Spasticity After Stroke
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Spasticity is a common complication after stroke where muscles become excessively tight. It can interfere with activities like dressing, hygiene, and mobility. Treatment involves therapeutic exercises, oral medications like baclofen and dantrolene, botulinum toxin injections into affected muscles, and intrathecal baclofen pumps for severe lower extremity spasticity. The goals are to improve positioning, mobility, pain, and prevent contractures while easing care requirements. A physiatrist can properly assess spasticity and coordinate multi-modal management tailored to individual patient goals.
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Spasticity After Stroke
- 1. Spasticity After Stroke Heather Walker, M.D. Assistant Professor Department of Physical Medicine & Rehabilitation UNC-Chapel Hill
- 5. Spasticity can be defined as increased tightness in affected muscles
- 16. Botulinum Toxin Type A (BOTOX ® ) : History of Development 1944 1920s 1895 Botulinum toxin type A first isolated Dr. Schantz begins investigation C. botulinum identified Dr. Scott initiates first therapeutic testing in humans 1978 1989 FDA approval of BOTOX ®
- 25. QUESTIONS???
Editor's Notes
- Detailed PT and OT evaluations provide specific information about the patient’s baseline status, so that changes can be documented as treatment progresses. This detailed information provides the framework for developing the therapy program. Comparison of pre- and post-intervention status can also be useful to justify payment for treatment from third party providers. Therapists can also provide helpful input on whether a patient might benefit from a specific type of intervention, working in conjunction with neurologists, physiatrists, orthopedists, and others involved in the patient’s care. Establishing realistic goals is crucial in determining which treatment or combination of treatments will be beneficial to a patient. Both short and long term goals must be established before a therapy treatment program begins. It is important to educate not only the patient but all family members and other caregivers who may be involved in the patient’s care. Providing the practical details of the planned surgical or medical intervention helps to educate them, allay fears of the unknown, and encourages them to work with the treatment team to develop reasonable goals and expectations. Patients and families often want and need to know the details, such as how long surgery will take, and what can be expected afterwards in terms of pain, swelling, and decreased mobility. Providing explicit information regarding the need for increased help with self-care activities, and how long that help will be needed, allows everyone to be better prepared. The PT/OT program needs to be coordinated with all other medical professionals involved in the patient’s care. This takes extra time and effort on everyone’s part, but definitely pays off in the long run.
- Stretching and ROM exercises are implemented for the purpose of decreasing contractures and increasing the dynamic range available for functional activities. Myofascial and joint mobilization should be added to the patient’s exercise program as indicated. Active assistive, active and resistive exercises improve strength and increase motor control. The patient who has undergone intervention to reduce spasticity often will demonstrate significant weakness in the previously spastic muscle(s); with less interference from spasticity and synergies, he can work more effectively on strengthening the involved muscles. The patient with severe spasticity may demonstrate involuntary co-contraction of muscles around a joint, impairing voluntary movement. However, voluntary co-contraction is an important component of volitional movement. It is used for proximal stabilization, allowing free distal purposeful movement. Co-contraction is also needed for “turn-around”, the transition from one movement to another. The program should include exercises that will increase the patient’s endurance as well. Improved endurance and more efficient movement will result in decreased energy expenditure.
- In slightly more than 100 years, our knowledge of botulinum toxin type A has expanded from the identification of the bacterium Clostridium botulinum to the commercialization of botulinum toxin type A, as BOTOX ® . C. botulinum was first identified in the late 1890s. In the 1920s a crude form of botulinum toxin type A was isolated by Dr. Herman Sommer and his colleagues at the University of California. Other scientists conducted further purification studies over the next 20 years. In 1944, Dr. Edward Schantz began his investigations with botulinum toxin type A (Schantz, Johnson, 1997). In the late 1960s, Dr. Alan Scott sought a substance that could be used to weaken eye muscles as an alternative to surgery for patients with strabismus. Dr. Schantz provided him with several substances to test, one of which was botulinum toxin type A 900 kD complex (Schantz, 1994). In the 1960s and 1970s, Drs. Schantz and Scott continued their research with botulinum toxin type A, including testing the compound in nonhuman animals. In 1978, Dr. Scott initiated the first tests of botulinum toxin type A in humans for the treatment of strabismus. In 1989, BOTOX ® was approved by the FDA (at that time the product was called Oculinum ).
- BOTOX ® is a focal therapeutic that is injected directly into muscles. It acts on peripheral cholinergic neurons to inhibit acetylcholine release, which reduces contractions and relaxes muscles. Local injection of BOTOX ® is associated with several advantages. First, treatment can be targeted to the specific muscles that are causing the symptoms. Second, when used at recommended doses, BOTOX ® is not expected to result in systemic, overt distant clinical effects. The beneficial effects of each injection last approximately 3 months, at which time patients may return for reinjection. Injections can be repeated as long as the patient continues to respond and doesn’t experience an allergic reaction.