There is no known cure for microcephaly. Treatment is symptomatic and supportive.

Although there is no cure for 13q deletion syndrome, symptoms can be managed, usually with the involvement of a neurologist, rehabilitation physician, occupational therapist, physiotherapist, psychotherapist, nutritionist, special education professional, and/or speech therapist. If the affected child's growth is particularly slow, growth hormone treatment can be used to augment growth. Plastic surgeries can repair cleft palates, and surgical repair or monitoring by a pediatric cardiologist can manage cardiac defects. Some skeletal, neurological, genitourinary, gastrointestinal, and ophthalmic abnormalities can be definitively treated with surgery. Endocrine abnormalities can often be managed medically. Special educators, speech and occupational therapists, and physiotherapists can help a child develop skills in and out of school.

Pregnant mothers are advised to take folic acid supplements to reduce risk of iniencephaly by up to 70%. Pregnant mothers are also advised not to take antiepileptic drugs, diuretics, antihistamines, and sulfa drugs, all of which have been associated with increased risk for neural tube defects.

Medical management of children with Trisomy 13 is planned on a case-by-case basis and depends on the individual circumstances of the patient. Treatment of Patau syndrome focuses on the particular physical problems with which each child is born. Many infants have difficulty surviving the first few days or weeks due to severe neurological problems or complex heart defects. Surgery may be necessary to repair heart defects or cleft lip and cleft palate. Physical, occupational, and speech therapy will help individuals with Patau syndrome reach their full developmental potential. Surviving children are described as happy and parents report that they enrich their lives. The cited study grouped Edwards syndrome, which is sometimes survivable beyond toddlerhood, along with Patau, hence the median age of 4 at the time of data collection.

There is no standard treatment for hydranencephaly. Treatment is symptomatic and supportive. Hydrocephalus may be treated with surgical treatment of a shunt, which often grants a much better prognosis and greater quality of life.

The prognosis for children with hydranencephaly is generally quite poor. Death often occurs in the first year of life, but other children may live several years.

Medical text identifies that hydranencephalic children simply have only their brain stem function remaining, thus leaving formal treatment options as symptomatic and supportive. Severe hydrocephalus causing macrocephaly, a larger than average head circumference, can easily be managed by placement of a shunt and often displays a misdiagnosis of another lesser variation of cephalic condition due to the blanketing nature of hydrocephalus. Plagiocephaly, the asymmetrical distortion of the skull, is another typical associated condition that is easily managed through positioning and strengthening exercises to prevent torticollis, a constant spasm or extreme tightening of the neck muscles.

Most fetuses with triploidy do not survive to birth, and those that do usually pass within days. As there is no treatment for Triploidy, palliative care is given if a baby survives to birth. If Triploidy is diagnosed during the pregnancy, termination is often offered as an option due to the additional health risks for the mother (preeclampsia, a life-threatening condition, or choriocarcinoma, a type of cancer). Should a mother decide to carry until term or until a spontaneous miscarriage occurs, doctors will monitor her closely in case either condition develops.

Mosaic triploidy has an improved prognosis, but affected individuals have moderate to severe cognitive disabilities.

At present, treatment for ring 18 is symptomatic, meaning that the focus is on treating the signs and symptoms of the conditions as they arise. To ensure early diagnosis and treatment, it is suggested that people with ring 18 undergo routine screenings for thyroid, hearing, and vision problems.

Currently, the most common form of treatment for SLOS involves dietary cholesterol supplementation. Anecdotal reports indicate that this has some benefits; it may result in increased growth, lower irritability, improved sociability, less self-injurious behaviour, less tactile defensiveness, fewer infections, more muscle tone, less photosensitivity and fewer autistic behaviours. Cholesterol supplementation begins at a dose of 40–50 mg/kg/day, increasing as needed. It is administered either through consuming foods high in cholesterol (eggs, cream, liver), or as purified food grade cholesterol. Younger children and infants may require tube feeding. However, dietary cholesterol does not reduce the levels of 7DHC, cannot cross the blood–brain barrier, and does not appear to improve developmental outcomes. One empirical study found that cholesterol supplementation did not improve developmental delay, regardless of the age at which it began. This is likely because most developmental delays stem from malformations of the brain, which dietary cholesterol cannot ameliorate due to its inability to cross the blood–brain barrier.

At present, treatment for 18p- is symptomatic, meaning that the focus is on treating the signs and symptoms of the conditions as they arise. To ensure early diagnosis and treatment, it is suggested that people with 18p- undergo routine screenings for hearing and vision problems.

Since newborns with iniencephaly so rarely survive past childbirth, a standard treatment does not exist.

HMG-CoA reductase inhibitors have been examined as treatment for SLOS. Given that this catalyzes the rate-limiting step in cholesterol synthesis, inhibiting it would reduce the buildup of toxic metabolites such as 7DHC. Simvastatin is a known inhibitor of HMG-CoA reductase, and most importantly is able to cross the blood–brain barrier. It has been reported to decrease the levels of 7DHC, as well as increase the levels of cholesterol. The increased cholesterol levels are due to simvastatin's effect on the expression of different genes. Simvastatin increases the expression of "DHCR7", likely leading to increased activity of DHCR7. It has also been shown to increase the expression of other genes involved in cholesterol synthesis and uptake. However, these benefits are dependent on the amount of residual cholesterol synthesis. Because some individuals possess less severe mutations and demonstrate some amount of DCHR7 activity, these people benefit the most from simvastatin therapy as they still have a partially functioning enzyme. For individuals that show no residual DCHR7 activity, such as those homozygous for null alleles or mutations, simvastatin therapy may actually be toxic. This highlights the importance of identifying the specific genotype of the SLOS patient before administering treatment. It is still unknown if simvastatin will improve the behavioural or learning deficits in SLOS.

Surgery is typically used to correct structural heart defects and syndactyly. Propanolol or beta-adrenergic blockers are often prescribed as well as insertion of a pacemaker to maintain proper heart rhythm. With the characterization of Timothy syndrome mutations indicating that they cause defects in calcium currents, it has been suggested that calcium channel blockers may be effective as a therapeutic agent.

Because newborns can breathe only through their nose, the main goal of postnatal treatment is to establish a proper airway. Primary surgical treatment of FND can already be performed at the age of 6 months, but most surgeons wait for the children to reach the age of 6 to 8 years. This decision is made because then the neurocranium and orbits have developed to 90% of their eventual form. Furthermore, the dental placement in the jaw has been finalized around this age.

Structural nasal deformities are corrected during or shortly after the facial bipartition surgery. In this procedure, bone grafts are used to reconstruct the nasal bridge. However, a second procedure is often needed after the development of the nose has been finalized (at the age of 14 years or even later).

Secondary rhinoplasty is based mainly on a nasal augmentation, since it has been proven better to add tissue to the nose than to remove tissue. This is caused by the minimal capacity of contraction of the nasal skin after surgery.

In rhinoplasty, the use of autografts (tissue from the same person as the surgery is performed on) is preferred. However, this is often made impossible by the relative damage done by previous surgery. In those cases, bone tissue from the skull or the ribs is used. However, this may give rise to serious complications such as fractures, resorption of the bone, or a flattened nasofacial angle.

To prevent these complications, an implant made out of alloplastic material could be considered. Implants take less surgery time, are limitlessly available and may have more favorable characteristics than autografts. However, possible risks are rejection, infection, migration of the implant, or unpredictable changes in the physical appearance in the long term.

At the age of skeletal maturity, orthognathic surgery may be needed because of the often hypoplastic maxilla. Skeletal maturity is usually reached around the age of 13 to 16. Orthognathic surgery engages in diagnosing and treating disorders of the face and teeth- and jaw position.

HPE is not a condition in which the brain deteriorates over time. Although serious seizure disorders, autonomic dysfunction, complicated endocrine disorders and other life-threatening conditions may sometimes be associated with HPE, the mere presence of HPE does not mean that these serious problems will occur or develop over time without any previous indication or warning. These abnormalities are usually recognized shortly after birth or early in life and only occur if areas of the brain controlling those functions are fused, malformed or absent.

Prognosis is dependent upon the degree of fusion and malformation of the brain, as well as other health complications that may be present.

The more severe forms of encephalopathy are usually fatal. This disorder consists of a spectrum of defects, malformations and associated abnormalities. Disability is based upon the degree in which the brain is affected. Moderate to severe defects may cause mental retardation, spastic quadriparesis, athetoid movements, endocrine disorders, epilepsy and other serious conditions; mild brain defects may only cause learning or behavior problems with few motor impairments.

Seizures may develop over time with the highest risk before 2 years of age and the onset of puberty. Most are managed with one medication or a combination of medications. Typically, seizures that are difficult to control appear soon after birth, requiring more aggressive medication combinations/doses.

Most children with HPE are at risk of having elevated blood sodium levels during moderate-severe illnesses, that alter fluid intake/output, even if they have no previous diagnosis of diabetes insipidus or hypernatremia.

Affected individuals have a somewhat shortened lifespan. The maximum described lifespan is 67 years. Adults with 13q deletion syndrome often need support services to maintain their activities of daily living, including adult day care services or housing services.

Numerous possible risk factors have been identified, including gestational diabetes, transplacental infections (the "TORCH complex"), first trimester bleeding, and a history of miscarriage. As well, the disorder is found twice as often in female babies. However, there appears to be no correlation between HPE and maternal age.

There is evidence of a correlation between HPE and the use of various drugs classified as being potentially unsafe for pregnant and lactating mothers. These include insulin, birth control pills, aspirin, lithium, thorazine, retinoic acid, and anticonvulsants. There is also a correlation between alcohol consumption and HPE, along with nicotine, the toxins in cigarettes and toxins in cigarette smoke when used during pregnancy.

MRI will help with the diagnosis of structural abnormality of the brain. Genetic testing may also be pursued.

Ethmocephaly is a type of cephalic disorder caused by holoprosencephaly. Ethmocephaly is the least common facial anomaly. It consists of a proboscis separating narrow-set eyes with an absent nose and microphthalmia (abnormal smallness of one or both eyes). Cebocephaly, another facial anomaly, is characterized by a small, flattened nose with a single nostril situated below incomplete or underdeveloped closely set eyes.

The least severe in the spectrum of facial anomalies is the median cleft lip, also called premaxillary agenesis.

Although the causes of most cases of holoprosencephaly remain unknown, some may be due to dominant or chromosome causes. Such chromosomal anomalies as trisomy 13 and trisomy 18 have been found in association with holoprosencephaly, or other neural tube defects. Genetic counseling and genetic testing, such as amniocentesis, is usually offered during a pregnancy if holoprosencephaly is detected. The recurrence risk depends on the underlying cause. If no cause is identified and the fetal chromosomes are normal, the chance to have another pregnancy affected with holoprosencephaly is about 6%.

There is no treatment for holoprosencephaly and the prognosis for individuals with the disorder is poor. Most of those who survive show no significant developmental gains. For children who survive, treatment is symptomatic. It is possible that improved management of diabetic pregnancies may help prevent holoprosencephaly, however there is no means of primary prevention.

Currently, research is focusing on identifying the role of the genes on 18p in causing the signs and symptoms associated with deletions of 18p. This will ultimately enable predictive genotyping.

TGIF-Mutations and deletions of this gene have been associated with holoprosencephaly. Penetrance is incomplete, meaning that a deletion of one copy of this gene is not in and of itself sufficient to cause holoprosencephaly. Ten to fifteen percent of people with 18p- have holoprosencephaly, suggesting that other genetic and environmental facts play a role in the etiology of holoprosencephaly in these individuals.

Prognosis is poor. Previous research suggested a 100% mortality rate for those with acrania. This disease is rare, occurring in 1 in 20,000 live births.

In order to better manage an acrania diagnosis, early detection is of extreme importance so that actions may be taken to help the mother and child. Families may choose either to terminate the pregnancy, or to carry the child to term. Acrania may cause a fetus to spontaneously abort before reaching term.

There is no cure for ONH; however, many therapeutic interventions exist for the care of its symptoms. These may include hormone replacement therapy for hypopituitarism, occupational, physical, and/or speech therapy for other issues, and services of a teacher of students with blindness/visually impairment. Special attention should be paid to early development of oral motor skills and acclimation to textured foods for children with texture aversion, or who are otherwise resistant to eating.

Sleep dysfunction can be ameliorated using melatonin in the evening in order to adjust a child's circadian clock.

Treatment for strabismus may include patching of the better eye, which may result in improved vision in the worse eye; however, this should be reserved for cases in which the potential for vision improvement in both eyes is felt to be good. Surgery to align the eyes can be performed once children with strabismus develop equal visual acuity in both eyes, most often after the age of three. Generally surgery results in improved appearance only and not in improved visual function.

More than 80% of children with Patau syndrome die within the first year of life. Children with the mosaic variation are usually affected to a lesser extent. In a retrospective Canadian study of 174 children with trisomy 13, median survival time was 12.5 days. One and ten year survival was 19.8% and 12.9% respectively.

Microcephaly is a medical condition in which the brain does not develop properly resulting in a smaller than normal head. Microcephaly may be present at birth or it may develop in the first few years of life. Often people with the disorder have an intellectual disability, poor motor function, poor speech, abnormal facial features, seizures, and dwarfism.

The disorder may stem from a wide variety of conditions that cause abnormal growth of the brain, or from syndromes associated with chromosomal abnormalities. A homozygous mutation in one of the "microcephalin" genes causes primary microcephaly. It serves as an important neurological indication or warning sign, but no uniformity exists in its definition. It is usually defined as a head circumference (HC) more than two standard deviations below the mean for age and sex. Some academics advocate defining it as head circumference more than three standard deviations below the mean for the age and sex.

There is no specific treatment that returns the head size to normal. In general, life expectancy for individuals with microcephaly is reduced and the prognosis for normal brain function is poor. Occasionally, some will grow normally and develop normal intelligence.

Cerebellar agenesis is a rare condition in which a brain develops without the cerebellum. The cerebellum controls smooth movement, and when it does not develop, the rest of the brain must compensate, which it cannot do completely. The condition is not fatal on its own, but people born without a cerebellum experience severe developmental delays, language deficits, and neurological abnormalities. As children with cerebellar agenesis get older, their movements usually improve. It can co-exist with other severe malformations of the central nervous system, like anencephaly, holoprosencephaly, and microencephaly.

The condition was first reported in 1831. 10 cases had been reported as of 1998. Agenesis of one half or another part of the cerebellum is more common than complete agenesis.

Cerebellar agenesis can be caused by mutations in the PTF1A gene.