More MS news articles for November 2000

Q&A on Multiple Sclerosis treatments

News staff writer
The Birmingham News

Dr. John N. Whitaker, chairman of the Department of Neurology at the University of Alabama at Birmingham and a former president of the American Neurological Association, is a nationally recognized expert on multiple sclerosis.

Whitaker, who is medical director and chairman of UAB's Multiple Sclerosis Center, recently answered questions about MS research and treatments of the future.

Where do we stand in the treatment of MS, given the introduction, beginning in 1993, of drugs that delay the disease.

It's a very different day now than it was eight years ago. We've made substantial headway in treating those early cases and slowing down the disability.

We're trying to keep the disease from progressing, and keep the nerve fibers from being damaged. I think making a decision to start a drug early, to try and delay or prevent future attacks and lessen the damage is certainly important.

What advances in treatments are being developed?

There are three major approaches to treatment: Reduce the number and intensity of attacks, which are called relapses; prevent progression of the disease; and treat symptoms, such as spasticity of the legs, fatigue, and bowel and bladder dysfunction.

Right now a form of cortisone is the preferred drug to manage relapses. Several other drugs are being looked at to not only lessen the length of an attack, but also to prevent future attacks. Steroids don't do that.

Another of the big changes in the next few years will be better application and understanding of MRI, or magnetic resonance imaging. MS is a long-term disease. It goes on for decades. You are trying to treat something now, hoping that 20 years from now the patient will be much better.

Trying to predict that is very difficult; we look for something called a surrogate marker. And the test for that primarily is MRI of the brain and spinal cord. MRI advances will allow us to modify the treatment of MS patients long before they show the disability that has been the common hallmark of this disease.

In regard to symptomatic relief, I think that you'll see drugs come along, in particular, to treat fatigue. That's one of the most bothersome symptoms that patients have. It's a fatigue that is probably not seen in quite the same way in other diseases.

How close are we to finding the cause of MS?

No. 1, the disease is probably more than one disease. Thus, different people within the large category of MS require different treatments. To understand that will require the study of pathology as well as the MRI. Secondly, we must understand the origin of the disease, which is the combination of genetics and exposure to something in the environment - we suspect it's a virus, but not the same virus in every instance. And finalization of the human genome project will give us a lot more insight in terms of picking out those genetic markers which require the most attention in understanding the disease and perhaps even treating it.

What's the outlook for an oral form of medication to slow progression of MS?

There is currently a multi center Phase III trial going on with oral Copaxone. The drug that has previously been injected every day has now been formulated into an oral tablet form and given by mouth.

This form of Copaxone seems to be well tolerated by patients and seems to have a remarkable effect on animals with the disease model. So the trial's going on right now. And we should have the result on that probably by the early part of 2002, which is a fast trial in MS. We're a part of that trial at UAB. The entry into that trial is among the fastest ever in MS. Patients really do not like giving themselves shots.

What about people who have had MS for years, are disabled and severely afflicted? Is there any help on the horizon?

We just have to realize that there are some things we cannot help. We are involved, along with the bone marrow transplant unit here, in a new trial using bone marrow transplantation for some of the most severely affected patients. There are also a number of highly experimental treatments going on around.

But those patients, by and large, have not only the myelin sheath affected, but the nerve fiber around which the sheath goes has also been badly damaged. So recovery or reversibility is unlikely to occur.

© 2000 The Birmingham News.