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PostPosted: Mon Sep 17, 2012 10:18 am 
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http://www.neurology.org/content/early/ ... d.abstract
Quote:
Association of cognitive dysfunction with neurocirculatory abnormalities in early Parkinson disease
Joong-Seok Kim, MD, PhD, Yoon-Sang Oh, MD, PhD, Kwang-Soo Lee, MD, PhD, Yeong-In Kim, MD, PhD, Dong-Won Yang, MD, PhD and David S. Goldstein, MD, PhD

From the Department of Neurology (J.-S.K., Y.-S.O., K.-S.L., Y.-I.K., D.-W.Y.), College of Medicine, The Catholic University of Korea, Seoul, Korea; and Clinical Neurocardiology Section (D.S.G.), Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.

ABSTRACT

Objective: Cognitive impairment and neurocirculatory abnormalities such as orthostatic hypotension (OH), supine hypertension (SH), and failure to decrease blood pressure at night (nondipping) occur relatively commonly in Parkinson disease (PD); however, whether cognitive dysfunction in early PD is related to neurocirculatory abnormalities has not been established. Cognitive dysfunction in PD is associated with white matter hyperintensities on MRI. We report results of an analysis of neuropsychological and hemodynamic parameters in patients with early PD.

Methods: Among 87 patients, 25 had normal cognition, 48 had mild cognitive impairment, and 14 had dementia, based on comprehensive neuropsychological tests. Orthostatic vital signs and ambulatory 24-hour blood pressure monitoring were recorded, and brain magnetic resonance scans were obtained for all patients.

Results: Cognitive impairment was associated with OH, SH, and white matter hyperintensities but not with nondipping. Dementia and white matter hyperintensities were common in SH. Of 13 patients with OH + SH, every one had mild cognitive impairment or dementia.

Conclusions: Cognitive dysfunction is related to neurocirculatory abnormalities, especially OH + SH, in early PD, raising the possibility that early detection and effective treatment of those abnormalities might slow the rate of cognitive decline.

This is Parkinson's and not MS, but of interest because of the vascular and neurological intersection.
Do orthostatic hypertension, supine hypertension, or failure to decrease blood pressure at night occur in MS or in CCSVI?


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PostPosted: Mon Sep 17, 2012 7:32 pm 
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Cece, interesting link.

As Dr. Sclafani has mentioned he sees low blood pressure in the patients he treats with MS.
Dr. Arata is interested in helping folks with Parkinson's through venoplasty of the IJV. His idea about stimulating the Vagus nerve is very interesting. Brain cell degeneration in Parkinson's seems to effect this nerve and the autonomic nervous system.
The link earlier this week talking about the discovery of the glymphatic system may be of interest.

I hope that Dr. Haacke or the Annette Funicello Foundation are conducting SWI MRI on Parkinson patients also. There may be more to neuro hemodymanics circulation than we know.

Thanks for all of your posts.

This below link is a bit off topic but I am still very fascinated in how emotion (stress) can lead to MS relapses, and how peoples faces turn red sometimes.

From the good Dr.'s at HHMI.....Why Does your Skin Go Red when you slap it.

http://www.askascientist.org/askascient ... ap_it.html


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PostPosted: Mon Sep 17, 2012 8:56 pm 
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At one point, it was suggested that CCSVI is a matter of hypertension instead of insufficency. Dr. Tucker shared some ideas also how the refluxed flow, when it met up with a wave of oncoming flow, would cause a focal point of hypertension right where the two waves met, where the pressure was the combined amount of both the reflux wave and the incoming wave. (I may not be doing justice to his ideas.) The focal hypertension weakens the blood-brain barrier and leads to a cascade of ill effects.

The glymphatic system was interesting but seems to be moving the focus away from the jugulars and the CSF and the blood-brain barrier.
The effect of a slap is all capillaries, isn't it? But vasodilatation is good for flow, vasoconstriction is bad...


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PostPosted: Tue Sep 18, 2012 8:59 am 
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Cece wrote:
The focal hypertension weakens the blood-brain barrier and leads to a cascade of ill effects.

The glymphatic system was interesting but seems to be moving the focus away from the jugulars and the CSF and the blood-brain barrier. ...



Yes, I think glymphatic system will play a bigger role in Alzheimer patients. I in no way want to distract from the CCSVI research being conducted. Having just finished Marie Rhodes book I am such a strong believer in CCSVI as the cause for MS. What are the odds that a doctor in Italy would have a theory and then 40 some people from the other side of the world would visit a doctor at Stanford, and low and behold, have the condition he described? What are the odds of that?

After reading her book it has me looking at the research community completely differently when it comes to chronic degenerative disease. I feel all of these diseases will be better understood when their disease process is properly described, like Dr. Zamboni has done. All of the gene nock outs we do on mice and rational drug discoveries can't do anything if the disease process isn't understood. I am looking for a few more breakthrough discoveries in "disease process" similiar to CCSVI theroy.


Cece wrote:
The effect of a slap is all capillaries, isn't it? But vasodilatation is good for flow, vasoconstriction is bad...



I think you have probably described how stress hurts folks with CCSVI. Stress causes further vasoconstriction? Thank you for your comments.

Rogan


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