Oligoclonal immunoglobulins

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

MINI STROKES

Postby Gordon » Mon Jun 07, 2010 8:41 pm

MINI STROKES ??? IS THIS WHAT YOU ARE SAYING

THIS CONCEPT MAKES SO MUCH SENSE.
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Postby cheerleader » Mon Jun 07, 2010 9:13 pm

More like venous infarcts or venous strokes--but yup, Gordon. We know how these happen due to thrombosis in the jugular vein/sinus---but the research compiled on this thread by several different posters points to how CCSVI could create transient ischemic events, or mini-strokes.

Sharon posted this new medical hypothesis on another thread....it carries on this idea of venous infarcts created by jugular reflux...

http://www.ncbi.nlm.nih.gov/pubmed/20172657
Abstract
Leukoaraiosis (LA) is a major cause of vascular dementia and disability in the elderly. Age and hypertension are the most two important risk factors. Despite its clinical significance, the etiology is so far unclear. Chronic cerebral hypoperfusion associated with vasogenic edema, microbleeding or/and endothelial dysfunction found in LA favors venous ischemia, in stead of arterial ischemia, as its pathogenesis. The involved regions in LA, periventricular and subcortical regions, are the drainage territory of deep cerebral venous system and the watershed region between the superficial and deep cerebral venous system respectively. Adding the facts that periventricular venule collagenosis, and retinal and intraparenchymal venules dilatation are related to the severity of LA, cerebral venous hypertension caused by downstream venous outflow impairment might play a major role in the pathogenesis of LA. Internal jugular vein is the main venous outflow pathway for cerebral venous drainage. The frequency of jugular venous reflux (JVR) is increased with aging. Hypertension, which has a decreased venous distensibility, might further exacerbate the sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency caused by JVR. Clinically, JVR caused by a dural AV fistula does lead to cerebral hypoperfusion, white matter abnormalities, vasogenic edema and cognitive impairment in several published reports. JVR is suggested to play a key role in the pathogenesis of LA through a sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency, which might lead to chronic cerebral venous hypertensions, abnormal cerebral venules structural changes, decreased cerebral blood flow, endothelial dysfunction, and vasogenic edema in cerebral white matters. Copyright 2010 Elsevier Ltd. All rights reserved.



cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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