November 4 2011 - Mr. Speaker, I am pleased to present a petition regarding chronic cerebrospinal venous insufficiency, or CCSVI. Over 15,000 procedures have now been performed in over 60 countries. In May 2010, my colleague from St. Paul's and I brought the fight for clinical trials and the registry for CCSVI to Parliament. Almost a year later in March 2011, the government announced a registry, although it would not start until July 2012. In June 2011, at last the government announced clinical trials.

I want to be very clear. All we have right now is announcements. What we need is action. Canadians with MS cannot afford to wait.

The petitioners call for the Minister of Health to consult experts actively engaged in diagnosis and treatment of CCSVI, to undertake phase 3 clinical trials on an urgent basis with a large patient participation in multiple centres across Canada and to require follow-up care.

Kirsty Duncan

November 3 2011 - With respect to the venous system, and more particularly, chronic cerebrospinal venous insufficiency (CCSVI): (a) what, if any, steps is the government taking to address research questions regarding the venous system, including (i) what does the normal venous system look like, and, specifically, what does it look like in infants, children, and adults, (ii) can the veins, in particular the jugulars and the azygous, look normal, and the flow be abnormal, (iii) what is the normal range of flow through veins, in particular the jugulars and the azygous, (iv) how should normal range of flow through veins, in particular the jugulars and azygous, be defined, (v) what is the normal range of blood gases in veins, in particular the jugulars and the azygous, (vi) what causes venous pathology and when does it occur, (vii) theoretically, what is the complete range of possible vascular problems in the head, neck, chest, and spine, which ones might impact health, and specifically which ones might be linked to multiple sclerosis (MS), (viii) how does the complete range of possible vascular problems compare with those actually seen in patients, (ix) how should abnormal flow through veins, in particular the jugulars and the azygous, be defined, (x) how might abnormal blood gases in veins affect health in the short-term and long-term, (xi) what, if any, reflux is normal in veins, and, if some reflux is normal, what is the ‘tipping point’ to abnormal, (xii) can a catalogue of venous pathology (in the head, neck, chest and spine), abnormal flow, and potential health impacts be established, (xiii) what protects against abnormal venous pathology and abnormal flow, (xiv) who should receive venous protective measures, and when should protective measures be put in place;

(b) what, if any, steps is the government taking to address research questions regarding the venous system and MS, including, (i) can fluid mechanics predict where physiologic changes in the brain might occur, (ii) how does the neurologist’s understanding of flow through the brain compare with that of physicists, (iii) does decreased metabolism lead to hypoxia which may lead to endothelial damage and inflammation, (iv) what occurs first, inflammatory changes in the brain or iron deposition, (v) what role does reduced perfusion have in MS, (vi) does stenosis extra-cranially cause less perfusion in the brain, (vii) does stenosis extra-cranially cause morphological changes in the brain, (viii) do cerebral veins actually disappear over time, or is it merely a lack of flow that makes them look like they disappear in magnetic resonance imaging (MRI) studies; (ix) what, if any changes beyond lesions, occur in the spinal cord of MS patients, as a result of reduced vertebral flow, (x) do vertebral veins show a similar disappearance over time, (xi) what percentage of MS patients show evidence of venous pathology, as compared to 'normals', (xii) what other venous abnormalities might MS patients have (e.g., bladder, intestine, kidney), might these abnormalities play a role in their disease, and, if so, how should they be imaged and treated, (xiii) what percentage of MS patients show venous abnormalities below the chest (e.g., May Thurner syndrome), and does this have an impact on their disease, (xiv) how does the vascular system of someone with benign MS compare to that of someone with relapsing-remitting, primary progressive or secondary progressive MS;

(c) what, if any, steps is the government taking to address research questions regarding CCSVI and MS, including, (i) what is the prevalence of CCSVI in relapsing-remitting, primary progressive or secondary progressive MS, (ii) does CCSVI worsen over time with the progression of disease, (iii) does CCSVI play a role in MS, and, if so, how, (iv) is CCSVI specific to MS, (v) what are the potential health impacts of CCSVI in the short-term, medium-term and long-term, both with and without treatment;

(d) what, if any, steps is the government taking to address research questions regarding CCSVI diagnosis, including (i) how do the results of MRI compare with those of ultrasound for diagnosis of CCSVI, (ii) what is the best way to image the venous system and the best way to image venous pathology, (iii) what are the limitations of current diagnostic tools to image the venous system, (iv) should intravascular ultrasound be used, and what are the benefits and the risks, (v) what is the learning curve for the various diagnostic procedures, and what should practitioners undertake to become sufficiently accomplished, (vi) can a standardized protocol be established for diagnosing CCSVI in MS patients, and when should MS patients be tested for CCSVI, (vii) can a standardized system for describing lesions (e.g., type, location) be established, (viii) what should be the decision-making process regarding whether to treat or not to treat (e.g., anatomy, flow, etc.), (ix) should arterial, venous and CSF flow be monitored, how often, and for what purpose, (x) should lesions and iron load be monitored, how often, and for what purpose;

(e) what, if any, steps is the government taking to address research questions regarding CCSVI treatment, including (i) what timescale is useful for treatment of CCSVI, (ii) what are the benefits and risks associated with treatment of CCSVI, (iii) what are best practices for treating each identified vascular problem, (iv) how should a successful CCSVI treatment be defined (e.g., valvular correction, reduction in stenosis, increased flow, improved blood gases), (v) can malformed jugulars and azygous be treated to achieve normal flow, (vi) can malformed jugulars and azygous be treated to achieve a normal range of blood gases, (vii) can jugulars and azygous be sufficiently treated to make up for poor vertebral flow, and, if not, what procedures can be developed to improve vertebral flow, (viii) should stents be used, and, if so, under what circumstances, (ix) what are the immediate complications of CCSVI treatment, and in what percentage of treatments does each occur for each identified abnormality, (x) what is the best follow-up anti-coagulant therapy, what are the potential risks, and what is the prevalence of complications, (xi) what are the best follow-up therapies, including, brain plasticity exercises, nutrition, physiotherapy, speech therapy, etc., and which therapies have the best associated outcomes, (xii) what are late complications, what follow-up is necessary to determine late complications, and in what percentage of treatments does each occur for each identified abnormality, (xiii) what treatments are available should a stent be occluded, either through hyperplasia or thrombosis, (xiv) what is the success rate of each identified treatment for an occluded stent;

(f) what, if any, steps is the government taking to address research questions regarding determining the best CCSVI treatment, including, (i) is CCSVI treatment with the addition of pharmacological agents more efficacious than just the CCSVI procedure, (ii) what pharmacological agents could be used to treat venous inflammation, iron storage, and hydrocephaly, and could these agents be added to CCSVI treatment, (iii) what safe apparatuses could be developed to keep treated veins open, (iv) are vein grafts possible, and if so, on whom, and when should they be used, (v) is CCSVI treatment more efficacious with mesenchymal-derived or adipose-derived stem-cell infusion than just the CCSVI procedure alone, (vi) what methods might be added to reduce permeability of the blood-brain barrier, including pharmacological agents and stem cells, (vii) what are the effects of chelators on iron uptake and release from the brain, and might iron chelators be used as therapeutic agents;

(g) what, if any, steps is the government taking to address research questions regarding possible impacts of CCSVI treatment on MS patients, including (i) what impact does CCSVI treatment have on patients immediately, (ii) what impact does CCSVI treatment have on patients at 24 hours, 3 months, 6 months, 1 year, and 2 years, (iii) what does the magnetic resonance venography (MRV) of a treated patient look like at 24 hours, 3 months, 6 months, 1 year, and 2 years, (iv) what percentage of MS patients show functional improvement at 3 months, 6 months, 1 year, and 2 years, (v) what are the most appropriate scales to measure any health impacts following CCSVI treatment as reported by MS patients, (vi) do new scales have to be created to measure reported changes following treatment, (vii) which patients show the greatest improvement, and does early intervention allow for a better outcome, (viii) what are the treatment outcomes associated with each of the identified venous problems, (ix) what percentage of MS patients show a reduction in MS attacks and brain lesions following the CCSVI procedure, (x) what percentage of MS patients with little or mild blockage show improvement following the CCSVI procedure, (xi) for those MS patients whose conditions do not improve or become worse, why does this occur;

(h) what, if any, steps is the government taking to address research questions regarding CCSVI re-stenosis and diagnosis, including, (i) what is rate of stenosis for each identified vascular abnormality, (ii) what changes should patients be told to look for to in order to recognize whether they are possibly re-stenosing, (iii) what diagnostic methods should be used after treatment for CCSVI, (iv) what diagnostic methods should be used to look for re-stenosis, and at what timescales;

(i) what, if any, steps is the government taking to address research questions regarding secondary procedures for CCSVI, including, (i) are secondary procedures safe, and if so, how many, (ii) what should be the follow-up protocol for secondary procedures, (iii) should there be a methodology established regarding whether to do a secondary procedure or not; and

(j) what, if any, steps is the government taking to address research questions regarding prevention in the next generation, including, (i) do vascular issues develop in utero, during childhood, or later, and what would be the best methods to discover circulation problems at the earliest time possible to avoid health impacts at a later date, (ii) might vascular birthmarks and tumours be an indication of potential vascular problems, (iii) might skin discolouration, skin abnormalities, and even proliferation of moles be an indication of an autoimmune or neural condition, (iv) might giving vitamin D to pregnant mothers reduce the risk of children being born with, or developing, vascular problems and other conditions and, if so, what dosage is appropriate, (v) do antioxidants, vitamin D and omega 3 reduce vein inflammation, (vi) will giving children and adolescents vitamin D reduce the risk of developing vein inflammation and venous hypertension and, if so, what dosage is appropriate, and what quantity should be recommended for a child with a family history of CCSVI, vascular problems or MS, etc., (vii) what would be the optimum time to undertake CCSVI treatment to avoid health impacts at a later date?

Kirsty Duncan