Cerebral hypoperfusion linked to white matter lesions in the elderly.

When I had my first MRI, prior to my diagnosis, my neuro talked about the lesions and how you can get them with increasing age. They appear in the white matter. It is a condition known as leukoariosis (LA), which is a major cause of vascular dementia and disability in the elderly.

A taiwanese doctor, Dr Chung, has been carrying out research into the relationship between the jugular veins and transient global anmesia (TGA) and other neurological disorders. He has recently published two papers into aging and the jugular veins.

http://www.ncbi.nlm.nih.gov/pubmed/20800950
http://www.biomedsearch.com/nih/Pathogenesis-leukoaraiosis-Role-jugular-venous/20172657.html

The etiology is so far unclear. Chronic cerebral hypoperfusion associated with vasogenic edema, microbleeding or/and endothelial dysfunction found in LA favors venous ischemia, instead 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.

Dr Chung is postulating that slowed venous flow in the left jugular, more reflux and less drainage is the cause of these white matter lesions in the brain. While this is not CCSVI, nor is it MS, there is evidence out there that conditions thought of as neurological have in fact a vascular cause.