MS affects the nerve fibres of the central nervous system - the brain and spinal cord. These nerves gradually lose their ability to transmit electrical signals between the brain and body, causing symptoms which can include partial blindness, chronic fatigue, loss of mobility, loss of speech, and behavioural problems. In some cases symptoms are rapid and deadly.

I have witnessed the devastating effects of MS on my wife Gwen (below) who was stricken by this frightening disorder fifteen years ago, at the age of 32. I have watched a fit, healthy, young woman gradually being forced to come to terms with a fearfully debilitating illness.

What causes Multiple Sclerosis?

• MS is unpredictable and can strike anyone, even children.
• Around 250 new cases are diagnosed every day in the UK and the US.
• Over 85,000 people in the UK are affected by MS.
• One in a thousand people in the Western world have MS.
• Click here to read what it is like to live with MS on a daily basis

Multiple Sclerosis is a disorder that strikes the central nervous system, which consists of the brain and spinal cord. These organs control the movements and functions of the entire body. The nerves are surrounded by insulating matter called myelin, a soft, white, fatty substance that forms a protective sheath for the nerves. Multiple sclerosis is a disorder where the myelin breaks down and can slow down or even block the flow of signals to and from the central nervous system to the rest of the body, impairing such functions as vision, strength, or co-ordination. The symptoms of MS can be mild or severe, and can include partial blindness, chronic fatigue, loss of mobility, loss of speech, and behavioural problems. In a small number of cases symptoms are rapid and deadly.

The specific causes of MS remain a mystery.

Current clues to the cause of MS include:

Climate: Until recently it was believed that the farther countries are from the equator, the higher the incidence of MS. But Abramsky, chairman of the neurology department at Hadassah-University Hospital in Jerusalem's Ein Kerem and a leading clinician and researcher on MS, says this is not accurate, pointing out that there are countries with a lot of daylight and higher rates of MS, while Lapland - which is as north as one can get - has no MS at all.

Age: Studies of people who have lived in high risk areas for MS between the ages of 10 and 15 suggest that exposure to some factors (such as a virus) in the environment during that time makes one more susceptible to MS many years later.

Genetics: MS is more common in family members of MS patients than in families with no history of MS. The heightened incidence of MS is not strictly a hereditary disorder caused by one genetic defect. Many genes are likely to play a role.

Immunology: The immune system is composed of white blood cells that normally protect the body from viruses, bacteria, cancers, and other "foreign agents." However, this system may react abnormally in MS patients, and, in fact, may play a major role in the cause of multiple sclerosis. Lymphocytes are triggered or activated, then travel through the blood-brain barrier to enter the brain and set off a series of chemical and cellular events that lead to myelin damage.

Virus: One or more viruses may play a role in the cause of multiple sclerosis. Viruses may be the predisposing "environmental factor" in MS. MS is not contagious. Viral infections such as "colds" may increase the risk of a specific attack for those with MS. One theory postulates that exposure to a virus predisposes the body's immune system to malfunction and attack myelin. In this theory, many factors must act together. They include an environmental factor attacking a susceptible person, at a specific age. Other factors may also be necessary to set the stage for multiple sclerosis. For patients with primary-progressive MS, diagnosis usually occurs between the ages of 40 and 60.

For reasons presently unknown small patches on the myelin sheath are attacked and stripped in a way that is roughly analogous to what happens when an electrician peels a small piece of plastic insulation off an electric wire. Soon thereafter star-shaped neuralgia cells known as oligodendrocytes and astrocytes arrive on the scene to repair the damaged sites, but during this rebuilding process they cause scar tissue, known as gliotic plaques, to form. These plaques become hard and sclerotic (a sclerosis is a thickening or hardening of cellular tissue) and then begin to interfere with or obstruct the flow of nerve impulses that pass along the nerve cells. Normally, for example, nerve impulses travel along axonal pathways at around 225 miles an hour. When a section of myelin sheath is destroyed, however, nerve impulses are slowed down to half that speed or even less. This means that command messages sent from the brain do not arrive at their normal speed, and often become garbled or confused in the transmission. If a sclerotic plaque is small, about the size of a pinhole, the disturbances it produces may affect only a single function of the body. If large, an inch or longer, it may disturb several functions at once. If a plaque heals and then another forms elsewhere in the CNS (Central Nervous System), the type of symptom produced will change, along with its location in the body. If several plaques are active at the same time they will produce multiple disturbances.

Although multiple sclerosis is categorised as a neurological disorder, it is also a disorder of the immune system. For patients with multiple sclerosis, the immune system turns against the body instead of defending it, thus putting multiple sclerosis in the broader category of autoimmune diseases. In the case of multiple sclerosis, myelin is clearly the target of the immune system's attack. In multiple sclerosis patients, all of the immune system's components are involved in one way or another in this inadvertent attack on the brain's myelin. These components include B cells, T cells, macrophages, and all of the associated cytokines, the chemical mediators serving in this biological warfare. Many studies reveal a clear association between one particular cytokine, called tumor necrosis factor (TNF), and multiple sclerosis attacks. In a two-year study Dr. Romain Hentges and his colleagues measured the levels of TNF in the cerebrospinal fluid and serum and correlated those levels with the way the disorder progressed in each patient.

Why would patients with elevated TNF levels suffer more from multiple sclerosis attacks? When your brain is working properly, the body's own blood-brain barrier - the cellular and chemical guards that select which substances are granted permission to pass into the brain from the blood capillaries - keeps out invaders. However, one function of the TNF cytokine is to create passages for other components of the immune system to cross the blood-brain barrier and enter into the battle zone, much the way army engineers build roads and bridges to allow further reserve troops to enter a war zone. Without the help of TNF, the hand-to-hand combatants of our immune system - our microphages - could never make it into the front line trenches of the brain. This breakdown of the blood-brain barrier is the first rung on the ladder to multiple sclerosis attacks, for it is followed by inflammation, the breakdown of myelin, and the formation of hard fibrous material (the scars or sclerosis) on nerve fibres.

Most people with MS, about 75 to 85 percent, begin with relapsing/remitting MS (RRMS). It is the most typical presentation in younger patients. People with RRMS go through temporary periods when symptoms get worse. These periods are called relapses, exacerbations, or attacks, and they typically last a few weeks or months. Symptoms during relapse include numbness or tingling, partial loss of sight, fatigue, and bladder and bowel problems, among others. Eventually, the relapse ends, followed by subsequent improvement. Symptoms gradually disappear, a period called a remission. During a remission, MS is still active and can still progress. Damage to axons (nerve fibers) can still occur even though there are no symptoms. Patients typically have attacks every 1-2 years although it can be more or less frequent than this.

Approximately 10 years after onset, about 50% of people with RRMS will slowly progress to secondary progressive MS (SPMS). Within 25 years, about 90% of people with RRMS will progress to the secondary-progressive type. In this stage patients slowly and steadily get worse. They may occasionally still have an attack or relapse of MS or they may stop having relapses altogether. The key thing is that they enter a phase of progressive worsening after they initially had relapsing/remitting MS. With primary progressive MS, which affects about 15% of patients, there is progressive steady worsening without the patient ever having had an attack or relapse of MS.

In rare cases (only about 5% of people with MS), an individual seems to combine features of different types of MS. This is known as Progressive Relapsing MS (PRMS). It is characterized by a progressive course from the onset, with only occasional relapses later in the disease. However, the progression doesn't appear to significantly alter long-term outcome.

After one or two attacks with complete recovery, people with benign MS do not worsen with time and there is no permanent disability. Benign MS can only be identified when there is minimal disability ten to fifteen years after onset. Initially it would have been categorised as relapsing-remitting MS. Benign MS tends to be associated with less severe symptoms at onset (e.g. sensory).

Although no cure exists at present for MS, the frequency and severity of attacks in RRMS may be reduced through treatments with injectable medicines, either beta interferon (Avonex, Betaseron, or Rebif) or glatiramer acetate (Copaxone). These chemicals regulate the immune response, reduce the number of attacks by approximately one-third, and may also decrease the severity of some relapses. Not all patients respond to these medicines. In general when someone with relapsing-remitting MS does not respond to one of these drugs or cannot tolerate its side-effects, another is tried. It is also not known whether interferon and glatiramer acetate can be given together, but studies are underway to determine whether combination therapy is helpful.

For treatment of severe acute relapses, a short course of a steroid medicine (methylprednisolone intravenously followed by prednisone orally) is usually prescribed; this treatment has been found to speed recovery from attacks. It can also cause nasty side effects which should be read up on by anyone considering being treated by them.

Progressive MS symptoms are less responsive to these MS therapies, although there is a role for the interferons in patients with progressive MS who are also having superimposed relapses.

Mitoxantrone (Novantrone) is an immune modifying drug that has recently been approved for patients with secondary progressive MS; it has many side effects, including suppression of the immune system and effects on the heart, and its long-term effectiveness is still not known.

It is also important to emphasise that many symptoms of MS can be successfully treated, including spasticity, bladder symptoms, sexual problems, and depression; several medicines are also available for the treatment of fatigue, although these are only partially effective.

Regular exercise and a healthy lifestyle is essential for all MS patients Finally, a trusting and unhurried working relationship with physicians and other health care providers is needed to ensure that the many possible problems related to MS can be optimally managed

Click here to read what it is like to live with MS on a daily basis