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.

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 risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem. Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing. This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum.

For spontaneous ICH seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the insult, and half of the deaths occur in the first 2 days. Even though the majority of deaths occurs in the first days after ICH, survivors have a long term excess mortality of 27% compared to the general population.

It accounts for 20% of all cases of cerebrovascular disease in the United States, behind cerebral thrombosis (40%) and cerebral embolism (30%).

It is two or more times more common in black than white people.

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.

TBI is a leading cause of death and disability around the globe and presents a major worldwide social, economic, and health problem. It is the number one cause of coma, it plays the leading role in disability due to trauma, and is the leading cause of brain damage in children and young adults. In Europe it is responsible for more years of disability than any other cause. It also plays a significant role in half of trauma deaths.

Findings on the frequency of each level of severity vary based on the definitions and methods used in studies. A World Health Organization study estimated that between 70 and 90% of head injuries that receive treatment are mild, and a US study found that moderate and severe injuries each account for 10% of TBIs, with the rest mild.

The incidence of TBI varies by age, gender, region and other factors. Findings of incidence and prevalence in epidemiological studies vary based on such factors as which grades of severity are included, whether deaths are included, whether the study is restricted to hospitalized people, and the study's location. The annual incidence of mild TBI is difficult to determine but may be 100–600 people per 100,000.

Brain contusions and subarachnoid hemorrhages are commonly associated with IVH. The bleeding can involve the anterior communicating artery or the posterior communicating artery.

In both adults and infants, IVH can cause dangerous increases in ICP, damage to the brain tissue, and hydrocephalus.

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.

A cerebral laceration with large amounts of blood apparent on a CT scan is an indicator of poor prognosis. The progression and course of complications (health effects that result from but are distinct from the injury itself) do not appear to be affected by a cerebral laceration's location or a mass effect it causes.

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.

In the US, the case fatality rate is estimated to be 21% by 30 days after TBI. A study on Iraq War soldiers found that severe TBI carries a mortality of 30–50%. Deaths have declined due to improved treatments and systems for managing trauma in societies wealthy enough to provide modern emergency and neurosurgical services. The fraction of those who die after being hospitalized with TBI fell from almost half in the 1970s to about a quarter at the beginning of the 21st century. This decline in mortality has led to a concomitant increase in the number of people living with disabilities that result from TBI.

Biological, clinical, and demographic factors contribute to the likelihood that an injury will be fatal. In addition, outcome depends heavily on the cause of head injury. In the US, patients with fall-related TBIs have an 89% survival rate, while only 9% of patients with firearm-related TBIs survive. In the US, firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls. Of deaths from firearms, 75% are considered to be suicides.

The incidence of TBI is increasing globally, due largely to an increase in motor vehicle use in low- and middle-income countries. In developing countries, automobile use has increased faster than safety infrastructure could be introduced. In contrast, vehicle safety laws have decreased rates of TBI in high-income countries, which have seen decreases in traffic-related TBI since the 1970s. Each year in the United States, about two million people suffer a TBI, approximately 675,000 injuries are seen in the emergency department, and about 500,000 patients are hospitalized. The yearly incidence of TBI is estimated at 180–250 per 100,000 people in the US, 281 per 100,000 in France, 361 per 100,000 in South Africa, 322 per 100,000 in Australia, and 430 per 100,000 in England. In the European Union the yearly aggregate incidence of TBI hospitalizations and fatalities is estimated at 235 per 100,000.

Cerebral lacerations usually accompany other brain injuries and are often found with skull fractures on both sides of the head. Frequently occurring in the same areas as contusions, lacerations are particularly common in the inferior frontal lobes and the poles of the temporal lobes. When associated with diffuse axonal injury, the corpus callosum and the brain stem are common locations for laceration. Lacerations are very common in penetrating and perforating head trauma and frequently accompany skull fractures; however, they may also occur in the absence of skull fracture. Lacerations, which may result when brain tissue is stretched, are associated with intraparenchymal bleeding (bleeding into the brain tissue).

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.

The most common cause of intracranial epidural hematoma is traumatic, although spontaneous hemorrhage is known to occur. Hemorrhages commonly result from acceleration-deceleration trauma and transverse forces. The majority of bleeds originate from meningeal arteries, particularly in the temporal region. 10% of epidural bleeds may be venous, due to shearing injury from rotational forces. Epidural hematoma commonly results from a blow to the side of the head. The pterion region which overlies the middle meningeal artery is relatively weak and prone to injury. Thus only 20 to 30% of epidural hematomas occur outside the region of the temporal bone. The brain may be injured by prominences on the inside of the skull as it scrapes past them. Epidural hematoma is usually found on the same side of the brain that was impacted by the blow, but on very rare occasions it can be due to a contrecoup injury.

It is not known whether PTS increase the likelihood of developing PTE. Early PTS, while not necessarily epileptic in nature, are associated with a higher risk of PTE. However, PTS do not indicate that development of epilepsy is certain to occur, and it is difficult to isolate PTS from severity of injury as a factor in PTE development. About 3% of patients with no early seizures develop late PTE; this number is 25% in those who do have early PTS, and the distinction is greater if other risk factors for developing PTE are excluded. Seizures that occur immediately after an insult are commonly believed not to confer an increased risk of recurring seizures, but evidence from at least one study has suggested that both immediate and early seizures may be risk factors for late seizures. Early seizures may be less of a predictor for PTE in children; while as many as a third of adults with early seizures develop PTE, the portion of children with early PTS who have late seizures is less than one fifth in children and may be as low as one tenth. The incidence of late seizures is about half that in adults with comparable injuries.

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.

The chances that a person will suffer PTS are influenced by factors involving the injury and the person. The largest risks for PTS are having an altered level of consciousness for a protracted time after the injury, severe injuries with focal lesions, and fractures. The single largest risk for PTS is penetrating head trauma, which carries a 35 to 50% risk of seizures within 15 years. If a fragment of metal remains within the skull after injury, the risk of both early and late PTS may be increased. Head trauma survivors who abused alcohol before the injury are also at higher risk for developing seizures.

Occurrence of seizures varies widely even among people with similar injuries. It is not known whether genetics play a role in PTS risk. Studies have had conflicting results with regard to the question of whether people with PTS are more likely to have family members with seizures, which would suggest a genetic role in PTS. Most studies have found that epilepsy in family members does not significantly increase the risk of PTS. People with the ApoE-ε4 allele may also be at higher risk for late PTS.

Risks for late PTS include hydrocephalus, reduced blood flow to the temporal lobes of the brain, brain contusions, subdural hematomas, a torn dura mater, and focal neurological deficits. PTA that lasts for longer than 24 hours after the injury is a risk factor for both early and late PTS. Up to 86% of people who have one late post-traumatic seizure have another within two years.

DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse such as in shaken baby syndrome.

Immediate disconnection of axons could be observed in severe brain injury, but the major damage of DAI is delayed secondary axon disconnections slowly developed over an extended time course. Tracts of axons, which appear white due to myelination, are referred to as white matter. Lesions in both grey and white matters are found in postmortem brains in CT and MRI exams.

Besides mechanical breaking of the axonal cytoskeleton, DAI pathology also includes secondary physiological changes such as interrupted axonal transport, progressive swellings and degeneration. Recent studies have linked these changes to twisting and misalignment of broken axon microtubules, as well as tau and APP deposition.

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.

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury, and is a major cause of unconsciousness and persistent vegetative state after severe head trauma. It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.

DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.

The nature of the head trauma also influences the risk of PTE. People who suffer depressed skull fractures, penetrating head trauma, early PTS, and intracerebral and subdural haematomas due to the TBI are especially likely to suffer PTE, which occurs in more than 30% of people with any one of these findings. About 50% of patients with penetrating head trauma develop PTE, and missile injuries and loss of brain volume are associated with an especially high likelihood of developing the condition. Injuries that occur in military settings carry higher-than-usual risk for PTE, probably because they more commonly involve penetrating brain injury and brain damage over a more widespread area. Intracranial hematomas, in which blood accumulates inside the skull, are one of the most important risk factors for PTE. Subdural hematoma confers a higher risk of PTE than does epidural hematoma, possibly because it causes more damage to brain tissue. Repeated intracranial surgery confers a high risk for late PTE, possibly because people who need more surgery are more likely to have factors associated with worse brain trauma such as large hematomas or cerebral swelling. In addition, the chances of developing PTE differ by the location of the brain lesion: brain contusion that occurs on in one or the other of the frontal lobes has been found to carry a 20% PTE risk, while a contusion in one of the parietal lobes carries a 19% risk and one in a temporal lobe carries a 16% chance. When contusions occur in both hemispheres, the risk is 26% for the frontal lobes, 66% for the parietal, and 31% for the temporal.

Elderly people are the most rapidly growing demographic in developed nations. Although they sustain traumatic injury less commonly than children and young adults, the mortality rate for trauma in the elderly is higher than in younger people. In the United States, this population accounts for 14% of all traumatic injuries, of which a majority are secondary to falls.

The more severe the brain trauma is, the more likely a person is to suffer late PTE. Evidence suggests that mild head injuries do not confer an increased risk of developing PTE, while more severe types do. In simple mild TBI, the risk for PTE is about 1.5 times that of the uninjured population. By some estimates, as many as half of sufferers of severe brain trauma experience PTE; other estimates place the risk at 5% for all TBI patients and 15–20% for severe TBI. One study found that the 30-year risk of developing PTE was 2.1% for mild TBI, 4.2% for moderate, and 16.7% for severe injuries, as shown in the chart at right.

Closed head injury is a type of traumatic brain injury in which the skull and dura mater remain intact. Closed-head injuries are the leading cause of death in children under 4 years old and the most common cause of physical disability and cognitive impairment in young people. Overall, closed-head injuries and other forms of mild traumatic brain injury account for about 75% of the estimated 1.7 million brain injuries that occur annually in the United States. Brain injuries such as closed-head injuries may result in lifelong physical, cognitive, or psychological impairment and, thus, are of utmost concern with regards to public health.

Virtually all organ systems experience a progressive decline in function as a result of the aging process. One example is a decline in circulatory system function caused in part by thickening of the cardiac muscle. This can lead to congestive heart failure or pulmonary edema.

Atrophy of the brain begins to accelerate at around seventy years of age, which leads to a significant reduction in brain mass. Since the skull does not decrease in size with the brain, there is significant space between the two when this occurs which puts the elderly at a higher risk of a subdural hematoma after sustaining a closed head injury. The reduction of brain size can lead to issues with eyesight, cognition and hearing.