STILL STALKING MS
It comes like a thief. By attacking the nervous system, it steals mobility and independence from many of its victims. And it cheats by mimicking other neurological diseases. Many decades after medical science first noticed the disease, multiple sclerosis still eludes "capture' by those seeking causes and hunting possible cures for a disease that preys on some 2 million people worldwide.
Added to this evasive trickery is increasing concern that the focus on a relative newcomer called AIDS will dilute efforts to fight disorders like multiple sclerosis. Yet scientists at last month's meeting in Washington, D.C., of the International Federation of Multiple Sclerosis Societies discussed their varied research results in hopeful terms, convinced that data on other diseases will also bolster knowledge about multiple sclerosis. Tying together results from diverse research projects, however, may prove as challenging as solving the mysteries of multiple sclerosis has been in the past.
It is well established that certain cellular changes in the brain and spinal cord result in the many faces of multiple sclerosis. Nerve-cell extensions called axons are coated with a fatty sheath of myelin, produced by cells called oligodendrocytes (see drawing). These large cells send out thin fingers of myelin that wrap around axons in concentric circles to form the sheaths--which are conduits for messages between the central nervous system and the rest of the body.
But if the myelin sheath is destroyed by scavenging cells from the immune system, scar-like areas called plaques are formed (see photos). With their demyelinated nerve cells, the plaques disrupt proper nerve transmission. This short-circuiting phenomenon leads to a broad range of symptoms in multiple sclerosis, the most common of the demyelinating disorders. Symptoms like weakness, tremors and impaired vision usually first appear between the ages of 20 and 40 years of age, with twice as many women as men developing the disease. The complex course of the disease ranges from mild to severe, and is either progressive or chronic with relapses and remissions-- sometimes changing from one form to the other.
Among the experimental treatments being tested now for multiple sclerosis are transplanting myelin-producing oligodendrocytes into animals' brains and using drugs that "fiddle with' electrical impulses in the brain so messages can be transmitted without myelin, according to Byron Waksman of the New York-based National Multiple Sclerosis Society. He says the ultimate goal is a vaccine for those at risk of developing multiple sclerosis. But it is doubtful that this goal will be achieved by taking a straight-and-narrow approach to research.
Scientific discovery in multiple sclerosis has followed a convoluted route, passing through the fields of genetics, virology and immunology. On the basis of data from this research, many now believe that viral infection serves as an environmental "trigger' in the disease, activating a malfunctioning immune system in those already genetically predisposed to it. At last month's meeting, scientists presented recent data supporting this multifaceted theory.
Early evidence for a genetic component in multiple sclerosis came from family and twin studies done by federal agencies. Among those early results was the observation that there is a higher frequency of the disease among identical twins than among nonidentical twins. Also supporting genetics as a factor was a series of epidemiologic surveys showing that the disease is concentrated in certain parts of the world. It is very rare among those living near the equator, for example, and most common in the temperate zones of Canada, the United States, South America and Europe.
There also are unexplained pockets of both the disease and resistance to it. On the Shetland and Orkney Islands near Scotland, the percentage of the population with the disease at any given time is three times the prevalence seen in nearby countries. …