How MS Develops
MS was once considered to be strictly an inflammatory disease of the central nervous system (CNS; the brain and spinal cord). During an MS relapse, a flare-up in the body’s immune system causes inflammation and swelling in the CNS. For example, inflammation of the optic nerve (leading to the eye) can cause vision problems and eye pain, a condition known as optic neuritis. Inflammation of the sensory or motor nerves can produce sensory symptoms, such as tingling or numbness, or motor (i.e. muscle) symptoms, such as weakness or spasms. As the inflammatory flare-up subsides, these symptoms tend to go away (or "remit") either completely or partially. This is why the most common form of MS is called relapsing-remitting MS: episodes of relapses are followed by periods of remission.
One of the great mysteries of MS
What triggers these inflammatory flare-ups? That mystery still hasn’t been solved but a number of key factors appear to be involved. There may be an initial trigger, such as a virus or some other toxic factor, which "turns on" the immune system, although a specific trigger has not been isolated.
Once the immune system is activated in people with MS, there are two key problems. Activated cells of the immune system migrate from the body into the CNS across what is known as the blood-brain barrier (BBB), a physical barrier of tightly-packed cells that is there to screen out injurious substances from entering the brain. Once inside the CNS, these activated immune cells, called T cells, attack the body’s own tissues. This is why MS is believed to be an autoimmune disorder.
The second problem is that once the attack gets underway, it doesn’t switch off as it should. Normally, when the immune system detects a foreign invader, such as a virus or a bacterium, it signals a red alert and attacks it with its arsenal of weapons. Once the invader has been killed or inactivated, the immune system shuts down the attack and goes back to its role of patrolling the body.
In MS, the inflammatory response persists. Prolonged inflammation is very injurious to the delicate nerve fibres (or axons) in the CNS. Immune cells can damage the nerves’ protective covering, called myelin. Immune cells can directly attack the myelin, or they can release toxic chemicals that erode it. Either way, the myelin begins to deteriorate, a process called demyelination. Just as damaged insulation can cause a wire to short-circuit, damaged myelin disrupts the messages traveling along the nerve fibers. The "short-circuits" are experienced as MS symptoms, such as tingling, numbness or pain.
The body fights back
Fortunately, the body has the ability to repair damaged myelin, a process called remyelination. As the myelin is rebuilt, it re-insulates the wiring and re-establishes normal nerve functioning. This is what is happening during periods of remission.
Unfortunately, this process of remyelination isn’t perfect. The body may not be able to fix the damage completely. With repeated episodes of damage and repair throughout the course of MS, the body’s repair mechanisms appear to falter. The cells responsible for remyelination, called oligodendrocytes, aren’t able to keep up with the amount of nerve damage that’s occurring. It could also be that their repair job in laying down new myelin isn’t as good as the original. The amount of damage starts to accumulate.
It isn’t clear why this happens but genetic factors probably play a role. MS is believed to have a genetic component, although no "MS gene" has been discovered and MS isn’t transmitted the way other genetic diseases (e.g. cystic fibrosis, Tay Sachs, etc.) are passed from parent to child. Instead, some individuals may inherit certain genetic propensities that influence their immune system response or their body’s ability to repair damage.
To use an analogy, you don’t always get a terrible cold after being exposed to a virus. If you are healthy, well-rested and eating properly, your immune system may be able to fight off the infection. If you are run-down, you are more likely to get sick. In a similar way, there may be genetically-influenced factors that enable your body to recover from an inflammatory flare-up. Or there may be other factors that impair your self-repair mechanisms. MS is a complex disease and the role of genetic factors isn’t fully understood yet. If such factors do exist, they may explain, in part, why some people with MS have little disability and others become severely disabled during their lifetime.