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Chronic cerebrospinal venous insufficiency
Classification and external resources
ICD-10 I87.2
ICD-9 459.81
DiseasesDB 13734
MeSH D014689

Chronic cerebro-spinal venous insufficiency (CCSVI) is a hypothesized syndrome in which the flow of blood in the cervical and thoracic veins, from the central nervous system (CNS) to the heart, is compromised and less efficient. It is proposed that insufficient venous blood flow, in turn, promotes development of brain dysfunction, especially multiple sclerosis.

The reported blood flow compromises involve both reduced and intermittently reversed (reflux) flow velocities in the cerebral veins, changed brain capillary dynamics (altering the blood-brain barrier), and are reportedly associated with stenosis of the jugular and azygos veins. Such a vascular picture was described by Paolo Zamboni in 2008, who also reported an association of CCSVI with multiple sclerosis (MS). The hypothesis has generated optimism, especially from patients, for more effective treatment options for Multiple Sclerosis. It has also been received with skepticism by some in the medical community, as well as efforts by some institutions to support research into it.

Contents

History

This syndrome was described on 2008. The venous hypothesis has mainly been advocated by researcher Paolo Zamboni. According to Zamboni, CCSVI had a high sensitivity and specificity differentiating healthy individuals from those with multiple sclerosis. The study included progressive variants of MS, but excluded non-standard forms such as Balo concentric sclerosis and diffuse myelinoclastic sclerosis.[1] The first international symposium took place in 2009, at Bologna, Italy.[2] The causes of the venous insufficiencies were discussed, and venous stenosis due to developmental abnormalities has been established as the primary cause of CCSVI by the International Phlebology Union.[3][4]

Symptoms and consequences

theoretical flow of blood in the veins of the neck and head in CCSVI, showing possible relationship with Dawson fingers

Potential consequences of the syndrome could be hypoxia, delayed perfusion, reduced drainage of the catabolites and increased transmural pressure,[5] and iron deposits around the cerebral veins.[6][7]

It has been theorized that the malformed blood vessels caused increased deposition of iron in the brain, which in turn triggers autoimmunity and degeneration of the nerve's myelin sheath (the causes of MS have long been related to autoimmunity, but the cause of the autoimmune reaction itself is not yet known).

This has resulted in a theory that CCSVI is present in a subtype of MS patients.[citation needed]

Pathophysiology

A vascular component in MS had been cited previously in immunohistological analysis,[8] including that hemodynamic abnormalities precede sub-cortical gray matter changes in multiple sclerosis,[9] raising the possibility that MS could be a hemodynamic disorder or involve a hemodynamic component.[10][11] Normal appearing brain tissues (NAWM, NAGM) have been found in MS, in which lesions are expected to appear.[12][13] They show a primary vascular injury.[14]

Diagnosis

CCSVI was first found using extracranial and transcranial doppler sonography[1].

Treatment

The syndrome, when it is due to stenosis, could be treated by balloon angioplasty and preliminary treatment results in MS patients have been published [15]

Research directions

A larger study is ongoing at Buffalo Neuroimaging Analysis Center to study the relationship between CCSVI and MS with a press release claiming preliminary results supporting the link.[16]

The Multiple Sclerosis Society of Canada has committed to funding further experimental trials on the hypothesis, though the head of the organization noted the results were promising but preliminary.[17]

MRV may be of use for diagnosis.[18]

Reception

The hypothesis has generated optimism, especially from patients, for more effective treatment options for Multiple Sclerosis. It has been received with caution or skepticism by some experts, who found it to rely on too limited data to support at least some of the following claims: (a) that the syndrome actually exists; (b) that it could be causative of (or a co-factor in) Multiple Sclerosis; (c) that vascular treatments for the syndrome would prevent or reduce the incidence of Multiple Sclerosis. The neurology community has criticized the methodology of Zamboni's research and recommends not to use the proposed treatment until its effectiveness is confirmed by controlled studies, the need for which has been recognized by the scientific bodies engaged in MS research.[19][20]

See also

References

  1. ^ a b Zamboni P, Galeotti R, Menegatti E, et al. (April 2009). "Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis". J. Neurol. Neurosurg. Psychiatr. 80 (4): 392–9. doi:10.1136/jnnp.2008.157164. PMID 19060024. PMC 2647682. http://jnnp.bmj.com/cgi/content/full/80/4/392. 
  2. ^ Rossini, F (2009-09-08). "Venous Function And Multiple Sclerosis" (doc). Fondazione Hilarescere. http://www.fondazionehilarescere.org/cst/eng/090908/1_CSTgenerale_8sett09_eng.doc. Retrieved 2009-12-03. 
  3. ^ Lee BB, Bergan J, Gloviczki P, Laredo J, Loose DA, Mattassi R, Parsi K, Villavicencio JL, Zamboni P. Diagnosis and treatment of venous malformations Consensus Document of the International Union of Phlebology [1]
  4. ^ "Bologna conference notes". http://www.keepandshare.com/doc/view.php?id=1370985&da=y. Retrieved 2009-12-03. 
  5. ^ Franceschi C (April 2009). "The unsolved puzzle of multiple sclerosis and venous function". J. Neurol. Neurosurg. Psychiatr. 80 (4): 358. doi:10.1136/jnnp.2008.168179. PMID 19289474. 
  6. ^ Zamboni P (November 2006). "The big idea: iron-dependent inflammation in venous disease and proposed parallels in multiple sclerosis". J R Soc Med 99 (11): 589–93. doi:10.1258/jrsm.99.11.589. PMID 17082306. PMC 1633548. http://www.jrsm.org/cgi/pmidlookup?view=long&pmid=17082306. 
  7. ^ Singh AV, Zamboni P (December 2009). "Anomalous venous blood flow and iron deposition in multiple sclerosis". J. Cereb. Blood Flow Metab. 29 (12): 1867–78. doi:10.1038/jcbfm.2009.180. PMID 19724286. 
  8. ^ Minagar A, Jy W, Jimenez JJ, Alexander JS (2006). "Multiple sclerosis as a vascular disease". Neurol. Res. 28 (3): 230–5. doi:10.1179/016164106X98080. PMID 16687046. 
  9. ^ Varga AW, Johnson G, Babb JS, Herbert J, Grossman RI, Inglese M (July 2009). "White matter hemodynamic abnormalities precede sub-cortical gray matter changes in multiple sclerosis". J. Neurol. Sci. 282 (1-2): 28–33. doi:10.1016/j.jns.2008.12.036. PMID 19181347. 
  10. ^ Simka M (May 2009). "Blood brain barrier compromise with endothelial inflammation may lead to autoimmune loss of myelin during multiple sclerosis". Curr Neurovasc Res 6 (2): 132–9. PMID 19442163. 
  11. ^ Ge Y, Zohrabian VM, Grossman RI (June 2008). "Seven-tesla magnetic resonance imaging: new vision of microvascular abnormalities in multiple sclerosis". Arch. Neurol. 65 (6): 812–6. doi:10.1001/archneur.65.6.812. PMID 18541803. 
  12. ^ van der Valk P, Amor S (June 2009). "Preactive lesions in multiple sclerosis". Curr. Opin. Neurol. 22 (3): 207–13. doi:10.1097/WCO.0b013e32832b4c76. PMID 19417567. 
  13. ^ Goodkin DE, Rooney WD, Sloan R, et al. (December 1998). "A serial study of new MS lesions and the white matter from which they arise". Neurology 51 (6): 1689–97. PMID 9855524. http://www.neurology.org/cgi/content/abstract/51/6/1689. 
  14. ^ M. Filippi, G. Comi, and M. Rovaris, eds. New York: Springer; (2004). "Normal-appearing White and Grey Matter Damage in Multiple Sclerosis. Book review.". AJRN. http://www.ajnr.org/cgi/content/full/27/4/945. 
  15. ^ Zamboni P, Galeotti R, Menegatti E, et al. (December 2009). "A prospective open-label study of endovascular treatment of chronic cerebrospinal venous insufficiency". J. Vasc. Surg. 50 (6): 1348–58.e1–3. doi:10.1016/j.jvs.2009.07.096. PMID 19958985. http://linkinghub.elsevier.com/retrieve/pii/S0741-5214(09)01568-7. 
  16. ^ "First Blinded Study of Venous Insufficiency Prevalence in MS Shows Promising Results". University of Buffalo. 2010-02-10. http://www.buffalo.edu/news/10937. Retrieved 2010-02-16. 
  17. ^ Picard, A (2009-11-23). "MS group to fund research into 'liberation procedure'". The Globe and Mail. http://www.theglobeandmail.com/news/national/ms-group-to-fund-research-into-liberation-procedure/article1374954/. Retrieved 2009-12-29. 
  18. ^ Neurovascular Imaging Center of Excellence review
  19. ^ Khan, 0 et al. (12 February 2010). "Chronic cerebrospinal venous insufficiency and multiple sclerosis". Annals of Neurology. http://www3.interscience.wiley.com/journal/123283159/abstract. Retrieved 2010-03-05. 
  20. ^ Susan Jeffrey (2009-12-03). "Endovascular Treatment of Cerebrospinal Venous Insufficiency Safe, May Provide Benefit in MS". Medscape. http://www.medscape.com/viewarticle/713367. Retrieved 2010-01-27. 

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