You are in: eMedicine Specialties > Orthopedic Surgery > FOOT AND ANKLE Toe WalkingArticle Last Updated: Oct 5, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Edwards P Schwentker, MD, Professor, Departments of Orthopedics and Rehabilitation and Pediatrics, Pennsylvania State College of Medicine Editors: John S Early, MD, Clinical Professor of Orthopedic Surgery, Department of Orthopedics, University of Texas Southwestern Medical School; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Shepard R Hurwitz, MD, Director of Clinical Services, Department of Orthopedic Surgery, University of Virginia School of Medicine; Director, Division of Foot and Ankle Surgery, Department of Orthopedic Surgery, University of Virginia Health System; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of Orthopedic Surgery, University of Missouri Author and Editor Disclosure Synonyms and related keywords: equinus contracture, idiopathic toe walking, habitual toe walking, congenital short Achilles tendon, muscle spasticity, paralytic muscle disorder, jumper's gait, neuromuscular disease, cerebral palsy, paralytic muscle disease, Duchenne muscular dystrophy INTRODUCTIONSection 2 of 12
  Toe walking has multiple etiologies ranging from idiosyncratic habit to profound neuromuscular disease. The spectrum of management options extends from mere observation to operations that may involve the lengthening of multiple tendons in the same lower extremity. In dealing with this entity, the underlying pathophysiology for each case must be understood to ensure that the treatment is appropriate to the specific etiology. History of the ProcedureTenotomies are among the oldest procedures in orthopedics. It would be impossible to date the first lengthening of a heel cord. The multilevel percutaneous lengthening was described by Delpech in 1823 in France. ProblemToe walking may be a sign of a serious condition, such as profound neuromuscular disease. FrequencyThe most common cause of toe walking is cerebral palsy, which affects 1-7 per 1000 children, but toe walking occurs in fewer than 50% of these patients. Reports vary greatly regarding the incidence of the various types of cerebral palsy. (Also, see the eMedicine article Cerebral Palsy.) A second cause is paralytic muscle disease, most typically represented by Duchenne muscular dystrophy, which has an incidence of 1 per 3500 live male births. All children with Duchenne muscular dystrophy walk on their toes. Finally, toe walking may be idiopathic. No studies report the incidence of this condition. The author saw 8 patients with idiopathic toe walking out of 1160 new patient visits in his pediatric orthopedic specialty practice, but this population is significantly filtered through the referral process. EtiologyAt the benign end of the spectrum is the condition called idiopathic toe walking. This entity has also been termed habitual toe walking and congenital short Achilles tendon. The diagnosis is made by excluding all neuromuscular pathologies. Idiopathic toe walking first appears in a toddler as walking begins. Many children start out on their toes. Some give up this apparent habit pattern; others do not. Those who persist merit attention. A more common cause of toe walking is muscle spasticity. Spasticity of the muscles of the lower extremity may have multiple causes. The common denominator is a lesion within the pyramidal tract of the central nervous system. The most common cause of this is spastic cerebral palsy, in which the lesion is a deficit in the motor cortex, resulting from either a failure of development or, more rarely, from a birth injury. Less commonly in children, the insult to the motor cortex may occur after birth as a result of a cerebral vascular accident. Lower extremity spasticity may also result from damage to the fiber tracts from the motor cortex within the spinal cord. Spinal cord lesions may be congenital, traumatic, or otherwise acquired. It is important to determine the underlying etiology of muscle spasticity as precisely as possible and to understand how this alters the dynamics of gait before proceeding with treatment. (Also, see the eMedicine article The last of the 3 etiologies is paralytic muscle disease, a loss of muscle caused by loss of anterior horn cells or by a destructive process of the muscle. The classic example is Duchenne muscular dystrophy. This progressive loss of muscle tissue is associated with fibrosis. Because the plantar flexor muscles at the ankle are about 6 times more powerful than are the dorsiflexors, this fibrosis leads to a fixed contracture in plantarflexion (ie, equinus). Less common paralytic muscle diseases that may lead to toe walking include some of the other types of muscular dystrophies and some of the congenital myopathies. Again, as with spasticity, an understanding of the dynamics of gait is critical before proceeding with treatment. PathophysiologyIdiopathic toe walking results from a congenital shortness of the tendon or from a habit pattern of toe walking that leads to a fixed contracture of the Achilles tendon. Young patients who display idiopathic toe walking invariably have symmetrical involvement. The extent to which their ankles are plantarflexed in gait typically is more than any tendon contracture would require. Many patients can stand flat if prompted to do so, and with an occasional patient, the examiner can demonstrate a normal range of passive dorsiflexion. Regardless of the initial status of the heel cord, the contracture progresses with time. A long-standing equinus contracture can then lead to a valgus deformity of the hindfoot, another undesirable consequence. Two mechanisms for toe walking may result from lower extremity muscle spasticity. The first is a spastic contracture of the heel cord. Muscles that are more spastic have been shown to grow less than do muscles that are less spastic. If the gastrocnemius and the soleus are excessively spastic, a fixed equinus results. This consequence is seen most typically in spastic hemiplegia, the form of cerebral palsy that involves 1 side of the body and in which the foot and ankle usually are more involved than is the proximal limb musculature. Lower extremity spasticity may also involve the proximal joints in addition to the foot and ankle. Spastic diplegia is a form of cerebral palsy that involves both lower extremities and spares, to a relative extent, the upper extremities. Typically, there is a uniform involvement of hip, knee, and ankle in spastic diplegia. Spasticity of the hip flexors and the knee flexors causes an abnormality of gait in which the hip and knee are constantly flexed and the patient bears weight upon the toes and forefoot. This abnormality has been called a jumper's gait. The toe walking may be associated with spasticity of the ankle plantar flexors, but it is in part secondary to the flexion of the hip and knee. If hip and knee are flexed in stance and the ankle is held at a right angle (ie, plantigrade), the patient bears weight on the toes and forefoot, even though the ankle itself is not in equinus. Understanding the dynamics of the gait abnormality is important in treating toe walking associated with muscle spasticity. Is the toe walking caused by spasticity of the ankle plantar flexors alone, or must the surgeon also deal with spasticity at the knee and hip? Toe walking in paralytic muscle disease is caused by the replacement of muscle by fibrous tissue as the muscle deteriorates. All muscles are involved, but plantar flexors remain stronger than do dorsiflexors, favoring the development of equinus. Patients with paralytic muscle disease also walk on their toes to compensate for weakness of the knee extensors. In Duchenne muscular dystrophy, as a classic example, the weakness in the limb is greater proximally than distally. The quadriceps becomes weak, which threatens knee stability. The ankle plantar flexors remain relatively strong. By walking on the forefoot, the patient generates an extension moment at the knee that helps to stabilize the knee. To help understand this phenomenon, stand on the toes of 1 lower extremity. The knee is felt being pushed into extension. Once again, the dynamics of the patient's gait must be understood before treatment is instituted. ClinicalThe patient with idiopathic toe walking presents as a toddler as walking begins. The child otherwise appears completely normal and begins to walk at a normal age (anytime up to age 18 mo). The deep tendon reflexes are normal. No pathologic reflexes are present. Often, the patient can walk flatfooted if prompted. There may be a variable degree of tightness of the plantar flexors of the ankle that restricts passive dorsiflexion. Inspection and palpation of the thoracolumbar spine reveals normal findings. The child walks and runs on the toes, particularly when he or she is unaware of being observed. Balance and coordination are otherwise appropriate to the patient's age. Toe walking invariably is symmetrical in involvement. Asymmetry eliminates the diagnosis of idiopathic toe walking. The presentation of toe walking in a patient with muscle spasticity depends on the underlying cause and time of onset of the spasticity. If the condition is congenital, as it will be in the case of cerebral palsy, developmental milestones, including the onset of walking, can be expected to be significantly delayed. Muscle spasticity is apparent at the time of the initial evaluation and has an anatomic distribution that reflects the extent of the lesion of the motor cortex. The deep-tendon reflexes are hyperactive. While muscle contractures can worsen with time, it is important with cerebral palsy to understand that the underlying neurological lesion is static and nonprogressive. A patient with cerebral palsy may have associated cognitive defects, but those are separate from the diagnosis of cerebral palsy, which is by definition a disorder of the motor system alone. Patients with other causes of spasticity may present later in life with acquired toe walking. The history may adequately document an etiology, such as a stroke or spinal cord injury, that occurred abruptly. However, the onset may instead have been gradual, as might be seen with a spinal cord tumor or diastematomyelia (in which the presentation may be unilateral). A thorough examination to include the spine is required. The underlying cause may be far more significant to the patient's well-being than is the effect of the toe walking itself. In addition to determining the underlying cause of the muscle spasticity, the examiner must fully evaluate the dynamics of gait (that is, how the spasticity is causing the toe walking). Muscle function must be evaluated at all joints in the lower extremity. A patient with toe walking secondary to a paralytic muscle disease presents later, usually after the primary diagnosis has been well established. The clinical picture varies, depending on the primary diagnosis. Specific to the toe walking, the examiner must evaluate the strength of all of the muscles of the lower extremities to determine the degree to which the equinus may be compensating for weakness of knee extension. The patient's overall prognosis must be considered in the decision-making process, but if there is doubt with a paralytic muscle disease, the physician always should err on the side of optimism. Physical examination The most valuable diagnostic procedure is the physical examination. For a patient with suspected idiopathic toe walking, the examination should be directed to rule out all other possible causes. For a patient with muscle spasticity, determine the anatomic distribution of the spasticity. To what extent is the toe walking secondary to contracture of the Achilles tendon and to what extent is it secondary to spasticity of the hamstring muscles and the hip flexor muscles causing a jumper's gait? For a patient with paralytic muscle disease, preoperatively determine the contribution of the equinus to knee stability. INDICATIONSSection 3 of 12
Specific indications for treatment for each of the different causes of toe walking are discussed in Treatment. To make the proper decisions regarding treatment options, the surgeon must first determine if the toe walking should be treated at all. If it is to be treated, the decision must be made whether it can be corrected nonoperatively and, if surgery is required, whether a simple heel cord tenotomy will suffice or whether the treatment must involve multiple muscles within the lower extremities. RELEVANT ANATOMYSection 4 of 12
The most common operative procedure for the treatment of toe walking is lengthening of the Achilles tendon. The surgeon should understand the particular anatomy of this tendon, which serves the gastrocnemius and soleus muscles. The gastrocnemius takes its origin from the distal femur and inserts into the calcaneus through the Achilles tendon. By doing so, it effectively crosses the knee and ankle joints. The gastrocnemius is a major plantar flexor of the ankle and a minor flexor of the knee. The soleus originates from the posterior surfaces of the tibia and the fibula. It, too, inserts into the calcaneus by way of the Achilles tendon. The only action of the soleus is to plantarflex the ankle. It is possible to differentiate the contributions of the gastrocnemius and soleus muscles to an equinus contracture by passively dorsiflexing the patient's ankle with the knee in flexion. If the equinus significantly increases when the knee is then extended, this finding suggests that the gastrocnemius is tighter than the soleus. The examiner should be aware, however, that the dynamic actions of the 2 muscles in gait may not correlate with this passive test in patients with muscle spasticity. The Achilles tendon is formed by a blending of the distal aponeuroses of the gastrocnemius and the soleus. From the point where the 2 aponeuroses join to the insertion distally into the calcaneus, the Achilles tendon extends some 4-8 cm, depending on the patient's size. With some variability as the fibers of the tendon traverse this distance, they rotate approximately 90º degrees in the axial plane. The fibers that are medial proximally are posterior distally. The lateral fibers proximally become the anterior fibers distally. Understanding this rotation of the fibers helps in planning the percutaneous lengthening procedure discussed in Surgical Therapy. CONTRAINDICATIONSSection 5 of 12
There are instances in which each of the modalities that have been devised for the treatment of toe walking is inappropriate or frankly contraindicated. These instances are discussed along with the details of treatment options in Treatment. WORKUPSection 6 of 12
Imaging Studies
Other Tests
TREATMENTSection 7 of 12
Medical TherapyNonoperative treatment of toe walking includes observation, stretching, casting, and orthotics. A toddler with idiopathic toe walking who has just begun to walk and who is without fixed contractures should simply be observed. For many patients, this conditions represents a temporary habit pattern. The patient should be monitored at 6-month intervals. If progressive heel cord contractures are detected or if the pattern does not spontaneously resolve by age 3 years, treatment should be considered. Stretching of the Achilles tendon in idiopathic toe walking offers a limited chance of success, but it may be politic to begin with this modality when parents initially are reluctant to accept more invasive treatment. For any chance of success, however, stretching must employ the patient's own body weight. Even in a child, these lower extremity muscles are too powerful to allow effective stretch by parents or therapists with simple passive dorsiflexion. The parents should be taught to help the child stretch by having the child stand with the forefoot elevated on a small block so that the heel may drop downward. The parents steady the child and add gentle pressure to the stretching process. In a second technique, the patient leans forward against a counter, with feet together and pointed straight forward, knees straight, and hips extended. Again, the parents assist by steadying the child and adding gentle pressure. Progressive stretch is accomplished by increasing the distance from the counter. It should be stressed to the parents that they must be involved. Even older children do not effectively perform such exercises unassisted. Serial casting is an effective technique for gaining stretch of the Achilles tendon.1 The child should be placed in a below-the-knee plaster or fiberglass cast while the knee is flexed. This is accomplished most easily with the child prone and the knee bent while an assistant pushes gently downward on the forefoot. Once the cast has set, the gastrocnemius component will stretch further as the knee extends. These casts should be changed weekly to progressively increase the range of dorsiflexion. Between cast changes, the child can walk fairly effectively with cast boots. The author's preferred method of nonoperative treatment for idiopathic toe walking employs an articulated molded ankle-foot orthosis (MAFO) (see Image 1). This appliance is cosmetically acceptable, fits in a regular shoe, allows nearly normal ambulation, and prevents plantarflexion while allowing full dorsiflexion. With an articulated MAFO, the heel cord is stretched with every step. These devices are worn during all waking hours for a minimum of 6 months. MAFOs must be custom fabricated and, hence, cost several hundred dollars apiece, but they can be expected to fit for 12-18 months. Often, the toe walking habit pattern disappears after MAFOs have been worn for this length of time. For toe walking that is secondary to muscle spasticity, stretching alone invariably is ineffective. Serial casting can be used to lengthen the Achilles tendon, but the contracture will recur rapidly unless the patient is maintained in an MAFO. An articulated MAFO is an effective appliance for preventing the progressive spastic equinus that occurs with growth, providing it is applied consistently. If a patient with spasticity continues to toe walk when MAFOs are discontinued after the patient reaches skeletal maturity, operative lengthening may then be considered so that the orthosis can be discontinued. After skeletal maturity, equinus in a patient who is spastic is less likely to progress. For toe walking associated with paralytic muscle disease, the use of regular stretching and orthoses together should be considered. Both modalities of nonoperative treatment are preferable to operative lengthening, as the latter must weaken the muscle. Prolonged use of serial casts also weakens muscles and should be avoided. Surgical TherapyIf conservative measures fail to correct idiopathic toe walking after about 12 months, consider operative lengthening. This procedure can be performed under a brief anesthetic by either an open or percutaneous technique.2 Perform an open heel-cord lengthening through a medial incision 6-8 cm in length, stopping distally just proximal to the tendon's insertion into the calcaneus. Avoid a straight posterior approach, because the skin scar may contract and limit dorsiflexion. Open the sheath and incise the tendon longitudinally over the full length of the exposure, dividing the tendon into 2 equal halves. Detach one half proximally and the other distally in a Z fashion. Allow the tendon to lengthen to the degree desired, and suture the 2 halves back together in the lengthened state. Follow this repair with a standard skin closure, and immobilize the patient in a below-the-knee walking cast for 6 weeks. The author prefers a percutaneous lengthening of the Achilles tendon for most patients with idiopathic toe walking. To perform this technique, have an assistant hold the patient's foot and ankle in maximum dorsiflexion after the skin is prepared. A thin-bladed tenotomy knife is inserted through a small medial stab wound 5-8 cm above the calcaneal insertion, depending on the size of the patient. By feel, divide the medial half of the proximal tendon. Make a second medial stab wound just above the distal insertion, and there, divide the anterior half of the tendon. If the tendon has rotated a full 90º over this length, half of the fibers will have been cut proximally and the other half will have been cut distally. The assistant will feel the tendon give, and the equinus contracture may then be corrected. After covering the wounds with small dressings, apply the below-the-knee cast. Control the amount of correction by immobilizing the foot and ankle in the cast in more or less dorsiflexion. If the tendon fails to part with 2 incisions, make a third stab wound from straight posterior, halfway between the first 2 incisions. Through this, cut the lateral half of the fibers until the tendon gives. Open and percutaneous techniques are applicable to patients with toe walking secondary to muscle spasticity. As indicated, however, before simply lengthening the Achilles tendon in a patient with spasticity, it is critical to determine if a component of the toe walking is caused by spastic flexion of the knee and possibly also of the hip. Observe the patient in gait. Is the ankle truly in equinus, or is the patient bearing weight on the forefoot because the knee is flexed? If the latter is true, do not lengthen the heel cord. Doing so will change a jumper's gait into a crouch gait and worsen the patient's ability to walk. To appropriately treat such a patient, consider lengthening the hamstrings and possibly the hip flexors. Management of this complex multiple-joint situation is beyond the scope of this article. Patients with spasticity with unilateral involvement, or spastic hemiplegia, usually have true equinus. If the patient walks with the knee no more than slightly flexed and the ankle is in definite plantarflexion, the heel cord safely may be lengthened. If the ankle can be brought passively to neutral with the knee flexed, but the ankle thrusts into equinus as the knee is extended, consider release of the gastrocnemius insertion alone. This release is performed through the gastrocnemius aponeurosis just before it joins the aponeurosis of the soleus to form the Achilles tendon proper. If the ankle remains in significant equinus despite knee flexion, lengthen the entire tendon as described above, either with an open Z technique or percutaneously. Heel cord lengthening can be considered in a patient with paralytic muscle disease who walks on the toes, but only if the knee extends fully and the quadriceps muscle has normal or near-normal strength. If the patient is using toe walking to generate an extension moment at the knee to compensate for a weak quadriceps, lengthening the heel cord will cause a premature loss of ambulation. All patients with Duchenne muscular dystrophy during their last few years of ambulation employ toe walking to compensate for weak knee extensors. Management of toe walking in such patients must be confined to nonoperative modalities. Postoperative detailsAfter a heel cord has been lengthened with either an open or a percutaneous technique, the patient should be immobilized in a below-the-knee walking cast for 6 weeks. The position of the ankle is critical if the operation was performed percutaneously, because the position determines the degree to which the tendon is lengthened. The ankle should be placed in more dorsiflexion to increase length, and in more plantarflexion to minimize lengthening. Follow-upFollowing cast removal, the patient may resume walking as tolerated. A patient with idiopathic toe walking will be unable to toe walk and will run flatfooted immediately out of casts. Warn the parents preoperatively that this weakness is to be expected. The gastrocnemius and the soleus will regain strength slowly over the subsequent few months, and the ability to toe walk and to run usually will return. Monitor the patient for at least 6 months after these abilities are regained to ensure that toe walking does not recur. If it recurs, place the patient in articulated MAFOs. Immature patients with spasticity or paralytic muscle disease should be monitored closely after heel cord lengthening. With growth or continued muscle fibrosis, contractures are prone to recur. Prescribe stretching and/or orthotics as needed to prevent recurrence. For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center. Also, see eMedicine's patient education article Cast Care. COMPLICATIONSSection 8 of 12
The chief concern following operative heel cord lengthening for a patient with idiopathic toe walking is recurrence. This is a rare complication, but if it occurs, the author recommends using an articulated MAFO for up to a year before considering repeat operative lengthening. The diagnostic workup should be repeated for any patient whose contractures have recurred as a means of looking for signs of neuromuscular disease or intraspinal pathology that might not have initially been evident. Recurrence following operative heel cord lengthening also is possible in patients with spastic or paralytic muscle disease. The appropriate application of orthotics should prevent this complication in most cases. A more serious complication for patients with toe walking secondary to spasticity or paralytic muscle disease is postoperative deterioration or loss of ambulation. Such complications can be avoided by careful preoperative evaluation of the appropriateness of heel cord lengthening. If function is adversely impacted by tendon lengthening, the foot and ankle should be supported with an orthosis. OUTCOME AND PROGNOSISSection 9 of 12
Patients with idiopathic toe walking who have spontaneously discontinued toe walking or who, following operative or nonoperative treatment, remain down on their heels for more than 1 year can be considered cured. Late recurrence is unlikely, and there should be no adverse late effects from any treatment employed. The prognosis for patients with spasticity or paralytic muscle disease is less predictable. These patients deserve follow-up indefinitely, as recurrence remains a risk. FUTURE AND CONTROVERSIESSection 10 of 12
Some controversies exist regarding the use of gait analysis in diagnosis (see Other Tests). MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Article Last Updated: Oct 5, 2007 | |||||||
