Review of electrical stimulation, botulinum toxin, and their combination for spastic drop foot

Abstract

Abstract-Spastic drop foot is a functional impairment causing significant morbidity and mortality. Multiple treatments are available for this condition, but it is often not clear which treatment or combination of treatments is optimal for a given patient. One relatively recent therapy is the use of functional electrical stimulation to stimulate the peroneal nerve. Another is the use of botulinum toxin injections in the spastic ankle plantar flexors. While reasons exist to think these two treatments might work effectively in combination, there is no clear consensus in the literature. In this article, I review the background of the pathophysiology of spastic drop foot and its treatment options. I present some of the theoretical reasons why functional electrical stimulation and botulinum toxin injections could work synergistically and present a literature review on the topic. Recommendations for future research are discussed.Key words: ankle, botulinum toxins, chemodenervation, drop foot, functional electrical stimulation, gait, muscle spasticity, neurorehabilitation, peroneal nerve stimulation, upper motor neuron syndrome. SPASTIC DROP FOOTSpastic drop foot is a functional impairment causing significant morbidity by impairing gait, limiting activities of daily living, and contributing to injuries [1]. Spastic drop foot exists when, due to a combination of weakness of the ankle dorsiflexors (primarily tibialis anterior) and spasticity of the ankle plantar flexors (primarily gastrocnemius and soleus), the ankle has a predisposition for staying pathologically plantar flexed. Due to associated weakness of ankle evertors (e.g., peroneal musculature) and/or spasticity of invertors (e.g., tibialis posterior), pathological foot inversion is also often associated [2][3].Because ankle dorsiflexion during the swing phase of gait is essential for foot clearance, drop foot can lead to falls and injury [1]. In addition, with drop foot, foot-floor contact in stance phase can happen initially at the forefoot (as opposed to at the heel in nondisabled gait) and limited dorsiflexion can prevent forward progression of the tibia, resulting in hyperextension of the knee and limited forward translation of the body [4]. Those affected often develop pathological compensatory gaits to attempt to compensate for spastic drop foot. One of these, referred to as "steppage gait," involves abnormally flexing the hip and bending the knee to attempt to get the foot to clear the ground [5]. Other patients will hike their hip on the side of the spastic ankle with each swing phase or circumduct the lower limb to aid in foot clearance [6].Abbreviations: AAN = American Academy of Neurology, AFO = ankle-foot orthosis, BTA = botulinum toxin type A, BTB = botulinum toxin type B, BTX = botulinum toxin, CMAP = compound muscle action potential, CNS = central nervous system, FES = functional electrical stimulation, MS = multiple sclerosis, PNS = peroneal nerve stimulation, SCI = spinal cord injury, TBI = traumatic brain injury, UMNS = upper motor neuron syndro...

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“…whereas the 'dynamic' model, although allowing greater mobility at the joint, has a bulky appearance and is expensive. It has also been shown that orthotic devices may lead to pressure sore formation, and impede the ability to generate a standing torque from a seated position or to climb stairs [42].…”

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