Nyheder

[Lisa.T]

Er dit hoved skruet rigtigt på?


http://us1.campaign-archive2.com/?u=646d7fd51cbebd959c3a5b033&id=097d32f148&e=2a5edb0cf7

[bitte Mormor]

Jeg har ofte tænkt på, om det var mit hoved, der var kommet til at sidde skævt på kroppen, eller det i virkeligheden er startet med, at kroppen har vokset sig ud af balance med hovedet. Koblingen melem hoved og krop i hjernestammen føles i hverttilfælde meget væsentlig i mit forhold til verden og min sygdom.
birte

[Lisa.T]

Dette er godt nok henvendt til hjertepatienter, men det kan have betydning her også. Der er et nyt blodfortyndende middel, der gør det mere sikkert, hvis patienten tidligere har fået en stent. Det er åbenbart et problem, hvis en stent-patient skal gen-opereres, stenten er problematisk. Det nye middel gør det mere sikkert at operere igen:


http://dailyqi.com/?p=47704


Jeg havde problemer første gang jeg skulle ind på linket, jeg håber det virker her. Ellers prøv igen.....

[Lisa.T]

Der er sket en positiv udvikling i at forskerne kan forstå sammenhæng med ccsvi og MS.

http://www.prnewswire.com/news-releases/research-teams-report-on-18-months-of-progress-from-ms-societies-initial-studies-on-ccsvi-and-ms-138221444.html


Stykket er et langt, det vil fylde rigtig meget at bringe det her. Jeg har ganske vist kun skimmet, men der er gode nyheder. Det går fremad.

[helleho]

Her undersøgelse fra Toronto omkring risici ved CCSVI indgreb, som vurderes minimal 

Artiklen er fundet på FB - på siden CCSVI tracking, hvor der er nyhedsopslag dagligt fra hele verden - kan anbefales

Complications and Safety of Jugular and Azygos Angioplasty in CCSVI Patients with MS - M. Magnano
.by CCSVI in MS Toronto on Saturday, 28 January 2012 at 18:07.Purpose: In spite of the lack of confirmed data on the real value of transluminal angioplasty for the treatment of MS symptoms in patients reported positive to chronic cerebrospinal venous insufficiency (CCSVI) with ultrasound duplex scan, many patients have been so far treated in many countries. Purpose of this study is to evaluate the safety of procedure.

 

Materials and Methods: In our institution we have performed 380 jugular angioplasties since November 2010 on 380 patients, mostly (85%) bilateral. 20% of patients had also azygos angioplasty in the same session. All patients were MS patients symptomatic. CIS patients were not included. Age was from 19 years old to 65 years old. All patients were diagnosed CCSVI using ultrasound color duplex scan using the so called “Zamboni method” with at least 2 points positive out of 5 on the Venous Hemodynamic Insufficiency Severity Score scale. In our patient series there was no known coagulation disease or vasculitis or other known venous abnormalities other than the CCSVI. We performed in all patients venous access using 8F introducer in 90% of cases in the left groin. Phlebography of left iliac, iliolumbar, renal, azygos, vertebrale, and internal jugular vein performed in all patients. Angioplasty was performed using semi compliant high pressure balloons. All patients were administered low-molecular- weight (LMW) heparin for 3 weeks and included in a follow up program with ultrasound duplex scan after 1 month and 3 months.

 

Results: The complications reported were mainly in the access site (25 local hematoma not needing any further surgery, 1 case severe hematoma with skin ulcer probably due to long compression, 1 case long thrombosis of common iliac vein in the access side with pulmonary embolism needing long hospitalization and long anti-coagulating therapy) and in the jugular district (8 cases subacute thrombosis that were treated with prolonged LMW heparin for 2 months). We discovered that thrombosis was more common when using oversized balloons. We never observed venous rupture both in jugular and azygos district.

 

Conclusions: We concluded that CCSVI is a safe procedure with a low complication rate and no mortality rate. We suggest to not oversize balloon diameter, specially on hypoplastic veins.

[Lisa.T]

Dr. Zamboni søger finansiering af sit projekt:

http://bravedreams.ccsvi-sm.org/en

[Lisa.T]

Metaller i hjernen:


http://online.wsj.com/article/SB10001424052970204740904577192901072611524.html


Nederst er en hjælpsom oversigt.

[Lisa.T]

Her er en liste med, hvilke forsøg med ccsvi, der er i gang og planlagt:

http://www.clinicaltrials.gov/ct2/results?term=Ccsvi

[Lisa.T]

Mulig vaccine mod autoimmune sygdomme. Det synes jeg er rigtig gode nyheder. Hvis jeg regner MS for autoimmun, så lider jeg af to autoimmune sygdomme, og hvis man i fremtiden kan vaccinere mod flere af dem, så bliver livet lettere. For sent for mit vedkommende, men godt for fremtidens mennesker.


http://nocamels.com/2012/01/new-vaccine-tested-against-autoimmune-diseases/?t=New+Vaccine+Tested+Against+Autoimmune+Diseases

[Lisa.T]

Nyt forsøg bekræfter, at MS-patienter har overskud af jern i hjernen.


http://www.sciencedirect.com/science/article/pii/S0720048X12000046

[Anders]

der er så meget man ikke kan forså.. dette link er fra 2009.... men man er først lige begyndt at høre om det i det sidste år... igen.. OH but why

http://www.farma.ku.dk/index.php/Peptider-som-vaccine-mod-scler/7846/0/

[Lisa.T]

Jamen, jeg har egentlig aldrig været i tvivl. Det gælder sikkert alle m-firmaer. Og det gælder sikkert også for ms-medicin.

http://nyhederne.tv2.dk/article.php/id-47955765:medicinalfirmaer-modarbejder-fri-forskning.html

[Lisa.T]

Det lyder som gode nyheder for Jason Watt. Måske også for os:

http://www.eurekalert.org/pub_releases/2012-02/w-npr020112.php

[Lisa.T]

Dette er en rigtig spændende artikel, som jeg har fundet på fb. Jeg er nødt til at bringe den i sin helhed, da et link ikke vil virke for dem, der ikke er på fb. Der er både godt og skidt - men læs selv:



A new direction for MS research?
af CCSVI in Multiple Sclerosis den 6. februar 2012 kl. 16:40

--Marie Rhodes, author of CCSVI as the Cause of Multiple Sclerosis:

The Science Behind the Controversial Theory (McFarland Health Topics)

 

It is widely assumed that relapses and their accompanying worsening of symptoms are eventually the cause of long term progression. This is why 2 year studies that show a drug reduces relapses are thought to indicate long term success for the MS patient.

 

Relapses are caused by demyelination which is accompanied by inflammation.  That just means that if you looked at the lesion area under a microscope you would see that the myelin coating had come off of the nerve and there are immune system cells in the area.  The nerves are exposed and bare; that is what causes the loss of function in a relapse. 

 

The thing is that new myelin re-coats the nerve as the body heals the area.   Because of this,  EDSS scores swing wildly during the relapsing remitting phase of the disease and tend to drop if the relapses can be stopped for long enough for the healing process to complete.  Inflammation isn't good for brain tissue.

 

Progressive loss of function is different.  The progressive losses that occur later as the SPMS phase sets in are permanent--the nerves themselves degenerate; they aren't just bare and exposed. 

 

The reason this is significant is that short-term studies using new drugs on relapsing remitting patients which show a positive result on EDSS scores are often extrapolated out in time to suggest that the treatment in question slows progression.  Yet this is entirely an assumption; it depends on the assumption that relapses cause secondary progression years later. 

 

Research tells us something different.

 

"Multiple sclerosis (MS) is the most frequent chronic, disabling neurological disease in young adults in France. Descriptions of the natural history of large cohorts have provided extensive information about the overall course and prognosis of MS, but individual prognosis remains a major challenge for researchers. Recent studies suggest that the clinical phenotype of MS is mostly age-related and that relapses play a minimal role in the long-term accumulation of disability."

link 

 

and from another team:

 

"and further evidence supports the dissociation between relapses and long-term disability."

link

 

This idea that relapses are not associated with later disease progression is becoming more widely accepted among researchers and academics. 

 

Reducing relapses is an important therapeutic goal.  It results in a better quality of life and stabilization of the disease in early years.  And there are savings in hospital costs, lost work time and the unutterable pain and fear of living with an arm or leg that is "out" for a few weeks.  These are really important things.

 

But it's not right to pretend today's drugs do something that they do not--to pretend that they make a big difference in the progressive phase of the disease or that they prevent it.  They don't.  In fact a recent study on the quality adjusted life year for MS drugs reveals that it takes 800,000 dollars worth of current DMD--and many years--for the patient to recieve one "better" year due to the use of that drug. link

 

Some folks have suggested that the current therapies "work" and this disproves CCSVI, but patients themselves who discover that they are progressing after years of available DMDs may question the idea that simply suppressing immune system function (which modern medicine is very good at) will ever result in anything close to a cure.

 

And such patients would find themselves in good company.  My book details some of the published research that discusses this:

 

"Today's standard therapies reduce this inflammatory activity.  Conversely, the progressive phase of the disease is caused by degeneration and loss of nerves themselves and increasingly researchers are identifying degeneration as a separate problem and not simply a result of inflammation that occurred earlier.  Stem cell transplants are the most radical and aggressive version of immune system suppression, yet even this approach seems to allow continued degenerative loss of nerves" (CCSVI as the Cause of Multiple Sclerosis p 83)

link to book

 

If MS is primarily a degenerative process, we need to understand what causes this loss of nerve tissue.  CCSVI offers the first new direction of research that may result in better understanding of the actual MS process in a generation.

 

Does hypoxia result in degenerative loss of oligodendrocytes and subsequent scavenging immune system activation as Barnett and Prineas suggest? (Barnett and Prineas 2004, Barnett et al 2006, Henderson et al 2009)

 

Since venous insufficiency causes hypoxia-- is Prineas and Barnett's hypoxia in MS brains caused by CCSVI?  And is THAT the initial step in an MS lesion?  Does it take having the right genes and the right immune system for CCSVI to cause an MS lesion?  It doesn't have to be CCSVI vs. the traditional view--it is probably a combination.

 

If science is going to answer new questions about MS they have to stop spending all their energy and resources insisting that auto-immune inflammation is the whole story.

 

They also need to stop pretending that CCSVI advocates are throwing away everything that good objective science has already revealed about MS so they can begin to see where current MS research meshes beautifully with CCSVI theory. My book does that by reviewing the current understanding of MS and showing those areas where this matches with CCSVI.  I am an MS patient and working hard to do everything I can to see that this new model gets a fair shake from the powers that be.

 

We're all here for this same reason, and I am grateful for every one of you. 

Thanks for all you do to help.

Marie

 

[Lisa.T]

Om placebo - stærke sager:


http://www.miller-mccune.com/health/placebo-effect-stronger-than-we-thought-38717/