International Journal of MS Care
page 1, Volume 3, Issue 4
Robert M. Herndon, MD
Dr. Herndon is Director of the Department of Neurology at the Veterans Affairs Medical Center in Jackson, Mississippi; Professor of Neurology at the University of Mississippi Medical Center; and Editor-in-Chief of the International Journal of MS Care.
Suggested citation: Management of Spasticity in Multiple Sclerosis. Herndon, RM. Int J MS Care. December 2001;3(4).
Spasticity in multiple sclerosis (MS) can be a blessing or a curse. It is a blessing in that it adds strength to the support muscles that hold us erect against gravity when those muscles have been weakened due to loss of input from the upper motor neurons. When we look at strength in a spastic leg, we find that the weakest muscles are those that pick up the leg (ie, the hip and knee flexors and the ankle dorsiflexors). The strongest muscles are the quadriceps, which extend the knees; the glutei, which extend the hip; and the gastroc-solei, which plantar flex the ankle. Picking up the leg is typically much more difficult than standing. One aspect of spasticity is loss of the precision of muscle control. It is hard to partially relax a spastic muscle; consequently, going down stairs is typically more difficult for patients than going up stairs. The muscle is strong enough to lift the body’s weight, but when an attempt is made to bend the hip and knee, the muscle is likely to give way because the gradations in contraction necessary to hold one’s weight with the knee bent cannot be accomplished.
The resulting stiffness and abnormal pull on joints from spasticity can cause many problems, including abnormal stresses on joints, particularly the knees; muscle pain and soreness; and flexor and extensor spasms. Flexor spasms, in which the knees pull up to the chest periodically or with a minimal stimulus, can be troublesome and make sitting in a chair difficult. Extensor spasms, which cause the body and legs to extend, can push an individual out of his or her chair or cause the individual to tip over backwards. Spasticity in the adductor muscles of the legs makes perineal hygiene difficult, interferes with sexual activity, and can cause pressure problems where the knees rub together.
Management of spasticity can be helpful, but considerable care must be taken. Available medical treatments include baclofen, tizanidine, dantrolene, and diazepam. All of these are sedating at therapeutic doses, and many patients cannot get adequate muscle relaxation without too much sedation. Additionally, all of these medications cause weakness, so that adequate control of spasticity almost invariably causes some weakness in addition to some sedation. The dose of a muscle relaxant used to manage spasticity is “enough and not too much.” The goal is to reduce spasticity without causing too much weakness.
In those patients who cannot get adequate muscle relaxation without too much sedation, intrathecal baclofen may be a useful option. By providing a high local concentration in the lumbar cord with a very low systemic concentration, muscle relaxation can be accomplished without sedation.
As indicated in the paper by Jarrett
et al, a goal-oriented approach is important. Individuals who are to undergo
intrathecal baclofen therapy need to understand what the therapy can and
cannot do. It will not improve the tradeoff between spasticity and weakness.
Added weakness in the legs may make standing more difficult or impossible
while improving other problems caused by the spasticity. However, with
a clear understanding of what can be accomplished, most patients in whom
intrathecal therapy is indicated will be happy with the results.
© 2001 International Journal of MS Care