Dr. Aron Buchman is a neurologist at Rush University in Chicago. For the past 20 years, he has been studying the aging brain and subtle changes that come before Alzheimers and Parkinsons diagnoses. Here is the press regarding his most recent study, which looks at the brains after the participants have passed---
http://www.eurekalert.org/pub_releases/2011-09/rumc-soa082911.php
Signs of aging may be linked to undetected blocked brain blood vessels
Many common signs of aging, such as shaking hands, stooped posture and walking slower, may be due to tiny blocked vessels in the brain that can't be detected by current technology.
In a study reported in Stroke: Journal of the American Heart Association, researchers from Rush University Medical Center, Chicago, examined brain autopsies of older people and found:
Microscopic lesions or infarcts — too small to be detected using brain imaging — were in 30 percent of the brains of people who had no diagnosed brain disease or stroke.
Those who had the most trouble walking had multiple brain lesions. Two-thirds of the people had at least one blood vessel abnormality, suggesting a possible link between the blocked vessels and the familiar signs of aging.
"This is very surprising," said Dr. Aron S. Buchman, lead author of the study and associate professor of neurological sciences at Rush. "The public health implications are significant because we are not identifying the 30 percent who have undiagnosed small vessel disease that is not picked up by current technology. We need additional tools in order to identify this population."
In 1994, the researchers began conducting annual exams of 1,100 older nuns and priests for signs of aging. The participants also donated their brains for examination after death. This study provides results on the first 418 brain autopsies (61 percent women, average 88 years old at death).
Although Parkinson's disease occurs in only 5 percent of older people, at least half of people 85 and older have mild symptoms associated with the disease.
Before the study, researchers believed that something more common, such as microscopic blocked vessels, might be causing the physical decline. The study's autopsies found the small lesions could only be seen under a microscope after participants died. The lesions couldn't be detected by current scans.
During the annual exams of the nuns and priests, researchers used the motor skills portion of a Parkinson's disease survey to assess their physical abilities. Researchers observed and rated the participants'
Balance, Ability to maintain posture, Walking speed, Ability to get in and out of chairs, Ability to make turns when walking, Sense of dizziness.
"Often the mild motor symptoms are considered an expected part of aging," said Buchman, who is also a member of the Rush Alzheimer's Disease Center. "We should not accept this as normal aging. We should try to fix it and understand it. If there is an underlying cause, we can intervene and perhaps lessen the impact."
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How does this relate to CCSVI?
One important similarity is microvascular brain abnormalities in both the elderly and pwMS. Just as Rindfleisch noted microscopic engorged vessels inside MS lesions in the brains of deceased MS patients, the Rush doctors note blocked vessels and microscopic lesions in the brains of the elderly with "mild motor symptoms." From 1863 and Rindfleisch to 2011 and Rush University....our technology notes these microscopic vascular changes in the brain after death.
Thanks to new technology, microvascular abnormalities have been found in vivo (meaning, in living pwMS) using the new, higher powered 7Tesla MRI machines. I hope the Rush researchers might utilize 7Tesla technology, to see if these vascular changes in the elderly are detectable. Because they are in MS:
Seven-Tesla magnetic resonance imaging: new vision of microvascular abnormalities in multiple sclerosis.
We demonstrated markedly enhanced detection of unique microvascular involvement associated with most of the visualized MS lesions with abnormal signals on and around the venous wall on 7-T compared with 3-T MRI.
These findings, which have never been shown on conventional fields of MRI, not only allow for direct evidence of vascular pathogenesis in MS in vivo but also have important implications for monitoring lesion activity and therapeutic response.
http://www.ncbi.nlm.nih.gov/pubmed/18541803
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Another common avenue of research in the elderly and pwMS is the jugular vein
Dr. Chung is a Taiwanese researcher who has been looking at jugular vein valve problems for the past 15 years. He has a theory as to why these blocked vessels occur in the brains of the elderly. He has postited that white matter lesions in their brains are due to jugular blockage and venous ischemia.
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.
http://www.ncbi.nlm.nih.gov/pubmed/20172657
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Before my Dad passed in 2010, he had been diagnosed with LA. He showed white matter lesions in his brain on MRI. He had trouble with balance, was slowing and showing signs of Parkinsons. He eventually took a bad fall, hit his head and died at the age of 78. Too soon for his wife, me, my brother and his many friends. I asked Dad's neurologist what was the difference between my father's brain lesions and my husband's, who had MS. Well, his neuro replied, your father is older....we know that his lesions are related to aging. Your husband is too young for LA. He has MS.
Again, I ask---what is the difference? Why can't it be the same mechanism for the elderly as the young? Why can't it be jugular venous insufficiency, edema, endothelial damage, microvascular abnormalities and white matter lesions in both instances? My husband felt like his MS was aging him way before his time. He was fatigued, dizzy, and he couldn't take the heat. After venoplasty, he regained energy, balance and lost his heat intolerence.
Our plea to MS researchers--- Please look at Dr. Chung's research. Please study the vasculature. Look at Dr. Buchman's research in the elderly. Look to other disease models. Work with the International Society of Neurovascular Diseases. Now. EAE is not MS. The connections continue, and we are reading the research.
Joan
the cerebral vascular system