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.

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.

Major risk factors for cerebral infarction are generally the same as for atherosclerosis: high blood pressure, Diabetes mellitus, tobacco smoking, obesity, and dyslipidemia. The American Heart Association/American Stroke Association (AHA/ASA) recommends controlling these risk factors in order to prevent stroke. The AHA/ASA guidelines also provide information on how to prevent stroke if someone has more specific concerns, such as Sickle-cell disease or pregnancy. It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study.

Traumatic injury to an extremity may produce partial or total occlusion of a vessel from compression, shearing or laceration. Acute arterial occlusion may develop as a result of arterial dissection in the carotid artery or aorta or as a result of iatrogenic arterial injury (e.g., after angiography).

The thrombi may dislodge and may travel anywhere in the circulatory system, where they may lead to pulmonary embolus, an acute arterial occlusion causing the oxygen and blood supply distal to the embolus to decrease suddenly. The degree and extent of symptoms depend on the size and location of the obstruction, the occurrence of clot fragmentation with embolism to smaller vessels, and the degree of peripheral arterial disease (PAD).

- Thromboembolism (blood clots)

- Embolism (foreign bodies in the circulation, e.g. amniotic fluid embolism)

Although there is a lack of robust studies demonstrating the efficacy of lifestyle changes in preventing TIA, many medical professionals recommend them. These include:

- Avoiding smoking

- Cutting down on fats to help reduce the amount of plaque build up

- Eating a healthy diet including plenty of fruits and vegetables

- Limiting sodium in the diet, thereby reducing blood pressure

- Exercising regularly

- Moderating intake of alcohol, stimulants, sympathomimetics, etc.

- Maintaining a healthy weight

In addition, it is important to control any underlying medical conditions that may increase the risk of stroke or TIA, including:

- Hypertension

- High cholesterol

- Diabetes mellitus

- Atrial fibrillation

By definition, TIAs are transient, self-resolving, and do not cause permanent impairment. However, they are associated with an increased risk of subsequent ischemic strokes, which can be permanently disabling. Therefore, management centers around the prevention of future ischemic strokes and addressing any modifiable risk factors. The optimal regimen depends on the underlying cause of the TIA.

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.

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.

Hemodynamic impairment is thought to be the cause of deep watershed infarcts, characterized by a rosary-like pattern. However new studies have shown that microembolism might also contribute to the development of deep watershed infarcts. The dual contribution of hemodynamic impairment and microembolism would result in different treatment for patients with these specific infarcts.

Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive blood sugar control has been shown to reduce small blood vessel complications such as kidney damage and damage to the retina of the eye it has not been shown to reduce large blood vessel complications such as stroke.

A sharp drop in blood pressure is the most frequent cause of watershed infarcts. The most frequent location for a watershed stroke is the region between the anterior cerebral artery and middle cerebral artery. These events caused by hypotension do not usually cause the blood vessel to rupture.

Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half. It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.

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.

Whether a cerebral infarction is thrombotic or embolic based, its pathophysiology, or the observed conditions and underlying mechanisms of the disease. In thrombotic ischemic stroke, a thrombus forms and blocks blood flow. A thrombus forms when the endothelium is activated by a variety of signals to result in platelet aggregation in the artery. This clump of platelets interacts with fibrin to form a platelet plug. This platelet plug grows into a thrombus, resulting in a stenotic artery. Thrombotic ischemia can occur in large or small blood vessels. In large vessels, the most common causes of thrombi are atherosclerosis and vasoconstriction. In small vessels, the most common cause is lipohyalinosis. Lipohyalinosis is when high blood pressure and aging causes a build-up of fatty hyaline matter in blood vessels. Atheroma formation can also cause small vessel thrombotic ischemic stroke.

An embolic stroke refers to the blockage of an artery by an embolus, a traveling particle or debris in the arterial bloodstream originating elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis). The embolus may be of cardiac origin due to Atrial fibrillation, Patent foramen ovale or from atherosclerotic plaque of another (or the same) large artery. Cerebral artery gas embolism (e.g. during ascent from a SCUBA dive) is also a possible cause of infarction (Levvett & Millar, 2008)

The fact that the ischemic cascade involves a number of steps has led doctors to suspect that neuroprotectants such as calcium channel blockers or glutamate antagonists could be produced to interrupt the cascade at a single one of the steps, blocking the downstream effects. Though initial trials for such neuroprotective drugs led many to be hopeful, until recently, human clinical trials with neuroprotectants such as NMDA receptor antagonists were unsuccessful.

On October 7, 2003, a U.S. patent number 6630507 entitled "Cannabinoids as Antioxidants and Neuroprotectants" was awarded to the United States Department of Health and Human Services, based on research carried out at the National Institute of Mental Health (NIMH), and the National Institute of Neurological Disorders and Stroke (NINDS). This patent claims that cannabinoids are "useful in the treatment and prophylaxis of wide variety of oxidation associated diseases such as ischemia, inflammatory ... and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma..."

On November 17, 2011, in accordance with 35 U.S.C. 209(c)(1) and 37 CFR part 404.7(a)(1)(i), the National Institutes of Health, Department of Health and Human Services, published in the Federal Register, that it is contemplating the grant of an exclusive patent license to practice the invention embodied in U.S. Patent 6,630,507, entitled “Cannabinoids as antioxidants and neuroprotectants” and PCT Application Serial No. PCT/US99/08769 and foreign equivalents thereof, entitled “Cannabinoids as antioxidants and neuroprotectants” [HHS Ref. No. E-287-1997/2] to KannaLife Sciences Inc., which has offices in New York, U.S. This patent and its foreign counterparts have been assigned to the Government of the United States of America. The prospective exclusive license territory may be worldwide, and the field of use may be limited to: The development and sale of cannabinoid(s) and cannabidiol(s) based therapeutics as antioxidants and neuroprotectants for use and delivery in humans, for the treatment of hepatic encephalopathy, as claimed in the Licensed Patent Rights.

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.

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 major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.

Diseases associated with cerebral atherosclerosis include:

- Hypertensive arteriopathy

This pathological process involves the thickening and damage of arteriole walls. It mainly affects the ends of the arterioles which are located in the deep gray nuclei and deep white matter of the brain. It is thought that this is what causes cerebral microbleeds in deep brain regions. This small vessel damage can also reduce the clearance of amyloid-β, thereby increasing the likelihood of CAA.

Diseases cerebral atherosclerosis and associated diseases can cause are:

- Alzheimer's disease

Alzheimer's disease is a form of dementia that entails brain atrophy. Cerebral amyloid angiopathy is found in 90% of the cases at autopsy, with 25% being severe CAA.

- Cerebral microbleeds (CMB)

Cerebral microbleeds have been observed during recent studies on dementia sufferers using MRI.

- Stroke

Strokes occur from the sudden loss of blood flow to an area of the brain. The loss of flow is generally either from a blockage or hemorrhage. Studies of postmortem stroke cases have shown that intracranial athreosclerotic plaque build up occurred in over half of the individuals and over one third of the overall cases had stenotic build up.

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.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

Cerebral hypoxia is a form of hypoxia (reduced supply of oxygen), specifically involving the brain; when the brain is completely deprived of oxygen, it is called "cerebral anoxia". There are four categories of cerebral hypoxia; they are, in order of severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury.

Cases of total oxygen deprivation are termed "anoxia", which can be hypoxic in origin (reduced oxygen availability) or ischemic in origin (oxygen deprivation due to a disruption in blood flow). Brain injury as a result of oxygen deprivation either due to hypoxic or anoxic mechanisms are generally termed hypoxic/anoxic injuries (HAI). Hypoxic ischemic encephalopathy (HIE) is a condition that occurs when the entire brain is deprived of an adequate oxygen supply, but the deprivation is not total. While HIE is associated in most cases with oxygen deprivation in the neonate due to birth asphyxia, it can occur in all age groups, and is often a complication of cardiac arrest.

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).

Asymptomatic individuals with intracranial stenosis are typically told to take over the counter platelet inhibitors like aspirin whereas those with symptomatic presentation are prescribed anti-coagulation medications. For asymptomatic persons the idea is to stop the buildup of plaque from continuing. They are not experiencing symptoms; however if more build up occurs it is likely they will. For symptomatic individuals it is necessary to try and reduce the amount of stenosis. The anti-coagulation medications reduce the likelihood of further buildup while also trying to break down the current build up on the surface without an embolism forming. For those with severe stenosis that are at risk for impending stroke endovascular treatment is used. Depending on the individual and the location of the stenosis there are multiple treatments that can be undertaken. These include angioplasty, stent insertion, or bypass the blocked area.