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Managing Spasticity in MS

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Vol. 13 •Issue 7 • Page 65
Managing Spasticity in MS

Botulinum toxin injections can effectively treat spasticity, which affects 47 percent of the MS population.

Nearly 9,000 new cases of multiple sclerosis (MS) are diagnosed each year in the United States, affecting more than 250,000 people and their families.1 MS is a chronic, progressive disease of the central nervous system that's probably autoimmune in nature.

After decades of disappointing progress, recent research has uncovered new treatments that arrest or slow progression of certain MS subtypes. Even with these great strides, it's difficult to deter the late, debilitating stages of the disease or determine how long it may take to find a cure. Until that cure arrives, helping people maximize and maintain quality of life and mobility remains a cornerstone of treatment.

Disabling Symptoms

MS brings an array of disabling symptoms, among them fatigue, depression, sleep disturbances, tremors, ataxia, dizziness, visual changes, weakness, pain and spasticity.2,3

Spasticity in the upper and lower extremities often contributes to pain, joint contractures and skin breakdown. In addition, it can significantly limit ambulation, activities of daily living (ADLs) and perineal hygiene.

Spasticity is one of the most common complications, and it occurs at some point in the disease process in approximately 47 percent of people with MS.4 Spasticity is velocity dependent resistance (tone) with passive stretch of a muscle, a "clasp-knife" response. However, pathophysiology and manifestations are likely more complicated. Patients complain of muscle stiffness, which occurs at rest (static tone) or during activity (dynamic tone).

Measuring Spasticity

Spasticity severity, regardless of etiology, is measured using the Ashworth scale and, more commonly, the modified Ashworth scale (MAS.) These measures are ordinal scales ranging from 0 (no tone) to 4 (unable to passively move a joint). When assigning clinical significance to scores, raters should recognize the inherent daily and hourly variability of tone and various patient factors, such as being in a supine vs. upright position, talking and stress. These factors may increase tone.

Mild spasticity may not affect function. However, in severe forms, joints can become completely immobile and frozen, which leads to pain, immobility and problems with self-care and hygiene.

Making the clinical distinction between a fixed contracture and an MAS of 4 can be difficult, since both scenarios produce an immovable joint. Diagnostic peripheral nerve blocks using a short-acting anesthetic, such as polocaine or bupivicaine, can help distinguish between severe tone and a fixed contracture.5

Spasticity Scenarios

Spasticity in MS occurs as spastic hemiparesis (arm and leg on one side), spastic paraparesis (both legs) or spastic quadraparesis (all four extremities.) The first two scenarios can present in ambulatory patients; spastic quadraparesis develops in later stages of MS.

To select a proper treatment strategy, clinicians must understand the implications of generalized and focal spasticity. Generalized spasticity affects several muscle groups in two or more limbs; focal spasticity affects only a few muscles in one or two limbs. A generalized distribution is more common in people with MS, but the two can occur together.

For example, with mild spastic paraparesis (generalized), dynamic adductor tone (focal) may cause a scissoring-type gait and gait instability. In nonambulatory patients with para- or quadraparesis, severe bilateral adductor muscle spasticity can lead to significant limits in perineal hygiene, bladder catheterization or skin care. In both cases, treatment of focal spasticity can play a vital role in the setting of generalized tone.

Managing spasticity includes physical and occupational therapy, oral medications, botulinum toxin (BT) injections, and nerve or motor point blocks using phenol or alcohol. Surgery includes orthopedic release or placing an intrathecal bacolfen pump.

BT injections are symptomatic treatments only. Therefore, they don't affect the underlying disease course. Approved by the Food and Drug Administration for tortocollis and blephrospasm, BT for spasticity is an "off-label" use of the medication. Only a few serotypes of BT are used clinically. The most common agents are botulinum toxin A (Botox® or Dysport®, which isn't available in the United States) and type B (Myobloc®). The basic BT mechanism temporarily inhibits release of the neurotransmitter acetylcholine into the neuromuscular junction, which causes muscle relaxation. Side effects slightly differ between types. Mild flu-like symptoms occur with type A; dry mouth can accompany type B.6 BT is also used in MS for bladder management and painful spasms.7

A rehab team often plays a critical role in BT treatment. At our facility, a team of physiatrists, physical therapists and occupational therapists assesses MS patients with spasticity. An assessment includes documenting static and dynamic tone during activities, such as walking or self-care. Using gait laboratories and motion analysis during these evaluations can help, if these methods are available.

Focus on Function

The concept of "primary impairment that leads to disability" is crucial to spasticity assessments. Other symptoms, such as weakness, poor balance or incoordination, may be more significant issues to ambulation or self-care than spasticity. If this is the case, BT or other treatment approaches to spasticity probably will not improve function.

If spasticity is a significant limitation, the rehab team should determine which specific muscles affect functional activities. Again, the distribution can be generalized, focal or mixed. BT works best when functionally significant spasticity involves only a few key muscles in one or two extremities.

Treatment for generalized distribution of tone can include oral medication or a trial of intrathecal bacolfen (ITB.) Nerve blocks or motor point blocks also can improve focal tone, depending on the involved muscle groups or accessibility of the peripheral nerve to the muscle group. In some cases, BT may be appropriate to treat patients who decline or can't tolerate oral medications, phenol or ITB.

Referral to Rehab

Patients can be referred to physical and occupational therapy before treatment to help delineate functionally significant muscles to target injections. After BT treatment, rehab can focus on range of motion, gait retraining and functional upper extremity activities to restore movement and strength that was previously prohibited by severe muscle stiffness.

After identifying the functionally significant muscle, a physician must determine the correct dose of BT, which is injected into one to four sites in affected muscles using a small-diameter needle. This allows precise localization. The dose and number of sites depend on muscle size and BT dilution. The injection is guided by direct electrical stimulation, with visual confirmation of muscle contraction or electromyographic guidance with auditory feedback.

Only a few studies have examined using BT in MS.7,8 Snow et al. injected 400 units of Botox into hip adductor muscles in a double-blind, randomized crossover study. While the study showed statistically significant improvements in tone and hygiene, BT didn't affect muscle spasm frequency. (The study, however, didn't use standardized outcome measures—a shortcoming.)

In another study, Grazko and colleagues treated four people with MS among a larger group of 12 with Botox.9 They focused on hamstrings, elbow flexors and adductor muscles. Although they didn't include functional measures, they reported a consistent two-point drop in an Ashworth score in treated muscle groups.

In a larger sample size, Hyman et al. studied Dysport in 74 patients with advanced MS and adductor muscle spasticity.10 Patients who received BT improved passive range of motion, MAS scores and perineal hygiene. They observed mild side effects in 55 percent of Dysport patients and 63 percent of placebo patients. Interestingly, the placebo groups also showed substantial improvements. While these findings are encouraging, clinicians need to continue studying functionally oriented outcome measures.

Reducing tone is the starting point to improve all functional activities, such as walking, transfers, self care, hygiene and skin care. For people with MS, that can make all the difference to maximizing quality of life.

References

1. Barnes, M.P., Kent, R.M., Semlyen, J.K., & McMullen, K.M. (2003). Spasticity in multiple sclerosis. Neurorehabilitative Neural Repair, 17, 66-70.

2. Brashear, A. et al. (2002). Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke. New England Journal of Medicine, 347, 395-4000.

3. Glenn, M.B. (1990). Nerve blocks. In M.B. Glenn & J. Whyte (Eds.), The practical management of spasticity in children and adults (pp. 227-258). Philadelphia: Lea and Febiger.

4. Grazko, M.A., Polo, K.B., & Jabbari, B. (1995). Botulinum toxin A from spasticity, muscle spasms, and rigidity. Neurology, 45, 712-717.

5. Hyman, N. et al. (2000). Botulinum toxin (Dysport®) treatment of hip adductor spasticity in multiple sclerosis: A prospective, randomized, double blind, placebo controlled, dose range study. Journal of Neurology, Neurosurgery and Psychiatry, 68, 707-712.

6. Moore, A.P. (2002). Botulinum toxin A (BoNT-A) for spasticity in adults. What is the evidence? European Journal of Neurology, 9(suppl), 42-47.

7. Restivo, D.A. et al. (2003). Botulinum toxin treatment of painful tonic spasms in multiple sclerosis. Neurology, 61, 719-720.

8. Noseworthy, J.H. (2003). Management of multiple sclerosis: Current trials and future options. Current Opinion in Neurology, 16, 289-297.

9. Snow, B.J., Tsui, J.K.C., Bhatt, M.H., & Varlas, M. (1990). Treatment of spasticity with botulinum toxin: A double blind study. Annals of Neurology, 28, 512-515.

10. Thompson, A.J. (2001). Symptomatic management and rehabilitation in multiple sclerosis. Journal of Neurology, Neurosurgery and Psychiatry, 71 (suppl), ii22-ii27.

Michael W. O'Dell, MD, is professor of clinical rehabilitation medicine at the Weill Medical College of Cornell University in New York. He's associate chief and medical director of inpatient rehabilitation in the department of rehabilitation medicine at New York-Presbyterian Hospital. Dr. O'Dell also works with the Nancy Davis Foundation Center Without Walls, a national network of the top six MS research centers, based in Los Angeles. The foundation's collaboration of physicians, scientists and clinicians develops research programs and therapeutic approaches for MS. Gina Sauro, PT, and Lisa Rivera, OTR/L, are on staff at New York-Presbyterian Hospital and contributed to the article.




     

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