Dr. Frohman and Normal Pressure Hydrocephalus

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

Postby SammyJo » Sat Sep 19, 2009 9:12 pm

I was doing a little research earlier this year for a friend who had suspected NPH, and we determined that one of the top treatment centers was Columbia, Dr. Guy McKhann
http://cumc.columbia.edu/dept/nsg/ct/hydrocephalus.html

On the interdiscipline advantage, like Frohman bringing up NPH. We need a high powered investigative team of assorted specialists, will this just happen naturally, something the docs will do themselves, or does it come from MS patients requesting this?

On the pragmatic front for early adopters, at least with PPMS, would Dr. Dake's assessment include CSF pressure, or is that something he'd look for in the neurologist's assessment. If you've never had a lumbar puncture, would the pressure issue be missed?

Thank you Marie & Cheer, I started reading extensive info you've compiled when I heard about CCSVI 9/15, my records were in the mail to Stanford 2 days later. Yes, all the unknowns deserve due caution, this is serious business. But very exciting.
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Postby gibbledygook » Sun Sep 20, 2009 8:19 am

Cheereo, the research you have posted and discussed offers us all invaluable information about the complexities and problems of different fluid-containing parts of the brain. I expect that something similar to NPH may be occuring to the CSF which might affect a proportion of people with MS. ...We need more Dakes in this world!
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby radeck » Sun Sep 20, 2009 8:35 am

Thanks for the insights.

mrhodes40 wrote: It is not making sense to me that collapsed veins are the explanation for stenosis... :? are you saying they are collapsed not stenosed... or that the collapse causes stenosis ...or that the stenosis makes veins collapse downstream from the stenosis itself?


I was just trying to help out coming up with explanation for a re-stenosis away from a stent. As this is not congenital, and beyond the reaches of CNS pressure, I thought one explanation would be that the vein collapsed because there is too large of a pressure gradient between the inside and outside of the vein in that area. I thought that lack of 40% of veins throughout an average MS brain could be a reason for that.
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Postby LR1234 » Sun Sep 20, 2009 8:37 am

erased as I didn't write it on the right board!
Last edited by LR1234 on Sun Sep 20, 2009 9:42 am, edited 1 time in total.
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Postby gibbledygook » Sun Sep 20, 2009 8:42 am

Here's something on the ventricles:

1: Acta Radiol. 2008 Jun;49(5):570-9. LinksRate of ventricular enlargement in multiple sclerosis: a nine-year magnetic resonance imaging follow-up study.
Martola J, Stawiarz L, Fredrikson S, Hillert J, Bergstrom J, Flodmark O, Aspelin P, Kristoffersen Wiberg M.
Division of Radiology, Department of Clinical Science, Intervention, and Technology, Karolinska Institute, Stockholm, Sweden. juha.martola@ki.se

BACKGROUND: In multiple sclerosis (MS), brain atrophy assessed by linear measurements of ventricular widths has been reported to be well correlated with three-dimensional (3D) measurements. Therefore, serial linear measurements with no need for advanced 3D evaluation may be proven to be robust markers of irreversible, destructive changes. PURPOSE: To evaluate the rate of supratentorial ventricular enlargement representing four decades of disease span. MATERIAL AND METHODS: 37 MS patients with disease duration at baseline ranging from 1 to 33 years were included. The mean time of the individual magnetic resonance imaging (MRI) follow-up was 9.25 years (range 7.3-10 years). Enlargement rate of the third and lateral ventricles was studied over time by applying three linear measurements on axial 5-mm T1-weighted MRI images. RESULTS: Progression of supratentorial ventricular widths during 9 years' follow-up was found. The mean annual width increase of the third ventricle was 0.20 mm (P<0.001, 95% confidence interval [CI] 0.15-0.25), for the frontal horn width 0.32 mm (P<0.001, 95% CI 0.23-0.40), and increase of the intercaudate distance was 0.26 mm (P<0.001, 95% CI 0.19-0.33). The association between these three measurements and disability status persisted at the time of follow-up. CONCLUSION: We found uniform ventricular enlargement progression during four decades of disease span, suggesting unchanging total brain atrophy progression over time.

PMID: 18568545 [PubMed - indexed for MEDLINE

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1: Neuroimage. 2007 Nov 15;38(3):529-37. Epub 2007 Aug 16. LinksRegional brain atrophy development is related to specific aspects of clinical dysfunction in multiple sclerosis.
Jasperse B, Vrenken H, Sanz-Arigita E, de Groot V, Smith SM, Polman CH, Barkhof F.
Department of Neurology, VU University Medical Center, Boelelaan 1117, PO Box 7057, 1007 MB, Amsterdam, The Netherlands. mms.jasperse@vumc.nl

Brain atrophy in multiple sclerosis (MS) is thought to reflect irreversible tissue damage leading to persistent clinical deficit. Little is known about the rate of atrophy in specific brain regions in relation to specific clinical deficits. We determined the displacement of the brain surface between two T1-weighted MRI images obtained at baseline and after a median follow-up time of 2.2 years for 79 recently diagnosed, mildly disabled MS patients. Voxel- and cluster-wise permutation-based statistics were used to identify brain regions in which atrophy development was significantly related to Expanded Disability Status Scale (EDSS), Timed Walk Test (TWT), Paced Auditory Serial Addition Test (PASAT) and 9-Hole Peg Test (HPT). Clusters were considered significant at a corrected cluster-wise p-value of 0.05. Worse EDSS change-score and worse follow-up EDSS were related to atrophy development of periventricular and brainstem regions and right-sided parietal, occipital and temporal regions. Worse PASAT at follow-up was significantly related to atrophy of the ventricles. A worse TWT change-score and worse follow-up TWT were exclusively related to atrophy around the ventricles and of the brainstem. Worse HPT change-score and worse follow-up HPT of either arm were significantly related to the atrophy of widely distributed peripheral regions, as well as atrophy of periventricular and brainstem regions. Our findings suggest that decline in ambulatory function is related to atrophy of central brain regions exclusively, whereas decline in neurologically more complex tasks for coordinated hand function is related to atrophy of both central and
and peripheral brain regions.

PMID: 17889567 [PubMed - indexed for MEDLINE
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I wonder how the blocked jugular could lead to all this ventricular damage..
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby cheerleader » Sun Sep 20, 2009 9:29 am

Hey Gibs-
Read up on the SWI and lesions thread. Dr. Mark Haacke and his team find alot of iron deposition and hypoxic tissue death in MS brains. Basically damaged brain tissue- which is why gray matter damage and atrophy are seen in MS brains.

The reflux from blocked jugulars is very damaging to the brain tissue. As far as how CSF complicates this picture, it may be as simple as just creating even more pressure in an already stressed brain.
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http://ccsviinms.blogspot.com
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Postby gibbledygook » Sun Sep 20, 2009 9:46 am

Hi Cheereo,

I have indeed read quite a bit on the SWI section. I'm not sure that the iron deposition can explain the expansion of the ventricles or am I missing something?! It seems that disturbance of the CSF would be a more likely explanation. I'm very interested by the NPF story and wonder if there might be something like that going on in addition to the iron/stenoses etc. :roll:
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby mrhodes40 » Sun Sep 20, 2009 10:13 am

I'll play devil's advocate here for how ventricles might enlarge without NPH. The skull is a certain size, therefore the contents of the skull have to stay constant in terms of volume or the brain would slosh around--and that would damage it. Therefore the blood, brain, and CSF together must always equal the volume of the skull. If there is tissue loss---atrophy--something else has to get bigger to make up the difference. I believe that is the standard explanation for why the ventricles enlarge in MS, atrophy is well documented.

I like the possibility of a side issue/co factor of NPH better as an explanation and am grateful they are already on it!!
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
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Postby gibbledygook » Mon Sep 21, 2009 4:07 am

Marie, what a great explanation. My god these ventricles, which look so solid in the diagrams could just be like plastic bags full of liquid. Mmm. All fascinating stuff.

Let's hope that skydog's restenosis can be fully fixed.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby cheerleader » Mon Sep 21, 2009 7:35 am

Agree! Marie's got it...atrophy. Nature abhors a vacuum...a loss of volume from one area will increase volume from another. After Jeff was stented and had that horrendous headache, Dr. D talked with Dr. Z about why...and D. Z explained that the fluid levels in Jeff's brain had dramatically changed, like a sponge being wrung out. It took several days for the body to sort it out and rebalance- so his brain was not "sloshing about" after the blood had a quicker exit.

sorry for clouding the water, but I also hope there are answers as to Mark's restenosis...(germs, Marie?)
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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby mrhodes40 » Mon Sep 21, 2009 12:43 pm

germs?


I do not know. It seems possible to me but there is not any histology yet showing that in any stenotic lesions so.....my guess is as good as anyone elses... :roll:

I did mention the idea of stenosis and germs to all kinds of docs (stratton wheldon simka) so these folks should be looking for that possibility. Mark's restenosis is incredible to think about.........it does not appear to be common though luckily.
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
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Diagnosed with both NPH and MS

Postby gfrl » Fri May 28, 2010 5:57 pm

Aloha:
I am an otherwise healthy 65 yo woman from Hawaii.
I was dx with NPH in 2005 and had a programmable shunt implanted 2006; triad of symptoms: falling; wobbly; UI.
next 6 months symptoms resolved; however, became increasingly wobbly; gait imbalance; UI; depression 2007 to present;
2009 dx MS (RR); "numerous lesions brain, neck, spinal cord
RX: Copaxone; Provigil; Buproprion; Prozac; Folic Acid; B12

Are there others with both diagnosis?
HI doctors say I'm the only one, but it cannot be... :idea:
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Re: Diagnosed with both NPH and MS

Postby cheerleader » Fri May 28, 2010 6:04 pm

gfrl wrote:Aloha:
I am an otherwise healthy 65 yo woman from Hawaii.
I was dx with NPH in 2005 and had a programmable shunt implanted 2006; triad of symptoms: falling; wobbly; UI.
next 6 months symptoms resolved; however, became increasingly wobbly; gait imbalance; UI; depression 2007 to present;
2009 dx MS (RR); "numerous lesions brain, neck, spinal cord
RX: Copaxone; Provigil; Buproprion; Prozac; Folic Acid; B12

Are there others with both diagnosis?
HI doctors say I'm the only one, but it cannot be... :idea:


Welcome, gfr...
I don't remember seeing another MSer with NPH on here, but maybe someone will chime in. If I were you, I'd look into CCSVI. You've already been diagnosed with a pressure issue, maybe there's something going on in your extracranial veins, as well? Bring Dr. Zamboni's research to your neuro/vascular doc or whoever treated you for NPH. One thing Dr. Zamboni has noticed is that cerebrospinal fluid levels are affected with CCSVI. Here's the paper for you:
http://www.fondazionehilarescere.org/pdf/VHISS-CSF.pdf

all the best,
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby 1eye » Mon May 31, 2010 5:29 pm

This is right. We should not need to get MD credentials. My brother had hydrocephalus and still has his shunt even though there's nothing in it now. It goes inside one of his jugulars, and what it used to do was depressurize the CSF in his brain ventricles.

We were both born with malformations. His affected him right away, and mine waited 40 years. But they are both congenital. The brain is too complex for the likes of me to understand. But there are those who do. For Bill it was a very forward-thinking neurosurgeon in 1962. For me, who knows?

The brain and spinal column surround veins, arteries, nerves and spinal fluid. The brain also has brain tissue. Inside the bone case, both skull and spine, the volume is more or less constant. That means whenever one expands, whichever is weakest must contract, to allow for the unchanging volume. My brain mass has been decreasing. That allows for expansion of existing veins and the addition of collateral veins.

The whole fluid system is very complex, changing as it does when I lie down. The vein and artery complex is a closed system. Even changes in how fat I am have an affect. I will leave it to experts to try to understand mine. But the thing we should all learn is that these are congenital, and everybody is different.

When I was in grade school, I heard you could drive a nail with a bottle. Mr. Wizard told me. I took a Prel bottle (they were glass then) and filled it under the tap, and put he lid on, so that there was NO AIR, just water. Since water is not compressible, it might as well have been a brick. I drove nails with it all day. Veins and arteries are more pliable, so they may change their shape, but the whole system is closed, so if you blow up a balloon in one place, you may increase the pressure (and/or volume) somewhere else. In other words, a vein, or even an artery, or inside a fixed bone chamber, all kinds of stuff, some more compressible than others.

It's a complex system. I hope whoever operates on me knows what they are doing.
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
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Postby cheerleader » Mon Jul 18, 2011 11:42 pm

bump...in light of the continuing discussion on NPH by Dr. Salvi at the AAC CCSVI symposium...cerebrospinal fluid is part of this equation.
cheer
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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