The prevention of the complications mentioned above plays an important role in the discussion about the timing of the surgery. The general consensus is now to perform surgery in late infancy, i.e. between six and twelve months. In this time frame the efficacy of surgery is enhanced due to several reasons:

- The bone is still more malleable and can be remodelled relatively 'simply' by greenstick fractures of the bone. At approximately one year of age the bone has become more mineralized and brittle and needs to be fastened to the surrounding bone with sutures or an absorbable plate.

- Reshaping of the cranial vault most commonly means excision of the bones and adjustment of the shape. Replacement of the bones can leave 'gaps' which are readily re-ossified before the age of one year, but need bony filling thereafter.

The reason why most surgeons will not intervene until after the age of six months is the greater risk that blood loss poses before this age. If possible it is preferred to wait until after three months of age when the anaesthetic risks are decreased.

Surgery is not performed in early childhood in every country. In some countries surgical intervention can take place in the late teens.

It is important that families seek out a Pediatric Craniofacial Physician who has experience with craniosynostosis for proper diagnosis, surgical care, and followup.

Environmental factors refer for example to maternal smoking and the maternal exposure to amine-containing drugs. Several research groups have found evidence that these environmental factors are responsible for an increase in the risk of craniosynostosis, likely through effects on fibroblast growth factor receptor genes.

On the other hand, a recent evaluation of valproic acid (an anti-epilepticum), which has been implicated as a causative agent, has shown no association with craniosynostosis.

Certain medication (like amine-containing drugs) can increase the risk of craniosynostosis when taken during pregnancy, these are so-called teratogenic factors.

Surgery is needed to prevent the closing of the coronal sutures from damaging brain development. In particular, surgeries for the LeFort III or monobloc midface distraction osteogenesis which detaches the midface or the entire upper face, respectively, from the rest of the skull, are performed in order to reposition them in the correct plane. These surgeries are performed by both plastic and oral and maxillofacial (OMS) surgeons, often in collaboration.

Dolichocephaly (derived from the Ancient Greek δολιχός, meaning "long") is a condition where the head is longer than would be expected, relative to its width. In humans, scaphocephaly is a form of dolichocephaly.

Dolicocephalic dogs (such as German Shepherds) have elongated noses. This makes them vulnerable to fungal diseases of the nose such as aspergillosis. In humans the anterior–posterior diameter (length) of dolichocephaly head is more than the transverse diameter (width). It has an incidence of 1 in every 4,200 babies.

It can present be in cases of Sensenbrenner syndrome, Crouzon syndrome, Sotos syndrome as well as Marfan syndrome.

Although dolichocephaly may be associated with some other abnormalities, alone it is just a normal variation; unless symptomatic, it is not a cause for concern. Early diagnosis can be made by X-ray or ultrasonography. Treatment is not essential.

There is no standard treatment for the hand malformations in Apert due to the differences and severity in clinical manifestations in different patients. Every patient should therefore be individually approached and treated, aiming at an adequate balance between hand functionality and aesthetics.

However, some guidelines can be given depending on the severity of the deformities.

In general it is initially recommended to release the first and fourth interdigital spaces, thus releasing the border rays.

This makes it possible for the child to grasp things by hand, a very important function for the child's development. Later the second and third interdigital spaces have to be released.

Because there are three handtypes in Apert, all with their own deformities, they all need a different approach regarding their treatment:

- Type I hand usually needs only the interdigital web space release. First web release is rarely needed but often its deepening is necessary. Thumb clynodactyly correction will be needed.

- In type II hands it is recommended to release the first and fifth rays in the beginning, then the second and the third interdigital web spaces have to be freed. The clynodactyly of the thumb has to be corrected as well. The lengthening of the thumb phalanx may be needed, thus increasing the first web space. In both type I and type II, the recurrent syndactyly of the second web space will occur because of a pseudoepiphysis at the base of the index metacarpal. This should be corrected by later revisions.

- Type III hands are the most challenging to treat because of their complexity. First of all, it is advised to release the first and fourth webspace, thus converting it to type I hand. The treatment of macerations and nail-bed infections should also be done in the beginning. For increasing of the first web space, lengthening of the thumb can be done. It is suggested that in severe cases an amputation of the index finger should be considered. However, before making this decision, it is important to weigh the potential improvement to be achieved against the possible psychological problems of the child later due to the aesthetics of the hand. Later, the second and/or third interdigital web space should be released.

With growing of a child and respectively the hands, secondary revisions are needed to treat the contractures and to improve the aesthetics.

Each child is different and it entirely depends on which sutures are fused and how it is affecting the child as to how it is treated. Some children have severe breathing issues due to shallow mid face and may require a tracheostomy. All should be treated at a specialist centre. Cranio bands are not used in the UK.

Surgery is typically used to prevent the closure of sutures of the skull from damaging the brain's development. Without surgery, blindness and mental retardation are typical outcomes. Craniofacial surgery is a discipline of both plastic surgery and oral and maxillofacial surgery (OMFS) . To move the orbits forward, craniofacial surgeons expose the skull and orbits and reshape the bone. To treat the midface deficiency, craniofacial surgeons can move the lower orbit and midface bones forward. For jaw surgery, either plastic surgeons or OMFS surgeons can perform these operations.

Crouzon patients tend to have multiple sutures involved, most specifically bilateral coronal craniosynostoses, and either open vault surgery or strip craniectomy (if child is under 6 months) can be performed. In the later scenario, a helmet is worn for several months following surgery.

Once treated for the cranial vault symptoms, Crouzon patients generally go on to live a normal lifespan.

Incidence of Crouzon syndrome is currently estimated to occur in 1.6 out of every 100,000 people. There is a greater frequency in families with a history of the disorder, but that doesn't mean that everyone in the family is affected (as referred to above).

In terms of management, unless the syndrome results in other medical problems, treatment for endocrine dysfunction associated with pituitary malfunction is symptomatic and thus supportive;however, in some cases, surgery may be needed.

This syndrome was first described by Lehman et al. in 1977. This paper described a 14-year-old girl with a number of unusual findings. Her mother shared some of the same findings. Since then over a dozen additional cases have been reported.

The lateral meningocele syndrome is a very rare skeletal disorder with facial anomalies, hypotonia and meningocele-related neurologic dysfunction.

Empty sella syndrome (abbreviated ESS) is where the pituitary gland shrinks or becomes flattened, filling the sella turcica with cerebrospinal fluid on imaging instead of the normal pituitary. ESS can be found in the diagnostic workup of pituitary disorders, or as an incidental finding when imaging the brain.

Treatments are usually based on the individuals symptoms that are displayed. The seizures are controlled with anticonvulsant medication. For the behavior problems, the doctors proscribe to a few medications and behavioral modification routines that involve therapists and other types of therapy. Even if mental retardation is severe, it does not seem to shorten the lifespan of the patient or to get worse with age.

Preventive maintenance therapy for the oral effects of TDO involve frequent dental cleanings, professional application of desensitizing medication, diet counseling, and oral hygiene instructions in proper home care and maintenance; medicated dental rinses and toothpastes are also prescribed as people suffering from TDO are more prone to oral hard tissue disease and early tooth loss. If restorative dentistry is performed without orthodontics to correct the protrusion of the lower jaw, a dental night guard worn at bedtimes on the upper or lower teeth to protect them from the effects of grinding may be recommended.

In extreme cases, tooth loss is inevitable, and the patient will consult with a prosthodontist to determine tooth replacement options such as dental implants, or partial dentures. There is no cure for TDO, but managing its oral and systemic affects is key to having the most favorable outcome from the disease. As the person affected by TDO ages, increased bone fractures may occur. The person suffering from TDO should watch for any pimple like masses on the gum tissue, pain or soreness in the teeth and gums, broken or chipped teeth, feeling of water in the ear or severe pain in the extremities which could indicate fracture.

The hair, teeth, and skeletal side effects of TDO are lifelong, and treatment is used to manage those effects. A person with TDO has the same life expectancy as a person without TDO. There are no cures or medications used to treat systemic effects of TDO, but medications for the frequent ear and dental infections can be used to manage its symptoms. A team based approach between dental specialists, oral and maxillofacial surgeons, and physicians is necessary for treating the systemic effects and improves the prognosis. It is also recommended for affected individuals to seek counseling to be better able to cope with any psychosocial problems due to oral and facial abnormalities that occur with TDO.

At home, a person suffering from TDO may be instructed to use frequent deep conditioning treatments and low manipulation hair styling to control shedding and hair loss. Clinical treatment involves the use of radiology to determine the effects that TDO has had on the surrounding teeth and bone structures. A series of appointments with the healthcare team are usually necessary to correct TDO abnormalities with treatment duration lasting from several months to through full oral-facial maturation stages.

Endodontic procedures are routinely recommended due to treatdental pulp exposure or periodontal abscess. Maxillofacial surgery may be required to establish a more appropriate mastication, skeletal, and esthetic relationship vertically between the teeth to improve functioning. Esthetic procedures such as dental crown (dentistry) or veneer (dentistry) are often performed to improve the physical look of the teeth and to strengthen the weak enamel caused by TDO.

Sensenbrenner syndrome (OMIM #218330) is a rare (less than 20 cases reported by 2010) multisystem disease first described in 1975. It is inherited in an autosomal recessive fashion, and a number of genes appear to be responsible. Three genes responsible have been identified: intraflagellar transport (IFT)122 (WDR10), IFT43 — a subunit of the IFT complex A machinery of primary cilia, and WDR35 (IFT121: TULP4)

It is also known as Sensenbrenner–Dorst–Owens syndrome, Levin Syndrome I and cranioectodermal dysplasia (CED)

Smith–Fineman–Myers syndrome (SFMS1), congenital disorder that causes birth defects. This syndrome was named after 3 men, Richard D. Smith, Robert M. Fineman and Gart G. Myers who discovered it around 1980.

The American Heart Association made the following recommendations for Marfan's patients with no or mild aortic dilation:

- Probably permissible activities: bowling, golf, skating (but not ice hockey), snorkeling, brisk walking, treadmill, stationary biking, modest hiking, and doubles tennis.

- Intermediate risk: basketball (both full- and half-court), racquetball, squash, running (sprinting and jogging), skiing (downhill and cross-country), soccer, singles tennis, touch (flag) football, baseball, softball, biking, lap swimming, motorcycling, and horseback riding.

- High risk: bodybuilding, weightlifting (non-free and free weights), ice hockey, rock climbing, windsurfing, surfing, and scuba diving.

Management often includes the use of beta blockers such as propranolol or if not tolerated calcium channel blockers or ACE inhibitors.

Since angiotensin II receptor antagonists (ARBs) also reduce TGF-β, these drugs have been tested in a small sample of young, severely affected people with Marfan syndrome. In some, the growth of the aorta was reduced. However, a recent study published in NEJM demonstrated similar cardiac outcomes between the ARB, losartan, and the more established beta blocker therapy, atenolol.

These are pleomorphic and include

- dolichocephaly (with or without sagittal suture synostosis)

- microcephaly

- pre- and postnatal growth retardation

- brachydactyly

- narrow thorax

- rhizomelic dwarfism

- epicanthal folds

- hypodontia and/or microdontia

- sparse, slow-growing, hyperpigmented, fine hair

- nail dysplasia

- hypohydrosis

- chronic renal failure

- heart defects

- liver fibrosis

- visual deficits

- photophobia

- hypoplasia of the posterior corpus callosum

- aberrant calcium homeostasis

Electroretinography shows gross abnormalities.

Two fetuses of 19 and 23 weeks gestation have also been reported. They showed acromesomelic shortening, craniofacial characteristics with absence of craniosynostosis, small kidneys with tubular and glomerular microscopic cysts, persistent ductal plate with portal fibrosis in the liver, small adrenals, an enlarged cisterna magna and a posterior fossa cyst.