Jos laskimoteoria osottautuu todeksi, voisiko se olla Nobel-tasoinen saavutus? kilpailua ja kateutta?

Kun erekki toit näitä laskimoasioita esille niin ajattelin; vouhotusta, mutta näyttösi perusteella alan vähitellen taipua. Tiede etenee aina uuden paradikman kautta. D-vitamiiniin uskon jo täysillä. Päiväannoksetkin ovat nousseet.

Hyvä bongaus THC4MS, raudan kertyminen ja sen seurauksen on nyt varmastikin tutkijoita kiinnostava seikka.. varsinkin kun asiassa on vielä paljon tutkittavaa ja selvitettävää. Tuo rautakertymien ja oligodenrosyyttien kuolema on vilahdellut aiemminkin teksteissä. Rautakertymiin keskittynyt tutkija Mark Haacke pohdiskeli keväällä 2009 julkaistussa tuotoksessaan, että miten/mistä rauta kertyy ja esitti että rautapitoisuudet olisivat hyvä biomarkkeri ms-taudin etenemisen suhteen.

Characterizing iron deposition in multiple sclerosis lesions using susceptibility weighted imaging

The source of iron deposition may be myelin/oligodendrocyte debris (17), concentrated iron in the macrophages (that phagocytize the destructed myelin/oligodendrocyte), or the product of hemorrhages from damaged brain vessels. The mechanism of direct damage to the brain by iron might be related to oxidative stress and the generation of toxic free radicals (12). The amount of iron deposition could reflect the extent of tissue damage, thus iron could be used as a biomarker to predict clinical outcome. This is a reasonable hypothesis given recent findings (27), which show very clear iron deposition encircling dilated veins in MS. The source of this iron is still unclear, but it could result from microhemorrhaging and hemosiderin buildup (27). Additionally, our results appear to indicate that chronic lesions may vanish on T2WI in some instances. If this is the case, then it may explain why the number of lesions on T2WI has not been very specific to the severity of the disease.
...
Brain iron accumulation has been shown histologically in MS and recently, an iron increase from 24% to 39.5% was reported in the deep gray matter in MS patients compared to control subjects (25,26).

Tuo Mark Haacke on ÄIJÄ! Ja antaa aivan varmasti osaltaan merkittävän panoksen MS-tutkimukseen ja CCSVI:n liittyen.

Edelliseen liittyen löysin EAE-hiiri tutkimuksen vuodelta -98, jossa pohdittiin rautakertymien muodostumista - liittyen oligodendrosyyttien vaurioihin. Iron deposits in the central nervous system of SJL mice with experimental allergic encephalomyelitis

Iron has been proposed to promote oxidative tissue damage in multiple sclerosis (MS). In order to gain insights about how iron gets processed during MS, the deposition of iron was investigated in the CNS of mice with experimental allergic encephalomyelitis (EAE), which is a commonly used animal model of MS...
...
Thus, each of the stained features in EAE animals could be due to the extravasation of blood which occurs in the SJL model of EAE, although some of the iron could have originated from myelin and oligodendrocytes damaged during EAE.

Medscape on julkaissut mielenkiintoisen artikkelin: (en ole nyt varma onko linkitetty jo tänne

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From Medscape Medical News

Endovascular Treatment of Cerebrospinal Venous Insufficiency Safe, May Provide Benefit in MS

Susan Jeffrey


December 3, 2009 — New data from a pilot open-label study suggest that endovascular treatment of strictures in extracranial cerebrospinal veins is safe in patients with multiple sclerosis (MS) and may provide some neurological benefit for these patients, researchers conclude.

The controversial approach, which has recently been making headlines in consumer media outlets, proposes that narrowing in the veins draining the brain, called chronic cerebrospinal venous insufficiency (CCVI), may be an early step in the disease process causing MS, and further, this narrowing may respond to simple angioplasty.


Left: location of venous stenosis with relative rate found in CCVI associated with multiple sclerosis. Right: the minimally invasive technique of balloon angioplasty eliminates the stricture in the cerebral venous system.
Lead author Paolo Zamboni, MD, director of the Vascular Diseases Center at the University of Ferrara, Italy, emphasized that the current report should be viewed as an interesting finding that urgently requires replication by other groups.

"What we know is that MS is very complex and multifactorial," Dr. Zamboni told Medscape Neurology. "I have identified an unknown factor and possible treatment for this factor."

The study is published as an online article in the December issue of the Journal of Vascular Surgery.

CCVI and MS

In a previous study published online in December 2008, Dr. Zamboni and colleagues assessed venous outflow routes in 65 patients with clinically definite MS (CDMS) and 235 control patients using a combined transcranial and extracranial color Doppler high-resolution examination. They reported that CDMS and venous outflow abnormalities were "dramatically" associated, with an odds ratio of 43 (95% confidence interval, 29 - 65; P < .0001).

Venography showed the presence of multiple severe extracranial stenoses affecting the principal venous segments in the patients with MS but not the control patients. "This provides a picture of chronic cerebrospinal venous insufficiency with 4 different patterns of distribution of stenosis and substitute circle," the authors write. "Moreover, relapsing-remitting and secondary progressive courses were associated with CCVI patterns significantly different from those of primary progressive (P < .0001)" (Zamboni P, et al. J Neurol Neurosurg Psychiatry 2009;80:392-399).

In an editorial accompanying that publication, Claude Franceschi, MD, from Saint Joseph and Pitié-Salpétrière Hospitals in Paris wrote that, "in light of the association between such a previously overlooked vascular picture and MS, a further stimulating research field is opened by this article. This should be addressed in understanding the contribution of venous drainage to the different aspects of inflammation, autoimmunity and neurodegeneration characterising the intriguing puzzle of MS" (Franceschi C. J Neurol Neurosurg Psychiatry 2009;80:358).

Dr. Zamboni stressed that this association between venous stenoses in extracranial arteries and MS is not contradictory to what is already known about the disease. "What I've found is a previously unknown factor, widely diffuse in my MS population, which could trigger or facilitate both immune reaction and inflammation," he told Medscape Neurology. "If you have elevated pressure and difficulty of drainage in the brain, you have the possibility of extravazation of blood components crossing the blood–brain barrier, and this could trigger inflammation and also immune reaction."

Restenosis a Problem

In the current report, the researchers describe the safety and early outcomes in these same patients after endovascular treatment of stenoses in the internal jugular vein and the azygous vein.

Of the 65 patients, 35 had relapsing-remitting disease, 20 had secondary-progressive disease, and 10 had primary progressive MS. All underwent percutaneous transluminal angioplasty to address strictures in these veins. All procedures were done as day surgery under local anesthesia, and no operative or postoperative complications were seen, including vessel rupture, thrombosis, or adverse effects from contrast.

Postoperative headache was reported in 6 patients, which resolved spontaneously, and minor hemorrhages with hematoma occurred at vascular access sites "occasionally," the authors report.

After the procedure, venous pressure was significantly lower in the internal jugular and azygous veins (P < .001). Stenoses in these venous pathways "were never found to be isolated," the researchers note, but always combined in the internal jugular, azygous veins, or lumbar system in 4 main patterns of distribution.

At a mean follow-up of 18 months, the risk for restenosis after intervention was higher in the internal jugular vein, Dr. Zamboni noted, with a patency rate of 53% compared with 96% in azygous veins (95% confidence interval, 3.5 - 72.5; P < .0001).

Patency at follow-up depended on the type of obstruction faced, including membranous obstructions, twisting, and hypoplasia. A stent was placed in 1 patient to resolve a twisted vein, but a second case retwisted, the authors note.

Using the patients as their own control, the researchers found improvement with treatment on some clinical outcome measures after the intervention, particularly for the relapsing-remitting patients. In this group, 27% were relapse-free before surgery and 50% were so after treatment (P < .001). Gadolinium-enhancing lesions on magnetic resonance imaging (MRI) fell from 50% to 12% (P < .001).

Significant improvement over the preoperative assessment was seen at 1 year on the Multiple Sclerosis Functional Composite again for relapsing-remitting patients (P < .008), but not among those with a secondary or primary progressive course.

Physical quality-of-life measures also improved significantly in relapsing-remitting MS patients and in primary-progressive patients, with a positive trend among those with secondary progressive disease. Mental quality of life also was significantly improved for the relapsing-remitting and primary progressive groups, but not for those with secondary progressive MS.

The authors conclude that although improved endovascular techniques are needed to approach the internal jugular vein, "the results of this pilot study warrant a subsequent randomized control study."

It is possible that the addition of stents to this endovascular approach that he calls the "liberation procedure" may improve outcomes, Dr. Zamboni noted. "However, the results are really interesting, if you think that all treated patients were already under the best treatment for MS and had adjunctive neurological benefits from the liberation procedure compared to the previous 2 years."

Mixed Response From Neurology Community

Asked for comment on these findings, Lily Jung, MD, from the Swedish Neuroscience Institute, Seattle, Washington, speaking on behalf of the American Academy of Neurology, was cautious in her assessment. She feels some of the strong claims in the current report are not supported by the data.

For example, the number of patients in the report is small, "and to make the correlation between the patterns of venous obstruction and the categories of MS is a real stretch," Dr. Jung said. Assessment was done by unblinded neurologists, which is "not ideal." She also noted that the MRI results used different techniques, different protocols, and different study intervals.

We would welcome some randomized, controlled, double-blinded studies...but before then would not be encouraging our patients to jump in with both feet to do this procedure.

"The bottom line is that my colleagues and I have been flooded by calls and emails from patients who have been led by the publicity around this article to believe that there is a cure for MS, and to make such a claim with such preliminary results is premature," Dr. Jung said. "We would welcome some randomized, controlled, double-blinded studies to look at the issue, but before then would not be encouraging our patients to jump in with both feet to do this procedure, which has significant risks and has not been proven to be safe."

As a vascular interventionalist, Dr. Zamboni says he is keen to collaborate with neurologists in the setting of MS, but acknowledged that his work has had a mixed response from the neurology community. Some, he says, have been excited and at least curious, which in his view is important in research. Researchers from institutions including Stanford, Harvard, the Mayo Clinic, and others have asked to discuss the technique so that they may attempt to reproduce these findings in their own populations.

To the contrary, of course, I've also found big opposition, but I think that probably it is a prejudgement.

"To the contrary, of course, I've also found big opposition, but I think that probably it is a prejudgement, and they have not read the paper carefully," he said. "But it's not important. What is important is to have other people interested in doing the research and understanding more."

The first step will be to understand how widespread the presence of CCVI is among patients with MS, he said. "We need to test patients very rapidly to have the epidemiological data, which are very important."

Already, Dr. Zamboni is collaborating with Robert Zivadinov, MD, and colleagues at Buffalo General Hospital in New York on an open-label, MRI-blinded study of 16 relapsing-remitting patients with MS with confirmed strictures in the cerebrospinal venous outflow routes. Half — 4 randomly selected patients in Italy and 4 in New York — will undergo early intervention to address the blockages at 3 months, and 8 patients will have a delayed procedure at 6 months of follow-up.

beddgelert kirjoitti on 01.12.2009 - 12:19:20:



Ja Aamulehdessä .

Hauskaa oli käydä työterveyslääkärillä perjantaina ja hän alkoi tohkeissaan kertomaan tästä "uudesta" tutkimuksesta .

Lainaus:


Kaikista eniten ärsyttää se tämä lause:

Dr Zamboni's most recently published work examined CCSVI in 65 people and suggested that 50 per cent of people with relapsing remitting MS were relapse-free for 18 months.

Tämä samainen lause hieman eri tavalla kirjoitettuna on melkein joka paikassa, MUTTA siinä jätetään AINA mainitsematta se että he jotka saivat relapseja, heille ahtaumat olivat tulleet uudestaan!.

On se vaan jännä miten tämä CCSVI tuntuu jakavan mielipiteet näin mustavalkoisesti, puolesta ja vastaan. Positiivisesti suhtautuvat ammattilaiset ovat käsitykseni mukaan niitä, jotka ovat tutustuneet aiheeseen ja joiden alaan CCSVI paremmin sopii eli verisuoni asiantuntijat. Tutkimuksellisesti Buffalon yliopisto on kyllä poikkeuksellinen yksikkö ja sen tutkijathan ovat kirjoitelleet mm. rautakertymistä jo vuosikausia takaperin, joten Zambonin teoriat/tutkimukset sopivat heille kuin nyrkki silmään. Kaikista negatiivisimmin ja pahimmillaan kiukkuisen kielteisesti on suhtauduttu neurologian kentältä. En voi kuin hämmästellä kuinka rohkeasti tieteellistä arvostusta nauttineet neurotutkijat (kuten professori Alastair Compston) ampuvat CCSVI:n alas. On paljon mahdollista että julkisuudessa sanotut seikat kääntyvät itseään vastaan - entä jos laskimohäiriöt ovatkin MS-taudin syy ja perusta? Entä jos tästä avautuukin kokonaan uusi ja ratkaiseva tutkimushaara? Ok, täytyy muistaa että aihe on edelleenkin erittäin tuore.. mutta paljon on tapahtunut parin viimeisen kuukauden aikana. Jännää, mitähän seuraavat kuukaudet tuovat tullessaan? En tiedä olenko liian optimisti, mutta olen vakuuttunut että kaikkinensa suunta on oikea.