An endovascular treatment of Chronic Cerebro-Spinal Venous Insufficiency in multiple sclerosis patients - 6 month follow-up results.
ABSTRACT In this study, the mid-term results (6 month follow-up) of the endovascular treatment in patients with Chronic Cerebro-Spinal Venous Insufficiency (CCSVI) and multiple sclerosis (MS) were prospectively evaluated.
Thirty-six patients with confirmed MS and CCSVI underwent endovascular treatment by the means of the uni- or bilateral jugular vein angioplasty with optional stent placement. All the patients completed 6 month follow-up. Their MS-related disability status and quality of life were evaluated 1, 3 and 6 months postoperatively by means of the following scales: Expanded Disability Status Scale (EDSS), Multiple Sclerosis Impact Scale (MSIS-29), Epworth Sleepiness Scale (ESS), Heat Intolerance scale (HIS) and Fatigue Severity Scale (FSS). For patency and restenosis rate assessment, the control US duplex Doppler examination was used.
Six months after the procedure, restenosis in post-PTA jugular veins was found in 33% of cases. Among 17 patients who underwent stent implantation into the jugular vein, restenosis or partial in-stent thrombosis was identified in 55% of the cases. At the 6 month follow-up appointment, there was no significant improvement in the EDSS or the ESS. The endovascular treatment of the CCSVI improved the quality of life according to the MSIS-29 scale but only up to 3 months after the procedure (with no differences in the 6 month follow-up assessment). Six months after the jugular vein angioplasty (with or without stent placement), a statistically significant improvement was observed only in the FSS and the HIS.
The endovascular treatment in patients with MS and concomitant CCSVI did not have an influence on the patient's neurological condition; however, in the mid-term follow-up, an improvement in some quality-of-life parameters was observed.
- SourceAvailable from: Marian Simka
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- "Of note, despite successful decompression of the vein, we did not observe clinical improvement in this patient. However, it is already known that only a subset of MS patients benefits from restoration of proper venous outflow after endovascular treatment for CCSVI [29, 30]. Patients with more severe disability, like our patient, were less likely to improve. "
ABSTRACT: We describe a multiple sclerosis patient presenting with compression of the internal jugular vein caused by aberrant omohyoid muscle. Previously this patient underwent balloon angioplasty of the same internal jugular vein. Ten months after this endovascular procedure, Doppler sonography revealed totally collapsed middle part of the treated vein with no outflow detected. Still, the vein widened and the flow was restored when the patient's mouth opened. Thus, the abnormality was likely to be caused by muscular compression. Surgical exploration confirmed that an atypical omohyoid muscle was squeezing the vein. Consequently, pathological muscle was transected. Sonographic control three weeks after surgical procedure revealed a decompressed vein with fully restored venous outflow. Although such a muscular compression can be successfully managed surgically, future research has to establish its clinical relevance.10/2012; 2012:293568. DOI:10.1155/2012/293568
- Annals of Indian Academy of Neurology 01/2012; 15(1):2-5. DOI:10.4103/0972-2327.93266 · 0.60 Impact Factor
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ABSTRACT: The discovery of stenoses in the azygous and internal jugular veins, the so-called chronic cerebrospinal venous insufficiency that accompanies multiple sclerosis, has enabled the reinterpretation of knowledge about this neurologic disease. Pathologic venous outflow from the central nervous system appears to lead to two main problems. Firstly, it disassembles the blood-brain barrier and may allow the penetration of nervous parenchyma by glutamate and leukocytes. Secondly, it may result in significant hypoperfusion of the brain and spinal cord. These two overlapping pathologies are likely to trigger plaques through caspase-1-driven pyroptosis of oligodendrocytes and to evoke neurodegeneration via glutamate excitotoxicity. Moreover, brain hypoperfusion may lead to chronic fatigue and other global neurologic symptoms. It is hoped that this review will help to elucidate new strategies and treatments for multiple sclerosis and will show new avenues for the research on this debilitating disease.Reviews on Recent Clinical Trials 02/2012; 7(2):93-9. DOI:10.2174/157488712800100198 · 1.07 Impact Factor