Sunday, 30 September 2012

Unrelated Blogger Comments September 2

Sometimes you what to say something that is unrelated to the threads. This is a spot for You. Previous comments can be got at on the posts on the right of the main page. 


Gavin Giovannoni said...
Re: "Ground fish dumplings at Le Poelon d'Or is a nice place to start. 29 rue des Remparts d'Ainay (+33 (0)4 78 42 43 42)."

Thanks for your recommendations; I will pre-book.

Re big pharma wining and dining neurologists in Michelin-starred restaurants; those days are long gone and buried. The new ABPI guidelines, and the UK bribery act, prohibit such extravagance. If we do take the opportunity to eat at the best Lyon has to offer, it will at our own expense and in the company of good friends.
Anonymous said...
Dear MouseDoc

thanks for bringing Haute Couture (pardon, Mouse Couture) to this blog :-)) Finally... Are there any other outfits?

Btw, the original was Audrey Hepburn in "Funny Face" for those who love old movies.
MouseDoctor said...
I do have another frock for that special occasion:-).

However, Prof G got banned from taking any more pics, these outfits can be seen at Mouse Couture II in San Fransisco
Anonymous said...
This time a more serious question than frocks;-)

When doctors talk about lesions they say 'oh, it's dead brain cells' how do they know from looking at MRI if the spots are dead or indeed re-myelinated cells? Both look white, don't they? How can somebody know without an autopsy know how much of the brain has repaired itself? Thanks.
Gavin Giovannoni said...
The post-mortem MRI studies have taught us that if a lesion that is white on a T2-MRI and black or gray on a T1-MRI then it is associated with loss of axons and nerve cells. There is on caveat in that new lesions can repair themselves, i.e go from being black, to gray and then disappear. So we have to do serial scans to make sure the black or gray hole is long-standing or chronic. Similarly, MRI lesions with reduced MTR (magnetization transfer ratios) are more likely to me demyelinated. So there are ways to look at lesions using MRI and tell something about the pathological attributes. The MRI folk are clever, very clever, but they can't get to the cause of MS. MRI is a tool to help diagnose and monitor MS, but it needs other tools in parallel to pin down the cause of the disease.
Roshni said...
Pls explain the white knight posts and why we can't comment there
Anonymous said...
I asked myself the same thing this morning. Hmmm, he is into something. I sense a Hitchcock-like suspense in the blogosphere. MouseDoc report - what's going on???
MouseDoctor said...
This is a post in response to a comment made by a BLOGGER late last month.

Too early to allow comments in case the knights ride off into the sunset or more likely they get assassins' daggers in their backs that stops their quest and Too much attention make wake the sleeping giant

Now that's cryptic
Roshni said...
Ok we'll have to wait for more explanation
Don't listen to the people who ask you to stop
Anonymous said...
I have been reading about EBV in the aetiology MS with interest. There is certainly some intriguing evidence and (anecdotally) i had a confirmed diagnosis of EBV 2 years before my first ms symptoms.

I am however confused about how much significance the negative predictive value adds to the argument. If there is such a universal exposure to EBV in the general population (95%), then surely we would be expect to find very few MSers (if any in a sample population) to be seronegative for EBV ... as is the case.

Where am i going wrong? Please enlighten.
MouseDoctor said...
If you do not have EBV you do not get MS.

There are less (or no if causal) that are virus negative than is found in the general population

However if you have EBV as most of the population does it does not mean you will get MS, but if it is causal then you need to have EBV to trigger the MS in someone who has gene variants that make you susceptible to getting MS in some one you has the environmental factors, e.g. smokers, vitamin D levels. Without the trigger the gun never fires.
Anonymous said...
There seems to be a group of patients that have a relatively benign RRMS course (maybe 1 or 2 relapses only) but then still go on to develop SPMS.

Why do you think this is? Is it because they are still experiencing sub-clinical attacks and therefore accumulation of disability or do you think there is something different going on?
Gavin Giovannoni said...
Re: "There seems to be a group of patients that have a relatively benign RRMS course (maybe 1 or 2 relapses only) but then still go on to develop SPMS. Why do you think this is? Is it because they are still experiencing sub-clinical attacks and therefore accumulation of disability or do you think there is something different going on?"

This is what will be answered with the alemtuzumab trials. If the MSers who have been treated early with this drug turn out to have benign MS and don't develop SPMS after 2--30 years then the former is correct. If they comeback with SPMS then the latter is correct. The problem we face is can we afford to wait to find out the answer to this question? VV is clearly prepared to wait as he is convinced that relapse and MRI activity make no difference. I am not sure his correct, which is why I am a strong advocate of early aggressive treatment.

25 comments:

  1. James Bostrom SAID

    Monday, September 17, 2012 6:26:00 AM

    While some MS patients who have had the liberation therapy are reporting long-term benefits from having the procedure, there are just as many for whom the ‘liberation therapy’ has failed as an effective therapeutic intervention. This doesn’t mean that these patients didn’t have some immediate benefits once the neck veins were opened; most did, but over time the veins restenosed again and their MS symptoms returned. In fact, having seen their MS symptoms almost totally disappear however briefly once their veins were cleared, patients who have restenosed want it done over again, as many times as necessary in some cases. However, there is now a new and growing subset of MS patients who have had vein widening venoplasty multiple times, usually to less beneficial effect each time, leading to the later discovery of so much intraluminal scar tissue by the second, third, or fourth attempt at re-opening the veins that the procedure cannot be performed again

    THEN LINKS REMOVED...IT SOUNDS LIKE AN ADVERT.
    SO PLEASE FEEL FREE TO IGNORE.

    VENOPLASTY WOULD BECOME AN INDUSTRY AND IF YOU DID IT MORE THAN A FEW TIMES A YEAR WOULD COST NO LESS THAN THE INTERFERONS ETC. IF TRUE THEN SOME CLINICAL TRIALS ARE DOOMED BECUASE THE UNIT IT OF ASSESSMENT IS OVER A YEAR OR MORE

    ReplyDelete
  2. UNBELIEVABLE I HAVE FOLLOWED THE LINKS I REMOVED FROM THE ABOVE ADVERT....IT WAS PLUGGING CCSVI AND STEM CELLS....SO TWO UNVALIDATED TREATMENTS AND LINKED TO A CCSVI CLINIC SO IF YOU READ THE ABOVE IT IS AN INDITEMENT OF THE CCSVI INDUSTRY BY THE CCSVI INDUSTRY AS IT SAYS THE PROCEDURE IS OF LIMITED LONGEVITY AND CAUSES SCARRING. I AM SURE THERE WILL BE READERS OUT THERE WITH DIFFERNT EXPERIENCES.

    ReplyDelete
  3. Prof G - do you know how much dimethyl fumarate (in mg) per day is the recommended dosis for BG-12?

    ReplyDelete
  4. Ok, Prof G, that's what I don't understand sorry (I'm daft) - is it 240 mg for a whole day administered twice or it is 2x240mg so 480mg per day? I read conflicting stuff on that.

    ReplyDelete
    Replies
    1. 2 x 240mg = 480mg per day; e.g. 240mg at 8am in the morning and 240mg at 8pm in the evening.

      Delete
    2. Thank you - last question: is it really necessary to take it in the evening and not lets say at midday or in the afternoon. I'm asking because of the side-effects (stomach pains) which come after intake and can disrupt one's sleep.

      Delete
    3. I'll let Prof G anwser this specifically

      However, the reason for twice a day is to keep the drug levels at state that they constant and are still active, so the time interval is probably more important than when you start. When you take a drug you get a spike in the blood and then the druug wanes as it is broken down and at a certain time it will get to a stage where the levels are too low to be effective. This is why you need a second dose. However food can sometimes absorption of the drug and in some cases it influences side effects.

      Drugs have a so called half life and thiss is given as a time. In this time half of it is broken down, just like some radio active compounds have half-lifes but in there case it is not hours but thousands of years

      Delete
  5. Thank you MouseDoc. I'll take it in the morning and in the early evening - hopefully it works with no side-effects. I take the medication with food, however, because otherwise I would not be able to endure the stomach pains (they are quite painful).

    Hopefully the food doesn't diminish the drug effect??

    ReplyDelete
  6. I thought that the fumerate drug they use for psoriasis was generally only given for about 6 months or so because of the GI problems it causes, whereas BG12 has been formulated to try and overcome this? If you've got stomach pains, aren't you concerned that it could be damaging your GI tract?

    ReplyDelete
  7. The BG12 pahse III results have been published today in New England Journal on trials lasting a few years we will see the incidence of GI problems.

    ReplyDelete
  8. Can we pls go back to the old way when to read comments a small new window would open up rather than having to load an entire new page in order to read and respond to comments?

    ReplyDelete
  9. Any thoughts on the mGluR4 proof of concept trial results for EAE that has been PR'd today?

    ReplyDelete
  10. Any thoughts on the mGluR4 proof of concept trial results for EAE

    Yes this is company marketing and is about raising product awareness and importantly money. About 2 years ago a group from Italy reported that stimulating mGLUR4 glutamate ( a nerve transmitter) receptor could inhibit EAE. The company with some of the original scientists on board has made another version of a drug against the same target and low and beyond they report that it does the same thing..This is smashing. If it is just being done in EAE animals there is some years to go before it will be in MS but I'll look at the original study

    ReplyDelete
  11. Can we pls go back to the old way when to read comments a small new window would open up.

    IS THAT BETTER?

    HAVING THE COMMENTS EMBEDDED ALLOWED ME TO GET AT THEM FROM A KINDLE WHEN I WAS AWAY

    ReplyDelete
  12. Brother, you sound angry. Please don't be.

    This way of reading and responding to comments is way better. I like to use my PC for surfing the internet, therefore, this is a much better way for getting to the blog.

    ReplyDelete
  13. I have taken caps lock off...I was not angry, sorry if I appeared that way.

    I suspect that this system may not stay in place as powers greater than me feel that it is easier to reply the other way...sorry

    ReplyDelete
  14. I was reading an article on the mechanism of action of Vitamin D and it stated(among other things) it 'enhances the innate immune system primarily by its ability to stimulate cathelicidin, an anti microbial peptide important in defence against invading organisms' If one of the causes of MS is a virus, could this stuff be preventing some people from becoming MSers in the first place,and has its use been looked at in the context of MS?

    ReplyDelete
  15. In the news today is an account of a transcription profiling "of periphral blood mononuclear cells" which denoted people as either MS-A or MS-B; one group has a 40% lower risk of relapse than the other. Significant developement?

    ReplyDelete
  16. Sounds interesting. we'll take a look
    Link is http://stm.sciencemag.org/content/4/153/153ra131.full

    ReplyDelete
  17. Do you agree with this statement
    "Tremor in MS patients could be considered as an advanced consequence of the disease and its presence suggests a more aggressive course."

    It is from this recent article http://www.tremorjournal.org/index.php/tremor/article/view/109

    ReplyDelete
  18. I would think that tremor is an advanced consequence of the disease, indicating quite severe damage in the nerves affecting the affected area. This will be as a result of neurodegeration but I'm not sure it suggests an aggressive course per se as it could be possible to get a lot of degeneration in one particular area whilst other areas might be spared.
    We see similar things in our mice,
    spasticity is much more common than tremor, which also usually accompanies a spastic limb.
    Tremors are much more difficult to treat.

    ReplyDelete
  19. Advances in MS:

    Aren't we at the stage now with the newest DMDs where, if all neurologists were truly competent, we could say that we have successfully made the impact of the disease considerably less, albeit not negligible? If all newly diagnosed RRMSers on the McDonald criteria (with all CISers receiving 6 monthly MRIs to get conversion at the earliest possible time) were given (say) Alemtuzumab (but this could equally apply to others) regardless of their lack of diability at that point, then that would dramatically change the natural history of MS, wouldn't it?. For 15-20 years at least, stability and lack of progression for many, many years would be the statistical norm and, if stability is applied to those with EDSS 0, then the impact of MS on those newly dianosed would be minimal for many, many years. We'd have to wait and see, of course, whether SPMS still raised its head 15-20 years down the line (and therefore continue to look for neuroprotective DMDs) but, at the very least, such a blanket approach would transform the impact of RRMS. Yes, some people would be risk averse so wouldn't go along with this but I can't understand why this wouldn't be the standard approach and the impact this would have on the condition as we know it on a population level would be enormous wouldn't it? I realise that these new drugs are not a 'cure' per se and aren't perfect for everyone but why aren' we talking about the potential for substantially reducing the impact of RRMS on all those newly diagnosed by such a widespread 'standard' treatment approach?

    ReplyDelete
  20. Re: "Aren't we at the stage now with the newest DMDs where,..."

    Yes, I agree. This is the strategy of aggressive early treatment. It is nor for everyone as it would be paternalistic to expect all MSers to take-up this option, but it would be great if we could offer this option up front!

    ReplyDelete
  21. Is there really a connection between MS and Schizophrenia.I have the timings of childhood onset MS and prodromal schizophrenia

    ReplyDelete

Please note that all comments are moderated and any personal or marketing-related submissions will not be shown.