Spasticity is characterized by increased muscle tone, exaggerated tendon jerks, and poor control of voluntary movement that occurs as part of an upper motor neuron syndrome. Patients with spasticity are at high risk of sustaining rheologic changes to the involved muscles, ultimately leading to contractures and painful limb deformities. The principal goal of spasticity management is to prevent irreversible soft-tissue changes and tendon contractures by maintaining muscle length and normal limb positioning.
Treatment options ranging from conservative to aggressive measures, including physical and occupational therapies; oral and intrathecal medications; surgery; and focal chemical denervation with phenol, alcohol, and botulinum neurotoxin (BoNT). Therapy is dictated by the duration, distribution, and severity of disease. Management of spasticity is driven by patient needs and long-term functional goals (Figure 1, page 672).
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FIGURE 1 Algorithm for the management of spasticity with botulinum toxin. The development of a spasticity management program begins with an evaluation of the upper motor neuron syndrome and the determination that spasticity is interfering with patient function. By carefully defining the goals of treatment, the components of the treatment plan are established. For some patients (e.g., those with spinal cord injury), an important initial treatment may be the removal of noxious stimuli, such as tight orthotics or ingrown toenails. Range-of-motion exercises are indicated for almost all patients to prevent contrac-ture. Oral medications, phenol neurolysis, surgery, and intrathecal baclofen may be useful in properly chosen patients. Botulinum toxin (BTX) therapy is often the appropriate treatment for patients with spasticity who have focal, dynamic (not fixed) contracture, if spasticity is interfering with function. Careful definition of the goals of BTX therapy is necessary before treatment proceeds.The clinical team helps patients and caregivers identify and clarify goals, and it evaluates the suitability of BTX to meet these goals. Outcome measures, selected for their relevance to the expected benefits of treatment, are applied before the first injection and then again at an appropriate interval following treatment. An initial dose may be determined from the accompanying dosing chart, but most clinicians adapt and modify these guidelines based upon the individual patient’s response to therapy. In the treatment of spasticity, BTX injection is almost never used as monotherapy, and adjunctive treatments including physical interventions (range-of-motion exercises, serial casting, or strengthening programs) are instituted or modified after the injection.
BoNT exists as seven immunologically distinct serotypes— A, B, C1, D, E, F, and G. These serotypes are produced by the anaerobic, gram-positive, spore-forming bacterium Clostridium botulinum. Three principal clinical formulations of BoNT are in use worldwide:
- two BoNT-A formulations: Botox (Allergan, Inc.) and Dys-port (Ipsen, Ltd.)
- a BoNT-B formulation, Myobloc/Neurobloc (Solstice Neurosciences, Inc.)
Of these, Botox and Myobloc have been approved by the Food and Drug Administration (FDA) for clinical use in the U.S., although neither agent is indicated for the treatment of spas-ticity. These formulations are unique and should not be considered generic equivalents or interchangeable, because they differ in manufacturing, units of activity, and clinical potency.
When the goals of BTX treatment have been defined and outcome measures chosen, evaluation of the treatment’s success should be straightforward.When the goals of patients or caregivers have not been met despite functional improvement, the clinical team works with them to re-evaluate their expectations. When the functional or technical goals of treatment have not been met, some modification of muscle selection, injection technique, or adjunctive therapies might be needed. Continued lack of efficacy even with optimal technique and muscle selection suggests that the patient was poorly selected for BTX therapy, the technical goals were inappropriate, or the patient was resistant to BTX. Antibody or frontalis muscle testing may be indicated in this situation. Successful treatment does not obviate the need for re-evaluation of goals, the treatment program, or the dose and injection site.These matters are routinely considered at the follow-up visit, and adjustments made as needed or desired. As always, patients and caregivers remain at the center of the decision-making process. ADL = activities of daily living; CP = cerebral palsy; CVA = cerebro-vascular accident; MS = multiple sclerosis; OT = occupational therapy; PT = physical therapy; SCI = spinal cord injury; TBI = traumatic brain injury. (Adapted from The We Move Spasticity Study Group. In: Mayer NH,Simpson DM, eds. Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin. New York: 2002. Reprinted with permission from We Move,2006.)
Clinically, BoNT is administered intramuscularly. It reduces neuromuscular transmission by modulating the release of acetyl-choline and other vesicular neuropeptides from nerve termi-nals. It is safe and effective in the treatment of various conditions characterized by muscle overactivity such as cervical dystonia. Its safety and efficacy in the treatment of adult focal spasticity are discussed in this evidenced-based review.