Objective: To present interdisciplinary practical guidance for the assessment and treatment of spastic equinovarus foot after stroke.
Results: Clinical examination and diagnostic nerve block with anaesthetics determine the relative role of the factors leading to spastic equinovarus foot after stroke: calf spasticity, triceps surae – Achilles tendon complex shortening and dorsiflexor muscles weakness and/or imbalance. Diagnostic nerve block is a mandatory step in determining the cause(s) of, and the most appropriate treatment(s) for, spastic equinovarus foot. Based on interdisciplinary discussion, and according to a patient-oriented goal approach, a medical and/or surgical treatment plan is proposed in association with a rehabilitation programme. Spasticity is treated with botulinum toxin or phenol–alcohol chemodenervation and neurotomy, shortening is treated by stretching and muscle-tendon lengthening, and weakness is treated by ankle-foot orthosis, functional electrical stimulation and tendon transfer. These treatments are frequently combined.
Conclusion: Based on 20 years of interdisciplinary expertise of management of the spastic foot, guidance was established to clarify a complex problem in order to help clinicians treat spastic equinovarus foot. This work should be the first step in a more global international consensus.
Stroke is the third most common cause of death and the primary cause of severe disability in industrialized countries. Following stroke, approximately 80% of patients regain walking function with decreased gait velocity and asymmetrical gait pattern (1). Spastic equinovarus foot (SEVF) is one of the most common disabling deformities observed among hemiplegic patients. SEVF is frequently associated with other kinematic gait abnormalities, such as stiff knee gait, genu recurvatum, and painful claw toes. SEVF deformity forces the patient to increase their hip and knee flexion in the swing phase. If they are unable to do this (e.g. if they have associated stiff knee gait), the patient will present a hip circumbduction in the swing phase. Correction of such equinus may therefore improve distal as well as proximal gait disturbances.
SEVF deformity has 4 main causes (2, 3). The first is spasticity of the calf muscles (soleus, gastrocnemius, tibialis posterior, flexor digitorum and flexor hallucis longus muscles), responsible for SEVF in the stance phase of gait and for painful toe curling with callosities on the pulp and dorsum of the toes. The peroneus longus and brevis muscles may also be spastic (often with clonus), but such spasticity is useful to limit the varus and stabilize the ankle. Secondly, the spastic muscles have a tendency to remain in a shortened position for prolonged periods, which, in turn, results in soft-tissue changes and contractures, leading to a fixed deformity (4). Thirdly, weakness of the ankle dorsiflexor muscles (tibialis anterior, extensor digitorum and hallucis muscles) as well as the peroneus longus and brevis muscles is responsible for drop-foot in the swing phase of gait. Such weakness is often emphasized by triceps spastic co-contraction and/or contracture. The weakness also affects the triceps surae muscles, leading to a lack of propulsion at the end of the stance phase of gait. Lastly, an imbalance between the tibialis anterior and the peroneus muscles leads to varus of the hind-foot in the swing phase, as peroneus activation must compensate for physiological varus positioning related to contraction of the tibialis anterior. In such a case, the foot will be placed in an unstable varus position during the swing phase and at the beginning of the stance phase.
The respective role of the main causes of SEVF (spasticity, shortening, weakness, and imbalance) varies from patient to patient, and therapeutic decisions are therefore challenging. Indeed, as emphasized by Fuller, the causes of SEVF are varied and complex, due to a variety of deforming forces, and thus a single procedure does not exist to correct all deformities (3). Hence there is a need for guidance and guidelines.
Treatments for SEVF described in the literature are multimodal and include rehabilitation, orthosis, botulinum toxin (BoNT-A) injections, alcohol and phenol nerve blocks, functional neurosurgery (selective neurotomy and intrathecal baclofen therapy) and orthopaedic surgery (tendon transfer, tendon lengthening and bone surgery) (5). SEVF rehabilitation programmes include strengthening of the tibialis anterior and peroneus muscles, electrical stimulation, stretching of the triceps surae to reduce spasticity and prevent contracture, and gait and balance training. Modern therapeutic approaches, such as task-oriented strategy and treadmill with bodyweight support, are promoted. Several publications support the effectiveness of these treatments in SEVF (6–8). However, only 3 studies have compared different treatment options (9–11). A systematic review of surgical correction in adult patients with stroke emphasized the need to compare treatments in order to generate evidence on which to base algorithms (8). In fact, no practical guidelines are available for use in daily practice. Evidence regarding choice of treatment is poor, thus therapeutic decision-making is based on professional personal preferences and beliefs rather than on scientific evidence. An interdisciplinary approach with a physical medicine and rehabilitation (PMR) specialist and rehabilitation team, neurosurgeon, and orthopaedic surgeon is therefore mandatory in order to optimize treatments.
The aim of this paper is to present and discuss the Mont-Godinne interdisciplinary guidance (Fig. 1), based on the existing literature and on 20 years of experience of an interdisciplinary medical and surgical approach to SEVF.