Commentary Nothing confounds a parent or grandparent more than watching their young child walk “abnormally.” Whether the concern is flat feet, in-toeing, or bowed legs, most of our orthopaedic care of these children consists of education and reassurance. However, when the family complains that their child is walking on his or her toes, red flags go up in the clinician’s mind. Does the child have cerebral palsy that has not been diagnosed, does the patient have muscular dystrophy, or is this a case of idiopathic or habitual toe-walking? The first two questions can be answered by means of a careful history and physical examination and treated appropriately, but idiopathic toe-walking is a conundrum. What are its causes and what are the best ways to treat this perplexing and relatively common condition1?

It is clear to me that idiopathic toe-walking is a neurologically based diagnosis. Many of the children are on the autism spectrum2, and many have speech and language delays3. There is the hypothesis that this condition may be a sensory processing dysfunction4 or even a form of dyspraxia. Regardless of the etiology, the treating physician is faced with many different options: night splinting, serial casts, chemodenervation, and, in cases with fixed contractures, surgical lengthening of the gastrocnemius-soleus complex.

The authors of this excellent Level-I study from the Karolinska Institute in Sweden randomized their patients into two groups based on the most frequently used treatments for idiopathic toe-walking: serial casts, and chemodenervation with botulinum toxin A combined with serial casts. Each of the children had a thorough evaluation by an orthopaedic surgeon, a neurologist, and a physical therapist to ensure that there were no other diagnoses besides idiopathic toe-walking. A screening questionnaire was given to ascertain any neuropsychiatric diagnoses as well. Physical examination parameters, three-dimensional gait analysis, and parental perception of toe-walking frequency were utilized as outcome measures.

Weaknesses of some of the prospective studies in this area include the fact that several different people applied the casts, an inadequate amount of botulinum toxin A was given, a low number of patients, and inadequate follow-up. Engström et al. addressed and overcame all of these shortcomings, and I believe that this enhanced their study. One criticism and possible problem with the paper is that it does not indicate how much botulinum toxin A the patients actually received or how much the children weighed. Twelve units per kilogram is a total body dose. I would be surprised if the authors gave that total dose to just the gastrocnemius-soleus muscle complex, but if they did, they should have indicated this. Since these were older children (mean, age nine years), a dose of 12 U/kg means that the authors could have been injecting a large amount of botulinum toxin A into the gastrocnemius-soleus complex muscle group.