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| ORIGINAL ARTICLE |
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| Year : 2022 | Volume
: 5
| Issue : 4 | Page : 156-160 |
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Medico-surgical management of the spastic equinovarus foot deformity in adults: A retrospective series of 622 patients
Thierry Deltombe1, Thomas Gavray1, Olivier Van Roy1, Delphine Wautier2, Thierry Gustin3
1 Department of Physical Medicine and Rehabilitation, CHU UCL Namur Site Godinne, Yvoir, Belgium
2 Department of Orthopaedic Surgery, CHU UCL Namur Site Godinne, Yvoir, Belgium
3 Department of Neurosurgery, CHU UCL Namur Site Godinne, Yvoir, Belgium
| Date of Submission | 21-Sep-2022 |
| Date of Decision | 07-Nov-2022 |
| Date of Acceptance | 21-Nov-2022 |
| Date of Web Publication | 15-Dec-2022 |
Correspondence Address:
Prof. Thierry Deltombe
Department of Physical Medicine and Rehabilitation, CHU UCL Namur Site Godinne, B-5530 Yvoir
Belgium
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijprm.JISPRM-000182
Objective: This study aimed to determine the frequency of spastic equinovarus foot (SEF) treatments. Materials and Methods: the medical files of 622 patients treated for SEF were reviewed. Results: SEF resulted from stroke in 66%. The most frequent pattern was equinovarus in 56%, knee recurvatum in 55%, and claw toes in 41%. Patients benefited from surgical treatment in 59%, including neurotomy in 22%, tendon surgery in 12%, and a combined surgery in 25%. Conclusion: Surgery was performed in 59% of the cases. The type of treatment was influenced by the preoperative diagnostic nerve block assessment.
Keywords: Equinovarus foot, motor nerve block, muscle spasticity, neuro-orthopedics, neurotomy
How to cite this article:
Deltombe T, Gavray T, Van Roy O, Wautier D, Gustin T. Medico-surgical management of the spastic equinovarus foot deformity in adults: A retrospective series of 622 patients. J Int Soc Phys Rehabil Med 2022;5:156-60 |
How to cite this URL:
Deltombe T, Gavray T, Van Roy O, Wautier D, Gustin T. Medico-surgical management of the spastic equinovarus foot deformity in adults: A retrospective series of 622 patients. J Int Soc Phys Rehabil Med [serial online] 2022 [cited 2023 May 28];5:156-60. Available from: https://www.jisprm.org/text.asp?2022/5/4/156/363883 |
| Introduction | |  |
Lesions of the central nervous system (CNS) involving the corticospinal pathways may lead to the deforming spastic paresis syndrome with a neurological and a muscle component.[1] This syndrome includes a lack of voluntary motor command (paresis), a loss of muscle extensibility leading to muscle shortening (deforming) and a muscle spasticity (spastic). The prevalence of spastic muscle overactivity (SMO) 6 months after stroke is estimated between 22% and 46%.[2]
Spastic equinovarus foot (SEF) is one of the most common deformities among patients affected by a spastic paresis syndrome, with an incidence estimated at 18% of stroke survivors.[3] The SEF is responsible for foot instability and pain, forcing the patient to hip circumduction in the swing phase of gait when associated with a stiff knee gait. Patients frequently need ankle foot orthosis (AFO) and/or crutch for walking.[4] SEF deformity may be due to plantarflexors (soleus, gastrocnemius, tibialis posterior and flexor digitorum longus and brevis muscles) SMO that can be treated by botulinum toxin (BoNT) injections or neurotomy and/or contracture that can be treated by intensive stretching or muscle-tendon surgical lengthening.[5] SEF may also be due to dorsiflexor muscle weakness as well as the imbalance between tibialis anterior and fibularis muscles that can be treated by strengthening, AFO, functional electrical stimulation, or tendon transfer.[6] Appropriate treatment of the three components of SEF (paresis, SMO, and shortening) is essential to improve the patient condition in the three domains (impairment–activity–participation and quality of life) of the WHO International Classification of Functioning.[7] However, the reasons leading to SEF differ from patient to patient, explaining why a single procedure does not exist to correct all the deformities.[4],[8] Therefore, a precise determination of the respective responsibility of these different causes is mandatory before proposing a treatment, especially with surgery. Such a determination can be obtained by means of a diagnostic nerve block (DNB) with anesthetics that consists of injecting a small dose (usually 1 or 2 ml) of local anesthetics at the level of the motor nerve. The DNB can be performed at the level of the tibial nerve or of the motor nerve branches innervating the soleus, gastrocnemius, and tibialis posterior muscles. DNB eliminates SMO after a few minutes and for several hours, allowing assessment of the respective contribution of the different spastic muscles, the degree of muscle shortening, and the weakness of the antagonistic muscles. This explains why DNB is recommended in the SEF assessment.[4],[9]
Even if medical and surgical options are described in the literature,[4],[5],[6],[10],[11],[12] no study assesses the influence of DNB on the therapeutic decision and the relative frequency of each therapeutic option in clinical practice.
The aim of the present study was to retrospectively evaluate the medical and surgical treatments proposed and performed in relation to the DNB assessment.
| Materials and Methods | | |
We conducted a retrospective analysis of the patients assessed for a spastic foot deformity consecutive to a CNS lesion.
Participants
The medical files of the patients who underwent a DNB for a SEF assessment between April 1996 and July 2020 were analyzed. The available data included in the patient medical file necessary for the inclusion in the study were: age, sex, etiology of the CNS lesion, affected side, pathological foot pattern in the stance phase of gait, complaint (s) expressed by the patient, previous treatments, DNB assessment, targeted motor nerves branches during DNB, ankle kinematics improvement in the stance phase of gait obtained after the DNB completion (no improvement, incomplete improvement and complete correction consisting in a heel contact with an ankle dorsal flexion > 90° in stance phase) and the medical and/or surgical treatments proposed and performed. The medical and/or surgical treatments were chosen according to the results obtained after DNB based on an interdisciplinary discussion and a patient-oriented goal approach following a published guidance pathway established by our interdisciplinary group.[6] SMO is treated by BoNT or phenol–alcohol chemodenervation and neurotomy, shortening by stretching and muscle-tendon lengthening and weakness by AFO, functional electrical stimulation, and tendon transfer. These treatments are frequently combined.[6],[7] The medical treatments included oral medications, orthosis, BoNT injections, and alcohol neurolysis, while the surgical treatments included neurotomy and tendon lengthening and/or transfer. The neural treaments defined those that were acting on muscle overactivity, such as oral medications, BoNT injections, alcohol neurolysis, and neurotomy, while the nonneural treatments defined those were acting on muscle shortening, such as orthosis and tendon surgery.
Statistical analysis
We performed a descriptive statistical analysis. The correlation between the improvement obtained after the DNB and the type of treatment was performed with Pearson Ki-Carré (IBM SPSS Statistics for Windows, Version 27.0. Armonk, NY, USA). The types of treatment were divided according to whether they act at the level of the neural spastic component (BoNT, alcohol neurolysis, and neurotomy) and/or at the level of the nonneural muscle component (tendon surgery and orthosis).
Ethic
The study has been approved by the institutional local Ethic Committee (internal N°214/2020).
| Results | | |
From April 1996 to July 2020, 1290 patients suffering from SEF benefited from a DNB assessment. Of these 1290 medical files, 622 included all the necessary data and were analyzed.
Patients were male in 54% (n = 336) and female in 46% (n = 286). The spastic paresis syndrome affected the right side in 44% (n = 272), the left side in 46% (n = 289), and both sides in 10% (n = 61). The CNS lesion etiologies were stroke in 66% (n = 414) from the ischemic origin in 43% (n = 271) or hemorrhagic origin in 23% (n = 143), traumatic brain injury in 14% (n = 85), spinal cord disease in 6% (n = 36), cerebral palsy in 4% (n = 24), multiple sclerosis in 3% (n = 19), brain tumor in 2% (n = 12), and others in 5% (n = 32). The complaints expressed by the patients were foot instability in 67% (n = 416), foot pain in 27% (n = 165), poor AFO tolerance in 23% (n = 140), low walking speed in 11% (n = 68) and knee pain in 6% (n = 39). The pathological gait patterns were equinovarus in 56% (n = 348), isolated equinus in 38% (n = 236), and isolated varus in 6% (n = 38). The associated pathological gait patterns were knee recurvatum in 55% (n = 342) and claw toes in 41% (n = 253). The treatments previously performed before the DNB assessment were physical therapy in 89% (n = 551), AFO and orthotic shoes in 55% (n = 344), oral medications in 34% (n = 212), BoNT injections in 18% (n = 112), surgery in 6% (n = 35), no treatment in 5% (n = 28), and alcohol neurolysis in 1% (n = 8).
The DNB assessment was performed only once in 86% of the patients (n = 535), twice in 13% (n = 79) and three times in the same patients during different sessions in 1% (n = 8). When a second or third DNB was performed, it was usually targeting the flexor hallucis and digitorum muscles for an additional claw toes assessment.
The DNB was performed at the level of the tibial nerve trunk at the upper part of the popliteal fossa in 10% of cases (n = 60%). Most of the time, DNB targeted one or several motor nerve branches innervating different muscles. The soleus nerve was targeted in 90% (n = 561), the tibialis posterior nerve in 43% (n = 266), the gastrocnemius medialis and lateralis nerves in 19% (n = 116), the flexor digitorum longus nerve in 4% (n = 26), the flexor hallucis longus nerve or muscle in 2% (n = 15) and the extensor hallucis longus muscle in 1% (n = 4). The DNB assessment provided no improvement in ankle kinematics in the stance phase of gait in 17% (n = 107), a partial improvement in 57% (n = 353), and a complete correction of the foot deformity in 26% (n = 162).
[Table 1] lists the type and frequency of the treatments performed after the DNB assessment. A medical treatment was performed in 69% (n = 430), a surgical treatment was performed in 59% (n = 367) while no treatment was proposed or performed in 7% (n = 44). Interestingly, 34% (n = 211) only had a medical treatment, 35% (n = 219) had a medical treatment, followed by a surgical one, while 24% (n = 148) were directly operated. A treatment of the SMO neural component (BoNT-alcohol neurolysis-neurotomy) was performed in 47% (n = 292), a treatment of the muscular nonneural component (tendon surgery-orthosis) in 7% (n = 46), and a combined treatment of the neural and nonneural component in 34% (n = 211).
There was a strong and significant correlation between the improvement obtained after DNB and the treatment performed (K-carré = 178.152; P < 0.001; V de Cramer = 0.403). A neural treatment was more frequently performed in case of partial or complete improvement after DNB, and a nonneural treatment was more frequently performed when the DNB provided no improvement.
[Table 2] lists the type and frequency of the medical treatments. The medical treatments consisted of BoNT injections in 48% (n = 299), orthosis in 41% (n = 252), oral medication in 5% (n = 30), and alcohol neurolysis in 2% (n = 15). Among the 299 patients treated with BoNT injections, the soleus muscle was targeted in 91% (n = 271), the tibialis posterior in 39% (n = 116), the gastrocnemius lateralis and medialis in 36% (n = 107), the flexor hallucis longus in 30% (n = 91), the flexor digitorum longus in 27% (n = 81), and the extensor hallucis longus in 4% (n = 11).
[Table 3] lists the type and frequency of the surgical treatments. A neurotomy was performed in 47% (n = 292) alone in 22% (n = 136), in association with an Achilles tendon lengthening in 14% (n = 85), in association with a split anterior tibial tendon transfer onto the fibularis tendon Split anterior tibialis tendon transfer (SPLATT) in 8% (n = 48) and with both Achilles tendon lengthening and SPLATT in 3% (n = 20). An Achilles tendon lengthening was performed in 22% (n = 134) alone in 1.3% (n = 8) or in association with neurotomy and SPLATT in 3% (n = 20). An additional toe flexors tenotomy was performed in 28% (n = 177).
[Table 4] lists the type of motor nerve branches targeted during the neurotomy procedure, whether it was performed alone or in combination with a tendon surgery. Among the 292 patients treated by neurotomy, the soleus nerve was treated in almost all the cases, while the tibialis posterior nerve was treated in 76% (n = 223). Notably, the flexor digitorum longus nerve was treated in only 2% (n = 7). | Table 4: Type of motor nerve branches targeted during the neurotomy (n=292)
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| Discussion | | |
Until now, no study has discussed the frequency of the different types of treatment applied in the case of disabling SEF. We present the largest series of patients assessed and treated for SEF.
In line with the literature, the most frequent etiology was ischemic stroke, hemorrhagic stroke, and traumatic brain injury.[3] The most frequent complaints expressed by patients were foot instability, pain at the foot and/or knee and difficulties to tolerate AFO. The most frequent patterns were equinovarus followed by isolated equinus and isolated varus. Associated knee recurvatum in the stance phase of gait and claw toes were frequent.[13],[14] Most of the patients had multipattern problems, including SEF. Before our intervention, nearly all the patients had already benefited from physical therapy, AFO prescription, and BoNT injections. Surprisingly, one-third of the patients took antispastic oral medications, but their efficiency to reduce spasticity is poorly documented.[15]
As DNB was an inclusion criterion, all the patients benefited from a DNB assessment. In available guidance, the DNB is the cornerstone of SEF management.[6],[9] Interestingly, DNB is recommended by French guidelines.[9] In most of the cases, DNB was performed selectively to target motor nerve branches. Among these, the soleus motor branch was the most frequently targeted nerve confirming Decq's finding that the soleus muscle spasticity was mainly responsible for SEF.[16] The other branches innervating the tibialis posterior (in case of varus) and/or the gastrocnemius medialis and lateralis (in case of insufficient improvement after soleus block) were frequently blocked. Logically, the muscles injected with BoNT and the motor nerve branches selected during neurotomy were identical to those targeted during the DNB assessment. Indeed, it has been demonstrated that DNB can predict the spasticity reduction and ankle kinematics improvement obtained after BoNT injections and neurotomy.[17],[18]
After DNB, most of the patients noticed partial or complete SEF improvement, while one-sixth had no improvement, mainly because of a predominant muscle contracture. DNB not only helps to determine the respective responsibility of the different spastic muscles in the deformity but also to differentiate the neural (SMO improved by DNB to be treated by BoNT or neurotomy) from the nonneural (muscle shortening not improved by DNB to be treated by muscle-tendon lengthening) component.
The most frequent medical treatments were BoNT injections and AFO. BoNT is now considered the first-line treatment of SEF to reduce muscle tone and to improve walking speed and community ambulation.[19] In agreement with the DNB assessment, the soleus muscle was the most frequently injected muscle, followed by the tibialis posterior, the gastrocnemii and the flexor digitorum muscles. As tibial nerve alcohol, neurolysis is associated with a 30% risk of dysesthesia and neuropathic pain interfering with gait, we preferred BoNT injections that have a safer profile.[20] Alone or in combination with BoNT, AFO improves the ankle and knee kinematics, kinetics, and energy cost of walking in stroke survivors.[21] However, the AFO is sometimes difficult to install (especially in stroke patients with only one valid hand), explaining why AFO removal is a frequent goal expressed by patients. Among the patients who benefited from a medical treatment, half of them will be surgically treated later.
Surgical management of SEF was a frequent therapeutic option. As pointed out by Allart et al., the therapeutic modalities of SEF, including surgical strategy, are very heterogeneous, with few case series published explaining the lack of consensus.[4] In the largest available series, Carda et al. demonstrated that tendon surgery is a safe and effective procedure to improve ankle kinematic and gait kinetic.[22] When DNB completely corrects SEF, an isolated neural treatment including BoNT (as a long-lasting block test), followed by neurotomy is proposed. Selective neurotomy consists of a partial section of the motor nerve branches innervating spastic muscles allowing a permanent reduction in spasticity. Bollens et al. demonstrated that neurotomy is a safe procedure that permanently reduces SMO and improves ankle kinematics during gait.[23],[24] Notably, the flexor digitorum longus SMO was not treated by neurotomy because of the risk of foot neuropathic pain related to the injury of sensory fibers that are closely mixed with motor fibers at the level of the surgical approach.[25] In the case of claw toes, tendon surgery is therefore preferred to neurotomy. When DNB only partially improved the SEF, a combined treatment of SMO and muscle contracture is proposed. In our series, surgery included by order of frequency selective tibial neurotomy (targeting the neural component), followed by toe flexors tenotomy, Achilles tendon lengthening, and SPLATT (targeting the nonneural component). Each procedure was performed alone or in combination according to the results obtained after DNB and available guidance.[6]
This work has several limitations. First, this is a retrospective chart review of prospective data. Even if, since the beginning of our practice, data of each patient who benefited from a DNB were collected in our database, some results were missing, explaining why only 622 among 1290 patients were included in the present study. Second, the improvement observed after DNB resulted from a global and subjective analysis (no improvement, partial improvement, or complete improvement). We did not perform a specific analysis of spasticity reduction, ankle range of motion, and gait kinematics improvement because it would have reduced the number of included patients. Furthermore, the effects of treatments on spasticity, range of motion, and gait have already been studied previously. The main objective of the study was to determine the frequency of the different treatments in clinical practice. Third, the study analyzed data of patients treated over a long period. Our medical practice may have changed over time. Finally, this is a monocentric review by an interdisciplinary team. As we know, the practice may vary from one team to another.
Financial support and sponsorship
Nil.
Conflicts of interest
Thierry Deltombe has served as investigator, speaker and advisor for Abbvie, Ipsen and Merz.
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[Table 1], [Table 2], [Table 3], [Table 4]
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