Ischemic Stroke

An ischemic stroke is death of an area of brain tissue (cerebral infarction) resulting from an inadequate supply of blood and oxygen to the brain due to blockage of an artery.

Ischemic stroke usually results when an artery to the brain is blocked, often by a blood clot or a fatty deposit due to atherosclerosis. Symptoms occur suddenly and may include muscle weakness, paralysis, lost or abnormal sensation on one side of the body, difficulty speaking, confusion, problems with vision, dizziness, and loss of balance and coordination. Diagnosis is usually based on symptoms and results of a physical examination, imaging tests, and blood tests. Treatment may include drugs to break up blood clots or to make blood less likely to clot and surgery, followed by rehabilitation. About one third of people recover all or most of normal function after an ischemic stroke.

Causes An ischemic stroke typically results from blockage of an artery that supplies the brain, most commonly a branch of one of the internal carotid arteries. Commonly, blockages are blood clots (thrombi) or pieces of fatty deposits (atheromas, or plaques) due to atherosclerosis. Such blockages often occur in the following ways:

By forming in and blocking an artery: An atheroma in the wall of an artery may accumulate more fatty material and become large enough to block the artery. Or a blood clot can form and block the artery when an atheroma ruptures (see Atherosclerosis: How Atherosclerosis Develops ). Clots tend to form on a ruptured atheroma because the atheroma narrows the artery and slows blood flow through it, like a clogged pipe slows the flow of water. Slow-moving blood is more likely to clot. A large clot can block enough blood flowing through the narrowed artery that brain cells supplied by that artery die. By traveling to another artery: A blood clot in the heart, a piece of an atheroma, or a blood clot in the wall of an artery can break off and travel through the bloodstream (becoming an embolus). The embolus may then

lodge in an artery that supplies the brain and block blood flow there. (Embolism refers to blockage of arteries by materials that travel through the bloodstream to another part of the body.) Such blockages are more likely to occur where arteries are already narrowed by fatty deposits. Several conditions besides rupture of an atheroma can trigger or promote the formation of blood clots, increasing the risk of blockage by a blood clot, such as the following:

Heart-related problems: Blood clots may form in the heart or on a heart valve (including artificial valves). Strokes due to such blood clots are most common among people who have recently had heart surgery and people who have a heart valve disorder or an abnormal heart rhythm (arrhythmia), especially a fast, irregular heart rhythm called atrial fibrillation. Blood disorders: Some disorders, such as an excess of red blood cells (polycythemia), make blood thick, increasing the risk of blood clots. Some disorders, such as antiphospholipid syndrome and a high homocysteine level in the blood (hyperhomocysteinemia), make blood more likely to clot. Oral contraceptives: Taking oral contraceptives, particularly those with a high estrogen dose, increases the risk of blood clots.

Another common cause of ischemic strokes is a lacunar infarction. In lacunar infarction, one of the small arteries deep in the brain becomes blocked by a mixture of fat and connective tissuea blood clot is not the cause. This disorder is called lipohyalinosis and tends to occur in older people with diabetes or poorly controlled high blood pressure. Lipohyalinosis is different from atherosclerosis, but both disorders can cause blockage of arteries. Only a small part of the brain is damaged in lacunar infarction. Rarely, small pieces of fat from the marrow of a broken long bone, such as a leg bone, are released into the bloodstream. These pieces can clump together and block an artery. The resulting disorder, called fat embolism syndrome, may resemble a stroke. An ischemic stroke can also result from any disorder that reduces the amount of blood or oxygen supplied to the brain, such as severe blood loss or very low blood pressure. Occasionally, an ischemic stroke occurs when blood flow to the brain is normal but the blood does not contain enough oxygen. Disorders that reduce the oxygen content of blood include a severe deficiency of red blood cells (anemia), suffocation, and carbon monoxide poisoning. Usually, brain damage in such cases is widespread (diffuse), and coma results.
An ischemic stroke can occur if inflammation of blood vessels (vasculitis) or infection (such as herpes simplex) narrows blood vessels

that supply the brain. Migraine headaches or drugs such as cocaine and amphetamines can cause spasm of the arteries, which can narrow the arteries supplying the brain and cause a stroke.

Clogs and Clots: Causes of Ischemic Stroke

When an artery that carries blood to the brain becomes clogged or blocked, an ischemic stroke can occur. Arteries may be blocked by fatty deposits (atheromas, or plaques) due to atherosclerosis. Arteries in the neck, particularly the internal carotid arteries, are a common site for atheromas. Arteries may also be blocked by a blood clot (thrombus). Blood clots may form on an atheroma in an artery. Clots may also form in the heart of people with a heart disorder. Part of a clot may break off and travel through the bloodstream (becoming an embolus). It may then block an artery that supplies blood to the brain, such as one of the cerebral arteries. Symptoms Usually, symptoms occur suddenly and are often most severe a few minutes after they start because most ischemic strokes begin suddenly, develop rapidly, and cause death of brain tissue within minutes to hours. Then, most strokes become stable, causing little or no further damage. Strokes that remain stable for 2 to 3 days are called completed strokes. Sudden blockage by an embolus is most likely to cause this kind of stroke. Less commonly, symptoms develop slowly. They result from strokes that continue to worsen for several hours to a day or two, as a steadily enlarging area of brain tissue dies. Such strokes are called evolving strokes. The progression of

symptoms and damage is usually interrupted by somewhat stable periods, during which the area temporarily stops enlarging or some improvement occurs. Such strokes are usually due to the formation of clots in a narrowed artery. Many different symptoms can occur, depending on which artery is blocked and thus which part of the brain is deprived of blood and oxygen (see Brain Dysfunction: Brain Dysfunction by Location). When the arteries that branch from the internal carotid artery (which carry blood along the front of the neck to the brain) are affected, the following are most common:

Blindness in one eye Inability to see out of the same side in both eyes Abnormal sensations, weakness, or paralysis in one arm or leg or on one side of the body

When the arteries that branch from the vertebral arteries (which carry blood along the back of the neck to the brain) are affected, the following are most common:

Dizziness and vertigo Double vision Generalized weakness on both sides of the body

Many other symptoms, such as difficulty speaking (for example, slurred speech), impaired consciousness (such as confusion), loss of coordination, and urinary incontinence, can occur. Severe strokes may lead to stupor or coma. In addition, strokes, even milder ones, can cause depression or an inability to control emotions. For example, people may cry or laugh inappropriately. If symptoms, particularly impaired consciousness, worsen during the first 2 to 3 days, the cause is often swelling due to excess fluid (edema) in the brain. Symptoms usually lessen within a few days, as the fluid is absorbed. Nonetheless, the swelling is particularly dangerous because the skull does not expand. The resulting increase in pressure can cause the brain to shift, further impairing brain function, even if the area directly damaged by the stroke does not enlarge. If the pressure becomes very high, the brain may be forced downward in the skull, through the rigid structures that separate the brain into compartments. The resulting disorder is called herniation (see Head Injuries:Overview of Head Injuries ).

Strokes can lead to other problems. If swallowing is difficult, people may not eat enough and become malnourished. Food, saliva, or vomit may be inhaled (aspirated) into the lungs, resulting in aspiration pneumonia. Being in one position too long can result in pressure sores and lead to muscle loss. Not being able to move the legs can result in the formation of blood clots in deep veins of the legs and groin (deep vein thrombosis). Clots can break off, travel through the bloodstream, and block an artery to a lung (a disorder called pulmonary embolism). People may have difficulty sleeping. The losses and problems resulting from the stroke may make people depressed. Diagnosis Turbulent Blood Flow

Doctors can usually diagnose an ischemic stroke based on the history of events and results of a physical examination. Doctors can usually identify which artery in the brain is blocked based on symptoms (see Brain Dysfunction:Overview of Brain Dysfunction ). For example, weakness or paralysis of the left leg suggests blockage of the artery supplying the area on the right side of the brain that controls the left leg's muscle movements. Computed tomography (CT) is usually done first. CT helps distinguish an ischemic stroke from a hemorrhagic stroke, a brain tumor, an abscess, and other structural abnormalities. Doctors also measure the blood sugar level to rule out a low blood sugar level (hypoglycemia), which can cause similar symptoms. If available, diffusion magnetic resonance imaging (MRI), which can detect ischemic strokes within minutes of their start, may be done next. Identifying the precise cause of the stroke is important. If the blockage is a blood clot, another stroke is very likely unless the underlying disorder is corrected. For example, if blood clots result from an abnormal heart rhythm, treating that disorder can prevent new clots from forming and causing another stroke. Tests for causes may include the following:

Electrocardiography (ECG) to look for abnormal heart rhythms Continuous ECG monitoring (done at home or in the hospitalsee Diagnosis of Heart and Blood Vessel Disorders: Continuous Ambulatory Electrocardiography) to record the heart rate and rhythm continuously for 24 hours (or more), which may detect abnormal heart rhythms that occur

unpredictably or briefly

Echocardiography to check the heart for blood clots, pumping or structural abnormalities, and valve disorders Imaging testscolor Doppler ultrasonography, magnetic resonance angiography, CT angiography, or cerebral (standard) angiographyto determine whether arteries, especially the internal carotid arteries, are blocked or narrowed Blood tests to check for anemia, polycythemia, blood clotting disorders, vasculitis, and some infections (such as heart valve infections and syphilis) and for risk factors such as high cholesterol levels or diabetes

Imaging tests enable doctors to determine how narrowed the carotid arteries are and thus to estimate the risk of a subsequent stroke or TIA. Such information helps determine which treatments are needed. For cerebral angiography, a thin, flexible tube (catheter) is inserted into an artery, usually in the groin, and threaded through the aorta to an artery in the neck (see Common Imaging Tests: Angiography). Then, a dye is injected to outline the artery. Thus, this test is more invasive than other tests that provide images of the brain's blood supply. However, it provides more information. Cerebral angiography may be done before atheromas are removed surgically or when vasculitis is suspected. Rarely, a spinal tap (lumbar puncture) is donefor example, after CT, when doctors still need to determine whether strokelike symptoms are due to an infection or whether a subarachnoid hemorrhage is present (see Stroke (CVA): Subarachnoid Hemorrhage). This procedure is done only if doctors are sure that the brain is not under excess pressure (usually determined by CT or MRI). Prognosis About 10% of people who have an ischemic stroke recover almost all normal function, and about 25% recover most of it. About 40% of people have moderate to severe impairments requiring special care, and about 10% require care in a nursing home or other long-term care facility. Some people are physically and mentally devastated and unable to move, speak, or eat normally. About 20% of people who have a stroke die in the hospital. The proportion is higher among older people. About 25% of people who recover from a stroke have another stroke within 5 years. Subsequent strokes impair function further. During the first few days after an ischemic stroke, doctors usually cannot predict whether a person will improve or worsen. Younger people and people who start improving quickly are likely to recover more fully. About 50% of people with

one-sided paralysis and most of those with less severe symptoms recover some function by the time they leave the hospital, and they can eventually take care of their basic needs. They can think clearly and walk adequately, although use of the affected arm or leg may be limited. Use of an arm is more often limited than use of a leg. Most impairments still present after 12 months are permanent. Treatment People who have any symptom suggesting an ischemic stroke should go to an emergency department immediately. The earlier the treatment, the better are the chances for recovery. The first priority is to restore the person's breathing, heart rate, blood pressure (if low), and temperature to normal. An intravenous line is inserted to provide drugs and fluids when needed. If the person has a fever, it may be lowered using acetaminophen , ibuprofen , or a cooling blanket. An increase in body temperature by even a few degrees can dramatically worsen brain damage due to an ischemic stroke. Generally, doctors do not immediately treat high blood pressure unless it is very high (over 220/120 mm Hg) because, when arteries are narrowed, blood pressure must be higher than normal to push enough blood through them to the brain. However, very high blood pressure can injure the heart, kidneys, and eyes and must be lowered. If a stroke is very severe, drugs such as mannitol may be given to reduce swelling and the increased pressure in the brain. Some people need a ventilator to breathe adequately. Specific treatment of stroke may include drugs to break up blood clots (thrombolytic drugs), drugs to make blood less likely to clot (antiplatelet drugs and anticoagulants), and surgery, followed by rehabilitation. Thrombolytic (Fibrinolytic) Drugs: In certain circumstances, a drug called tissue plasminogen activator (tPA) is given intravenously to break up clots and help restore blood flow to the brain. Because tPA can cause bleeding in the brain and elsewhere, it should not be given to people with certain conditions, such as the following:

A past occurrence of a hemorrhagic stroke, a bulge (aneurysm) in an artery to the brain, other structural abnormalities in the brain, or a brain tumor A seizure when the stroke began

A tendency to bleed Recent major surgery Recent bleeding (hemorrhage) in the gastrointestinal or urinary tract A recent head injury or other serious trauma A very high or very low blood sugar level A heart infection Current use of an anticoagulant (warfarin )

A large ischemic stroke Blood pressure that remains high after treatment with an antihypertensive drug Symptoms that are resolving quickly

Before tPA is given, CT is done to rule out bleeding in the brain. To be effective and safe, tPA, given intravenously, must be started within 3 hours of the beginning of an ischemic stroke. After 3 hours, most of the damage to the brain cannot be reversed, and the risk of bleeding outweighs the possible benefit of the drug. However, pinpointing when the stroke began may be difficult. So doctors assume that the stroke began the last time a person was known to be well. For example, if a person awakens with symptoms of a stroke, doctors assume the stroke began when the person was last seen awake and well. Thus, tPA can be used in only a few people who have had a stroke. If people arrive at the hospital 3 to 6 hours (occasionally, up to 18 hours) after the stroke began, they may be given tPA or another thrombolytic drug. But the drug must be given through a catheter instead. For this treatment, doctors make an incision in the skin, usually in the groin, and insert a catheter into an artery. The catheter is then threaded through the aorta and other arteries, to the clot. The clot is partly broken up with the catheter wire and then injected with tPA. This treatment is usually available only at specialized stroke centers. Antiplatelet Drugs and Anticoagulants: If a thrombolytic drug cannot be used, most people are given aspirin (an antiplatelet drug) as soon as they get to the hospital. If symptoms seem to be worsening, anticoagulants such as heparin are occasionally used, but their effectiveness has not been proved. Antiplatelet drugs make platelets less likely to clump and form clots. Anticoagulants inhibit proteins in blood that help it to clot

(clotting factors). Regardless of the initial treatment, long-term treatment usually consists of aspirin or another antiplatelet drug to reduce the risk of blood clots and thus of subsequent strokes (see Stroke (CVA): Prevention). People who have atrial fibrillation or a heart valve disorder are given anticoagulants (such as warfarin ) instead of antiplatelet drugs, which do not seem to prevent blood clots from forming in the heart. Occasionally, people at high risk of another stroke are given both aspirin and warfarin . If people have been given a thrombolytic drug, doctors usually wait at least 24 hours before antiplatelet drugs or anticoagulants are started because these drugs add to the already increased risk of bleeding in the brain. Anticoagulants are not given to people who have uncontrolled high blood pressure or who have had a hemorrhagic stroke. Surgery: Once an ischemic stroke is completed, surgical removal of atheromas or clots (endarterectomy) in an internal carotid artery may be done. Carotid endarterectomy can help if all of the following are present:

The stroke resulted from narrowing of a carotid artery by more than 70%. Some brain tissue supplied by the affected artery still functions after the stroke. The person's life expectancy is at least 5 years.

In such people, carotid endarterectomy may reduce the risk of subsequent strokes. It also reestablishes the blood supply to the affected area, but it cannot restore lost function because some brain tissue is dead. For carotid endarterectomy, a general anesthetic or a local anesthetic (to numb the neck area) may be used. If people remain awake during the operation, the surgeon can better evaluate how the brain is functioning. The surgeon makes an incision in the neck over the area of the artery that contains the blockage and an incision in the artery. The blockage is removed, and the incisions are closed. For a few days afterwards, the neck may hurt, and swallowing may be difficult. Most people can stay in the hospital 1 or 2 days. Heavy lifting should be avoided for about 3 weeks. After several weeks, people can resume their usual activities.

Carotid endarterectomy can trigger a stroke because the operation may dislodge clots or other material that can then travel through the bloodstream and block an artery. However, after the operation, the risk of stroke is lower for several years than it is when drugs are used. In other narrowed arteries, such as the vertebral arteries, endarterectomy may not be possible because the operation is riskier to perform in these arteries than in the internal carotid arteries. People should find a surgeon who is experienced doing this operation and who has a low rate of serious complications (such as heart attack, stroke, and death) after the operation. If people cannot find such a surgeon, the risks of endarterectomy outweigh its expected benefits. Stents: If endarterectomy is too risky, a less invasive procedure can be done: A wire mesh tube (stent) with an umbrella filter may be placed in the carotid artery. The stent helps keep the artery open, and the filter catches blood clots and prevents them from reaching the brain and causing a stroke. The filter is similar to one used to prevent pulmonary embolism (see Venous Disorders: Umbrellas: One Way to Prevent Pulmonary Embolism ). After a local anesthetic is given, a catheter is inserted through a small incision into a large artery near the groin or in the arm and is threaded to the internal carotid artery in the neck. A dye that can be seen on x-rays (radiopaque dye) is injected, and x-rays are taken so that the narrowed area can be located. After the stent and filter are placed, the catheter is removed. People remain awake for the procedure, which usually takes 1 to 2 hours. The procedure appears to be as safe as endarterectomy and is almost as effective in preventing strokes and death. Other Treatments: Another option being studied is a tiny corkscrew-shaped device that is attached to a catheter, threaded to the clot, and used to snag the clot. The clot is then drawn out through the catheter. This treatment may be useful for people who cannot be given tPA. Treatment of Problems Due to Strokes: Measures to prevent aspiration pneumonia (see Pneumonia: Aspiration Pneumonia) and pressure sores (see Pressure Sores: Prevention) are started early. Heparin, injected under the skin, may be given to help prevent deep vein thrombosis (see Venous Disorders: Deep Vein Thrombosis (DVT)). People are closely monitored to determine whether the esophagus, bladder, and intestines are functioning. Often, other disorders such as heart failure, abnormal heart rhythms, and lung infections must be treated. High blood pressure is often treated after the stroke has been stabilized. Because a stroke often causes mood changes, especially depression, family members or friends should inform the doctor if the person seems depressed. Depression can be treated with drug therapy and psychotherapy (see Mood

Disorders: Prognosis and Treatment). Last full review/revision November 2007 by Elias A. Giraldo, MD, MS

Patofisiologi Stroke Non Hemoragik

Stroke iskemik terjadi karena hilangnya suplai darah ke salah satu bagian otak dan mengakibatkan terjadinya ischemic cascade. ischemic cascade adalah suatu rangkaian reaksi biokimia yang terjadi setelah sel atau jaringan aerob mengalami iskemi. Iskemi sangat berbahaya bagi sel dan jaringan, terutama sel syaraf yang tidak memiliki cadangan energi yang banyak. Jaringan otak akan berhenti berfungsi jika tidak mendapat oksigen lebih dari 60-90 detik. Ketika pembuluh darah serebral terhambat, otak akan kekurangan energi, sehingga harus melakukan respirasi anaerob di tempat terjadinya iskemi. Proses ini menghasilkan sedikit energi dan asam laktat yang dapat mengiritasi sel. Keseimbangan asam basa yang ada di otak akan terganggu dengan adanya asam laktat. Area iskemi ini disebut "ischemic penumbra". ATP tidak dapat diproduksi pada sel otak yang kekurangan oksigen dan glukosa sehingga sel tidak melaksanakan proses yang seharusnya dilakukan seperti contohnya pompa ion yang penting untuk kehidupan sel. Hal tersebut menyebabkan ketidakseimbangan jumlah neurotransmiter glutamat dan kalsium yang merupakan salah satu penyebab kerusakan sistem saraf. Konsentrasi glutamat di luar sel saraf seharusnya terjaga dalam jumlah yang kecil yang dipengaruhi oleh pompa ion. Pompa ion yang tidak dapat bekerja mengakibatkan reuptake glutamat tidak berjalan dengan lancar. Glutamat bekerja pada reseptor (terutama NMDA reseptor) di sel saraf untuk menghasilkan influks kalsium ke dalam sel. Kalsium di dalam sel dapat mengaktifasi enzim yang bisa menghancurkan protein, lipid, dan materi nuklear sel. Influks kalsium juga akan mengganggu mitokondria sehingga sel semakin kehilangan energi dan memicu kematian sel melalui apoptosis. Iskemi juga menginduksi produksi radikal bebas oksigen dan zat reaktif lain. Zat-zat tersebut dapat bereaksi dan merusak berbagai sel dan jaringan, termasuk jaringan endotelium pembuluh darah. Proses tersebut sama pada berbagai iskemi jaringan. Namun, jaringan otak sangat rentan terhadap proses tersebut karena sel otak tidak memiliki cadangan nutrisi yang banyak dan sangat tergantung pada respirasi aerob. Selain mengakibatkan kerusakan sel otak, iskemi dan infark dapat merusak struktur dari jaringan otak, sawar darah otak, dan pembuluh darah melalui pelepasan matrix metalloprotease yang merupakan enzim yang tergantung pada zinc dan kalsium yang dapat menghancurkan kolagen, asam hialuronat, dan berbagai elemen dari jaringan konektif. Adanya zat-zat yang bisa menghancurkan jaringan sangat berbahaya bagi sawar darah otak. Sawar darah otak yang rusak bisa mengalami kebocoran sehingga molekul ukuran besar seperti albumin dapat masuk ke dalam otak. Albumin dapat menarik air ke jaringan otak dari pembuluh darah melalui osmosis yang disebut juga vasogenic edema. Edema ini akan menyebabkan kerusakan otak lebih lanjut melalui tekanan pada jaringan otak. Zat lain yang muncul saat terjadi iskemi adalah radikal bebas yang juga berbahaya bagi sel. Sistem imun juga akan teraktifasi oleh infark serebral dan dapat memperparah cedera yang disebabkan infark. Deb P, Sharma S, Hassan KM. "Pathophysiologic mechanisms of acute ischemic stroke: An

overview with emphasis on therapeutic significance beyond thrombolysis". Pathophysiology. January 12, 2010. http://www.ncbi.nlm.nih.gov/pubmed/20074922

Practice Essentials
Stroke is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Strokes are classified as either hemorrhagic or ischemic. Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke.

Essential update: New AHA/ASA guidelines for acute stroke treatment

The American Heart Association (AHA) and American Stroke Association (ASA) released new guidelines for the early management of acute ischemic stroke in January 2013. New features of the guidelines include a focus on the importance of stroke systems of care, a recommendation for the use of tissue plasminogen activator (t-PA) in selected patients presenting within 3 to 4.5 hours of symptom onset, and a recommendation for door-to-needle times within 60 minutes of hospital arrival in patients eligible for thrombolysis.[1, 2]

Signs and symptoms

Although signs and symptoms of stroke can occur alone, they are more likely to occur in combination. Common stroke signs and symptoms include the following:

Abrupt onset of hemiparesis, monoparesis, or quadriparesis Acute hemisensory loss Complete or partial hemianopia, monocular or binocular visual loss, or diplopia Visual field deficits Diplopia Dysarthria Ataxia Vertigo Nystagmus Aphasia Sudden decrease in the level of consciousness

In younger patients, a history of recent trauma, coagulopathies, illicit drug use (especially cocaine), migraines, or use of oral contraceptives should be elicited.

See Clinical Presentation for more detail.

Diagnosis
With the availability of thrombolytic therapy for acute ischemic stroke in selected patients, the physician must be able to perform a brief, but accurate, neurologic examination on patients with suspected stroke syndromes. Essential components of the neurologic examination include evaluations of the following:

Cranial nerves Motor function Sensory function Cerebellar function Gait Deep tendon reflexes Mental status level of consciousness

The patients skull and spine also should be examined, and signs of meningismus should be sought. Laboratory studies Laboratory tests performed in the diagnosis and evaluation of ischemic stroke include the following:

Complete blood cell count: The CBC count serves as a baseline study and may reveal a cause for the stroke (eg, polycythemia, thrombocytosis, thrombocytopenia, leukemia) or provide evidence of concurrent illness (eg, anemia) Basic chemistry panel: The chemistry panel serves as a baseline study and may reveal a stroke mimic (eg, hypoglycemia, hyponatremia) or provide evidence of concurrent illness (eg, diabetes, renal insufficiency) Coagulation studies: Coagulation studies may reveal a coagulopathy and are useful when thrombolytics or anticoagulants are to be used Cardiac biomarkers: Cardiac biomarkers are important because of the association of cerebral vascular disease and coronary artery disease Toxicology screening: Toxicology screening may assist in identifying intoxicated patients with symptoms/behavior mimicking stroke syndromes

Pregnancy testing: A urine pregnancy test should be obtained for all women of childbearing age with stroke symptoms; recombinant tissue-type plasminogen activator (rt-PA) is a pregnancy class C agent Arterial blood gas analysis: Although infrequent in patients with suspected hypoxemia, arterial blood gas defines the severity of hypoxemia and may be used to detect acid-base disturbances

Imaging studies Imaging in ischemic stroke can involve the following modalities:

Several types of magnetic resonance imaging Several types of computed tomography scanning Angiography Ultrasonography Radiology Echocardiography Nuclear imaging

Lumbar puncture A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the CT scan is negative but the clinical suspicion remains high See Workup for more detail.

Management
Ischemic stroke therapies include the following:

Thrombolytic therapy: Thrombolytics restore cerebral blood flow among some patients with acute ischemic stroke and may lead to improvement or resolution of neurologic deficits Antiplatelet agents: The International Stroke Trial and the Chinese Acute Stroke Trial (CAST) demonstrated modest benefit from the use of aspirin in the setting of acute ischemic stroke[3, 4] Mechanical thrombolysis: Involves the endovascular treatment of acute ischemic stroke

Stroke prevention

Primary stroke prevention refers to the treatment of individuals with no previous history of stroke. Measures may include use of the following:

Platelet antiaggregants 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (ie, statins) Exercise

Secondary prevention refers to the treatment of individuals who have already had a stroke. Measures may include use of the following:

Platelet antiaggregants Antihypertensives HMG-CoA reductase inhibitors (statins) Lifestyle interventions

See Treatment and Medication for more detail.

Image library

Vascular distributions: ACA infarction. Diffusion-weighted image on the left demonstrates high signal in the paramedian frontal and high parietal regions. The opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger ACA infarction involving the left paramedian frontal and posterior parietal regions. There is also infarction of the lateral temporoparietal regions bilaterally (both MCA distributions), greater on the left indicating multivessel involvement suggesting emboli.

Background
Stroke is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Also previously called cerebrovascular accident (CVA) or stroke syndrome, stroke is a nonspecific term encompassing a heterogeneous group of pathophysiologic causes. Broadly, however, strokes are classified as either hemorrhagic or ischemic. Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke. (Prior literature indicated that only 8-18% of strokes are hemorrhagic, but a retrospective review from a stroke center found that 40.9% of 757 strokes included in the study were hemorrhagic.[5] )

Based on the system of categorizing stroke developed in the multicenter Trial of Org 10172 in Acute Stroke Treatment (TOAST), ischemic strokes may be divided into the following 3 major subtypes[6] :

Large artery infarction: Thrombotic strokes are caused by in situ occlusions on atherosclerotic lesions in the carotid, vertebrobasilar, and cerebral arteries, typically proximal to major branches. Small-vessel, or lacunar, infarction Cardioembolic infarction: Cardiogenic emboli are a common source of recurrent stroke. They may account for up to 20% of acute strokes and have been reported to have the highest 1-month mortality. (See Pathophysiology.)

The National Institute of Neurologic Disorders and Stroke (NINDS) recombinant tissue-type plasminogen activator (rt-PA) stroke study group first reported that the early administration of rtPA benefited carefully selected patients with acute ischemic stroke.[7] The trials outcome led to the long-standing goal of t-PA administration within a 3-hour window for a patient deemed likely to benefit from thrombolytic intervention. Encouraged by this breakthrough study and the subsequent approval by the US Food and Drug Administration (FDA) of the use of t-PA in acute ischemic stroke, many medical professionals now consider acute ischemic stroke to be a medical emergency that may be amenable to treatment. Thrombolytic therapy administered between 3 and 4.5 hours after the onset of symptoms was found to be efficacious in improving neurologic outcomes in the European Cooperative Acute Stroke Study III (ECASS III), suggesting a wider time window for the administration of thrombolytics.[8] Based on this and other data, in May 2009, the American Heart Association and the American Stroke Association guidelines for the administration of rt-PA were revised to expand the treatment window from 3 to 4.5 hours.[9] This indication has not yet been FDA approved. Understanding of the pathophysiology, clinical presentation, and evaluation of the stroke patient is essential, as is knowledge of the therapeutic armamentarium currently available to treat acute ischemic stroke, which includes supportive care, treatment of neurologic complications, antiplatelet therapy, glycemic control, blood pressure control, prevention of hyperthermia, and thrombolytic therapy. (See Treatment and Management.) See the images below.

Axial noncontrast computed tomography (NCCT) demonstrates diffuse hypodensity in the right lentiform nucleus with mass effect upon the frontal horn of the right lateral ventricle in this 70-year-old female with history of left-sided weakness for several

hours duration. Magnetic Resonance Imaging (MRI) was subsequently obtained in the same patient as in the above image. An axial T2 FLAIR image (left) demonstrates high signal in the lentiform nucleus with mass effect. The axial diffusion weighted image (middle) demonstrates high signal in the same area with corresponding low signal on the apparent diffusion coefficient (ADC) maps, consistent with true restricted diffusion and an acute infarction. Maximum intensity projection from a 3D time-of-flight magnetic resonance angiogram (MRA, right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).

Anatomy
The brain is the most metabolically active organ in the body. While representing only 2% of the body's mass, it requires 15-20% of the total resting cardiac output to provide the necessary glucose and oxygen for its metabolism. See the Cardiac Output calculator. Knowledge of cerebrovascular arterial anatomy and the territories supplied by each is useful in determining which vessels are involved in acute stroke. Atypical patterns that do not conform to a vascular distribution may indicate a diagnosis other than ischemic stroke, such as venous infarction.

Arterial distributions
The cerebral hemispheres are supplied by 3 paired major arteries, specifically, the anterior, middle, and posterior cerebral arteries. The anterior and middle cerebral arteries carry the anterior circulation and arise from the supraclinoid internal carotid arteries. The anterior cerebral artery (ACA) supplies the medial portion of the frontal and parietal lobes and anterior portions of basal ganglia and anterior internal capsule. The middle cerebral artery (MCA) supplies the lateral portions of the frontal

and parietal lobes, as well as the anterior and lateral portions of the temporal lobes, and gives rise to perforating branches to the globus pallidus, putamen and internal capsule. The posterior cerebral arteries arise from the basilar artery and carry the posterior circulation. The posterior cerebral artery (PCA) gives rise to perforating branches that supply the thalami and brainstem and the cortical branches to the posterior and medial temporal lobes and occipital lobes. The cerebellar hemispheres are supplied inferiorly by the posterior inferior cerebellar artery (PICA) arising from the vertebral artery, superiorly by the superior cerebellar artery, and anterolaterally by the anterior inferior cerebellar artery (AICA) from the basilar artery. The cerebral vasculature is seen in the images below. The images after Table 1 demonstrate cerebral artery infarction.

Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The MCA can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches) and M4 (distal cortical branches on the lateral hemispheric convexities).

Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the ICA bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the MCA with the apex representing the Sylvian point.

Table 1. Vascular Supply to the Brain (Open Table in a new window) VASCULAR TERRITORY Structures Supplied Anterior Circulation (Carotid) Anterior Cerebral Artery Cortical branches: medial frontal and parietal lobe

Medial lenticulostriate branches: caudate head, globus pallidus, anterior limb of internal capsule

Middle Cerebral Artery

Cortical branches: lateral frontal and parietal lobes lateral and anterior temporal lobe

Lateral lenticulostriate branches: globus pallidus and putamen, internal capsule

Anterior Choroidal Artery Posterior Circulation (Vertebrobasilar) Posterior Cerebral Artery

Optic tracts, medial temporal lobe, ventrolateral thalamus, corona radiata, posterior limb of the internal capsule

Cortical branches: occipital lobes, medial and posterior temporal and parietal lobes

Perforating branches: brainstem, posterior thalamus and midbrain

Posterior Inferior Cerebellar Inferior vermis; posterior and inferior cerebellar hemispheres Artery Anterior Inferior Cerebellar Anterolateral cerebellum Artery Superior Cerebellar Artery Superior vermis; superior cerebellum

The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The MCA (red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal and anterior temporal lobes, insula and basal ganglia. The ACA (blue) supplies the medial frontal and parietal lobes. The PCA (green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.

Vascular distributions: MCA infarction. Noncontrast CT demonstrates a large acute infarction in the MCA territory involving the lateral surfaces of the left frontal, parietal, and temporal lobes, as well as the left insular and subinsular regions, with mass effect and rightward midline shift. There is sparing of the caudate head and at least part of the lentiform nucleus and internal capsule, which receive blood supply from the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of involvement of the medial frontal lobe (ACA territory), thalami and paramedian occipital lobe (PCA territory).

Vascular distributions: ACA infarction. Diffusion-weighted image on the left demonstrates high signal in the paramedian frontal and high parietal regions. The opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger ACA infarction involving the left paramedian frontal and posterior parietal regions. There is also infarction of the lateral temporoparietal regions bilaterally (both MCA distributions), greater on the left indicating multivessel involvement suggesting emboli.

Vascular distributions: PCA infarction. The noncontrast CT

images demonstrate PCA distribution infarction involving the right occipital and inferomedial temporal lobes. The image on the right demonstrates additional involvement of the thalamus,

also part of the PCA territory. Vascular distributions: anterior choroidal artery infarction. The diffusion-weighted image (left) demonstrates high signal with associated signal dropout on the apparent diffusion coefficient (ADC) map involving the posterior limb of the internal capsule. This is the typical distribution of the anterior choroidal artery, the last branch of the internal carotid artery before bifurcating into the anterior and middle cerebral arteries. The anterior choroidal artery may also arise from the MCA.

Pathophysiology
Acute ischemic strokes are the result of vascular occlusion secondary to thromboembolic disease (see Etiology). Ischemia results in cell hypoxia and depletion of cellular adenosine triphosphate (ATP). Without ATP, energy failure results in an inability to maintain ionic gradients across the cell membrane and cell depolarization. With an influx of sodium and calcium ions and passive inflow of water into the cell, cytotoxic edema results.[10, 11, 12]

Ischemic core and penumbra

An acute vascular occlusion produces heterogeneous regions of ischemia in the affected vascular territory. The quantity of local blood flow is made up of any residual flow in the major arterial source and the collateral supply, if any. Regions of the brain with CBF lower than 10 mL/100g of tissue/min are referred to collectively as the core, and these cells are presumed to die within minutes of stroke onset. Zones of decreased or marginal perfusion (CBF < 25 mL/100g of tissue/min) are collectively called the ischemic penumbra. Tissue in the penumbra can remain viable for several hours because of marginal tissue perfusion.

Ischemic cascade
On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted and membrane ion-transport systems fail. The resulting influx of calcium leads to the release of a number of neurotransmitters, including large quantities of glutamate, which in turn activates N -methyl-D-aspartate (NMDA) and other excitatory receptors on other neurons. These neurons then become depolarized, causing further calcium influx, further glutamate release, and local amplification of the initial ischemic insult. This massive calcium influx also activates various degradative enzymes, leading to the destruction of the cell membrane and other essential neuronal structures.[13]

Free radicals, arachidonic acid, and nitric oxide are generated by this process, which leads to further neuronal damage. Ischemia also directly results in dysfunction of the cerebral vasculature, with breakdown of the blood-brain barrier occurring within 4-6 hours after infarction. Following the barriers breakdown, proteins and water flood into the extracellular space, leading to vasogenic edema. Vasogenic edema produces greater levels of brain swelling and mass effect that peaks at 3-5 days and resolves over the next several weeks with resorption of water and proteins.[14, 15] Within hours to days after a stroke, specific genes are activated, leading to the formation of cytokines and other factors that, in turn, cause further inflammation and microcirculatory compromise.[13] Ultimately, the ischemic penumbra is consumed by these progressive insults, coalescing with the infarcted core, often within hours of the onset of the stroke. Infarction results in the death of astrocytes as well as the supporting oligodendroglia and microglia cells. The infarcted tissue eventually undergoes liquefaction necrosis and is removed by macrophages with the development of parenchymal volume loss. A well-circumscribed region of cerebrospinal fluidlike low density is eventually seen, consisting of encephalomalacia and cystic change. The evolution of these chronic changes may be seen in the weeks to months following the infarction.

Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage. This is estimated to occur in 5% of uncomplicated ischemic strokes, in the absence of thrombolytics. Hemorrhagic transformation is not always associated with neurologic decline and ranges from small petechial hemorrhages to hematomas requiring evacuation. Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed producing petechial hemorrhage or more frank intraparenchymal hematoma.[10, 16, 17] Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days post ictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size.[10, 18, 7] Hemorrhagic transformation is also more likely following administration of t-PA, with noncontrast computed tomography (NCCT) scanning demonstrating areas of hypodensity.[19, 20, 21]

Poststroke cerebral edema and seizures

Although significant cerebral edema can occur after anterior circulation ischemic stroke, it is thought to be somewhat rare (10-20%).[22] Edema and herniation are the most common causes of early death in patients with hemispheric stroke.

Seizures occur in 2-23% of patients within the first days after stroke.[22] A fraction of patients who have experienced stroke develop chronic seizure disorders.

Etiology
Ischemic strokes result from events that limit or stop blood flow, such as extracranial or intracranial thrombosis embolism, thrombosis in situ, or relative hypoperfusion. As blood flow decreases, neurons cease functioning, and irreversible neuronal ischemia and injury begin at blood flow rates of less than 18 mL/100 g of tissue/min.

Risk factors
Risk factors for ischemic stroke include modifiable and nonmodifiable etiologies. Identification of risk factors in each patient can uncover clues to the cause of the stroke and the most appropriate treatment and secondary prevention plan. Nonmodifiable risk factors include the following:

Age Race Sex Ethnicity History of migraine headaches Sickle cell disease Fibromuscular dysplasia Heredity

Modifiable risk factors include the following:

Hypertension (the most important) Diabetes mellitus Cardiac disease - Atrial fibrillation, valvular disease, mitral stenosis, and structural anomalies allowing right to left shunting, such as a patent foramen ovale and atrial and ventricular enlargement Hypercholesterolemia Transient ischemic attacks (TIAs) Carotid stenosis

Hyperhomocystinemia Lifestyle issues - Excessive alcohol intake, tobacco use, illicit drug use, obesity, physical inactivity Oral contraceptive use

Among the types of cardiac disease that increase stroke risk are atrial fibrillation, valvular disease, mitral stenosis, and structural anomalies allowing right-to-left shunting, such as a patent foramen ovale and atrial and ventricular enlargement. TIA is a transient neurologic deficit with no evidence of an ischemic lesion on neuroimaging. Roughly 80% resolve within 60 minutes.[23] TIA can result from the aforementioned mechanisms of stroke. Data suggest that roughly 10% of patients with TIA suffer stroke within 90 days and half of these patients suffer stroke within 2 days.[24, 25]

Genetic and inflammatory mechanisms

Evidence continues to accumulate to suggest important roles for inflammation and genetic factors in the process of atherosclerosis and, specifically, in stroke. According to the current paradigm, atherosclerosis is not a bland cholesterol storage disease, as previously thought, but a dynamic, chronic, inflammatory condition caused by a response to endothelial injury. Traditional risk factors, such as oxidized low-density lipoprotein (LDL) and smoking, contribute to this injury. It has been suggested, however, that infections may also contribute to endothelial injury and atherosclerosis. Host genetic factors, moreover, may modify the response to these environmental challenges, although inherited risk for stroke is likely multigenic. Even so, specific single-gene disorders with stroke as a component of the phenotype demonstrate the potency of genetics in determining stroke risk. For more information, see Genetic and Inflammatory Mechanisms in Stroke. In addition, complete information on the following metabolic disease and stroke can be found in the main articles:

Metabolic Disease and Stroke - Methylmalonic Acidemia Metabolic Disease and Stroke - Homocystinuria/Homocysteinemia Metabolic Disease and Stroke - Fabry Disease Metabolic Disease and Stroke MELAS Metabolic Disease and Stroke - Hyperglycemia/Hypoglycemia

Flow disturbances

Stroke symptoms can result from inadequate cerebral blood flow due to decreased blood pressure (and specifically, decreased cerebral perfusion pressure) or as a result of hematologic hyperviscosity due to sickle cell disease or other hematologic illnesses, such as multiple myeloma and polycythemia vera. In these instances, cerebral injury may occur in the presence of damage to other organ systems. For more information, see Blood Dyscrasias and Stroke.

Large-artery occlusion
Large-artery occlusion typically results from embolization of atherosclerotic debris originating from the common or internal carotid arteries or from a cardiac source. A smaller number of large-artery occlusions may arise from plaque ulceration and in situ thrombosis. Large-vessel ischemic strokes more commonly affect the MCA territory with the ACA territory affected to a lesser degree. (See the images below.)

Noncontrast CT in this 52-year-old male with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity and sulcal effacement involving the left anterior and middle cerebral artery territories consistent with acute infarction. There are scattered curvilinear areas of hyperdensity noted suggestive of developing petechial

hemorrhage in this large area of infarction. MRA in the same patient as in the above image (left) demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal MCA trunk and attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high signal confirmed to be true restricted diffusion on the ADC map consistent with acute

infarction. MIP image from a CTA demonstrates a filling defect or highgrade stenosis at the branching point of the right MCA trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.

Lacunar strokes
Lacunar strokes represent 13-20% of all ischemic strokes. They occur when the penetrating branches of the MCA, the lenticulostriate arteries, or the penetrating branches of the circle of Willis, vertebral artery, or basilar artery become occluded. (See the image below.)

Axial noncontrast CT demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in this 60-year-old male with new onset of rightsided weakness. The lesion demonstrates high signal on the FLAIR sequence (middle image) and diffusion-weighted MRI (right image), with low signal on the ADC maps indicating an acute lacunar infarction. Lacunar infarcts are typically no more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata, brainstem and cerebellum. Causes of lacunar infarcts include the following:

Microatheroma Lipohyalinosis Fibrinoid necrosis secondary to hypertension or vasculitis Hyaline arteriosclerosis Amyloid angiopathy

The great majority are related to hypertension.

Embolic strokes

Cardiogenic emboli may account for up to 20% of acute strokes. Emboli may arise from the heart, the extracranial arteries, or, rarely, the right-sided circulation (paradoxical emboli) with subsequent passage through a patent foramen ovale. The sources of cardiogenic emboli include the following:

Valvular thrombi (eg, in mitral stenosis or endocarditis or from use of a prosthetic valve) Mural thrombi (eg, in myocardial infarction [MI], atrial fibrillation [AF], dilated cardiomyopathy, or severe congestive heart failure [CHF]) Atrial myxoma

MI is associated with a 2-3% incidence of embolic strokes, of which 85% occur in the first month after MI.[26] Embolic strokes tend to have a sudden onset, and neuroimaging may demonstrate previous infarcts in several vascular territories or calcific emboli. Risk factors include atrial fibrillation and recent cardiac surgery. Cardioembolic strokes may be isolated, multiple and in a single hemisphere, or scattered and bilateral; the latter 2 types indicate multiple vascular distributions and are more specific for cardioembolism. Multiple and bilateral infarcts can be the result of embolic showers or recurrent emboli. Other possibilities for single and bilateral hemispheric infarctions include emboli originating from the aortic arch and diffuse thrombotic or inflammatory processes that can lead to multiple small-vessel occlusions.[27, 28] (See the image below.)

Cardioembolic stroke: Axial diffusion-weighted images demonstrate scattered foci of high signal in the subcortical and deep white matter bilaterally in a patient with a known cardiac source for embolization. An area of low signal in the left gangliocapsular region may be secondary to prior hemorrhage or subacute to chronic lacunar infarct. Recurrent strokes are most commonly secondary to cardioembolic phenomenon. For more information, see Cardioembolic Stroke.

Thrombotic strokes
Thrombogenic factors may include injury to and loss of endothelial cells, exposing the subendothelium, and platelet activation by the subendothelium, activation of the clotting cascade, inhibition of fibrinolysis, and blood stasis. Thrombotic strokes are generally thought to originate on ruptured atherosclerotic plaques. Arterial stenosis can cause turbulent blood flow, which can increase the risk for thrombus formation, atherosclerosis (ie, ulcerated plaques), and platelet adherence; all cause the formation of blood clots that either embolize or occlude the artery.

Intracranial atherosclerosis may be the cause in patients with widespread atherosclerosis. In other patients, especially younger patients, other causes should be considered, including the following[29, 10] : Hypercoagulable states (eg, antiphospholipid antibodies, protein C deficiency, protein S deficiency, pregnancy)

Sickle cell disease Fibromuscular dysplasia Arterial dissections Vasoconstriction associated with substance abuse

Watershed infarcts
Vascular watershed, or border-zone, infarctions occur at the most distal areas between arterial territories. They are believed to be secondary to embolic phenomenon or due to severe hypoperfusion, such as in carotid occlusion or prolonged hypotension.[30, 31, 32]

MRI was obtained to evaluate this 62-year-old hypertensive and diabetic male with a history of transient episodes of right-sided weakness and aphasia. The FLAIR image (left) demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter, bilaterally. This configuration is typical for deep border-zone or watershed infarction, in this case the anterior and posterior MCA watershed areas. The left sided infarcts have corresponding low signal on the ADC map (right), signifying acuity. An old left posterior parietal infarct is noted as well.

Epidemiology
Stroke is the leading cause of disability and the third leading cause of death in the United States.
[33]

More than 700,000 persons per year suffer a first-time stroke in the United States, with 20% of these individuals dying within the first year after the stroke. If current trends continue, this number is projected to reach 1 million per year by the year 2050.[34] The global incidence of stroke is unknown.

Stroke incidence by race and sex

In the United States, blacks have an age-adjusted risk of death from stroke that is 1.49 times that of whites.[35] Hispanics have a lower overall incidence of stroke than whites and blacks but more frequent lacunar strokes and stroke at an earlier age. Men are at higher risk for stroke than women; white males have a stroke incidence of 62.8 per 100,000, with death being the final outcome in 26.3% of cases, while women have a stroke incidence of 59 per 100,000 and a death rate of 39.2%.

Stroke and age

Although stroke often is considered a disease of elderly persons, one third of strokes occur in persons younger than 65 years.[34] Risk of stroke increases with age, especially in patients older than 64 years, in whom 75% of all strokes occur.

Prognosis
The prognosis after acute ischemic stroke varies greatly, depending on the stroke severity and on the patients premorbid condition, age, and poststroke complications.[6] Some patients experience hemorrhagic transformation of their infarct (See Pathophysiology). This is estimated to occur in 5% of uncomplicated ischemic strokes, in the absence of thrombolytics. Hemorrhagic transformation is not always associated with neurologic decline and ranges from small petechial hemorrhages to hematomas requiring evacuation. In the Framingham and Rochester stroke studies, the overall mortality rate at 30 days after stroke was 28%, the mortality rate at 30 days after ischemic stroke was 19%, and the 1-year survival rate for patients with ischemic stroke was 77%. In the United States, 20% of individuals die within the first year after a first-time stroke, as previously mentioned. Cardiogenic emboli are associated with the highest 1-month mortality in patients with acute stroke. In stroke survivors from the Framingham Heart Study, 31% needed help caring for themselves, 20% needed help when walking, and 71% had impaired vocational capacity in long-term followup. The presence of CT scan evidence of infarction early in presentation has been associated with poor outcome and with an increased propensity for hemorrhagic transformation after thrombolytics.[7, 36, 37]

Acute ischemic stroke has been associated with acute cardiac dysfunction and arrhythmia, which then correlate with worse functional outcome and morbidity at 3 months. Data suggest that severe hyperglycemia is independently associated with poor outcome and reduced reperfusion in thrombolysis, as well as extension of the infarcted territory.[38, 39, 40] To see complete information on Motor Recovery in Stroke, please go to the main article by clicking here.

Patient Education
Public education must involve all age groups. Incorporating stroke into basic life support (BLS) and cardiopulmonary resuscitation (CPR) curricula is just one way to reach a younger audience. Avenues to reach an audience with a higher stroke risk include using local churches, employers, and senior organizations to promote stroke awareness. The American Stroke Association advises the public to be aware of the symptoms of stroke that are easily recognized and to call 911 immediately. These symptoms include the following:

Sudden numbness or weakness of face, arm, or leg, especially on 1 side of the body Sudden confusion Sudden difficulty in speaking or understanding Sudden deterioration of vision in 1 or both eyes Sudden difficulty in walking, dizziness, and loss of balance or coordination Sudden, severe headache with no known cause

For excellent patient education resources, visit eMedicineHealth's Stroke Center. In addition, see eMedicineHealth's patient education articles Stroke, Transient Ischemic Attack (Mini-stroke),and Stroke-Related Dementia.
BAB II TINJAUAN PUSTAKA A. Definisi

Stroke atau serangan otak adalah sindrom klinis yang awal timbulnya mendadak, progresif, cepat, berupa defisit neurologis fokal dan atau global, yang berlangsung 24 jam atau lebih atau langsung menimbulkan kematian, dan semata-mata di sebabkan oleh gangguan peredaran darah otak non traumatik. 9 Stroke non hemoragik didefinisikan sebagai sekumpulan tanda klinik yang berkembang oleh sebab vaskular. Gejala ini berlangsung 24 jam atau lebih pada

umumnya terjadi akibat berkurangnya aliran darah ke otak, yang menyebabkan cacat atau kematian.10 Stroke non hemoragik sekitar 85%, yang terjadi akibat obstruksi atau bekuan di satu atau lebih arteri besar pada sirkulasi serebrum. Obstruksi dapat disebabkan oleh bekuan (trombus) yang terbentuk di dalam suatu pembuluh otak atau pembuluh atau organ distal. Trombus yang terlepas dapat menjadi embolus. 11 B. Etiologi

Stroke non hemoragik bisa terjadi akibat suatu dari dua mekanisme patogenik yaitu trombosis serebri atau emboli serebri.12 Trombosis serebri menunjukkan oklusi trombotik arteri karotis atau cabangnya, biasanya karena arterosklerosis yang mendasari. Proses ini sering timbul selama tidur dan bisa menyebabkan stroke mendadak dan lengkap. Defisit neurologi bisa timbul progresif dalam beberapa jam atau intermiten dalam beberapa jam atau hari.12 Emboli serebri terjadi akibat oklusi arteria karotis atau vetebralis atau cabangnya oleh trombus atau embolisasi materi lain dari sumber proksimal, seperti bifurkasio arteri karotis atau jantung. Emboli dari bifurkasio karotis biasanya akibat perdarahan ke dalam plak atau ulserasi di atasnya di sertai trombus yang tumpang tindih atau pelepasan materi ateromatosa dari plak sendiri. Embolisme serebri sering di mulai mendadak, tanpa tanda-tanda disertai nyeri kepala berdenyut. 12 C. Klasifikasi

Stroke sebagai diagnosis klinis untuk gambaran manifestasi lesi vaskular serebral, dapat di bagi dalam : 1. Stroke non hemoragik yang mencakup 13 a. b. c. d. TIA (Transient Ischemic Attack) Stroke in-evolution Stroke trombotik Stroke embolik

e. Stroke akibat komperesi terhadap arteri oleh proses di luar arteri seperti tumor, abses, granuloma. 2. Berdasarkan subtipe penyebab11 a. b. Stroke lakunar Stroke trombotik pembuluh besar

c. d. D.

Stroke embolik Stroke kriptogenik Faktor risiko

Ada beberapa faktor risiko stroke yang sering teridentifikasi pada stroke non hemoragik, diantaranya yaitu faktor risiko yang tidak dapat di modifikasi dan yang dapat di modifikasi. Penelitian yang dilakukan Rismanto (2006) di RSUD Prof. Dr. Margono Soekarjo Purwokerto mengenai gambaran faktor-faktor risiko penderita stroke menunjukan faktor risiko terbesar adalah hipertensi 57,24%, diikuti dengan diabetes melitus 19,31% dan hiperkolesterol 8,97%. 15,16 Faktor risiko yang tidak dapat dimodifikasi :15,16 1. Usia Pada umumnya risiko terjadinya stroke mulai usia 35 tahun dan akan meningkat dua kali dalam dekade berikutnya. 40% berumur 65 tahun dan hampir 13% berumur di bawah 45 tahun. Menurut Kiking Ritarwan (2002), dari penelitianya terhadap 45 kasus stroke didapatkan yang mengalami stroke non hemoragik lebih banyak pada tentan umur 45-65 tahun.16,17 2. Jenis kelamin Menurut data dari 28 rumah sakit di Indonesia, ternyata bahwa kaum pria lebih banyak menderita stroke di banding kaum wanita, sedangkan perbedaan angka kematianya masih belum jelas. Penelitian yang di lakukan oleh Indah Manutsih Utami (2002) di RSUD Kabupaten Kudus mengenai gambaran faktor-faktor risiko yang terdapat pada penderita stroke menunjukan bahwa jumlah kasus terbanyak jenis kelamin laki-laki 58,4% dari penelitianya terhadap 197 pasien stroke non hemoragik.16,18 3. Heriditer Gen berperan besar dalam beberapa faktor risiko stroke, misalnya hipertensi, penyakit jantung, diabetes melitus dan kelainan pembuluh darah, dan riwayat stroke dalam keluarga, terutama jika dua atau lebih anggota keluarga pernah mengalami stroke pada usia kurang dari 65 tahun, meningkatkan risiko terkena stroke. Menurut penelitian Tsong Hai Lee di Taiwan pada tahun 1997-2001 riwayat stroke pada keluarga meningkatkan risiko terkena stroke sebesar 29,3%. 5 4. Rasa atau etnik

Orang kulit hitam lebih banyak menderita stroke dari pada kulit putih. Data sementara di Indonesia, suku Padang lebih banyak menderita dari pada suku Jawa (khususnya Yogyakarta). 16

Faktor risiko yang dapat dimodifikasi : 1. Riwayat stroke Seseorang yang pernah memiliki riwayat stoke sebelumnya dalam waktu lima tahun kemungkinan akan terserang stroke kembali sebanyak 35% sampai 42%. 16 2. Hipertensi Hipertensi meningkatkan risiko terjadinya stroke sebanyak empat sampai enam kali ini sering di sebut the silent killer dan merupakan risiko utama terjadinya stroke non hemoragik dan stroke hemoragik. Berdasarkan Klasifikasi menurut JNC 7 yang dimaksud dengan tekanan darah tinggai apabila tekanan darah lebih tinggi dari 140/90 mmHg, makin tinggi tekanan darah kemungkinan stroke makin besar karena mempermudah terjadinya kerusakan pada dinding pembuluh darah, sehingga mempermudah terjadinya penyumbatan atau perdarahan otak. 16,19 3. Penyakit jantung Penyakit jantung koroner, kelainan katup jantung, infeksi otot jantung, paska oprasi jantung juga memperbesar risiko stroke, yang paling sering menyebabkan stroke adalah fibrilasi atrium, karena memudahkan terjadinya pengumpulan darah di jantung dan dapat lepas hingga menyumbat pembuluh darah otak. 16 4. (DM) Diabetes melitus Kadar gulakosa dalam darah tinggi dapat mengakibatkan kerusakan endotel pembuluh darah yang berlangsung secara progresif. Menurut penelitian Siregar F (2002) di RSUD Haji Adam Malik Medan dengan desain case control, penderita diabetes melitus mempunyai risiko terkena stroke 3,39 kali dibandingkan dengan yang tidak menderita diabetes mellitus.16,5 5. TIA Merupakan serangan-serangan defisit neurologik yang mendadak dan singkat akibat iskemik otak fokal yang cenderung membaik dengan kecepatan dan tingkat penyembuhan berfariasi tapi biasanya 24 jam. Satu dari seratus orang dewasa di perkirakan akan mengalami paling sedikit satu kali TIA seumur hidup mereka, jika diobati dengan benar, sekitar 1/10 dari para pasien ini akan mengalami stroke dalam 3,5 bulan setelah serangan pertama, dan sekitar 1/3 akan terkena stroke dalam lima tahun setelah serangan pertama. 11,20 6. Hiperkolesterol Lipid plasma yaitu kolesterol, trigliserida, fosfolipid, dan asam lemak bebas. Kolesterol dan trigliserida adalah jenis lipid yang relatif mempunyai makna klinis penting sehubungan dengan aterogenesis. Lipid tidak larut dalam plasma sehingga lipid terikat dengan protein sebagai mekanisme transpor dalam serum, ikatan ini

menghasilkan empat kelas utama lipuprotein yaitu kilomikron, lipoprotein densitas sangat rendah (VLDL), lipoprotein densitas rendah (LDL), dan lipoprotein densitas tinggi (HDL). Dari keempat lipo protein LDL yang paling tinggi kadar kolesterolnya, VLDL paling tinggi kadar trigliseridanya, kadar protein tertinggi terdapat pada HDL. Hiperlipidemia menyatakan peningkatan kolesterol dan atau trigliserida serum di atas batas normal, kondisi ini secara langsung atau tidak langsung meningkatkan risiko stroke, merusak dinding pembuluh darah dan juga menyebabkan penyakit jantung koroner. Kadar kolesterol total >200mg/dl, LDL >100mg/dl, HDL <40mg/dl, trigliserida >150mg/dl dan trigliserida >150mg/dl akan membentuk plak di dalam pembuluh darah baik di jantung maupun di otak. Menurut Dedy Kristofer (2010), dari penelitianya 43 pasien, di dapatkan hiperkolesterolemia 34,9%, hipertrigliserida 4,7%, HDL yang rendah 53,5%, dan LDL yang tinggi 69,8%. 21,16,22 7. Obesitas Obesitas berhubungan erat dengan hipertensi, dislipidemia, dan diabetes melitus. Prevalensinya meningkat dengan bertambahnya umur. Obesitas merupakan predisposisi penyakit jantung koroner dan stroke. Mengukur adanya obesitas dengan cara mencari body mass index (BMI) yaitu berat badan dalam kilogram dibagi tinggi badan dalam meter dikuadratkan. Normal BMI antara 18,50-24,99 kg/m2, overweight BMI antara 25-29,99 kg/m2 selebihnya adalah obesitas.16,23 8. Merokok Merokok meningkatkan risiko terjadinya stroke hampir dua kali lipat, dan perokok pasif berisiko terkena stroke 1,2 kali lebih besar. Nikotin dan karbondioksida yang ada pada rokok menyebabkan kelainan pada dinding pembuluh darah, di samping itu juga mempengaruhi komposisi darah sehingga mempermudah terjadinya proses gumpalan darah. Berdasarkan penelitian Siregar F (2002) di RSUD Haji Adam Malik Medan kebiasaan merokok meningkatkan risiko terkena stroke sebesar empat kali.16,5 E. Patofisiologi

Otak terdiri dari sel-sel otak yang disebut neuron, sel-sel penunjang yang dikenal sebagai sel glia, cairan serebrospinal, dan pembuluh darah. Semua orang memiliki jumlah neuron yang sama sekitar 100 miliar, tetapi koneksi di antara berbagi neuron berbeda-beda. Pada orang dewasa, otak membentuk hanya sekitar 2% (1200-1400 gram) dari berat tubuh total, tetapi mengkonsumsi sekitar 20% oksigen dan 50% glukosa yang ada di dalam darah arterial. Dalam jumlah normal darah yang mengalir ke otak sebanyak 50-60ml per 100 gram jaringan otak per menit. Jumlah darah yang diperlukan untuk seluruh otak adalah 700-840 ml/menit, dari jumlah darah itu di salurkan melalui arteri karotis interna yang terdiri dari arteri karotis (dekstra dan sinistra), yang menyalurkan darah ke bagian depan otak disebut sebagai sirkulasi arteri serebrum anterior, yang kedua adalah vertebrobasiler, yang memasok darah ke bagian belakang otak disebut sebagai

sirkulasi arteri serebrum posterior, selanjutnya sirkulasi arteri serebrum anterior bertemu dengan sirkulasi arteri serebrum posterior membentuk suatu sirkulus Willisi.5,13 Gangguan pasokan darah otak dapat terjadi dimana saja di dalam arteri-arteri yang membentuk sirkulus willisi serta cabang-cabangnya. Secara umum, apabila aliran darah ke jaringan otak terputus 15 sampai 20 menit, akan terjadi infark atau kematian jaringan. Perlu di ingat bahwa oklusi di suatu arteri tidak selalu menyebabkan infark di daerah otak yang di perdarahi oleh arteri tersebut dikarenakan masih terdapat sirkulasi kolateral yang memadai ke daerah tersebut. Proses patologik yang sering mendasari dari berbagi proses yang terjadi di dalam pembuluh darah yang memperdarhai otak diantaranya dapat berupa : 11 1. Keadaan penyakit pada pembuluh darah itu sendiri, seperti pada aterosklerosis dan thrombosis. 2. Berkurangnya perfusi akibat gangguan status aliran darah, misalnya syok atau hiperviskositas darah. 3. Gangguan aliran darah akibat bekuan atau embolus infeksi yang berasal dari jantung atau pembuluh ekstrakranium. Dari gangguan pasokan darah yang ada di otak tersebut dapat menjadikan terjadinya kelainian-kelainan neurologi tergantung bagian otak mana yang tidak mendapat suplai darah, yang diantaranya dapat terjani kelainan di system motorik, sensorik, fungsi luhur, yang lebih jelasnya tergantung saraf bagian mana yang terkena. F. Gejala klinis

Gejala stroke non hemoragik yang timbul akibat gangguan peredaran darah di otak bergantung pada berat ringannya gangguan pembuluh darah dan lokasi tempat gangguan peredaran darah terjadi, kesadaran biasanya tidak mengalami penurunan, menurut penelitian Rusdi Lamsudi pada tahun 1989-1991 stroke non hemoragik tidak terdapat hubungan dengan terjadinya penurunan kesadaran, kesadaran seseorang dapat di nilai dengan menggunakan skala koma Glasgow yaitu :5,9,24 ]

Tabel 2.1. Skala koma Glasgow.9 Buka mata (E) Respon motorik (M) Respon verbal (V)

1. Tidak ada respons 2. Respons dengan rangsangan nyeri 3. Buka mata dengan perintah 5. Buka mata spontan

1. Tidak ada gerakan 2. Ekstensi abnormal

1. Tidak ada suara 2. Mengerang

4. Fleksi abnormal 3.

Bicara kacau

5. Menghindari nyeri

4. Disorientasi tempat dan waktu

6. Melokalisir nyeri5. Orientasi baik dan sesuai 7. Mengikuti perintah

Penilaian skor skala koma Glasgow : a. b. c. Koma (GCS = 3-8) Konfusi, lateragi atau stupor (GCS = 9-14) Sadar penuh, atentif dan orientatif (GCS = 15)

Gangguan yang biasanya terjadi yaitu gangguan mototik ( hemiparese), sensorik (anestesia, hiperestesia, parastesia/geringgingan , gerakan yang canggung serta simpang siur, gangguan nervus kranial, saraf otonom (gangguan miksi, defeksi, salvias), fungsi luhur (bahasa, orientasi, memori, emosi) yang merupakan sifat khas manusia, dan gangguan koordinasi (sidrom serebelar) :5,13 1. Disekuilibrium yaitu keseimbangan tubuh yang terganggu yang terlihat seseorang akan jatuh ke depan, samping atau belakang sewaktu berdiri 2. Diskoordinasi muskular yang diantaranya, asinergia, dismetria dan seterusnya. Asinergia ialah kesimpangsiuran kontraksi otot-otot dalam mewujudkan suatu corak gerakan. Dekomposisi gerakan atau gangguan lokomotorik dimana dalam suatu gerakan urutan kontraksi otot-otot baik secara volunter atau reflektorik tidak dilaksanakan lagi. Disdiadokokinesis tidak biasa gerak cepat yang arahnya berlawanan contohnya pronasi dan supinasi. Dismetria, terganggunya memulai dan menghentikan gerakan.

3.

Tremor (gemetar), bisa diawal gerakan dan bisa juga di akhir gerakan

4. Ataksia berjalan dimana kedua tungkai melangkah secara simpangsiur dan kedua kaki ditelapakkanya secara acak-acakan. Ataksia seluruh badan dalam hal ini badan yang tidak bersandar tidak dapat memelihara sikap yang mantap sehingga bergoyang-goyang. Tabel 2.2. Gangguan nervus kranial.25 Nervus kranial I: Olfaktorius II: Optikus III: Okulomotorius Fungsi Penciuman Penglihatan Gerak mata; kontriksi pupil; akomodasi Penemuan klinis dengan lesi Anosmia (hilangnya daya penghidu) Amaurosis Diplopia (penglihatan kembar), ptosis; midriasis; hilangnya akomodasi Diplopia mati rasa pada wajah; kelemahan otot rahang Diplopia Hilangnya kemampuan mengecap pada dua pertiga anterior lidah; mulut kering; hilangnya lakrimasi; paralisis otot wajah Tuli; tinitus(berdenging terus menerus); vertigo; nitagmus

IV: Troklearis V: Trigeminus

Gerak mata Sensasi umum wajah, kulit kepala, dan gigi; gerak mengunyah Gerak mata Pengecapan; sensasi umum pada platum dan telinga luar; sekresi kelenjar lakrimalis, submandibula dan sublingual; ekspresi wajah

VI: Abdusen VII: Fasialis

VIII: Pendengaran; Vestibulokoklea keseimbangan ris IX: Glosofaringeus

Pengecapan; sensasi Hilangnya daya umum pada faring dan pengecapan pada telinga; mengangkat sepertiga posterior palatum; sekresi kelenjar lidah; anestesi pada parotis farings; mulut kering

sebagian X: Vagus Pengecapan; sensasi umum pada farings, laring dan telinga; menelan; fonasi; parasimpatis untuk jantung dan visera abdomen Disfagia (gangguan menelan) suara parau; paralisis palatum

XI: Asesorius Spinal XII: Hipoglosus

Fonasi; gerakan kepala; Suara parau; leher dan bahu kelemahan otot kepala, leher dan bahu Gerak lidah Kelemahan dan pelayuan lidah

Gejala klinis tersering yang terjadi yaitu hemiparese yang dimana Pendeita stroke non hemoragik yang mengalami infrak bagian hemisfer otak kiri akan mengakibatkan terjadinya kelumpuhan pada sebalah kanan, dan begitu pula sebaliknya dan sebagian juga terjadi Hemiparese dupleks, pendeita stroke non hemoragik yang mengalami hemiparesesi dupleks akan mengakibatkan terjadinya kelemahan pada kedua bagian tubuh sekaligus bahkan dapat sampai mengakibatkan kelumpuhan.26 Penelitian yang dilakukan Sri Andriani Sinaga (2008) terhadap 281 pasien stroke di Rumah Sakit Haji Medan di dapatkan hemiparese sinistra yaitu 46,3%, diikuti oleh hemiparese dekstra 31,7%, tidak tercatat sebanyak 14,2% dan hemiparesese dupleks 7,8%. Gambaran klinis utama yang berkaitan dengan insufisiensi arteri ke otak mungkin berkaitan dengan pengelompokan gejala dan tanda berikut yang tercantum dan disebut sindrom neurovaskular :5,11 1. Arteri karotis interna (sirkulasi anterior : gejala biasanya unilateral)

a. Dapat terjadi kebutaan satu mata di sisi arteria karotis yang terkena, akibat insufisiensi arteri retinalis b. Gejala sensorik dan motorik di ekstremitas kontralateral karena insufisiensi arteria serebri media c. Lesi dapat terjadi di daerah antara arteria serebri anterior dan media atau arteria serebri media. Gejala mula-mula timbul di ekstremitas atas dan mungkin mengenai wajah. Apabila lesi di hemisfer dominan, maka terjadi afasia ekspresif karena keterlibatan daerah bicara motorik Broca.

2. a. b.

Arteri serebri media (tersering) Hemiparese atau monoparese kontralateral (biasanya mengenai lengan) Kadang-kadang hemianopsia (kebutaan) kontralateral

c. Afasia global (apabila hemisfer dominan terkena): gangguan semua fungsi yang berkaitan dengan bicara dan komunikasi d. 3. a. b. c. 4. a. b. c. d. e. f. g. h. i. j. 5. a. b. c. d. G. Disfasia Arteri serebri anterior (kebingungan adalah gejala utama) Kelumpuhan kontralateral yang lebih besar di tungkai Defisit sensorik kontralateral Demensia, gerakan menggenggam, reflek patologis Sistem vertebrobasilaris (sirkulasi posterior: manifestasi biasanya bilateral) Kelumpuhan di satu atau empat ekstremitas Meningkatnya reflek tendon Ataksia Tanda Babinski bilateral Gejala-gejala serebelum, seperti tremor intention, vertigo Disfagia Disartria Rasa baal di wajah, mulut, atau lidah Sinkop, stupor, koma, pusing, gangguan daya ingat, disorientasi Gangguan penglihatan dan pendengaran Arteri serebri posterior Koma Hemiparese kontralateral Afasia visual atau buta kata (aleksia) Kelumpuhan saraf kranialis ketiga: hemianopsia, koreoatetosis. Pemeriksaan fisik

Tujuan pemeriksaan fisik adalah untuk mendeteksi penyebab stroke ekstrakranial, memisahkan stroke dengan kelainan lain yang menyerupai stroke, dan menentukan beratnya defisit neurologi yang dialami, pemeriksaan neurologik terdiri dari penilaian hal-hal berikut ini :25 1. a. b. c. d. e. f. g. h. i. j. k. l. 2. Status mental Tingkat kesadaran Bicara Orientasi Pengetahuan kejadian-kejadian mutakhir Pertimbangan Abstraksi Kosakata Respons emosional Daya ingat Berhitung Pengenalan benda Praksis (integrasi aktivitas motorik). Nervus kranial

a. Nervus olfaktorius diperiksa tajamnya penciuman dengan satu lubang hidung pasien ditutup, sementara bahan penciuman diletakan pada lubang hidung kemudian di suruh membedakan bau. b. Nervus optikus yang diperikasa adalah ketajaman penglihatan dan pemeriksaan oftalmoskopi. c. Nervus okulomotorius yang diperiksa adalah reflek pupil dan akomodasi.

d. Nervus troklearis dengan cara melihat pergerakan bola mata keatas, bawah, kiri, kanan, lateral, diagonal. e. Nervus trigeminus dengan cara melakukan pemeriksaan reflek kornea dengan menempelkan benang tipis ke kornea yang normalnya pasien akan menutup mata, Pemeriksaan cabang sensoris pasa bagian pipi, pemeriksaan cabang motorik pada pipi.

f. Nervus abdusen dengan cara pasien di suruh menggerakan sisi mata ke samping kiri dan kanan. g. Nervus fasialis di dapatkan hilangnya kemampuan mengecap pada dua pertiga anterior lidah, mulut kering, paralisis otot wajah. h. Nervus vestibulokoklearis yang di periksa adalah pendengaran, keseimbangan, dan pengetahuan tentang posisi tubuh. i. Nervus glosofaringeus di periksa daya pengecapan pada sepertiga posterior lidah anestesi pada farings mulut kering sebagian. j. Nervus vagus dengan cara memeriksa cara menelan.

k. Nervus asesorius dengan cara memeriksa kekuatan pada muskulus sternokleudomastoideus, pasien di suruh memutar kepala sesuai tahanan yang di berikan si pemeriksa. l. Nervus hipoglosus bisa dengan melihat kekuatan lidah, lidah di julurkan ke luar jika ada kelainan maka lidah akan membelok ke sisi lesi. 3. a. Fungsi motorik Masa otot bisa dengan inspeksi.

b. Kekuatan otot, dengan menyuruh pasien bergerak secara aktif melawan tahanan, bandingkan dengan sisi yang lain. Sekala yang lazim digunakan yaitu 0: tidak ada kontraksi, 1: hanya ada sedikit kontraksi, 2: gerakan yang dibatasi oleh gravitasi, 3: gerakan melawan gravitasi, 4: gerakan melawan gravitasi dengan sedikit tahanan, 5: gerakan melawan gravitasi dengan tahanan penuh (normal). c. Tonus otot dengan membandingkan gerakan pasif pada otot itu bandingkan dengan sisi yang lain, lesi neuron motorik atas terjadi peningkatan tonus tetapi sebaliknya lesi pada neuron motorik bawah menyebabkan penurunan tonus otot. 4. Reflek

Ada dua jenis reflek yang di periksa yaitu reflek renggang, atau tendo profunda, dan reflek superfisial. Reflek renggang diantaranya yaitu reflek biseps, brakioradialis, triseps, patela dan achiles bisa dinilai berdasarkan sekala 0-4+ yaitu 0: tak ada respon, 1+: berkurang, 2+: normal, 3+: meningkat, 4+: hiperaktif. Jika reflek hiperaktif merupakan ciri penyakit traktus ekstrapiramidalis, kelainan elektrolit, hipertiroidisme dan kelainan metabolik, sedangkan jika reflek berkurangnya reflek merupakan ciri kelainan sel kornu anterior dan miopati. Reflek superfisial yang abnormal yaitu reflek babinski, reflek chaddock, reflek openheim. Reflek babinski untuk menguji radiks saraf pada lumbal lima sampai sacrum dua, dengan menggores bagian telapak kaki bagian lateral dari tumit ke arah pangkal jari-jari kaki melengkung ke medial, maka akan terjadi dorsifleksi ibu jari kakai dengan

penyebaran jari-jari lainya. Reflek chaddock akan terjadi dorsofleksi ketika sisi lateral kaki di gores. Reflek openheim dengan penekanan tulang kering yang akan menyebabkan dorsofeksi ibu jari kaki. 5. a. b. c. d. e. 6. Fungsi sensorik Sentuhan ringan Sensasi nyeri Sensasi getar Propriosepsis (sensasi posisi) Lokalisasi taktil. Fungsi serebelar

a. Tes jari ke hidung jika terjadi gangguan di serebelum maka akan melewati sasaran secara terus menerus dan kadang di sertai tremor. b. Tes tumit kelutut, pasien di suruh menggeserkan tumit suatu ekstremitas bawah menuruni tulang kering ekstremitas bawah lainya dengan dimulai dari lutut, dalam keadaan penyakit serebelum tumitnya bergoyang-goyang dari sisi ke sisi. c. Gerakan yang berganti-ganti dengan cepat.

d. Tes Romberg dengan cara menyuruh pasien berdiri di depan pemeriksa, dengan kaki di rapatkan sehingga kedua tumit dan jari-jari kaki saling bersentuhan tes ini positif jika pasien mulai bergoyang-goyang dan harus memindahkan kakinya untuk keseimbangan. e. Gaya berjalan. Hemiplegi cenderung menyeret kakinya. parkinson cenderung berjalan dengan langkah pendek, diseret, kepala membungkuk dengan punggung membungkuk dan tergesa-gesa. Ataksia serebelum berjalan dengan langkah kaki berdasar lebar, kedua kakinya sangat jauh terpisah ketika berjalan. Foot drop dengan gaya berjalan seperti menampar yang khas. Ataksia sensoris yaitu berjalan dengan langkah-langkah yang tinggi. H. Pemeriksaan laboratorium dan teknik pencitraan

Pemeriksaan laboratorium standar biasanya di gunakan untuk menentukan etiologi yang mencakup urinalisis, darah lengkap, kimia darah, dan serologi. Pemeriksaan yang sering dilakukan untuk menentukan etiologi yaitu pemeriksaan kadar gula darah, dan pemeriksaan lipid untuk melihat faktor risiko dislipidemia : 1. Gula darah

Tabel 2.3. Kadar glukosa darah. 9

Kriteria diagnostik DM Bukan DM Belum pasti (mg/dl) DM (mg/dl) Kadar glukosa darah sewaktu Plasma Vena Darah kapiler Kadar glukosa darah puasa Plasma vena Darah <110 <90 110 125 90 109 >126 >110 <110 <90 110 199 90 199 >200 >200 DM (mg/dl)

Diabetes melitus merupakan faktor risiko untuk stroke, namun tidak sekuat hipertensi. Gatler menyatakan bahwa penderita stroke aterotrombotik di jumpai 30% dengan diabetes mellitus. Diabetes melitus mampu menebalkan pembuluh darah otak yang besar, menebalnya pembuluh darah otak akan mempersempit diameter pembuluh darah otak dan akan mengganggu kelancaran aliran darah otak di samping itu, diabetes melitus dapat mempercepat terjadinya aterosklerosis (pengerasan pembuluh darah) yang lebih berat sehingga berpengaruh terhadap terjadinya stroke.5,26 2. Profil lipid

Tabel 2.4. Kadar Lipid Serum Normal. 22 Kolesterol Total Optimal Diinginkan Tinggi LDL Optimal Mendekati optimal Diinginkan Tinggi < 100 100 129 130 159 160 189 (mg/dl) < 200 200 239 240

Sangat tinggi HDL Rendah Tinggi Trigliserida Optimal Diinginkan Tinggi Sangat tinggi

190

< 40 60

< 150 150 199 200 449 500

LDL adalah lipoprotein yang paling banyak mengandung kolesterol. LDL merupakan komponen utama kolesterol serum yang menyebabkan peningkatan risiko aterosklerosis, HDL berperan memobilisasi kolesterol dari ateroma yang sudah ada dan memindahkannya ke hati untuk diekskresikan ke empedu , oleh karena itu kadar HDL yang tinggi mempunyai efek protektif dan dengan cara inilah kolesterol dapat di turunkan, namun penurunan kadar HDL merupakan faktor yang meningkatkan terjadinya aterosklerosis dan stroke. 22 Pemeriksaan lain yang dapat di lakukan adalah dengan menggunakan teknik pencitraan diantaranya yaitu :27,11 1. CT scan

Untuk mendeteksi perdarahan intra kranium, tapi kurang peka untuk mendeteksi stroke non hemoragik ringan, terutama pada tahap paling awal. CT scan dapat memberi hasil tidak memperlihatkan adanya kerusakan hingga separuh dari semua kasus stroke non hemoragik.20 2. MRI (magnetic resonance imaging)

Lebih sensitif dibandingkan dg CT scan dalam mendeteksi stroke non hemoragik rigan, bahkan pada stadium dini, meskipun tidak pada setiap kasus. Alat ini kurang peka dibandingkan dengan CT scan dalam mendeteksi perdarahan intrakranium ringan.20 3. Ultrasonografi dan MRA (magnetic resonance angiography)

Pemindaian arteri karotis dilakukan dengan ultrasonografi (menggunakan gelombang suara untuk menciptakan citra), MRA digunakan untuk mencari kemungkinan penyempitan arteri atau bekuan di arteri utama, MRA khususnya

bermanfaat untuk mengidentifikasi aneurisma intrakranium dan malformasi pembuluh darah otak.2 4. Angiografi otak

Merupakan penyuntikan suatu bahan yang tampak dalam citra sinar-X ke dalam arteri-arteri otak. Pemotretan dengan sinar-X kemudian dapat memperlihatkan pembuluh-pembuluh darah di leher dan kepala. 20

I.

Penatalaksanaan

Waktu merupakan hal terpenting dalam penatalaksanaan stroke non hemoragik yang di perlukan pengobatan sedini mungkin, karena jeda terapi dari stroke hanya 3-6 jam. Penatalaksanaan yang cepat, tepat dan cermat memegang peranan besar dalam menentukan hasil akhir pengobatan. 9 1. Prinsip penatalaksanaan stroke non hemoragik

a. Memulihkan iskemik akut yang sedang berlangsung (3-6 jam pertama) menggunakan trombolisis dengan rt-PA (recombinan tissue-plasminogen activator ). Ini hanya boleh di berikan dengan waktu onset <3 jam dan hasil CT scan normal, tetapi obat ini sangat mahal dan hanya dapat di lakukan di rumah sakit yang fasilitasnya lengkap. b. Mencegah perburukan neurologis dengan jeda waktu sampai 72 jam yang diantaranya yaitu : 1) Edema yang progresif dan pembengkakan akibat infark. Terapi dengan manitol dan hindari cairan hipotonik. 2) Ekstensi teritori infark, terapinya dengan heparin yang dapat mencegah trombosis yang progresif dan optimalisasi volume dan tekanan darah yang dapat menyerupai kegagalan perfusi. 3) Konversi hemoragis, msalah ini dapat di lihat dari CT scan, tiga faktor utama adalah usia lanjut, ukuran infark yang besar, dan hipertensi akut, ini tak boleh di beri antikoagulan selama 43-72 jam pertama, bila ada hipertensi beri obat antihipertensi. c. Mencegah stroke berulang dini dalam 30 hari sejak onset gejala stroke terapi dengan heparin. 2. Protokol penatalaksanaan stroke non hemoragik akut

a. Pertimbangan rt-PA intravena 0,9 mg/kgBB (dosis maksimum 90 mg) 10% di berikan bolus intravena sisanya diberikan per drip dalam wakti 1 jam jika onset di pastikan <3 jam dan hasil CT scan tidak memperlihatkan infrak yang luas. b. Pemantauan irama jantung untuk pasien dengan aritmia jantung atau iskemia miokard, bila terdapat fibrilasi atrium respons cepat maka dapat diberikan digoksin 0,125-0,5 mg intravena atau verapamil 5-10 mg intravena atau amiodaron 200 mg drips dalam 12 jam. c. Tekanan darah tidak boleh cepat-cepat diturunkan sebab dapat memperluas infrak dan perburukan neurologis. Pedoman penatalaksanaan hipertensi bila terdapat salah satu hal berikut : 1) Hipertensi diobati jika terdapat kegawat daruratan hipertensi neurologis seperti, iskemia miokard akut, edema paru kardiogenik, hipertensi maligna (retinopati), nefropati hipertensif, diseksi aorta. 2) Hipertensi diobati jika tekanan darah sangat tinggi pada tiga kali pengukuran selang 15 menit dimana sistolik >220 mmHg, diastolik >120 mmHg, tekanan arteri rata-rata >140 mmHg. 3) Pasien adalah kandidat trombolisis intravena dengan rt-PA dimana tekanan darah sistolik >180 mmHg dan diastolik >110 mmHg. Dengan obat-obat antihipertensi labetalol, ACE, nifedipin. Nifedifin sublingual harus dipantau ketat setiap 15 menit karena penurunan darahnya sangat drastis. Pengobatan lain jika tekanan darah masih sulit di turunkan maka harus diberikan nitroprusid intravena, 50 mg/250 ml dekstrosa 5% dalam air (200 mg/ml) dengan kecepatan 3 ml/jam (10 mg/menit) dan dititrasi sampai tekanan darah yang di inginkan. Alternatif lain dapat diberikan nitrogliserin drip 10-20 mg/menit, bila di jumpai tekanan darah yang rendah pada stroke maka harus di naikkan dengan dopamin atau debutamin drips. d. Pertimbangkan observasi di unit rawat intensif pada pasien dengan tanda klinis atau radiologis adanya infrak yang masif, kesadaran menurun, gangguan pernafasan atau stroke dalam evolusi. e. Pertimbangkan konsul ke bedah saraf untuk infrak yang luas.

f. Pertimbangkan sken resonasi magnetik pada pasien dengan stroke vetebrobasiler atau sirkulasi posterior atau infrak yang tidak nyata pada CT scan. g. Pertimbangkan pemberian heparin intravena di mulai dosis 800 unit/jam, 20.000 unit dalam 500 ml salin normal dengan kecepatan 20 ml/jam, sampai masa tromboplastin parsial mendekati 1,5 kontrol pada kondisi : 1) Kemungkinan besar stroke kardioemboli

2) 3) 4) 5)

TIA atau infrak karena stenosis arteri karotis Stroke dalam evolusi Diseksi arteri Trombosis sinus dura

Heparin merupakan kontraindikasi relatif pada infrak yang luas. Pasien stroke non hemoragik dengan infrak miokard baru, fibrilasi atrium, penyakit katup jantung atau trombus intrakardiak harus diberikan antikoagulan oral (warfarin) sampai minimal satu tahun. Perawatan umum untuk mempertahankan kenyamanan dan jalan nafas yang adekuat sangatlah penting. Pastikan pasien bisa menelan dengan aman dan jaga pasien agar tetap mendapat hidrasi dan nutrisi. Menelan harus di nilai (perhatikan saat pasien mencoba untuk minum, dan jika terdapat kesulitan cairan harus di berikan melalui selang lambung atau intravena. Beberapa obat telah terbukti bermanfaat untuk pengobatan penyakit serebrovaskular, obat-obatan ini dapat dikelompokkan atas tiga kelompok yaitu obat a ntikoagulansia, penghambat trombosit dan trombolitika :27 1. Antikoagulansia adalah zat yang dapat mencegah pembekuan darah dan di gunakan pada keadaan dimana terdapat kecenderungan darah untuk membeku. Obat yang termasuk golongan ini yaitu heparin dan kumarin. 28 2. Penghambat trombosit adalah obat yang dapat menghambat agregasi trombosit sehingga menyebabkan terhambatnya pembentukan trombus yang terutama sering ditemukan pada sistem arteri. Obat yang termasuk golongan ini adalah aspirin, dipiridamol, tiklopidin, idobufen, epoprostenol, clopidogrel. 28 3. Trombolitika juga disebut fimbrinolitika berkhasiat melarutkan trombus diberikan 3 jam setelah infark otak, jika lebih dari itu dapat menyebabkan perdarahan otak, obat yang termasuk golongan ini adalah streptokinase, alteplase, urokinase, dan reteplase.28 Pengobatan juga di tujukan untuk pencegahan dan pengobatan komplikasi yang muncul sesuai kebutuhan. Sebagian besar pasien stroke perlu melakukan pengontrolan perkembangn kesehatan di rumah sakit kembali, di samping melakukan pemulihan dan rehabilitasi sendiri di rumah dengan bantuan anggota keluarga dan ahli terapi. Penelitian yang dilakukan Sri Andriani (2008) terhadap 281 pasien stroke di Rumah Sakit Haji Medan di dapatkan 60% berobat jalan, 23,8% meninggal dan sisanya pulang atas permintaan sendiri. 28,5 J. Komplikasi

Kebanyakan morbiditas dan mortilitas stroke berkaitan dengan komplikasi non neurologis yang dapat di minimalkan dengan perawatan umum, komplikasikomplikasi tersebut yaitu :9 1. Demam, yang dapat mengeksaserbasi cedera otak iskemik dan harus di obati secara agresif dengan antipiretik atau kompres dingin. Penyebab demam biasanya adalah pneumonia aspirasi, kultur darah dan urin kemudian beri antibiotik intravena sesuai hasil kultur. 2. Kekurangan nutrisi, bila pasien sadar dan tidak memiliki risiko aspirasi maka dapat dilakukan pemberian makanan secara oral, tetapi jika pasien tidak sadar atau memiliki risiko aspirasi beri makanan secara enteral melalui pipa nasoduodenal ukuran kecil dalam 24 jam pertama setelah onset stroke. 3. Hipovolemia, dapat di koreksi dengan kristaloid isotonis. Cairan hipotonis (dekstrosa 5% dalam air, larutan NaCl 0,45 %) dapat memperberat edema serebri dan harus di hindari. 4. Hiperglikemi dan hipoglikemi, ini dapat lakukan terapi setiap 6 jam selama 35 hari sejak onset stoke : a. b. c. d. e. f. g. h. 5. < 50 mg/dl 50-100 mg/dl 100-200 mg/dl 200-250 mg/dl 250-300 mg/dl 300-350 mg/dl 350-400 mg/dl > 400 mg/dl : dekstrosa 40% 50 ml bolus intravena : dekstrosa 5 % dalam NaCl 0,9 %, 500 ml dalam 6 jam : pengobatan (-), NaCl 0,9 % atau Ringer laktat : insulin 4 unit intravena : insulin 8 unit intravena : insulin 12 unit intravena : insulin 16 unit intravena : insulin 20 unit intravena

Atelektasis paru, dapat di cegah dengan fisioterapi dada setiap 4 jam

6. Dekubitus, dicegah dengan perubahan posisi tubuh setiap 2 jam, kontraktur dilakukan latihan gerakan sendi anggota badan secara pasif 4 kali sehari, pemendekan tendo achiles di lakukan splin tumit untuk mempertahankan pergelangan kaki dalam posisi dorsofleksi. 7. Defisit sensorik, kognitif, memori, bahasa, emosi serta visuospasial harus di lakukan neurorestorasi dini. 8. Trombosis vena dalam, di cegah dengan pemberian heparin 5000 unit atau fraksiparin 0,3 cc setiap 12 jam selama 5-10 hari.

9. Infeksi vesika, pembentukan batu, gangguan sfingter vesika biasanya di karenakan pemasangan kateter urin menetap, latihan vesika harus segera di lakukan sedini mungkin bila pasien sudah sadar. K. Pencegahan

Pencegahan primer dapat dilakukan dengan menghindari rokok, stres mental, alkohol, kegemukan, konsumsi garam berlebih, obat-obat golongan amfetamin, kokain dan sejenisnya. Mengurangi kolesterol dan lemak dalam makanan. Menggendaliakan hipertensi, diabetes melitus, penyakit jantung, penyakit vaskular aterosklerotik lainya. Perbanyak konsumsi gizi seimbang dan olahraga teratur. 9 Pencegahan skunder dengan cara memodifikasi gaya hidup yang berisiko seperti hipertensi dengan diet dan obat antihipertensi, diabetes melitus dengan diet dan obat hipoglikemik oral atau insulin, penyakit jantung dengan antikoagulan oral, dislipidemia dengan diet rendah lemak dan obat antidislipidemia, berhenti merokok, hindari kegemukan dan kurang gerak. 9 L. Prognosis

Prognosis stroke dipengaruhi oleh sifat dan tingkat keparahan defisit neurologis yang dihasilkan. usia pasien, penyebab stroke, gangguan medis yang terjadi bersamaan juga mempengaruhi prognosis. Secara keseluruhan, kurang dari 80% pasien dengan stroke bertahan selama paling sedikit 1 bulan, dan didapatkan tingkat kelangsungan hidup dalam 10 tahun sekitar 35%. pasien yang selamat dari periode akut, sekitar satu setengah samapai dua pertiga kembali fungsi independen, sementara sekitar 15% memerlukan perawatan institusional. Di Indonesia, diperkirakan setiap tahun terjadi 500.000 penduduk terkena serangan stroke, dan sekitar 25% atau 125.000 orang meninggal dan sisanya mengalami cacat ringan atau berat. Sebanyak 28,5% penderita stroke meninggal dunia, sisanya menderita kelumpuhan sebagian maupun total. Hanya 15% saja yang dapat sembuh total dari serangan stroke dan kecacatan. 29,30,31,32