[Abstract] Crouzon first reported this disease in 1921, so it is called Crouzon syndrome, also known as parrot head syndrome, Virchow syndrome, congenital acromegaly, narrow skull syndrome, etc. It is a syndrome mainly characterized by premature closure of cranial suture, hypoplasia and protrusion of the eye. The syndrome is mainly characterized by premature closure of cranial sutures, hypoplasia and protruding eyes. Some scholars believe that the cause of premature closure of the cranial suture and other bone merging abnormalities is due to the abnormal joining or abnormal separation of the ossification centers of the two bones caused by the mutation of the bud germ plasma; Crouzon believes that the premature closure is caused by the inflammation of the bone suture area during the fetal period. [Clinical manifestations] The clinical picture is mostly seen in males. Patients may present with cranial anomalies, oral and maxillofacial anomalies, and ocular anomalies, even in combination with other bone anomalies. Cranial anomalies: Due to the premature closure of the cranial suture, especially the coronal suture, the growth of the skull and maxilla is restricted, causing acromegaly, short head deformity or triangular head deformity, compensating for the frontal area with a pronounced elevated bulge, while the bony union of the suture cannot adapt to the increase in the volume of the rapidly developing skull and brain, resulting in hydrocephalus, mental retardation, and in severe cases, increased intracranial pressure, headache, vomiting, and even seizures; Oral and maxillofacial anomalies: mainly maxillary dysplasia, relative protrusion of the mandible, which makes the upper and lower jaws in a reverse perturbed state, protrusion of the nose in the shape of a parrot’s beak, V-shaped increase in the palatal arch to become sharp, sometimes combined with cleft palate, cleft lip, recession of the entire middle of the face, crowded maxillary teeth, short upper lip, sagging lower lip, sometimes not appearing mandibular protrusion, but the relative formation of mandibular hypoplasia, appearing mandatory mouth breathing, etc.; eye and ear anomalies The eyes and ears have progressive vision loss, shallow eye sockets, protruding eyeballs, light blue sclera, widened spacing between the eyes, exotropia, downward sloping eye fissures, nystagmus, and also optic neuritis or optic papillary edema due to optic nerve compression, visual field atrophy above, secondary optic nerve atrophy, and even blindness, etc. They can also be accompanied by other eye diseases, such as cataract, glaucoma, lens ectasia, iris defect, etc.; bilateral external ear canal atresia, hearing Other: some may have spina bifida, juxtaposition of fingers (toes), congenital heart disease, etc. X-ray examination: bony connection of skull sutures, skull base, maxilla and skull to mandible size disproportion, enlarged pituitary fossa. Laboratory examination: increased cerebrospinal fluid pressure [Treatment] Early craniomandibular surgery to open the bony closed sutures and widen the volume of the cranial cavity to reduce the extrusion on the cranial development and the restriction on the development of the maxilla, especially those with obvious family genetic predisposition, the craniomandibular development of infants should be observed early; after surgery to open the affected cranial sutures, artificial anti-ossification materials, such as polyethylene, can be filled, such as the optic nerve papillae If there are symptoms of intracranial hypertension such as optic nerve papillae, it is an indication for surgery; if proptosis has appeared, orbital decompression is feasible. If the external auditory canal is atretic, external auricular atlas should be performed early. [Prognosis] The lesion will not progress after cranial development is completed (8 years old).