[ARTICLE] Spotlight on botulinum toxin and its potential in the treatment of stroke-related spasticity – Full Text HTML/PDF

Abstract: Poststroke spasticity affects up to one-half of stroke patients and has debilitating effects, contributing to diminished activities of daily living, quality of life, pain, and functional impairments. Botulinum toxin (BoNT) is proven to be safe and effective in the treatment of focal poststroke spasticity. The aim of this review is to highlight BoNT and its potential in the treatment of upper and lower limb poststroke spasticity. We review evidence for the efficacy of BoNT type A and B formulations and address considerations of optimal injection technique, patient and caregiver satisfaction, and potential adverse effects of BoNT.

Introduction

Spasticity is a velocity-dependent increase in muscle tone as a part of the upper motor neuron syndrome and is seen in a wide variety of neurologic diseases including stroke.1 Poststroke spasticity can develop as early as 1 week after stroke,2 and it is estimated to occur in up to one-half of stroke survivors.3 The most frequent predictors of spasticity include weakness and reduced motor control.2 Long-term spasticity may lead to tendon contractures and limb deformities that can cause significant pain and functional impairment. Depending on the location of the spasticity, this can impact mobility, activities of daily living such as toileting, dressing, and transferring, and quality of life (QoL) and increase the dependence on caregivers.4

The aim of the treatment in poststroke spasticity is focused on muscle limb overactivity reduction. Treatment modalities are used to alleviate spasticity including physical therapy, systemic and intrathecal medications, and surgery. Systemic medications can be helpful if spasticity is generalized. Agents such as baclofen (gamma-aminobutyric acid [GABA]-B receptor agonist) diazepam (GABA-A receptor agonist), dantrolene (decreases calcium release from skeletal muscle sarcoplasmic reticulum), or tizanidine (TZD; alpha-2 adrenergic receptor agonist) often have systemic side effects such as dry mouth, dizziness, sedation, or generalized weakness.5 After several months of treatment, tolerance may develop to systemic medications.

Chemodenervation and neurolytic procedures with alcohol or phenol may be utilized as second-line management. These techniques are more localized and are injected perineurally to destroy the nerve causing spasticity. The effect may be limited by partial nerve regeneration and adverse effects such as bladder, bowel, and sexual dysfunction.6 Intrathecal baclofen acts on GABA receptors in the lumbar spinal cord and may improve walking speed and functional mobility in poststroke spasticity. However, this therapy is invasive and limited by side effects including nausea, vomiting, and urinary retention. Overdosing may lead to death.7,8

The aim of this review is to highlight botulinum toxin (BoNT) and its potential in the treatment of upper and lower limb poststroke spasticity. Optimal treatment may include BoNT injections into focal muscles in conjunction with an integrated multidisciplinary team approach and intensive rehabilitation programs or to help utilize affected muscles.9 Higher-intensity rehabilitation programs (≥3 1-hour weekly session for ~10 weeks) may help patients achieve more upper limb goals following BoNT injections for spasticity when compared with usual care programs (≤2 1-hour weekly sessions).10 A recent consensus panel of 44 neurologists and physiatrists with experience in BoNT therapy recommended starting a rehabilitation program during the first week after BoNT injection therapy.11

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