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Review of electrical stimulation, botulinum toxin, and their combination for spastic drop foot. Ari Jacob Levi Wilkenfeld, MD, PhD. Aim Review pathophysiology of spastic drop foot and its treatment options.
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Review of electrical stimulation, botulinum toxin, and their combination for spastic drop foot Ari Jacob Levi Wilkenfeld, MD, PhD
Aim • Review pathophysiology of spastic drop foot and its treatment options. • Present theoretical reasons why functional electrical stimulation (ES) and botulinum toxin (BTX) injections could work synergistically. • Relevance • There are reasons to think functional ES and BTX injections might work effectively in combination, but no clear consensus exists in literature.
Background • Spastic drop foot • Weak ankle dorsiflexors and spastic ankle plantar flexors predispose ankle to stay pathologically plantar flexed. • Functional ES • Uses electric current to activate muscles and nerves that are weak/paralyzed but still have intact lower motor neurons and musculature. • BTX • Prevents acetylcholine release at presynaptic terminal, thus impairing neuromuscular transmission and inducing weakness.
Treatment • 4 mechanisms by which ES might increase antispasticity effect of BTX. • Animal experiments: BTX’s paralytic effect starts earlier when toxin uptake is increased with ES. • Moving muscle through flexion/extension cycles could help mechanically spread toxin. • Direct effects of ES on tone reduction. • Simultaneously addressing positive and negative components of upper motor neuron syndrome could lead to increased functional gains in gait.
Conclusions • For ES: Evidence of decreased spasticity. • But, e.g., whether stimulation should be over spastic muscle or its antagonist, how long effect lasts, and whether it works during gait must be clarified. • For BTX: Evidence of decreased tone. • But evidence lacking for improved gait. • ES+BTX: Evidence that ES of muscle may increase efficacy of BTX. • However, large controlled studies examining relative effects are lacking.