There is no single factor that is consistently found in the prenatal history of individuals affected with amyoplasia and, in some cases, there is no known cause of the disorder.

Amyoplasia is a sporadic condition that occurs due to lack of fetal movement in the womb. There is no specific gene that is known to cause the disorder. It is thought to be multifactorial, meaning that numerous genes and environmental factors play a role in its development. The recurrence risk is minimal for siblings or children of affected individuals. There have been no reports of recurrent cases of amyoplasia in a family.

The fetal akinesia in amyoplasia is thought to be caused by various maternal and fetal abnormalities. In some cases, the mother's uterus does not allow for adequate fetal movement because of a lack of amniotic fluid, known as oligohydramnios, or an abnormal shape to the uterus, called a bicornuate uterus.

There may also be a myogenic cause to the fetal akinesia, meaning that fetal muscles do not develop properly due to a muscle disease (for example, a congenital muscular dystrophy). Similarly, connective tissue tendon and skeletal defects may contribute to the fetal akinesia and be the primary cause of amyoplasia. Additionally, malformations may occur in the central nervous system and/or spinal cord that can lead to a lack of fetal movement in utero. This neurogenic cause is often accompanied by a wide range of other conditions. Other causes of fetal akinesia may include a maternal fever during pregnancy or a virus.

Arthrogryposis could also be caused by intrinsic factors. This includes molecular, muscle- and connective tissue development disorders or neurological abnormalities.

The malformations of arthrogryposis can be secondary to environmental factors such as: decreased intrauterine movement, oligohydramnios (low volume or abnormal distribution of intrauterine fluid), and defects in the fetal blood supply. Other causes could be: hyperthermia, limb immobilization and viral infections. Myasthenia gravis of the mother leads also in rare cases to arthrogryposis. The major cause in humans is fetal akinesia. However, this is disputed lately.

Surgery may be necessary to address the congenital deformities frequently occurring in conjunction with arthrogryposis. Surgery on feet, knees, hips, elbows and wrists may also be useful if more range of motion is needed after therapy has achieved maximum results. In some cases, tendon transfers can improve function. Congenital deformities of the feet, hips and spine may require surgical correction at or about one year of age.

Fetal entities: First twin 17-30%; Second twin 28-39%; Stillborn 26%; Prader-Willi syndrome 50%, Werdnig-Hoffman syndrome 10%; Smith-Lemli-Opitz syndrome 40%; Fetal alcohol syndrome 40%; Potter anomaly 36%; Zellweger syndrome 27%; Myotonic dystrophy 21%, 13 trisomy syndrome 12%; 18 trisomy syndrome 43%; 21 trisomy syndrome 5%; de Lange syndrome 10%; Anencephalus 6-18%, Spina bifida 20-30%; Congenital Hydrocephalus 24-37%; Osteogenesis imperfecta 33.3%; Amyoplasia 33.3%; Achondrogenesis 33.3%; Amelia 50%; Craniosynostosis 8%; Sacral agenesis 30.4%; Arthrogriposis multiplex congenita 33.3; Congenital dislocation of the hip 33.3%; Hereditary sensory neuropathy type III 25%; Centronuclear myoptathy 16.7%; Multiple pituitary hormone deficiency 50%; Isolated pituitary hormone deficiency 20%; Ectopic posterior pituitary gland 33.3%; Congenital bilateral perisilvian syndrome 33.3; Symmetric fetal growth restriction 40%; Asymmetric fetal growth restriction 40%; Nonimmune hydrops fetalis 15%; Atresio ani 18.2%; Microcephalus 15.4%; Omphalocele 12.5%; Prematurity 40%

Placental and amniotic fluid entities: Amniotic sheet perpendicular to the placenta 50%; Cornual-fundal implantation of the placenta 30%; Placenta previa 12.5%; Oligohydramnios 17%; Polyhydramnios 15.8%; MATERNAL ENTITIES: Uterus arcuatus 22.6%; Uterus unicornuatus 33.3%; Uterus bicornuatus 34.8%; Uterus didelphys 30-41%; Uterus septus 45.8%; Leimyoma uteri 9-20%; Spinal cord injury 10%; Carriers of Duchenne muscular dystrophy 17%

Combination of two medical entities: First twin in uterus with two bodies 14.29%; Second twin in uterus with two bodies 18.52%.

Also, women with previous Caesarean deliveries have a risk of breech presentation at term twice that of women with previous vaginal deliveries.

The highest possible probability of breech presentation of 50% indicates that breech presentation is a consequence of random filling of the intrauterine space, with the same probability of breech and cephalic presentation in a longitudinally elongated uterus.

In twin pregnancies, it is very common for one or both babies to be in the breech position. Most often twin babies do not have the chance to turn around because they are born prematurely. If both babies are in the breech position and the mother has gone into labour early, a cesarean section may be the best option. About 30-40% of twin pregnancies result in only one baby being in the breech position. If this is the case, the babies can be born vaginally. After the first baby who is not in the breech position is delivered, the baby who is presented in the breech position may turn itself around, if this does not happen another procedure may performed called the breech extraction. The breech extraction is the procedure that involves the obstetrician grabbing the second twin's feet and pulling him/her into the birth canal. This will help with delivering the second twin vaginally. However, if the second twin is larger than the first, complications with delivering the second twin vaginally may arise and a cesarean section should be performed. At times, the first twin (the twin closest to the birth canal) can be in the breech position with the second twin being in the cephalic position (vertical). When this occurs, risks of complications are higher than normal. In particular, a serious complication known as Locked twins. This is when both babies interlock their chins during labour. When this happens a cesarean section should be performed immediately.