It's an issue I've previously written about.
The latest studies yet again demonstrate that these vein blockages are unlikely to be the cause of MS:
Several new studies are pointing against narrowed neck veins as being the primary culprit in causing multiple sclerosis.
(...)
Now, results of a study that involved Doppler ultrasounds of 499 subjects, led by Dr. Robert Zivadinov of the University of Buffalo, N.Y., have been published in the journal Neurology.
The prevalence of CCSVI was 56 per cent for patients with MS, 42 per cent in patients with other neurologic diseases, 38 per cent in those with clinically isolated syndrome that can be a precursor to MS and 23 per cent in healthy controls.
"Our findings are consistent with an increased prevalence of CCSVI in MS but with modest sensitivity/specificity," the researchers concluded.
"Our findings point against CCSVI having a primary causative role in the development of MS."
(...)
An accompanying editorial in the journal says the study suggests that CCSVI, as defined using ultrasound of the intracranial and extracranial venous system, is not likely to be a primary causal process in MS.
(...)
A number of other smaller studies on the subject were presented this week at the meeting.
A study led by Katayoun Alikhani of Calgary included 67 people at the city's University Hospital who underwent magnetic resonance venography of their neck veins.
Among the findings: vein abnormalities were found in 20 per cent of those with MS and 20 per cent of those without MS.
"This first independent Canadian MRV study confirms neck vein abnormalities are infrequent and independent of the diagnosis of MS," the researchers wrote in their conclusion, noting that larger, controlled, blinded and more comprehensive studies are underway.
Another group in Europe assessed whether the venous drainage from the brain was impaired in 94 patients with MS and 20 healthy control subjects. Their findings provided compelling evidence against a significant role of cerebro-cervical venous congestion in the pathogenesis of MS, they concluded.
What's also of note is that Dr. Zivadinov had previously seemed to be quite supportive of Paolo Zamboni's CCVSI theory.
Now these are just the most recent but certainly not the only studies casting doubt on the CCSVI theory. Some of the others include:
This (a study Dr. Zivadinov was also involved in):
No significant differences in the extracranial venous systems between MS patients and HC subjects were detected by using MR venography.
This:
Chronic cerebrospinal venous insufficiency (CCSVI) has been postulated as a cause for multiple sclerosis (MS). Venous pressure assessments have not been made. Intracranial venous pressure was assessed using ophthalmodynamometry in 29 MS patients and compared with 28 healthy controls and 19 cases with elevated intracranial pressure (ICP). MS and control subjects had normal venous pressures (mean 15.5 resp. 15.1 cmHg). Only cases with intracranial pressure pathology had elevated venous pressures (mean 28.8 cmHg). There is no evidence of an increased intracranial venous pressure in MS patients.
This:
This triple-blinded extra- and transcranial duplex sonographic assessment of cervical and cerebral veins does not provide supportive evidence for the presence of CCSVI in MS patients. The findings cast serious doubt on the concept of CCSVI in MS
This:
...we studied 21 relapsing-remitting multiple sclerosis cases and 20 healthy controls with phase-contrast magnetic resonance imaging. In addition, in multiple sclerosis cases we performed contrast-enhanced magnetic resonance angiography. We found no differences regarding internal jugular venous outflow, aqueductal cerebrospinal fluid flow, or the presence of internal jugular blood reflux. Three of 21 cases had internal jugular vein stenoses. In conclusion, we found no evidence confirming the suggested vascular multiple sclerosis hypothesis
This:
Findings suggestive of anomalies of the cranial venous outflow anatomy were frequently observed in both MS patients and healthy controls. Given the normal intracranial venous flow quantification results, it is likely that these findings reflect anatomical variants of venous drainage rather than clinically relevant venous outflow obstructions.
This:
Our results challenge the hypothesis that cerebral venous congestion plays a significant role in the pathogenesis of MS. Future studies should elucidate the difference between patients and healthy subjects in BVF regulation.
This:
Our findings do not support a cause-effect relationship between CCSVI and pMS. Further studies are warranted to clarify whether CCSVI is associated with later disease stages and characterizes the progressive forms of MS.
None of this necessarily closes the door on the CCSVI theory, although it certainly would imply that Zamboni's initial findings are not reliable. More research, though, is warranted to see what if any relationship there is between MS and these blockages. It could be that MS is causing CCSVI as opposed to the other way around.
It's unfortunate, though, that as much attention as the CCSVI theory gets in the media and from politicians, these studies do not seem to be included in much of the coverage.
What's also unfortunate is that other important research on MS (that has nothing to do with CCSVI) seems to get overlooked, as well.
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