A number of studies have shown that tobacco use is a significant factor in miscarriages among pregnant smokers, and that it contributes to a number of other threats to the health of the fetus. Smoking and pregnancy, combined, cause twice the risk of premature rupture of membranes, placental abruption and placenta previa. Also, it causes 30% higher odds of the baby being born prematurely.

Prenatal cocaine exposure is associated with, for example, premature birth, birth defects and attention deficit disorder.

A recent study on cocaine in Prenatal Drug Exposure(2008) explores how the differences between children who were exposed to drugs prenatal and those with non-drug prenatal exposure differ at the age of five.

Many of the side effects from the children who were exposed to the recreational drug being cocaine had side effects including the following; lack in school readiness, slower impulse control and lack in visual attention.

While any number of injuries may occur during the birthing process. A number of specific conditions are well described. Brachial plexus palsy occurs in 0.4 to 5.1 infants per 1000 live birth. Head trauma and brain damage during delivery can lead to a number of conditions include: caput succedaneum, cephalohematoma, subgaleal hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, epidural hemorrhage, and intraventricular hemorrhage.

The most common fracture during delivery is that of the clavicle (0.5%).

Genetics plays a role in having a baby born with LGA. Taller, heavier parents tend to have larger babies. Babies born to an obese mother have greatly increased chances of LGA.

Sequelae can occur in both the mother and the infant after a traumatic birth.

Birth trauma is uncommon in the Western world in relation to rates in the third world. In the West injury occurs in 1.1% of C-sections.

There are believed to be links with polyhydramnios (excessive amniotic sac fluid). If one has excessive amniotic fluid, microsomia is more likely, since there is no room for the baby to grow. Preterm labor is also highly likely for polyhydramnios.

A longitudinal study done on prenatal stress and gender roles showed that prenatal stress only plays a small part in the gender roles the offspring takes on and mentions it has more to do with older siblings, maternal use of alcohol and/or tobacco, maternal education, and the observance or teaching of “traditional sex roles” from the parents.

Prenatal stress (or prenatal maternal stress) is exposure of an expectant mother to stress, which can be caused by stressful life events or by environmental hardships. The resulting changes to the mother's hormonal and immune system may harm the fetus's (and after birth, the infant's) immune function and brain development.

Prenatal stress is shown to have several affects in fetal brain development. In the hippocampus of adult male rats, prenatal stress has shown to decrease the rate of proliferation and cell death in the hypothalamus-pituitary axis. Prenatal stressed animals have prolonged corticosterone response. Removing the adrenal glands of the mother eliminates the effect of the pup's corticosterone response. Supplementing the adrenalectamized mother with corticosterone, rescued the hypothalamic-pituitary-axis response to maternal stress for prenatally stressed offspring. Prenatal stress caused high glucocorticoids, which in turn affects the hypothalamic-pituitary-axis negative feedback.

A study by García-Cáceres et al. showed that prenatal stress decreases cell turnover and proliferation in the hypothalamus of adult rats, which reduces structural plasticity and reduces the response to stress in adulthood. This study also showed that when prenatally stressed rats were stressed in adulthood the females showed an increase in corticotropin-releasing hormone suggesting it to be an up-regulation in the hypothalamic-pituitary adrenal axis. Males showed no elevation of corticosterone levels. Increase in adrenocorticotropic hormone with no effect of adult stress and a decrease in the corticotropin-releasing hormone mRNA in the hypothalamus showed a down-regulation. The author concludes that this makes prenatally stressed females less reactive to later life stressors than males.

Most pregnancies that are diagnosed with confined placental mosaicism continue to term with no complications and the children develop normally.

However, some pregnancies with CPM experience prenatal or perinatal complications. The pregnancy loss rate in pregnancies with confined placental mosaicism, diagnosed by chorionic villus sampling, is higher than among pregnancies without placental mosaicism. It may be that sometimes the presence of significant numbers of abnormal cells in the placenta interferes with proper placental function. An impaired placenta cannot support the pregnancy and this may lead to the loss of a chromosomally normal baby. On the other hand, an apparently normal diploid fetus may experience problems with growth or development due to the effects of uniparental disomy (UPD). Intrauterine growth restriction (IUGR) has been reported in a number of CPM cases. In follow-up studies adequate postnatal catch-up growth has been demonstrated, which may suggest a placental cause of the IUGR.

When predicting the likely effects (if any) of CPM detected in the first trimester, several potentially interactive factors may be playing a role, including:

- "Origin of error:" Somatic errors are associated with lower levels of trisomy in the placenta and are expected usually to involve only one cell line (i.e.: the trophoblast cells or the villus stroma cells). Somatic errors are thus less likely than meiotic errors to be associated with either ultrasound abnormalities, growth problems or detectable levels of trisomy in small samples of prenatal CVS. Currently, there is no evidence that somatic errors, which lead to confined placental trisomy, are of any clinical consequence. Errors of meiotic origin are correlated with higher levels of trisomy in placental tissues and may be associated with adverse pregnancy outcome. The cell type in which the abnormality is seen is also an important factor in determining the risk of fetal involvement. The villus stroma or mesenchymal core is more likely than the cytotrophoblast to be reflective of the fetal genotype.

- "Level of mosaicism:" There is a correlation between a high number of aneuploid cells detected at CVS with poor pregnancy progress. This includes an association between high levels of abnormal cells in placental tissue and concerns with the growth of the baby. However, it is not accurate to use these associations to try to predict pregnancy outcome based on the percent of trisomic cells in a first trimester CVS result.

- "Specific chromosomes:" The influence of CPM on fetal growth is chromosome specific. Certain chromosomes carry imprinted genes involved in growth or placental function, which may contribute to impaired pregnancy progress when CPM is detected. Different chromosomes are observed at different frequencies depending on the type of CPM observed. The pregnancy outcome is strongly chromosome specific. The most frequently seen trisomic cells in confined placental mosaicism involve chromosomes 2, 3, 7, 8 and 16. The next frequently involved are 9, 13, 15, 18, 20 and 22. It has been observed that CPM involving the sex chromosomes usually has no adverse effects on fetal development. The common autosomal trisomies (21, 18, 13) made up a smaller number of cases of mosaicism detected on CVS, but were more often confirmed in fetal tissue (19%). On the other hand, the uncommon autosomal trisomies accounted for a greater number of placental mosaicism cases, but were less often confirmed in fetal tissue (3.2%). When CPM is detected on CVS involving certain chromosomes which are known or suspected to carry imprinted genes, molecular investigations should be performed to exclude fetal UPD. We will explore chromosome specific cases in the chromosome specific section.

- "Type of chromosome abnormality:" The factor that had the highest predictive value as to whether the fetus was affected or not was the type of chromosome abnormality. Marker chromosomes were more often confirmed in the fetus than trisomies. For example, of 28 cases of mosaic polyploidy detected on CVS, fetal mosaicism was confirmed in only one case. This is compared to marker chromosomes detected on CVS, in which mosaicism was confirmed in 1/4 of the fetuses.

Cannabis consumption in pregnancy might be associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits. The American Congress of Obstetricians and Gynecologists recommended that cannabis use be stopped before and during pregnancy, Cannabis is the most commonly used illicit substance

among pregnant women.

Although it is difficult to draw firm conclusions, there is some evidence that prenatal exposure to marijuana may be associated with deficits in language, attention, cognitive performance, and delinquent behaviors. THC exposure in rats during the prenatal developmental phase may cause epigenetic changes in gene expression, but there is limited knowledge about the risk for psychiatric disorders because of ethical barriers to studying the developing human brain. While animal studies cannot take into account factors that could influence the effects of cannabis on human maternal exposure, such as environmental and social factors, a 2011 review of rodent studies by Campolongo "et al." said there was "... increasing evidence from animal studies showing that cannabinoid drugs ... induce enduring neurobehavioral abnormalities in the exposed offspring ..." Campolongo "et al." added that "clinical studies report hyperactivity, cognitive impairments and altered emotionality in humans exposed in utero to cannabis". Martin "et al." investigated recent trends in substance abuse treatment admissions for cannabis use in pregnancy in the US, based on Treatment Episodes Data Set (TEDS) from 1992 to 2012, and discovered that, while the proportion of treatment admissions for pregnant women was stable (about 4%), the admissions for women who were pregnant and reported any marijuana use grew from 29% to 43%. A 2015 review found that cannabis use by pregnant mothers impaired brain maturation in their children, and that it also predisposed their children to neurodevelopmental disorders.

Amount, frequency, and timing of prenatal alcohol use can dramatically impact the other three key features of FASD. While consensus exists that alcohol is a teratogen, there is no clear consensus as to what level of exposure is toxic. The CDC guidelines are silent on these elements diagnostically. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30-day period.

"The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as "high risk" and "some risk". It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg female drinking six to eight beers in one sitting.

For many adopted or adults and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.

There is no known definitive single mechanism that causes colpocephaly. However, researchers believe there are many possible causes of colpocephaly. It is a common symptom of other neurological disorders in newborns, can be caused as a result of shunt treatment of hydrocephalus, developmental disorders in premature infants, due to intrauterine disturbances during pregnancy, genetic disorders, underdevelopment or lack of white matter in the cerebrum, and exposure of the mother and the developing fetus to medications, infections, radiation, or toxic substances. Also, it is usually more common in premature infants than in full-term infants, especially in babies born with hypoxia or lung immaturity.

Some of the central nervous system disorders which are associated with colpocephaly are as follows:

- polymicrogyria

- Periventricular leukomalacia (PVL)

- intraventricular hemorrhage

- Hydrocephalus

- schizencephaly

- microgyria

- microcephaly

- Pierre-Robin syndrome

- Neurofibromatosis

Often colpocephaly occurs as a result of hydrocephalus. Hydrocephalus is the accumulation of cerebrospinal fluid (CSF) in the ventricles or in the subarachnoid space over the brain. The increased pressure due to this condition dilates occipital horns causing colpocephaly.

The most generally accepted theory is that of neuronal migration disorders occurring during the second to fifth months of fetal life. Neuronal migration disorders are caused by abnormal migration, proliferation, and organization of neurons during early brain development. During the seventh week of gestation, neurons start proliferating in the germinal matrix which is located in the subependymal layer of the walls of the lateral ventricles. During the eighth week of gestation, the neurons then start migrating from the germinal zone to cortex along specialized radial glial fibers. Next, neurons organize themselves into layers and form synaptic contacts with other neurons present in the cortex. Under normal conditions, the neurons forming a germinal layer around ventricles migrate to the surface of the brain and form the cerebral cortex and basal ganglia. If this process is abnormal or disturbed it could result in the enlargement of the occipital horns of the lateral ventricles. Common prenatal disturbances that have been shown to disturb the neuronal migration process include the following:

- continuation of oral contraceptives

- exposure to alcohol

- intrauterine malnutrition

- intrauterine infections such as toxoplasmosis

- maternal drug ingestion during early pregnancy such as corticosteroids, salbutamol, and theophylline

Researchers also believe that these factors can cause destruction of neural elements that have previously been normally formed.

It is suggested that the underdevelopment or lack of white matter in the developing fetus could be a cause of colpocephaly. The partial or complete absence of white matter, also known as agenesis of the corpus callosum results in anatomic malformations that can lead to colpocephaly. This starts to occur around the middle of the second month to the fifth month of pregnancy. The lateral ventricles are formed as large cavities of the telencephalic vesicle. The size of the ventricles are decreased in normal development after the formation of the Foramen of Magendie, which decompresses the ventricular cavities. Myelination of the ventricular walls and association fibers of the corpus callosum and the calcarine fissure helps shape the occipital horns. In cases where this developmental process is interrupted, occipital horns are disproportionately enlarged.

Colpocephaly has been associated with chromosomal abnormalities such as trisomy 8 mosaic and trisomy 9 mosaic. A few reports of genetically transmitted colpocephaly are also found in literature. Some of these are of two siblings, monozygotic twins, and non-identical twins. The authors suggest a genetic origin with an autosomal or X-linked recessive inheritance rather than resulting from early prenatal disturbances.

Mosaic trisomy 16, a rare chromosomal disorder, is compatible with life, therefore a baby can be born alive. This happens when only some of the cells in the body contain the extra copy of chromosome 16. Some of the consequences include slow growth before birth.

During prenatal diagnosis the levels of trisomy in fetal-placental tissues can be analyzed. These levels can be predictors of outcomes in mosaic trisomy 16 pregnancies. In a study of prenatal diagnosis cases, there were 66% live births with an average 35.7 weeks gestational age. About 45% of them had malformations. The most common malformations were CSD, ASD, and hypospadias. However, trisomy 16 does not always result in anatomical abnormalities.

Confined placental mosaicism (CPM) represents a discrepancy between the chromosomal makeup of the cells in the placenta and the cells in the baby. CPM was first described by Kalousek and Dill in 1983. CPM is diagnosed when some trisomic cells are detected on chorionic villus sampling and only normal cells are found on a subsequent prenatal test, such as amniocentesis or fetal blood sampling. In theory, CPM is when the trisomic cells are found only in the placenta. CPM is detected in approximately 1-2% of ongoing pregnancies that are studied by chorionic villus sampling (CVS) at 10 to 12 weeks of pregnancy. Chorionic villus sampling is a prenatal procedure which involves a placental biopsy. Most commonly when CPM is found it represents a trisomic cell line in the placenta and a normal diploid chromosome complement in the baby. However, the fetus is involved in about 10% of cases.

Common causes of head injury are motor vehicle traffic collisions, home and occupational accidents, falls, and assaults. Wilson's disease has also been indicative of head injury. According to the United States CDC, 32% of traumatic brain injuries (another, more specific, term for head injuries) are caused by falls, 10% by assaults, 16.5% by being struck or against something, 17% by motor vehicle accidents, 21% by other/unknown ways. In addition, the highest rate of injury is among children ages 0–14 and adults age 65 and older.

The non-immune form of hydrops fetalis has many causes including:

- Iron deficiency anemia

- Paroxysmal supraventricular tachycardia resulting in heart failure

- Deficiency of the enzyme beta-glucuronidase. This enzyme deficiency is the cause of the lysosomal storage disease called mucopolysaccharidosis type VII.

- Congenital disorders of glycosylation

- Parvovirus B19 (fifth disease) infection of the pregnant woman

- Cytomegalovirus in mother

- Congenital pulmonary airway malformation

- Maternal syphilis and maternal diabetes mellitus

- Alpha-thalassemia can also cause hydrops fetalis when all four of the genetic loci for α globin are deleted or affected by mutation. This is termed Hb Barts (consists of y-4 tetramers).

- Uncommonly, Niemann-Pick disease Type C (NPC) and Gaucher disease type 2 can present with hydrops fetalis.

- Turner Syndrome

- Tumors, the most common type of fetal tumor being teratoma, particularly a sacrococcygeal teratoma.

- Twin-twin transfusion syndrome in pregnancies in which twins share a single placenta (hydrops affects the recipient twin)

- Maternal hyperthyroidism

- Fetal cardiac defects and skeletal defects

- Noonan syndrome

- Mirror syndrome, in which fetal and placental hydrops develops in association with maternal preeclampsia, edema and hypertension

The role of the endocannabinoid system (ECS) in female fertility has long been suspected and studied. Most studies through 2013 linking development of the fetus and cannabis show effects of consumption during the gestational period, but abnormalities in the endocannabinoid system during the phase of placental development are also linked with problems in pregnancy. According to Sun and Dey (2012), endocannabinoid signaling plays a role in "female reproductive events, including preimplantation embryo development, oviductal embryo transport, embryo implantation, placentation, and parturition". Karusu "et al" (2011) said that a "clear correlation ... in the actual reproductive tissues of miscarrying versus healthy women has yet to be established. However, the adverse effects of marijuana smoke and THC on reproductive functions point to processes that are modulated by ECS."

Keimpema and colleagues (2011) said, "Prenatal cannabis exposure can lead to growth defects during formation of the nervous system"; "[c]annabis impacts the formation and functions of neuronal circuitries by targeting cannabinoid receptors ... By indiscriminately prolonging the "switched-on" period of cannabinoid receptors, cannabis can hijack endocannabinoid signals to evoke molecular rearrangements, leading to the erroneous wiring of neuronal networks". A report prepared for the Australian National Council on Drugs concluded cannabis and other cannabinoids are contraindicated in pregnancy as they may interact with the endocannabinoid system.

As many as 50–70% of people who survive traffic accidents have facial trauma. In most developed countries, violence from other people has replaced vehicle collisions as the main cause of maxillofacial trauma; however in many developing countries traffic accidents remain the major cause. Increased use of seat belts and airbags has been credited with a reduction in the incidence of maxillofacial trauma, but fractures of the mandible (the jawbone) are not decreased by these protective measures. The risk of maxillofacial trauma is decreased by a factor of two with use of motorcycle helmets. A decline in facial bone fractures due to vehicle accidents is thought to be due to seat belt and drunk driving laws, strictly enforced speed limits and use of airbags. In vehicle accidents, drivers and front seat passengers are at highest risk for facial trauma.

Facial fractures are distributed in a fairly normal curve by age, with a peak incidence occurring between ages 20 and 40, and children under 12 suffering only 5–10% of all facial fractures. Most facial trauma in children involves lacerations and soft tissue injuries. There are several reasons for the lower incidence of facial fractures in children: the face is smaller in relation to the rest of the head, children are less often in some situations associated with facial fractures such as occupational and motor vehicle hazards, there is a lower proportion of cortical bone to cancellous bone in children's faces, poorly developed sinuses make the bones stronger, and fat pads provide protection for the facial bones.

Head and brain injuries are commonly associated with facial trauma, particularly that of the upper face; brain injury occurs in 15–48% of people with maxillofacial trauma. Coexisting injuries can affect treatment of facial trauma; for example they may be emergent and need to be treated before facial injuries. People with trauma above the level of the collar bones are considered to be at high risk for cervical spine injuries (spinal injuries in the neck) and special precautions must be taken to avoid movement of the spine, which could worsen a spinal injury.

Complications are likely to result in cases of excess blood loss or punctures to certain organs, possibly leading to shock. Swelling and bruising may result, more so in high-impact injuries. Pain in the affected areas may differ where severity of impact increases its likelihood and may radiate if symptoms are aggravated when one moves around.

In children with uncomplicated minor head injuries the risk of intra cranial bleeding over the next year is rare at 2 cases per 1 million. In some cases transient neurological disturbances may occur, lasting minutes to hours. Malignant post traumatic cerebral swelling can develop unexpectedly in stable patients after an injury, as can post traumatic seizures. Recovery in children with neurologic deficits will vary. Children with neurologic deficits who improve daily are more likely to recover, while those who are vegetative for months are less likely to improve. Most patients without deficits have full recovery. However, persons who sustain head trauma resulting in unconsciousness for an hour or more have twice the risk of developing Alzheimer's disease later in life.

Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain radiating to the arms are signs of cervical spine injury and merit spinal immobilization via application of a cervical collar and possibly a long board.If the neurological exam is normal this is reassuring. Reassessment is needed if there is a worsening headache, seizure, one sided weakness, or has persistent vomiting.

To combat overuse of Head CT Scans yielding negative intracranial hemorrhage, which unnecessarily expose patients to radiation and increase time in the hospital and cost of the visit, multiple clinical decision support rules have been developed to help clinicians weigh the option to scan a patient with a head injury. Among these are the Canadian Head CT rule, the PECARN Head Injury/Trauma Algorithm, and the New Orleans/Charity Head Injury/Trauma Rule all help clinicians make these decisions using easily obtained information and noninvasive practices.

Mortality rates in patients with pelvic fractures are between 10 and 16 percent. However, death is typically due to associated trauma affecting other organs, such as the brain. Death rates due to complications directly related to pelvic fractures, such as bleeding, are relatively low.

Vehicle-related SCI is prevented with measures including societal and individual efforts to reduce driving under the influence of drugs or alcohol, distracted driving, and drowsy driving. Other efforts include increasing road safety (such as marking hazards and adding lighting) and vehicle safety, both to prevent accidents (such as routine maintenance and antilock brakes) and to mitigate the damage of crashes (such as head restraints, air bags, seat belts, and child safety seats). Falls can be prevented by making changes to the environment, such as nonslip materials and grab bars in bathtubs and showers, railings for stairs, child and safety gates for windows. Gun-related injuries can be prevented with conflict resolution training, gun safety education campaigns, and changes to the technology of guns (such as trigger locks) to improve their safety. Sports injuries can be prevented with changes to sports rules and equipment to increase safety, and education campaigns to reduce risky practices such as diving into water of unknown depth or head-first tackling in association football.

Colpocephaly is usually non-fatal. There has been relatively little research conducted to improve treatments for colpocephaly, and there is no known definitive treatment of colpocephaly yet. Specific treatment depends on associated symptoms and the degree of dysfunction. Anticonvulsant medications can be given to prevent seizure complications, and physical therapy is used to prevent contractures (shrinkage or shortening of muscles) in patients that have limited mobility. Patients can also undergo surgeries for stiff joints to improve motor function. The prognosis for individuals with colpocephaly depends on the severity of the associated conditions and the degree of abnormal brain development.

A rare case of colpocephaly is described in literature which is associated with macrocephaly instead of microcephaly. Increased intracranial pressure was also found in the condition. Similar symptoms (absence of corpus callosum and increased head circumference) were noted as in the case of colpocephaly that is associated with microcephaly. A bi-ventricular peritoneal shunt was performed, which greatly improved the symptoms of the condition. Ventriculo-peritoneal shunts are used to drain the fluid into the peritoneal cavity.