Multiple Sclerosis

Definition

Multiple sclerosis (MS) is a chronic autoimmune disorder affecting movement, sensation, and bodily functions. It is caused by destruction of the myelin sheath (insulation) covering nerve fibers (neurons) in the central nervous system (brain and spinal cord).

Description

MS is a nerve disorder caused by destruction of the insulating layer surrounding neurons in the brain and spinal cord. This insulation, called myelin, helps electrical signals pass quickly and smoothly between the brain and the rest of the body. When the myelin is destroyed neuronal messages are sent more slowly and less efficiently. Patches of scar tissue, called plaque, form over the affected areas, further disrupting neuronal communication. The symptoms of MS occur when the brain and spinal cord nerves no longer communicate properly with other parts of the body. MS causes a wide variety of symptoms and can affect vision, balance, strength, sensation, coordination, and bodily functions.

Multiple sclerosis affects more than a quarter of a million people in the United States. Most people have their first symptoms between the ages of 20 and 40 years; symptoms rarely begin before 15 years or after 60 years of age. Women are almost twice as likely as men to get MS, especially in their early years. People of northern European heritage are more likely to be affected than people of other racial backgrounds, and MS rates are higher in the United States, Canada, and Northern Europe than in other parts of the world. MS is very rare among Asians, North and South American natives, and Eskimos. Between 10% and 20% of people with MS have a benign type, meaning their symptoms progress very little over the course of their lives.

Causes

Multiple sclerosis is an autoimmune disease, meaning its cause is due to an attack by the body's own immune system. For unknown reasons immune cells attack and destroy the myelin sheath that insulates neurons in the brain and spinal cord. This myelin sheath, created by other brain cells called glia, speeds transmission and prevents electrical activity in one cell from short-circuiting to another cell. Disruption of communication between the brain and other parts of the body prevents normal passage of sensations and control messages, leading to the symptoms of MS. The demyelinated areas appear as plaques, small round areas of gray neurons without the white myelin covering. The progression of symptoms is correlated with development of new plaques in the portion of the brain or spinal cord controlling the affected areas. Because there appears to be no pattern in the appearance of new plaques, the progression of MS is unpredictable.

Despite considerable research the trigger for this autoimmune destruction is still unknown. At various times evidence has pointed to genes, environmental factors, viruses, or a combination of these factors.

The risk of developing MS is higher if another family member is affected, suggesting the influence of genetic factors. In addition, the higher prevalence of MS among people of northern European ancestry suggests some genetic susceptibility.

The role of an environmental factor is suggested by studies of the effect of migration on the risk of developing MS. Age plays an important role in determining this change in risk. Young people in low-risk groups who move into countries with higher MS rates display the risk rates of their new surroundings, while older migrants retain the risk of their original home country. One interpretation of these studies is that an environmental factor, either protective or harmful, is acquired in early life. The risk of disease later in life reflects the effects of the early environment.

These same data can be used to support the involvement of a slow-acting virus, one that is acquired early on but begins its destructive effects much later. Slow viruses are known to cause other diseases, including Creutzfeldt-Jakob disease and bovine spongiform encephalopathy ("mad cow" disease). In addition, viruses have been implicated in other autoimmune diseases. Many claims have been made for the role of viruses, slow or otherwise, as the trigger for MS; however, as of 2001, no strong candidate has emerged.

How a virus could trigger the autoimmune reaction is also unclear. There are two main models of virally induced autoimmunity. The first suggests the immune system is actually attacking a virus (one too well hidden for detection in the laboratory), and the myelin damage is an unintentional consequence of fighting the infection. The second model suggests the immune system mistakes myelin for a viral protein encountered during a prior infection. Primed for the attack, the immune system destroys myelin because it resembles the previously recognized viral invader.

Either of these models allows a role for genetic factors, since certain genes can increase the likelihood of autoimmunity. Environmental factors, as well, might change the sensitivity of the immune system or interact with myelin to provide the trigger for the secondary immune response. Possible environmental triggers that have been invoked in MS include viral infection, trauma, electrical injury, and chemical exposure—although controlled studies have not supported a causative role.