Twists and turns in the MS research trails
Hi, I am Mark Baker, a university lecturer, and I teach neuroscience to medical and science students at QMUL. I am also a member of Barts MS and have maintained an interest in MS over many years. I have been involved in research investigating the mechanisms of excitability in normal and diseased nerve, involved in pain signalling and the effects of demyelination. What do I mean by the mechanisms of excitability? I mean that amazing characteristic that allows some specialized cells to generate impulses that are used for signalling, so in nerve this characteristic allows us to feel things and work our muscles.
MS is a disease targeting nerve fibres in the brain. When I first became interested in what was going on in MS, as a student, the condition was thought of as mainly a demyelinating disease, but no longer. Well within my lifetime, the understanding has evolved, and MS is now thought of a demyelinating disease, but also a neurodegenerative disease. The emphasis now has changed.
When this kind of thing happens it is important for science and medicine, and ultimately patients, because light can be shed into what were darkened corners and questions asked that had not been asked before. This whole process of discovery is about real people in a lab or clinic somewhere asking questions and noticing something perhaps for the first time, and then reporting it, but the question asked arises out of the knowledge base, at that time, and I guess it is important to appreciate that. I can think of another example in MS research when ideas have fundamentally changed, and of course, there may be others.
An idea that was of some importance in the 1980s developed directly from the known temperature-dependent symptoms in MS. Many people reading this post will have temperature dependent symptoms that are serious enough for them to have to try to keep out of hot places, for example.
One result that is not disputed and had stemmed from the basic science of physiology was that the nerve impulse got briefer when the temperature increased, and what was shown in elegant experiments was that when the myelin was damaged in nerve, having a briefer impulse made the impulse more likely to fail.
This failure of impulse conduction along nerves in the brain and spinal cord with raised temperature, following demyelination, is the classical explanation for the appearance of new symptoms and exacerbation of existing ones with a rising core body temperature.
One way of trying to do something about this was to try to make the nerve impulse longer by using drugs that block proteins in nerves called potassium channels. There have been several clinical trials and potassium channel blockers are still under investigation to determine any useful effects.
The irony is that the widening of nerve impulses that provided the way into this area of research cannot be the basis of the useful therapeutic effect under investigation now, because the concentration of the drug that is necessary and safe for beneficial effects on walking is far lower than that required to make the nerve impulse longer.
Do you have temperature-dependent symptoms?
If so, what do you do about them? Have you found any strategy or treatment effective?
Let me know in the comments
What else you would like to know about the basic science behind MS?