MS is a disease of the brain and spinal cord, which are also known as the central nervous system (CNS), characterized by an inflammatory, demyelinating condition. In inflammation, a wound typically gets hot, swollen, and painful, because the immune system sends in white cells. These secrete messenger chemicals that cause the inflammation and dispose of bacteria, debris and foreign substances in the wound.
Demyelination is a disorder affecting the myelin sheath around nerves. Nerve cells in the CNS have many branches, or axons, which communicate with other nerve cells via charges that look like electrical impulses. Myelin, a fatty substance, is produced when specialized cells (oligodendrocytes) wrap themselves around the axons, like layers of an onion. Myelin is fatty because the outer coating or membrane of every cell is made up largely of fat, so when the cell wraps itself around the axon, the multiple layers form a fatty sheath.
The qualities of the fat that makes up this membrane depend on fats consumed in the diet. The signals passing down the axons are not really electrical, but they appear to be because of the rapid movement of charged particles called ions. These are minerals like sodium, potassium, calcium, magnesium and so on; again, these largely come from diet.
So dietary factors like fat and mineral consumption are also important for day-to-day nerve conduction. Demyelination occurs when some of the myelin is broken down. In inflammatory demyelination, the myelin is broken down as a consequence of inflammation.
Here’s the typical sequence of events:
Symptoms depend on what the affected nerve cells connect to. If they are:
Because some swelling of the surrounding nervous tissue is associated with this inflammation, nerve transmission through nearby axons will also be affected. As the swelling subsides, nerve cells that aren’t seriously injured (but have become dysfunctional because of inflammation) start to work again. So there is almost always some recovery for this reason alone.
Limited repair of damaged nerve cells takes place, with some remyelination, particularly early in the disease, so the MS symptoms settle a bit more. There is growing evidence that remyelination occurs throughout the disease and is considerably more prominent than we have realized to date.1
That’s why the area of numbness or tingling is likely to get smaller and the weakness is likely to improve over time, as lesions heal and scar, and the uninjured nerves recover.
Recovery is often incomplete, however, and less severe symptoms remain in the same part of the body. These typically wax and wane, depending on numerous factors, temperature chief among them. The warmer they get, the more poorly the nerves function. So heat tends to make these residual symptoms worse for most people, although cold is more of a problem for some.
Although heat makes the nerves conduct more slowly and worsens MS symptoms, it does not actually damage nerves. So exercising is fine, even if it temporarily worsens symptoms.
Gradually, as more and more lesions occur in the CNS, more and more pathways are knocked out, and a gradual decline in function becomes evident. Many lesions occur in ‘silent’ parts of the brain and are not noticed. The obvious ones occur in the spinal cord or nerves leading to the eye, where virtually all nerves are essential for things like sensation, power, balance, vision and so on. So even a small lesion here is usually noticed.
Much research is being done on how the CNS attempts to repair lesions. The nervous system has an amazing capacity not only to regenerate so that impulses can ‘detour’ around the damaged lesion, but in the brain, changes occur which involve recruitment of new nerve cells and pathways to compensate for what is missing.2 When there are only a few lesions, the CNS is extremely good at regeneration and compensation, even if there isn’t much remyelination. However, if the process continues, these compensatory mechanisms become overwhelmed and progressive disability occurs.
That is why OMS’s focus is on stabilizing the disease early and preventing further damage.
1. Patani R, Balaratnam M, Vora A, et al. Remyelination can be extensive in multiple sclerosis despite a long disease course. Neuropathol Appl Neurobiol 2007
2. Kerschensteiner M, Bareyre FM, Buddeberg BS, et al. Remodeling of axonal connections contributes to recovery in an animal model of multiple sclerosis. J Exp Med 2004; 200:1027-1038