Botulinum toxin for the management of muscle overactivity and spasticity after stroke

Abstract

Stroke is a major cause of disability involving the arm and leg. This disability results from the upper motoneuron syndrome (UMN) evident after stroke. It is commonly associated with spasticity and muscle overactivity, which can lead to abnormal limb posturing that interferes with active and passive function. The origin of limb deformity in patients with UMN is based on the concept of unbalanced agonist and antagonist muscle forces acting across joints. In the past decade, botulinum toxin A (BTX-A) a new medication that modifies muscle force and, hence, can treat muscle imbalance, has become available and has renewed interest in the management of muscle overactivity and spasticity after stroke. A reduction in muscle tone, painful spasms, and improved functionality can be obtained. Research and clinical reports support the concept that chemodenervation with BTX-A is an excellent intervention for treating focal muscle overactivity and spasticity secondary to stroke. Many muscles differing in size, shape, and location have been injected, and clinical effectiveness is particularly notable in elbow flexors, ankle plantar flexors, and smaller limb muscles, such as intrinsics of the hand and wrist. Smaller muscles are readily accessible for injection and require smaller amounts of toxin.