Idiopathic Toe Walking: An Update on Natural History, Diagnosis, and Treatment : JAAOS - Journal of the American Academy of Orthopaedic Surgeons

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Reviews: Review Article

Idiopathic Toe Walking: An Update on Natural History, Diagnosis, and Treatment

Bauer, Jeremy P. MD; Sienko, Susan PhD; Davids, Jon R. MD

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Journal of the American Academy of Orthopaedic Surgeons: November 15, 2022 - Volume 30 - Issue 22 - p e1419-e1430
doi: 10.5435/JAAOS-D-22-00419
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Toe walking (TW) in children is a common presenting report in both pediatric and orthopaedic clinics and includes developmental, benign, and more serious conditions. TW is defined as a child whose initial foot contact pattern is on the forefoot, rather than the normal heel strike. On the initial evaluation of a child with TW, it is imperative for the practitioner to understand the cause of the TW. The differential diagnosis for TW ranges in severity from children who toe walk as part of normal development to children with contractures (congenital or acquired) and neurologic or neuromuscular conditions. The latter group includes cerebral palsy (CP), muscular dystrophy, spinal dysraphism and tethered cord syndrome, hereditary spastic paraplegia, and hereditary motor sensory neuropathies.1 In the absence of another cause of the TW, a diagnosis of idiopathic toe walking (ITW) is made. TW can represent a phase of normal ambulatory development during early development, with spontaneous normalization in nearly 80% of children who toe walk by the age of 10 years.2 It has also been shown that there is a strong family history in some children who toe walk and an association with sensory processing issues and autism spectrum disorders.3 In such cases, this leads to the question as to whether this diagnosis is truly “idiopathic” and perhaps has a true underlying neurologic cause. Persistent TW in children older than 3 years often results in parental concern, provoking multiple medical visits, and a range of interventions including physical therapy (PT), stretching (SC), botulinum toxin A (BTX-A) injections, and surgery.2

Children who continue to toe walk beyond the age of 5 years are described as having persistent idiopathic toe walking (ITWp). ITWp is used to describe persistent walking in a toe-toe pattern and can include both children with and without a contracture at the ankle. Sorting through the differential diagnosis of ITW can be challenging, and the lack of consensus in the literature regarding ITW terminology further confounds the issue.

It is helpful to recognize several categories of children who fall under the commonly used terminology umbrella of ITW. These include children younger than 5 years who have no contracture but walk on their toes, children older than 5 years with persistent TW, and TW secondary to a congenital or acquired contracture. Having a clear nomenclature helps to delineate the different forms of ITW, which then has different implications for treatment (Figure 1). For example, a 3-year-old child with ITW and full range of motion (ROM) is expected to resolve spontaneously without any treatment,2 whereas an older child with ITWp and a contracture may need intervention.

Figure 1:
Flowchart showing an outline of the proposed nomenclature of idiopathic toe walking.

The goal of this review was for the reader to gain a better understanding of the nature, natural history, and clinical consequences of ITW to best determine which children need treatment.

Natural History

ITW is a common pediatric condition with a prevalence of 5% to 24% in children.2-4 ITW often resolves spontaneously, and therefore, many think that it does not warrant any attention. However, given the large number of children with ITWp presenting for evaluation in orthopaedic practice, it is evident that not all children resolve spontaneously. Engstrom and Tedroff5 followed a cohort of typically developing children aged 5 years in Sweden and found the prevalence of TW among children presenting for a well-child visit to be 1.9% (26/1,401), with another 2.6% (37/1,401) reporting a history of TW that had spontaneously resolved. When they followed these children to the age of 8 years, another 23% (6/26) resolved and by the age of 10 years, another 27% (7/26), leaving only 13 children who still toe walked or had surgery to address TW.2 In their cohort, only one child developed a contracture. However, Sobel et al4 found that ankle ROM decreased with increasing age in their study of children with TW, with only one child older than 6 years with dorsiflexion greater than 0° at follow-up. Engelbert et al found a 9% prevalence of ITW (21/348) and joint contracture, with another 3% cases (9/348) who toe walked without contracture.6 Children with ITW were greater than 3 times more likely to have a contracture of ≤0° dorsiflexion than those with a normal gait pattern.7 Williams et al8 found that in children with ITW, there was a higher incidence of motor and sensory challenges than expected. Little is written on the long-term sequela of untreated TW; however, abnormal talar morphology, including the lack of a talar recess, has been documented in 66% of children with ITW and loss of talar roundness in 30% of children with ITW.9


Because a family history of TW is reported in many children with ITW, there is a strong possibility that a subset of children may have a genetic cause of the condition.4,5,10,11 Pomarino et al12 found that ITW is seen predominantly in boys and hypothesized that there may be an autosomal X-linked recessive inheritance pattern accounting for 30% to 70% of reported cases of ITW.

Using whole genome sequencing, Pomarino et al13 identified two groups of toe walkers based on clinical findings and gene modifications. Patients defined as having ITW type I have a late onset of the gait abnormality of TW, normal reflexes until the age of 14 years, hypertrophy of the calf muscle, pes cavus, and delayed language development. The clinical features of ITW type I also include bilateral footdrop and general gait abnormalities. This clinical phenotype has been associated with changes in the PMP22, EGR2, and AIFM1 genes.13 By contrast, patients defined as having ITW type II display early onset of TW and hypertrophy of the calf muscle and have at least one other family member who displays similar symptoms. Approximately 52% of children who toe walk have type II ITW, spend approximately 70% of the time walking on their forefoot, and have been linked to changes in multiple genes.13 Many of the genes identified as being linked to ITW have also been reported to being associated with both autosomal dominant mutations in CMT1 and CMT2 genes (genes initially associated with Charcot-Marie-Tooth neuropathy), in addition to autosomal recessive variants CMT4, CMT2, CMTRI, and CMTX.14 Because children with ITW may have a genetic component, understanding the genetic determinants may help clarify the natural history and guide clinical decision making. No standard genetic testing recommendations exist for the diagnosis of ITW, although testing for other neurologic causes of TW is common.


In addition to understanding the natural history of ITW (and determining whether the child's TW will resolve without treatment or will become persistent), the other challenge is in making the diagnosis itself. Although no single clinical finding is pathognomonic, Table 1 outlines some common history and physical examination findings that help direct a diagnosis.

Table 1 - Outlines History and Physical Examination Findings That Would Lead to a Diagnosis Other Than ITW
Historical Findings Diagnostic Considerations
Premature birth/perinatal complication CP
Delayed motor milestones CP, neuromuscular disorders, and others
Progressive toe walking Tethered cord, diastematomyelia, MD, and HSP
Treatment refractory CP, tethered cord, and dystonia
Incontinence/constipation Tethered cord and diastematomyelia
Leg and back pain Tethered cord and diastematomyelia
Sensory processing disorder or autism spectrum disorder ITW
Variable TW with varus foot posturing Dystonia
Worsening throughout the day Dopa-responsive dystonia
Family history of similar condition HSP, HSMN/peripheral neuropathy, and MDs
 Physical examination findings
 Dorsal midline skin lesions Tethered cord and diastematomyelia
 Calf hypertrophy and proximal muscle weakness Duchenne muscular dystrophy, and other MDs
 UMN findings (spasticity, hyperflexia, and Babinski) HSP, CP, and spinal cord lesion
 Unilateral Structural: limb-length discrepancy; hip dysplasia, arteriovenous malformation, and trauma; or neurologic: hemiplegic CP, peripheral neuropathy, and spinal cord
 Calf hypertrophy and proximal muscle weakness Duchenne muscular dystrophy and other MDs
 LMN (cavus, muscle atrophy/weakness, sensory loss, and hyporeflexia) Neuropathy
 Popliteal angle May differentiate between CP and ITW
CP = cerebral palsy, HSP = hereditary spastic paraplegia, ITW = idiopathic toe walking, TW = toe walking, UMN = upper motor neuron

Because of the large differential diagnosis and the possibility of a genetic cause, the initial workup of a child with ITW must include a thorough history and physical examination, particularly looking at the general development, timing of the TW, and whether the TW is intermittent or worsening. Of note though, the history of prematurity alone is unable to distinguish between CP and ITW.15 When history or physical examination findings are abnormal, a consultation with a neurologist is warranted. Haynes et al3 found in their series of children with abnormal or asymmetric ITW referred to pediatric neurology from pediatric orthopaedics, 62% were determined to have an underlying pathologic cause. If those children with autism and ADHD are excluded, the diagnosis of a pathologic cause was still 47%. An important finding was that 71% of children with asymmetric TW had an eventual diagnosis of hemiplegic CP.3

Although no single examination measurement is diagnostic, a comprehensive examination, including the foot, spine, general gait, and ROM, and neurologic examination are important. On visual gait examination, it is important to determine whether the child can walk in a heel-toe manner when asked. Although this can be distressing/frustrating to the caregiver, it is a reassuring sign to the clinician because it demonstrates that the child has normal motor control and does not have a plantar flexion contracture that precludes heel contact during gait. Other observational gait parameters to include are ataxia, Trendelenburg, or arm posturing that occurs when running, which may be a sign of mild hemiplegic CP. The Gower maneuver is important to assess for signs of primary muscle pathology such as muscular dystrophy. Examination of the foot is conducted in both standing and seated positions to look for cavus deformity and to assess for signs of persistent TW such as increased forefoot and decreased hindfoot callosity and widening of the forefoot (Figure 2). The two most important ROM parameters are the popliteal angle and ankle dorsiflexion with the knee extended and flexed (Silfverskiold test) (Figure 3) with the subtalar joint held in a neutral position to avoid apparent dorsiflexion from occurring through either the subtalar or midtarsal joint.16 There is a range in the literature as to what is considered a contracture (between 0° and 10° dorsiflexion), and we define a contracture as less than 5° dorsiflexion.17 The spinal examination is important to assess for any asymmetry, hairy patches, or other signs of spinal dysraphism that would be indicative of a primary spinal etiology. Finally, the neurologic examination should include assessment of strength, reflexes, spasticity, selective motor control, and upper motor neuron signs such as Hoffman or Babinski.

Figure 2:
A, Lateral foot photograph showing plantar flexion contracture and increased arch height. B, Photograph showing posterior and mirror views of forefoot pressure distribution and relative widening of the forefoot compared with the hindfoot.
Figure 3:
A, Photographs showing Silfverskiold examination demonstrating increased dorsiflexion of the ankle when the knee is flexed. B, With the knee extended, the ankle is in equinus consistent with the isolated contracture of the gastrocnemius muscle.

The primary purpose of the clinical history and physical examination is to exclude other disease processes that may be associated with a TW gait pattern. Within this paradigm, ITW can be considered a diagnosis of exclusion because there is no pathognomonic finding on clinical history or physical examination. Although the phenotype of ITW can be variable, the diagnosis can be made with confidence once the other possible diagnoses have been excluded.


Quantitative Gait Analysis

Quantitative gait analysis (QGA) has been used to discriminate between ITWp and CP. Children with ITW have kinematic, kinetic, and dynamic electromyography profiles that are similar to typically developing children when asked to walk on their heels, but are distinct relative to children with CP.18

The main kinematic changes in children with ITW occur at the ankle and knee. During the stance phase, the ankle exhibits more plantar flexion than typically developing children or children with CP. In the swing phase, there is initial motion toward dorsiflexion, followed by a sudden plantar flexion wave midway through the swing phase, resulting in prepositioning the foot to have a toe strike at the subsequent initial contact in the stance phase19 (Figure 4). Knee extension in stance has been studied and found to have either normal19 or mild knee hyperextension,19,20 whereas there is increased knee flexion in the stance phase in children with mild spastic diplegic CP.19

Figure 4:
A, Graph showing ankle kinematics. The x-axis represents the ankle ROM, and the y-axis represents the percentage of the gait cycle. The y-axis is divided by a red line that separates the stance phase from the swing phase. The gray band is the laboratory normative value for typically developing children. The black arrow shows that the foot lands in plantar flexion and has no first rocker. The ankle achieves limited dorsiflexion with weight acceptance (second rocker) and has a limited arc of the third rocker. The red arrow demonstrates that the ankle goes into plantar flexion at late swing after an initial wave of dorsiflexion in the swing phase. B, Graph showing ankle kinetics. The x-axis represents the ankle moments measured in Nm/kg, and the y-axis represents the percentage of the gait cycle. The y-axis is divided by a red line that separates the stance phase from the swing phase. It shows a “double bump” arc consistent with an initial plantar flexion moment (blue arrow) instead of the typical dorsiflexion moment.

The sagittal plane ankle kinetic profile of children has shown an absence of the internal dorsiflexor moment at initial contact, consistent with an absence of the first rocker19 (Figure 4). The stance phase ankle moment profile was characterized by a bimodal shape, with an elevated midstance plantar flexor moment, followed by a diminished plantar flexor moment at terminal stance. The ankle power profile in children with ITW was characterized by a loading response power absorption phase, a midstance power generation phase, and a diminished terminal stance ankle power generation phase.

Dynamic electromyography has also been used to distinguish between ITW and CP with the “coactivation test.”15 The child is asked to simultaneously extend their knee and dorsiflex the ankle, and if there is EMG activation of the gastrocnemius, it is indicative of CP. A study using QGA, comparing self-selected versus best walk (ie, when asked to walk with feet flat on the ground), determined that 70% of children were able to normalize some but not all the stance and swing variables, and only 7% were truly able to completely normalize their gait.19

A classification scheme for gait patterns seen in children with ITW by Alvarez et al,21 based on kinematic and kinetic parameters, where type 1 is mild and type 3 is severe has been proposed. This classification is based on three primary criteria: presence of a first ankle rocker, presence of an early third ankle rocker, and a predominant early ankle moment. The utility (reliability and sensitivity to change follow intervention) of this classification has yet to be established.22 QGA, if available, should be considered to establish or confirm the diagnosis of ITW, assess the severity of gait disruption in these children, determine the need for nonsurgical or surgical management, and assess the outcomes after intervention.20,23-26

Radiographic Evaluation

When a foot clinically has increased cavus or forefoot width, a standing AP and lateral radiographs of the foot to assess for the degree of cavus deformity, which may guide treatment (ie, plantar fascia release for cavus >10°). Measuring the calcaneal pitch helps to determine whether the child has a primarily equinus or cavus deformity, but caution must be taken to ensure that the tibia is perpendicular to the ground. For this reason, the tibiocalcaneal angle is a more accurate measurement. The degree of cavus can also be determined by measuring the Meary angle. The AP view is useful to document the degree of forefoot deformity by measuring the forefoot splay (Figure 5).27

Figure 5:
Radiographs showing A, AP of the foot, showing an increased forefoot width compared with the hindfoot. B, Three measurements are demonstrated. White arc: Meary angle or the lateral talus: The first metatarsal angle shows the degree of cavus deformity. Yellow arc: tibial: The calcaneal angle shows that the calcaneus is in equinus. Red arc: Calcaneal pitch appears normal because the tibia is not perpendicular to the floor.

Treatment For Persistent Toe Walkers

Once the diagnosis has been established, the treatment for children with ITWp is based on the assessment of age (skeletally immature or mature), ROM, absence or presence of a fixed contracture of the gastrocnemius-soleus complex (GSC), and foot shape (normal, increased, or decreased arch). For children with a normal ROM yet persistent TW, the treatment is primarily nonsurgical, including bracing and PT. For children with ITWp and limited ROM, the treatment is focused on improving the ROM (casting or surgery), maintaining the improvement (braces), and normalizing gait (PT). Our treatment algorithm is based off the available evidence and presented in Figure 6.

Figure 6:
Flowchart showing the treatment algorithm for a child presenting with toe walking.


Stretching is a main stay of PT, although the evidence that ROM is improved to a clinically significant amount is lacking. A Cochrane review showed an average improvement of ROM of 2° in neurologic conditions and only 1° in non-neurologic conditions.28 Liu found less than 2° improvement of ROM after a stretching protocol, with no change in the injury rate.29 However, there may be a role of stretching to preserve ROM obtained after surgery or casting and for gait training after treatment. There is not sufficient evidence for the use of biofeedback devices as a treatment of TW.30


Ankle foot orthoses (AFOs) are often used both in children with ITWp with adequate ROM and in those who have had treatment to improve their ROM by surgery and/or casting. Any AFO should be designed to prevent excessive plantar flexion. This can be done with a posterior leaf spring (PLS) AFO or a hinged/articulated AFO (HAFO) with a plantar flexion stop. A small trial evaluating both a HAFO and a custom rigid foot orthotic found that the HAFO did better at normalizing gait while it was being used, although the simple orthosis maintained better heel-toe gait 6 weeks after cessation.31 A study by Bartoletta found that the use of an AFO had an odds ratio of nearly four for the likelihood of a successful outcome after both surgical and nonsurgical treatments.6 A HAFO was used for nearly 6 months in a study by Berger, who found that TW that persisted greater than 50% of the time was found in 36% of the children at 24 months.32 Driano found that the use of footwear modifications in childhood had negative effects, so any footwear or orthotic treatment must be carefully weighed against the natural history of TW.33 For children with ITWp older than 5 years, with dorsiflexion ROM >10° with the knee extended, the authors recommend the use of a PLS AFO along with PT to help break the pattern of TW. Although HAFO with a plantar flexion stop will work similarly, we find the PLS to fit better into shoe wear and still allow dorsiflexion during stance when designed properly.


There is notable heterogeneity of cast treatment in the literature (duration of each cast, goal ROM, and postcast bracing treatment and therapy) with very few high-quality studies published. When serial casting (SC) is done, casts should be applied with the subtalar joint held in neutral to slight inversion to avoid causing a midfoot break. Because the child is allowed to walk in the casts, they must be well padded to avoid heel pressure sores. The casts are then changed at 1- to 2-week intervals until dorsiflexion of greater than 10° with the knee extended is achieved (Figure 7). When the last cast is removed, the child is usually transitioned to an AFO and continues PT for maintaining the ROM and gait training. Although the evidence is not clear that SC will result in long-term normalization of gait, it does seem to have relatively few complications other than skin ulceration.11,34 Eastwood found that 41 children treated with casting spent a mean 70% of the time TW after treatment. Although only 22% had developed a normal gait, no difference was found compared with the observation cohort.35 Stricker similarly showed little difference between observation and casting, yet the more severe group that had surgery had a better improvement of ROM compared with the casting group.11 By contrast, Thielemann found that in 10 children treated by casting, their gait was no different than a cohort of typically developing children at a 6-month follow-up.36 A study by Davies grouped children who received both casting and casting + BTX-A together and compared them with a group of children who had inactive treatment (stretching).37 At an average of 13 years of follow-up, they found that the casting group had improved dynamic dorsiflexion ROM and a decreased severity of TW, but 52% of the children in the casting group had self-reported TW compared with 45% in the inactive group. A systematic review concluded that there was preliminary evidence that casting improves ROM, ankle kinetics, and kinematics, but the results do not seem to be long lasting.38 Although the best evidence is level 3, casting does seem to have short-term benefits with relatively few complications. The authors offer SC for children between 5 and 12 years with ROM at the ankle from −10° to +10° as presented in our protocol in Figure 6.

Figure 7:
A, Photograph showing the posterior view of a child undergoing serial casting. The subtalar joint is held in a neutral position to a slightly inverted position to avoid dorsiflexion through the midfoot. B, Photograph showing the lateral view of a child's final serial cast. A heel post is added to ensure heel contact, especially early in the casting process. A rigid toe plate extends to the end of the toes, allowing for free toe extension.

Botulinum Toxin A

Two recent randomized controlled trials have evaluated the off-label use of BTX-A for the treatment of ITW.37,39 Satila randomized children to a stretching, night splint, and firm shoe group and a similar group plus BTX-A administered at 6-month intervals.39 At the follow-up, there were no differences in dorsiflexion ROM or ability to walk with a heel strike. In addition, 22 of the 30 children in the BTX-A group reported 38 adverse events. Engstrom randomized children to either a walking cast group or a walking cast plus a single injection of BTX-A group.37 They found no difference in the severity of TW between the groups, and no parent reported difference in the frequency of TW. Dorsiflexion ROM improved similarly for both groups and was maintained at the 12-month follow-up. With two level I studies, the literature does not support the use of BTX-A for the treatment of ITW.


When the degree of deformity is more severe, surgical intervention is indicated. The authors recommend surgery for the following indications: contracture >10°; child is unable to normalize their gait; persistent pain; skeletal changes apparent; or for milder contractures when SC is not an option because of compliance. Surgical lengthening can be undertaken at any of the three surgical zones of the GSC40 (to correct hindfoot equinus) and at the level of the plantar fascia (to correct midfoot cavus).41 Although gastrocnemius-driven equinus is more common in children with CP than ITWp, it is important to use the Silfverskiold test preoperatively to evaluate the contribution of the gastrocnemius to the degree of equinus present. When the gastrocnemius is determined to be the primary cause of the equinus contracture, a proximal release of just the gastrocnemius (zone 1 lengthening) may be done40 (Figure 8). When the contribution of the equinus is from both the soleus and the gastrocnemius, then a zone 2 or zone 3 lengthening can be conducted. It is our preference to lengthen the Achilles tendon, lengthening in either an open or mini-open approach to control the degree of correction during the operation to avoid overlengthening and weakness (Figure 9). It is important to determine preoperatively whether a cavus deformity is present in addition to equinus. Although it is orthopaedic dogma that you cannot conduct a plantar fascia release concomitantly with a GSC lengthening, it is experienced that there is often enough residual tightness of the posterior ankle capsule to give leverage to stretch the foot after release. We routinely conduct the cavus correction by plantar fascia release first and then use intraoperative stress fluoroscopy to determine the magnitude of the equinus deformity to select the proper zone for surgical lengthening of the GSC. Postoperatively, the child is placed in a weight-bearing below-knee cast and is transitioned to an AFO at the 4- to 6-week mark.

Figure 8:
Illustrations showing three zones of calf lengthening. The more proximal the zone, the more selective (ie, gastrocnemius only) the lengthening. The more distal the zone, the greater the possible lengthening of both the gastrocnemius and the soleus. Used with permission.
Figure 9:
Intraoperative photographs of a child undergoing a mini-open white slide. The ankle is held in maximum dorsiflexion. A, Proximal incision is marked with the direction of hemisection outlined (posterior). A distal cut is marked, and the medial 50% is transected percutaneously. The dotted line represents a typical open incision location and option if mini open is unsuccessful. B, Plantaris tendon is identified, and 1 cm is resected. C, Posterior 50% of the Achilles tendon cut. D, Final dorsiflexion is improved. Note the skin divot distally where the medial tendon was cut.

Like the data on casting, there is notable heterogeneity of the research methods and outcome measurements, making it difficult to compare studies. In general, the outcomes after zone 2 or 3 lengthening are effective, with most children achieving a heel toe gait pattern, which is maintained at follow up. A study looking at zone 2 lengthening in children with ITWp showed improved passive ankle dorsiflexion by an average of 14.1° with the entire cohort achieving a least neutral dorsiflexion.42 Westberry et al26 evaluated 26 children with severe TW who had undergone zone 2 (9 children) and zone 3 (15 children) lengthenings and found that the 15 children who underwent a zone 3 lengthening had a more severe deformity and eight underwent a concomitant plantar fascia release. For the children who received a zone 2 lengthening, passive ankle dorsiflexion improved 11.4° to a final mean of 6.6°, compared with an improvement of 22.7° for a final mean dorsiflexion of 4.8° in those undergoing a zone 3 lengthening. Using the Alvarez classification,21 they found that all patients were classified as type 3 severe, preoperatively; however, after intervention, 19% improved to a type 1 mild and 75% improved to a type 2 moderate. No cases of overlengthening or recurrence in the zone 3 group were observed, whereas there were children in the zone 2 group who required additional surgery for recurrence.

McMulkin evaluated their long-term outcomes in eight children treated with zone 2 and zone 3 lengthenings.43 At the 5-year follow-up, seven of the eight children maintained a first rocker in stance although dorsiflexion worsened over the period. Jahn evaluated muscle tendon lengths in a group of 14 children with TW and found that ROM and muscle tendon unit lengths improved postoperatively and the degree of change was correlated with the degree of preoperative deformity.44 In a study of 24 children with ITW, the ROM was improved by 9.8°, and while the ROM was within the range of normal values, the peak dorsiflexion at initial contact, stance, and swing all remained lower than the laboratory-based normative data.25 By contrast, Hemo found that after zone 3 lengthening, ROM was normalized and stance and swing dorsiflexion improved to laboratory-based normative data. However, three children did not achieve a first rocker.20

Something to note and preemptively educate the caregivers on is an external foot progression, which is often noted after surgery or casting. This is, in part, due to the difficulty in assessing tibial torsion with the ankle held in plantar flexion and the potential unlocking of the subtalar joint after the GSC contracture is resolved.

In summary, it seems that at 1 year, most children maintain their passive ankle dorsiflexion with their knee extended, although not all children achieve normal ankle kinematics. We recommend a zone 3 lengthening in children without a markedly positive Silfverskiold examination because there is less recurrence of TW without any notable risk of weakness. Although ROM does decrease with time, TW does not return in most children.


Most of the young children who toe walk with a normal ROM will eventually normalize their gait. When the TW persists (ITWp), they often present to an orthopaedic clinic for evaluation. In this situation, it is important to rule out any underlying etiology that may cause the TW before making the diagnosis of ITW. Referral to a neurologist, physiatrist, or developmental pediatrician is recommended when either the history or physical examination is abnormal. Although the quality of the available evidence is low, treatment is often necessary. We have made recommendations based off the best available evidence. For children without contracture, initial management should consist of PT and reassurance. If a child still toe walks despite PT and observation and continues to have normal ROM, an AFO may be reasonable to help normalize the gait. In children with a mild contracture, either SC or surgery is an appropriate option to improve the child's gait. Although some advocate SC in larger deformities, we recommend surgical lengthening for children with more severe contractures.


References printed in bold type are those published within the past 5 years.

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