Preventive Neurology


Avid readers of this blog will have probably noticed that Prof G has been increasingly focusing on new initiatives recently. One of these is Preventive Neurology – as part of this we have received a large grant to set up a Preventive Neurology Unit, based at the Wolfson Institute of Preventive Medicine within QMUL. 

But what does preventive neurology have to do with MS, given that we can’t even be sure as to the cause of MS? And how will this work? 

Having been away from QMUL and Barts-MS for a few years, I’ve now taken up a post as a Senior Lecturer in the Preventive Neurology Unit to develop strategies to prevent MS. So I thought I’d introduce some of these, and how the unit might work towards this over the next few years. 

Firstly what do we mean by preventing MS? The most obvious interpretation of this is preventing MS from actually developing, which would be fantastic, but is clearly a very long term goal. I think it is also important to think about how we can prevent disability from developing in people who already have MS – not just MS-related physical disability, but cognitive problems, and also other health problems that can increase disability such as fractures. 

In terms of preventing MS from developing, we are looking at risk factors that have previously been associated with MS development; and one of the most interesting of these is infection with the Epstein-Barr virus, EBV. As many of you will know, if we look hard enough we find evidence of EBV infection in (almost) 100% people with MS, but only about 95% of controls without MS. Looking at this the other way round, if you haven’t been infected with EBV you are extremely unlikely (i.e. it is almost impossible) to get MS. It is also clear that if you have symptomatic infection (infectious mononucleosis, or glandular fever) your risk of MS is even higher. 

We don’t understand why, when infected, it is that some people do get MS and others don’t and this is something that we need to understand better and that we are working on. We also need to look at whether treating infectious mononucleosis, and/or suppressing the levels of EBV in the blood after infection have any effect on MS risk or MS activity. 

One of the ways that we can start to do this is by looking at people who haven’t yet developed MS who may go on to do so in the future, and following them up over a long period of time to see who develops MS, and then go back and look at what has happened before their MS developed. We know that the people at highest risk of developing MS are relatives of people who have MS, and we would be keen to work with people with MS and their relatives to work out how we can do this. This study is something that will take many years, and will also need the help of all of the MS community to have enough people enrolled in such a study to make it meaningful. So if readers of the blog have any comments/suggestions it would be great to hear them, either via the blog or via email ( 

By DrRuth

About the author

Rebecca Aldam


  • "if you haven’t been infected with EBV you are extremely unlikely (i.e. it is almost impossible) to get MS."

    You are confusing CDMS with MS. The only data available regarding temporal association of EBV and MS refer to the clinical manifestation of the disease, that is CDMS. However, early MS symptoms can precede CDMS for over a decade, whereas early, silent and still unknown pathological workings can take place long before any MS-like detectable symptom.

    Your assumption that EBV infection comes first is at least unsupported, if not totally wrong. So before go on and spend money trying to prevent EBV infection, you should first prove beyond doubt that a disease of unknown etiology comes after a well defined infection. This is the futility of any preventive measure.

    • Thanks. I agree that most studies are done in CDMS. We’ve looked at >1000 people with clinically isolated syndrome, and found the same thing. Also the ascherio group showed that in army recruits, all the EBV negative recruits seroconverted (ie became infected) some time before any clinical symptoms.

      One of the studies that we are looking to do is to gather a high risk (for MS) group of people and follow them for years, to see who does (and who doesn’t) get MS. This will hopefully help us to answer this question, but it will take many years…

    • I don't think it's futile.
      I had IM around 04 months before the first clinical manifestations of MS, so for me and others I'm sure it's plausible, logical and dingo yes of investment in research. Waste of time is precisely not researching something that can be or give a definitive answer.
      If this were the case, we would not ask for Vitamin D and MS, or so many people, despite the already proven ineffectiveness of this technique, would not insist on CCSV.

    • "04 months before"

      "MS patients had significantly higher risk of presenting up to 10 years prior to index date with gastric, intestinal, urinary and anorectal disturbances, anxiety, depression, insomnia, fatigue, headache and various types of pain."

      Druth, suppose i am diagnosed with MS this year and my first MS-related episode dates back 10 years. When did my MS start?

    • You’ve hit upon one of the disconnects that makes MS research tricky – the date of MS diagnosis can be very different from first symptoms.
      And yes, there are people with MS who have symptoms dating back years prior to dx, and often have many lesions on scan at diagnosis. And there are others who, when diagnosed, have only 2-3 lesions all of which have been symptomatic and don’t have this “prodrome”. They both have MS, may have the same date of diagnosis, but their date of onset may be very different. All of this makes what I’m trying to do difficult, but doesn’t mean that we shouldn’t be doing it!

  • Are all EBV infections equal? Are there possibly "nastier" variants which unleash different responses in the host?

    • Good question – honestly, I don’t know for sure. But some people in families do, and some don’t, get MS, despite presumably being infected with the same strain of EBV. My theory is that it’s the persons response to EBV, but i could be wrong. It seems to be something about the interaction though. We need to look at both EBV related and human related factors though – as you point out.

    • "Are all EBV infections equal"

      Guess not

      Ebv can cause Hodgkin lymphoma, naso-pharyngeal cancer (a type of head and neck cancer) and Burkitts lymphoma.

      Most people get infected with EBV as a child and stay infected for life without ever experiencing any symptoms. That’s why reducing the risk of EBV linked cancers is difficult, because most people are infected without knowing it, and we can’t predict who will develop cancer and who won’t.

      Some researchers think that the best way forward would be to develop a vaccine that can either prevent the initial infection, or at least stop EBV linked cancers developing. We don’t have a vaccine to do this yet. To promote research in this area, Cancer Research UK has made the eradication of EBV linked cancers one of its Grand Challenges.

  • I have 2 brothers and a sister. We all have MS except for our youngest brother. He fell off a balcony when he was two and required an emergency splenectomy. My theory is that the lack of a spleen somehow affected his immune system in a way protecting him from MS. I don't have a biology background but is there any scientific plausability to my theory? (I realize he could just have been lucky)

  • some amazing pessimism above. we may well be able to prevent MS if we can identify risk factors. it would be worth it for future generation. I don't think anyone is 'born with MS'. I think you have risk factors for it and bad luck and then you catch it/develop it

  • Thanks! This is how I think about it too… and if we (as clinicians/scientists) were too pessimistic we’d never take the risks needed to advance scientific knowledge. So not going to be put off (for now)

  • Me, my sister, my aunt and my uncle have (had) MS. My daughter had EBV and IM at the age of 16. I am sad to say that she would be someone to follw up.



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