Preventive measures against pre-eclampsia have been heavily studied. Because the pathogenesis of pre-eclampsia is not completely understood, prevention remains a complex issue. Below are some of the currently accepted recommendations.

Supplementation with a balanced protein and energy diet does not appear to reduce the risk of pre-eclampsia. Further, there is no evidence that changing salt intake has an effect.

Supplementation with antioxidants such as vitamin C, D and E has no effect on pre-eclampsia incidence; therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.

Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of pre-eclampsia.

In most cases Ballantyne syndrome causes fetal or neonatal death and in contrast, maternal involvement is limited at the most to preeclampsia.

Although the exact etiopathogenetic mechanism of Ballantyne syndrome remains unknown, several authors have reported raised uric acid levels, anemia, and low hematocrit without hemolysis.

Miller-Dieker occurs in less than one in 100000 people and can occur in all races.

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

MDS was named for the two physicians, James Q. Miller and H. Dieker., who independently described the condition in the 1960s. The hallmark of MDS is lissencephaly, a condition in which the outer layer of the brain, the cerebral cortex, is abnormally thick and lacks the normal convolutions (gyri). In some areas of the brain, gyri are fewer in number but wider than normal (pachygyri). Other areas lack gyri entirely (agyri). Normally, during the third and fourth months of pregnancy, the brain cells in the baby multiply and move to the surface of the brain to form the cortex. Lissencephaly is caused by a failure of this nerve cell migration. MDS is often called Miller-Dieker lissencephaly syndrome.

JQ Miller described the disease and in 1969 H Dieker emphasized that it should also take the name lissencephaly syndrome because several malformations occur beyond the brain itself. When MDS was initially described, geneticists assumed it followed an autosomal recessive pattern of inheritance. In the early 1990s, several patients with Miller–Dieker syndrome were found to be missing a small portion of chromosome 17. (17p13.3) (a partial deletion).

Maternal mortality is a sentinel event to assess the quality of a health care system. The standard indicator is the Maternal Mortality Ratio, defined as the ratio of the number of maternal deaths per 100,000 live births. Due to improved health care the ratio has been declining steadily in developed countries. For example, in the UK 1952-1982 the ratio was halving every 10 years. In the European Union the ratio has now stabilized at around 10 to 20.

The small number of cases makes the evaluation of maternal mortality practically impossible Historically, the study of negative outcomes have been highly successful in preventing their causes, this strategy of prevention therefore faces difficulties when if the number of negative outcome drop to low levels. In the UK, for example, the most dramatic decline in maternal death was achieved in Rochdale, an industrial town in the poorest area of England. In 1928 the town had a Maternal Mortality Ratio of over 900 per 100,000 live births, more than double the national average of the time. An enquiry into the causes of the deaths reduced the ratio to 280 per 100,000 pregnancies by 1934, only six years later, then the lowest in the country.

The very low figures of maternal mortality have therefore stimulated an interest in investigating cases of life-threatening obstetric morbidity or maternal near miss. There are several advantages of investigating near miss events over events with fatal outcome

- near miss are more common than maternal deaths

- their review is likely to yield useful information on the same pathways that lead to severe morbidity and death,

- investigating the care received may be less threatening to providers because the woman survived

- one can learn from the women themselves since they can be interviewed about the care they received.

- all near misses should be interpreted as free lessons and opportunities to improve the quality of service provision

- it is also clear that maternal deaths merely are the tip of the iceberg of maternal disability. For every woman who dies, many more will survive but often suffer from lifelong disabilities.

The growing interest is reflected in an increasing number of systematic reviews on the prevalence of near miss. The studies and reviews span

- analytic attempts to define the concept more strictly,

- descriptive efforts to measure and quantify new indicators (prevalence) of near-miss for different geographical regions etc.

- explanatory efforts of the leading cause for morbidity

Post-maturity syndrome develops in about 20% of human pregnancies continuing past the expected dates. Features of post-maturity syndrome include oligohydramnios, meconium aspiration, macrosomia and fetal problems such as dry peeling skin, overgrown nails, abundant scalp hair, visible creases on palms and soles, minimal fat deposition and skin colour become green or yellow due to meconeum staining.

If there are no maternal or fetal complications, labour can be induced after assessing the favourability of the cervix and excluding cephalo-pelvic disproportions. Otherwise emergency lower segment Caesarean section (LSCS) should be made.

The syndrome was first described by Stewart H. Clifford in 1954.

Treatment of cause: Due to the genetic cause, no treatment of the cause is possible.

Treatment of manifestations: routine treatment of ophthalmologic, cardiac, and neurologic findings; speech, occupational, and physical therapies as appropriate; specialized learning programs to meet individual needs; antiepileptic drugs or antipsychotic medications as needed.

Surveillance: routine pediatric care; routine developmental assessments; monitoring of specific identified medical issues.

The World Health Organization defines a maternal near-miss case as "a woman who nearly died but survived a complication that occurred during pregnancy, childbirth or within 42 days of termination of pregnancy."

The caloric intake of children with SRS must be carefully controlled in order to provide the best opportunity for growth. If the child is unable to tolerate oral feeding, then enteral feeding may be used, such as the percutaneous endoscopic gastrostomy.

In children with limb-length differences or scoliosis, physiotherapy can alleviate the problems caused by these symptoms. In more severe cases, surgery to lengthen limbs may be required. To prevent aggravating posture difficulties children with leg length differences may require a raise in their shoe.

Growth hormone therapy is often prescribed as part of the treatment of SRS. The hormones are given by injection typically daily from the age of 2 years old through teenage years. It may be effective even when the patient does not have a growth hormone deficiency. Growth hormone therapy has been shown to increase the rate of growth in patients and consequently prompts 'catch up' growth. This may enable the child to begin their education at a normal height, improving their self-esteem and interaction with other children. The effect of growth hormone therapy on mature and final height is as yet uncertain. There are some theories suggesting that the therapy also assists with muscular development and managing hypoglycemia.

There are many factors that may influence childbearing age in women, although they are mostly correlations without certain causations.

Two studies show that generous parental leave allowances in Britain encourage young motherhood and that parental-leave allowance reduces postponement in Sweden.

If ongoing and rapid haemorrhage is occurring then immediate delivery of the foetus may be indicated if the fetus is sufficiently developed. If the haemorrhage has already occurred and now stopped, an inutero transfusion of red cells to the foetus may be recommended.

Exposure of spermatozoa to lifestyle, environmental and/or occupational hazards may increase the risk of aneuploidy. Cigarette smoke is a known aneugen (aneuploidy inducing agent). It is associated with increases in aneuploidy ranging from 1.5 to 3.0-fold. Other studies indicate factors such as alcohol consumption, occupational exposure to benzene, and exposure to the insecticides fenvalerate and carbaryl also increase aneuploidy.

A woman's risk of having a baby with chromosomal abnormalities increases with her age. Down syndrome is the most common chromosomal birth defect, and a woman's risk of having a baby with Down syndrome is:

- At age 20, 1 in 1,441

- At age 25, 1 in 1,383

- At age 30, 1 in 959

- At age 35, 1 in 338

- At age 40, 1 in 84

- At age 45, 1 in 32

- At age 50, 1 in 44

On several locations in the world people are studying on the subject of 1q21.1 deletion syndrome. The syndrome was identified for the first time with people with heart abnormalities. The syndrome has later been found with patients with autism and schizophrenia. Research is done on patients with a symptom of the syndrome, to find more patients with the syndrome.

There may be a relation between autism and schizophrenia. Literature shows that nine locations have been found on the DNA where the syndromes related to autism or schizophrenia can be found, the so-called "hotspots": 1q21.1, 3q29, 15q13.3, 16p11.2, 16p13.1, 16q21, 17p12, 21q11.2 and 21q13.3. With a number of hotspots both autism and schizophrenia were observed at that location. In other cases, either autism or schizophrenia has been seen.

Statistical research showed that schizophrenia is more common in combination with 1q21.1 deletion syndrome. On the other side, autism is significantly more common with 1q21.1 duplication syndrome. Further research confirmed that the odds on a relation between schizophrenia and deletions at 1q21.1, 3q29, 15q13.3, 22q11.21 en Neurexin 1 (NRXN1) and duplications at 16p11.2 are at 7.5% or higher.

Common variations in the BCL9 gene, which is in the distal area, confer risk of schizophrenia and may also be associated with bipolar disorder and major depressive disorder.

Research is done on 10–12 genes on 1q21.1 that produce DUF1220-locations. DUF1220 is an unknown protein, which is active in the neurons of the brain near the neocortex. Based on research on apes and other mammals, it is assumed that DUF1220 is related to cognitive development (man: 212 locations; chimpanzee: 37 locations; monkey: 30 locations; mouse: 1 location). It appears that the DUF1220-locations on 1q21.1 are in areas that are related to the size and the development of the brain. The aspect of the size and development of the brain is related to autism (macrocephaly) and schizophrenia (microcephaly). It has been proposed that a deletion or duplication of a gene that produces DUF1220-areas might cause growth and development disorders in the brain

Another relation between macrocephaly with duplications and microcephaly with deletions has been seen in research on the HYDIN Paralog or HYDIN2. This part of 1q21.1 is involved in the development of the brain. It is assumed to be a dosage-sensitive gene. When this gene is not available in the 1q21.1 area, it leads to microcephaly. HYDIN2 is a recent duplication (found only in humans) of the HYDIN gene found on 16q22.2.

Research on the genes CHD1L and PRKAB2 within lymphoblast cells lead to the conclusion that anomalies appear with the 1q21.1-deletionsyndrome:

- CHD1L is an enzyme which is involved in untangling the chromatides and the DNA repair system. With 1q21.1 deletion syndrome a disturbance occurs, which leads to increased DNA breaks. The role of CHD1L is similar to that of helicase with the Werner syndrome

- PRKAB2 is involved in maintaining the energy level of cells. With 1q21.1-deletion syndrome this function was attenuated.

GJA5 has been identified as the gene that is responsible for the phenotypes observed with congenital heart diseases on the 1q21.1 location. In case of a duplication of GJA5 tetralogy of Fallot is more common. In case of a deletion other congenital heart diseases than tetralogy of Fallot are more common.

Some infants are treated with 40% dextrose (a form of sugar) gel applied directly to the infant's mouth.

It is the goal of evolutionary medicine to find treatments for diseases that are informed by the evolutionary history of a disease. It has been suggested that gestational hypertension is linked to insulin resistance during pregnancy. Both the increase in blood sugar that can lead to gestational diabetes and the increase in blood pressure that can lead to gestational hypertension are mechanisms that mean to optimize the amount of nutrients that can be passed from maternal tissue to fetal tissue. It has been suggested that techniques used to combat insulin insensitivity might also prove beneficial to those suffering from gestational hypertension. Measures to avoid insulin resistance include avoiding obesity before pregnancy, minimizing weight gain during pregnancy, eating foods with low glycemic indexes, and exercising.

Those infants that have an increased risk of developing hypoglycemia shortly after birth are:

- preterm

- asphyxia

- cold stress

- congestive heart failure

- sepsis

- Rh disease

- discordant twin

- erythroblastosis fetalis

- polycythemia

- microphallus or midline defect

- respiratory disease

- maternal glucose IV

- maternal epidural

- postmaturity

- hyperinssulinnemia

- endocrine disorders

- inborn errors of metabolism

- diabetic mother

- maternal toxemia

- intrapartum fever

Since the syndrome is caused by a genetic mutation in the individual's DNA, a cure is not available. Treatment of the symptoms and management of the syndrome, however, is possible.

Depending on the manifestation, surgery, increased intake of glucose, special education, occupational therapy, speech therapy, and physical therapy are some methods of managing the syndrome and associated symptoms.

Genetic

- Inborn errors of metabolism

1. Congenital disorder of glycosylation

2. Mitochondrial disorders

3. Peroxisomal disorder

4. Glucose transporter defect

5. Menkes disease

6. Congenital disorders of amino acid metabolism

7. Organic acidemia

Syndromes

- Contiguous gene deletion

1. 17p13.3 deletion (Miller–Dieker syndrome)

- Single gene defects

1. Rett syndrome (primarily girls)

2. Nijmegen breakage syndrome

3. X-linked lissencephaly with abnormal genitalia

4. Aicardi–Goutières syndrome

5. Ataxia telangiectasia

6. Cohen syndrome

7. Cockayne syndrome

Acquired

- Disruptive injuries

1. Traumatic brain injury

2. Hypoxic-ischemic encephalopathy

3. Ischemic stroke

4. Hemorrhagic stroke

- Infections

1. Congenital HIV encephalopathy

2. Meningitis

3. Encephalitis

- Toxins

1. Lead poisoning

2. Chronic renal failure

- Deprivation

1. Hypothyroidism

2. Anemia

3. Congenital heart disease

4. Malnutrition

Genetic factors may play a role in causing some cases of microcephaly. Relationships have been found between autism, duplications of chromosomes, and macrocephaly on one side. On the other side, a relationship has been found between schizophrenia, deletions of chromosomes, and microcephaly. Moreover, an association has been established between common genetic variants within known microcephaly genes ("MCPH1, CDK5RAP2") and normal variation in brain structure as measured with magnetic resonance imaging (MRI)i.e., primarily brain cortical surface area and total brain volume.

The spread of Aedes mosquito-borne Zika virus has been implicated in increasing levels of congenital microcephaly by the International Society for Infectious Diseases and the US Centers for Disease Control and Prevention. Zika can spread from a pregnant woman to her fetus. This can result in other severe brain malformations and birth defects. A study published in The New England Journal of Medicine has documented a case in which they found evidence of the Zika virus in the brain of a fetus that displayed the morphology of microcephaly.

The treatment depends on the cause.

Severely anemic fetuses, including those with Rh disease and alpha thalassemia major, can be treated with blood transfusions while still in the womb. This treatment increases the chance that the fetus will survive until birth.

SGBS is similar to another overgrowth syndrome called Beckwith–Wiedemann syndrome.

SGBS Cells are a unique tool to study the function of Human adipocyte biology. These cells are similar to human primary preadipocytes, and may or may not become a popular model instead of Mouse 3T3-L1 cells to study the secretion and adipokine profile in the future. This cellular tool has been described and developed by Dr. Martin Wabitsch, University of Ulm, Germany.

Fetal microchimerism could have an implication on maternal health. Isolating cells in cultures can alter the properties of the stem cells, but in pregnancy the effects of fetal stem cells can be investigated without in vitro cultures. Once characterized and isolated, fetal cells that are able to cross the blood brain barrier could impact certain procedures. For example, isolating stem cells can be accomplished through taking them from sources like the umbilical cord. These fetal stem cells can be used in intravenous infusion to repair the brain tissue. Hormonal changes in pregnancy alter neurogenesis, which could create favorable environments for fetal cells to respond to injury.

The true function on fetal cells in mothers is not fully known, however, there have been reports of positive and negative health effects. The sharing of genes between the fetus and mother may lead to benefits. Due to not all genes being shared, health complications may arise as a result of resource allocation. During pregnancy, fetal cells are able to manipulate the maternal system to draw resources from the placenta, while the maternal system tries to limit it.