Diastasis recti (also known as abdominal separation) is commonly defined as a gap of roughly 2.7 cm or greater between the two sides of the rectus abdominis muscle. This condition has no associated morbidity or mortality.

The distance between the right and left rectus abdominis muscles is created by the stretching of the linea alba, a connective collagen sheath created by the aponeurosis insertions of the transverse abdominis, internal oblique, and external oblique.

Diastasis of this muscle occurs principally in two populations: newborns and pregnant women. It is also known to occur in men.

- In the newborn, the rectus abdominis is not fully developed and may not be sealed together at midline. Diastasis recti is more common in premature and black newborns.

- In pregnant or postpartum women, the condition is caused by the stretching of the rectus abdominis by the growing uterus. It is more common in multiparous women due to repeated episodes of stretching. When the defect occurs during pregnancy, the uterus can sometimes be seen bulging through the abdominal wall beneath the skin.

- Women are more susceptible to develop diastasis recti when over the age of 35, high birth weight of child, multiple birth pregnancy, and multiple pregnancies. Additional causes can be attributed to excessive abdominal exercises after the first trimester of pregnancy.

No treatment is necessary for women while they are still pregnant. In children, complications include development of an umbilical or ventral hernia, which is rare and can be corrected with surgery.

Alerting a medical professional is important when an infant displays signs of vomiting, redness or pain in the abdominal area.

Typically the separation of the abdominal muscles will lessen within the first 8 weeks after childbirth; however, the connective tissue remains stretched for many postpartum women. The weakening of the abdominal muscles and the reduced force transmission from the stretched linea alba may also make it difficult to lift objects, and cause lower back pain. Additional complications can manifest in weakened pelvic alignment and altered posture.

Haemorrhoids (piles) are swollen veins at or inside the anal area, resulting from impaired venous return, straining associated with constipation, or increased intra-abdominal pressure in later pregnancy. They are more common in pregnant than non-pregnant women. It is reported by 16% of women at 6 months postpartum. Most pregnant women in countries where the diet is not heavily fiber-based may develop hemorrhoids, although they will usually be asymptomatic. Hemorrhoids can cause bleeding, itching, soiling or pain, and they can become strangulated. Symptoms may resolve spontaneously after pregnancy, although hemorrhoids are also common in the days after childbirth. Conservative treatments for hemorrhoids in pregnancy include dietary modification, local treatments, bowel stimulants or depressants, or phlebotonics (to strengthen capillaries and improve microcirculation). Treatment with oral hydroxyethylrutosides may help improve first and second degree hemorrhoids, but more information on safety in pregnancy is needed. Other treatments and approaches have not been evaluated in pregnant women.

For most women, PGP resolves in weeks after delivery but for some it can last for years resulting in a reduced tolerance for weight bearing activities. PGP can take from 11 weeks, 6 months or even up to 2 years postpartum to subside. However, some research supports that the average time to complete recovery is 6.25 years, and the more severe the case is, the longer recovery period.

Overall, about 45% of all pregnant women and 25% of all women postpartum suffer from PGP. During pregnancy, serious pain occurs in about 25%, and severe disability in about 8% of patients. After pregnancy, problems are serious in about 7%. There is no correlation between age, culture, nationality and numbers of pregnancies that determine a higher incidence of PGP.

If a woman experiences PGP during one pregnancy, she is more likely to experience it in subsequent pregnancies; but the severity cannot be determined.

Pica is a craving for nonedible items such as dirt or clay. It is caused by iron deficiency which is normal during pregnancy and can be overcome with iron in prenatal vitamins or, if severe, parenteral iron

PGP in pregnancy seriously interferes with participation in society and activities of daily life; the average sick leave due to posterior pelvic pain during pregnancy is 7 to 12 weeks.

In some cases women with PGP may also experience emotional problems such as anxiety over the cause of pain, resentment, anger, lack of self-esteem, frustration and depression; she is three times more likely to suffer postpartum depressive symptoms. Other psychosocial risk factors associated with woman experiencing PGP include higher level of stress, low job satisfaction and poorer relationship with spouse.

An epigastric hernia is a type of hernia which may develop in the epigastrium (upper, central part of the abdomen). Epigastric hernias usually appear in adults.

Unlike the benign diastasis recti, epigastric hernia may trap fat and other tissues inside the opening of the hernia, causing pain and tissue damage.

Symptomatic epigastric hernias are repaired with surgery. Even if they are asymptomatic, they can be surgically corrected for cosmetic reasons. In general, cosmetic surgery on infants is delayed until the infant is older and better able to tolerate anaesthesia.

The precise cause is unknown, and has been much debated. In 1912 Moschcowitzl proposed that rectal prolapse was a sliding hernia through a pelvic fascial defect.

This theory was based on the observation that rectal prolapse patients have a mobile and unsupported pelvic floor, and a hernia sac of peritoneum from the Pouch of Douglas and rectal wall can be seen. Other adjacent structures can sometimes be seen in addition to the rectal prolapse. Although a pouch of Douglas hernia, originating in the cul de sac of Douglas, may protrude from the anus (via the anterior rectal wall), this is a different situation from rectal prolapse.

Shortly after the invention of defecography, In 1968 Broden and Snellman used cinedefecography to show that rectal prolapse begins as a circumferential intussusception of the rectum, which slowly increases over time. The leading edge of the intussusceptum may be located at 6–8 cm or at 15–18 cm from the anal verge. This proved an older theory from the 18th century by John Hunter and Albrecht von Haller that this condition is essentially a full-thickness rectal intussusception, beginning about 3 inches above the dentate line and protruding externally.

Since most patients with rectal prolapse have a long history of constipation, it is thought that prolonged, excessive and repetitive straining during defecation may predispose to rectal prolapse. Since rectal prolapse itself causes functional obstruction, more straining may result from a small prolapse, with increasing damage to the anatomy. This excessive straining may be due to predisposing pelvic floor dysfunction (e.g. obstructed defecation) and anatomical factors:

- Abnormally low descent of the peritoneum covering the anterior rectal wall

- poor posterior rectal fixation, resulting in loss of posterior fixation of the rectum to the sacral curve

- loss of the normal horizontal position of the rectum with lengthening (redundant rectosigmoid) and downward displacement of the sigmoid and rectum

- long rectal mesentery

- a deep cul-de-sac

- levator diastasis

- a patulous, weak anal sphincter

Some authors question whether these abnormalities are the cause, or secondary to the prolapse. Other predisposing factors/associated conditions include:

- pregnancy (although 35% of women who develop rectal prolapse are nulliparous (have never given birth)

- previous surgery (30-50% of females with the condition underwent previous gynecological surgery)

- pelvic neuropathies and neurological disease

- high gastrointestinal helminth loads (e.g. Whipworm)

- COPD

- cystic fibrosis

The association with uterine prolapse (10-25%) and cystocele (35%) may suggest that there is some underlying abnormality of the pelvic floor that affects multiple pelvic organs. Proximal bilateral pudendal neuropathy has been demonstrated in patients with rectal prolapse who have fecal incontinence. This finding was shown to be absent in healthy subjects, and may be the cause of denervation-related atrophy of the external anal sphincter. Some authors suggest that pudendal nerve damage is the cause for pelvic floor and anal sphincter weakening, and may be the underlying cause of a spectrum of pelvic floor disorders.

Sphincter function in rectal prolapse is almost always reduced. This may be the result of direct sphincter injury by chronic stretching of the prolapsing rectum. Alternatively, the intussuscepting rectum may lead to chronic stimulation of the rectoanal inhibitory reflex (RAIR - contraction of the external anal sphincter in response to stool in the rectum). The RAIR was shown to be absent or blunted. Squeeze (maximum voluntary contraction) pressures may be effected as well as the resting tone. This is most likely a denervation injury to the external anal sphincter.

The assumed mechanism of fecal incontinence in rectal prolapse is by the chronic stretch and trauma to the anal sphincters and the presence of a direct conduit (the intussusceptum) connecting rectum to the external environment which is not guarded by the sphincters.

The assumed mechanism of obstructed defecation is by disruption to the rectum and anal canal's ability to contract and fully evacuate rectal contents. The intussusceptum itself may mechanically obstruct the rectoanal lumen, creating a blockage that straining, anismus and colonic dysmotility exacerbate.

Some believe that internal rectal intussusception represents the initial form of a progressive spectrum of disorders the extreme of which is external rectal prolapse. The intermediary stages would be gradually increasing sizes of intussusception. However, internal intussusception rarely progresses to external rectal prolapse. The factors that result in a patient progressing from internal intussusception to a full thickness rectal prolapse remain unknown. Defecography studies demonstrated that degrees of internal intussusception are present in 40% of asymptomatic subjects, raising the possibility that it represents a normal variant in some, and may predispose patients to develop symptoms, or exacerbate other problems.

Rectal prolapse is a “falling down” of the rectum so that it is visible externally. The appearance is of a reddened, proboscis-like object through the anal sphincters. Patients find the condition embarrassing. The symptoms can be socially debilitating without treatment, but it is rarely life-threatening.

The true incidence of rectal prolapse is unknown, but it is thought to be uncommon. As most sufferers are elderly, the condition is generally under-reported. It may occur at any age, even in children, but there is peak onset in the fourth and seventh decades. Women over 50 are six times more likely to develop rectal prolapse than men. It is rare in men over 45 and in women under 20. When males are affected, they tend to be young and report significant bowel function symptoms, especially obstructed defecation, or have a predisposing disorder (e.g., congenital anal atresia). When children are affected, they are usually under the age of 3.

35% of women with rectal prolapse have never had children, suggesting that pregnancy and labour are not significant factors. Anatomical differences such as the wider pelvic outlet in females may explain the skewed gender distribution.

Associated conditions, especially in younger patients include autism, developmental delay syndromes and psychiatric conditions requiring several medications.

Assisted reproductive technology (ART) is a general term referring to methods used to achieve pregnancy by artificial or partially artificial means. According to the CDC, in general, ART procedures involve surgically removing eggs from a woman's ovaries, combining them with sperm in the laboratory, and returning them to the woman's body or donating them to another woman. ART has been associated with epigenetic syndromes, specifically BWS and Angelman syndrome. Three groups have shown an increased rate of ART conception in children with BWS. A retrospective case control study from Australia found a 1 in 4000 risk of BWS in their in-vitro population, several times higher than the general population. Another study found that children conceived by in vitro fertilisation (IVF) are three to four times more likely to develop the condition. No specific type of ART has been more closely associated with BWS. The mechanism by which ART produces this effect is still under investigation.

Most patients are diagnosed by the age of 10 years and Duane's is more common in girls (60 percent of the cases) than boys (40 percent of the cases). A French study reports that this syndrome accounts for 1.9% of the population of strabismic patients, 53.5% of patients are female, is unilateral in 78% of cases, and the left eye (71.9%) is affected more frequently than the right. Around 10–20% of cases are familial; these are more likely to be bilateral than non-familial Duane syndrome. Duane syndrome has no particular race predilection.

External forces such as falling from a horse or a car accident can result in this type of injury to the symphysis pubis.

Diastasis symphysis pubis is the separation of normally joined pubic bones, as in the dislocation of the bones, without a fracture.

Beckwith–Wiedemann syndrome has an estimated incidence of one in 13,700; about 300 children with BWS are born each year in the United States. The exact incidence of BWS is unknown because of the marked variability in the syndrome's presentation and difficulties with diagnosis. The number of reported infants born with BWS is most likely low because many are born with BWS, but have clinical features that are less prominent and therefore missed. BWS has been documented in a variety of ethnic groups and occurs equally in males and females.

Children conceived through In vitro fertilization have a three to fourfold increased chance of developing Beckwith–Wiedemann syndrome. It is thought that this is due to genes being turned on or off by the IVF procedures.

Congenital fibrosis of the extraocular muscles, or CFEOM, is a class of rare genetic disorders affecting one or more of the muscles that move the eyeballs. Individuals with CFEOM have varying degrees of ophthalmoplegia (an inability to move the eyes in one or more directions) and ptosis. The condition is present from birth and non-progressive, runs in families, and usually affects both eyes similarly. In the most common form, the superior recti are dysfunctional and the inferior recti, lacking proper opposition, pull the eyes down, forcing the head to be tilted upward in order to see straight ahead.

There are three types of CFEOM, numbered 1-3. CFEOM1, the most common type, is now known to be caused by one of several mutations in the KIF21A gene, while CFEOM2 is caused by mutations in the PHOX2A gene. CFEOM3 is caused by mutations in the TUBB3 gene.

CFEOM was first named in 1956, although papers describing conditions now known or assumed to be CFEOM appear in the medical literature as early as 1840. Due to its rarity, it has been independently cited numerous times under many different names.

The gene sal-like 4 (SALL4) or CHN1 ("chimerin") has became a mutated gene (protein) and it is also one of the cause of the body's Duane Syndrome.

Macrostomia, (from the Greek prefix "makro-" meaning "large" and from Greek , "mouth") refers to a mouth that is unusually wide.

Macrostomia is characterized as a physical abnormality that causes clefts to form on the face of affected individuals. These clefts can form on either or both sides of the face, but they are most commonly seen on the right cheek and have a higher rate of occurrence in males. Macrostomia is very irregular and on average occurs only once in every 150,000 to 300,000 live births. It's unusual for macrostomia to occur on its own and it is included as a symptom for many diseases including craniofacial microsomia. The clefts result from improper development and fusion of the mandibular and maxillary processes. The clefts cause problems with facial muscle development. The origin of macrostomia is not yet fully understood it could have multiple causes.

There are 4 distinct variations of macrostomia. Classifications are a complete lateral facial cleft, simple macrostomia, macrostomia with diastasis of the facial musculature, and isolated facial musculature diastasis. Each has a different physical appearance with varying levels of severity.

The cleft associated with macrostomia is associated with improper or failed fusion of the mandibular and maxillary processes during embryonic development. This can lead to a variety of abnormalities involving skin, subcutaneous tissue, facial muscles, and the mucous membrane. The severity of each abnormality can vary from minor to severe. Environmental contaminants may play a role in causing macrostomia. Many affected individuals were found in Lagos, an industrial area of Nigeria, where water supplies are known to be contaminated by improper disposal of industrial and domestic waste.

A compound elevated skull fracture is a rare type of skull fracture where the fractured bone is elevated above the intact outer table of the skull. This type of skull fracture is always compound in nature. It can be caused during an assault with a weapon where the initial blow penetrates the skull and the underlying meninges and, on withdrawal, the weapon lifts the fractured portion of the skull outward. It can also be caused the skull rotating while being struck in a case of blunt force trauma, the skull rotating while striking an inanimate object as in a fall, or it may occur during transfer of a patient after an initial compound head injury.

A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges—or runs through the paranasal sinuses and the middle ear structures, putting the outside environment in contact with the cranial cavity—is a compound fracture.

Compound fractures may either be clean or contaminated. Intracranial air (pneumocephalus) may occur in compound skull fractures.

The most serious complication of compound skull fractures is infection. Increased risk factors for infection include visible contamination, meningeal tear, loose bone fragments and presenting for treatment more than eight hours after initial injury.

Because the nerve emerges near the bottom of the brain, it is often the first nerve compressed when there is any rise in intracranial pressure. Different presentations of the condition, or associations with other conditions, can help to localize the site of the lesion along the VIth cranial nerve pathway.

The most common causes of VIth nerve palsy in adults are:

- More common: Vasculopathic (diabetes, hypertension, atherosclerosis), trauma, idiopathic.

- Less common: Increased intracranial pressure, giant cell arteritis, cavernous sinus mass (e.g. meningioma, Brain stem Glioblastoma aneurysm, metastasis), multiple sclerosis, sarcoidosis/vasculitis, postmyelography, lumbar puncture, stroke (usually not isolated), Chiari Malformation, hydrocephalus, intracranial hypertension, tuberculosis meningitis.

In children, Harley reports typical causes as traumatic, neoplastic (most commonly brainstem glioma), as well as idiopathic. Sixth nerve palsy causes the eyes to deviate inward (see: Pathophysiology of strabismus). Vallee et al. report that benign and rapidly recovering isolated VIth nerve palsy can occur in childhood, sometimes precipitated by ear, nose and throat infections.

The VIth nerve's course is short and lesions in the orbit rarely give rise to isolated VIth nerve palsies, but more typically involve one or more of the other extraocular muscle groups.

Ophthalmoparesis can result from disorders of various parts of the eye and nervous system:

- Infection around the eye. Ophthalmoplegia is an important finding in orbital cellulitis.

- The orbit of the eye, including mechanical restrictions of eye movement, as in Graves disease.

- The muscle, as in progressive external ophthalmoplegia or Kearns-Sayre syndrome.

- The neuromuscular junction, as in myasthenia gravis.

- The relevant cranial nerves (specifically the oculomotor, trochlear, and abducens), as in cavernous sinus syndrome or raised intracranial pressure.

- The brainstem nuclei of these nerves, as in certain patterns of brainstem stroke such as Foville's syndrome.

- White matter tracts connecting these nuclei, as in internuclear ophthalmoplegia, an occasional finding in multiple sclerosis.

- Dorsal midbrain structures, as in Parinaud's syndrome.

- Certain parts of the cerebral cortex (including the frontal eye fields), as in stroke.

- Toxic envenomation by mambas, taipans, and kraits.

Thiamine deficiency can cause ophthalmoparesis in susceptible persons; this is part of the syndrome called Wernicke encephalopathy. The causal pathway by which this occurs is unknown. Intoxication with certain substances, such as phenytoin, can also cause ophthalmoparesis.

Treatment and prognosis depend on the underlying condition. For example, in thiamine deficiency, treatment would be the immediate administration of vitamin B1.