Clubfoot The clubfoot is the most common of the upper motor neuron damage postures of the lower extremities, and it has the greatest impairment of walking function. The foot and ankle are turned inward and may be accompanied by downward toe flexion or claw toe. The lateral edge of the foot, especially the fifth metatarsal head, is usually pressed against the floor or against the footrest of a wheelchair when standing and walking. Skin lesions may develop at the fifth metatarsal head after prolonged pressure. A pattern of maintaining a clubfoot is often present throughout the support phase of the gait cycle. As the gait cycle progresses, inversion of the foot may increase during weight bearing, causing ankle instability. Restricted dorsiflexion during early and mid-support prevents the other calf from crossing in front of the supporting foot, often causing knee hyperextension, which may lead to compensatory hip flexion. At the end of the support phase and in the pre-swing phase, ankle dorsiflexion impairment prevents the foot from leaving the ground and advancing forward, resulting in much less power being generated by the ankle joint. In the swing phase, the horseshoe foot posture can lead to problems with limb contouring, while abnormal posture of the foot in the support phase can lead to unstable standing of the entire body. Therefore, this particular problem must be corrected, as should the clubfoot in patients with restricted walking ability. The pattern of clubfoot deformity is mostly caused by an imbalance in the forces produced by the muscles. The deformogenic forces that have the potential to cause this clubfoot posture include: anterior tibialis, posterior tibialis, long toe flexors, gastrocnemius, hallux valgus, long bunion, and internal foot muscles. Weakness of the long and short fibular muscles in the support phase, and weakness of the long toe extensors in the swing phase may also play a role. Clinical examination of the above mentioned muscles during walking, combined with dynamic electromyography (EMG) findings, can provide detailed insight into the rationale for the development of this deformity. Dynamic EMG findings often demonstrate that prolonged active time of the gastrocnemius and hallux complex muscles and the long toe flexors are the most common causes of ankle plantarflexion deformity. In individual cases, the electromyographic activity of the gastrocnemius and flounder muscles may differ and must be taken into account during treatment. Differences in activity between the medial and lateral gastrocnemius muscles are relatively rare. Inversion of the foot is usually the result of overactivity of the posterior tibial and/or anterior tibial muscles plus the gastrocnemius and hallux valgus muscles, and sometimes the bunion extensor muscles. If both the posterior tibial and anterior tibial muscles are responsible for the pronated foot deformity, it must be clarified which of these two muscles is the primary responsible muscle. A diagnostic nerve block with lidocaine is a useful way to block either the posterior tibial or peroneal nerve to exclude the action of either muscle, and then observe what changes in foot posture occur. It is important to note that decreased activity of the gastrocnemius-fibularis complex tends to enhance dorsiflexion in the supporting phase. When dorsiflexion is increased, the long toe flexors are tensed due to the tendon fixation effect, which creates an additional problem. Based on the clinical findings corresponding to the dynamic electromyography, a decision can now be made regarding the preferred treatment, which includes the injection of botulinum toxin into the posterior tibialis, gastrocnemius, hallux valgus and long toe flexor muscles. When there is significant contracture, a series of casts or surgical approaches may be required to address the shortening of the physical length of the soft tissue.