What Happens When the Blood Supply to a Certain Part is Blocked

What happens when the blood supply to a certain part is blocked?

Cellular Changes

Injury from ischemic stroke is the result of a complex series of cellular metabolic events that occur

rapidly after the interruption of nutrient blood flow to a region of the brain. The duration, severity, and

location of focal cerebral ischemia determine the extent of brain function and thus the severity of

stroke.

Shown is a summary of the cascade of cellular changes as ischemia progresses.

Neuronal Function: Importance of Oxygen and Glucose

Click Image to Enlarge

A neuron consists of a cell body, which contains a nucleus, and one or more extensions

protruding from the cell body. Dendrites receive nerve impulses from other neurons or from

sensory receptors. The axon carries the nerve impulses (action potential) away from the cell

body to another neuron or to an effector organ such as a muscle.

A stimulus affects the axon by changing the permeability of the axon to positive ions. The

influx of positive ions reduces the electrical potential across one segment of the membrane

(depolarization). The change in electrical potential in the first part of the axon triggers a

change in electrical potential in the adjacent segment of the axon such that the impulse

travels along the axon as a self-generating chain reaction.

At most synapses, arrival of the impulse at the presynaptic terminal leads to release of

neurotransmitter, which crosses the synapse to interact with receptors on the membrane of

the postsynaptic cell. This interaction opens ion-specific channels in the postsynaptic

membrane, changing the membrane’s permeability for positive ions.

The transient change in voltage induced by the action potential is determined by the

concentration of ions on either side of the cell membrane. Maintaining these ionic gradients

is an energy-consuming process that requires a constant supply of glucose and oxygen to

the neuron.

Inadequate Energy Supply

Lack of glucose and oxygen deplete the cellular energy stores required to maintain electrical

potentials and ion gradients.

In ischemic brain tissue, the membrane that surrounds each affected neuron becomes

“leaky,” and the cell loses potassium and adenosine triphosphate (ATP), the tissue’s medium

for energy exchange.

Energy failure is not the immediate cause of cell death, however, since all brain cells

tolerate loss of ATP for several minutes. In humans, it appears that 5 to 10 minutes of

complete occlusion is required for irreversible brain damage. In actuality, most strokes do

not involve a complete occlusion of blood flow, but even a partial occlusion, if allowed to

continue for a sufficient time, may produce irreversible brain damage.

Once blood flow to cerebral neurons diminishes, one or more branching mechanisms may

independently lead to brain cell death. These mechanisms may involve deterioration of ion

gradients or the effects of anaerobic metabolism.

With respect to the latter, anaerobic glycotic pathways are utilized in the affected region to

compensate for the loss of oxygen and provide a source of energy. However, this produces

damaging byproducts, including lactic acid and hydrogen ions, which accumulate in tissue in

proportion to the carbohydrate stores present at the outset of ischemia. Toxicity of

hydrogen ions, especially their ability to facilitate ferrous-iron-mediated free-radical

mechanisms, appears to irreversibly affect neuronal integrity.

Deterioration of Ion Gradients

Inadequate energy supply leads to deterioration of ion gradients. Anoxic depolarization (equilibration

of intracellular and extracellular ions) causes potassium to leave the cell and sodium, chloride, and

calcium ions to enter. It also stimulates the massive release of the amino acids glutamate and

aspartate, excitatory neurotransmitters in the brain.

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Glutamate further activates sodium and calcium ion channels in the neuron membrane.

As sodium and calcium ions rapidly accumulate within the cells, accompanied by an inflow of water,

cytotoxic edema causes rapid swelling of neurons and glia.

Activation of calcium channels results in further influx of calcium into the cell. One of the most

intensely studied calcium channels is the N-methyl-D aspartate (NMDA) channel.

Consequences of Calcium Overload

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Entry of calcium through the NMDA (and similar channels) can be devastating. First, attempts to get

rid of the excess calcium use up already scarce supplies of ATP. Second, excessive calcium influx

causes the disordered activation of a wide range of enzyme systems (proteases, lipases, and

nucleases). These enzymes and their metabolic products, such as oxygen free radicals, damage cell

membranes, genetic material, and structural proteins in the neurons, ultimately leading to cell death.

This sequence of events has been termed excitotoxicity because of the pivotal role of excitatory amino

acids such as glutamate.

Several agents are under investigation to block these steps.

The Ischemic Penumbra

Within the ischemic cerebrovascular bed, there are two major zones of injury: the core ischemic zone

and the “ischemic penumbra” (the term generally used to define ischemic but still viable cerebral

tissue).

In the core zone, which is an area of severe ischemia (blood flow below 10% to 25%), the loss of

oxygen and glucose results in rapid depletion of energy stores. Severe ischemia can result in necrosis

of neurons and also of supporting cellular elements (glial cells) within the severely ischemic area.

Brain cells within the penumbra, a rim of mild to moderately ischemic tissue lying between tissue that

is normally perfused and the area in which infarction is evolving, may remain viable for several hours.

That is because the penumbral zone is supplied with blood by collateral arteries anastomosing with

branches of the occluded vascular tree (see inset). However, even cells in this region will die if

reperfusion is not established during the early hours since collateral circulation is inadequate to

maintain the neuronal demand for oxygen and glucose indefinitely.

In this example, the ischemic penumbra is shown as a rim of tissue surrounding the severely ischemic

core lying within the vascular territory of the pre-Rolandic branch of the left middle cerebral artery.

The Rolandic artery is occluded by a thromboembolus. The extent of the penumbra varies directly with

the number and patency of collateral arteries.

The penumbra is where pharmacologic interventions are most likely to be effective. However, it may

also be possible to salvage cells within the severely ischemic core zone. Although severe ischemia kills

selectively vulnerable neurons, glial cells may be spared if blood flow is restored early. Therefore,

timely recanalization of the occluded vessel should theoretically restore perfusion in both the

penumbra and in the severely ischemic core. Partial recanalization should markedly reduce the size of

the penumbra as well.

Cerebral Infarction / Effects of Edema

Shown is a brain slice viewed from the back following a stroke. Blood flow to the region on

the left was interrupted due to a thrombus or embolus. The lack of blood flow resulted in

severe damage (infarct) to some of the brain tissue. The infarcted tissue caused fluids to

accumulate (edema) and result in swelling. The center of the brain is shifted to the right due

to swelling from the left.

The rigid container of the cranium allows limited room for expansion, and any condition that

causes an increase in volume of one or more structures within this vault will cause an

increase in intracranial pressure (ICP) or will shift one compartment of the brain, thereby

compressing others. As the pressure increases, the brain shifts or is distorted, compressing

neurons, nerve tracts, and cerebral arteries. A sustained increase in pressure causes

persistent ischemia, irreversible damage to brain cells, and potentially death.

Edema Formation

Ischemic brain edema is a combination of two major types of edema: cytotoxic (cellular) and

vasogenic [Fishman RA. Cerebrospinal Fluid in Diseases in the Nervous System. 2nd Ed.

Philadelphia, PA: W.B. Saunders Co; 1992:103-155]. Cytotoxic edema evolves over minutes

to hours and may be reversible, while the vasogenic phase occurs over hours to days, and is

considered an irreversibly damaging process.

Click Image to Enlarge

Cytotoxic edema is characterized by swelling of all the cellular elements of the brain

(shown). In the presence of acute cerebral ischemia, neurons, glia (indicated by astrocytes),

and endothelial cells swell within minutes of hypoxia due to failure of ATP-dependent ion

(sodium and calcium) transport. With the rapid accumulation of sodium within cells, water

follows to maintain osmotic equilibrium. Increased intracellular calcium activates

phospholipases and the release of arachidonic acid, leading to the release of oxygen-derived

free radicals and infarction.

Vasogenic edema (not shown) is characterized by an increase in extracellular fluid volume

due to increased permeability of brain capillary endothelial cells to macromolecular serum

proteins (e.g., albumin). Normally, the entry of plasma protein-containing fluid into the

extracellular space is limited by tight endothelial cell junctions, but in the presence of

massive injury, there is increased permeability of brain capillary endothelial cells to large

molecules. Vasogenic edema can displace the brain hemisphere and, when severe, lead to

cerebral herniation.

Acute hypoxia initially causes cytotoxic edema, followed within the next hours to days by

the development of vasogenic edema as infarction develops (Fishman, 1992). The delayed

onset of vasogenic edema suggests that time is needed for the defects in endothelial cell

function and permeability to develop.

http://www.strokecenter.org/professionals/brain-anatomy/cellular-injury-during-ischemia/edema-formation/

Brain ischemiaFrom Wikipedia, the free encyclopedia

Brain ischemia

CT scan slice of the brain showing a right-hemispheric cerebral infarct (left

side of image).

Classification and external resources

Specialty neurology, cardiology

ICD-10 G45.9, I67.8

ICD-9-CM 435X,437X

MeSH D002545

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]

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, andspeaking. The causes of brain ischemia vary from sickle cell anemia tocongenital 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 andZimmerman[disambiguation needed] demonstrated that ischemia induced inmammalian 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]

Contents

  [hide] 

1   Classification o 1.1   Focal brain ischemia

o 1.2   Global brain ischemia

2   Symptoms 3   Causes 4   Pathophysiology 5   Treatment 6   Management 7   Research 8   References 9   Bibliography 10   Further reading

Classification[edit]

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[edit]

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[edit]

Global brain ischemia occurs when blood flow to the brain is halted or drastically reduced. This is commonly caused bycardiac 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]

Symptoms[edit]

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[citation needed]. 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.[citation

needed] Late onset depression is increasingly seen as a distinct sub-type of depression, and can be detected with an MRI.[12]

Causes[edit]

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 ofheart 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.[citation needed] 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[edit]

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 ofadenosine 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 thecytosol, 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 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[edit]

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[edit]

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[edit]

Therapeutic hypothermia has been attempted to improve results post brain ischemia[citation needed]. 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.[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]

https://en.wikipedia.org/wiki/Brain_ischemia

What Is A Stroke?

Source:  MedicineNet.comMedical Author: Benjamin C. Wedro, MD, FAAEMMedical Editor: William C. Shiel Jr., MD, FACP, FACR

Stroke: What is it?A stroke, or cerebrovascular accident (CVA), occurs when blood supply to part of the brain is disrupted, causing brain cells to die. When blood flow to the brain is impaired, oxygen and glucose cannot be delivered to the brain. Blood flow can be compromised by a variety of mechanisms.Blockage of an artery

•Narrowing of the small arteries within the brain can cause a so-called lacunar stroke, (lacune=empty space). Blockage of a single arteriole can affect a tiny area of brain causing that tissue to die (infarct).•Hardening of the arteries (atherosclerosis) leading to the brain. There are four major blood vessels that supply the brain with blood. The anterior circulation of the brain that controls most motor, activity, sensation, thought, speech, and emotion is supplied by the carotid arteries. The posterior circulation, which supplies the brainstem and the cerebellum, controlling the automatic parts of brain function and coordination, is supplied by the vertebrobasilar arteries.

If these arteries become narrow as a result of atherosclerosis, plaque or cholesterol, debris can break off and float downstream, clogging the blood supply to a part of the brain. As opposed to lacunar strokes, larger parts of the brain can lose blood supply, and this may produce more symptoms than a lacunar stroke.

•Embolism to the brain from the heart. In situations in which blood clots form

within the heart, the potential exists for small clots to break off and travel (embolize) to the arteries in the brain and cause a stroke.Rupture of an artery (hemorrhage)•Cerebral hemorrhage (bleeding within the brain substance). The most common reason to have bleeding within the brain is uncontrolled high blood pressure. Other situations include aneurysms that leak or rupture or arteriovenous malformations (AVM) in which there is an abnormal collection of blood vessels that are fragile and can bleed.

What causes a stroke?

Blockage of an arteryThe blockage of an artery in the brain by a clot (thrombosis) is the most common cause of a stroke. The part of the brain that is supplied by the clotted blood vessel is then deprived of blood and oxygen. As a result of the deprived blood and oxygen, the cells of that part of the brain die. Typically, a clot forms in a small blood vessel within the brain that has been previously narrowed due to a variety of risk factors including:•high blood pressure (hypertension),•high cholesterol,•diabetes, and•smoking.Embolic strokeAnother type of stroke may occur when a blood clot or a piece of atherosclerotic plaque (cholesterol and calcium deposits on the wall of the inside of the heart or artery) breaks loose, travels through open arteries, and lodges in an artery of the brain. When this happens, the flow of oxygen-rich blood to the brain is blocked and a stroke occurs. This type of stroke is referred to as an embolic stroke. For example, a blood clot might originally form in the heart chamber as a result of an irregular heart rhythm, such as occurs in atrial fibrillation. Usually, these clots remain attached to the inner lining of the heart, but occasionally they can break off, travel through the blood stream, form a plug (embolism) in a brain artery, and cause a stroke. An embolism can also originate in a large artery (for example, the carotid artery, a major artery in the neck that supplies blood to the brain) and then travel downstream to clog a small artery within the brain.Cerebral hemorrhageA cerebral hemorrhage occurs when a blood vessel in the brain ruptures and bleeds into the surrounding brain tissue. A cerebral hemorrhage (bleeding in the brain) can cause a stroke by depriving blood and oxygen to parts of the

brain. Blood is also very irritating to the brain and can cause swelling of brain tissue (cerebral edema). Edema and the accumulation of blood from a cerebral hemorrhage increases pressure within the skull and causes further damage by squeezing the brain against the bony skull.Subarachnoid hemorrhageIn a subarachnoid hemorrhage, blood accumulates in the space beneath the arachnoid membrane that lines the brain. The blood originates from an abnormal blood vessel that leaks or ruptures. Often this is from an aneurysm (an abnormal ballooning out of the wall of the vessel). Subarachnoid hemorrhages usually cause a sudden, severe headache and stiff neck. If not recognized and treated, major neurological consequences, such as coma, and brain death will occur.VasculitisAnother rare cause of stroke is vasculitis, a condition in which the blood vessels become inflamed.Migraine headacheThere appears to be a very slight increased occurrence of stroke in people with migraine headache. The mechanism for migraine or vascular headaches includes narrowing of the brain blood vessels. Some migraine headache episodes can even mimic stroke with loss of function of one side of the body or vision or speech problems. Usually, the symptoms resolve as the headache resolves. What are the risk factors for stroke?

Overall, the most common risk factors for stroke are:•high blood pressure,•high cholesterol,•smoking,•diabetes and•increasing age.Heart rhythm disturbances like atrial fibrillation, patent foramen ovale, and heart valve disease can also be the cause.When strokes occur in younger individuals (less than 50 years old), less common risk factors are considered including illicit drugs, such as cocaine or amphetamines, ruptured aneurysms, and inherited (genetic) predispositions to blood clotting. An example of a genetic predisposition to stroke occurs in a rare condition called homocystinuria, in which there are excessive levels of the chemical homocystine in the body. Scientists are trying to determine whether the non-hereditary occurrence of high levels of homocystine at any age can predispose to stroke. What is a transient ischemic attack (TIA)?A transient ischemic attack (TIA) is a short-lived episode (less than 24 hours)

of temporary impairment to the brain that is caused by a loss of blood supply. A TIA causes a loss of function in the area of the body that is controlled by the portion of the brain affected. The loss of blood supply to the brain is most often caused by a clot that spontaneously forms in a blood vessel within the brain (thrombosis). However, it can also result from a clot that forms elsewhere in the body, dislodges from that location, and travels to lodge in an artery of the brain (emboli). A spasm and, rarely, a bleed are other causes of a TIA. Many people refer to a TIA as a "mini-stroke."Some TIAs develop slowly, while others develop rapidly. By definition, all TIAs resolve within 24 hours. Strokes take longer to resolve than TIAs, and with strokes, complete function may never return and reflect a more permanent and serious problem. Although most TIAs often last only a few minutes, all TIAs should be evaluated with the same urgency as a stroke in an effort to prevent recurrences and/or strokes. TIAs can occur once, multiple times, or precede a permanent stroke.A transient ischemic attack should be considered an emergency because there is no guarantee that the situation will resolve and function will return.  A TIA from a clot to the eye can cause temporary visual loss (amaurosis fugax), which is often described as the sensation of a curtain coming down. A TIA that involves the carotid artery (the largest blood vessel supplying the brain) can produce problems with movement or sensation on one side of the body, which is the side opposite to the actual blockage. An affected patient may experience paralysis of the arm, leg, and face, all on one side. Double vision, dizziness (vertigo), and loss of speech, understanding, and balance can also be symptoms depending on what part of the brain is lacking blood supply.

What is the impact of strokes?

In the United States, stroke is the third largest cause of death (behind heart disease and all forms of cancer). The cost of strokes is not just measured in the billions of dollars lost in work, hospitalization, and the care of survivors in nursing homes. The major cost or impact of a stroke is the loss of independence that occurs in 30% of the survivors. What was a self-sustaining and enjoyable lifestyle may lose most of its quality after a stroke and other family members can find themselves in a new role as caregivers.

What are stroke symptoms?

When brain cells are deprived of oxygen, they cease to perform their usual

tasks. The symptoms that follow a stroke depend on the area of the brain that has been affected and the amount of brain tissue damage.Small strokes may not cause any symptoms, but can still damage brain tissue. These strokes that do not cause symptoms are referred to as silent strokes. According to The U.S. National Institute of Neurological Disorders and Stroke (NINDS), these are the five major signs of stroke:

1.Sudden numbness or weakness of the face, arm or leg, especially on one side of the body. The loss of voluntary movement and/or sensation may be complete or partial. There may also be an associated tingling sensation in the affected area.

2.Sudden confusion or trouble speaking or understanding. Sometimes weakness in the muscles of the face can cause drooling.

3.Sudden trouble seeing in one or both eyes

4.Sudden trouble walking, dizziness, loss of balance or coordination

5.Sudden, severe headache with no known cause 

What should be done if you suspect you or someone else is having a stroke?

If any of the symptoms mentioned above suddenly appear, emergency medical attention should be sought. Therefore, the first action should be to call 911 (or whatever number activates the emergency medical response in your area). The family doctor and/or neurologist should also be contacted. However, the first priority is ensuring that the ambulance arrives as soon as possible. •The affected person should lie flat to promote an optimal blood flow to the brain.

•If drowsiness, unresponsiveness, or nausea are present, the person should be placed in the rescue position on their side to prevent choking should vomiting occur.

•Although aspirin plays a major role in stroke prevention (see below), once the symptoms of a stroke begin, it is generally recommended that additional

aspirin not be taken until the patient receives medical attention. If stroke is of the bleeding type, aspirin could theoretically make matters worse.Cincinnati Prehospital Stroke Scale (CPSS)According to a study by the University of North Carolina, three commands may be used to assess whether a person may be experiencing a stroke. Lay persons can command a potential stroke victim to:

1.Smile

2.Raise both arms

3.Speak a simple sentence

The three commands, known as the Cincinnati Prehospital Stroke Scale (CPSS), are used by health professionals as a simple first step in the assessment process for signs of stroke. If a person has trouble with any of these simple commands, emergency services (911) should be called immediately with a description of the situation, noting that you suspect the individual is having a stroke. 

How is a stroke diagnosed?

A stroke is a medical emergency. Anyone suspected of having a stroke should be taken to a medical facility immediately for evaluation and treatment. Initially, the doctor takes a medical history from the patient if he/she is alert or others familiar with the patient if they are available, and performs a physical examination. If a person has been seeing a particular doctor, it would be ideal for that doctor to participate in the assessment. Previous knowledge of the patient can improve the accuracy of the evaluation. A neurologist, a doctor specializing in disorders of the nervous system and diseases of the brain, will often assist in the diagnosis and management of stroke patients. Just because a person has slurred speech or weakness on one side of the body does not necessarily signal the occurrence of a stroke. There are many other possibilities that can be responsible for these symptoms. Other conditions that can mimic a stroke include: brain tumors, a brain abscess (a collection of pus in the brain caused by bacteria or a fungus), migraine headache, bleeding in the brain either spontaneously or from trauma, meningitis or encephalitis, an overdose of certain medications, or an imbalance of sodium, calcium, or glucose in the body can also cause changes in the nervous system that can mimic a stroke.

In the acute stroke evaluation, many things will occur at the same time. As the physician is taking the history and performing the physical examination, nursing staff will begin monitoring the patient's vital signs, getting blood tests, and performing an electrocardiogram (EKG or ECG). Part of the physical examination that is becoming standardized is the use of a stroke scale. There is a narrow time frame to intervene in an acute stroke with medications to reverse the loss of blood supply to part of the brain. The patient needs to be appropriately evaluated and stabilized before any clot-busting drugs can be potentially utilized.

Computerized tomography:In order to help determine the cause of a suspected stroke, a special x-ray test called a CT scan of the brain is often performed. A CT scan is used to look for bleeding or masses within the brain, a much different situation than stroke that is also treated differently.MRI scan:Magnetic resonance imaging (MRI) uses magnetic waves rather than x-rays to image the brain. The MRI images are much more detailed than those from CT, but this is not a first line test in stroke. While a CT scan may be completed within a few minutes, an MRI may take more than an hour to complete. An MRI may be performed later in the course of patient care if finer details are required for further medical decision making. People with certain medical devices (for example, pacemakers) or other metals within their body, cannot be subjected to the powerful magnetic field of an MRI.Other methods of MRI technology:An MRI scan can also be used to specifically view the blood vessels non-invasively (without using tubes or injections), a procedure called an MRA (magnetic resonance angiogram). Another MRI method called diffusion weighted imaging (DWI) is being offered in some medical centers. This technique can detect the area of abnormality minutes after the blood flow to a part of the brain has ceased, whereas a conventional MRI may not detect a stroke until up to six hours after it has started, and a CT scan sometimes cannot detect it until it is 12 to 24 hours old. Again, this is not a first line test in the evaluation of a stroke patient, when time is of the essence.Computerized tomography with angiography:Using dye that is injected into a vein in the arm, images of the blood vessels in the brain can give information regarding aneurysms or arteriovenous malformations. As well, other abnormalities of brain blood flow may be

evaluated. With increasingly sophisticated technology, CT angiography has supplanted conventional angiograms.Conventional angiogram:An angiogram is another test that is sometimes used to view the blood vessels. A long catheter tube is inserted into an artery (usually in the groin area) and dye is injected while x-rays are simultaneously taken. While an angiogram delivers some of the most detailed images of the blood vessel anatomy, it is also an invasive procedure and is used only when absolutely necessary. For example, an angiogram is done after a hemorrhage when the precise source of bleeding needs to be identified. It also is sometimes performed to accurately evaluate the condition of a carotid artery when surgery to unblock that blood vessel is contemplated.Carotid Doppler ultrasound:A carotid Doppler ultrasound is a non-invasive (without injections or placing tubes) method that uses sound waves to screen for narrowings and decreased blood flow in the carotid artery (the major artery in the neck that supplies blood to the brain).Heart tests:Certain tests to evaluate heart function are often performed in stroke patients to search for the source of an embolism. An echocardiogram is a sound wave test that is done by placing a microphone device on the chest or down the esophagus (transesophageal echocardiogram) in order to view the heart chambers. A Holter monitor is similar to a regular electrocardiogram (EKG), but the electrode stickers remain on the chest for 24 hours or longer in order to identify a faulty heart rhythm.Blood tests:Blood tests such as a sedimentation rate and C-reactive protein are done to look for signs of inflammation that can suggest inflamed arteries. Certain blood proteins that can increase the chance of stroke by thickening the blood are measured. These tests are performed to identify treatable causes of a stroke or to help prevent further injury. Screening blood tests looking for potential infection, anemia, kidney function, and electrolyte abnormalities may also be considered. What is the treatment of a stroke?Tissue plasminogen activator (TPA)There is opportunity to use alteplase (TPA) as a clot-buster drug to dissolve the blood clot that is causing the stroke. There is a narrow window of opportunity to use this drug. The earlier that it is given, the better the result and the less potential for the complication of bleeding into the brain.Present American Heart Association guidelines recommend that if used, TPA must be given within three hours after the onset of symptoms. Normally, TPA is

injected into a vein in he arm. The time frame for use can be extended to six hours if it is dripped directly into the blood vessel that is blocked. This is usually performed by an interventional radiologist, and not all hospitals have access to this technology.For posterior circulation strokes that involve the vertebrobasilar system, the time frame for treatment with TPA may be extended even further to 18 hours.Heparin and aspirinDrugs to thin the blood (anticoagulation; for example, heparin) are also sometimes used in treating stroke patients in the hopes of improving the patient's recovery. It is unclear, however, whether the use of anticoagulation improves the outcome from the current stroke or simply helps to prevent subsequent strokes (see below). In certain patients, aspirin given after the onset of a stroke does have a small, but measurable effect on recovery. The treating doctor will determine the medications to be used based upon a patient's specific needs.Managing other Medical ProblemsBlood pressure and cholesterol control are key to prevention of future stroke events. In transient ischemic attacks, the patient may be discharged with medications even if the blood pressure and cholesterol levels are acceptable. In an acute stroke, blood pressure will be tightly controlled to prevent further damage.In patients with diabetes, the blood sugar (glucose) level is often elevated after a stroke. Controlling the glucose level in these patients may minimize the size of a stroke. Finally, oxygen may administered to stroke patients when necessary.RehabilitationWhen a patient is no longer acutely ill after a stroke, the healthcare staff focuses on maximizing the patient's functional abilities. This is most often done in an inpatient rehabilitation hospital or in a special area of a general hospital. Rehabilitation can also take place at a nursing facility. The rehabilitation process can include some or all of the following: 1.speech therapy to relearn talking and swallowing;

2.occupational therapy to regain dexterity in the arms and hands; 3.physical therapy to improve strength and walking; and

4.family education to orient them in caring for their loved one at home and the challenges they will face. 

The goal is for the patient to resume as many, if not all, of their pre-stroke

activities and functions. Since a stroke involves the permanent loss of brain cells, a total return to the patient's pre-stroke status is unfortunately, not a realistic goal in many cases. When a stroke patient is ready to go home, a nurse may come to the home for a period of time until the family is familiar with caring for the patient and the procedures for giving various medications. Physical therapy may continue at home. Eventually, the patient is usually left at home with one or more caregivers, who now find their lives have changed in major ways. Caring for the stroke patient at home may be easy or very nearly impossible. At times, it becomes apparent that the patient must be placed in a board and care home or a skilled nursing facility because adequate care cannot be given at home despite the good intentions of the family. What complications can occur after a stroke?A stroke can become worse despite an early arrival at the hospital and appropriate medical treatment. It is not unusual for a stroke and a heart attack to occur at the same time or in very close proximity to each other. During the acute illness, swallowing may be affected. The weakness that affects the arm, leg, and side of the face can also impact the muscles of swallowing. A stroke that causes slurred speech seems to predispose the patient to abnormal swallowing mechanics. Should food and saliva enter the trachea instead of the esophagus when eating or swallowing, pneumonia or a lung infection can occur. Abnormal swallowing can also occur independently of slurred speech.Because a stroke often results in immobility, blood clots can develop in a leg vein (deep vein thrombosis). This poses a risk for a clot to travel upwards to and lodge in the lungs - a potentially life-threatening situation (pulmonary embolism). There are a number of ways in which the treating physician can help prevent these leg vein clots. Prolonged immobility can also lead to pressure sores (a breakdown of the skin, called decubitus ulcers), which can be prevented by frequent repositioning of the patient by the nurse or other caretakers.Stroke patients often have some problem with depression as part of the recovery process, which needs to be recognized and treated.The prognosis following a stroke is related to the severity of the stroke and how much of the brain has been damaged. Some patients return to a near-normal condition with minimal awkwardness or speech defects. Many stroke patients are left with permanent problems such as hemiplegia (weakness on one side of the body), aphasia (difficulty or the inability to speak), or incontinence of the bowel and/or bladder.A significant number of persons become unconscious and die following a major stroke. If a stroke has been massive or devastating to a person's

ability to think or function, the family is left with some very difficult decisions. In these cases, it is sometimes advisable to limit further medical intervention. It is often appropriate for the doctor and the patient's family to discuss and implement orders to not resuscitate the patient in the case of a cardiac arrest, since the quality of life for the patient would be so poor. In many cases, this decision is made somewhat easier if the patient has made such a request when well. What can be done to prevent a stroke?Risk factor reduction High blood pressure:The possibility of suffering a stroke can be markedly decreased by controlling the risk factors. The most important risk factor for stroke is high blood pressure. When a person's blood pressure is persistently too high, roughly greater than 130/85, the risk of a stroke increases in proportion to the degree by which the blood pressure is elevated. Controlling blood pressure in the normal range decreases the chances of a stroke.Smoking:Another important risk factor is cigarette or other tobacco use. Cigarettes cause the carotid arteries to develop severe atherosclerosis, which can lead to their closure and block the blood flow to the brain. Atherosclerosis in general, including involvement of the arteries that supply blood to the heart, is accelerated by smoking. So, when an individual smokes, the main question becomes - which will occur first; a stroke, heart attack, or lung cancer?Diabetes:Another risk factor for developing a stroke is diabetes mellitus. Diabetes causes the small vessels to close prematurely. When these blood vessels close in the brain, small (lacunar) strokes may occur. Good control of blood sugar is important in decreasing the risk of stroke in diabetic patients. An elevated level of blood cholesterol is also a risk factor for a stroke due to the eventual blockage of blood vessels (atherosclerosis). A healthy diet and medications can help normalize an elevated blood cholesterol level.Blood thinner/warfarin:An irregular heart beat (atrial fibrillation in particular) is associated with an increased risk of an embolic stroke, in which the blood clot travels from the heart, through the bloodstream, and into the brain. Warfarin (Coumadin) is a blood "thinner" that prevents the blood from clotting. This medication is often used in patients with atrial fibrillation to decrease this risk. Warfarin is also sometimes used to prevent the recurrence of a stroke in other situations, such as with certain other heart conditions and conditions in which the blood has a tendency to clot on its own (hypercoagulable states). Patients taking warfarin need to have periodic blood checks to make sure that their current dose is producing the desired effect. Patients on warfarin

also need to know that they are at increased risk for bleeding, either externally or internally.Aspirin and other antiplatelet therapy:Many stroke patients who do not require warfarin can use another class of medicines called "antiplatelet" drugs to reduce their risk of suffering another stroke. These medicines reduce the tendency of the blood to clot (clog) in the arteries. As a side effect, patients on these medicines usually have a higher likelihood of bleeding, but this risk is less than when taking an anticoagulant like warfarin. The most commonly prescribed first-choice antiplatelet agent for preventing a stroke recurrence is aspirin. If the patient has an adverse reaction to aspirin or has a stroke despite being on aspirin, newer antiplatelet preparations can be used [clopidogrel (Plavix), dipyridamole (Persantine).Carotid endarterectomy:In many cases, a person may suffer a TIA or a stroke that is caused by the narrowing or ulceration (sores) of the carotid arteries (the major arteries in the neck that supply blood to the brain). If left untreated, patients with these conditions have a high risk of experiencing a major stroke in the future. An operation that cleans out the carotid artery and restores normal blood flow is known as a carotid endarterectomy. This procedure has been shown to markedly reduce the incidence of a subsequent stroke. In patients who have a narrowed carotid artery, but no symptoms, this operation may be indicated in order to prevent the occurrence of a first stroke. What is in the future for stroke treatment?Currently, studies are being done on additional drugs that dissolve clots. These drugs are administered either in the veins (like TPA) or directly into the clogged artery. The goal of these studies is to determine which stroke patients might benefit from this new and aggressive form of treatment.New medications are also being tested that help slow the degeneration of the nerve cells that are deprived of oxygen during a stroke. These drugs are referred to as "neuroprotective" agents, an example of which is sipatrigine. Another example is chlormethiazole, which works by modifying the expression of genes within the brain. (Genes produce proteins that determine an individual's makeup.)Finally, stem cells, which have the potential to develop into a variety of different organs, are being used to try to replace brain cells damaged by a previous stroke. In many academic medical centers, some of these experimental agents may be offered in the setting of a clinical trial. While new therapies for the treatment of patients after a stroke are on the horizon, they are not yet perfect and may not restore complete function to a stroke

victim. Stroke At A Glance•Stroke is the sudden death of brain cells due to lack of oxygen.

•Stroke is caused by the blockage of blood flow or rupture of an artery to the brain.

•Sudden tingling, weakness, or paralysis on one side of the body or difficulty with balance, speaking, swallowing, or vision can be a symptom of a stroke.

•Any person suspected of having a stroke or TIA should present for emergency care immediately

•Clot-busting drugs like TPA can be used to reverse a stroke, but the time frame for their use is very narrow. Patients need to present for care as soon as possible so that TPA therapy can be considered.

•Stroke prevention involves minimizing risk factors, such as controlling high blood pressure, elevated cholesterol, tobacco abuse, and diabetes.http://www.thestrokefoundation.com/index.php/about-stroke/27-what-is-a-stroke

Stroke factsAlthough stroke is the fifth leading cause of death in America and a leading

cause of adult disability, many myths surround this disease. Test how much

you know about stroke today

MYTH FACTMYTH: Stroke cannot be prevented. FACT: Up to 80 percent of strokes are preventable.

MYTH: There is no treatment for stroke.FACT: At any sign of stroke call 9-1-1- immediately. Treatment may be available.

MYTH: Stroke only affects the elderly. FACT: Stroke can happen to anyone at any time.

MYTH: Stroke happens in the heart. FACT: Stroke is a "brain attack".

MYTH: Stroke recovery only happens for the first few months after a FACT: Stroke recovery is a lifelong process.

stroke.

MYTH: Strokes are rare.FACT: There are nearly 7 million stroke survivors in the U.S. Stroke is the 5th leading cause of death in the U.S.

MYTH: Strokes are not hereditary.FACT: Family history of stroke increases your chance for stroke. 

MYTH: If stroke symptoms go away, you don’t have to see a doctor.FACT: Temporary stroke symptoms are called transient ischemic attacks (TIA). They are warning signs prior to actual stroke and need to be taken seriously.

http://www.stroke.org/understand-stroke/what-stroke/stroke-facts

What function/s of the brain is/are lost?

The brain is an extremely complex organ that controls various body functions. If a stroke occurs and blood flow can't reach the region that controls a particular body function, that part of the body won't work as it should.

If the stroke occurs toward the back of the brain, for instance, it's likely that some disability involving vision will result. The effects of a stroke depend primarily on the location of the obstruction and the extent of brain tissue affected.

Right BrainThe effects of a stroke depend on several factors, including the location of the obstruction and how much brain tissue is affected. However, because one side of the brain controls the opposite side of the body, a stroke affecting one side will result in neurological complications on the side of the body it affects. For example, if the stroke occurs in the brain's right side, the left side of the body (and the left side of the face) will be affected, which could produce any or all of the following:

Paralysis on the left side of the body    Vision problems    Quick, inquisitive behavioral style    Memory loss

Left BrainIf the stroke occurs in the left side of the brain, the right side of the body will be affected, producing some or all of the following:

Paralysis on the right side of the body    Speech/language problems    Slow, cautious behavioral style    Memory loss

Brain StemWhen stroke occurs in the brain stem, depending on the severity of the injury, it can affect both sides of the body and may leave someone in a ‘locked-in’ state. When a locked-in state occurs, the patient is generally unable to speak or achieve any movement below the neck.

http://www.strokeassociation.org/STROKEORG/AboutStroke/EffectsofStroke/Effects-of-Stroke_UCM_308534_SubHomePage.jsp

How will the lost of blood supply be clinically manifested? (Clinical history and physical examination, neurologic examination findings)

Stroke Assessment Scales Overview

Taken from “Post-Stroke Rehabilitation: Assessment, Referral, and Patient Management Quick

Reference Guide Number 16″ published by the US Agency for Health Care Policy and Research.

TYPE NAME AND SOURCE

APPROXIMAT

E T IME TO

ADMIN ISTER STRENGTHS

WEAKNESSE

S

Level-of-consciousness scale Glasgow Coma Scale [a] 2 minutes

Simple, valid, reliable.

None observed.

Stroke deficit scales

NIH Stroke Scale [b] 2 minutes

Brief, reliable, can be administered by non-neurologists.

Low sensitivity.

Canadian Neurological Scale [c] 5 minutesBrief, valid, reliable.

Some useful measures omitted.

Global disability scale Rankin Scale [d, e] 5 minutes

Good for overall assessment of disability.

Walking is the only explicit assessment criterion. Low sensitivity.

Measures of disability/activities of dailyliving (ADL)

Barthel Index [f] 5-10 minutes

Widely used for stroke. Excellent validity and reliability.

Low sensitivity for high-level functioning.

Functional Independence Measure

40 minutes Widely used for stroke. 

“Ceiling” and “floor”

(FIM) [g]

Measuresmobility, ADL, cognition, functional communication. effects.

Mental status screening

Folstein Mini-Mental State Examination [h] 10 minutes

Widely used for screening.

Several functions with summed score. Maymisclassify patients with aphasia.

NeurobehavioralCognition Status Exam (NCSE) [i] 10 minutes

Predicts gainin Barthel Index scores.  Unrelated to age.

Does not distinguishright from left hemisphere. No reliability studies in stroke.No studies of factorial structure. Correlates with  education.

Assessment of motor function

Fugl-Meyer [j]30-40 minutes

Extensively evaluated measure. Good validity and reliabilityfor assessing sensorimotor function and balance.

Considered too complex and time-consuming by many.

Motor Assessment Scale [k] 15 minutes Good, brief assessment of movementand physical

Reliability assessed only in stablepatients.

mobility.Sensitivity not tested.

Motricity Index [l] 5 minutes

Brief assessment of motor functionof arm, leg, and trunk.

Sensitivity not tested.

Balance assessment Berg Balance Assessment [m] 10 minutes

Simple, well established with stroke patients,sensitive to change.

None observed.

Mobility assessment Rivermead Mobility Index [n] 5 minutes

Valid, brief, reliable test of physical mobility.

Sensitivity not tested.

Assessment of speech andlanguage functions

Boston DiagnosticAphasia Examination [o] 1-4 hours

Widely used, comprehensive,good  standardization data, sound theoretical rationale.

Time to administerlong; half of patients cannot be classified.

Porch Index ofCommunicative Ability (PICA) [p] 1/2-2 hours

Widely used, comprehensive,careful test development and standardization.

Time to administerlong. Special training required to administer. Inadequate samplingof language other than one word and single sentences.

Western aphasiaBattery [q]

1-4 hours Widely used, comprehensi

Time to administer

ve.

long. “Aphasia quotients” and “taxonomy”of aphasia not well validated.

Depression scales

Beck Depression Inventory (BDI) (BDI) [r] 10 minutes

Widely used, easily administered. Norms available.  Goodwith somatic symptoms.

Less useful in elderly and in patients with aphasia or neglect.Highrate of false positives.  Somatic items may not be dueto depression.

Center for Epidemiologic StudiesDepression (CES-D) [s]

< 15 minutes

Brief, easily administered, usefulin elderly, effective for screening in stroke population.

Not appropriate for aphasic patients.

Geriatric Depression Scale (GDS)[t] 10 minutes

Brief, easy to use with elderly,cognitively impaired, and those with visual or physical problemsor low motivation.

High false negative rates in minordepression.

Hamilton Depression Scale [u] < 30 minutes

Observer rated; frequently used

Multiple differing versions compromise

in stroke patients.

interobserver reliability.

Measures of instrumentalADL

PGC Instrumental Activities of Daily Living[v] 5-10 minutes

Measures broad base of information necessaryfor independent living.

Has not been tested in stroke patients.

Frenchay ActivitiesIndex [w]

10-15 minutes

Developed specificallyfor  stroke patients; assesses broad array of activities.

Sensitivity andinterobserver reliability not tested; sensitivity probably limited.

Family assessment

Family Assessment Device (FAD) [x] 30 minutes

Widely used in stroke. Computer scoring available. Excellentvalidity and reliability. Available in multiple languages.

Assessment subjective; sensitivity not tested; “ceiling”and “floor” effects.

Health status/ quality oflife measures

Medical Outcomes Study (MOS) 36-Item Short-FormHealth Survey [y]

10-15 minutes

Generic health status scale SF36 is improvedversion of SF20. Brief, can be self – administered or administeredby phone or interview. Widely used in the United States.

Possible “floor” effect in seriouslyill patients (especially for physical functioning), suggestsit should be supplemented by an ADL scale in  stroke patients.

Sickness ImpactProfile (SIP) [z]

20-30 minutes

Comprehensiveand well-evaluated. Broad range of items reduces “floor”or “ceiling” effects.

Time to administersomewhat long. Evaluates behavior rather than subjective health;needs questions on well-being, happiness, and satisfaction.

http://www.strokecenter.org/professionals/stroke-diagnosis/stroke-assessment-scales-overview/

Stroke Syndromes

Middle Cerebral Artery

Ataxic Hemiparesis Gerstmann Syndrome (Gerstmann Syndrome) Middle Cerebral Artery - Inferior Division Middle Aerebral Artery - Superior Division

Posterior Cerebral Artery

Alexia without Agraphia Balint Syndrome (Balint Syndrome) Claude Syndrome Cortical Blindness (Anton Syndome) Posterior Cerebral Artery - Unilateral Occipital Thalamic Pain Syndrome (Dejerine-Roussy Syndrome) Weber Syndrome (Weber Syndrome)

Anterior Inferior Cerebellar Artery

Lateral Pontine Syndrome (Marie-Foix Syndrome) Posterior Inferior Cerebellar Artery

Lateral Medullary Syndrome (Wallenberg Syndrome) Basilar Artery

Ataxic Hemiparesis

ANATOMY

Cerebral hemisphere: Posterior limb of external capsule, Pons: Basis pontis

VASCULAR

Middle cerebral artery: Small penetrating arteries

Basilar artery: Small penetrating arteries

Signs & Symptoms

S IDE MANIFESTAT ION COMMENTS

Contralateral Weakness – upper and lower extremity  

Contralateral Ataxia – arm and leg  

Notes

Weakness usually more prominent in leg than arm; extensor plantar response; no facial involvement or

dysarthria. Other locations include thalamocapsular lesions, red nucleus, anterior cerebral artery

distribution. Also called “homolateral ataxia and crural paresis.”

Cortical Blindness (Anton Syndome)

EPONYM

Anton Syndome

ANATOMY

Cerebral hemisphere: Bilateral occipital lobes

VASCULAR

Posterior cerebral artery: Bilateral

Basilar artery: Top of the basilar

Signs & Symptoms

S IDE MANIFESTAT ION COMMENTS

Both Visual loss – bilateral

Both Unawareness or denial of blindness

Inferior Medial Pontine Syndrome (Foville Syndrome)

Lateral Pontine Syndrome (Marie-Foix Syndrome) Locked-in Syndrome Medial Medullary Syndrome (Dejerine Syndrome) Ventral Pontine Syndrome (Raymond Syndrome) Ventral Pontine Syndrome (Millard-Gubler Syndrome)

Vertebral Artery

Lateral Medullary Syndrome (Wallenberg Syndrome) Medial Medullary Syndrome (Dejerine Syndrome)

Anterior Spinal Artery

Medial Sedullary Syndrome (Dejerine Syndrome)

About Magnetic Resonance Imaging

MRI provides a wealth of structural and biochemical

information about tissue (Hilal SK, Mohr JP, 1992. Dunbabin DW, Sandercock PAG, 1991.

Caplan LR. Stroke: a Clinical Approach. Boston, Butterworth-Heinemann, 1993, pp 99-150].

The technique is based on the interaction between radio frequency waves and the nuclei of

different atoms in the body in the presence of a strong magnetic field. Hydrogen (proton) is

the most common nuclear magnetic resonance-observable nucleus within the human body.

Clinically, water protons and fat protons are the most extensively imaged nuclei.

In the presence of the powerful magnetic field, the protons are susceptible to excitation by

selective radio frequency pulses. The energy from these pulses is absorbed and then

released until the tissue being scanned has completely reemitted the energy absorbed and

has undergone complete relaxation. The energy released from the excited tissue occurs

over a short period of time according to two relaxation constants known as T1 and T2. In T1-

weighted images, cerebrospinal fluid has a low-density relative to brain, while the fat has a

high-signal intensity. In T2-weighted images, cerebrospinal fluid has an increased signal

relative to brain, and fat has almost no signal.

Conventional MRI shows tomographic sections of the brain in multiple plans of proton

distribution modified by T1 and T2 relaxation times as well by a third type of image with a

balanced T1-and T2-weighting.

Ischemia alters water content in the brain cells, changing their response to a magnetic field.

Infarction prolongs the T1 and T2 relaxation films. Intracerebral hemorrhage (ICH) has

different appearances that are complex and depend on the duration of time since the bleed,

the strength of the magnetic field, and the settings used to obtain the images [Bruno A.

Geriatrics. 1993; 48;26].

MRI Compared to CT

This patient’s imaging studies show evolution of a left cerebral artery infarct on CT scan and

MRI.

Computed tomography of the head done 1/7/97 shows a hyperacute infarct, which is seen

only by the effacement of the cerebral sulci in the left parietal region and suggestion of loss

of grey/white distinction.

T2- weighted MRI scan shows no obvious signal abnormality.

Contrast-enhanced T1-weighted image shows slightly prominent intravascular contrast

enhancement within the branches of the left middle cerebral artery. Otherwise, the T1-

weighted images show no obvious abnormality.

One month later, on 2/7/97, the T2-weighted images show a typical wedge-shaped infarct in

the distribution of the left middle cerebral artery.

A contrast-enhanced T1-weighted image shows asymmetric intravascular contrast

enhancement. However, there is minimal parenchymal contrast enhancement of the wedge-

shaped left middle cerebral artery infarct in the left parietal lobe.

Non-contrast computed tomography of the head shows a hypodense left middle cerebral

artery distribution infarct involving the left parietal lobe. Minimal contrast enhancement is

seen.

Lateral radiograph of the left carotid angiogram shows complete occlusion of the left internal

carotid artery with minimal collateral flow via external carotid branches.

Frontal radiograph of the left carotid angiogram shows complete occlusion of the left internal

carotid artery with minimal collateral flow via external carotid branches.

On 2/20/97, sagittal T1-weighted images show marked contrast enhancement of the left

parietal infarct following contrast administration. The images also show enhancement in the

occipital and temporal lobes.

Axial T2-weighted images now show minimal signal changes with linear T2-hypointensity in

the gyri in the left parietal lobe, indicating minimal hemorrhagic component, but most of the

signal changes of T2-weighted images have resolved. Note high signal in the cavernous

carotid artery on the lowest slice, indicative of carotid occlusion.

Cerebral Angiography

Cerebral angiography is an invasive test that involves the injection of contrast media into the carotid

artery by means of a catheter. Radiographs are taken as the dye works its way through the cerebral

circulation. Angiography may be utilized to identify bleeding aneurysms, vasospasm, and

arteriovenous malformations, and to differentiate embolism from large artery thrombosis [Adams HP,

et al, 1994. Mohr JP, 1992]. Cerebral angiography provides information on both arteries and veins, with

sequential images showing arterial, capillary, and venous phases.

Click Image to Enlarge

The role of conventional angiography in the management of acute stroke is controversial. The test

itself is associated with a risk of stroke, since the catheter carrying the dye might dislodge plaque from

the carotid wall. In addition, patients may be allergic to the contrast dye, and the dye has been

associated with the development of renal failure, particularly when pre-existing kidney disease is

present. Presently, angiography is performed mainly in selected patients, especially those in whom

surgery (such as carotid endarterectomy or craniotomy for ruptured aneurysms or arteriovenous

malformations) is considered.

Click Image to Enlarge

Conventional angiography has been replaced by magnetic resonance angiography (MRA) in some

patients with cerebrovascular disease [Bruno A, 1993]. A noninvasive test, MRA permits the

visualization of blood flow in vessels without the need for catheters or contrast agents. The technology

can yield information regarding collateral blood flow and is nearly as effective as conventional

angiography in estimating disease at the carotid bifurcation.

This left common carotid angiogram shows complete occlusion of the left middle cerebral artery distal

to the origin of the anterior temporal branch.

Positron Emission Tomography

Click Image to Enlarge

These are PET glucose metabolic images (shown on the right) compared with X-ray computed

tomography (shown on the left) of a patient with aphasia. The studies were performed at two months

and four years following left hemisphere cerebral hemorrhage. Note that for both time frames, the

extent of cerebral hypometabolism (less black) is much greater than the actual lesion or residual

cavity (at late time). These studies demonstrate that the functional abnormality demonstrated with

PET typically exceeds that seen with structural imaging techniques such as X-ray, CT, or MRI and is a

more representative depiction of the underlying functional state of the brain and the resultant

abnormal behaviors it produces. [Metter EJ, et al. Arch Neurol. 1980;47:1235-38.]

Can the brain recover after a stroke? Through what mechanisms will brain cells regenerate?

Brain Plasticity

Brain plasticity, also known as neuroplasticity, suggests that the location of a given function in the brain (for example, speech) can move to another area of the brain. This transfer can be activated by repetitive learning.

In the case of stroke, brain plasticity refers to healthy brain cells taking over the functions of damaged brain cells.

This means that certain lost functions, such as speech and language, may reemerge as the result of intensive rehabilitation. 

Brian Plasticity and Stroke

Stroke can cause damage to parts of the brain responsible for thinking, learning, awareness, judgement, and problem solving.

Stroke survivors with thinking deficits may demonstrate:

Reduced concentration ability or lack of concentration

Processing new information slower

Trouble learning new tasks

Problems comprehending meaning

An inability to make plans

Very short attention spans

Deficits in short-term memory

Difficulty engaging in complex mental activities

All of these ailments are treated through speech and language therapy. Improvements in communication skills are commonly achieved through brain plasticity and intensive therapy (practicing on a daily basis).

How does Brain Plasticity Work?

After a stroke, how does the brain reorganize itself?

The answer to this question is not fully understood, although researchers have now found that adult brain cells can reorganize themslves following damage. 

The ability of nerve cells to respond in this way is called   plasticity.  

Plasticity refers to the brain's ability to repair and reorganize cells. This means having healthy cells of the brain taking over jobs that were previously carried out by brain cells which were destroyed.

This is done by sprouting of new synaptic connections and creating new pathways to unaffected parts of the brain.

The brain's plasticity appears to be greatest when we are young. You can probably recall how much easier it was to learn complex material, such as a foreign language or a musical instrument, when you were younger.

Of course our ability to learn new skills continues as we become adults. This indicates that the brain retains a certain level of plasticity throughout our lives.

However, the capability and speed of learning is likely to lessen as we age. In spite of this tendency, the brain can still assign learning to new, healthy areas of itself.

In other words, when neurons, the primary cells of the nervous system, are damaged by a stroke or brain injury, other neurons take over for them. This adaptive behavior allows us to reorganize the brain in an effort to recover lost skills.

Brain plasticity is why intensive therapy is such a critical element of stroke recovery.

During the time of natural recovery it's extremely beneficial to challenge your physical, and mental abilities. By doing so you are initiating changes within the brain that can lead to new areas taking over for damaged ones.

This is the reason why speech therapy, physical therapy, and occupational therapy are so important to a stroke patient. These activities can accelerate and enhance the stroke recovery process.

Discover how your highest potential can be realized! 

Forge New Pathways to Healthy Areas of the Brain

In order for new pathways to be formed, neurons must be stimulated. You can activate this growth by exercising your brain.

You exercised your brain throughout life as you learned new skills. Stroke recovery is no different. In order to relearn your speech and language skills you'll have to practice.

"Now an enormous amount of evidence uncovered in the past two decades finds that the brain never stops changing and adjusting.One line of research is showing that this flexibility can help maintain language processing even in the face of severe obstacles. 

Take advantage of your brain's flexibility by practicing your speech and language skills on a daily basis.

This is achieved by daily practice of:

Therapeutic Speech Exercises

Oral Motor Therapy

Therapeutic Language Activities

Word finding Strategies

The length and frequency of quality treatment absolutely makes a difference.

http://www.speech-therapy-on-video.com/brainplasticity.html

Name the three most important lessons you learned from the symposium?

Overview

Think of a stroke as a "brain attack" - it is an emergency! Because a stroke can damage brain tissue,

every minute counts. When symptoms appear call 911 immediately. 

A stroke occurs when the brain is deprived of the oxygen it needs due to an interruption of its blood

supply. Without oxygen brain cells die. The oxygen deprived area of brain tissue is called an infarct.

Depending on what area of the brain has been affected, a stroke can cause problems with speech,

behavior, thought patterns and memory, and may result in permanent brain damage, disability or death.

Blood supply of the brain

To understand stroke, it is helpful to understand the circulatory system of the brain (see Anatomy of the

Brain). Blood is carried to the brain by two paired arteries, the internal carotid arteries and the vertebral

arteries (Fig. 1). The internal carotid arteries supply the anterior (front) areas and the vertebral arteries

supply the posterior (back) areas of the brain. After passing through the skull, the right and left vertebral

arteries join together to form a single basilar artery. The basilar artery and the internal carotid arteries

“communicate” with each other in a ring at the base of the brain called the Circle of Willis. The middle

cerebral artery is the artery most often occluded in stroke.

Figure 1. Blood supply of the brain. Each artery supplies a specific area of the brain. Some areas are supplied by more than one artery.

What is a stroke?

Stroke is a sudden interruption of the blood supply to the brain. Most strokes are caused by an abrupt

blockage of an artery (ischemic stroke). Other strokes are caused by bleeding into brain tissue when a

blood vessel bursts (hemorrhagic stroke). The effects of a stroke depend on the severity and which area

of the brain is injured. Strokes may cause sudden weakness, loss of sensation, or difficulty with speaking,

seeing, or walking. Since different parts of the brain control different areas and functions, it is usually the

area immediately surrounding the stroke that is affected. Hemorrhagic strokes have a much higher death

rate than ischemic strokes.

Ischemic stroke - (most common - 83% of cases) is caused by a blockage of an artery from a blood clot

(thrombus) or from clogged blood vessels due to atherosclerosis (hardening of the arteries). In

atherosclerosis, cholesterol plaques are deposited within the walls of the arteries, narrowing the inside

diameter of the artery. As the artery narrows, less blood is able to pass to the brain and blood pressure

increases to meet the demands of the body. The normally smooth inner wall of the artery is now roughed

with plaque deposits causing blood cells to build up and form clots - called a thrombus (Fig. 2). Thrombus

build up usually occurs on large blood vessels of the neck and base of the brain.

Figure 2. An ischemic stroke is caused by a blocked artery to the brain either from the build-up of plaques within the artery wall or from a clot.

Embolic stroke - is caused when a clot breaks off from the artery wall it becomes an embolus, which can

travel farther down the bloodstream to block a smaller artery. Emboli usually come from the heart, where

different diseases cause clot formation.

Hemorrhagic stroke - (less common - 17% of cases) is caused by rupture or leaking of an artery either

within or around the brain. It can occur when a weakened blood vessel ruptures releasing blood into the

space surrounding the brain - this is called a subarachnoid hemorrhage (SAH). It can be caused by a

ruptured aneurysm (Fig. 3), arteriovenous malformation (AVM), or head trauma.

Figure 3. A hemorrhagic stroke can be caused by a ruptured aneurysm. Reduced bloodflow to brain tissue causes an infarct. As blood fills the spaces within the brain, a hematoma, or blood

clot, forms causing increased pressure on the brain.

Bleeding within the brain tissue itself is known as an intracerebral hemorrhage  (ICH) and is primarily

caused by hypertension (Fig. 4). Hypertension is an elevation of blood pressure which may cause tiny

arteries to burst inside the brain. 

Figure 4. A hemorrhagic stroke can be caused by rupture of tiny arteries within the brain tissue (intracerebral hemorrhage). As blood collects, a hematoma or blood clot forms causing increased

pressure on the brain. Hypertension is the leading cause of ICH.

What are the symptoms?

Stroke symptoms may occur alone or in combination and may last a few minutes or several hours. If you

or someone around you notice one or more of these warning signs, seek immediate medical attention.

Poor public knowledge of stroke warning signs and risk factors limits effective stroke intervention and

prevention [1]. Even if stroke symptoms disappear, they are a clear warning that a larger stroke may

follow.  

Sudden weakness or numbness of the face, arm or leg, usually on one side of the body  Difficulty speaking or understanding language  Decreased or blurred vision in one or both eyes  Sudden, severe headaches  Unexplained loss of balance or dizziness 

Transient Ischemic Attacks (TIAs)

Sometimes strokes are preceded by mini-strokes, called transient ischemic attacks (TIAs), that last

anywhere from a few minutes to several hours. TIAs result when blood flow to the brain is temporarily

interrupted and then restored. The symptoms resolve completely and the person returns to normal. TIAs

should not be ignored - they are an important warning sign. It is possible to have several TIAs before a

larger stroke occurs.

Who is affected?

Stroke is the third leading cause of death in the United States after diseases of the heart and all forms of

cancer. About 600,000 Americans have strokes each year. Someone has a stroke every 53 seconds.

Someone dies of a stroke every 3.3 minutes.

Risk factors you can't modify 

Age - as a person ages, the chance of stroke increases.  Gender - men are more likely than women to experience a stroke.  Race - African Americans face twice the risk of stroke as the Caucasian population. 

Risk factors you can modify

High blood pressure - the most dominant stroke risk factor and the easiest to modify is high blood pressure, or hypertension. Have your blood pressure checked regularly and keep it under control. 

Smoking - doubles your stroke risk. If you smoke, stop. 

Weight - Being over-weight predisposes you to high cholesterol, high blood pressure and diabetes, all of which increase stroke risk. If you are over weight, modify your diet and limit your intake of fatty foods. 

Diabetes - makes people susceptible to cardiovascular diseases, which can result in stroke. If you have diabetes, keep it well controlled. 

Prior stroke or TIA - increases your risk of having another stroke. Certain medications may decrease stroke risk if taken regularly. 

Heart disease - heart conditions, especially atrial fibrillation (an irregular heart beat), have a greater stroke risk. Certain medications may decrease the risk if taken regularly.

To learn your risk of experiencing a stroke in the next ten years take the Stroke Risk Assessment. Within

seconds you will receive a report of your stroke risk compared to the average stroke risk for Americans of

the same age and sex. The results are not meant to predict whether or not you will suffer a stroke, but to

assist you in assessing your risk of having a stroke. This assessment should accompany, not replace, a

routine physical examination by your family physician.

How is a diagnosis made?

When you or a loved one is brought to the emergency room with a stroke, the doctor will learn as much

about your symptoms, current and previous medical problems, current medications, family history, and

perform a physical exam. If you can't communicate, a family member or friend will be asked to provide

this information. Diagnostic tests are used to help the doctors determine whether they need to unblock a

clogged artery (in ischemic stroke) or stop the bleeding (in hemorrhagic stroke).

Lumbar puncture is an invasive procedure in which a hollow needle is inserted into the subarachnoid

space of the spinal canal to detect blood in the cerebrospinal fluid (CSF). If a hemorrhagic stroke is

suspected, the doctor may perform a lumbar puncture.

Computed Tomography (CT) scan is performed for both ischemic and hemorrhagic strokes. CT is a

safe, noninvasive X-ray to review the anatomical structures within the brain to see if there is any bleeding

in or around the brain. A newer technology called CT angiography involves the injection of contrast into

the blood stream to view the arteries of the brain and find blockages.

Angiogram is an invasive procedure in which a catheter is inserted into an artery and passed through the

blood vessels to the brain. Once the catheter is in place, contrast dye is injected into the bloodstream and

X-ray images are taken. This test is used to diagnose and determine the location of aneurysms and

AVMs.

Magnetic resonance imaging (MRI) scan is a noninvasive test that uses a magnetic field and

radiofrequency waves to give a detailed view of the soft tissues of your brain. An MRA (Magnetic

Resonance Angiogram) is the same non-invasive study, except it is also an angiogram, which means it

also examines the blood vessels, as well as the structures of the brain.

What treatments are available?

For many years, there was little hope for those suffering an ischemic stroke. However, recent

breakthroughs have led to new treatments that restore blood flow to the brain. Thus, reducing secondary

damage in the area surrounding the infarct, called the penumbra. In contrast, treatment for those suffering

a hemorrhagic stroke focuses on stopping the bleeding. In either case the person must get to a hospital

immediately for the treatments to work.

Ischemic stroke treatments

Clot buster drugs (t-PA) Blood thinners (anticoagulants) Angioplasty/stents Carotid endarterectomy

Hemorrhagic stroke treatments

see Subarachnoid hemorrhage (SAH) see Intracerebral hemorrhage  (ICH)

Clot buster drugs

Thrombolytic "clot-buster" drugs help restore blood flow by dissolving the clot blocking the artery. The

most common "clot-buster" drug is tissue plasminogen activator, or t-PA for short. T-PA is an enzyme

found naturally in the body that dissolves clots. Doctors inject extra t-PA into your blood stream to speed

up this process. To be effective, t-PA (Activase) should be given as quickly as possible. Patients who

received t-PA within 3 hours of onset of stroke symptoms were at least 33% more likely to recover from

their stroke with little or no disability after 3 months [2,3].

T-PA can also be delivered right at the clot site in a procedure called intra-arterial thrombolysis. In this

method the t-PA drug doesn’t have to travel through your entire body before reaching the clot. A doctor

called a Neuro Interventionalist performs this procedure during an angiogram. A very small catheter is

inserted into an artery in your groin and guided through your bloodstream up to the brain where the clot is

located. The t-PA drug is then released to dissolve the clot. The doctor also pushes the catheter back and

forth through the clot to help break it up. Typically this treatment option is only available at specialized

stroke care centers.

Blood thinners

Anticoagulants, or “blood thinners”, such as warfarin and antiplatelet agents such as aspirin, ticlopidine,

diprydamole, or clopidogrel interfere with the blood's ability to clot and can play an important role in

preventing stroke.

Angioplasty 

Angioplasty is used to open blood vessels narrowed or blocked by plaque build-up in atherosclerosis. A

Neuro Interventionalist performs the procedure during an angiogram. A catheter is inserted into an artery

in the groin and then passed through the blood vessels to the plaque build-up. The doctor guides the

catheter through the bloodstream while watching a fluoroscopy (a type of x-ray) monitor. Once positioned

correctly, a balloon is inflated to flatten the plaques against the wall and open the artery to restore blood

flow.

Carotid endarterectomy

Sometimes plaque build-up is too great to treat with angioplasty and the plaque must be removed through

surgery. A common area for build-up of plaques is at the common carotid arteries in the neck where the

internal and external carotid arteries branch. If the carotid artery is more than 70% blocked, a surgical

procedure called an endarterectomy may reduce your risk of stroke by 65% [4]. Through an incision in

your neck the carotid artery is opened and the plaque removed to restore blood flow.

Recovery

Each person's mental and physical deficits are unique. For example, someone who has a small stroke

may experience only minor deficits such as weakness of an arm or leg. On the other hand, someone who

has a larger stroke may be left paralyzed on one side or lose his/her ability to speak and process

language. Some of these deficits may disappear over time with healing and therapy. The recovery

process is long and may take weeks, months, or years to understand the level of deficits you incurred and

regain function. Rehabilitation professionals can help set up a treatment plan and help others understand

the stroke person's needs and help with daily living activities.

Aphasia is a total or partial loss of the ability to understand or use words. Caused by damage to the brain's language center, some people quickly and completely recover from aphasia after a stroke. Others may have permanent speech and language problems. Speech problems can range from trouble finding words to being unable to speak. Some people have problems understanding what others are saying or have trouble with reading, writing or math. In other cases, someone with aphasia may have trouble talking but can understand what others say.

Apraxia is the inability to control your muscles making movement uncoordinated and jerky. Dysarthria is a loss of control over muscles in the face and mouth. Their voice may sound

slurred, muffled, or hoarse. The mouth may droop on one side of face due to muscle weakness. Exercises can strengthen these muscles.

Dysphagia is difficulty swallowing making eating and drinking a challenge and choking a danger. Tongue and lip exercises can help regain control.

Paralysis is a loss of muscle function and sensation in an area of the body. Hemiparesis is a weakness of muscles on one side of the body. Improving posture, range of

motion, and strength can help regain control. Hemianopia is the loss of sight in half of visual field.

Preventing another stroke

The link between cardiovascular health and stroke is inseparable. Of the 700,000 people who suffer a

stroke each year, about 200,000 are recurrent attacks.

1. Take your medication every day as directed. Your medication helps to thin your blood and prevent clots.

2. Eat a healthy diet of foods low in fat, cholesterol, and salt.3. Control your blood pressure.4. Quit smoking.5. Exercise regularly. You’ll feel good about yourself, alleviate depression, and build muscle

strength.6. Get enough sleep and reduce stress.7. Limit your use of alcohol. It can be risky to drink alcohol if you take certain medications. Talk

to your doctor.8. Talk about your feelings. Sudden mood swings and depression are common and lessen with

time. A support group or counselor can help you and your family.

Clinical trials

Clinical trials are research studies in which new treatments—drugs, diagnostics, procedures, and other

therapies—are tested in people to see if they are safe and effective. Research is always being conducted

to improve the standard of medical care. Information about current clinical trials, including eligibility,

protocol, and locations, are found on the Web. Studies can be sponsored by the National Institutes of

Health (see clinicaltrials.gov) as well as private industry and pharmaceutical companies

(see www.centerwatch.com).

http://www.mayfieldclinic.com/pe-stroke.htm#.VgmIaHFViko

Brain healingFrom Wikipedia, the free encyclopedia

This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (October 2013)

Brain healing is the process that occurs after the brain has been damaged. If an individual survives brain damage, the brain has a remarkable ability to adapt. When cells in the brain are damaged and die, for instance by stroke, there will be no repair or scar formation for those cells. The brain tissue will undergo liquefactive necrosis, and a rim of gliosis will form around the damaged area.

Contents

  [hide] 

1   Scar formation 2   Formation of a glial membrane 3   Functional recovery 4   References

Scar formation[edit]

Apart from a small amount in the blood vessels, there are no fibroblasts in the brain. A scar is formed by fibroblasts producing collagen to repair an area, which will later contract. If scars did form in the brain, the contraction would cause even more damage.

Formation of a glial membrane[edit]

Around the edge of necrosis, astrocytes proliferate. These cells extend processes, and form a delicate rim of gliosis around the margin of damage. The empty space left by brain tissue fills up with cerebrospinal fluid.

Functional recovery[edit]

Brain injury will commonly be accompanied by acute swelling, which impairs function in brain tissue that remains alive. Resolution of swelling is an important factor for the individual's function to improve. The greatest factor in functional recovery after brain injury comes from the brain's ability to learn, called neuroplasticity. After injury, neuroplasticity allows intact areas of the brain to adapt and attempt to compensate for damaged parts of the brain. Although axons and theperipheral nervous system in the developing brain can regenerate, they cannot in the adult brain. This is partly because of factors produced by cells in the brain that inhibit this regeneration. Dendrites, however, will develop from intact axons, as part of the neuroplasticity process. After severe brain injury, improvement in function related to neuroplasticity is unlikely to occur without help from health professionals skilled in rehabilitation. Recent studies have found collagen is extensively distributed throughout the brain and may be essential in protecting the brain against degeneration such as that in Alzheimers[1][2]

Regeneration and repair after stroke

Following stroke, the neuronal circuitries that support

cognitive and sensory-motor functions are lost due to

neuronal death and dysfunction. Still, over a 3 to 6

months period, stroke patients regain some

neurological functions, albeit a majority remain

disabled to a significant degree (Duncan et al.,

2000). In man, recovery processes primarily engage

ipsilateral brain regions, and if damage is severe,

contralateral brain areas are involved as well (Ward,

2005). Recovery of function following transient MCAO

in the rat is complex, but it is clear that the

contralateral hemisphere is involved (Kim et al.,

2005, Biernaskie, et al., 2005).

From experimental studies it is evident that within hours after ischemia regenerative mechanisms are

activated in the brain and develop along with tissue demise (Liu et al., 2007; Rickhag et al, 2006). In

later stages, tissue edema is resolved, inflammation ceases, injured neurons are partially repaired,

neuronal pathways activated, and glia cells and neuroblasts migrate into peri-infarct areas. In surviving

tissue, growth-promoting as well as growth-inhibitory genes are activated (Kury et al., 2004;

Carmichael et al., 2005). Still, recovery is limited because of the restricted capacity for anatomical

reorganization of the brain. During the first four weeks of recovery after experimental stroke axonal

sprouting and spine growth is stimulated and some neuroblasts resume a neuronal phenotype,

accompanied by angiogenesis in the peri-infarct areas. The established novel neural networks are

stabilized by an experience-driven process. Hence, spontaneous functional recovery appears to involve

four distinct phases of cellular response that will be addressed in this application: (1) reactivation of

existing neural pathways, (2) activation of alternative existing pathways (3) formation of new

connections by axonal sprouting or neurogenesis and (4) consolidation of new neural networks

(Wieloch and Nikolich, 2006).

During recent years novel therapies that enhance recovery of function during the first month following

stroke have been proposed, including measures to activate brain plasticity, attenuate axonal growth

inhibition, and cortical stimulation and physical therapy. In the experimental setting, changing housing

environment or training is a strong stimulus of recovery of function. Housing injured animals in an

enriched environment (EE), starting 2-5 days after stroke stimulate functional recovery (Johansson,

2004), activates specific gene programs (Keyvani et al., 2004), enhances dendritic arborization and

spine density on the contralateral pyramidal neurons, (Johansson, 2004), and activates cell genesis

(Matsumori et al., 2005; Komitova et al., 2006). The relative importance of the different mechanisms

for recovery of function will be studied within the frame of the application.

Growth factors such as FGF, EPO and G-CSF also promote functional recovery. Erythropoietin enhances

motor skill when administered for 7 days starting 24 h after stroke (Wang et al., 2004), and similar

observations were seen following treatment with G-CSF (Shyu et al., 2004, Schneider et al., 2005) as

well as after heparin-binding epidermal growth factor-like growth factor delivered by adenoviral vector

(Sugiuras et al., 2004). Also, statins, when administered one day after injury, enhance functional

recovery (Chen et al., 2003). The mechanisms of the recovery-promoting properties of EFO and G-CSF

will be studied by the ESN consortium.

Certain motor skills recover within a few days after the lesion, suggesting that for such rapid recovery

of neuronal function the unmasking or activation of silent pathways or silent synapses must be

considered (Metz et al., 2005). At the cellular level, adaptive changes in neuronal morphology (axonal

growth, dendritic arborization, and spine remodeling) are seen in the contralateral cortex (Schallert et

al., 2000). These most certainly involve recovery of spine function, since ischemia causes spine

collapse and actin aggregation (Hasbani et al., 2001; Gisselsson et al., 2005). Axonal outgrowth is

limited by growth-inhibitors such as Nogo A (Buchli and Schwab; 2005). This inhibition can be

overcome by Nogo A antibodies (Seymour at al., 2005) or by blocking peptides or mutations (Lee et al.,

2004). Intrathecal delivery of Nogo A antibody for one month, starting as late as seven days after

ischemia, dramatically enhances functional recovery after stroke (Seymour at al., 2005), and is

associated with increased sprouting of cortico-rubral projections. The contribution of the individual

hemispheres for the recovery process will be explored within this project.

Cell genesis in neurogenic zones is stimulated following stroke (Arvidsson et al., 2002; Parent et al.,

2002). Neuroblasts are continuously generated up to 4 month after injury, providing a pool of cells that

potentially can develop into mature neurons (Thored et al., 2005). Neurogenesis is depressed by

inflammation occurring during recovery after stroke (Jakubs et al., 2007). Neuronal, glial, and

endothelial progenitor cells support plasticity of surviving neurons by releasing growth factors, or

providing cellular components (Zhang et al., 2005; Lu et al., 2003). In addition, angiogenesis is

prominent and may enhance vascularization of the surviving penumbra area as well as stimulating

neurogenesis (Busch et al., 2003).

http://www.europeanstrokenetwork.eu/index.php?option=com_content&view=article&id=38&Itemid=47

Rewiring Brains: Rehabilitation, Plasticity and TransplantsEach day we listen to new predictions about how the events of today or the future will cause the world to implode.  But, let’s assume we will once again navigate our way through these disastrous mine fields.  As we enter the second

decade of the new millennium will we not only be traveling to new destinations in space, but also repairing and rewiring human brains?  These are exciting times for patients with disabilities, as we perform experiments using stem cells and engineered nervous system cells.   Will we cure currently incurable diseases?  Will patients walk again?  Time will tell.

Most people have a basic understanding of how a fractured bone “knits” itself back together or a cut finger heals leaving only a small scar.   But, the healing that takes place after a stroke, brain or spinal cord injury is much more complex.

THE PLASTIC BRAINThe first thing that comes to mind is the “visible” man or woman that we could buy as a child and watch as the blue or red food coloring flowed in their blood vessels.  But, here “plastic” has a different meaning.  After any injury or stroke there is the potential for the brain to reorganize and repair itself; attempting to compensate for the cells that have been damaged or lost.  Once again we face the basic question:“Is it nature or nurture?”  Does the brain do all this by itself or can we influence how this reorganization takes place?  If we perform different types of physical, occupational or speech therapies on patients are we enhancing or hindering the brain’s recovery process?  The same is true for various drugs that we administer to patients at different times during their recovery. Some studies have suggested that amphetamines promote brain healing while benzodiazepines like diazepam will hinder it.H.L. Menken, the journalist and curmudgeon, said that, “For every complex problem there is a simple solution that does not work.” Just look at what goes on inside the brain after it has been damaged and you will see why repairing the brain, rehabilitation, is so complicated and difficult.

Brain cells may still be marginally functioning in an environment of inadequate blood or oxygen that needs to be corrected.

Like a swollen bruise, the brain may improve as its swelling and edema resolve.

After an injury or stroke there may be increased electrical activity in alternate pathways and areas of the brain that have been partially spared. Areas that may be able to assume new functions.

The brain may recruit “parallel” pathways and networks that perform similar functions. For example a part of the brain that controls shoulder movement may start to take over movement of the hand muscles.

Reorganization of both structural and chemical pathways may take place, much like rerouting a train away from a washed out rail bed. If the message can’t get through the old way, it may seek a new path.

For the most part we are an adaptable species and will naturally seek out behavioral strategies to compensate for what we have lost. For example, as we become more forgetful we may make more lists.

WHAT REHAB DOES ACCOMPLISHThe key is to look at the various mechanisms of recovery and to figure out how rehabilitation can positively influence each one.  The recovery process clearly has a component of natural biological recovery, for we know that people will improve to some degree without rehabilitation. Like school, rehabilitation brings to the table new learning and exercises that take people

to a higher functional level. Children who never go to school learn some skills while those with education develop much more sophisticated skills.

We have learned that exercise is more than just strengthening and keeping muscles moving.  Experimental evidence suggests that active functional therapies can recruit and open up new pathways in the brain.  In one study a group of normal people were taught to play a one handed piano exercise for five days, while another group was never shown the exercise.  Brain activity was measured at the beginning of the study and five days later.  Increased brain activity could be measured over the part of the brain that controlled the hand in those patients who performed the five days of exercises as compared to those who did not.

Much more elaborate experiments have been performed in primates.  A discrete stroke was created by closing off small vessels in the brain

that resulted in weakness of one of the monkey’s hands. One half of the monkeys received exercises with food rewards while the other half did not. The half that received “therapy” improved more rapidly, but more importantly, these studies suggested that the brain was truly “plastic.” The part of the brain that previously controlled shoulder movement had now taken over movement of the hand.  The brain had reorganized itself and done so more efficiently in those who received “monkey therapy.”  Research like this supports the notion that therapies can facilitate the opening of new pathways and “turn on” brain cells that previously were not primarily responsible for the movement of a particular part of the body.

Another study reported that animals placed in an “enriched environment” after a brain injury did better. They were given more “toys” and activity.  Repetitive use of an extremity enhanced recovery, as did increased cage size, companions, stimulation and increased activities. Physiological studies suggested that those animal receiving “rehab” were better able to reorganize the structures in their brains. Rehab made a difference!

These types of studies raise some interesting questions.  Should we primarily teach patients how to compensate for their deficits or should we focus our strategies on paralyzed muscles for prolonged periods of time? How long will it take to open up a new pathway and what is the best way to do it? If we bypass the usual movement patterns and substitute new methods of movement will we prevent the opening of parallel or collateral pathways?  How long do you have to work with a paralyzed muscle to turn on a collateral network or neuron and can it be done routinely in humans?

In our current health care environment we may never know the answers to many of these questions, for we are asked to discharge a patient from rehabilitation as soon as possible.  Clearly therapy should not go on for years, but it may be that we are writing off some patients too soon and sacrificing some potential gains.

Dr. Mary Dombovy, a stroke researcher summarized the problem —“It takes years of practice to become an accomplished pianist or a skilled craftsman or

athlete and one gains facility by practicing the piano not the flute.  Clinical observations indicate that determination and prolonged practice also underlie the higher level of recovery seen in some patients. Unfortunately, most neurologically impaired patients receive only a few weeks or at most a few months of rehabilitation, much of which may not be specific to their deficits.”THE HIGHTECH FUTUREWe know that after an injury there are early aborted attempts by the neurons and axons in the brain to regenerate and repair themselves.  The key is to create the proper environment so that these nerve cells and their connections will not only grow, but will also travel to the right place and make the proper connection.  If they do grow and make a wrong correction, there is not just the risk of an arm that will not move, but also that it will have an adverse effect such as spasticity.Research laboratories have been actively looking for ways to facilitate the healing process.  Here are few of the more promising methods.

Peripheral Nerve Bridges.  This is just what it sounds like-a splice between two separated nerves, much like we would splice together a television cable. These are more useful in spinal cord injury where long white matter tracts are interrupted.  For example, a spinal cord injury may interrupt the axons in the neck that carry movement and sensation down to the legs.   In rats with experimental spinal cord injuries, researchers have successfully taken pieces of large peripheral nerves from an extremity and used them to bridge this gap, restoring movements in the hind limbs.  Not only does this bridge provide a pathway for growth, but it may also release growth factors that assist in the survival of the surrounding nerve cells.

FETAL CELL TRANSPLANTS. Tissue taken from a fetus can be transplanted into a laboratory animal or human and it will continue to produce chemicals such as neurotransmitters.  The best known use is that of fetal tissue transplants in Parkinson’s patients, where the fetal cells produce dopamine in the brain and the patient’s function improves.  The problems with this approach are many. The clinical benefit is modest and the amount of fetal tissue available is limited.  New methods of acquiring stem cells that are less controversial will greatly enhance future research.GENETICALLY ENGINEERED TRANSPLANTS. The controversy over the use of fetal cells led to the use of genetically engineered cells.  Neural cells lines have been

developed from human tumor lines by treating the tumor cells so that they will  no longer divide and one does not have to worry about causing cancer.  When transplanted into the Central Nervous System they send out axons and acquire other characteristics of neurons.Within this group of cells are embryonic precursor cells.   These cells have the potential to become a variety of different cells when exposed to trophic growth factors. One of the problems is how to guide the regenerating axons into the right place.  In frogs and rats there appear to be “guidance cues” in the local environment where the cells are implanted that instruct the axons and neurons on how to make the right connection.   It was cells like these that were used in the first human motor neuron transplant.

http://www.richardsenelick.com/articles/rewiring-brains-rehabilitation-plasticity-and-transplants

What You Need to Know About Stroke

Table of Contents

Know Stroke

Why is Stroke an Emergency?

o What is a stroke?

o What causes a stroke?

o What disabilities can result from a stroke?

Know the Signs. Act in Time

o Stroke Symptoms

o What should you do?

Call 911

o A 911 Call Saved My Life.

Know Stroke Prevention

o What can you do to prevent a stroke?

WHY IS STROKE TREATMENT URGENT?

Where Can You Learn More About Stroke?

STROKE PREVENTION

o I Hope People Realize They Can Prevent Stroke.

Know Stroke

Each year in the United States, there are approximately 795,000 strokes. Stroke is the fourth leading cause of death in the country. And stroke causes more serious long-term disabilities than any other

disease. Nearly three-quarters of all strokes occur in people over the age of 65 and the risk of having a stroke more than doubles each decade after the age of 55.

For African Americans, stroke is more common and more deadly - even in young and middle-aged adults - than for any ethnic or other racial group in the United States.

Learning about stroke can help you act in time to save a co-worker, friend, or relative. And making changes in your lifestyle can help you prevent stroke.

Why is Stroke an Emergency?

New treatments are available that greatly reduce the damage caused by a stroke. But you need to arrive at the hospital within 60 minutes after symptoms start to prevent disability. Knowing stroke symptoms, calling 911 immediately, and getting to a hospital are critical.

What is a stroke?

A stroke is serious - just like a heart attack. A stroke is sometimes called a "brain attack." Most often, stroke occurs when blood flow to the brain stops because it is blocked by a clot. The brain cells in the immediate area begin to die because they stop getting the oxygen and nutrients they need to function.

What causes a stroke?

There are two kinds of stroke. The most common kind of stroke, called ischemic stroke, is caused by a blood clot that blocks or plugs a blood vessel in the brain. The other kind of stroke, called hemorrhagic stroke, is caused by a blood vessel that breaks and bleeds into the brain.

What disabilities can result from a stroke?

Stroke damage in the brain can affect the entire body - resulting in mild to severe disabilities. These include paralysis, problems with thinking, problems with speaking, and emotional problems.

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Know the Signs. Act in Time

Stroke Symptoms

Sudden numbness or weakness of the face, arm, or leg (especially on one side of the body)

Sudden confusion, trouble speaking or understanding speech

Sudden trouble seeing in one or both eyes

Sudden trouble walking, dizziness, loss of balance or coordination

Sudden severe headache with no known cause

What should you do?

Because stroke injures the brain, you may not realize that you are having a stroke. The people around you might not know it either. Your family, friends, or

neighbors may think you are confused. You may not be able to call 911 on your own. That's why everyone should know the signs of stroke - and know how to act fast.

Don't wait for the symptoms to improve or worsen. If you believe you are having a stroke - or someone you know is having a stroke - call 911 immediately. Making the decision to call for medical help can make the difference in avoiding a lifelong disability.

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Call 911

If you believe you are having a stroke - or someone you know is having a stroke - call 911 immediately.

A 911 Call Saved My Life.

When I walked into the locker room at work, I realized something was wrong. I couldn't speak. I tried to pick up my lock, but my right hand couldn't grab it. One of my co-workers noticed something was wrong and asked if I could write. With my left hand, I scribbled 911 on a piece of paper. Luckily, my friend knew the signs of stroke and got help. She called an ambulance, and I was rushed to the emergency room. The doctors ran some tests and put a drug into my IV. Within 10 minutes I could speak again. I didn't know a thing about stroke before I had one. Now, I make sure that all my family knows the signs of stroke so they can get help if they need it.

Ruth JuniousStroke Survivor

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Know Stroke Prevention

Conditions that can cause stroke are very common among African Americans. The best treatment for stroke is prevention. You can reduce your risk of having a stroke by taking action to improve your health.

What can you do to prevent a stroke?

While family history of stroke plays a role in your risk, there are many risk factors you can control.

If you have high blood pressure, work with your doctor to get it under control. Many people do not realize they have high blood pressure, which usually produces no symptoms but is a major risk factor for heart disease and stroke. Managing your high blood pressure is the most important thing you can do to avoid stroke.

If you smoke, quit.

If you have diabetes, learn how to manage it. As with high blood pressure, diabetes usually causes no symptoms but it increases the chance of stroke.

If you are overweight, start maintaining a healthy diet and exercising regularly.

WHY IS STROKE TREATMENT URGENT?

Every minute counts. The longer blood flow is cut off to the brain, the greater the damage. The most common kind of stroke, ischemic stroke, can be treated with a drug that dissolves clots blocking the blood flow. The window of opportunity to start treating stroke patients is three hours. But a person needs to be at the hospital within 60 minutes of having a stroke to be evaluated and receive treatment.

Where Can You Learn More About Stroke?

Talk to your doctor about your personal risk factors for having a stroke. For more information about stroke prevention and treatment, call the National Institute of Neurological Disorders and Stroke at 1-800-352-9424.

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STROKE PREVENTION

Manage your diabetes

Eat right

Control your high blood pressure

Exercise

Don't smoke

I Hope People Realize They Can Prevent Stroke.

I had a stroke when I was 49 years old. I am 67 now and have gone almost 20 years without another stroke. Until I had my stroke, I didn't do anything good for my health. I had high blood pressure, I was overweight, and I smoked. When bad things happen

to people, they tend to think "why me?" But, when I think about my stroke, I think "why not me?" I had all the risk factors and wasn't taking care of myself like I am now. I've learned a lot of important lessons from my stroke, which have caused me to change my eating habits, quit smoking, and really control my high blood pressure for the first time in my life. I hope people realize they can prevent stroke. It doesn't have to happen to them.

Ted TurnerStroke Survivor

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NIH Publication No. 10-5517

Back to Stroke Information Page.

Prepared by:Office of Communications and Public LiaisonNational Institute of Neurological Disorders and StrokeNational Institutes of HealthBethesda, MD 20892

NINDS health-related material is provided for information purposes only and does not necessarily represent endorsement by or an official position of the National Institute of Neurological Disorders and Stroke or any other Federal agency. Advice on the treatment or care of an individual patient should be obtained through consultation with a physician who has examined that patient or is familiar with that patient's medical history.

All NINDS-prepared information is in the public domain and may be freely copied. Credit to the NINDS or the NIH is appreciated.

Last updated June 18, 2013

http://www.ninds.nih.gov/disorders/stroke/stroke_needtoknow.htm#URGENT

Stroke Treatment: Time is Brain

Nearly 800,000 people in the U.S. suffer astroke each year. It is the number one cause of disability and the fourth leading cause of death, with 130,000 individuals dying as a result of stroke each year.

Unfortunately, many people don’t recognize the common symptoms of stroke – weakness on one side of the body, difficulty speaking, drooping on one side of the face, difficulty walking – and this can cause a delay in receiving treatment.

It turns out that the time that lapses from the onset of symptoms to the treatment for strokeis a huge factor in determining how significant its effect will be. The Wall Street Journal recently reported on the important advances in speeding treatment for stroke victims in their article, A Fast Track to Treatment for Stroke Patients.

The time between a stroke patient’s arrival in the emergency department and the time they receive treatment with tPA – a medication that dissolves blood clots – is referred to as door-to-needle time. Larger clots can be treated with endovascular methods, where a small tube is introduced into the blocked vessel and the clot removed. The American Stroke Association has established Target

Stroke, an initiative aimed at reducing this door-to-needle time for patients suffering a stroke.

Dr. Sean Lavine, MD of the Columbia Neurosurgery Endovascular Center explains, “Patients need to know that minimizing the time to treatment for stroke is key to improving their chances to have an excellent outcome, and that they should come to a designated stroke center such as ours staffed with physicians from the Columbia Neurosurgery Endovascular Center at the first sign of strokesymptoms.”

The door-to-needle time represents an area of rapid evolution in stroke treatment. Virtual stroke networks have been established so that experts can remotely diagnose stroke and expedite treatment. When it works well, treatment can be initialized as early as the ambulance ride to the hospital, and endovascular specialists can be waiting for the patient’s arrival.

http://www.columbianeurosurgery.org/2015/04/stroke-treatment-time-brain/

Nurses play a pivotal role in all phases of care of the stroke patient. The 2 phases of stroke care: (1) The emergency or hyperacute care phase,2,3 which includes the prehospital setting and the emergency department (ED), and (2) the acute care phase, which includes critical care units, intermediate care units, stroke units, and general medical units. Nurses are often responsible for the coordination of care throughout the continuum.4–9 Coordinated care of the patient results in improved outcomes, decreased lengths of stay, and decreased costs.10

Stroke is a complex disease that requires the efforts and skills of all members of the multidisciplinary team. In developing this comprehensive overview, the writing panel applied the rules of evidence and formulation of strength of evidence (recommendations) used by other AHA writing groups11 (Table 1). We also cross-reference other AHA guidelines as appropriate.http://stroke.ahajournals.org/content/40/8/2911.full