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Tuesday, August 31, 2010

A Must Read


With the advent of CCSVI as a major factor in multiple sclerosis, it has become painfully apparent that national MS societies do not have the best interests of persons with MS as their highest priority. This has taken many people by surprise because most people are under the assumption that the main concern of national MS societies is the well being of persons with MS. This assumption is not, and has never been, true. Perhaps one more benefit of the discovery of CCSVI as an important causal factor of MS, has been to expose the myth the national MS societies have people with MS as their #1 priority.

The Groups of the MS Societies

To understand the priorities of national MS societies, it is essential to understand the various groups which compose their structure. These groups are the scientific advisors, the staff members, the board members, and the members of the society who are mainly persons affected by MS. Each of these groups plays a very specific role in how a given national MS society functions.

The most important and influential group is the scientific advisors who determine the type of information the society provides to the members and to the public at large. They also determine what research will be done and what overall policies will be followed when it comes to lobbying efforts to influence government decisions. The scientific advisors are clinical neurologists who specialize in multiple sclerosis. Many of them also carry out research activities in addition to their clinical work.

The next important group is the paid staff of the society and, in the case of a large society, they can number in the hundreds. Their salary and benefit packages are on par with workers in similar jobs in both the private and public sectors. Importantly, the staff, for the most part, puts into action the policies and plans of the scientific advisors, that is, the neurologists. There is a very strict adherence to this and no deviation or independent thinking is tolerated. The staff members are like soldiers who do what they are told and are not expected to contribute to the scientific or public policies of the society. They are simply the “go-betweens”, the neurologists and the all those seeking information from the society. Notably, most staff members are not affected by MS.

By far the greatest responsibility of the staff is to raise money by running various fund raising projects. Most of staff time in spent on this critical activity which is understandable given the majority of the money raised goes to pay staff salaries and benefits. Staff members also arrange some programs for people with MS in terms of education but this activity is rather minor in terms of actual time and effort expended. The staff also fields questions from persons with MS and, as noted previously, the provided information is only that sanctioned by the scientific advisors (neurologists).

The board of directors of a given national society is most often composed of people who usually have good connections for fund raising from corporations or who have strong political connections. Usually a few persons with MS are included on a board but, in most cases, the majority of board members are not affected by MS. One or more staff members also usually are part of the board.

Most board members have at best a rudimentary understanding of science in general and the science of MS in specific. They have very little influence on any major policies of the society and, in most cases, simply rubber stamp the scientific and political policies determined by the neurologists and implemented by the staff. Their main responsibility seems to be ensuring that the society is on a firm financial footing and discussing the merits of proposed fund raising campaigns.

The final group in a national MS society consists of the members themselves and they, for the most part, are persons affected by MS. They are the consumers of the products of the society which consist mainly of information dictated by the neurologists and packaged by the staff. Such information is both hard copy and web-based. Some members act as volunteers and volunteer activities are related to both money raising activities and to helping other people with MS. The members essentially have no say in terms of the main policies of the society although on a local level they can help to get new member services initiated.

In summary, a national MS society spends most of its time raising money which is used to pay fund-raising costs, the salaries and benefits of the staff members, and substantial administrative expenses. Such expenses require about 80-85% of all money collected. The amount left over is mainly used to fund research projects approved by the scientific advisors (neurologists) and, not surprisingly, projects of former and current advisors usually are well funded. Proposals from “outsiders” don’t fare so well.

Past Situation

In the past, everything went along rather smoothly with the society advertising the need to raise money to cure MS, with such a cure being attainable through the research activities funded by the society. Given the severe disabilities sometimes associated with MS, the need for finding a cure for MS is not a hard sell, and the large MS societies raise tens of millions of dollars every year. In the 60 years this routine has been going on, the research funded by the societies has not brought us anywhere even remotely near the prospect of developing an effective treatment for MS. This impressive failure has only led to louder calls for more money for more research.

The scientific and medical information provided by a national MS society is entirely centred on drug therapies that have been approved for use. The staff members strongly advocate the use of such drug therapies and almost all other proposed therapies are ignored, discouraged and/or denigrated. The main government lobby efforts of the societies usually are to fight for the approved use of the drugs.

It is imperative to appreciate that most (often all) of the scientific advisors of the societies and the societies themselves have strong financial ties to the pharmaceutical companies which manufacture and market the approved drug therapies for MS. The most blatant of such ties is that of the NMSS of the United States. It partners with drug companies and gives substantial grants to them.

The existence of such financial ties readily accounts for the policy that only drug therapies are advocated and that the value of such therapies is never, ever remotely questioned. These financial ties also create a serious conflict of interest for the neurologists and MS societies when it comes to any proposed, non-drug therapy and that is one, big reason why non-drug therapies are ignored or downplayed by the societies.

There can be no doubt that the national MS societies are there mainly for the benefit of the neurologists (scientific advisors) in that they provides them much needed research funding. The societies also provide an excellent vehicle for promoting drug therapies which are financially very important for the neurologists. Of course the societies are also there for the benefit of the staff members who make a good living from keeping everything running smoothly and ensuring the information from the neurologists reaches the desired destinations.

Before the advent of CCSVI, the drug therapies were the only conventional medical therapies available. By advocating such therapies, the societies could easily claim to be acting in the best interests of persons with MS even though such advocacy was driven mainly by the best interests of the neurologists and the societies themselves. Whether or not the use of the current drugs is really in the best interests of persons with MS is a completely separate issue and will be explored in a separate document.

CCSVI Rocks the Boat

The sudden emergence of CCSVI as an important factor in MS, and the great promise of CCSVI treatment for slowing and perhaps even halting MS disease progression for many, have caused a great problem for MS societies around the world. Given all that we now know about CCSVI and its treatment, the national MS societies would best serve the interests of persons with MS by immediately funding a major, comprehensive research program which definitively tests the effectiveness of CCSVI relief in the next few years. Furthermore, it would also be in the best interests of persons with MS if the MS societies lobbied to have CCSVI treatment available as soon as possible given the health problems associated with having impaired venous drainage from the brain and the many hundreds of credible, experiential accounts of very significant positive changes following CCSVI treatment.

The MS societies have studiously avoided funding any clinical trial studies for CCSVI treatment as was clearly demonstrated by the rejection of proposals from top CCSVI researchers by North American national MS societies. (e.g. University of Buffalo, Stanford University, McMaster University). Notably, those who got their proposals accepted seem to have either very strong ties to the pharmaceutical industry (e.g. Wolinsky at U of Texas) or do not know what they are doing. A fine example of this latter category is Dr Kathleen Knox at the University of Saskatchewan who recently was quoted as saying “The biggest difficulty her team faces, is that they don’t know how to test patients to see if they have the blocked veins”. This is a stunning admission of incompetence and shows the type of researchers favoured by the national MS societies when it comes to CCSVI “research.

Some national MS societies are actively lobbying their respective government NOT to allow CCSVI treatment. A fine example of this is a recent letter the director of the Ontario division of the MS Society of Canada wrote to the Ontario Health Minister emphasizing that the province should not fund any CCSVI testing or treatment. The notice on the website of the Multiple Sclerosis Society of Canada says it all - “the MS Society does not recommend that people with MS be examined or treated for CCSVI outside of an established research protocol”. All in all, any thought that MS societies are acting in the best interests of persons of MS must be abandoned. So who’s best interests are they serving with their actions?

When it comes to CCSVI, the interests of the neurologists and the societies are best served by having CCSVI marginalized, by not funding any CCSVI treatment research, and by lobbying the government to not allow any treatment of impaired venous drainage in persons with MS despite the obvious health hazard such a condition represents. The reasons for such actions are straightforward.

If CCSVI treatment by venous angioplasty turns out to be far more effective than the current drug treatments, and there is every reason to expect it will be, then MS drug revenues will plummet precipitously. Such a huge loss of revenue will have a devastating effect on the financial well being of MS neurologists and the national MS societies themselves. Furthermore, persons with MS will be treated primarily by interventional radiologists, thus adding to the financial losses of the neurologists. There is no question that any activity which helps to bring the implementation of CCSVI treatment forward is not in the best interests of the neurologists and the national MS societies that they control and everyone is well aware of this indisputable but somewhat awkward fact.

Because of the advent of CCSVI, we now have an unprecedented situation of conflicting interests. What is in the best interests of persons with MS is clearly not in the best interests of both the neurologists who provide the scientific guidance for the MS societies and the staff of the societies who put into effect the policies of the neurologists.

The Current Reality

Not surprisingly, the best interests of the neurologists and the society staff members will always trump the best interests of the persons with MS. Thus the policies and actions of the national MS societies have been to avoid any funding of proposed CCSVI treatment studies and to lobby government bodies not to provide any CCSVI treatment. They also advise persons with MS not be tested or treated for CCSVI despite the obvious medical need for such treatment (blocked veins are hazardous to one’s health).

The neurologists and the MS societies also have instituted a policy of casting doubt on the validity of the CCSVI concept and on the safety of CCSVI treatment. This has even gone as far as blatant fear-mongering when it comes to having venous angioplasty to relieve CCSVI. One good example of this recently appeared in a governmental health report written by MS neurologists. The writers claimed that the only venous blockages that exist in persons with MS are clots caused by angioplasty and the only results of venous angioplasty are injuries to the vein. This is of course sheer nonsense but, as they say, truth is the first casualty in any war.

The current actions of the national MS societies regarding CCSVI are entirely rational once the structure of the societies is understood. The societies are acting in the best interests of the neurologists and staff members as they always have and always will. Unfortunately, when it comes to CCSVI, such actions are not in the best interests of persons with MS. However, it is the false perception that the national MS societies are there primarily to serve the best interests of persons with MS that has created the shock and disappointment with the current actions of the societies in regards to CCSVI. When it comes to the policies and actions of the national MS societies, persons with MS must fully realize that they are lower in priority than the neurologists and staff members. The CCSVI issue has clearly demonstrated this beyond any reasonable doubt.

Consequences of the Actions of the National MS societies

We now have sufficient data to say that, each day a person with MS suffers the consequences of impaired venous drainage, they are doing harm to themselves and such a reality has to be clearly understood. It has been said, “MS Never Sleeps” and one of the main reasons for this is that impaired venous drainage never sleeps and this serious pathology is causing problems every day for persons with MS. Thus it logically follows that every dollar the national MS societies raise is potentially doing harm to persons with MS because that dollar is potentially contributing to actions that are designed to delay the availability of CCSVI treatment for all persons with MS.

Given the above, it is clear that the interests of persons with MS would be best served by halting any support of national MS societies and by supporting groups which are actively promoting the need for CCSVI treatment research and government support for the availability of CCSVI treatment as soon as possible.


The advent of CCSVI has revealed the highest priorities of the national MS societies. These are actions and policies that are in the best interests of neurologists and society staff members. The interests of persons with MS are a distant third in this contest of competing interests. Continued support for national MS societies is potentially harmful for persons with MS because of the societies’ deliberate lack of appropriate and much needed actions regarding CCSVI. All persons affected by MS should be supporting organizations which are funding clinical trials to test the effectiveness of CCSVI treatment and which are lobbying governments to make CCSVI treatment widely available in the near future.

Saturday, August 28, 2010

Blood Flow and white matter lesions

by CCSVI in Multiple Sclerosis on Saturday, August 28, 2010 at 2:25am

Thanks to Jim for posting the research of Dr. Bernard Juurlink -a Saskatchewan researcher who proposed the theory of MS being created by slowed bloodflow in 1998---

Here's the story on Canada.com


Here's is Dr. Juurlink's proposal from 12 years ago--


Just wanted to write a post about this for my research geek friends on my favorite topic:

Hypoperfusion in the MS brain

Hypo-meaning under ot sub-par and perfusion- meaning the delivery of blood to the capillary bed.

In MS brains, there is a below normal delivery of blood into brain tissue. Neurologists have never given a good explanation. Here's a great paper that looks at this phenomena and tries to figure out why this is happening.

(terms to know -NAWM is normal appearing white matter, or healthy myelin.

Myelin is the protective white matter in your brain. Gray matter is the tissue below the myelin.

Ischemia means a lack of oxygen or hypoxia.)


"Accumulating evidence indicates that there is a decreased perfusion throughout the NAWM (normal appearing white matter) in patients with MS. It occurs in both relapsing–remitting and primary progressive MS, strongly suggesting that it represents an integral part of the disease process. Ischemic changes might be involved in the development of a subtype of focal demyelinating lesions (type III lesions). There appears to be a relationship between reduced white matter perfusion and cognitive dysfunction in patients with MS.

Ge et al (2005) interpreted the hypoperfusion in NAWM as a vasculopathy in the context of the perivascular inflammations that occur in focal MS lesions. However, although inflammatory infiltrates in MS are typically located around small- or medium-sized veins (Adams, 1989) and in the perivascular spaces surrounding arterioles (Gay, 2006; Gay et al, 1997), microvessel thrombosis is only exceptionally being observed within these lesions (Aboul-Enein and Lassmann, 2005; Wakefield et al, 1994)."

So, this paper comes pretty close to saying that this slowed perfusion and white matter lesions could be created by slowed blood flow and a lack of oxygen in the brain. This is exactly what Dr. Juurlink was proposing.

Here's a study that shows that white matter lesions in rats were formed when cerebral hypoperfusion was created in their brains.


"Cerebrovascular white matter lesions represent an age-related neurodegenerative condition that appears as a hyperintense signal on magnetic resonance images. These lesions are frequently observed in aging, hypertension and cerebrovascular disease, and are responsible for cognitive decline and gait disorders in the elderly population. In humans, cerebrovascular white matter lesions are accompanied by apoptosis of oligodendroglia, and have been thought to be caused by chronic cerebral ischemia. In the present study, we tested whether chronic cerebral hypoperfusion induces white matter lesions and apoptosis of oligodendroglia in the rat. Doppler flow meter analysis revealed an immediate reduction of cerebral blood flow ranging from 30% to 40% of that before operation; this remained at 52–64% between 7 and 30 days after operation. Transferrin-immunoreactive oligodendroglia decreased in number and the myelin became degenerated in the medial corpus callosum at 7 days and thereafter."

There is NO NEED for any auto- immune system activation to create white matter lesions or myelin destruction. NONE. Dr. Juurlink knew this. Many doctors who study stroke know this. All that is needed is slowed blood flow. Did you know that most elderly people have white matter lesions in their brains? We don't see them, because they are not routinely given MRIs. But it's a known fact that the aging brain has slower perfusion, slower circulation and decreased blood flow, resulting in less oxygenation. Why has the correlation of circulation in MS and other neurodegenerative diseases been ignored? This chaps my hide.

Here's a paper where they created white matter lesions in rats' brains by clamping their carotid arteries closed. Remember, the arteries bring the blood in, the veins take it out. Slowed perfusion can be created by slowed delivery of blood, or slowed removal. It works both ways.


Notice in this study, the first areas of white matter lesions were on the optic nerve after only THREE DAYS of ligation. This mimics the order of problems we see in pwMS. RRMS patients typically present with vision problems first and show white matter lesions.

"Cerebral white matter (WM) lesions are observed frequently in human ischemic cerebrovascular disease and have been thought to contribute to cognitive impairment. This type of lesion can be experimentally induced in rat brains under chronic cerebral hypoperfusion by the permanent occlusion of both common carotid arteries. However, it remains uncertain whether chronic ischemia can damage both the gray and white matter, and whether it can induce demyelination with or without axonal damage. Therefore, we examined axonal damage using immunohistochemistry for the amyloid β/A4 precursor protein (APP), chromogranin A (CgA) and demyelination using immunohistochemistry for the encephalitogenic peptide (EP) in this model. Severe WM lesions such as vacuolation and the loss of nerve fibers appeared in the optic nerve and optic tract after 3 days of ligation, and less intense changes were observed in the corpus callosum, internal capsule, and fiber bundles of the caudoputamen after 7 days with Klüver–Barrera and Bielschowsky staining. These WM lesions persisted even after 30 days. The APP, CgA, and EP-immunopositive fibers increased in number from 1 to 30 days after the ligation in the following WM regions: the optic nerve, optic tract, corpus callosum, internal capsule, and fiber bundles of the caudoputamen. "

When neurologists say that Dr. Zamboni's research is not based on fact....give them a lecture on hypoperfusion and white matter lesions. This is science, this is fact, this is real.


Saturday, August 7, 2010

Background Information on CCSVI all in one place!
Background Information on CCSVI
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system of unknown origin. Since the time of Charcot, a relationship between the cerebral veins and the inflammatory lesions associated with MS has been consistently reported (1,2). Observations have been made that the periventricular lesions of MS seem to extend along cerebral veins and that the cortical lesions occur within territory drained by cortical veins (1,3-5). Additional post-mortem studies have confirmed the relationship between the lesions of MS and the small veins of the CNS (6-8). For example, Fog showed that MS plaques arise from segments of large epiventricular veins and then extend into the cerebral hemispheres along the cerebral veins (6). In addition, Putnam showed plaques lined with gliotic tissue containing large veins, surrounded by hematogenous pigment (7). While these observations imply a connection between the cerebral veins and MS, this connection was felt to be interesting but was largely ignored.

As MRI became a primary way of evaluating patients with MS, the potential connection between the cerebral venous circulation and MS was once again observed. Studies showed that patients with MS have cerebral blood flow disturbances, including decreased cerebral blood flow, decreased cerebral blood volume, and a prolonged mean transit time (9-12). These findings were felt by some to be due to vascular pathology and not a result of decreased metabolic demand (10,13). However, the cause of the abnormal flow was never fully explained. MR venography has also been helpful in directly demonstrating the relationship between the inflammatory lesions of MS and the cerebral veins (14).

Histologic studies of the venous system in MS have potentially shed some light on this relationship. These studies have shown evidence of both pericapillary fibrin cuffs and perivenous iron deposits in the form of extracellular hemosiderin and iron-laden macrophages (8,15,16). In addition, MRI has been able to detect these perivenous iron deposits (17-19). Iron is known to be important for CNS physiology since it is a cofactor for neural metabolism and ATP production and because it is involved in myelination and oligodendrocyte development (20,21). In addition, a role for iron in the pathophysiology of senile toxicity and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease has been described (22-24), possibly due to oxidative stress and free-radical generation (18,25,26).

Interestingly, there appears to be a possible role for iron in the inflammation associated with MS, although investigations into this role are limited (20). For example, Grant, et al. found that the incidence of encephalomyelitis (EAE) in mice, which is often used as an experimental for MS, was 60-70% in mice with a normal iron level and in iron-overloaded mice, but 0% in iron-deficient mice, suggesting that iron-deficiency is protective against EAE (27). Similarly, Sfagos found higher levels of serum ferritin and soluble transferring receptors in active MS than in controls (28). Both of these findings support the hypothesis that local iron-overload may be the initial signal of the inflammatory chain in MS (2).

This relationship between the venous circulation and iron deposition has been better explored in patients with chronic venous insufficiency in the lower extremities (2). In the lower extremities, venous reflux and venous obstruction are known to cause multiple problems including varicose veins, edema, skin changes (including pigmentation, lipodermatosclerosis, etc.), and ultimately venous ulcers. Studies have demonstrated a relationship between tissue iron accumulation and the inflammatory changes associated with chronic venous insufficiency (29-32). In the lower extremities, venous stasis can lead to extravasation of red blood cells. The degradation of these cells causes iron to be released, ultimately leading to its incorporation into ferritin, hemosiderin deposition, and inflammatory change (2). In addition, both chronic venous reflux and local iron overload may activate matrix metalloprotease (MMP) in the vein wall, which can lead to the degradation of collagen, elastin, and laminin, resulting in tissue breakdown and ulcer formation (33-36). Finally, the presence of a pericapillary fibrin cuff has been shown around the lower extremity vasculature in these patients and is considered a marker of insufficient venous drainage.

One of the reasons why the correlation between venous abnormalities and MS has been explored recently is because histologic changes similar to those seen in chronic venous insufficiency of the lower extremities have been found in association with MS. A pericapillary fibrin cuff is consistently found in patients with MS (8,15,16), which is important since fibrin deposition is thought to exacerbate axonal injury in MS patients (37). In addition, it is known that MMP activation has a role in MS by digesting basement-membrane collagen and fibronectin, thereby facilitating the migration of cells and proteins into the CNS, perhaps inciting the inflammatory response characteristic of MS (38-40). Cellular migration may involve red blood cells and their degradation can lead to increased iron deposition. As stated previously, perivenous iron deposits have been found on both MR imaging studies and histologic studies in MS patients.

While the histologic findings described above seem to support similarities between MS and chronic venous insufficiency, recent descriptions of venous abnormalities in MS patients have lent additional support to the theory of Chronic Cerebrospinal Venous Insufficiency (CCSVI). Zamboni, et al used Doppler ultrasound to evaluate the venous circulation in patients with MS (41,42). The findings that were seen significantly more often in MS patients than in normal controls included constant reflux in the internal jugular and/or vertebral veins, reflux in the deep cerebral veins, indetectable flow in the internal jugular and/or vertebral veins, and a defined stenosis of the internal jugular veins. Patients with positive Doppler examinations were subsequently studied with selective venography, which showed that CCSVI is characterized by multiple extracranial stenoses involving the internal jugular and azygous veins (43). More recently, Zivadinov, et al reported on the preliminary data from the Combined Transcranial and Extracranial Venous Doppler Evaluation (CTEVD) study at the 2010 meeting of the American Academy of Neurology (44). This study evaluated 441 patients (280 patients with MS and 161 healthy controls) and found that the prevalence of CCSVI in MS patients was 56.4% and in healthy controls, it was 22.4%. When the 10.2% of subjects in which the results were borderline were excluded, the percentage of affected MS patients rose to 62.5% compared to 25.9% of healthy controls.

Zamboni, et al were able to define four main patterns of extracranial disease in MS patients based on involvement of the internal jugular and/or azygous veins. It was felt that these disease patterns may occur more frequently in different forms of MS (41,45). For example, the form involving the azygous vein may be more common in patients with the primary progressive form of MS, which correlates with the fact that spinal plaques are often seen in these patients. It was therefore theorized that the location of venous obstruction might play a key role in determining the clinical course of MS.

Importantly, the internal jugular and azygous veins represent the primary routes for venous outflow from the CNS. Extracranial Doppler studies have shown that the internal jugular veins are the predominant pathways for drainage when a patient is in the supine position and that the vertebral veins are the primary pathways when a patient is upright (46,47). When flow in the internal jugular veins and/or azygous vein is compromised, it can have physiologic implications for cerebral blood flow. Collateral vessels develop in order to prevent the development of intracranial venous hypertension (48,49). However, even with these collateral pathways in place, the venous drainage is insufficient and the transit time is prolonged, as confirmed by MR perfusion studies (10,48,49). This can lead to several problems. Since normal CSF circulation depends on efficient venous drainage from the CNS (50-52), insufficient venous drainage can lead to lower net CSF flow. This is supported by the increases in the volume of the lateral and third ventricles in MS patients (51). Insufficient venous drainage can also cause retrograde venous flow and reflux into the CNS (49), which has been demonstrated in the deep cerebral veins and transverse sinus in MS patients (53). Based on the Doppler studies performed by Zamboni, et al, the reflux occurs in any body position and without being elicited by a forced movement, which suggests that the reflux is due to a stenosis or occlusion as opposed to valvular incompetence (41).

The presence of chronic reflux and flow reversal in the cerebral venous system can lead to increases in the peak diastolic velocity of blood, which increases the resistance to flow (53). The microcirculation can then become overloaded and transmural pressure becomes increased (35,54). Even before any discussions about CCSVI, venous hypertension was thought to play a role in the pathogenesis of MS (55,56). It is thought that slight increases in venous pressure can lead to venous dilatation, which can potentially separate the endothelial cells forming the blood brain barrier (57). This can enable cells, including red blood cells, to pass through the blood brain barrier and initiate the perivenular inflammatory process that is seen in MS (2,53). In MS, changes in microcirculatory perfusion parameters on MRI have been shown to precede plaque formation (58). These ideas may explain the venous distribution of MS lesions.

With this in mind, Zamboni, et al treated 65 MS patients with CCSVI that was diagnosed on Doppler ultrasound (59). These patients underwent selective venography of the internal jugular and azygous veins from a common femoral vein approach. A significant stenosis was considered a venous lumen reduction >50%, which correlated with a pressure gradient of 2.2 cm/H20. All of these procedures were performed as outpatient procedures. All patients were treated with angioplasty, which led to improved luminal diameter and reduced venous pressures. Six patients reported a post-operative headache, which resolved spontaneously in all patients. No other operative or postoperative complications were reported. Patients were followed with repeat Doppler ultrasound and venography at 18 months. At the completion of follow-up 96% of lesions treated in the azygous vein were patent and 53% of lesions treated in the internal jugular veins were patent; many of these patients underwent secondary angioplasty but the long-term patency after this second intervention has not yet been studied. Zamboni also showed sustained clinical improvement in relapsing-remitting patients as evidenced by significant improvement in the Multiple Sclerosis Functional Composite (MSFC). However, only limited improvement was seen in patients with primary and secondary progressive MS. All of the relapsing-remitting patients with continued patency of the internal jugular and azygous veins at 18 months were relapse-free. In addition, there were reductions in enhancing lesions on the MRI studies performed in these patients one year after treatment. This study concluded that endovascular treatment of CCSVI using angioplasty is feasible and safe.

Friday, August 6, 2010

Taken from Melissa Medina's blog


This is what I and other MSers may have:

Visual Symptoms-
Symptom Description
Optic Neuritis Blurred vision, eye pain, loss of colour vision, blindness
Diplopia Double Vision
Nystagmus Jerky Eye Movements
Ocular Dysmetria Constant under- or overshooting eye movements
Internuclear Ophthalmoplegia Lack of coordination between the two eyes, nystagmus, diplopia
Movement and sound phosphenes Flashing lights when moving eyes or in response to a sudden noise
Afferent Pupillary Defect Abnormal pupil responses

Motor Symptoms-
Symptom Description
Paresis, Monoparesis, Paraparesis, Hemiparesis, Quadraparesis Muscle weakness - partial or mild paralysis
Plegia, Paraplegia, Hemiplegia, Tetraplegia, Quadraplegia Paralysis - Total or near total loss of

Muscle strength-
Spasticity Loss of muscle tone causing stiffness, pain and restricting free movement of affected limbs
Dysarthria Slurred speech and related speech problems
Muscle Atrophy Wasting of muscles due to lack of use
Spasms, Cramps Involuntary contraction of muscles
Hypotonia, Clonus Problems with posture
Myoclonus, Myokymia Jerking and twitching muscles, Tics
Restless Leg Syndrome Involuntary Leg Movements, especially bothersome at night
Footdrop Foot drags along floor during walking
Dysfunctional Reflexes MSRs, Babinski's, Hoffman's, Chaddock's

Sensory Symptoms-
Symptom Description
Paraesthesia Partial numbness, tingling, buzzing and vibration sensations
Anaesthesia Complete numbness/loss of sensation
Neuralgia, Neuropathic and Neurogenic pain Pain without apparent cause, burning, itching and electrical shock sensations
L'Hermitte's Electric shocks and buzzing sensations when moving head
Proprioceptive Dysfunction Loss of awareness of location of body parts
Trigeminal Neuralgia Facial pain

Coordination and Balance Symptoms-
Symptom Description
Ataxia Loss of coordination
Intention tremor Shaking when performing fine movements
Dysmetria Constant under- or overshooting limb movements
Vestibular Ataxia Abnormal balance function in the inner ear

Vertigo Nausea/vomitting/sensitivity to travel sickness from vestibular ataxia

Speech Ataxia Problems coordinating speech, stuttering

Dystonia Slow limb position feedback
Dysdiadochokinesia Loss of ability to produce rapidly alternating movements, for example to move to a rhythm

Bowel, Bladder and Sexual Symptoms
Symptom Description
Frequent Micturation, Bladder Spasticity Urinary urgency and incontinence
Flaccid Bladder, Detrusor-Sphincter Dyssynergia Urinary hesitancy and retention
Erectile Dysfunction Male and female impotence
Anorgasmy Inability to achieve orgasm
Retrograde ejaculation Ejaculating into the bladder
Frigidity Inability to become sexually aroused
Constipation Infrequent or irregular bowel movements
Fecal Urgency Bowel urgency
Fecal Incontinence Bowel incontinence

Cognitive Symptoms-
Symptom Description
Cognitive dysfunction Short-term and long-term memory problems, forgetfulness, slow word recall
Mood swings, emotional lability, euphoria
Bipolar syndrome
Aphasia, Dysphasia Impairments to speech comprehension and production


Heat intolerance- Uhthoff's Symptom Increase in severity of symptoms with heat

Inappropriately cold body parts

Gastroesophageal Reflux Acid reflux

Impaired sense of taste and smell

Epileptic seizures

Swallowing problems

Respiratory problems

Sleeping Disorders

Autonomic nervous system problems
Take Your Drugs:

In the face of so many “independent” studies which show that the main MS drugs are of no benefit, and in some case actually make MS sufferers worse. Why are Neuros still pushing them? Why the hard sell?

My friend was just at his Neuro, and from the time he went in the clinic front door, the reception staff were doing their drug sales pitch. These people aren’t even Doctors, yet they are pushing drugs. Isn’t that illegal?

Immediately following this ambush, his Neuro starts pushing the drugs again, and starts to make him feel guilty, irresponsible, and stupid for not taking any of them.

The Neurological community is the first to ram the idea down our throats that CCSVI must have concrete independent studies. They need proof. They basically say that they can’t trust that Zamboni dude, since his petty research is all a hoax. It’s just junk science. It’s all garbage.

Well lets call a spade a spade shall we. Who has the “junk science” now?

The monsters at Big Pharma are acting like a bunch of criminals. What else can you call them?

Their self-fulfilling gold ribbon studies are a hoax. Their glossy sales pitch, is nothing but an unethical fraud. They are robbing patients and governments of billions of dollars, when clearly selling bottles of murky Lake Ontario water, would clearly offer more medical benefits.

So what is going on? Multiple independent studies verify what I’m saying. They all say that the level of disability was no different in groups of patients who took “the drugs” as compared to matched groups who took nothing. These were long-term studies, which looked at their level of disability.

If the Neuros, slick Drug Dealers, and the supportive MS Society are demanding they need proof that CCSVI Treatment offers any benefit, then they bloody well must halt their unrelenting drug promotion and support, and start holding the drugs up to the same ethical standards they demand of CCSVI. Anything less is not acceptable.

From around the globe, in 2010 we have seen nearly 2,000 MS sufferers receive a simple 45-minute angioplasty treatment. We are seeing benefits, that are clearly unmatched by any other known MS treatment. We have seen lives saved.

For many with advanced cases of MS there is no other treatment option available!

The Neurological community has completely failed the very patients they are sworn to help. That’s a fact. We see it unfolding right before our eyes now.

The book on MS has been rewritten by Dr. Paolo Zamboni. It's the most amazing thing ever.

Now it’s time for the Neurological community to pick up that book, and read it too.


Ashton Embry - New Studies Show the MS Drugs Don’t Slow Progression:

Dr. Alastair Compston and the Drug Dealers:

The Independent - MS drug trial 'a fiasco'

UK scheme for MS drugs "a costly failure" - experts:

BMJ - Multiple sclerosis risk sharing scheme: a costly failure:

NHS 'has wasted millions on MS drugs which did nothing to help patients'

Interferons May NOT Be Good for Some People with MS:

CCSVI for Dummies: