Compared to the Ponseti method which uses rigid casts and braces, the French method uses tape which allows for some motion in the feet. Despite its goal to avoid surgery, the success rate varies and surgery may still be necessary. The Ponseti method is generally preferred over the French method. Surgery
If non-operative treatments are unsuccessful or achieve incomplete correction of the deformity, surgery is sometimes needed. Surgery was more common prior to the widespread acceptance of the Ponseti method. The extent of surgery depends on the severity of the deformity. Usually, surgery is done at 9 to 12 months of age and the goal is to correct all the components of the clubfoot deformity at the time of surgery. For feet with the typical components of deformity (cavus, forefoot adductus, hindfoot varus, and ankle equinus), the typical procedure is a Posteromedial Release (PMR) surgery. This is done through an incision across the medial side of the foot and ankle, that extends posteriorly, and sometimes around to the lateral side of the foot. In this procedure, it is typically necessary to release (cut) or lengthen the plantar fascia, several tendons, and joint capsules/ligaments. Typically, the important structures are exposed and then sequentially released until the foot can be brought to an appropriate plantigrade position. Specifically, it is important to bring the ankle to neutral, the heel into neutral, the midfoot aligned with the hindfoot (navicula aligned with the talus, and the cuboid aligned with the calcaneus).
The theory of fetal growth arrest was proposed by Von Volkmann in 1863, and has been verified by other authors since. According to this theory, intrinsic errors or environmental insults during gestation prevents the correction of a equinovarus to pronated foot. Other researchers hypothesize that clubfoot may derive from external insults during gestation. For example, a research study found an alarming high incidence of club foot and limb contractures associated with iatrogenic amniotic leakage cause by early amniocentesis between the 11th and 12th week of gestation.Intrinsic Factors

Chromosomal abnormalities found in 30% and 2% of complex clubfoot and isolated clubfoot respectively. These include trisomy 18, 13, 21, sex chromosome abnormalities, micro-deletions and duplications. Genetic Syndromes: Larsen, Gordon, Pierre-Robin, Meckel-Gruber, Roberts, Smith-Lemli-Opitz, TARP (Talipes equinovarus, Atrial septal defect, Robin sequence, Persistence of left superior vena cava). Skeletal Dysplasias: Ellis van Creveld syndrome, diastrophic dysplasia, chondrodysplasia punctata, camptomelic dysplasia, atelosteogenesis, and mesomelic dysplasia. Neuromuscular and Neurologic abnormalities: arthrogryposis multiplex congenita, myotonic dystrophy, spinal muscular atrophy,  neural tube defects, holoprosencephaly, and hydranencephaly. Genetics
Clubfoot can be diagnosed prenatally as early as 13 weeks of gestation via ultrasound. According to the Society of Maternal-Fetal Medicine, a diagnostic testing for genetic causes is recommended when clubfoot is diagnoses prenatally. If prenatal screening is suspicious for aneuploidy, karyotype analysis or chromosomal microarray (CMA) may be performed. However, if patients decline diagnostic testing, Cell-Free DNA is another screening option to identify high-risk pregnancies for aneuploidy and it is not diagnostic.