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The Uses of Botulinum Toxin in Multiple Sclerosis
August 2005—Since the approval in mid-2002 of Botulinum Toxin Type A for the temporary improvement of facial wrinkling, botulinum toxins have received a great deal of publicity. In addition to their cosmetic uses, however, the toxins have a variety of medical applications, including some for people with MS.
There are seven botulinum toxins (labeled A to G). All are powerful neurotoxins (poisons) that block the release of acetylcholine at the junction of nerves and muscles. Acetylcholine is a chemical that, among other things, signals muscles to contract. Blocking the acetylcholine results in the temporary relaxation of targeted muscles. This action of botulinum toxins makes them potentially useful in the treatment of MS-related muscle stiffness (spasticity) and urinary symptoms caused by detrusor-sphincter dyssyndergia1 or detrusor hyperreflexia2.
Botulinum toxin was first identified in 1897 as the cause of the type of food poisoning subsequently known as botulism. It wasn't until 1949 that botulinum toxin type A was shown to block signals at the neuromuscular junction. In 1989, the U.S. Food and Drug Administration (FDA) approved its use for the treatment of two muscle disorders of the eye (blepharospasm and strabismus). The botulinum toxin type A currently available in the United States is called Botox® (manufactured by Allergan, Inc.). Botulinum toxin type B is also being evaluated for use in spasticity and other conditions.
Although Allergan, Inc. has not applied for FDA approval of Botox® treatment of MS-related symptoms, many MS physicians now consider it an effective treatment option for certain types of problems. Botox® injections have been shown in clinical trials to relieve spasticity in individual muscles for up to three months, without any significant side effects. The toxin can be delivered by injection directly into an overactive muscle that has not responded to the first-line oral medications such as baclofen (Lioresal®) and tizanidine (Zanaflex®). While the oral medications continue to be the most effective strategy to manage generalized spasticity of the upper and lower limbs, Botox® is considered by many physicians to be an additional strategy for temporary management of severe spasticity in an isolated area.
Botox® has also demonstrated its usefulness in the management of certain types of urinary symptoms. Injected into the external urinary sphincter, Botox® helps to relieve the urinary urgency, frequency, dribbling, retention, and infections that can be caused by detrusor-sphincter dyssynergia. Treatment benefits, which typically last a minimum of three months, can relieve voiding problems and reduce a person's need for intermittent self-catheterization or an indwelling catheter. No significant complications or side effects have been reported. Most recently, Schurch and colleagues reported in the Journal of Urology (2005 Jul;174(1):196-200) on a small, placebo-controlled study of Botox Type A to treat urinary incontinence caused by detrusor hyperreflexia in people with spinal cord injury (N=53) and MS (N=6). Compared to the placebo group, patients receiving a single injection of either 200U or 300U of Botox into the detrusor muscle experienced a reduction in episodes of incontinence, improved bladder function, and improved quality of life over a six-month period, with no significant adverse effects.
Further, large-scale clinical trials are needed before FDA approval is sought for Botox as a treatment of MS-related symptoms. In the interim, some third-party payers may not cover the cost of Botox for treating spasticity or bladder dysfunction. People who seek treatment with Botox for either of these symptoms will need to cover the relatively high costs themselves.
If you have questions about the use of Botox® for the treatment of spasticity or urinary symptoms, please consult your healthcare provider.
1Detrusor-sphincter dyssynergia: A type of neurogenic bladder dysfunction in which simultaneous contractions of the bladder's detrusor muscle and external sphincter cause urine to be trapped in the bladder, resulting in symptoms of urinary urgency, hesitancy, dribbling, and incontinence.
2Detrusor hyperreflexia: A type of neurogenic bladder dysfunction, also referred to as urge incontinence, in which a sudden strong need to urinate, immediately followed by a contraction of the detrusor muscle of the bladder, results in an involuntary loss of urine.
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