Brain herniation is a potentially deadly side effect of very high pressure within the skull that occurs when a part of the brain is squeezed across structures within the skull. The brain can shift across such structures as the falx cerebri, the tentorium cerebelli, and even through the foramen magnum (the hole in the base of the skull through which the spinal cord connects with the brain). Herniation can be caused by a number of factors that cause a mass effect and increase intracranial pressure (ICP): these include traumatic brain injury, intracranial hemorrhage, or brain tumor.

Herniation can also occur in the absence of high ICP when mass lesions such as hematomas occur at the borders of brain compartments. In such cases local pressure is increased at the place where the herniation occurs, but this pressure is not transmitted to the rest of the brain, and therefore does not register as an increase in ICP.

Because herniation puts extreme pressure on parts of the brain and thereby cuts off the blood supply to various parts of the brain, it is often fatal. Therefore, extreme measures are taken in hospital settings to prevent the condition by reducing intracranial pressure, or decompressing (draining) a hematoma which is putting local pressure on a part of the brain.

A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

Treatment involves removal of the etiologic mass and decompressive craniectomy. Brain herniation can cause severe disability or death. In fact, when herniation is visible on a CT scan, the prognosis for a meaningful recovery of neurological function is poor. The patient may become paralyzed on the same side as the lesion causing the pressure, or damage to parts of the brain caused by herniation may cause paralysis on the side opposite the lesion. Damage to the midbrain, which contains the reticular activating network which regulates consciousness, will result in coma. Damage to the cardio-respiratory centers in the medulla oblongata will cause respiratory arrest and (secondarily) cardiac arrest. Current investigation is underway regarding the use of neuroprotective agents during the prolonged post-traumatic period of brain hypersensitivity associated with the syndrome.

A spontaneous CSF leak is idiopathic, meaning the cause in unknown. Various scientists and physicians have suggested that this condition may be the result of an underlying connective tissue disorder affecting the spinal dura. It may also run in families and be associated with aortic aneurysms and joint hypermobility. Up to two thirds of those afflicted demonstrate some type of generalized connective tissue disorder. Marfan syndrome, Ehlers-Danlos syndrome and autosomal dominant polycystic kidney disease are the three most common connective tissue disorders associated with SCSFLS.

Roughly 20% of patients with SCSFLS exhibit features of Marfan syndrome, including tall stature, hollowed chest (pectus excavatum), joint hypermobility and arched palate. However these patients do not exhibit any other Marfan syndrome presentations.

Surgery may be useful in those with a herniated disc that is causing significant pain radiating into the leg, significant leg weakness, bladder problems, or loss of bowel control. Discectomy (the partial removal of a disc that is causing leg pain) can provide pain relief sooner than nonsurgical treatments. Discectomy has better outcomes at one year but not at four to ten years. The less invasive microdiscectomy has not been shown to result in a significantly different outcome than regular discectomy with respect to pain. It might however have less risk of infection.

The presence of cauda equina syndrome (in which there is incontinence, weakness and genital numbness) is considered a medical emergency requiring immediate attention and possibly surgical decompression. Regarding the role of surgery for failed medical therapy in people without a significant neurological deficit, a Cochrane review concluded that "limited evidence is now available to support some aspects of surgical practice".

Most authors favour degeneration of the intervertebral disc as the major cause of spinal disc herniation and cite trauma as a low cause. Disc degeneration occurs both with degenerative disc disease and aging. With degeneration, the contents of the disc, the nucleus pulposus and anulus fibrosus, are exposed to altered loads. Specifically, the nucleus becomes fibrous and stiff and less able to bear load. The load is transferred to the anulus, which, if it fails to bear the increased load, can lead to the development of fissures. If the fissures reach the periphery of the anulus, the nuclear material can pass through as a disc herniation.

Disc herniations can result from general wear and tear, such as constant sitting or squatting, driving, or a sedentary lifestyle. However, herniations can also result from the lifting of heavy loads. Professional athletes, especially those playing contact sports such as American football, are prone to disc herniations as well. Within such an athletic context, herniation is often the result of sudden blunt impacts against, or abrupt bending or torsional movements of, the lower back. When the spine is straight, such as in standing or lying down, internal pressure is equalized on all parts of the discs. While sitting or bending to lift, internal pressure on a disc can move from 17 psi (lying down) to over 300 psi (lifting with a rounded back). . Herniation of the contents of the disc into the spinal canal often occurs when the anterior side (stomach side) of the disc is compressed while sitting or bending forward, and the contents (nucleus pulposus) get pressed against the tightly stretched and thinned membrane (anulus fibrosus) on the posterior side (back side) of the disc. The combination of membrane thinning from stretching and increased internal pressure (200 to 300 psi) results in the rupture of the confining membrane. The jelly-like contents of the disc then move into the spinal canal, pressing against the spinal nerves, which may produce intense and potentially disabling pain and other symptoms.

Several genes are also associated with intervertebral disc degeneration. Probable candidate genes like type I collagen (sp1 site), type IX collagen, vitamin D receptor, aggrecan, asporin, MMP3, interleukin-1 and interleukin-6 polymorphisms have been implicated in disc degeneration. Mutation in genes coding for proteins involved in the regulation of the extracellular matrix, such as MMP2 and THBS2, has been demonstrated to contribute to lumbar disc herniation.

The prevalence of congenital Chiari I malformation, defined as tonsilar herniations of 3 to 5 mm or greater, was previously believed to be in the range of one per 1000 births, but is likely much higher. Women are three times more likely than men to have a congenital Chiari malformation. Type II malformations are more prevalent in people of Celtic descent. A study using upright MRI found cerebellar tonsillar ectopia in 23% of adults with headache from motor-vehicle-accident head trauma. Upright MRI was more than twice as sensitive as standard MRI, likely because gravity affects cerebellar position.

Cases of congenital Chiari malformation may be explained by evolutionary and genetic factors. Typically, an infant's brain weighs around 400g at birth and triples to 1100-1400g by age 11. At the same time the cranium triples in volume from 500 cm to 1500 cm to accommodate the growing brain. During human evolution, the skull underwent numerous changes to accommodate the growing brain. The evolutionary changes included increased size and shape of the skull, decreased basal angle and basicranial length. These modifications resulted in significant reduction of the size of the posterior fossa in modern humans. In normal adults, the posterior fossa comprises 27% of the total intracranial space, while in adults with Chiari Type I, it is only 21%. If a modern brain is paired with a less modern skull, the posterior fossa may be too small, so that the only place where the cerebellum can expand is the foramen magnum, leading to development of Chiari Type I. H. neanderthalensis had platycephalic (flattened) skull. Some cases of Chiari are associated with platybasia (flattening of the skull base).

Anterior spinal artery syndrome (also known as "anterior spinal cord syndrome", or "Beck's syndrome") is a medical condition where the anterior spinal artery, the primary blood supply to the anterior portion of the spinal cord, is interrupted, causing ischemia or infarction of the spinal cord in the anterior two-thirds of the spinal cord and medulla oblongata. It is characterized by loss of motor function below the level of injury, loss of sensations carried by the anterior columns of the spinal cord (pain and temperature), and preservation of sensations carried by the posterior columns (fine touch, vibration and proprioception). Anterior spinal artery syndrome is the most common form of spinal cord infarction.

Due to the branches of the aorta that supply the anterior spinal artery, the most common causes are insufficiencies within the aorta. These include aortic aneurysms, dissections, direct trauma to the aorta, surgeries, and atherosclerosis. Acute disc herniation, cervical spondylosis, kyphoscoliosis, damage to the spinal column and neoplasia all could result in ischemia from anterior spinal artery occlusion leading to anterior cord syndrome. Other causes include vasculitis, polycythemia, sickle cell disease, decompression sickness, and collagen and elastin disorders.

The most widely accepted pathophysiological mechanism by which Chiari type I malformations occur is by a reduction or lack of development of the posterior fossa as a result of congenital or acquired disorders. Congenital causes include hydrocephalus, craniosynostosis (especially of the lambdoid suture), hyperostosis (such as craniometaphyseal dysplasia, osteopetrosis, erythroid hyperplasia), X-linked vitamin D-resistant rickets, and neurofibromatosis type I. Acquired disorders include space occupying lesions due to one of several potential causes ranging from brain tumors to hematomas.

Head trauma may cause cerebellar tonsillar ectopia, possibly because of dural strain. Additionally, ectopia may be present but asymptomatic until whiplash causes it to become symptomatic. Posterior fossa hypoplasia causes reduced cerebral and spinal compliance.

A significant complication of diaphragmatic rupture is traumatic diaphragmatic herniation: organs such as the stomach that herniate into the chest cavity and may be strangulated, losing their blood supply. Herniation of abdominal organs is present in 3–4% of people with abdominal trauma who present to a trauma center.

Diaphragmatic injuries are present in 1–7% of people with significant blunt trauma and an average of 3% of abdominal injuries.

A high body mass index may be associated with a higher risk of diaphragmatic rupture in people involved in vehicle accidents. It is rare for the diaphragm alone to be injured, especially in blunt trauma; other injuries are associated in as many as 80–100% of cases. In fact, if the diaphragm is injured, it is an indication that more severe injuries to organs may have occurred. Thus, the mortality after a diagnosis of diaphragmatic rupture is 17%, with most deaths due to lung complications. Common associated injuries include head injury, injuries to the aorta, fractures of the pelvis and long bones, and lacerations of the liver and spleen. Associated injuries occur in over three quarters of cases.

No set risk factors have been clearly defined for CES at this point in time. Individuals most at risk for disc herniation are the most likely to develop CES. Race has little influence with the notable exception that African Americans appear slightly less likely to develop CES than other groups; similarly, men are slightly more likely to develop CES than women. Middle age also appears to be a notable risk factor, as those populations are more likely to develop a herniated disc; heavy lifting can also be inferred as a risk factor for CES.

Direct trauma can also cause cauda equina syndrome. Most common causes include iatrogenic lumbar punctures, burst fractures resulting in posterior migration of fragments of the vertebral body, severe disc herniations, spinal anaesthesia involving trauma from catheters and high local anaesthetic concentrations around the cauda equina, penetrating trauma such as knife wounds or ballistic trauma.

An inheritable gene variation may cause increased susceptibility. People with a variation in a gene that encodes the cartilage intermediate-layer protein (CILP) were 1.6 times more likely to have the disease than persons without the variation. CILP is a normal component of disc tissue. The gene variant was hypothesized to disrupt normal building and maintenance of cartilage. However, this association was not replicated in a follow-up study of Finnish and Chinese individuals.

A deficiency of folate itself does not cause neural tube defects. The association seen between reduced neural tube defects and folic acid supplementation is due to a gene-environment interaction such as vulnerability caused by the C677T Methylenetetrahydrofolate reductase (MTHFR) variant. Supplementing folic acid during pregnancy reduces the prevalence of NTDs by not exposing this otherwise sub-clinical mutation to aggravating conditions. Other potential causes can include folate antimetabolites (such as methotrexate), mycotoxins in contaminated corn meal, arsenic, hyperthermia in early development, and radiation. Maternal obesity has also been found to be a risk factor for NTDs. Studies have shown that both maternal cigarette smoking and maternal exposure to secondhand smoke increased the risk for neural tube defects in offspring. A mechanism by which maternal exposure to cigarette smoke could increase NTD risk in offspring is suggested by several studies that show an association between cigarette smoking and elevations of homocysteine levels. Cigarette smoke during pregnancy, including secondhand exposure, can increase the risk of neural tube defects. All of the above may act by interference with some aspect of normal folic acid metabolism and folate linked methylation related cellular processes as there are multiple genes of this type associated with neural tube defects.

The application of MRI plays a significant role in the early diagnosis and treatment of SCIWORA in children and adults. Recently, systematic reviews on SCIWORA described the clinical and radiological patterns and correlations with neurological outcome.C.K. Boese und P. Lechler: "Spinal cord injury without radiologic abnormalities in adults: a systematic review." In: "Journal of Trauma and Acute Care Surgery." 78, 2015, S. 320-330 .Boese CK, Oppermann J, Siewe J, Eysel P, Scheyerer MJ, Lechler P.: "Spinal cord injury without radiologic abnormality in children: a systematic review and meta-analysis." In: "Journal of Trauma and Acute Care Surgery." 75, 2013. Boese and Lechler proposed a MRI-based classification for SCIWORA which correlated with the neurological outcome:

Grynfeltt-Lesshaft hernia is a herniation of abdominal contents through the back, specifically through the superior lumbar triangle, which is defined by the quadratus lumborum muscle, twelfth rib, and internal oblique muscle.

Intraventricular hemorrhage (IVH), also known as intraventricular bleeding, is a bleeding into the brain's ventricular system, where the cerebrospinal fluid is produced and circulates through towards the subarachnoid space. It can result from physical trauma or from hemorrhaging in stroke.

30% of intraventricular hemorrhage (IVH) are primary, confined to the ventricular system and typically caused by intraventricular trauma, aneurysm, vascular malformations, or tumors, particularly of the choroid plexus. However 70% of IVH are secondary in nature, resulting from an expansion of an existing intraparenchymal or subarachnoid hemorrhage. Intraventricular hemorrhage has been found to occur in 35% of moderate to severe traumatic brain injuries. Thus the hemorrhage usually does not occur without extensive associated damage, and so the outcome is rarely good.

Meningohydroencephalocoele (AmE: meningohydroencephalocele) is a form of meningocele (AmE) - a developmental abnormality of the central nervous system.

Like meningocoele, meningohydroencephalocoele is caused by defects in bone ossification; in particular, the intramembranous ossification related to the closure of infantile fontanelles. It refers to the protrusion of the meninges between the un-fused bones, to lie subcutaneously.

- Meningocoele - refers to herniation of meninges.

- Meningoencephalocoele refers to the condition if brain tissue is included with the meninges in the herniation.

- Meningohydroencephalocoele refers to the condition including meninges, brain tissue and part of the ventricular system in the herniation.

Encephalocoele defects occur in approximately 1 in 2000 live births.

Initial treatment in lumbar disc disease is one or two days of bedrest (although growing number of studies shows that it makes little difference) and pain relieving medications. In cases with ongoing pain despite conservative treatments, a surgical operation that will remove the compressing disc material, a microdiscectomy or discectomy may be recommended to treat a lumbar disc herniation.

Spinal cord injury without radiographic abnormality (SCIWORA) is a spinal cord injury (SCI) with no evidence of injury to the spinal column present on radiographs. Spinal column injury is trauma that causes fracture of the bone or instability of the ligaments in the spine; this can coexist with or result in injury to the spinal cord itself but each injury can occur without the other. Abnormalities might show up on magnetic resonance imaging (MRI), but the term was coined before MRI was in common use.

Inadequate levels of folate (vitamin B9) and vitamin B12 during pregnancy have been found to lead to increased risk of NTDs. Although both are part of the same biopathway, folate deficiency is much more common and therefore more of a concern. Folate is required for the production and maintenance of new cells, for DNA synthesis and RNA synthesis. Folate is needed to carry one carbon groups for methylation and nucleic acid synthesis. It has been hypothesized that the early human embryo may be particularly vulnerable to folate deficiency due to differences of the functional enzymes in this pathway during embryogenesis combined with high demand for post translational methylations of the cytoskeleton in neural cells during neural tube closure. Failure of post-translational methylation of the cytoskeleton, required for differentiation has been implicated in neural tube defects. Vitamin B is also an important receptor in the folate biopathway such that studies have shown deficiency in vitamin B contributes to risk of NTDs as well. There is substantial evidence that direct folic supplementation increases blood serum levels of bioavailable folate even though at least one study have shown slow and variable activity of dihydrofolate reductase in human liver. A diet rich in natural folate (350 μg/d) can show as much increase in plasma folate as taking low levels of folic acid (250 μg/d) in individuals However a comparison of general population outcomes across many countries with different approaches to increasing folate consumption has found that only general food fortification with folic acid reduces neural tube defects While there have been concerns about folic acid supplementation being linked to an increased risk for cancer, a systematic review in 2012 shows there is no evidence except in the case of prostate cancer which indicates a modest reduction in risk.

Prognosis is also very poor when IVH results from intracerebral hemorrhage related to high blood pressure and is even worse when hydrocephalus follows. It can result in dangerous increases in ICP and can cause potentially fatal brain herniation. Even independently, IVH can cause morbidity and mortality. First, intraventricular blood can lead to a clot in the CSF conduits blocking its flow and leading to obstructive hydrocephalus which may quickly result in increased intracranial pressure and death. Second, the breakdown products from the blood clot may generate an inflammatory response that damages the arachnoid granulations, inhibiting the regular reabsorption of CSF and resulting in permanent communicating hydrocephalus.

Nasal glial heterotopia is rare, while an encephalocele is uncommon. NGH usually presents in infancy, while encephalocele may present in older children and adults. It is seen in both genders equally.