European Journal of Neurology 2014, 21: 1053–1054
doi:10.1111/ene.12404
EDITORIAL
Managing spastic foot drop after stroke See paper by Fietzek et al. on page 1089. Spastic equinovarus foot commonly interferes with ambulation and thus limits progress in rehabilitation. The impairment is due to shortening and overactivity of the ankle flexor muscles (gastrocnemius, soleus or both), foot invertors (tibialis posterior and, occasionally, tibialis anterior as well) and toe flexors (flexor hallucis longus and brevis and flexor digitorum longus and brevis). It may also be associated with supination of the foot and the presence of a striatal great toe deformity. Its consequence is an inability to place the foot on the ground and thereby gain a stable base of support to carry out transfers and assist ambulation [1]. Untreated, it may go on to contracture development, falls and chronic pain from an injured ankle. The typical posture of a hemiplegic lower limb after a central nervous system injury is a plantarflexion and inversion posture in the foot, but it is important from the outset to differentiate a spastic equinovarus foot from the simple relative weakness of the evertor muscles (peroneus group) compared with that of the invertors. The two can be easily distinguished through clinical examination. Spastic pes equinus tends to come on during the middle of the swing phase of the gait cycle when the foot is free, whereas, in weakness, the peronei muscles do not control the foot as it strikes the ground at the end of swing phase and inversion takes place at the start of stance from unopposed invertor muscles, usually tibialis posterior. Spastic foot drop may be unilateral (e.g. after stroke) or bilateral, as in paraplegia or tetraplegia (after brain or spinal cord injury, e.g. trauma, multiple sclerosis). It may occur also when there are other factors, such as perceptual problems, sensory neglect or, early on after a brain injury or stroke, learned non-use, when the subject learns to compensate with the non-affected limb. The aim of treatment is to allow the whole foot to be in contact with the ground during stance phase and to act as a stable platform, so that the muscles controlling the hip and knee joint can work effectively and ensure that controlled movement is permitted. This is the aim of rehabilitation interventions, in which there has been renewed interest in devising those that will have an impact on gait function. Treatment is directed at the spasticity causing the foot drop as well as the mechanical defect. It is thus important to distinguish between it and weakness. There is good evidence of the effectiveness of ankle foot orthoses and functional electrical stimulation to correct foot drop, but tibialis posterior m. spasticity © 2014 The Author(s) European Journal of Neurology © 2014 EAN
causing varus deformity can interfere with the patient’s tolerance of the device. Stimulating the common peroneal nerve electrically to produce a dorsiflexor force is the basis of functional electrical stimulation and reduces the need for wearing an ankle-foot orthosis [2]. Both are practical, long-term and cost-effective treatments for dropped foot [3,4]. As a result, a combined approach with botulinum toxin is useful to reduce the activity of (or ‘switch off’) those muscles causing the equinus or equinovarus deformity [4]. Most studies of botulinum toxin treatment in spastic pes equinovarus have been aimed at impairment control. BOTOX® (Allergan Inc., Irvine, CA, USA) at a dose of 300 U administered to the ankle flexors was shown to be effective in reducing hypertonia and muscle spasms and was well tolerated for the treatment of lower limb spasticity in adult patients [5,6]. Fietzek et al. [7] have also shown that early intervention has a better effect compared with starting treatment later on and this supports current thinking in clinical circles. It confirms the effect of botulinum toxin on spasticity and that it has little effect where the equinovarus posture is caused by imbalance between the stronger plantar flexors and weak dorsiflexors. The combination of botulinum toxin and physical treatment has recently been shown for the first time to allow patients to meet their goals for improved ambulation in comparison with placebo and physical treatment, when directed specifically at ankle plantar flexor muscles and tibialis posterior muscle [8]. When clear, objective and measurable goals for treatment exist, even the placebo group of patients improve, but the addition of botulinum toxin was significantly better. Surgical solutions fall into two categories. Neurosurgery is directed at treating spasticity through selective peripheral neurotomy/neurectomy (or, less commonly, dorsal root entry zone procedure) to reduce a and c motor neuron activity to diminish neuromuscular stimulation and spasticity. Orthopaedic surgery, on the other hand, can help the mechanical effects of the foot drop [9]. Split tibialis anterior tendon transfers restore effective dorsiflexion, whereby a tendon from a functioning tibialis anterior muscle is transposed laterally to allow foot eversion. Also a tibialis posterior tendon can be moved anteriorly to effect dorsiflexion [9]. If there is little active function in the lower leg, fusing the ankle and subtalar joint provides a very effective solution to stabilizing the foot, as well as giving pain-free function.
1053
1054
Editorial
Anthony B. Ward North Staffordshire Rehabilitation Centre, Haywood Hospital, Stoke-on-Trent, UK
5.
(e-mail: [email protected])
References 1. Simpson KJ, Jiang P. Foot landing position during gait influences ground reaction forces. Clin Biomech 1999; 14: 396–402. 2. Everaert DG, Stein RB, Abrams GM, et al. Effect of a foot-drop stimulator and ankle-foot orthosis on walking performance after stroke: a multicenter randomized controlled trial. Neurorehabilitation & Neural Repair 2013; 27: 579–591. 3. Taylor P, Humphreys L, Swain I. The long-term costeffectiveness of the use of functional electrical stimulation for the correction of dropped foot due to upper motor neuron lesion. J Rehabil Med 2013; 45: 154–160. 4. Johnson CA, Burridge JH, Strike PW, Wood DE, Swain ID. The effect of combined use of botulinum toxin type A and functional electric stimulation in the treatment of
6.
7.
8.
9.
spastic drop foot after stroke: a preliminary investigation. Arch Phys Med Rehabil 2004; 85: 902–909. Kaji R, Osako Y, Suyama K, et al. Botulinum toxin type A in post-stroke lower limb spasticity: a multicenter, double-blind, placebo-controlled trial. J Neurol 2010; 257: 1330–1337. Dunne JW, Gracies JM, Hayes M, Zeman B, Singer BJ, and on behalf of the Multicentre Study Group. A prospective, multicentre, randomized, double-blind, placebocontrolled trial of onabotulinumtoxinA to treat plantarflexor/invertor overactivity after stroke. Clinical Rehabilitation 2012; 26: 787–797. Fietzek UM, Kossmehl P, Schelosky L, Ebersbach G, Wissel J. Early botulinum toxin treatment for spastic pes equinovarus a randomized double-blind placebo-controlled study. Eur J Neurol 2014; 21: 1089–1095. Ward AB, Wissel J, Borg J, et al. Functional goal achievement in post-stroke spasticity patients: the BOTOX Economic Spasticity Trial (BEST). J Rehabil Med 2014; 46: 504–513. Surgery Lawrence SJ, Botte MJ. Management of the adult, spastic, equinovarus foot deformity. Foot Ankle Int 1994; 15: 340–346.
© 2014 The Author(s) European Journal of Neurology © 2014 EAN
doi:10.1111/ene.12404
EDITORIAL
Managing spastic foot drop after stroke See paper by Fietzek et al. on page 1089. Spastic equinovarus foot commonly interferes with ambulation and thus limits progress in rehabilitation. The impairment is due to shortening and overactivity of the ankle flexor muscles (gastrocnemius, soleus or both), foot invertors (tibialis posterior and, occasionally, tibialis anterior as well) and toe flexors (flexor hallucis longus and brevis and flexor digitorum longus and brevis). It may also be associated with supination of the foot and the presence of a striatal great toe deformity. Its consequence is an inability to place the foot on the ground and thereby gain a stable base of support to carry out transfers and assist ambulation [1]. Untreated, it may go on to contracture development, falls and chronic pain from an injured ankle. The typical posture of a hemiplegic lower limb after a central nervous system injury is a plantarflexion and inversion posture in the foot, but it is important from the outset to differentiate a spastic equinovarus foot from the simple relative weakness of the evertor muscles (peroneus group) compared with that of the invertors. The two can be easily distinguished through clinical examination. Spastic pes equinus tends to come on during the middle of the swing phase of the gait cycle when the foot is free, whereas, in weakness, the peronei muscles do not control the foot as it strikes the ground at the end of swing phase and inversion takes place at the start of stance from unopposed invertor muscles, usually tibialis posterior. Spastic foot drop may be unilateral (e.g. after stroke) or bilateral, as in paraplegia or tetraplegia (after brain or spinal cord injury, e.g. trauma, multiple sclerosis). It may occur also when there are other factors, such as perceptual problems, sensory neglect or, early on after a brain injury or stroke, learned non-use, when the subject learns to compensate with the non-affected limb. The aim of treatment is to allow the whole foot to be in contact with the ground during stance phase and to act as a stable platform, so that the muscles controlling the hip and knee joint can work effectively and ensure that controlled movement is permitted. This is the aim of rehabilitation interventions, in which there has been renewed interest in devising those that will have an impact on gait function. Treatment is directed at the spasticity causing the foot drop as well as the mechanical defect. It is thus important to distinguish between it and weakness. There is good evidence of the effectiveness of ankle foot orthoses and functional electrical stimulation to correct foot drop, but tibialis posterior m. spasticity © 2014 The Author(s) European Journal of Neurology © 2014 EAN
causing varus deformity can interfere with the patient’s tolerance of the device. Stimulating the common peroneal nerve electrically to produce a dorsiflexor force is the basis of functional electrical stimulation and reduces the need for wearing an ankle-foot orthosis [2]. Both are practical, long-term and cost-effective treatments for dropped foot [3,4]. As a result, a combined approach with botulinum toxin is useful to reduce the activity of (or ‘switch off’) those muscles causing the equinus or equinovarus deformity [4]. Most studies of botulinum toxin treatment in spastic pes equinovarus have been aimed at impairment control. BOTOX® (Allergan Inc., Irvine, CA, USA) at a dose of 300 U administered to the ankle flexors was shown to be effective in reducing hypertonia and muscle spasms and was well tolerated for the treatment of lower limb spasticity in adult patients [5,6]. Fietzek et al. [7] have also shown that early intervention has a better effect compared with starting treatment later on and this supports current thinking in clinical circles. It confirms the effect of botulinum toxin on spasticity and that it has little effect where the equinovarus posture is caused by imbalance between the stronger plantar flexors and weak dorsiflexors. The combination of botulinum toxin and physical treatment has recently been shown for the first time to allow patients to meet their goals for improved ambulation in comparison with placebo and physical treatment, when directed specifically at ankle plantar flexor muscles and tibialis posterior muscle [8]. When clear, objective and measurable goals for treatment exist, even the placebo group of patients improve, but the addition of botulinum toxin was significantly better. Surgical solutions fall into two categories. Neurosurgery is directed at treating spasticity through selective peripheral neurotomy/neurectomy (or, less commonly, dorsal root entry zone procedure) to reduce a and c motor neuron activity to diminish neuromuscular stimulation and spasticity. Orthopaedic surgery, on the other hand, can help the mechanical effects of the foot drop [9]. Split tibialis anterior tendon transfers restore effective dorsiflexion, whereby a tendon from a functioning tibialis anterior muscle is transposed laterally to allow foot eversion. Also a tibialis posterior tendon can be moved anteriorly to effect dorsiflexion [9]. If there is little active function in the lower leg, fusing the ankle and subtalar joint provides a very effective solution to stabilizing the foot, as well as giving pain-free function.
1053
1054
Editorial
Anthony B. Ward North Staffordshire Rehabilitation Centre, Haywood Hospital, Stoke-on-Trent, UK
5.
(e-mail: [email protected])
References 1. Simpson KJ, Jiang P. Foot landing position during gait influences ground reaction forces. Clin Biomech 1999; 14: 396–402. 2. Everaert DG, Stein RB, Abrams GM, et al. Effect of a foot-drop stimulator and ankle-foot orthosis on walking performance after stroke: a multicenter randomized controlled trial. Neurorehabilitation & Neural Repair 2013; 27: 579–591. 3. Taylor P, Humphreys L, Swain I. The long-term costeffectiveness of the use of functional electrical stimulation for the correction of dropped foot due to upper motor neuron lesion. J Rehabil Med 2013; 45: 154–160. 4. Johnson CA, Burridge JH, Strike PW, Wood DE, Swain ID. The effect of combined use of botulinum toxin type A and functional electric stimulation in the treatment of
6.
7.
8.
9.
spastic drop foot after stroke: a preliminary investigation. Arch Phys Med Rehabil 2004; 85: 902–909. Kaji R, Osako Y, Suyama K, et al. Botulinum toxin type A in post-stroke lower limb spasticity: a multicenter, double-blind, placebo-controlled trial. J Neurol 2010; 257: 1330–1337. Dunne JW, Gracies JM, Hayes M, Zeman B, Singer BJ, and on behalf of the Multicentre Study Group. A prospective, multicentre, randomized, double-blind, placebocontrolled trial of onabotulinumtoxinA to treat plantarflexor/invertor overactivity after stroke. Clinical Rehabilitation 2012; 26: 787–797. Fietzek UM, Kossmehl P, Schelosky L, Ebersbach G, Wissel J. Early botulinum toxin treatment for spastic pes equinovarus a randomized double-blind placebo-controlled study. Eur J Neurol 2014; 21: 1089–1095. Ward AB, Wissel J, Borg J, et al. Functional goal achievement in post-stroke spasticity patients: the BOTOX Economic Spasticity Trial (BEST). J Rehabil Med 2014; 46: 504–513. Surgery Lawrence SJ, Botte MJ. Management of the adult, spastic, equinovarus foot deformity. Foot Ankle Int 1994; 15: 340–346.
© 2014 The Author(s) European Journal of Neurology © 2014 EAN
