Can you give some advice on what is the recommended treatment for pregnant MS patients postpartum? What are their options if they want to breastfeed?
We typically recommend 4-6 weeks of breast-feeding before recommencing DMTs. However, there is data that IFNbeta, GA and natalizumab are safe whilst breast-feeding. DMF, based in its MOA, is also very likely to be safe. Most of the other monoclonals are likely to be safe; they will get across into breast milk in very low concentrations and are unlikely to be absorbed to any degree in the gut of the neonate. The low concentrations that do get across in the milk are likely to be denatured by acid in the stomach and digested by enzymes in the intestines.
I have recently been diagnosed with RRMS and I have been advised to take Tecfidera. I am however anxious about this as I know I have EBV in my system as I had Glandular Fever as a child and I don't want the EBV to be able to cause more damage by using a drug that suppresses my immune system. Ocrelizumad sounds very promising, I hope that the EMA doee licence this drug. In the mean time I would really appreciate hearing your advice on if EBV can effect MS when taking disease modifying drugs such as Tecfidera. My neurologist and the MS nurses have said they cannot comment on this. Best wishes and thank you for providing this platform, your work is inspirational.
Prof G,What dose of Rituximab do you believe would be sufficient to dampen the B-cell overshoot 6 months post Lem? Also, would you base administration on the B-cell counts (wait for them to rise) or would you just administer it at the 6 month mark?
ProfG proposed a study We have submitted a paper that may shed some light on your questions
Using rituximab 6-months post-alemtuzumb may be too late. In our proposal we wanted to administer it within the first 4 weeks.
Thank you. At what dose? I am having Lemtrada round #2 soon and am asking my neurologist for that small dose of Rituximab. For me though I feel that the overshoot flared my disease at 7 months post round #1. I want to dampen the b-cell hyper proliferation so that it doesn't happen again. My neurologist is concerned about suppressing my immune system too much, but I don't think he realises how small the dose of Rituximab would be.
We think the overshoot may relate to the chances of secondary autoimmunity, which run around 50%. As to re-curence of MS, if Genzyme supply the data we want then we can address this.
Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Diseasehttp://dx.doi.org.sci-hub.io/10.3390/pathogens6010002Charcot 2? Much Ado about Nothing?
Prof G,could you please clarify.(1) For a long time you are saying that RRMS, SPMS and PPMS are the same disease.(2) Yet, you are advocating early aggressive treatment of RRMS as it may benefit long-term. May be my logic is flawed, but I can’t see how both this statements could be true at the same time.Isn’t it strange to expect aggressive treatments to have any long term benefits in RRMS when there are PPMSers in whom progrssion kicks in at the age of ~40 after a period of subtle focal inflammation , subtle enough not to be noticed (do RRMSers treated with alemz/tysabri early accumulate less damage?)
Yes, this is a very good question... does alemtuzumab/natalizumab early stop the progression to SPMS?Because ( as mentioned a few days ago on this blog), rituximab started at a low level of disability did not deliver and the patient progressed anyway with new spinal cord lesions. So, do people treated with Lemtrada/Tysabri develop SPMS anyway? (Relapses do not bother me that much, they are mostly sensory in nature and go over in a matter of weeks. If I am to go on Lem/Tys I want to know it is actually going to help in the long run).
Does air pollution have nothing to do with MS?This study suggests that living near major roads increased the risk of developing dementia, but did not present an apparent risk of developing MS or Parkinson's disease.Http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)32399-6/abstract
An interesting publication:Cocapture of cognate and bystander antigens can activate autoreactive B cellshttp://www.pnas.org/content/early/2017/01/04/1614472114This is not molecular mimicry, rather lack of precision in localizing membrane-embedded antigens. Any comments?
On this blog I read promising studies on Ocrelizumab. My neuro has said that it is all hype and not get to get my hopes up and it is just pharma changing the name of an old drug Rituximab so that they will make more money. He says it will just do the same as Rituximab. To be honest I feel that I trust more of what is said on this site compared to what I am told by my neurologist.
Re: "Ocrelizumab ..... is just Pharma changing the name of an old drug Rituximab."This is not correct, ocleriluzmab is a more humanised monoclonal antibody. It binds to a different part of the CD20 molecule on B-cells and its so called Fc portion is different to Rituxumab. All these properties make ocrelizumab a different drug and some of these properties arguably make it better than Rituximab. We will only know if it is better than rituximab if we do a head-to-head study. This is something that we the MS community should consider doing as soon as ocrelizumab is launched.
Pharma are developin gcerlizumab so they can make money, rituximab is coming out of patent life, however as ProfG says it is humanised rather than chimeric and so is better suited to repeated injections
If I were to do a trial, I would suggest rituximab against alemtuzumab as an induction therapy, the main differences between ocrelizumab and rituximab will be tolerability.
Thankyou, I will print this off and show to my neurologist.
When used topically (!) a new Alzheimer's drug that targets tau regrows teeth by boosting stem cell production (!!)http://www.nature.com/articles/srep39654
Ramiel Nagel a dental health educator writes about how teeth can remineralize and repair naturally by modifying your diet. I've not read much about it but it sounds interesting. So I wonder about diet and myelin repair in MS, if it helps in some way.
What is the rumble in the jungle?
The rumble in the jungle refers to the next 'burning debate' at the ECTRIMS-ACTRIMS meeting in Paris later this year. Please the following post:http://multiple-sclerosis-research.blogspot.com/2017/01/researchspeak-who-trumps-who-t-cell-or.htmlThe idea is to get the big beasts of the MS world to debate whether MS is a T or B cell mediated disease. If you are young, you may not recall the 'rumble in the jungle'; it is probably the most historic boxing matches in history. The following is the opening paragraph from Wikipedia: The Rumble in the Jungle was a historic boxing event in Kinshasa, Zaire (now Democratic Republic of the Congo) on October 30, 1974 (at 4:00 am). Held at the 20th of May Stadium (now the Stade Tata Raphaël), it pitted the undefeated world heavyweight champion George Foreman against challenger Muhammad Ali, a former heavyweight champion. The attendance was 60,000. Ali won by knockout, putting Foreman down just before the end of the eighth round. It has been called "arguably the greatest sporting event of the 20th century".Debating is almost a sport in the UK and the analogy with boxing is not a bad one. We have already sent-out debater and referee invitations for the rumble. Let's hope we can get two MS big beasts to fight each other and an impartial match referee to take them to task on their claims.
My question is probably naïve but do certain kinds of music help improve walking ability in some pwMS? I ask this as I have seen a video of a person with Parkinson's disease and their gait improves quite a bit when they listen to music they can find the rhythm with. I know Parkinson's and MS are different.
Previous research has noted that music can improve gait in several pathological conditions, including Parkinson's disease, Huntington's disease and stroke(Nombela 2013). Perhaps pwMS could try listening to music when doing the Timed 25 Foot Walking Test at home and see if there are improvements.
On the latest episode of QI the host Sandi Toksvig said that you can prevent muscle loss in an arm encased in plaster by visualising moving those muscles. I couldn't find much online on the subject but there were some articles reporting 'evidence' of trial participants improving muscular and cognitive strength over time by imagining carrying out tasks.What do you think about this?
I'm very curious to understand the gender variations involving MS. Would Galanin gene polymorphism have any role in the differences in manifestation or development of MS for each sex, where the polymorphism of the galanin gene, varying inversely for women and men, could give more concrete clues to predict who would develop the disease, and in what way, if more "soft" or more aggressive? Https://www.ncbi.nlm.nih.gov/pubmed/27870457
Was made aware of this through a newsletter from DMSG just now and thought to post it here in case others are interested - a study looking at safety of Gadolinium MRI during pregnancy (according to this study, it's NOT safe in pregnancy to use gadolinium): https://www.ncbi.nlm.nih.gov/pubmed/27599330
Synesthesia is found in 4.4% of the population, as a lower estimate, which is equivalent to 1 in 23 people. But a little research seems to indicate synesthesia may be higher in pwMS than the general population. What do you think? Interesting stuff. So I asked myself what colour is middle C on the piano? I say yellow. Synesthesia is a neurological phenomenon in which stimulation of one sensory or cognitive pathway leads to automatic, involuntary experiences in a second sensory or cognitive pathway.
Not as rare as you think: http://teachneuro.blogspot.co.uk/2012/01/synesthesia-not-as-rare-as-you-think.html
Just seen this UK story - http://www.bbc.co.uk/news/health-38669588What does this mean for those of us already on pricey DMTs ?Thanks
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