Ask the Doctor
By Dr. Jack Burks
Chief Medical Officer for MSAA
Does Age Affect Long-Term Therapy?
(Note: The questions below were sent in by two different clients.)
Q: (a) I was diagnosed with MS in 2003. I was on Avonex for three years, then Copaxone for seven years. I had no relapses and only mild further deterioration overall. My neurologist, an MS specialist, recently took me off my disease-modifying therapy because I turned 60 years of age. Can you comment on the relationship of age to the effectiveness of a long-term therapy?
(b) Is it true that after someone has been living with MS for 20 or 30 years, the need for one of the available disease-modifying drug therapies diminishes? After three or more decades of MS, does the course of the disease typically slow down or even stop in a significant number of cases, if any?
A: You have both asked a very controversial question. Does MS naturally “burn out” at a certain age and does the need for treatment go away? The subject is debated often and very little scientific data are available. In my many years of MS experience, I have found much variability exists between patients.
Before the discovery of DMTs, I thought many patients had slowing of their disease course after age 60 or 65. They clearly had fewer relapses, and the disease progression slowed. However, many still had disease progression and some continued to have relapses.
This leads to another very controversial question. If you stop having relapses, should you stop your disease-modifying therapy? The majority of neurologists with whom I discuss this issue say that they do not stop treatment. They believe that the reason the relapses have stopped, and the disability is less than expected, is because these drugs are working. Therefore, stopping the effective drug will expose a patient to a possible worsening of his or her disease.
In regard to the first question (a), your neurologist has a different viewpoint. I respect your neurologist’s position, but I am resistant to stopping a treatment that may be responsible for a good outcome, especially if the patient is tolerating the drug well. Stopping the drug may increase MS damage, and we may have more trouble getting this new disease activity under control. More research is needed before I would feel “safe” in withdrawing treatment. Is it worth taking the gamble?
I believe that this decision, like other MS-treatment choices, should be a “shared decision” between the doctor and the patient. There is no “one size fits all” with MS treatments. Most disease-modifying therapies are only in the body for a few days. If you do stop your Copaxone, I would suggest close monitoring for a possible increase in your MS disease activity, including an MRI evaluation. Should it occur, the MRI may detect early disease re-activation.
Q: In an earlier issue of The Motivator, I read that a woman was having trouble confirming if she has MS. I have been experiencing the same problem for the past two years. I am still getting tested, and even though the MRI showed that I have lesions, the doctors have told me that this is due to my diabetes. Do people with diabetes have brain lesions similar to people with MS?
A: Sometimes it is difficult to distinguish between MS and diabetes with brain lesions as shown on an MRI. However, many details can help to differentiate the two conditions. Some patients with diabetes may have MRI brain lesions due to small areas of ischemia (decreased blood flow), which may be confused with MS damage and vice versa. Often the neuro-radiologist can differentiate MS lesions from those with diabetes, when considering details such as lesion size, location, and with MS, their enhancement with gadolinium dye.
MRI damage seen in the spinal cord is most likely MS. Do you have lesions in your spinal cord? Spinal fluid analysis can often help to separate the two diseases, as can the responses in an eye test called “visual evoked potentials.” Additionally, MS usually causes relapses or attacks that affect various parts of the body. Diabetes lesions are often but not always “silent,” with no obvious flare-ups (relapses). MS symptoms usually begin before age 40, while lesions with diabetes often develop later.
In summary, while there is not one specific test for MS, findings from your medical/ neurological history, physical examination, MRI of the brain and spinal cord, spinal fluid analysis, visual evoked response test, and other tests can usually allow an MS expert to sort out the diseases. I also want to note that some MS patients also have diabetes, so these individuals would need to be treated for both illnesses. An opinion from a neurologist/MS expert is best in this type of situation.
Q: I am a 77-year-old mother of five. Two of my sons have died (one as a newborn) and another at age 27 (autopsy showed multiple blood clots). My surviving son is 57, disabled with heart problems, and has many symptoms of MS, but has not been diagnosed. My two daughters, ages 58 and 51, both have advanced MS — one with relapsing-remitting MS and the other with progressive MS.
My older children have a different father than my younger children. My first husband died in a car accident, and my second husband (also deceased) had Parkinson’s disease, as did his father. While I have no signs of MS, my maternal grandmother had a condition that may have been MS and left her bedridden for many years. Has the medical community come to any conclusions as to whether or not MS is hereditary?
A: This is an important question and thank you for bringing it our readers’ attention. Yes, a connection does exist between genetic factors, environmental factors, and infectious factors relating to the risk of getting MS.
Specifically, about 400 genes, mostly related to the regulation of the immune system, have been identified as being associated with MS susceptibility. This is a small number of genes compared to the entire gene pool.
What is the overall risk in the United States? Generally, the risk of MS in our country is about one in 1,000 people. If a close, blood relative has MS, the risk increases to 1 to 2 percent. If a non-identical twin has MS, the risk is 2 to 5 percent. For identical twins, if one has MS, the other twin has about a 30-percent risk for developing MS.
Caucasians have a higher risk than non-Caucasians. Women have a higher risk than men. Other risk factors may be related to a virus or viruses. Epstein-Barr virus is a leading candidate for association with MS risk. Smokers have a higher risk than non-smokers. And people with low vitamin D have a higher risk than people with normal Vitamin D.
In summary, many risk factors have been associated with MS. While genetics is among these factors, so far, no single “MS gene” has been found. Nonetheless, other risk factors can be lessened by not smoking and treating a Vitamin D deficiency with prescribed supplements. Research continues into the risk factors for MS.
Jack Burks, MD is the chief medical officer for MSAA. He is an international MS neurologist, writer, lecturer, and researcher, who assists with the development of new MS therapies and advises patients, families, MS organizations, and healthcare groups. Dr. Burks is a clinical professor of neurology at the Florida International University in Miami and has authored textbooks, chapters, and articles on MS.
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