Brain ischemia, also known as cerebral ischemia, occurs when there is insufficient blood flow to the brain, depriving brain tissue of oxygen. This can lead to brain damage or stroke. There are two types - focal ischemia, which is confined to a specific brain region, and global ischemia, which affects wide areas of brain tissue. Symptoms vary depending on the location of ischemia and can include vision problems, weakness, and difficulty speaking. Causes include conditions like sickle cell anemia that increase risk of blood clots, as well as issues that decrease blood flow such as low blood pressure from heart attacks. Treatment aims to restore blood flow and oxygen supply to the brain to limit damage.

1. BRAIN ISCHEMIA presentation by Mwebaza Victor MBchB
CT scan slice of the brain showing a right-hemispheric cerebral infarct (left side of image).
Brain ischemia (aka cerebral ischemia, cerebrovascular ischemia) is a condition in which there is
insufficient blood flow to the brain to meet metabolic demand.[1] This leads to poor oxygen supply or
cerebral hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke.[2] It is a
sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.[3]
Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis.[4]

2. There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and
global ischemia, which encompasses wide areas of brain tissue.
The main symptoms involve impairments in vision, body movement, and speaking. The causes of brain
ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can
include unconsciousness, blindness, problems with coordination, and weakness in the body. Other
effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain
damage.
An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an
interruption in flow for more than a few minutes generally results in irreversible brain damage.[5] In
1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to
an hour can be at least partially recovered. Accordingly, this discovery raised the possibility of
intervening after brain ischemia before the damage becomes irreversible.[6]
Classification
The broad term, "stroke" can be divided into three categories: brain ischemia, subarachnoid
hemorrhage and intracerebral hemorrhage. Brain ischemia can be further subdivided, by cause, into
thrombotic, embolic, and hypoperfusion.[3] Thrombotic and embolic are generally focal or multifocal in
nature while hypoperfusion affects the brain globally.
Focal brain ischemia
Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel.[7] Focal brain ischemia
reduces blood flow to a specific brain region, increasing the risk of cell death to that particular area.[8] It
can be either caused by thrombosis or embolism.
Global brain ischemia
Global brain ischemia occurs when blood flow to the brain is halted or drastically reduced. This is
commonly caused by cardiac arrest. If sufficient circulation is restored within a short period of time,
symptoms may be transient. However, if a significant amount of time passes before restoration, brain
damage may be permanent. While reperfusion may be essential to protecting as much brain tissue as
possible, it may also lead to reperfusion injury. Reperfusion injury is classified as the damage that ensues
after restoration of blood supply to ischemic tissue.[7]

3. Symptoms
The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation.
Ischemia within the arteries branching from the internal carotid artery may result in symptoms such as
blindness in one eye, weakness in one arm or leg, or weakness in one entire side of the body. Ischemia
within the arteries branching from the vertebral arteries in the back of the brain may result in symptoms
such as dizziness, vertigo, double vision, or weakness on both sides of the body . Other symptoms
include difficulty speaking, slurred speech, and the loss of coordination.[9] The symptoms of brain
ischemia range from mild to severe. Further, symptoms can last from a few seconds to a few minutes or
extended periods of time. If the brain becomes damaged irreversibly and infarction occurs, the
symptoms may be permanent.[10]
Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness, brain
damage or death, mediated by the ischemic cascade.[11]
Multiple cerebral ischemic events may lead to subcortical ischemic depression, also known as vascular
depression. This condition is most commonly seen in elderly depressed patients. Late onset depression
is increasingly seen as a distinct sub-type of depression, and can be detected with an MRI.[12]
Causes
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.

4. 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 pathological 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.[13]
Pathophysiology
During brain ischemia, the brain cannot perform aerobic metabolism due to the loss of oxygen and
substrate. The brain is not able to switch to anaerobic metabolism and because it does not have any
long term energy stored the levels of adenosine triphosphate (ATP) drop rapidly and approach zero
within 4 minutes. In the absence of biochemical energy, cells begin to lose the ability to maintain
electrochemical gradients. Consequently, there is a massive influx of calcium into the cytosol, a massive
release of glutamate from synaptic vesicles, lipolysis, calpain activation, and the arrest of protein
synthesis.[14] Additionally, removal of metabolic wastes is slowed.[15] The interruption of blood flow to

5. the brain for ten seconds results in the immediate loss of consciousness. The interruption of blood flow
for twenty seconds results in the stopping of electrical activity.[5] An area called a penumbra, may result,
wherein neurons do not receive enough blood to communicate, however do receive sufficient
oxygenation to avoid cell death for a short period of time.[16]
Treatment
Alteplase (tpa) is an effective medication for acute ischemic stroke. When given within 3 hours,
treatment with tpa significantly improves the probability of a favourable outcome versus treatment with
placebo.
The outcome of brain ischemia is influenced by the quality of subsequent supportive care. Systemic
blood pressure (or slightly above) should be maintained so that cerebral blood flow is restored. Also,
hypoxaemia and hypercapnia should be avoided. Seizures can induce more damage; accordingly,
anticonvulsants should be prescribed and should a seizure occur, aggressive treatment should be
undertaken. Hyperglycaemia should also be avoided during brain ischemia.[17]
Management
When someone presents with an ischemic event, treatment of the underlying cause is critical for
prevention of further episodes.
Anticoagulation with warfarin or heparin may be used if the patient has atrial fibrillation.
Operative procedures such as carotid endarterectomy and carotid stenting may be performed if the
patient has a significant amount of plaque in the carotid arteries associated with the local ischemic
events.
Research
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.

6. 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.[18] Potential causes of brain hypoxia are suffocation, carbon monoxide
poisoning, severe anemia, and use of drugs such as cocaine and other amphetamines.[9] 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.[18]
THE CIRCLE OF WILLIS

7. The circle of Willis (also called Willis' circle, loop of Willis, cerebral arterial circle, and Willis polygon) is a
circulatory anastomosis that supplies blood to the brain and surrounding structures. It is named after
Thomas Willis (1621–1675), an English physician.[1]

8. Structure
The circle of Willis is a part of the cerebral circulation and is composed of the following arteries:[2]
Anterior cerebral artery (left and right)
Anterior communicating artery
Internal carotid artery (left and right)
Posterior cerebral artery (left and right)
Posterior communicating artery (left and right)
Basilar artery
The middle cerebral arteries, supplying the brain, are not considered part of the circle.
Origin of arteries
The left and right internal carotid arteries arise from the left and right common carotid arteries.
The posterior communicating artery is given off as a branch of the internal carotid artery just before it
divides into its terminal branches - the anterior and middle cerebral arteries. The anterior cerebral
artery forms the anterolateral portion of the circle of Willis, while the middle cerebral artery does not
contribute to the circle.
The right and left posterior cerebral arteries arise from the basilar artery, which is formed by the left and
right vertebral arteries. The vertebral arteries arise from the subclavian arteries.
The anterior communicating artery connects the two anterior cerebral arteries and could be said to arise
from either the left or right side.
All arteries involved give off cortical and central branches. The central branches supply the interior of
the circle of Willis, more specifically, the Interpeduncular fossa. The cortical branches are named for the
area they supply. Since they do not directly affect the circle of Willis, they are not dealt with here.

9. Variation
Considerable anatomic variation exists in the circle of Willis. Based on a study of 1413 brains, the classic
anatomy of the circle is only seen in 34.5% of cases.[3] In one common variation the proximal part of the
posterior cerebral artery is narrow and its ipsilateral posterior communicating artery is large, so the
internal carotid artery supplies the posterior cerebrum. In another variation the anterior communicating
artery is a large vessel, such that a single internal carotid supplies both anterior cerebral arteries.
Function
The arrangement of the brain's arteries into the circle of Willis creates redundancies or collaterals in the
cerebral circulation. If one part of the circle becomes blocked or narrowed (stenosed) or one of the
arteries supplying the circle is blocked or narrowed, blood flow from the other blood vessels can often
preserve the cerebral perfusion well enough to avoid the symptoms of ischemia.[4]
Clinical significance
Aneurysms
Circle of Willis with the most common locations of ruptured aneurysms marked
Main article: Subarachnoid haemorrhage
Subclavian steal syndrome
The redundancies that the circle of Willis introduce can also lead to reduced cerebral perfusion.[5][6] In
subclavian steal syndrome, blood is "stolen" from the circle of Willis to preserve blood flow to the upper
limb. Subclavian steal syndrome results from a proximal stenosis (narrowing) of the subclavian artery, an
artery supplied by the aorta which is also the same blood vessel that eventually feeds the circle of Willis
via the vertebral artery.
by MWEBAZA VICTOR