PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

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

PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby dania » Tue Sep 13, 2011 5:00 pm

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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby 1eye » Tue Sep 13, 2011 6:27 pm

Mechanical difficulties may be the cause of many syndromes, especially in conditions which are late-onset. Once an individual has passed the time of life when reproduction most often occurs, they no longer have Darwin on their side. A human can have many children, but things start to wear out eventually, and there is a peak which we all slide down the other side of. Some of us are fortunate to have been born in the middle of a population peak as well. We have more help with these problems than we otherwise would, from contemporaries and their children. In a sense we are still lucky. I don't know which helps more, the demographic bulge or the steady increase in population. Too bad some don't live to see things like this.
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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby Cece » Tue Feb 11, 2014 6:08 pm

I thought there was a longer CCSVI in Parkinsons thread but I couldn't find it.
This was presented at ISNVD 2014. Program book is here: http://www.isnvdconference.org/program/ ... -book.html
Chronic Cerebro-Spinal Venous Insufficiency and Parkinson’s Disease: The Presence of Abnormal Flow and White Matter Hyperintensities

E. Mark Haacke, Ph.D.1,2, Manju Liu1, Haibo Xu3, David Utriainen2 1 Department of Biomedical Engineering, Wayne State University, Detroit MI 48201, USA. 2 Magnetic Resonance Innovations, Inc., Detroit, MI 48202, USA. 3 Department of Radiology, Union Hospital,Wuhan, China

Background and Objective: Idiopathic Parkinson's disease (IPD) is one of those neurodegenerative diseases where the cause remains unknown. Many clinically diagnosed cases of IPD are associated with cerebrovascular disease and white matter hyperintensities (WMH). The presence of high iron content in the basal ganglia and midbrain in multiple sclerosis (MS) and the potential role of extracranial flow abnormalities in the venous system stimulated us to consider the possibility that patients with IPD might also have similar venous abnormalities. Therefore, the purpose of this study was to investigate the presence of transverse sinus and extracranial venous flow abnormalities in IPD patients and their relationship with brain WMH.

Methods: Twenty-three IPD patients and 23 age-matched normal controls were recruited from the same site in Wuhan, China. Each patient and subject had conventional MR structural and angiographic brain scans. In addition, blood flow in the extracranial vessels was quantified at C6/C7 with 2D phase- contrast (PC) imaging. The cross sections and flow were measured using SPIN (signal processing in NMR). The internal jugular vein (IJV) flow was normalized by the total arterial flow. Venous structures were evaluated with 2D-time-of-flight (TOF). WMH volume was quantified with T2 weighted fluid attenuated inversion recovery (FLAIR). The ratio of the flow in the dominant IJV and the sub-dominant IJV (Fd/Fsd) was calculated for each case. The IPD and normal subjects were classified using both the MR TOF and PC images into four categories: 1) missing transverse sinus and partially missing IJVs on the TOF images with high Fd/Fsd; 2) missing transverse sinus and stenotic IJVs with high Fd/Fsd; 3) reduced flow in the sub-dominant IJV with high Fd/Fsd; and 4) normal flow and no stenosis.

Results: When broken into the above 4 categories with categories 1 through 3 combined, a significant difference in the distribution of the IPD patients and normal controls (χ2=7.7, p<0.01) was observed. Venous abnormalities (categories 1, 2 and 3) were seen in 57% of IPD subjects and only in 30% of controls. Patients with venous abnormalities tended to show higher volume WMH. In IPD subjects, category type correlated with both flow abnormalities and WMH.

Discussion and Conclusion: A major fraction of IPD patients appear to have abnormal venous anatomy and flow on the left side of the brain and neck and the flow abnormalities in particular appear to correlate with WMH volume. Although having WMH is not a standard clinical diagnostic criterion for IPD, in this study cohort, 21 patients showed WMH, 5 had very high WMH volume (more than 10,000mm3) and of these 4 had a high visual Schelten’s score (greater than 9). According to many in vivo imaging studies, 30% to 55% of PD patients show WMHs. An MRI-pathological correlation study by Gao et al. (Alzheimer's and Dementia. 2008;4(4):T368-T9) demonstrated that focal and periventricular hyperintensities (PVH) often relate to venules. They proposed that venous collagenosis dilates the veins, making them macroscopic and causing venous insufficiency with consequent vessel leakage and vasogenic edema. Despite this evidence, a larger study is needed to validate these findings at other sites.

They found venous abnormalities in 57% of Parkinsons patients and only 30% of controls.
Also very interesting is the Gao study discussed at the end. They demonstrated that focal and periventricular hyperintensities often relate to venules. What is the difference between that sort of periventricular hyperintensity and a periventricular white matter MS lesion? How do you undo venous collagenosis?
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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby cheerleader » Wed Feb 12, 2014 3:06 pm

There's an interesting connection between the press release dania linked at the start of this thread, and what Dr. Haacke has been finding---
pulsatile vascular compression.

Dr. Jannetta's MRIs showed an intracranial problem--compression of the cerebral peduncles.

Based on this case, Dr. Jannetta and his colleagues at AGH conducted a blinded MRI study analyzing the brains of 20 patients with Parkinson’s and 20 healthy control subjects. The study showed that 78 percent of the Parkinson’s Disease patients had visible arterial compression/distortion of one or both cerebral penduncles. Of the study’s 20 control subjects, just two had low grade compression of the cerebral penduncle and one of those was subsequently diagnosed with Parkinson’s.
- See more at: http://www.wpahs.org/news/9-8-2011/mri- ... QS54T.dpuf

Beginning in 1966, a growing number of cranial nerve and brainstem syndromes have been reported to be caused by pulsatile vascular compression, arterial or venous or both. These include such apparently disparate problems as trigeminal neuralgia3–5 (both typical and atypical), hemifacial spasm,6,7 Meniere’s disease,8 disabling positional vertigo,9 glossopharyngeal neuralgia,10–12 Bell’s palsy,13 essential hypertension14–17 and type 2 diabetes.18,19 This knowledge of the above entities, although known and accepted in the neurosurgical community, have not penetrated into the general medicine literature. Beginning in the same year (1966), treatment of the pulsatile compression (microvascular decompression) was developed. These findings and treatments were possible because of the use of then new technology, and the magnification, lighting and recording capabilities of the surgical binocular microscope.13–19

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3207233/

He's treated one PD patient with decompression brain surgery--and saw some success, wants to do more studies.
But what if this pulsatile compression is part of an overall edemic situation, due to restricted extracranial venous flow?

Dr. Haacke first noted CCSVI in Parkinson's in 2010:
A member of the ISNVD and founding President, Dr. Mark Haacke, presented research at the 2nd Annual ISNVD conference. His paper, which has been submitted for publication , looked at 21 patients with Parkinson’s. These participants were imaged by MRV, and 15 of them (71%) had abnormal venous structures and/or blood flow. All participants with CCSVI exhibited the same pattern: reduced flow on the left side and abnormal left transverse sinus and jugular vein, with the right internal jugular carrying most of the flow out of the brain.

http://ccsvi.org/index.php/the-basics/c ... l-diseases

we're at the beginning, sports fans,
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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby Rogan » Thu Feb 13, 2014 10:24 pm

Cheerleader, thanks for these amazing updates…

Are all of these Parkinson's researchers at U Penn and Allegheny General Hospital?

These are very serious Neurosurgeons.

I wonder if they believe what Michael Flanagan (uprightdoc.com) has discussed. That Parkinson’s is a compression of the lower brain stem into the bony part of the skull. If I recall correctly Dr. Flanagan called these:

Chiari malformation (kee-AH-ree mal-for-MAY-shun) is a condition in which brain tissue extends into your spinal canal. It occurs when part of your skull is abnormally small or misshapen, pressing on your brain and forcing it downward.

Also, if I further recall Dr. Flanagan talked about how this issue isn't seen on a standard MRI. Lying down doesn't show this problem. Very interesting if true, that it must be seen from upright MRI.

Also Dr. Haacke is seeing left side vein issues as well with Parkinson's patients. I wonder like you do if

pulsatile compression is part of an overall edemic situation, due to restricted extracranial venous flow?


My question, which is way over my head is the quote from Peter J Jannetta and Donald Whiting's paper…

"Following the vascular decompression of the trigeminal nerve, the midbrain was decompressed by mobilizing and repositioning the posterior cerebral artery The patient's Parkinson's signs disappeared over a 48-hour period. "


What the hell is "vascular decompression of the trigeminal nerve, the midbrain was decompressed by mobilizing and repositioning the posterior cerebral artery"

Are they moving things around in the brain through surgery? Do these actions help venous flow?

Is this stuff safe?

Thank god for brave surgeons, may they heal us all. Just amazing stuff….
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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby cheerleader » Fri Feb 14, 2014 1:57 pm

Rogan wrote:
My question, which is way over my head is the quote from Peter J Jannetta and Donald Whiting's paper…

"Following the vascular decompression of the trigeminal nerve, the midbrain was decompressed by mobilizing and repositioning the posterior cerebral artery The patient's Parkinson's signs disappeared over a 48-hour period. "


What the hell is "vascular decompression of the trigeminal nerve, the midbrain was decompressed by mobilizing and repositioning the posterior cerebral artery"
Are they moving things around in the brain through surgery? Do these actions help venous flow?
Is this stuff safe?
Thank god for brave surgeons, may they heal us all. Just amazing stuff….


Hi Rogan--It's open brain surgery--the surgeon moves the artery so that it is no longer putting pressure on the trigeminal nerve, and inserts a sponge to keep some distance between them. Here's more on the procedure:
http://www.mayfieldclinic.com/PE-MVD.htm#.Uv6ADXnaFwQ

Here's more on vascular compression disorders--they can be arterial or venous.
http://radiopaedia.org/articles/vascula ... -disorders
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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby Rogan » Sun Feb 16, 2014 4:21 pm

Cheerleader this is just amazing news! Another Dr. Zamboni maybe buried in the sea of data out there.

From this link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3207233/
Neurol Int. 2011 July 5; 3(2): e7.
Parkinson’s disease: an inquiry into the etiology and treatment
Peter J. Jannetta, Donald M. Whiting, Lynn H. Fletcher, Joseph K. Hobbs, Jon Brillman, Matthew Quigley, Melanie Fukui, and Robert Williams


Why is this not front page news. I hope money is being thrown at this like crazy?

Parkinson's cured for 18 months until the brain compression occurs again. Do you know how many people suffer from this?

70+% folks with Parkingson's have brain compression issues! Fine maybe 30% of folks with Parkinson's have something else
10% of normals have brain compression....who knows maybe some people don't mind this or they are on their way to Parkinsons.

This could be just huge!!!!!

Now for the info as it relates to CCSVI and MS. If folks whom don't receive relief from venoplasty, could a "sponge" be inserted in them to keep the clavical from pinching the IJV?

From this link http://radiopaedia.org/articles/vascular-compression-disorders
Vascular compression disorders are numerous and can be divided into those cases where a vascular structure is the "compress-er" or the "compress-ee" . Some conditions fall into both categories, where one vessel compresses another


Here was the original press release of Jannetta's and other's discovery. A full trial was planned in 2011. I wonder how it is going?

A multi-center clinical trial to further explore the AGH team's premise has already been organized and is slated to begin later this year.

SOURCE Allegheny General Hospital

http://www.prnewswire.com/news-releases/mri-study-suggests-brain-blood-vessel-abnormality-may-be-factor-in-parkinsons-disease-129441163.html


http://forum.parkinson.org/index.php?/topic/11605-mri-study-suggests-brain-blood-vessel-abnormality-may-be-factor-in-pd/?hl=jannetta

This has a further discussion of this....
http://forum.parkinson.org/index.php?/topic/11652-question-about-recent-pd-news/?hl=jannetta

From the kind Dr. Okun on that site

Other scientists, reviewing these findings, have pointed out that the blood vessels image only very small diameters. The MRI protocol that they used may not be optimal to examine such small blood vessels, and especially their compressive effects. It would definitely be very difficult to see straining artery walls using this MRI technique. The authors may however be inferring that there is pressure by seeing that the blood vessels are located closer to regions of interest in the brainstem in people with PD. One problem with that observation is that reduced brain volume in this region is an established aspect of PD, and when the brain moves, so too can the blood vessels. When the structures shift in PD it is not because of pressure-- it is because of slow neurodegeneration and consequent shrinking. Finally, one must remember the anatomy and that those blood vessels normally course by the brainstem and provide blood and nutrition to those areas of the brain--being close to the areas of the brain does not prove compression---and when we do see compression there are usually unilateral motoric neurological examination findings evident on exam. The argument for compression and symptoms based on the MRI findings is speculative. There are several well-established biological explanations that offer attractive alternatives to Jannetta's findings.


and this....

http://forum.parkinson.org/index.php?/topic/12877-arterial-compression-in-parkinsons-dr-jannettas-discovery/?hl=jannetta

From Jackie:
Is it just me or does this discovery seem to put into question the long-standing belief that dopamine-producing cells are dead? if the cells are dead (as opposed to dormant, disabled, etc) than how does one explain the (rather instantaneous - 48 hrs) elimination of PD symptoms? if the dopamine cells ARE in fact dead and (assuming) the body CAN regenerate enough cells to eliminate symptoms, this would take presumably longer than 48 hrs to accomplish. So how does removing the toxic condition (the compression in the mid-brain) cause dopamine levels to spike back to normal? Maybe those cells that we thought were dead, were actually only disabled.....does anyone else find this interesting?


and this....

http://forum.parkinson.org/index.php?/topic/11625-cerebral-penduncle-pinched-artery/?hl=jannetta
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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby cheerleader » Sun Feb 16, 2014 5:15 pm

Rogan--thanks for the links! The researchers at ISNVD were discussing the fact that the vascular connection to all diseases of neurodegeneration is finally being explored---now that we have better imaging modalities, and we can see the brain's vasculature better than ever. 7Tesla MRI can view the microvasculature, and there are changes happening before demyelination or tissue loss in MS. There are cerebral perfusion changes, and restricted venous return in Parkinson's, Alzheimer's, and MS. And vascular surgeons are discussing the best ways to deal with the extrinsic compression issues (from muscles and bones that press on veins) to intracranial issues. Each case is unique.

Here is the difficulty: Drug trials are much easier to run and more lucrative. Drug trials have the support of drug companies, and the connections to labs around the globe. Universities love to get money for pharma clinical trials.
Vascular procedures are almost impossible to double-blind placebo control trial--and raising the money for them is exceedingly difficult. Plus, drug companies don't want vascular research to succeed. They want you to take a pill. That's why the new MS drugs are addressing blood flow, not the immune system.
http://ccsviinms.blogspot.com/2013/08/m ... blood.html

it's a problem, but not impossible to overcome. If we support the researchers of the ISNVD--anything is possible.
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Re: PARKINSON'S DISEASE BLOOD VESSEL ABNORMALITY

Postby Rogan » Sun Feb 16, 2014 5:44 pm

Yes, thank you for your efforts to expand the treatment options beyond medication.

The one huge thing we have in our favor is everyone at some point gets sick from something.

So the odds that powerful decision makers in NIH, FDA, etc. , know loved ones or are themselves going to get sick is 100%.

The news did pick on Jannetta's discovery. Just amazing future ahead of us.

http://www.youtube.com/watch?v=Nn3NYhnqGzY&list=PLP0irnIX4X7wEMii1sH4Weje3evUp_JSf&index=1

and on CBS

http://pittsburgh.cbslocal.com/2011/09/08/local-discovery-could-lead-to-parkinson%E2%80%99s-breakthrough/

I will try to find out how his multi-site clinical trial is going. Sounds like his first patient was cured for 4 years. Now her artery on the other side is needing the same procedure as her left. Sounds familiar to some here at CCSVI on ThisISMS.
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