Multiple Sclerosis : Treatment, Part 2

by Food and Drug Administration (FDA)

(Page 3 of 3)

"The most important thing in MS is not so much reducing flare-ups as preventing ultimate disability," Woodcock says. "We think the MRI lesions may be an indicator of disease progression and hope that Betaseron may prove to curtail disability as well as relapses. Post-market testing of the biologic will look into the relationships among treatment, MRI findings, and disability."

McFarland adds, "The study showed that over two years, the probability of not having a flare-up was 30 percent in patients on Betaseron as opposed to 20 percent for those on placebo. The figures don't knock you off your feet," he says, "but when you consider that every time you have an exacerbation you may accumulate some permanent disability, the results are significant."

Preliminary studies of another product, Copolymer 1, show this drug, too, may reduce the frequency of MS episodes. Now being tested in large-scale trials, Copolymer 1 has been available since January 1993 under a treatment IND — a special category that, under certain circumstances, allows patients with serious or life-threatening diseases early access to experimental drugs and biologics. Other possible new treatments under study include monoclonal antibodies, cytokines (chemicals produced by immune cells), and general immunosuppressive drugs.

Other current treatments — those most commonly used before Betaseron became available — are corticosteroids (prednisone or dexamethasone, for example) and the hormone ACTH, which stimulates the body to produce steroids. These drugs are given during flare-ups to help reduce inflammation and swelling, but they don't prevent new attacks. Often, McFarland says, steroids are given intravenously in high doses the first few days and then orally, tapering the dose for the next two to three weeks.

To ease symptoms, doctors can prescribe muscle relaxants like Lioresal or Atrofen (baclofen) for spasms and stiffness. Anticonvulsives such as Tegretol or Atretol (carbamazepine) can relieve facial pain and twitching, and Ditropan (oxybutynin), an antispasmodic that relaxes the bladder, may be given for incontinence.

Physical therapists can also help patients work on their muscle strength and coordination, balance, and stamina. Occupational therapists can introduce patients to devices that ease their lives in small and large ways, helping with everyday tasks of dressing and eating, for example.

For information on multiple sclerosis support groups and physician referrals, contact your local chapter of the National Multiple Sclerosis Society. For general information, write to the society's headquarters at 733 Third Avenue, Sixth Floor, New York, NY 10017.

Culprit Hard to Nail

Over the years, scientists looking for the cause of multiple sclerosis (MS) have pointed fingers at many possible culprits, but lacked sufficient evidence to nail any one with certainty.

The prime suspects include genes, viruses, and flaws in the immune system. Interest is also focused on a breach in the blood brain barrier, the gatekeeper that controls what substances pass from the blood into the nervous system.

MS is not a purely genetic disease, but its lower incidence or near total absence in some populations suggests genes influence susceptibility. For instance, Native Americans and African Americans have a lower incidence than European Americans living in the same region.

Also, the incidence in families is somewhat higher than expected in the general population. MS risk is difficult to calculate, partly because regional prevalence rates vary greatly and because risk varies with age, declining sharply after age 50. Based on an area with a high prevalence rate, the risk for people 20 to 50 years old has been calculated at 0.1 to 0.2 percent. In families with a history of the disease, the risk may be 2 percent or more — a 10- to 20-fold increase. And if a monozygotic (identical) twin has MS, the risk to the other twin — who shares the same genetic makeup — rises to 25 to 30 percent.

Experts believe MS is an autoimmune disease, in which the body mistakenly reacts against itself. A healthy immune system is finely tuned to respond to foreign substances, launching an attack to produce antibodies against the invader and then calling off the troops when the job is done. In autoimmune diseases, something goes awry and the system attacks the body's own tissues — myelin, in the case of MS. One theory proposes that the cells responsible for down-regulating immune activity are deficient in people with MS, allowing it to attack the central nervous system.

Finally, there has long been speculation that something in the environment provokes the problem in multiple sclerosis. Several observations support this idea. MS is more common in colder and temperate climates than in warmer ones. In the United States, it is more prevalent in the North than the South, and it is more common in northern Europe than southern Europe. People who migrate from a high-incidence area to a low-incidence area — or vice versa — before age 15 take on the risk of the new area. After age 15, they keep the risk of their area of origin. This suggests something that exerts an influence around the time of puberty.

Some evidence for a virus as a possible cause of MS comes from descriptions of disease clusters. One of the better known examples is the occurrence in the Faroe Islands between Iceland and Scandinavia. Before 1940, there were no known cases of MS in these islands, but shortly after World War II, a small epidemic of the disease occurred. The number of cases continued to climb for many years after. The island population had been relatively isolated before British troops arrived during the war. Some investigators believe the British, who are at high risk for MS, inadvertently spread a virus or other infectious agent they had brought with them.

Researchers have studied a possible link between MS and various viruses but have failed to find evidence of any specific one causing the disease. Still, there is interest in the prospect that one or more viruses may trigger an autoimmune response leading to the disease.

About the Author

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