also any antibiotics...

...Huge amount of knowledge required to support the other half of the picture of injuries and misalignments, imo...

...inflammation and scaring is a breeding ground for many pathogens that grow in volume over time and the symptoms appear at differing time frames depending on the body status and the bacterial load.


It is not necessary to have pathogens, breakdown or for anything to cross the blood brain barrier in order to cause neurodegenerative conditions. Inflammation and autoimmune reactions alone can cause damage by the chemicals they release.

The effects of compressive neuropathy are well understood. The cause of neurological symptoms, such as cranial nerves signs as well as brain atrophy in non-communicating childhood hydrocephalus is primarily due to abnormal shear forces and compression. The problem is corrected by increasing the drainage capacity with an internal or external shunt. Hydrocephalus in adults due to Chiari malformations and tumors cause similar neurological signs and symptoms due to shear forces and compression. Traumatic brain injuries likewise cause mechanical strains such as compression and shear forces due to the brain shifting inside the skull, as well as violent inversion flows that can damage nerves. They also cause swelling from edema which causes compression problems similar to hydrocephalus. Strokes cause cell death and neurodegenerative conditions due to a disruption in blood flow. It also sets off an ischemic cascade that releases destructive chemcials into the brain that are not pathogens. Ischemica atrophy is a major cause of Alzheimer's. My theory is that chronic ischemia, edema and hydrocephalus can cause neurodegenerative conditions.

There is a huge amount of knowledge in radiology, neurology and orthopedics to support the connection between trauma, misalignments of the spine and nerve injuries. In addition to traumatic brain injuries, the impact of macro strain types of misalignments of the spine, such as fractures, dislocations, scoliosis, spondylosis and lateral and central stenosis are well understood. They are primarlly due to compression. The compressive impact of Chiari malformations are also well known. The signs and symptoms all correlate clearly with the patients history, exam findings and images.
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Re: CCSVI and CCVBP

Postby NZer1 » Sat Oct 06, 2012 12:32 pm

uprightdoc wrote:
NZer1 wrote:...there has to be an entrance to the BBB for the issues to be symptomatic once there is infection load and immune system reaction/inflammation and that process enables the pathogen to spread by stealth means of replicating the DNA of the immune system and also any antibiotics...

...Huge amount of knowledge required to support the other half of the picture of injuries and misalignments, imo...

...inflammation and scaring is a breeding ground for many pathogens that grow in volume over time and the symptoms appear at differing time frames depending on the body status and the bacterial load.


It is not necessary to have pathogens, breakdown or for anything to cross the blood brain barrier in order to cause neurodegenerative conditions. Inflammation and autoimmune reactions alone can cause damage by the chemicals they release.

The effects of compressive neuropathy are well understood. The cause of neurological symptoms, such as cranial nerves signs as well as brain atrophy in non-communicating childhood hydrocephalus is primarily due to abnormal shear forces and compression. The problem is corrected by increasing the drainage capacity with an internal or external shunt. Hydrocephalus in adults due to Chiari malformations and tumors cause similar neurological signs and symptoms due to shear forces and compression. Traumatic brain injuries likewise cause mechanical strains such as compression and shear forces due to the brain shifting inside the skull, as well as violent inversion flows that can damage nerves. They also cause swelling from edema which causes compression problems similar to hydrocephalus. Strokes cause cell death and neurodegenerative conditions due to a disruption in blood flow. It also sets off an ischemic cascade that releases destructive chemcials into the brain that are not pathogens. Ischemica atrophy is a major cause of Alzheimer's. My theory is that chronic ischemia, edema and hydrocephalus can cause neurodegenerative conditions.

There is a huge amount of knowledge in radiology, neurology and orthopedics to support the connection between trauma, misalignments of the spine and nerve injuries. In addition to traumatic brain injuries, the impact of macro strain types of misalignments of the spine, such as fractures, dislocations, scoliosis, spondylosis and lateral and central stenosis are well understood. They are primarlly due to compression. The compressive impact of Chiari malformations are also well known. The signs and symptoms all correlate clearly with the patients history, exam findings and images.


Dr the one missing link is the 'connection' between the injuries and outcomes and the symptoms.
My experience so far has me believing that the body felt symptoms I have are not directly caused by 'lesions'.
Until this connection is made some how we are guessing!

This is what I am wanting to learn about and help the understanding along so that our diseases are manageable in a way that stops progression most of all!

Regards,
Nigel
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Re: CCSVI and CCVBP

Postby uprightdoc » Sat Oct 06, 2012 1:33 pm

Good point Nigel.

Lesions are typically found in the supratentorial area above the posterior fossa but many symptoms come from structures located in the posterior fossa. The cause of hyperintensity signal lesions isn't always clear. They can be due to infarction, infection, ischemia and edema. In this regard strokes can cause ischemic hyperintensity signals and edema in one area of the brain, such as the thalmaus for example, but signs and symptoms of cranial nerve involvement, such as with sight, speech and swallowing that have nothing to do with the area of ischemia. Instead, the cranial nerve signs are caused by brain swelling (edema) and increased intracranial pressure that cause compression and shear stresses. In some cases, severe edema can displace the brain and cause it to herniate beneath or through the connective tissues that divide the vault into compartments. Increased intracranial pressure can also cause the brain to herniate down into the foramen magnum similar to a Chiari malformation, which can also be caused by decreased pressure in the cord such as from a spinal tap. Chiari malformations cause obstruction to blood and CSF flow into and out of the brain. A decrease in blood flow in the vertebral-basilar artery due to a Chiari malformation can cause downstream problems, such as ischemic hyperintensity signals to show up in the cerebellum, pons, midbrain, thalamus and hypothalamus. The diplacement of the brain also causes tension and compression stress on nerve structures in the posterior fossa. Additionally, it causes blockage of CSF and normal pressure hydrocephalus which causes similar problems to edema.
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Re: CCSVI and CCVBP

Postby NZer1 » Sat Oct 06, 2012 2:13 pm

Thanks Dr.
I have searched for research etc that actually 'proves' that the symptom part is connected to the lesion. As yet the only link has been the talk about CPn where it has become intracellular in the immune system and or is within muscle tissue particularly where there has been inflammation.
The action of intracellular infections using ATP/depleting energy and also controlling apoptosis of the host is as close as I can find a link when I work from the 'expression' of symptom end of searching.
I hear the other explanation/theory from the brain end as you have mentioned and in literature.

I want the two pathways to meet so that the association goes beyond theory.

I am seeing that MS may be unique in its causes and that the action of entry across the BBB can vary, the time from crossing the BBB to symptom expression is also a big grey area. It can be days or it can be years to see on MRI lesions that can be associated to MS. My example was 2 years from symptom onset to visible lesions! So who came first the male or female?

So many times I see things that surprise me in the way the research has been halted instead of following the leads that have been exposed from tests and trials. Following in search of monetary gain instead of Health gain.
Franz Schelling and yourself have incredible focus and staying powers!

Because of the Internet and the access to past research it appears some connections are being made across time and space in the research library, connections that are avoiding monetary blocks!
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Re: CCSVI and CCVBP

Postby uprightdoc » Sat Oct 06, 2012 2:45 pm

Your welcome Nigel. If you want to connect ischemic hyperintensity signal type lesions to symptoms you should look into strokes. If you want to connect edema hyperintensity signals to symptoms you should look into traumatic brain injuries.

I think we are getting to a point where the different theories coincide. What we need to do is to triage the information to determine the best diagnosis and treatment that goes beyond the confines of the MS label. Most patients with MS have co-morbidities the same as other patients. Untreated co-morbidities can make MS worse. Infections can be a cause or co-morbidity. Most cases of MS I have consulted with are associated with significant history of trauma and spinal problems. Some cases of MS are clearly due to infections. As I mentioned previosly, I believe MS in the Faroe Islands was started by viruses and pathogens introduced into previously a unexposed population by innoculated British soilders that caused acute disseminated encephalomyelitis. About a third of the cases of MS I have consulted with are what I classify as migraine variants. Migraines involve too many issues to go into here but bacteria and pathogens certainly play a role. It takes good detective work to determine the different causes.
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Re: CCSVI and CCVBP

Postby NZer1 » Sat Oct 06, 2012 3:29 pm

I hear you in regard to dissecting the symptoms and working from that end.

I find often that when there is a technique or treatment used in MS the Neurologic approach is to say that when there is improvement for any reason the MS tag should be removed.

Shifting sand approach so that the reason for the MS tag remains invisible!

The connection by symptoms changing because of vascular flow improvement, a group of symptoms that commonly change, is a group way of dissecting the parts of the whole. These parts may be found to be incidental and cross to many diseases. This is the trend I am seeing, interlinked diseases eg ALs, PD, MS and so on.

As the layers of groupings are collected and then separated I believe there will be a core that is left that will create the newest understands in all these diseases.

Combinations are being found, eg injury, alignment, congenital, vascular, arterial, genetics, diet, geographic influences, heredity, the grouping of combinations and then following the path that they create to symptoms will only come from the breaking down into collectives.

I think that CCSVI is a big step in the right direction of finding more commonalities. That will need to be looked at for cross over links and then looked at again and again. There seems to be too many options to give clarity in understanding. Things need to be minimised to be understood in Human Terms. It is a Reductionist way of looking and there is the risk of believing that there will be a one hit wonder cure, and that is where money will influence the direction of knowledge finding.

Money causes stops and starts in Medical knowledge paths.

That's probably why people with the disease or people with loved ones will maintain the momentum of the search for answers.

Bla Bla, I'll fall off my Soap Box now and go out into the Sun,

Nigel
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Re: CCSVI and CCVBP

Postby uprightdoc » Sun Oct 07, 2012 4:54 am

Nigel,
It sounds to me like we are on the same page. It takes a dedicated doctor with good detective skills to decipher a patient's history, exam and labs findings in order to make a diagnosis and determine the correct course of treatment. Every patient is different. I have consulted with many patients with volumes of information from some of the best clinics, doctors and labs in the world. The problem is no one takes the time to put all the information together in a way that paints a clear picture of the patient's anatomy, physiology and pathology. Patients with infections or autoimmune-inflammatory conditions generally have compelling evidence in their history, physical exam and lab findings. Patients with spinal problems likewise generally have equally compelling evidence of significant trauma or other causes of structural problems in their history and exams and image studies. Patients with genetic issues such as design flaws in the skull or spine usually have strong evidence as well.

There are core issue that are coming to light that all point to a common link in the cause of neurodegeneartive conditions. It has to do with circulation in the brain and cord. It is highly unlikely that athletes with history of head trauma get dementia, Alzheimer's, Parkinson's, MS or ALS due to a virus or a bacteria. Instead, the problem stems from the long-term effects of traumatic brain injury and subsequent swelling, infarction and scar tissues. Further evidence is mounting that whiplash and other types of spinal trauma similarly play a role in neurodegenerative conditions due their impact on blood and CSF flow to the brain and cord, not to mention scar tissue.

As an aside my condition began with a root canal and neurotoxin I was given without my knowledge or consent. If you are interested you can google the dangers of root canals and sequestered bacteria as per Dr. Weston Price. It is a controversial topic that most patients aren't privy to. The neurotoxin was an anesthetic that breaks down in the plasma not the liver like most anesthetics by an enzyme that many patients with autoimmune-inflammatory conditions lack in their complement immune system. This sets off a chain reaction. Despite my background, it took me awhile to connect the dots until it all hit the fan after a dental visit about two years ago. Once I knew the cause I was able to address the problem with good results. I wrote a small book about it for a limited audience of dental victims but it goes into autoimmune-inflammatory conditions that effect many people. We will publish after we do the migraine book, which addresses similar issues.
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Re: CCSVI and CCVBP

Postby NZer1 » Mon Oct 08, 2012 12:55 pm

Hi,
Dr the difference in the time process of many diseases and the understanding of what is happening in a lead up must be clue to what we are wanting to learn.
For instance a stroke with rapid onset and rapid symptom expression and also with a time window of treatment giving benefit is very different to the patterns of for instance MS. The slow build and continuing progression of symptoms must be a clue to the burden or load of 'something'.
The rapid leakage of blood into the CNS in a Stroke compared with a slow and continuous weep with inflammation and immune system attempt to manage the ongoing accumulation of deficits.
I believe there is an infectious agent that is able to enter injury regions because of damage to tissues in particular, learning that CPn does enter immune cells and inflammation is a fertile ground has given me a personal experience now that I have started the ABx that is showing me the die off of the Bacteria in muscle tissue from past injuries. These same areas are where there 'MS' symptoms occur.
In my opinion there is something about the infectious agent theory that needs to be revisited because the understandings of Vascular involvement make the progression part of symptoms a secondary aspect in many of the de-generative multi-faceted diseases we are looking into.

Disability from accumulation of load of both an infectious intracellular agent and the immune system activation seems to be getting over looked.

The actions that allow the burden to ingress and progress have been found, the parts of the whole are not acknowledged collectively which is going to complete the picture of understanding.

I haven't worded this very well sorry, brain fade!

Regards,
Nigel
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Re: CCSVI and CCVBP

Postby NZer1 » Mon Oct 08, 2012 1:40 pm

This is a quote from a Question and Answer news feed I get in my inbox; http://www.msanswers.ca/QuestionView.aspx?L=2&QID=1143
"Both MS and Lupus are auto-immune diseases. That is, the person’s own immune system is attacking their body. In MS, it attacks the nerve myelin in the brain and spinal cord. In Lupus, it involves joints, skin, organs, and brain. "

This is what I mean by Medical Specialities needing to talk and share ideas.
If the "autoimmune" reaction is 'behind' the BBB it is called MS, if it is outside the BBB it is called Lupus.
That has to be a HUGE clue!
The thing that hasn't been thought of yet is that a. it isn't 'autoimmune' and b. it is the same 'agent' operating in different parts of the body. The load and action that causes the disability is variable to the region effected and the search for what it is or could be has not gone far enough yet. Very few Micro-Biologists are speaking out about there findings, Stratton is one and Wheldon is another that have looked at MS and infections. If there was more investigation into cellular content in the 'disabled' areas there might be a paradigm shift!
Look at all to find the links!
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Re: CCSVI and CCVBP

Postby uprightdoc » Mon Oct 08, 2012 2:17 pm

Hi Nigel,
The reason why neurodegenerative diseases show up later in life is because it takes time for tissues to breakdown. In this regard, some neurotoxins can kill you quickly. Others such as alchohol and cocaine damage the brain slowly, as do pesticides. In contrast to strokes, traumatic brain injuries cause internal damage in the brain that decreases blood flow through the damaged area. Chronic ischemia can lead to tissue degeneration. Tissue degeneration stimulates the immune system to attack and get rid of bad tissues, which is one of the theories regarding the role of viruses, bacteria and autoimmune reactions in Alzheimer's and other neurodegenerative diseases. Chronic inflammation releases chemical, such as cytokines. Cytokines stimulate the liver to produce a protein that reduces iron utilization, which further reduce oxygenation of tissues. I further suspect that chronic ischemia can cause a cascade of degenerative processes similar to the ischemic (glutamate) cascade which follows a stroke. Likewise, it also takes time in many cases for the spine to breakdown before it begins to effect nerves. Similarly, the circulatory system also breaksdown slowly. People can get strokes and heart attacks without warning. Hypertension also damages tissues slowly without any noticable signs and symptoms. In addition to the heart, hypertension effects the brain. Among other things it causes pulse pressure waves that are driven into the brain and damage it. Glaucoma is a pressure problems that insidously destroys the optic nerve. Normal pressure hydrocephalus similarly destroys the brain.

There has been a great deal of research into viral, bacterial, fugal and other pathogens in neurodegenerative diseases for decades. It was suspected that Alzheimer's disease was caused by the same latent viruses and bacteria back when I first started my research. Pathogens get out of balance in illness and old age and attack weak tissues.

Is there a way that you can clinically determine if the muscle aches are due to die off from the bacteria and the release of endotoxins and not an adverse reaction? As I recall, some of the cases I read were still unloading toxins months and in some cases years later. Among other things, antibiotics cause gastritis and colitis (irritation/inflammation). Chronic inflammation decreases iron utilization and oxygenation of tissues. Muscles use a lot of blood. Inadequate blood flow leads to anerobic metabolites, such as lactic acid, which causes muscles to ache and cramp.
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Re: CCSVI and CCVBP

Postby NZer1 » Mon Oct 08, 2012 3:12 pm

My favourite thing at the moment is understanding intracellular infections where the apoptosis of the host cell is changed to suit the bacteria and then the ATP drain on the host cell. This effect is happening everywhere in our bodies, yes it is a balancing act by our diet and exercise to keep the table in our favour so that we naturally manage the bacteria volume with antioxidants and natural antibiotics in our varied diet. So much diet change has happened with food storage methods that the issues of an unfresh food diet nowadays is greater than 50 years ago and more so 100 years ago when we ate whole fresh foods etc.
The effect of bacteria in the Human ageing process is not looked at deeply enough. Bacteria are now in greater number, have little to stop them multiplying in a natural food way, they can evolve their DNA and become resistant to our chemical bombing with mono antibiotics in less than our life time and they need us as much as we need them!
I think that the ageing process is where we use natural life processes to remove wastes and dead cells that suits and requires bacteria and viruses. We underestimate the involvement of bacteria in our lives. We seem to over look the volume increase of bacteria in our ageing bodies. Wear and tear in our bodies is a volume increase of sites of all sorts of things and the living cells in the healing and waste removal process go looking for more sustenance after they have achieved their job.
Hence the theory of autoimmune 'disease'. A intracellular infection that has evolved in a short space of time by replicating foreign/attacking DNA into its own and enabling resistant mutations of its 'self' to survive. The autoimmune theory is a misunderstanding of what is happening at cellular level over time.

So the diseases such as MS and ALs are examples of assumptions in our Health process.

Need to get some Vit D,
Nigel
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Re: CCSVI and CCVBP

Postby NZer1 » Mon Oct 08, 2012 4:03 pm

Scar tissue is another interest at the moment.

Anacroiditosis is one special interest. What modifies the DNA of the scar tissue to grow in excess and to mutate? Adhering to different cell layers and disrupting nerve flow, vascular flow and CSF flow?

If the intracellular infection is also entering the immune system cells is that then modifying the environment of cells in the region of the healing process?

Scar tissue doesn't grow back in a replication of the original, so does that mean that other cells will be modified in the immune process, such as nerve conduction cells and motor cells.
My experience on this one is that after a deep cut on the wrist/thumb area I now have altered nerve conduction. Sensation and strength are changed. So when there is healing are we going to have irreparable nerve damage particularly if scar tissue forms.

**If there is inflammation and immune system involvement and we have an infection of an intracellular bacteria or virus are we needing to understand more about the process at a DNA sharing level of a pathogen? **

Regards,
Nigel
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Re: CCSVI and CCVBP

Postby NZer1 » Tue Oct 09, 2012 1:28 am

Interesting find in my inbox!
From
CCSVI at UBC MS Clinic - Information and Support
Opening of tight junctions in the blood brain barrier are the beginning of the "vicious cycle" leading to disease:

Summary

The blood-brain barrier (BBB) is a highly specialized brain endothelial structure of the fully differentiated neurovascular system. In concert with pericytes, astrocytes, and microglia, the BBB separates components of the circulating blood from neurons. Moreover, the BBB maintains the chemical composition of the neuronal “milieu,” which is required for proper functioning of neuronal circuits, synaptic transmission, synaptic remodeling, angiogenesis, and neurogenesis in the adult brain. BBB breakdown, due to disruption of the tight junctions, altered transport of molecules between blood and brain and brain and blood, aberrant angiogenesis, vessel regression, brain hypoperfusion, and inflammatory responses, may initiate and/or contribute to a “vicious circle” of the disease process, resulting in progressive synaptic and neuronal dysfunction and loss in disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, and others. These findings support developments of new therapeutic approaches for chronic neurodegenerative disorders directed at the BBB and other nonneuronal cells of the neurovascular unit.
http://www.cell.com/neuron/retrieve/pii ... 7308000342
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Re: CCSVI and CCVBP

Postby uprightdoc » Tue Oct 09, 2012 3:41 am

Thanks Nigel. It's the best and most thorough paper I have read on the BBB so far. Among other things it covers many issues I have covered previously in my book, as well as on my blog, website and this thread including: ischemia, strokes, hypertension, glutamate, excitotoxicity, CSF's role as lymph system, microvascular pathology (vascular AD and PD), head injuries, toxins such as insecticides in PD, inflammation, autoimmunity etc.. One important fact that was left out of the discussion however, is that the circumventricular organs, such as the posterior pituitary, pineal gland, area postrema, lamina terminalis etc. have an incomplete BBB. My next book is on migraines and the arterial side of neurodegenerative diseases. The craniocerivcal spine can effect blood flow to the brain and cord. Ischemia is a major cause of neurodegenerative diseases.
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Re: CCSVI and CCVBP

Postby uprightdoc » Tue Oct 09, 2012 8:20 am

Thanks again Nigel. I just finished reading the paper for a second time and will probably read it many times more. It fits perfectly with my research including stroke rehabilitation. I may contact Dr. Zlocovik. We share the same interests and we are on the same page.
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