Mild and moderate cerebral hypoxia generally has no impact beyond the episode of hypoxia; on the other hand, the outcome of severe cerebral hypoxia will depend on the success of damage control, amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. A general consequence may be epilepsy. The long-term effects will depend on the purpose of that portion of the brain. Damage to the Broca's area and the Wernicke's area of the brain (left side) typically causes problems with speech and language. Damage to the right side of the brain may interfere with the ability to express emotions or interpret what one sees. Damage on either side can cause paralysis of the opposite side of the body.

The effects of certain kinds of severe generalized hypoxias may take time to develop. For example, the long-term effects of serious carbon monoxide poisoning usually may take several weeks to appear. Recent research suggests this may be due to an autoimmune response caused by carbon monoxide-induced changes in the myelin sheath surrounding neurons.

If hypoxia results in coma, the length of unconsciousness is often indicative of long-term damage. In some cases coma can give the brain an opportunity to heal and regenerate, but, in general, the longer a coma, the greater the likelihood that the person will remain in a vegetative state until death. Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.

Long-term comas can have a significant impact on a patient's families. Families of coma victims often have idealized images of the outcome based on Hollywood movie depictions of coma. Adjusting to the realities of ventilators, feeding tubes, bedsores, and muscle wasting may be difficult. Treatment decision often involve complex ethical choices and can strain family dynamics.

Hypoxic-anoxic events may affect the fetus at various stages of fetal development, during labor and delivery and in the postnatal period. Problems during pregnancy may include preeclampsia, maternal diabetes with vascular disease, congenital fetal infections, drug/alcohol abuse, severe fetal anemia, cardiac disease, lung malformations, or problems with blood flow to the placenta.

Problems during labor and delivery can include umbilical cord occlusion, torsion or prolapse, rupture of the placenta or uterus, excessive bleeding from the placenta, abnormal fetal position such as the breech position, prolonged late stages of labor, or very low blood pressure in the mother. Problems after delivery can include severe prematurity, severe lung or heart disease, serious infections, trauma to the brain or skull, congenital malformations of the brain or very low blood pressure in the baby and due to suffocation in cases of Münchausen syndrome by proxy.

The severity of a neonatal hypoxic-ischaemic brain injury may be assessed using Sarnat staging, which is based on clinical presentation and EEG findings, and also using MRI.

Some evidence suggests that magnesium sulfate administered to mothers prior to early preterm birth reduces the risk of cerebral palsy in surviving neonates. Due to the risk of adverse effects treatments may have, it is unlikely that treatments to prevent neonatal strokes or other hypoxic events would be given routinely to pregnant women without evidence that their fetus was at extreme risk or has already suffered an injury or stroke. This approach might be more acceptable if the pharmacologic agents were endogenously occurring substances (those that occur naturally in an organism), such as creatine or melatonin, with no adverse side-effects.

Because of the period of high neuronal plasticity in the months after birth, it may be possible to improve the neuronal environment immediately after birth in neonates considered to be at risk of neonatal stroke. This may be done by enhancing the growth of axons and dendrites, synaptogenesis and myelination of axons with systemic injections of neurotrophins or growth factors which can cross the blood–brain barrier.

Of the infants that survive, there may be as many as 1 million a year that develop cerebral palsy, learning difficulties or other disabilities. Cerebral palsy is the most common physical disability in childhood, and it is characterized by a lack of control of movement. Other neurological defects that can occur after a neonatal stroke include hemiparesis and hemi-sensory impairments Some studies suggest that when tested as toddlers and preschoolers, children who previously had neonatal strokes fall within normal ranges of cognitive development. Less is known about longer-term cognitive outcome, but there has been evidence that cognitive deficits may emerge later in childhood when more complex cognitive processes are expected to develop.

In the United States, intrauterine hypoxia and birth asphyxia were listed together as the tenth leading cause of neonatal death.

This refers specifically to hypoxic states where the arterial content of oxygen is insufficient. This can be caused by alterations in respiratory drive, such as in respiratory alkalosis, physiological or pathological shunting of blood, diseases interfering in lung function resulting in a ventilation-perfusion mismatch, such as a pulmonary embolus, or alterations in the partial pressure of oxygen in the environment or lung alveoli, such as may occur at altitude or when diving.

Carbon monoxide competes with oxygen for binding sites on hemoglobin molecules. As carbon monoxide binds with hemoglobin hundreds of times tighter than oxygen, it can prevent the carriage of oxygen.

Carbon monoxide poisoning can occur acutely, as with smoke intoxication, or over a period of time, as with cigarette smoking. Due to physiological processes, carbon monoxide is maintained at a resting level of 4–6 ppm. This is increased in urban areas (7–13 ppm) and in smokers (20–40 ppm). A carbon monoxide level of 40 ppm is equivalent to a reduction in hemoglobin levels of 10 g/L.

CO has a second toxic effect, namely removing the allosteric shift of the oxygen dissociation curve and shifting the foot of the curve to the left. In so doing, the hemoglobin is less likely to release its oxygens at the peripheral tissues. Certain abnormal hemoglobin variants also have higher than normal affinity for oxygen, and so are also poor at delivering oxygen to the periphery.

IH/BA is also a causitive factor in cardiac and circulatory birth defects the sixth most expensive condition, as well as premature birth and low birth weight the second most expensive and it is one of the contributing factors to infant respiratory distress syndrome (RDS) also known as hyaline membrane disease, the most expensive medical condition to treat and the number one cause of infant mortality.

Therapeutic hypothermia has been attempted to improve results post brain ischemia . This procedure was suggested to be beneficial based on its effects post cardiac arrest. Evidence supporting the use of therapeutic hypothermia after brain ischemia, however, is limited.

A closely related disease to brain ischemia is brain hypoxia. Brain hypoxia is the condition in which there is a decrease in the oxygen supply to the brain even in the presence of adequate blood flow. If hypoxia lasts for long periods of time, coma, seizures, and even brain death may occur. Symptoms of brain hypoxia are similar to ischemia and include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination. Potential causes of brain hypoxia are suffocation, carbon monoxide poisoning, severe anemia, and use of drugs such as cocaine and other amphetamines. Other causes associated with brain hypoxia include drowning, strangling, choking, cardiac arrest, head trauma, and complications during general anesthesia. Treatment strategies for brain hypoxia vary depending on the original cause of injury, primary and/or secondary.

Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison their healthy counterparts.

Sickle cell anemia may cause brain ischemia associated with the irregularly shaped blood cells. Sickle shaped blood cells clot more easily than normal blood cells, impeding blood flow to the brain.

Compression of blood vessels may also lead to brain ischemia, by blocking the arteries that carry oxygen to the brain. Tumors are one cause of blood vessel compression.

Ventricular tachycardia represents a series of irregular heartbeats that may cause the heart to completely shut down resulting in cessation of oxygen flow. Further, irregular heartbeats may result in formation of blood clots, thus leading to oxygen deprivation to all organs.

Blockage of arteries due to plaque buildup may also result in ischemia. Even a small amount of plaque build up can result in the narrowing of passageways, causing that area to become more prone to blood clots. Large blood clots can also cause ischemia by blocking blood flow.

A heart attack can also cause brain ischemia due to the correlation that exists between heart attack and low blood pressure. Extremely low blood pressure usually represents the inadequate oxygenation of tissues. Untreated heart attacks may slow blood flow enough that blood may start to clot and prevent the flow of blood to the brain or other major organs. Extremely low blood pressure can also result from drug overdose and reactions to drugs. Therefore, brain ischemia can result from events other than heart attacks.

Congenital heart defects may also cause brain ischemia due to the lack of appropriate artery formation and connection. People with congenital heart defects may also be prone to blood clots.

Other events that may result in brain ischemia include cardiorespiratory arrest, stroke, and severe irreversible brain damage.

Recently, Moyamoya disease has also been identified as a potential cause for brain ischemia. Moyamoya disease is an extremely rare cerebrovascular condition that limits blood circulation to the brain, consequently leading to oxygen deprivation.

Those patients who survive initial hospitalization are likely to recover from Grinker's Myelinopathy, but may take up to a year or longer. Age seems to be a factor in the time for recovery, as one study indicated that the mean age of patients who recovered within one year was 10 years younger than that of patients who did not. For most patients, a recovery time of 3–6 months is typical. Even after recovering, however, some symptoms may persist, including cognitive deficits or Parkinsonian symptoms that can be treated separately.

HACE occurs in 0.5% to 1% of people who climb or trek between and . In some unusual cases, up to 30% of members of expeditions have suffered from the condition. The condition is seldom seen below , but in some rare cases it has developed as low as . The condition generally does not occur until an individual has spent 48 hours at an altitude of .

Patients with HACE should be brought to lower altitudes and provided supplemental oxygen, and rapid descent is sometimes needed to prevent mortality. Early recognition is important because as the condition progresses patients are unable to descend without assistance. Dexamethasone should also be administered, although it fails to ameliorate some symptoms that can be cured by descending to a lower altitude. It can also mask symptoms, and they sometimes resume upon discontinuation. Dexamethasone's prevention of angiogenesis may explain why it treats HACE well. Three studies that examined how mice and rat brains react to hypoxia gave some credence to this idea.

If available, supplemental oxygen can be used as an adjunctive therapy, or when descent is not possible. FiO2 should be titrated to maintain arterial oxygen saturation of greater than 90%, bearing in mind that oxygen supply is often limited in high altitude clinics/environments.

In addition to oxygen therapy, a portable hyperbaric chamber (Gamow bag) can by used as a temporary measure in the treatment of HACE. These devices simulate a decrease in altitude of up to 7000 ft, but they are resource intensive and symptoms will often return after discontinuation of the device. Portable hyperbaric chambers should not be used in place of descent or evacuation to definitive care.

Diuretics may be helpful, but pose risks outside of a hospital environment. Sildenafil and tadalafil may help HACE, but there is little evidence of their efficacy. Theophylline is also theorized to help the condition.

Although AMS is not life-threatening, HACE is usually fatal within 24 hours if untreated. Without treatment, the patient will enter a coma and then die. In some cases, patients have died within a few hours, and a few have survived for two days. Descriptions of fatal cases often involve climbers who continue ascending while suffering from the condition's symptoms.

Recovery varies between days and weeks, but most recover in a few days. After the condition is successfully treated, it is possible for climbers to reascend. Dexamethesone should be discontinued, but continual acetazolamide is recommended. In one study, it took patients between one week and one month to display a normal CT scan after suffering from HACE.

Cerebral edema can result from brain trauma or from nontraumatic causes such as ischemic stroke, cancer, or brain inflammation due to meningitis or encephalitis.

Vasogenic edema caused by amyloid-modifying treatments, such as monoclonal antibodies, is known as ARIA-E (amyloid-related imaging abnormalities edema).

The blood–brain barrier (BBB) or the blood–cerebrospinal fluid (CSF) barrier may break down, allowing fluid to accumulate in the brain's extracellular space.

Altered metabolism may cause brain cells to retain water, and dilution of the blood plasma may cause excess water to move into brain cells.

Fast travel to high altitude without proper acclimatization can cause high-altitude cerebral edema (HACE).

Prognostics factors:

Lower Glasgow coma scale score, higher pulse rate, higher respiratory rate and lower arterial oxygen saturation level is prognostic features of in-hospital mortality rate in acute ischemic stroke.

A 2008 bulletin from the World Health Organization estimates that 900,000 total infants die each year from birth asphyxia, making it a leading cause of death for newborns.

In the United States, intrauterine hypoxia and birth asphyxia was listed as the tenth leading cause of neonatal death.

Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain.

Overall, the relative incidence of neonatal encephalopathy is estimated to be between 2 and 9 per 1000 term births. 40% to 60% of affected infants die by 2 years old or have severe disabilities. In 2013 it was estimated to have resulted in 644,000 deaths down from 874,000 deaths in 1990.

Ischemia: A decreased or restriction of circulating blood flow to a region of the brain which deprives neurons of the necessary substrates (primarily glucose); represents 80% of all strokes. A thrombus or embolus plugs an artery so there is a reduction or cessation of blood flow. This hypoxia or anoxia leads to neuronal injury, which is known as a stroke. The death of neurons leads to a so-called softening of the cerebrum in the affected area.

Hemorrhage: Intracerebral hemorrhage occurs in deep penetrating vessels and disrupts the connecting pathways, causing a localized pressure injury and in turn injury to brain tissue in the affected area. Hemorrhaging can occur in instances of embolic ischemia, in which the previously obstructed region spontaneously restores blood flow. This is known as a hemorrhagic infarction and a resulting red infarct occurs, which points to a type of cerebral softening known as red softening.

Cases of cerebral softening in infancy versus in adulthood are much more severe due to an infant's inability to sufficiently recover brain tissue loss or compensate the loss with other parts of the brain. Adults can more easily compensate and correct for the loss of tissue use and therefore the mortality likelihood in an adult with cerebral softening is less than in an infant.

Shunting refers to blood that bypasses the pulmonary circulation, meaning that the blood does not receive oxygen from the alveoli. In general, a shunt may be within the heart or lungs, and cannot be corrected by administering oxygen alone. Shunting may occur in normal states:

- Anatomic shunting, occurring via the bronchial circulation, which provides blood to the tissues of the lung. Shunting also occurs by the smallest cardiac veins, which empty directly into the left ventricle.

- Physiological shunts, occur due to the effect of gravity. The highest concentration of blood in the pulmonary circulation occurs in the bases of the pulmonary tree compared to the highest pressure of gas in the apexes of the lungs. Alveoli may not be ventilated in shallow breathing.

Shunting may also occur in disease states:

- Acute lung injury and adult respiratory distress syndrome, which may cause alveolar collapse. This will increase the amount of physiological shunting, and unlike many forms of shunting, can be managed by administering 100% Oxygen.

- Pathological shunts such as patent ductus arteriosus, patent foramen ovale, and atrial septal defects or ventricular septal defects. These states are when blood from the right side of the heart moves straight to the left side, without first passing through the lungs. This is known as a right-to-left shunt, which is often congenital in origin.

The main cause of the neurological disorders is believed to be demyelination of the cerebral hemispheres, though there is currently no widely accepted consensus on why. The most commonly accepted theories for the cause of demyelination include hypoxia and cerebral edema due to carbon monoxide toxicity, drug overdose, or cerebral blood vessel damage, and a disruption of myelin-producing pathways.

Acquired cerebrovascular diseases are those that are obtained throughout a person's life that may be preventable by controlling risk factors. The incidence of cerebrovascular disease increases as an individual ages. Causes of acquired cerebrovascular disease include atherosclerosis, embolism, aneurysms, and arterial dissections. Atherosclerosis leads to narrowing of blood vessels and less perfusion to the brain, and it also increases the risk of thrombosis, or a blockage of an artery, within the brain. Major modifiable risk factors for atherosclerosis include:

Controlling these risk factors can reduce the incidence of atherosclerosis and stroke. Atrial fibrillation is also a major risk factor for strokes. Atrial fibrillation causes blood clots to form within the heart, which may travel to the arteries within the brain and cause an embolism. The embolism prevents blood flow to the brain, which leads to a stroke.

An aneurysm is an abnormal bulging of small sections of arteries, which increases the risk of artery rupture. Intracranial aneurysms are a leading cause of subarachnoid hemorrhage, or bleeding around the brain within the subarachnoid space. There are various hereditary disorders associated with intracranial aneurysms, such as Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, and familial hyperaldosteronism type I. However, individuals without these disorders may also obtain aneurysms. The American Heart Association and American Stroke Association recommend controlling modifiable risk factors including smoking and hypertension.

Arterial dissections are tears of the internal lining of arteries, often associated with trauma. Dissections within the carotid arteries or vertebral arteries may compromise blood flow to the brain due to thrombosis, and dissections increase the risk of vessel rupture.

This refers to a disruption in the ventilation/perfusion equilibrium. Oxygen entering the lungs typically diffuses across the alveolar-capillary membrane into blood. However this equilibration does not occur when the alveolus is insufficiently ventilated, and as a consequence the blood exiting that alveolus is relatively hypoxemic. When such blood is added to blood from well ventilated alveoli, the mix has a lower oxygen partial pressure than the alveolar air, and so the A-a difference develops. Examples of states that can cause a ventilation-perfusion mismatch include:

- Exercise. Whilst modest activity and exercise improves ventilation-perfusion matching, hypoxemia may develop during intense exercise as a result of preexisting lung diseases. During exercise, almost half of the hypoxemia is due to diffusion limitations (again, on average).

- Aging. An increasingly poor match between ventilation and perfusion is seen with age, as well as a decreased ability to compensate for hypoxic states.

- Disease that affect the pulmonary interstitum can also result in hypoxia, by affecting the ability of oxygen to diffuse into arteries. An example of these diseases is pulmonary fibrosis, where even at rest a fifth of the hypoxemia is due to diffusion limitations (on average).

- Diseases that result in acute or chronic respiratory distress can result in hypoxia. These diseases can be acute in onset (such as obstruction by inhaling something or a pulmonary embolus) or chronic (such as chronic obstructive pulmonary disease).

- Cirrhosis can be complicated by refractory hypoxemia due to high rates of blood flow through the lung, resulting in ventilation-perfusion mismatch.

Preventing or delaying premature birth is considered the most important step in decreasing the risk of PVL. Common methods for preventing a premature birth include self-care techniques (dietary and lifestyle decisions), bed rest, and prescribed anti-contraction medications. Avoiding premature birth allows the fetus to develop further, strengthening the systems affected during the development of PVL.

An emphasis on prenatal health and regular medical examinations of the mother can also notably decrease the risk of PVL. Prompt diagnosis and treatment of maternal infection during gestation reduces the likelihood of large inflammatory responses. Additionally, treatment of infection with steroids (especially in the 24–34 weeks of gestation) have been indicated in decreasing the risk of PVL.

It has also been suggested that avoiding maternal cocaine usage and any maternal-fetal blood flow alterations can decrease the risk of PVL. Episodes of hypotension or decreased blood flow to the infant can cause white matter damage.