1. Hematoma theory. As early as 1838, Stromeyer proposed that the sternocleidomastoid muscle was damaged during delivery and the hematoma formed in the muscle as a result of mechanization. 1897, Hilderbrand described myofiber degeneration in the sternocleidomastoid mass, but no iron-containing heme was found. 1965, Armstrong reported that among 35 cases of oblique neck, 32 cases had sternocleidomastoid hematoma, and microscopic examination of 25 In 1965, Armstrong reported that 32 out of 35 cases of trapezius had sternocleidomas, and 25 % of them had iron-containing hemoglobin on microscopic examination, suggesting hematoma absorption. In recent years, most scholars have found no traces of hemorrhage in the early and late lesioned muscles, and there is no trauma in the muscle sections, so there is a negative attitude towards whether the muscle tissue is fibrotic due to normal birth injury tear. In recent years, the rate of breech delivery has decreased significantly, and most of the children with this disease were delivered by normal delivery or cesarean section, and many of them were found to have crooked neck and facial asymmetry at birth, which was later confirmed to be myotonic squint. The muscle specimens operated on at the age of 10 months to 1 year showed swollen and hyaline degeneration of the muscle fibers, which also did not correspond to the pathological process following normal muscle fiber tearing. Therefore, it is believed that the muscle hematoma caused by trauma during childbirth is the cause of the disease and should be reawakened. 2. The theory of venous obstruction. In 1930, Middeton, through animal experiments, pointed out that the cause of sternocleidomastoid muscle fibrosis is the obstruction of intramuscular venous return after muscle injury. brooks, in animal experiments in dogs, studied the pathological changes caused by muscle blood circulation disorders, completely occluding the main veins of the muscle, but retaining the intact arteries, resulting in muscle fiber edema, degeneration and acute inflammation, and finally muscle fiber necrosis and This results in edema, degeneration and acute inflammation of the muscle fibers, which are eventually necrotic and replaced by fibrous tissue. This result is similar to the changes seen in myotonic levator. If only the artery is permanently occluded, it can cause extreme muscle atrophy and necrosis, neither of which can cause fibrosis of the muscle tissue. The same conclusion was later obtained from similar experiments by Tepson and Middleton, and in the experiments by Brooks et al, the same myotonic leptomeninges could be seen after birth in those with no history of trauma at the time of delivery. Therefore, it is believed that the onset of congenital myotrabismus may be due to the fact that the head and neck have been in a position of excessive lateral flexion and compression in utero for a long time, which may block the compression of the main veins of the sternocleidomastoid muscle or occlude only a part of the veins of this muscle by compression, while the arterial blood supply may still be open, resulting in the obstruction of venous return to this muscle and causing edema and degeneration of the muscle fibers. Regardless of whether there is a history of difficult delivery or trauma, the muscle fibers are eventually replaced by fibrous tissues, resulting in muscle contracture leading to myotonic squamous neck. 3.The theory of arterial obstruction. In 1948, Chandler proposed that due to improper position of the fetus in utero, the sternocleidomastoid muscle was compressed with ischemia, resulting in fibrosis of this muscle. The superior thyroid artery is a terminal branch that supplies the sternal head and middle muscle belly of the sternocleidomastoid muscle. When the fetus is delivered in utero, especially through the birth canal, there is usually forward flexion, lateral bending and rotation of the head, resulting in torsion of the middle sternocleidomastoid muscle, narrowing and occlusion of the artery, and if this persists for some time, the muscle becomes ischemic and edematous leading to interventricular syndrome and finally muscle fibrosis and contracture. davids found signal of the affected sternocleidomastoid muscle and forearm and calf by MRI in 10 cases of congenital myotonic squamous neck The signal of fascial interval syndrome was similar, and the disease was considered to be possibly related to the sequelae of interval syndrome. Dissection was also performed on 3 adult cadavers, demonstrating the presence of intact interventricular compartments in and around the sternocleidomastoid muscle. Intraoperatively, intramuscular injections and pressure measurements were performed on the sternocleidomastoid muscle in three cases of congenital myotonic neck, and the muscle was found to indeed have an interventricular compartment. When the head and neck of the cadaver were flexed forward, bent sideways and rotated, it was found that the middle of the ipsilateral sternocleidomastoid muscle was kinked, which was thought to be the mechanism of sternocleidomastoid muscle injury. 4. Genetic theory. In 1927, Hellstadins suggested that there might be a genetic factor in the occurrence of sternocleidomastoid muscle, and in 1951, Reye suggested that it was caused by congenital defects in muscle development, which induced muscle injury and ischemia in utero or during delivery. The incidence of congenital myotubercular deformity is high in children with congenital myotubercular dislocation and acetabular dysplasia, and congenital myotubercular deformity is found in 7-10% of congenital hip dislocation and acetabular dysplasia, both of which occur on the same side. Tavill reported a case of familial infantile sternocleidomas, and it was confirmed that two generations of his family had myotuberculosis in infancy, thus suggesting a familial susceptibility to the development of congenital myotuberculosis. Schmalbruch et al. also reported a case of congenital myotonic dystrophy of the sternocleidomastoid, forearm and tibial muscles in which all three generations of the family had the disease, with autosomal dominant inheritance. Therefore, this disease may be related to genetic factors or congenital malformations. 5.The hyperextension theory. Some scholars believe that congenital factors and environmental factors lead to congenital dysplasia of the sternocleidomastoid muscle, and that the muscle is overstretched (overload by external forces and gravity) during childbirth, resulting in reactive granulation tissue and clinical appearance of sternocleidomastoid masses. It is characterized by detachment of the muscle fibers from the original fiber bundle, fusion, impaired circulation, interstitial edema of the muscle fibers, highly progressive degeneration of the muscle fibers and formation of granulation tissue between the muscle fibers, later progressive fibrosis, becoming scar tissue, contracture of the sternocleidomastoid muscle on the affected side, and later the typical oblique neck. In conclusion, the cause of congenital myotonic levator is the fibrosis and contracture of the sternocleidomastoid muscle on the affected side. In addition to the above mentioned theories, there are also theories of intrauterine load, inflammation, fetal movement, etc. Among them, the theory of hematoma of birth injury has been rejected by most scholars, and it is believed that the pathogenesis of congenital myotonic levator is caused by various factors, and the blood circulation disorder of the muscle is the direct cause of the pathogenesis, but the congenital pathogenic factors cannot be excluded. The exact etiology and pathogenesis need to be further studied.