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.

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.

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.

Final outcomes for people with SCSFLS remain poorly studied. Symptoms may resolve in as little as two weeks, or persist for months. Less commonly, patients may suffer from unremitting symptoms for many years. People with chronic SCSFLS may be disabled and unable to work. Recurrent CSF leak at an alternate site after recent repair is common.

According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.

Although the group of people at risk for SAH is younger than the population usually affected by stroke, the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage. The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55. Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.

Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage. However, lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption. Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked. Some protection of uncertain significance is conferred by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. There is likely an inverse relationship between total serum cholesterol and the risk of non-traumatic SAH, though confirmation of this association is hindered by a lack of studies. Approximately 4 percent of aneurysmal bleeds occur after sexual intercourse and 10 percent of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.

Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture.

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).

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.

Because the shunt systems are too expensive for most people in developing countries, such people often die without getting a shunt. Worse, the rate of revision in shunt systems adds to the cost of shunting many times. Looking at this point, a study compares shunt systems and highlights the role of low-cost shunt systems in most of the developing countries. It compares the Chhabra shunt system to shunt systems from developed countries.

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.

SAH is often associated with a poor outcome. The death rate (mortality) for SAH is between 40 and 50 percent, but trends for survival are improving. Of those that survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever. Delay in diagnosis of minor SAH (mistaking the sudden headache for migraine) contributes to poor outcome. Factors found on admission that are associated with poorer outcome include poorer neurological grade; systolic hypertension; a previous diagnosis of heart attack or SAH; liver disease; more blood and larger aneurysm on the initial CT scan; location of an aneurysm in the posterior circulation; and higher age. Factors that carry a worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from vasospasm, development of intracerebral hematoma, or intraventricular hemorrhage (bleeding into the ventricles of the brain) and presence of fever on the eighth day of admission.

So-called "angiogram-negative subarachnoid hemorrhage", SAH that does not show an aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysm; however, it is still associated with a risk of ischemia, rebleeding, and hydrocephalus. Perimesencephalic SAH (bleeding around the mesencephalon in the brain), however, has a very low rate of rebleeding or delayed ischemia, and the prognosis of this subtype is excellent.

The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding. It is difficult to isolate the effects of SAH from those of other aspects of traumatic brain injury; it is unknown whether the presence of subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred. People with moderate and severe traumatic brain injury who have SAH when admitted to a hospital have as much as twice the risk of dying as those who do not. They also have a higher risk of severe disability and persistent vegetative state, and traumatic SAH has been correlated with other markers of poor outcome such as post traumatic epilepsy, hydrocephalus, and longer stays in the intensive care unit. However, more than 90 percent of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12 have a good outcome.

There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of the gene encoding apolipoprotein E that also plays a role in Alzheimer's disease) seems to increase risk for delayed ischemia and a worse outcome. The occurrence of hyperglycemia (high blood sugars) after an episode of SAH confers a higher risk of poor outcome.

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.

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.

Epidural hematoma is when bleeding occurs between the tough outer membrane covering the brain and the skull. Often there is loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again. Other symptoms may include headache, confusion, vomiting, and an inability to move parts of the body. Complications may include seizures.

The cause is typically head injury that results in a break of the temporal bone and bleeding from the middle meningeal artery. Occasionally it can occur as a result of a bleeding disorder or blood vessel malformation. Diagnosis is typically by a CT scan or MRI. When this condition occurs in the spine it is known as a spinal epidural hematoma.

Treatment in generally by urgent surgery in the form of a craniotomy or burr hole. Without treatment death typically results. The condition occurs in one to four percent of head injuries. Typically it occurs in young adults. Males are more often affected than females.

Communicating hydrocephalus, also known as non-obstructive hydrocephalus, is caused by impaired cerebrospinal fluid reabsorption in the absence of any CSF-flow obstruction between the ventricles and subarachnoid space. It has been theorized that this is due to functional impairment of the arachnoidal granulations (also called arachnoid granulations or Pacchioni's granulations), which are located along the superior sagittal sinus and is the site of cerebrospinal fluid reabsorption back into the venous system. Various neurologic conditions may result in communicating hydrocephalus, including subarachnoid/intraventricular hemorrhage, meningitis and congenital absence of arachnoid villi. Scarring and fibrosis of the subarachnoid space following infectious, inflammatory, or hemorrhagic events can also prevent resorption of CSF, causing diffuse ventricular dilatation.

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.

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.

Disc herniation can occur in any disc in the spine, but the two most common forms are lumbar disc herniation and cervical disc herniation. The former is the most common, causing lower back pain (lumbago) and often leg pain as well, in which case it is commonly referred to as sciatica. Lumbar disc herniation occurs 15 times more often than cervical (neck) disc herniation, and it is one of the most common causes of lower back pain. The cervical discs are affected 8% of the time and the upper-to-mid-back (thoracic) discs only 1–2% of the time.

The following locations have no discs and are therefore exempt from the risk of disc herniation: the upper two cervical intervertebral spaces, the sacrum, and the coccyx. Most disc herniations occur when a person is in their thirties or forties when the nucleus pulposus is still a gelatin-like substance. With age the nucleus pulposus changes ("dries out") and the risk of herniation is greatly reduced. After age 50 or 60, osteoarthritic degeneration (spondylosis) or spinal stenosis are more likely causes of low back pain or leg pain.

- 4.8% males and 2.5% females older than 35 experience sciatica during their lifetime.

- Of all individuals, 60% to 80% experience back pain during their lifetime.

- In 14%, pain lasts more than 2 weeks.

- Generally, males have a slightly higher incidence than females.

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".

Cerebral contusion, Latin "contusio cerebri", a form of traumatic brain injury, is a bruise of the brain tissue. Like bruises in other tissues, cerebral contusion can be associated with multiple microhemorrhages, small blood vessel leaks into brain tissue. Contusion occurs in 20–30% of severe head injuries. A cerebral laceration is a similar injury except that, according to their respective definitions, the pia-arachnoid membranes are torn over the site of injury in laceration and are not torn in contusion. The injury can cause a decline in mental function in the long term and in the emergency setting may result in brain herniation, a life-threatening condition in which parts of the brain are squeezed past parts of the skull. Thus treatment aims to prevent dangerous rises in intracranial pressure, the pressure within the skull.

Contusions are likely to heal on their own without medical intervention.

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.

Since cerebral swelling presents a danger to the patient, treatment of cerebral contusion aims to prevent swelling. Measures to avoid swelling include prevention of hypotension (low blood pressure), hyponatremia (insufficient sodium), and hypercapnia (increased carbon dioxide in the blood). Due to the danger of increased intracranial pressure, surgery may be necessary to reduce it. People with cerebral contusion may require intensive care and close monitoring.

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:

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.

Intracranial hemorrhage (ICH), also known as intracranial bleed, is bleeding within the skull. It includes intracerebral bleeds (intraventricular bleeds and intraparenchymal bleeds), subarachnoid bleeds, epidural bleeds, and subdural bleeds.

Intracerebral bleeding affects 2.5 per 10,000 people each year.

Intracranial hemorrhage is a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. Severe increases in intracranial pressure (ICP) can cause brain herniation, in which parts of the brain are squeezed past structures in the skull.