What is ITW?

Idiopathic  toe walking (ITW) is a developmental gait disorder characterized by the child habitually walking on the toes, in the absence of any specific muscular or neurological disorder.   

General characteristics

Habitual toe walkers usually adopt a toe-walking gait from the onset of independent walking. They walk independently bilaterally on the  toes within the typical age range (Sala et al 1999, Sobel et al 1997)  

The child may spontaneously walk with a heel strike gait some of the time, and most children can adopt a heel-strike gait pattern when instructed to do so. However, the pattern of muscle activation differs from that of typically developing children (Crenna 2005).  (See Gait Kinematics and EMG studies below.) 

The majority stand plantigrade (Sobel et al 1997).  They tend to stand with the feet wide apart and turned out. 

Muscle tone, deep tendon reflexes, and sensation are normal. (Sala et al, 1999.) Muscle strength and endurance, when tested in functional movements patterns is often poor. 

Children who toe walk often have family members who also toe walk, with a familial incidence of up to 32% (Hemo et al, 2006) 

Etiology

The etiology of idiopathic toe walking is not known.  The tendency to walk on the toes is usually ascribed to shortening of the calf muscles and Achilles tendon. However,  although some children have marked restriction of dorsiflexion, in many children the degree of restriction is only mild. 

A study by Furrer et al (reported by Sala) noted children who are assessed at a younger age are less likely to have limitation of dorsiflexion than older children, lending support to the idea that the child develops tightness in the tendo achilles a result of persistent toe walking, rather than this tighness being the cause of the toe walking.  

Sensory modulation disorders have been proposed as a reason for a child walking on the toes. However there is no evidence for this claim (Williams, 2010)

Infants learning to walk do not have a consistent heel-toe gait: this is only established after  several months of independent walking experience as the child learns to control the many different aspects of the stance and swing phases of a mature gait pattern. The question that has not been addressed by researchers is why some children do not develop a typical heel-toe sequence during the stance phase of walking. 

Clinically children who present with toe walking in most cases also have generalised joint hypermobility, with associated muscle weakness and paradoxical tightness in two joint muscle and fascial structures of the lower quadrant.(Versfeld 2016)  This gives rise to restricted range of hip adduction and lateral rotation with the hip in extension which has an affect on lower limb alignment in walking.   See Idiopathic Toe Walking:  A practical Approach

Most children with generalized joint hypermobility walk with a heel-toe gait. So the question remains as to why some children toe walk while others do not. 

Children on the autistic spectrum have a higher incidence of toe walking than neuro-typical  children (Brown 2011).  This may be related to the postural  and coordination difficulties experienced by children on the autistic spectrum (Bhat et al 2011, Wyat et al 2011).  Generalised joint hypermobility is also common in ASD (Shetreat-Klein  2014).

Gait kinematics in toe walkers

Crenna et al (2005)  used kinematic, kinetic and EMG analysis to compare the spontaneous heel-contact gait patterns of 13 children classified as habitual toe walkers (HTWs) and age-matched controls.  "In the HTWs, the incidence of spontaneous heel-contact strides during a single recording session ranged from 15% to 92%, with no correlation with age, passive ankle joint excursion, walking speed and trial order." 

"Hallmarks of the heel-contact strides were premature heel-rise, reversal of the second rocker, relative shortening of the loading response and anticipation and enhancement of the electromyographic (EMG) activity normally observed in the triceps surae (TS) during the first half of the stance phase. This variant of the locomotor program is different from the walking patterns observed in normally developing toddlers and children with cerebral palsy (CP). It does not necessarily reflect a functional adaptation to changes in the rheological properties of the muscle–tendon complex."

Crenna et al also looked at the difference in EMG recordings of the muscle action in HTW when walking with a  heel contact gait.  "The most striking changes marking the heel-contact gait of HTWs were seen at 10–30% of the stride cycle. Dynamic EMG studies have shown that during this phase the forward rotation of the shank and the simultaneous progression of the COP are normally controlled by a lengthening contraction of the TS (the TSa component), with EMG silence on the antagonists TA  (Crenna 2001) 

 "In the heel-contact strides of HTWs, TSa proved to be most often prematurely recruited, with an increase in relative amplitude, and frequently followed by a definite silent period, while the reciprocal EMG silence was usually preserved. The prematurely augmented plantar-flexor torque resulting from these changes might well be responsible for the rapid progression of the COP toward the metatarsal heads and the shortening of the weight-acceptance phase. Moreover, the enhanced TSa in the bi-articular knee-flexor gastrocnemii was congruent with a premature rise of the heel and early plantar-flexion of the foot. Indeed, TSa activity attained a peak between 13% and 16% of the stride, which, taking into account the electro-mechanical delay [29], is consistent with the achievement of maximum mechanical effect at around 20% of the stride. The increased braking of the forward rotation of the shank, produced by the augmented TSa component, may produce knee hyperextension. The absence of hyper- extension in the children tested indicates a protective action of the gastrocnemii and possibly of the hamstrings, but the latter was not analysed in this study. "

Differential diagnosis 

Mild diplegic cerebral palsy.  There are differences in the patterns of muscle recruitment, and in particular the co-activation of antagonisitc muscles is commonly seen in CP but not in ITW (Policy 2001).  Muscle tone, deep tendon reflexes, and sensation are normal. (Sala 1999)
Duchenne muscular dystrophy
Spinal conditions such as syringomyelia  can present with equinus contractures and/or toe walking
Tethered cord syndrome may present as gait abnormalities and subtle neurological signs.  
Muscular skeletal disorders of the lower limbs (injuries, infection) present as acute onset of toe walking, usually in one leg. Idiopathic toe walking does not have an acute onset and is always bilateral. 

Intervention strategies

 In a review idiopathic toe walking Sala et al concluded: The efficacy of different treatment modalities is unclear. Improvement has been reported with exercises, serial casting,and surgery.

Comparisons across studies are difficult because clinical criteria for the use of each type of treatment are usually not provided. Generally, surgical intervention is used for only the worst cases when significant plantarflexor contractures are present.

​Hagland reported on a series of patients who had received one injection of botulinum toxin: 

"The purpose of this study was to investigate whether botulinum toxin A (BTX) improves the walking pattern in ITW as examined with 3-D gait analysis. 

"A consecutive series of 15 children (aged 5–13 years) were enrolled in the study. The children underwent a 3-D gait analysis prior to treatment with a total of 6 units/kg bodyweight Botox? in the calf muscles and an exercise program. The gait analysis was repeated 3 weeks and 3, 6, and 12 months after treatment. A classification of toe-walking severity was made before treatment and after 12 months.The parents rated the perceived amount of toe-walking prior to treatment and 6 and 12 months after treatment. 
Eleven children completed the 12-month follow-up. The gait analysis results displayed a significant improvement, indicating decreased plantarflexion angle at initial contact and during swing phase and increased dorsiflexion angle during midstance at all post-treatment testing instances. According to the parents’ perception of toe- walking, 3/11 children followed for 12 months had ceased toe-walking completely, 4/11 decreased toe-walking, and 4/11 continued toe-walking. After 6–12 months, the toe- walking severity classification improved in 9 of the 14 children for whom data could be assessed." 

​Hagland (2010)concluded that a single injection of BTX in combination with an exercise program can improve the walking pattern in children with ITW seen at gait analysis, but the obvious goal of ceasing toe-walking is only occasionally reached.

Serial casting has been shown to be effective in two recent studies. Fox et al (2006) reported improvement in 60 % of cases treated by serial casting. 

References

Barrow, W. J., Jaworski, M., & Accardo, P. J. (2011). Persistent Toe Walking in Autism. Journal of Child Neurology, 26(5), 26-29

​Bhat, A.N., Landa, R.J. & Galloway, J.C., 2011. Current perspectives on motor functioning in infants, children, and adults with autism spectrum disorders. Physical therapy, 91(7), pp.1116-29.  PDF

​Crenna, P., Fedrizzi, E., Andreucci, E., Frigo, C., & Bono, R. (2005). The heel-contact gait pattern of habitual toe walkers. Gait and Posture 21, 311-317

​Crenna P, Do MC, Brénière Y. (2001) Motor programmes for the termination of gait in humans: organisation and velocity-dependent adaptation. J Physiol (Lond)537:1059–72.

Fox A, Deakin S, Pettigrew G, Paton R. (2006) Serial casting in the treatment of idiopathic toe-walkers and review of the literature.  Acta Orthop Belg. 2006 Dec;72(6):722-30

​Furrer F, Deonna T. (1982) Persistent toe-walking in children: a comprehensive clinical study of 28 cases. Helvetica Paediatrica Acta 37: 301–16.

Haglund-a, Y. (2010). Does botulinum toxin A improve the walking pattern in children with idiopathic toe-walking? Journal Of Pediatric Orthopedics, 301-308.

Hemo Y, Macdessi SJ, Pierce RA, Aiona MD and Sussman MD. Outcome of patients after Achilles tendon lengthening for treatment of idiopathic toe walking.  Journal of Pediatric Orthopedics. 2006; 26:336-340

Policy, J. F., Torburn, L., Rinsky, L. A., Rose, J., & D, P. (2001). Electromyographic Test to Differentiate Mild Diplegic Cerebral Palsy and Idiopathic Toe-Walking. Journal of Pediatrics 21: 784-789.

​Sala DA, Shulman LH, Kennedy RF, Grant AD, Chu ML.(1999)  Idiopathic toe-walking: a review. Dev Med Child Neurol.41(12):846-8

Shetreat-Klein M, Shinnar S, Rapin I. Abnormalities of joint mobility and gait in children with autism spectrum disorders. Brain Dev. 2014 Feb;36(2):91-6. doi: 10.1016/j.braindev.2012.02.005. Epub 2012 Mar 7. PubMed PMID: 22401670.

​Shulman LH, Sala DA, Chu MLY, McCaul PR, Sandler BJ. (1997) Developmental implications of idiopathic toe walking. Journal of Pediatrics 130: 541–6.

​Sobel E, Caselli MA, Velez Z. (1997) Effect of persistent toe walking on ankle equinus. Analysis of 60 idiopathic toe walkers. J Am Podiatr Med Assoc. 87(1):17-22

Williams, C. M., Tinley, P., & Curtin, M. (2010). Idiopathic toe walking and sensory processing dysfunction. J Foot Ankle Res. 2010 Aug 16;3:16.

​Whyatt CP, Craig CM. (2011) Motor Skills in Children Aged 7-10 Years, diagnosed with Autism Spectrum Disorder. J Autism Dev Disord. 2011 Dec 17. [Epub ahead of print]