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.
Engström et al. found that a high percentage (58%) of the children had a family history of toe-walking, and that there was no clinically relevant difference between the two different treatment regimens in the short (three-month) or longer (twelve-month) term, as demonstrated by parental reports, physical examination, or gait analysis. They did not provide the results of the neuropsychiatric studies in the present study, as they had recently reported them in another journal5, but they indicated that the neuropsychiatric findings had no effect on the eventual outcomes of the treatment of the toe-walking.
On the basis of this well-conceived and well-executed study, the authors concluded that both treatments improved toe-walking at both the three and the twelve-month time interval, yet thirty-eight of forty-seven children still walked on their toes to a variable extent after treatment. This is not a ringing endorsement of cast treatment, but the authors thought that the amount of time that the children were walking on their toes decreased in both groups.
What do casts do to decrease the incidence of toe-walking? There are several theories. Obviously, if there is a contracture, the use of serial casts makes sense. However, none of the patients in this study had contractures. If the toe-walking is due to a dyspraxia, then perhaps just placing the foot in the proper position will lead to learning in the brain through pattern recognition. If it is a sensory processing dysfunction, then placing a cast leads to a constant sensory input that the child eventually incorporates into a more normal gait pattern. Of course, no one knows how casts work when a patient does not have a contracture, but this study and many others have shown some clinical improvement in some patients after cast treatment.
The main conclusion is that botulinum toxin A probably has no role in the treatment of idiopathic toe-walking. This should come as no surprise as the main use of botulinum toxin A is to treat spasticity. It does weaken the muscle in the short term, but since placing the limb in a cast also weakens the muscle, it never seemed appropriate to me to add botulinum toxin A to the treatment of idiopathic toe-walking. However, my perception that many clinicians were injecting this neurotoxin into patients for this condition and that there was a chance that it did not change the outcome was supported by this paper. I believe that this paper supports not injecting botulinum-A toxin into the gastrocnemius-soleus muscle complex of children with idiopathic toe-walking.