Patients with congenital vertical talus often exhibit loss of arch or plantar bulge, with the medial and metatarsal sides of the foot appearing very pronounced due to the prominence of the talar head here. 1. Etiology It is generally believed that this deformity is formed in the first three months of embryonic life. Clinically, there are two types of deformities: arcuate and associated. The latter is a congenital disorder such as spinal cord bulge, polyarticular contracture, neurofibromatosis, and trichromatosis13-15,18. The pathogenesis of the arcuate vertical talus is unknown. It has been proposed that it is due to impaired embryonic development of the foot. bitsila experimented with young rabbits and simultaneously severed the long toe extensor, anterior tibial muscle and transverse calf ligament, and caused shortening of the gastrocnemius muscle, resulting in a successful animal model of the vertical talus. Thus, he proposed that primary soft tissue lesions are the main factor in causing this deformity. Some other scholars found that the incidence of certain families and twins was significantly higher than that of the general population, which was thought to be related to genetic factors. 2.Pathological changes Pathological changes can be divided into bony deformity and soft tissue lesions. The bony deformity is mainly a joint between the navicular bone and the dorsal aspect of the talar neck, which locks the talus in a vertical position. The talar head is flattened or oval above, the talar neck is hypoplastic and shortened, and an articular surface is formed dorsally. The proximal articular surface of the navicular bone is tilted towards the metatarsal side. The heel bone is displaced posteriorly and laterally. The anterior portion of the heel is laterally deflected and flexed to the metatarsal side. The talar process is hypoplastic and loses its role in supporting the talus. The lateral column of the foot is depressed and the medial column is relatively longer. There are also significant changes in the soft tissues. Contracture of the tibial navicular ligament and the dorsal talofibular ligament is the main factor affecting the repositioning. Contracture of the divergent lateral ligaments caused foot abduction. Contracture of the heel talofibular ligament and heel peroneal ligament prevented the heel from being repositioned to the posterior lateral displacement. In contrast, the heel navicular metatarsal ligament, talofibular ligament and medial joint capsule are elongated. The anterior tibialis, long toe, long extensor, short peroneal muscle and triceps calf muscle are hypertonic due to contracture. The peroneus longus and tibialis posterior tendons move to the front of the ankle and act as dorsal extensors. 3. Pathogenesis Talofibular dislocation may develop in utero since the third trimester of pregnancy, while the adjacent subtrochanteric, intertarsal and ankle subluxations are secondary. It may occur singly or as a part of a generalized multiple deformity. The tarsal navicular bone forms an articulation with the dorsal aspect of the talar neck, giving the talus a vertical shape. The talar head is deformed, the talar neck is shortened, and the talus is dislocated posteriorly and laterally in a sagging fashion. The talus is convex on the plantar aspect of the foot. There are corresponding changes in other intertarsal joints. The anterior bundle of the deltoid ligament, the dorsal talofibular ligament, the heel dice ligament, the talofibular ligament and the heel fibular ligament are contracted to varying degrees, while the posterior capsules of the ankle and subtalar joints are shortened and the heel navicular ligament is stretched and relaxed. The calf muscles (anterior tibialis, m long extensors, long toe extensors, calf triceps, etc.) were contracted; the posterior tibialis and peroneus longus were displaced forward and became dorsiflexors.