CCSVI monthly January

Epub: Carraro et al. Optic Nerve and its Arterial-Venous Vascularization: An Ultrasonologic Study in Multiple SclerosisPatients and Healthy Controls.J Neuroimaging. 2012 Dec. doi: 10.1111/j.1552-6569.2012.00758.x.

BACKGROUND: Recent studies suggest that alterations in the cerebrospinal venous system may play a role in multiple sclerosis (MS) and that chronic cerebrospinal venous insufficiency correlates with clinical features of MS patients.

OBJECTIVES: To evaluate the vascularization of optic nerve (ONr) and measure ONe thickness by color Doppler ultrasonography in MS patients with and without previous optic neuritis (ONe).

SUBJECTS AND METHODS: We assessed flow variables in the ophthalmic artery, central retinal artery, and central retinal vein and measured the diameter of ONe in 46 relapsing-remitting MS patients and 37 healthy controls (HC). Twenty-two MS patients had previous ONe and 24 MS patients had not. Patients with acute ONe were not included. We examined and compared 63 unaffected and 29 affected eyes of MS patients with 74 control eyes.

RESULTS: Regarding flow variables, we did not find any significant difference between HC, MS affected, and unaffected eyes. Comparing ONr diameters, we found a progressive significant thinning of the ONr from HC to MS patients without and with past ONe.

CONCLUSIONS: We found no significant alteration in the arterial-venous vascularization of both affected and unaffected ONr compared with HC. We demonstrated the possibility to detect ONr atrophy in MS patients.

Not exactly CCSVI but does not find a vascular abnormality at the centre of the problem.

No prblem with the plumbing here. 

Simka et al. Multiple sclerosis, an unlikely cause of chronic cerebrospinal venous insufficiency: retrospective analysis of catheter venography. JRSM Short Rep. 2012;3(8):56. doi: 10.1258/shorts.2011.010146.

OBJECTIVES: It is unknown if a relationship exists between multiple sclerosis and chronic cerebrospinal venous insufficiency and if this venous pathology is a causal factor for multiple sclerosis or is a product of a neurological disease. Even so, one should expect that if multiple sclerosis were the cause for venous lesions, then patients with an extended history of the disease would present with a more severe venous pathology. 

DESIGN: Retrospective analysis of catheter venography of the azygous and internal jugular veins, and duration of clinical history of the disease inmultiple sclerosis patients. 

PARTICIPANTS: 353 multiple sclerosis patients, with duration of the disease: 0.5-41 years (median: 10 years).

MAIN OUTCOME MEASURES: We performed statistical analysis of the correlations between the duration of multiple sclerosis and the degree and number of venous lesions revealed using catheter venography.

RESULTS: We observed weak, statistically insignificant correlations (This means no correlation) between the severity of chronic cerebrospinal venous insufficiency and the duration of multiple sclerosis. For the cumulated scores of venous lesions, Spearman and Kendall’s tau correlation coefficients were 0.03 and 0.02, respectively; for maximal scores of venous lesions, coefficients were 0.06 and 0.05, while for the number of diseased veins they were 0.007 and 0.006, respectively. Consequently, this analysis did not yield any data supporting the idea that MS is the cause of venous lesions.

CONCLUSION: The results of our survey indicated that venous malformations are most likely congenital, and multiple sclerosis had no significant impact on the development of venous pathology.

More and more evidence piles up against CCSVI as a causative factor in MS.

Epub: Alroughani et al. Treatment of Chronic Cerebro-Spinal Venous Insufficiency in Multiple Sclerosis: A retrospective study. Int J Neurosci. 2013 Jan.

Background: Chronic Cerebro-Spinal Venous Insufficiency (CCSVI) has been proposed to be associated with Multiple Sclerosis (MS). Zamboni et al reported significant improvement in neurological outcomes in MS patients who underwent Percutaneous Transluminal Angioplasty (PTA). 

Objectives: To retrospectively evaluate the neurological outcomes in MS patients who underwent PTA. 

Method: Relapsing remitting MS patients who underwent PTA and completed at least one year post PTA were assessed. Patients with clinically isolated syndrome or progressive forms of MS were excluded. Primary endpoint was the proportion of relapse-free patients at one year. Secondary endpoints were change in mean EDSS score and proportion of patients with new MRI activity (defined as either Gadolinium-enhancing or new T2 lesions) at one year.

Results: 45 patients satisfied the inclusion criteria. Females constituted 71.1%. The mean age and mean disease duration were 33.76 and 7.16 years respectively. At one-year post-PTA, the proportion of relapse-free patients decreased from 84.44% to 66.67% (p = 0.085) whereas the mean EDSS score increased (p = 0.017). The proportion of patients with new MRI activity increased significantly from 17.78% to 44.44% (p = 0.012). 35.6% of patients stopped their DMTs. There was no difference among the patients who stopped their DMTs with respect to relapses, EDSS score or new MRI activity.

Conclusion: The study revealed that PTA in relapsing remitting MS patients was not associated with any neurological improvement. However, there was an increase in disease activity irrespective of the adherence to DMTs.

So not much evidence of any improvement here, but without a placebo control group this tells us not a lot because what would have happened in their was no treatment. However, it does not look encouraging. The worse thing is that the expectation leads to the CCSVIer stopping their DMT, with the risk of disease recurrence.

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  • It looks as if your prediction that CCSVI does not exist may be coming true. I wonder what all the CCSVI activists are going to do with their spare time when CCSVI gets assigned to the archives of MS history?

  • That study done by Simka showed that CCSVI abnormalities are not the result of MS – that means that perhaps these lesions are there before MS. Studies done with venography show that 90-100 % MS people have those abnormalities.

  • The optic nerve goes from the back of the eye till the centre of the brain. Thinning of the optic nerve can be caused by traumatic lesions far away from the eye. Reversed blood flow caused by extracranial venous obstructions releases its energy mainly in the periventricular veins (where most MS lesions are to be found). So the best place to search for retrograde flow is the vein system between the periventricular veins and the extracranial obstructed veins. Eye vasculature is NOT in that region. What is more, the retrograde flow is not constant but sporadic. One should monitor blood flow for a sufficient amount of time and under normal daily activities to catch it.

    The designers of the study were either ignorant of CCSVI basics or were just trying to create a negative fuss against it. Unfortunately they seem to have succeeded.

  • I can't hear the 'Fat Lady' singing just yet. The 'Auto immune ' Theory has run and run without proof for at least 60 years.
    None of the above studies are conclusive, you can spin those untill you're dizzy, if that's your thang.
    What will answer the questions will be exhaustive research combined with modern imaging techniques and not poorly designed trials. Untill one understands fully the sublect it is inconceivable to come up with ways to prove or disprove, don't get being too premature will you, you might be left with egg all over your face (or worse).

    Regards as Always

  • I look forward to there being a treatment effect especially for all those people who have paid alot fot this treatment. Will there ever be a study good enough to satisfy you?

    Egg on face is not a worry for me right or wrong

    • "Will there ever be a study good enough to satisfy you?"

      I just posed specific concerns about the value of the study. Are you willing to discuss them instead of answering with taglines?

    • I would think that the more than 20 Canadian physicians with MS who have sought this treatment, including a Canadian neurologist would differ. I think the lack of efficacy of the MS medications touted by the neurological community would better represent the "egg on the face" scenario.

      Anyway, I would have to agree with Mr. Clarke….I don't hear the fat lady singing yet either. If it took decades to develop the conventional therapies for MS using the autoimmune model, it will take many years to understand the role of the veins of MS patients.

      As for the question, "Will there ever be a study good enough to satisfy you?", one could ask the same question of the proponents of the unproven auto-immune theory. Please give a reference where the autoimmune theory was proven without question…..actually, don't waste your time….I know as well as you that it doesn't exist.

    • Yes there are studies were treatment with myelin basic protein peptides stimulated MBP reactive cells and made MS worse in some cases.

      Sorry have not got time to discuss, you had your opertunity and said you were too busy…ditto.

  • ..but there are quite many pilot studies, where initial results are promising, 50-70 % operated has got better guality of life. My friend got his life back, fatique disappeared over two years ago. This is the right direction..

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