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.

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