presentation of stroke

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• What is a stroke? A Mayo Clinic expert explains

Learn more from neurologist Robert D. Brown, Jr. M.D., M.P.H.

I'm Dr. Robert Brown, neurologist at Mayo Clinic. In this video, we'll cover the basics of a stroke. What is it, who it happens to, the symptoms, diagnosis, and treatment. Whether you're looking for answers for yourself or someone you love, we're here to give you the best information available. You've likely heard the term stroke before. They affect about 800,000 people in the United States each year. Strokes happen in two ways. In the first, a blocked artery can cut off blood to an area of the brain. And this is known as an ischemic stroke. 85% of strokes are of this type. The second type of stroke happens when a blood vessel can leak or burst. So the blood spills into the brain tissue or surrounding the brain. And this is called a hemorrhagic stroke. Prompt treatment can reduce brain damage and the likelihood of death or disability. So if you or someone you know is experiencing a stroke, you should call 911 and seek emergency medical care right away.

Anyone can have a stroke, but some things put you at higher risk. And some things can lower your risk. If you're 55 and older, if you're African-American, if you're a man, or if you have a family history of strokes or heart attacks, your chances of having a stroke are higher. Being overweight, physically inactive, drinking alcohol heavily, recreational drug use. Those who smoke, have high blood pressure or high cholesterol, have poorly controlled diabetes, suffer from obstructive sleep apnea, or have certain forms of heart disease are at greater risk as well.

Look for these signs and symptoms if you think you or someone you know is having a stroke: Sudden trouble speaking and understanding what others are saying. Paralysis or numbness of the face, arm or leg on one side of the body. Problems seeing in one or both eyes, trouble walking, and a loss of balance. Now many strokes are not associated with headache, but a sudden and severe headache can sometimes occur with some types of stroke. If you notice any of these, even if they come and go or disappear completely, seek emergency medical attention or call 911. Don't wait to see if symptoms stop, for every minute counts.

Once you get to the hospital, your emergency team will review your symptoms and complete a physical exam. They will use several tests to help them figure out what type of stroke you're having and determine the best treatment for the stroke. This could include a CT scan or MRI scan, which are pictures of the brain and arteries, a carotid ultrasound, which is a soundwave test of the carotid arteries which provide blood flow to the front parts of the brain, and blood tests.

Once your doctors can determine if you're having an ischemic or hemorrhagic stroke, they'll be able to figure out the best treatment. If you're suffering an ischemic stroke, it's important to restore blood flow to your brain as quickly as possible, providing the oxygen and other nutrients your brain cells need to survive. To do this, doctors may use an intravenous clot buster medicine, dissolving the clot that is obstructing the blood flow or they may perform an emergency endovascular procedure. This involves advancing a tiny plastic tube called a catheter up into the brain arteries, allowing the blockage in the artery to be removed directly. Unlike ischemic strokes, the goal for treating a hemorrhagic stroke is to control the bleeding and reduce pressure in the brain. Doctors may use emergency medicines to lower the blood pressure, prevent blood vessel spasms, encourage clotting and prevent seizures. Or, if the bleeding is severe, surgery may be performed to remove the blood that is in the brain.

Every stroke is different, and so every person's road to recovery is different. Management of a stroke often involves a care team with several specialties. This may include a neurologist and a physical medicine and rehabilitation physician, among others. Now, in the end, our goal is to help you recover as much function as possible so that you can live independently. A stroke is a life-changing event that can affect you emotionally as much as it can physically. You may feel helpless, frustrated, or depressed. So look for help and support from friends and family. Accept that recovery will take hard work and most of all time. Strive for a new normal and remember to celebrate your progress. If you'd like to learn even more about strokes, watch our other related videos or visit mayoclinic.org. We wish you all the best.

An ischemic stroke occurs when the blood supply to part of the brain is blocked or reduced. This prevents brain tissue from getting oxygen and nutrients. Brain cells begin to die in minutes. Another type of stroke is a hemorrhagic stroke. It occurs when a blood vessel in the brain leaks or bursts and causes bleeding in the brain. The blood increases pressure on brain cells and damages them.

A stroke is a medical emergency. It's crucial to get medical treatment right away. Getting emergency medical help quickly can reduce brain damage and other stroke complications.

The good news is that fewer Americans die of stroke now than in the past. Effective treatments also can help prevent disability from stroke.

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If you or someone you're with may be having a stroke, pay attention to the time the symptoms began. Some treatments are most effective when given soon after a stroke begins.

Symptoms of stroke include:

• Trouble speaking and understanding what others are saying. A person having a stroke may be confused, slur words or may not be able to understand speech.
• Numbness, weakness or paralysis in the face, arm or leg. This often affects just one side of the body. The person can try to raise both arms over the head. If one arm begins to fall, it may be a sign of a stroke. Also, one side of the mouth may droop when trying to smile.
• Problems seeing in one or both eyes. The person may suddenly have blurred or blackened vision in one or both eyes. Or the person may see double.
• Headache. A sudden, severe headache may be a symptom of a stroke. Vomiting, dizziness and a change in consciousness may occur with the headache.
• Trouble walking. Someone having a stroke may stumble or lose balance or coordination.

When to see a doctor

Seek immediate medical attention if you notice any symptoms of a stroke, even if they seem to come and go or they disappear completely. Think "FAST" and do the following:

• Face. Ask the person to smile. Does one side of the face droop?
• Arms. Ask the person to raise both arms. Does one arm drift downward? Or is one arm unable to rise?
• Speech. Ask the person to repeat a simple phrase. Is the person's speech slurred or different from usual?
• Time. If you see any of these signs, call 911 or emergency medical help right away.

Call 911 or your local emergency number immediately. Don't wait to see if symptoms stop. Every minute counts. The longer a stroke goes untreated, the greater the potential for brain damage and disability.

If you're with someone you suspect is having a stroke, watch the person carefully while waiting for emergency assistance.

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There are two main causes of stroke. An ischemic stroke is caused by a blocked artery in the brain. A hemorrhagic stroke is caused by leaking or bursting of a blood vessel in the brain. Some people may have only a temporary disruption of blood flow to the brain, known as a transient ischemic attack (TIA). A TIA doesn't cause lasting symptoms.

• Ischemic stroke

An ischemic stroke occurs when a blood clot, known as a thrombus, blocks or plugs an artery leading to the brain. A blood clot often forms in arteries damaged by a buildup of plaques, known as atherosclerosis. It can occur in the carotid artery of the neck as well as other arteries.

This is the most common type of stroke. It happens when the brain's blood vessels become narrowed or blocked. This causes reduced blood flow, known as ischemia. Blocked or narrowed blood vessels can be caused by fatty deposits that build up in blood vessels. Or they can be caused by blood clots or other debris that travel through the bloodstream, most often from the heart. An ischemic stroke occurs when fatty deposits, blood clots or other debris become lodged in the blood vessels in the brain.

Some early research shows that COVID-19 infection may increase the risk of ischemic stroke, but more study is needed.

Hemorrhagic stroke

Hemorrhagic stroke occurs when a blood vessel in the brain leaks or ruptures. Bleeding inside the brain, known as a brain hemorrhage, can result from many conditions that affect the blood vessels. Factors related to hemorrhagic stroke include:

• High blood pressure that's not under control.
• Overtreatment with blood thinners, also known as anticoagulants.
• Bulges at weak spots in the blood vessel walls, known as aneurysms.
• Head trauma, such as from a car accident.
• Protein deposits in blood vessel walls that lead to weakness in the vessel wall. This is known as cerebral amyloid angiopathy.
• Ischemic stroke that leads to a brain hemorrhage.

A less common cause of bleeding in the brain is the rupture of an arteriovenous malformation (AVM). An AVM is an irregular tangle of thin-walled blood vessels.

Transient ischemic attack

A transient ischemic attack (TIA) is a temporary period of symptoms similar to those of a stroke. But a TIA doesn't cause permanent damage. A TIA is caused by a temporary decrease in blood supply to part of the brain. The decrease may last as little as five minutes. A transient ischemic attack is sometimes known as a ministroke.

A TIA occurs when a blood clot or fatty deposit reduces or blocks blood flow to part of the nervous system.

Seek emergency care even if you think you've had a TIA . It's not possible to tell if you're having a stroke or TIA based only on the symptoms. If you've had a TIA , it means you may have a partially blocked or narrowed artery leading to the brain. Having a TIA increases your risk of having a stroke later.

Risk factors

Many factors can increase the risk of stroke. Potentially treatable stroke risk factors include:

Lifestyle risk factors

• Being overweight or obese.
• Physical inactivity.
• Heavy or binge drinking.
• Use of illegal drugs such as cocaine and methamphetamine.

Medical risk factors

• High blood pressure.
• Cigarette smoking or secondhand smoke exposure.
• High cholesterol.
• Obstructive sleep apnea.
• Cardiovascular disease, including heart failure, heart defects, heart infection or irregular heart rhythm, such as atrial fibrillation.
• Personal or family history of stroke, heart attack or transient ischemic attack.
• COVID-19 infection.

Other factors associated with a higher risk of stroke include:

• Age — People age 55 or older have a higher risk of stroke than do younger people.
• Race or ethnicity — African American and Hispanic people have a higher risk of stroke than do people of other races or ethnicities.
• Sex — Men have a higher risk of stroke than do women. Women are usually older when they have strokes, and they're more likely to die of strokes than are men.
• Hormones — Taking birth control pills or hormone therapies that include estrogen can increase risk.

Complications

A stroke can sometimes cause temporary or permanent disabilities. Complications depend on how long the brain lacks blood flow and which part is affected. Complications may include:

• Loss of muscle movement, known as paralysis. You may become paralyzed on one side of the body. Or you may lose control of certain muscles, such as those on one side of the face or one arm.
• Trouble talking or swallowing. A stroke might affect the muscles in the mouth and throat. This can make it hard to talk clearly, swallow or eat. You also may have trouble with language, including speaking or understanding speech, reading or writing.
• Memory loss or trouble thinking. Many people who have had strokes experience some memory loss. Others may have trouble thinking, reasoning, making judgments and understanding concepts.
• Emotional symptoms. People who have had strokes may have more trouble controlling their emotions. Or they may develop depression.
• Pain. Pain, numbness or other feelings may occur in the parts of the body affected by stroke. If a stroke causes you to lose feeling in the left arm, you may develop a tingling sensation in that arm.
• Changes in behavior and self-care. People who have had strokes may become more withdrawn. They also may need help with grooming and daily chores.

You can take steps to prevent a stroke. It's important to know your stroke risk factors and follow the advice of your healthcare professional about healthy lifestyle strategies. If you've had a stroke, these measures might help prevent another stroke. If you have had a transient ischemic attack (TIA), these steps can help lower your risk of a stroke. The follow-up care you receive in the hospital and afterward also may play a role.

Many stroke prevention strategies are the same as strategies to prevent heart disease. In general, healthy lifestyle recommendations include:

• Control high blood pressure, known as hypertension. This is one of the most important things you can do to reduce your stroke risk. If you've had a stroke, lowering your blood pressure can help prevent a TIA or stroke in the future. Healthy lifestyle changes and medicines often are used to treat high blood pressure.
• Lower the amount of cholesterol and saturated fat in your diet. Eating less cholesterol and fat, especially saturated fats and trans fats, may reduce buildup in the arteries. If you can't control your cholesterol through dietary changes alone, you may need a cholesterol-lowering medicine.
• Quit tobacco use. Smoking raises the risk of stroke for smokers and nonsmokers exposed to secondhand smoke. Quitting lowers your risk of stroke.
• Manage diabetes. Diet, exercise and losing weight can help you keep your blood sugar in a healthy range. If lifestyle factors aren't enough to control blood sugar, you may be prescribed diabetes medicine.
• Maintain a healthy weight. Being overweight contributes to other stroke risk factors, such as high blood pressure, cardiovascular disease and diabetes.
• Eat a diet rich in fruits and vegetables. Eating five or more servings of fruits or vegetables every day may reduce the risk of stroke. The Mediterranean diet, which emphasizes olive oil, fruit, nuts, vegetables and whole grains, may be helpful.
• Exercise regularly. Aerobic exercise reduces the risk of stroke in many ways. Exercise can lower blood pressure, increase the levels of good cholesterol, and improve the overall health of the blood vessels and heart. It also helps you lose weight, control diabetes and reduce stress. Gradually work up to at least 30 minutes of moderate physical activity on most or all days of the week. The American Heart association recommends getting 150 minutes of moderate-intensity aerobic activity or 75 minutes of vigorous aerobic activity a week. Moderate intensity activities can include walking, jogging, swimming and bicycling.
• Drink alcohol in moderation, if at all. Drinking large amounts of alcohol increases the risk of high blood pressure, ischemic strokes and hemorrhagic strokes. Alcohol also may interact with other medicines you're taking. However, drinking small to moderate amounts of alcohol may help prevent ischemic stroke and decrease the blood's clotting tendency. A small to moderate amount is about one drink a day. Talk to your healthcare professional about what's appropriate for you.
• Treat obstructive sleep apnea (OSA). OSA is a sleep disorder that causes you to stop breathing for short periods several times during sleep. Your healthcare professional may recommend a sleep study if you have symptoms of OSA . Treatment includes a device that delivers positive airway pressure through a mask to keep the airway open while you sleep.
• Don't use illicit drugs. Certain illicit drugs such as cocaine and methamphetamine are established risk factors for a TIA or a stroke.

Preventive medicines

If you have had an ischemic stroke, you may need medicines to help lower your risk of having another stroke. If you have had a TIA , medicines can lower your risk of having a stroke in the future. These medicines may include:

Anti-platelet drugs. Platelets are cells in the blood that form clots. Anti-platelet medicines make these cells less sticky and less likely to clot. The most commonly used anti-platelet medicine is aspirin. Your healthcare professional can recommend the right dose of aspirin for you.

If you've had a TIA or minor stroke, you may take both an aspirin and an anti-platelet medicine such as clopidogrel (Plavix). These medicines may be prescribed for a period of time to reduce the risk of another stroke. If you can't take aspirin, you may be prescribed clopidogrel alone. Ticagrelor (Brilinta) is another anti-platelet medicine that can be used for stroke prevention.

Blooding-thinning medicines, known as anticoagulants. These medicines reduce blood clotting. Heparin is a fast-acting anticoagulant that may be used short-term in the hospital.

Slower acting warfarin (Jantoven) may be used over a longer term. Warfarin is a powerful blood-thinning medicine, so you need to take it exactly as directed and watch for side effects. You also need regular blood tests to monitor warfarin's effects.

Several newer blood-thinning medicines are available to prevent strokes in people who have a high risk. These medicines include dabigatran (Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis) and edoxaban (Savaysa). They work faster than warfarin and usually don't require regular blood tests or monitoring by your healthcare professional. These medicines also are associated with a lower risk of bleeding complications compared to warfarin.

Stroke care at Mayo Clinic

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• Oliveira-Filho J, et al. Initial assessment and management of acute stroke. https://www.uptodate.com/contents/search. Accessed Sept. 13, 2023.
• About stroke. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/healthy_living.htm. Accessed Sept. 13, 2023.
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• Rehab therapy after a stroke. American Stroke Association. https://www.stroke.org/en/life-after-stroke/stroke-rehab/rehab-therapy-after-a-stroke. Accessed Sept. 13, 2023.
• Arteriovenous malformations (AVMs). National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/health-information/disorders/arteriovenous-malformations-avms?search-term=arterial#. Accessed Oct. 2, 2023.
• Cerebral aneurysms. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/disorders/patient-caregiver-education/fact-sheets/cerebral-aneurysms-fact-sheet. Accessed Sept. 13, 2023.
• Transient ischemic attack. Merck Manual Professional Version. https://www.merckmanuals.com/professional/neurologic-disorders/stroke/transient-ischemic-attack-tia?query=transient%20ischemic%20attack#. Accessed Sept. 13, 2023.
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• Rose NS, et al. Overview of secondary prevention of ischemic stroke. https://www.uptodate.com/contents/search. Accessed Sept. 13, 2023.
• Prevent stroke: What you can do. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/prevention.htm#print. Accessed Sept. 13, 2023.
• Know your risk for stroke. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/risk_factors.htm#. Accessed Oct. 2, 2023.
• Powers WJ, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke — A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2019; doi:10.1161/STR.0000000000000211.
• Papadakis MA, et al., eds. Quick Medical Diagnosis & Treatment 2023. McGraw Hill; 2023. https://accessmedicine.mhmedical.com. Accessed Sept. 13, 2023.
• Tsao CW, et al. Heart disease and stroke statistics — 2023 update: A report from the American Heart Association. Circulation. 2023; doi:10.1161/CIR.0000000000001123.
• Grotta JC, et al., eds. Stroke: Pathophysiology, Diagnosis, and Management. 7th ed. Elsevier, 2022. https://www.clinicalkey.com. Accessed Sept. 15, 2023.
• Suppah M, et al. An evidence-based approach to anticoagulation therapy comparing direct oral anticoagulants and vitamin K antagonists in patients with atrial fibrillation and bioprosthetic valves: A systematic review, meta-analysis and network meta-analysis. American Journal of Cardiology. 2023; doi:10.1016/j.amjcard.2023.07.141.
• Tyagi K, et al. Neurological manifestations of SARS-CoV-2: Complexity, mechanism and associated disorders. European Journal of Medical Research. 2023; doi:10.1186/s40001-023-01293-2.
• Siegler JE, et al. Cerebrovascular disease in COVID-19. Viruses. 2023; doi:10.3390/v15071598.
• Lombardo M, et al. Health effects of red wine consumption: A narrative review of an issue that still deserves debate. Nutrients. 2023; doi:10.3390/nu15081921.
• Jim J. Complications of carotid endarterectomy. https://www.uptodate.com/contents/search. Accessed Oct. 2, 2023.
• Van Nimwegan D, et al. Interventions for improving psychosocial well-being after stroke: A systematic review. International Journal of Nursing Studies. 2023; doi:10.1016/j.ijnurstu. 2023.104492 .
• Hasan TF, et al. Diagnosis and management of acute ischemic stroke. Mayo Clinic Proceedings. 2018; doi:10.1016/j.mayocp.2018.02.013.
• Ami TR. Allscripts EPSi. Mayo Clinic. Sept. 4, 2023.
• Barrett KM, et al. Ambulance-based assessment of NIH stroke scale with telemedicine: A feasibility pilot study. Journal of Telemedicine and Telecare. 2017; doi:10.1177/1357633X16648490.
• Sener U, et al. Ischemic stroke in patients with malignancy. Mayo Clinic Proceedings. 2022; doi:10.1016/j.mayocp.2022.09.003.
• Quality check. The Joint Commission. https://www.qualitycheck.org/search/?keyword=mayo%20clinic. Accessed Oct. 4, 2023.
• Quality care you can trust. American Heart Association. https://www.heart.org/en/professional/quality-improvement/hospital-maps. Accessed Oct. 4, 2023.
• Attig JM. Allscripts EPSi. Mayo Clinic. Oct. 9, 2023.
• How much physical activity do you need? American Heart Association. https://www.heart.org/en/healthy-living/fitness/fitness-basics/aha-recs-for-physical-activity-infographic. Accessed Oct. 12, 2023.
• Graff-Radford J (expert opinion). Mayo Clinic. Oct. 11, 2023.
• Healthcare. DNV Healthcare USA, Inc. https://www.dnvhealthcareportal.com/hospitals?search_type=and&q=mayo+clinic&c=&c=20806&c=&c=&prSubmit=Search. Accessed Nov. 1, 2023.
• Brain hemisphere connections
• Cerebral angiogram
• CT scan of brain tissue damaged by stroke
• Stroke rehabilitation
• Strokes FAQ Neurologist Robert D. Brown, Jr. M.D., M.P.H., answers the most frequently asked questions about strokes.
• Typing with Brain Waves

Associated Procedures

• Carotid angioplasty and stenting
• Carotid endarterectomy
• Carotid ultrasound
• Coronary angioplasty and stents
• Echocardiogram
• Home enteral nutrition

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Ischemic stroke.

Channing Hui ; Prasanna Tadi ; Mahammed Z. Khan Suheb ; Laryssa Patti .

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Last Update: April 20, 2024 .

• Continuing Education Activity

Acute stroke, previously known as a cerebrovascular accident (CVA), represents a critical medical emergency characterized by the sudden onset of focal neurological deficits within a vascular territory stemming from underlying cerebrovascular pathologies. As the most common type of stroke, ischemic strokes pose a significant burden on public health systems and individuals alike. With its pervasive impact across diverse patient populations, strokes constitute a significant source of morbidity and mortality worldwide. Understanding the underlying mechanisms, risk factors, and management strategies is crucial in mitigating the impact of this pervasive neurological condition.

This course provides a comprehensive overview of the evaluation and management of ischemic stroke, offering participants invaluable insights into the nuances of care delivery for this complex condition. From early recognition to evidence-based treatment modalities, participants will explore key strategies to optimize patient outcomes and minimize long-term sequelae. Moreover, the course highlights the pivotal role of an interprofessional team in promptly recognizing and effectively managing ischemic strokes, emphasizing the importance of collaborative efforts among healthcare professionals from various specialties.

• Apply anatomical anatomy to facilitate the proper treatment of acute ischemic stroke.
• Assess acute ischemic stroke using the current NIH stroke scale to measure the severity of ischemic stroke.
• Implement the recommended management of acute ischemic stroke, including immediate interventions, mitigation of sequelae, and subacute management.
• Collaborate with an interprofessional team to improve care coordination and communication while managing patients affected by acute and subacute ischemic strokes.
• Introduction

Acute stroke is the acute onset of focal neurological deficits in a vascular territory affecting the brain, retina, or spinal cord due to underlying cerebrovascular diseases. [1] Stroke is prevalent across patient populations and can significantly cause morbidity and mortality. Strokes are categorized as ischemic and hemorrhagic. Hemorrhagic strokes can further be classified as intracerebral and subarachnoid hemorrhage. Among ischemic strokes, the Trial Org 10172 in Acute Stroke Treatment (TOAST) classification is used to subdivide the categories that include the following:

• Cardioembolism                                                                                                                      
• Small vessel occlusion                                                                                                                
• Large artery atherosclerosis                                                                                                            
• Stroke of undetermined etiology
• Stroke of other determined etiology (possible or probable depending on the results of ancillary studies)  [2]

A crucial aspect of classification involves the physician's ability to designate a specific subtype diagnosis as probable or possible, depending on the level of certainty. A diagnosis is considered "probable" when clinical findings, neuroimaging data, and results of diagnostic studies align with a particular subtype, and other potential causes have been ruled out. On the other hand, a diagnosis is labeled as "possible" when clinical findings and neuroimaging data suggest a specific subtype, but additional studies have not been conducted. Given that many patients undergo a limited number of diagnostic tests, the categorizations of probable and possible allow the physician to establish as precise a subgroup diagnosis as possible.

The etiology of ischemic stroke is a thrombotic or embolic event that causes an impairment of blood flow to an area of the brain. In a thrombotic event, the blood flow to the brain is obstructed within the blood vessel due to a thrombus (clot) within the vessel itself, usually secondary to atherosclerotic disease, arterial dissection, fibromuscular dysplasia, or inflammatory conditions. In an embolic event, debris from elsewhere in the body blocks blood flow through the affected vessel. The source of emboli can be the proximal artery, such as an atherosclerotic plaque in the internal carotid artery, causing an artery-to-artery embolic stroke distally from any proximal source, commonly from the heart. Occasionally, the source may be from the right side of the circulation, going through a right-to-left shunt, such as a patent foramen ovale, towards the cerebral arterial system. The etiology of stroke affects both prognosis and outcomes. [3] [4]

Cardioembolism:  This group comprises patients with arterial blockages likely caused by an embolism originating in the heart. Cardiac sources are categorized into high-risk and medium-risk groups based on their propensity for embolism. At least 1 cardiac source of an embolus must be identified to consider a possible or probable diagnosis of cardioembolic stroke. Clinical and brain imaging findings resemble those described for large-artery atherosclerosis. Evidence of a previous transient ischemic attack (TIA) or stroke in more than 1 vascular territory or systemic embolisms supports a clinical diagnosis of cardiogenic stroke. Possible large artery atherosclerotic sources of thrombosis or embolism should be ruled out. A stroke occurring in a patient with a medium-risk cardiac source of embolism and no other apparent cause of stroke is categorized as a possible cardioembolic stroke. [5]

Large artery atherosclerosis:  These patients will exhibit clinical and brain imaging findings indicating either significant (> 50%) narrowing or complete blockage of a major brain artery or branch cortical artery, likely due to atherosclerosis. Clinical manifestations may include symptoms of cerebral cortical impairment (eg, aphasia, neglect, or limited motor function) or dysfunction of the brainstem or cerebellum. The presence of intermittent claudication history, TIAs in the same vascular territory, a carotid bruit, or weakened pulses can aid in confirming the clinical diagnosis. Lesions in the cortex, cerebellum, brainstem, or subcortical hemispheric infarctions larger than 1.5 cm in diameter observed on computed tomography (CT) or magnetic resonance imaging (MRI) indicate potential large artery atherosclerotic origin. Additional supportive evidence through duplex imaging or arteriography demonstrating more than 50% stenosis of a relevant intracranial or extracranial artery is necessary. Diagnostic evaluations should rule out potential sources of cardiogenic embolism. A diagnosis of stroke attributed to large artery atherosclerosis cannot be established if duplex or arteriographic studies appear normal or only reveal minimal changes. [6]

Small vessel occlusion:  This category encompasses patients with strokes commonly classified as lacunar infarcts in other systems. Patients in this group should present with 1 of the typical clinical lacunar syndromes and should not exhibit signs of cerebral cortical dysfunction. A history of diabetes mellitus or hypertension supports the clinical diagnosis. Additionally, patients should have normal CT scan or MRI findings or demonstrate a relevant brainstem or subcortical hemisphere lesion with a diameter of <1.5 cm. The absence of potential cardiac sources for embolism is expected, and evaluation of the major extracranial arteries should not reveal stenosis >50% in an artery on the same side. [7]

Stroke of undetermined etiology:  In numerous cases, determining the cause of a stroke proves challenging. Some patients undergo extensive evaluation yet yield no likely etiology. Others undergo only a cursory evaluation, resulting in an undetermined cause. This category also encompasses patients with 2 or more potential causes of stroke, making it difficult for physicians to reach a definitive diagnosis. For instance, a patient presenting with a medium-risk cardiac source of embolism alongside another potential cause of stroke would be classified as having a stroke of undetermined etiology. Similarly, a patient with atrial fibrillation and ipsilateral carotid stenosis of 50%, or one with a traditional lacunar syndrome and ipsilateral carotid stenosis of 50%, would fall into this category. [8]

Stroke of other determined etiology:  This group consists of patients with uncommon stroke causes, such as nonatherosclerotic vasculopathies, hypercoagulable states, or hematologic disorders. Patients in this category should exhibit clinical symptoms and CT or MRI findings indicative of acute ischemic stroke, regardless of the size or location of the lesion. Diagnostic tests, such as blood tests or arteriography, should reveal 1 of these unusual stroke causes. Other studies should be conducted to rule out cardiac sources of embolism and large artery atherosclerosis. [9]

• Epidemiology

In 2021, stroke accounted for 1 in 6 deaths from cardiovascular disease, with someone in the US experiencing a stroke every 40 seconds, resulting in a stroke-related death every 3 minutes and 14 seconds. [10] Annually, over 795,000 Americans suffer from a stroke, of which approximately 610,000 are initial occurrences. [10] Nearly a quarter of these strokes, roughly 185,000 cases, occur in individuals with a history of previous strokes. Ischemic strokes, blocking blood flow to the brain, constitute about 87% of all strokes. According to the Framingham Heart Study, stroke incidence has declined. However, the cohort was predominantly a White population. [11] [12] [13]

The financial burden of stroke in the US amounted to nearly $56.5 billion between 2018 and 2019, covering healthcare expenses, medication, and lost productivity due to missed workdays. Stroke stands as a primary contributor to severe long-term disability, particularly affecting mobility in over half of stroke survivors aged 65 and older. [14]

Disparities in stroke incidence and outcomes exist across racial and ethnic groups, with non-Hispanic Black adults facing nearly twice the risk of a first stroke compared to White adults, and both non-Hispanic Black and Pacific Islander adults exhibiting the highest stroke-related mortality rates. Moreover, the death rate attributed to stroke rose from 38.8 per 100,000 in 2020 to 41.1 per 100,000 in 2021. [15]

• Pathophysiology

In thrombosis, an obstructive process prevents blood flow to regions of the brain. The most common risk factor is large vessel atherosclerosis. Other risk factors include vasculitides and arterial dissection.

Embolic events occur when a clot originates from another location in the body. Most commonly, the clot's source is the heart's valve or chambers, for example, when a clot forms within the atria in atrial fibrillation and dislodges into the arterial vascular supply. Less frequent sources include venous, septic, air, or fat emboli.

Lacunar infarcts are usually seen in the subcortical areas of the brain supplied by small penetrating or perforating arteries, usually without collaterals. These include the lenticulostriate arteries from the middle cerebral artery, the thalamic perforators from the posterior cerebral artery, and the paramedian branches from the basilar artery. The underlying pathology of these penetrating arteries is small vessel arteriolosclerosis caused by hypertension, aging, smoking, diabetes, and other conventional vascular risk factors. [16]

Cerbral Autoregulation 

Under physiological conditions, cerebral blood flow is primarily regulated by the resistance within the cerebral blood vessels, which correlates directly with their diameter. Vasodilation results in increased blood volume within the brain and heightened cerebral blood flow, while vasoconstriction produces the opposite effect. [17] Additionally, cerebral blood flow is influenced by fluctuations in cerebral perfusion pressure.

Cerebral autoregulation denotes the ability to maintain relatively stable cerebral blood flow despite moderate shifts in perfusion pressure. [17] [18] The precise mechanisms underlying autoregulation remain incompletely understood and likely involve multiple pathways. Evidence suggests that the smooth muscle in cerebral vessels reacts directly to changes in perfusion pressure by contracting with pressure elevation and relaxing with pressure reduction. Furthermore, decreases in cerebral blood flow may prompt blood vessel dilation by releasing vasoactive substances, although the specific molecules responsible have yet to be identified. Nitric oxide released by endothelial cells also appears to contribute to autoregulation.

Ordinarily, cerebral blood flow regulation through autoregulation operates within a mean arterial pressure (MAP) range of 60 to 150 mm Hg, albeit with individual variations in upper and lower limits. Beyond this range, the brain's ability to compensate for perfusion pressure changes diminishes, causing cerebral blood flow to rise or fall passively in response to pressure fluctuations. This passive response poses a risk of ischemia at low pressures and edema at high pressures.

During certain pathological conditions, such as ischemic stroke, cerebral autoregulation becomes impaired. As cerebral perfusion pressure declines, cerebral blood vessels dilate to augment cerebral blood flow. [19]  However, if the decrease in perfusion pressure exceeds the brain's compensatory capacity, cerebral blood flow diminishes. Initially, an increase in the oxygen extraction fraction occurs to sustain oxygen delivery to the brain. Subsequently, as cerebral blood flow continues to decrease, additional mechanisms come into play.

Protein synthesis is inhibited below a cerebral blood flow rate of 50 mL/100 g/min. Protein synthesis ceases altogether at 35 mL/100 g/min, and there is a transient increase in glucose utilization. When cerebral blood flow drops to 25 mL/100 g/min, glucose utilization declines significantly, and anaerobic glycolysis ensues, resulting in tissue acidosis due to lactic acid accumulation. Neuronal electrical failure occurs at a cerebral blood flow of 16 to 18 mL/100 g/min, followed by failure of membrane ion homeostasis at 10 to 12 mL/100 g/min. [19] This threshold typically marks the onset of infarction.

In hypertensive individuals, autoregulation adapts to operate at higher arterial pressures. Lowering blood pressure to normal levels in such individuals could exacerbate autoregulation dysfunction during stroke, leading to further reductions in cerebral blood flow.

Concept of the Ischemic Penumbra

During an acute ischemic stroke, the brain tissue that relies exclusively on 1 artery for its blood supply will suffer an infarct, forming what is known as the infarct core. [20] Surrounding this core is an area of brain tissue called the ischemic penumbra, which maintains some blood supply through collateral circulation. However, as swelling from the infarction grows, the penumbra diminishes, and the infarct core expands. Under normal conditions, cerebral perfusion is approximately 50 mL/100 g/min. Brain cells begin to die when perfusion drops below 30%, equivalent to <15 mL/100 g/min. Hence, when blood flow is reduced but remains above 30% of the normal rate, the brain tissue is ischemic but not infarcted, highlighting the critical principle that "time is brain." This principle underscores the importance of timely revascularization treatments in acute ischemic stroke, given the distinct time windows for intervention based on these physiological insights. [21] [22] [23]

Ischemic Stroke Syndromes

Ischemic strokes can present in predetermined syndromes due to decreased blood flow to particular areas of the brain that correlate to exam findings—allowing clinicians to predict the site of the brain vasculature that can be affected.

Middle Cerebral Artery (MCA) Infarction

The MCA is the most common artery involved in stroke (see Images. Left MCA Territory Infarction and Right-Sided MDA 'Cord Sign' Harbingering Acute Infection). The MCA is divided into 4 segments (M1, M2, M3, and M4) and supplies a large area of the lateral surface of the brain, part of the basal ganglia, and the internal capsule. The M1 (horizontal) segment gives off the lenticulostriate arteries, which supply the basal ganglia and internal capsule. The M1 segment continues to the M2 (Sylvian) segment and supplies the insula, superior temporal lobe, parietal lobe, and inferolateral frontal lobe. [24]

The MCA distribution involves the lateral cerebral cortex. MCA syndrome is best explained by understanding the homunculus of the cerebral cortex, in which the lateral portion contains motor and sensory functions that involve the face and upper extremities. MCA infarctions classically present with contralateral hemiparesis, facial paralysis, and sensory loss in the face and upper extremities. The lower extremities may be involved, especially when the deep brain structures are involved, but upper extremity symptoms usually predominate. In addition, gaze preferences towards the side of the lesion may be seen. Additional symptoms include the following:  

• Dysarthria is characterized by difficulty phonating due to the physical weakness of the facial muscles. Dysarthria does not have much localizing value in acute stroke, as both cortical and subcortical infarcts can cause dysarthria. Dominant and nondominant hemisphere strokes can also cause dysarthria. The most severe form of dysarthria is anarthria, during which the patient will have no speech output. Dysarthria is often misinterpreted as aphasia.
• Neglect is when the patient seems to "ignore" a hemisphere of their world due to an inability to see that area. Neglect is a nondominant cortical sensory dysfunction. Extinction or inability to perceive double simultaneous stimuli is a bedside test commonly performed for a nondominant cortical lesion.
• Visual field loss occurs in MCA infarcts because the branches of the MCA supply the optic radiations. A more limited ischemic stroke affecting the parietal lobe may cause contralateral inferior quadrantanopia. In contrast, a limited temporal lobe infarct will result in a contralateral superior quadrantanopia (pie-in-the-sky).
• Aphasia, or the inability to produce or understand language, is caused by injury to the language areas of the dominant hemisphere of the brain, which are supplied by the dominant MCA.

Anterior Cerebral Artery (ACA) Infarction

The ACA supplies blood to the medial areas of the frontal, prefrontal, primary motor, primary sensory, and supplemental motor cortices. These are areas corresponding to the lower extremities in the cortical homunculus. Pure ACA infarcts are uncommon because of the good collateral blood supply. The sensory and motor cortices receive sensory information and control the contralateral lower extremity movement. The ACA distribution involves the medial cerebral cortex. The clinical presentation of an ACA infarction includes contralateral sensory and motor deficits in the lower extremity. The upper extremity and face are spared. [25]

Posterior Cerebral Artery (PCA) Infarction

The superficial PCA supplies the occipital lobe and the medial portion of the temporal lobe. The deep PCA supplies the thalamus and other posterior deep structures of the brain. The occipital lobe is the location of the visual cortex. The thalamus is the main relaying center for ascending and descending nervous networks. The most common cause of a PCA infarct is an atherothrombotic lesion in the vertebral artery. [26]

PCA infarctions can be divided into deep and superficial categories based on the PCA supply. If the deep segments of the PCA are involved, the symptoms are mainly related to thalamic dysfunction. The symptoms may include hypersomnolence, cognitive deficits, ocular findings, hypoesthesia, and ataxia. Larger infarcts that involve the deep structures can lead to hemisensory loss and hemiparesis due to the involvement of the thalamus and the adjacent internal capsule. Superficial infarcts present mainly with contralateral homonymous hemianopia, often with macular sparing. Rarely, bilateral PCA infarcts present with amnesia and cortical blindness. [27] [28]  In many posterior circulation strokes, symptomatology can be subtle; therefore, healthcare providers should have a low index of suspicion and obtain imaging and neurology consultations earlier (see Image. Axial Section on Noncontrast CT Head Shows Left PCA Ischemic Stroke and No Hemorrhage). [29]

Vertebrobasilar Infarction

The vertebrobasilar region of the brain is supplied by the 2 vertebral arteries and the basilar artery as they course the anterior surface of the pons. The vertebral arteries arise from their respective subclavian artery, course through the transverse foramina of the upper 6 cervical vertebrae, and enter the skull through the foramen magnum. The main branches of each vertebral artery are the posterior cerebellar artery (PICA) and the anterior spinal artery. The vertebral arteries terminate by merging to form the basilar artery. The basilar artery bifurcates into 2 posterior cerebral arteries, which join the circle of Willis. In addition to the paramedian penetrating branches, the basilar artery gives rise to the anterior inferior cerebellar artery and the superior cerebellar artery. These arteries supply the cerebellum and brainstem. [30]

The clinical presentation includes ataxia, vertigo, headache, vomiting, oropharyngeal dysfunction, visual field deficits, and abnormal oculomotor findings. Patterns of clinical presentation vary depending on the location and the infarction pattern of embolism or atherosclerosis. [31] [32]

Cerebellar Infarction

Patients may present with ataxia, nausea, vomiting, headache, dysarthria, and vertigo symptoms. In addition, edema and rapid clinical deterioration can complicate cerebellar infarction. [31]

Lacunar Infarction

Lacunar infarcts result from the occlusion of small perforating or penetrating arteries. By definition, these infarcts are smaller than 1 centimeter in diameter. See StatPearls' companion reference, " Lacunar Stroke ," for more information. [33]   Lacunar infarction can present with a pure motor or sensory loss, sensorimotor deficit, or ataxic-hemiparesis. [34] [35] [36]

• History and Physical

Ischemic strokes manifest suddenly, making it crucial to determine the time when symptoms first appeared. If the exact moment of symptom onset is unknown, clinicians use the time the patient was last observed in their usual state of health, free from new neurological symptoms, as a reference point. This established timeline is critical for deciding the appropriateness of administering intravenous (IV) thrombolytics. Another vital aspect of the clinical assessment involves investigating potential underlying causes to anticipate the stroke's mechanism. Factors to consider include common vascular risk factors such as hypertension, a history of stroke or TIAs, smoking, and diabetes. Additionally, a history of cardiac diseases, notably atrial fibrillation, recent myocardial infarction, and cardiomyopathy, should be ascertained by the treating clinician. Factors like a history of neck injury, recent chiropractic manipulations, and signs of hypercoagulopathy also play a significant role in the evaluation. [37]

A neurological examination is crucial for all patients suspected of having a stroke. Monitoring vital signs and heart rhythms is essential, as is listening for a neck bruit, which can indicate vascular abnormalities. The National Institutes of Health Stroke Scale (NIHSS)  [See NIH Stroke Scale] is the standard tool for assessing stroke severity, featuring 11 categories and scores ranging from 0 to 42. [38] [39]  These categories include the level of consciousness (LOC) instructions, LOC questions, LOC commands, gaze direction, vision, facial symmetry, arm and leg motor skills, limb coordination, sensory perception, language abilities, speech clarity, and attention to both sides of the body (see  Table 1.  National Institutes of Health Stroke Scale). The stroke scale should be performed in a specified order, basing each score on the patient's performance during the examination rather than on predicted abilities.

Table 1. National Institutes of Health Stroke Scale.

An organized stroke protocol is highly recommended to expedite evaluation. [38] The door-to-needle time of 60 minutes is recommended for acute ischemic stroke patients who qualify for thrombolytics. [38]

The goals in the initial phase include the following:

• Ensuring medical stability, with particular attention to airway, breathing, and circulation
• Quickly reversing any conditions that are contributing to the patient's problem
• Determining if the patient is a candidate for IV thrombolytic therapy or endovascular thrombectomy
• Moving toward uncovering the pathophysiologic basis of the patient's neurologic symptoms

The initial evaluation of any patient is airway, breathing, circulation, and vital signs. Patients may present with respiratory abnormalities from elevated intracranial pressure (ICP) and are at risk of aspiration and asphyxiation. Endotracheal intubation may be necessary to ensure adequate oxygenation and ventilation.

A fingerstick glucose check should be performed, as hypoglycemia can easily be ruled out as a cause of neurological abnormalities.

A plain CT head is recommended for patients within 20 minutes of presentation to rule out hemorrhage. In stroke centers or hospitals that can provide emergency care, vascular imaging should be considered for possible endovascular intervention. However, endovascular intervention should not delay the administration of thrombolytics. [38]

Diffusion-weighted imaging (DWI) is a specialized MRI technique that measures the diffusion of water molecules within tissue. DWI is particularly sensitive for detecting acute ischemic strokes due to its ability to reveal cytotoxic edema—a hallmark of acute infarction—within minutes after stroke onset. DWI can indicate a brain infarction much earlier than other MRI sequences, such as Fluid-Attenuated Inversion Recovery (FLAIR). While a DWI scan can show abnormalities within minutes of a stroke, a FLAIR sequence might take approximately 4.5 hours to reveal signs of a brain infarction. If DWI shows signs of a stroke while the FLAIR sequence does not, it suggests that the ischemic stroke occurred <4.5 hours ago. This timing is crucial because patients with strokes <4.5 hours old may be eligible for early IV thrombolysis, potentially reversing the neurological deficits. [40]

Other diagnostic tests include an electrocardiogram (ECG), troponin levels, complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine (Cr), and coagulation factors. The healthcare provider should evaluate an ECG and troponin because stroke is often associated with coronary artery disease. A CBC may reveal anemia or indicate infection. Healthcare providers should correct electrolyte abnormalities, which can cause altered mental status and could cloud the diagnosis of ischemic stroke. BUN and Cr should be monitored as contrast studies may worsen kidney function. Coagulation factors, including PT, PTT, and INR, should also be drawn as elevated levels may suggest a cause of hemorrhagic stroke. [38]

For institutions without expert imaging interpretation, the US Food and Drug Administration (FDA) highly recommends using a teleradiology system for image interpretation for suspected stroke patients. Rapid imaging interpretation assists with the decision to administer IV alteplase. A discussion and agreement between telestroke neurologists and radiologists is highly recommended. In areas that do not have an in-house stroke team or telestroke protocol, a telephone consultation may be considered to administer thrombolytics. The level of evidence for this recommendation is limited. [41] [42] [43]

• Treatment / Management

The goal of therapy in acute ischemic stroke is to preserve tissue in areas where perfusion is decreased but sufficient to avoid infarction. Tissue in this area of oligemia is preserved by restoring blood flow to the compromised regions and improving collateral flow. Recanalization strategies include IV recombinant tissue-type plasminogen activator and mechanical thrombectomy. Restoring blood flow can minimize the effects of ischemia only if performed quickly. The use of endovascular techniques has been used successfully in selected patients to treat acute ischemic stroke. Another consideration is neuroprotective agents, but none have been shown to improve clinical outcomes.

Essential treatments that have been shown in controlled trials to be efficacious in acute ischemic stroke treatment in different patient groups include the following:

Acute Reperfusion Therapy

• IV alteplase (within 4.5 hours of stroke onset):  The American Heart Association (AHA)/American Stroke Association (ASA) recommends IV alteplase (TPA) for patients who satisfy inclusion criteria and have symptom onset or last known baseline within 3 hours. [44] IV TPA should be administered at 0.9 mg/kg, with a maximum dose of 90 mg. The first 10% of the dose is given as a bolus over the first minute, and the remainder is given over the next 60 minutes. The time has been extended to 4.5 hours for selected candidates. Inclusion criteria include diagnosis of ischemic stroke with "measurable neurological deficit," symptom onset within 3 hours before treatment, and age 18 years or older. [44] Healthcare providers should review the exclusion criteria for thrombolytics before administering TPA. According to the FDA, the contraindications to IV thrombolysis include active internal bleeding, recent intracranial surgery or severe head trauma, intracranial conditions that may increase the risk of bleeding, bleeding diathesis, severe uncontrolled hypertension, current intracranial hemorrhage, subarachnoid hemorrhage, and a history of a recent stroke. Healthcare providers must consider the treatment benefits and risks for patients who present between 3 hours and 4.5 hours from symptom onset. Additional relative exclusion criteria for this patient category include age older than 80 years, NIHSS >25, oral anticoagulant use, and a history of diabetes and prior ischemic stroke. [44]
• MRI-guided thrombolysis for stroke with unknown time of onset:  Most of these patients wake up with an acute stroke. The patients will be ineligible for IV thrombolytic therapy because their last known normal will be at bedtime. The WAKE-UP Stroke Trial used the mismatch between a positive DWI MRI sequence showing an acute ischemic infarction and a negative FLAIR MRI sequence indicating that the infarct occurs within 4.5 hours of the MRI. DWI is positive within 30 minutes of an acute infarct. FLAIR sequence will not be positive until about 4.5 hours after an acute infarct. The mismatch indicates that the stroke occurred within 4.5 hours, and therefore, IV thrombolytic will be indicated. The WAKE-UP Stroke Trial confirmed the positive result. [40] [45]
• IV tenecteplase (within 4.5 hours of stroke onset):  Another fibrinolytic agent, tenecteplase (TNK), may be considered an alternative to alteplase. TNK has advantages over TPA with its longer half-life and can be administered as a single intramuscular (IM) dose rather than a 1-hour IV infusion of TPA. TNK can be given at a dose of 30 to 50 mg IV bolus over 5 sec once (based on weight). TNK is also cheaper to deliver because it is given as a single IM dose. TNK has become the fibrinolytic agent of choice for many stroke centers, especially during the COVID-19 pandemic. Recent studies have shown that TNK appeared to have efficacy and safety profiles similar to TPA. [46] [47]  The 2023 AHA guidelines state that choosing TNK over TPA in patients without contraindications for IV fibrinolytic who are also eligible to undergo mechanical thrombectomy may be reasonable. [38]  A dose of 0.4 mg/kg, compared to 0.25 mg/kg, showed no advantage.
• Mechanical thrombectomy (within 6 hours of stroke onset):  Mechanical thrombectomy should be considered in all patients, even those who received fibrinolytic therapy. The AHA/ASA guidelines do not recommend observation for a response after IV TPA in patients considered for mechanical thrombectomy. [44] In recent years, significant advancements have been made in acute stroke care. Multiple stroke trials in 2015 showed that endovascular thrombectomy in the first 6 hours is much better than standard medical care in patients with large vessel occlusion (LVO) in the arteries of the proximal anterior circulation. These benefits are sustained irrespective of geographical location and patient characteristics. [48] [49]
• Mechanical thrombectomy with perfusion study (within 16 to 24 hours of stroke onset):  Perfusion imaging studies (CT perfusion or MR perfusion) can define the areas of the brain that are ischemic but not infarcted, the ischemic penumbra. Depending on the size of the penumbra relative to the ischemic core, good amounts of brain tissue can be salvaged by restoring blood flow in cases of LVO identified on CT or MR angiogram, resulting in better clinical outcomes. In 2018, a significant paradigm shift occurred in stroke care. The DAWN trial showed significant benefits of endovascular thrombectomy in patients with LVO in the arteries of the proximal anterior circulation. This trial extended the stroke window to 24 hours in selected patients using perfusion imaging. Subsequently, more patients can be treated, even up to 24 hours. [50] Mechanical thrombectomy is recommended within 6 to 16 hours of the last known normal in selected patients with LVO with acute ischemic stroke in the anterior circulation and meets other DAWN and DEFUSE 3 criteria. In selected patients who meet the DAWN criteria, mechanical thrombectomy is reasonable within 24 hours of the last known normal. [50] [51]
• Endovascular therapy (thrombectomy) for acute ischemic stroke with large infarct:  Two large trials published in 2023, the ANGEL ASPECT Trial and the SELECT 2 Trial, showed positive results with endovascular thrombectomy therapy for patients with large ischemic strokes due to LVO and an Alberta Stroke Program Early CT Score (ASPECTS) of 3 to 5. The patients presented within 24 hours of the last known normal. Their NIHSS score is >6. The outcomes are better among patients treated with thrombectomy than those on standard medical therapy. [52] [53]    Definition of LVO:  Intracranial internal carotid artery, middle cerebral artery (M1), basilar artery, and posterior cerebral artery (P1) occlusion  [54] Determining ASPECTS:  This is a 10-point score system for acute middle cerebral artery territory ischemic stroke. One point will be deducted from 10 with an area of the brain infarcted, as shown on CT. Therefore, the smaller the number, the larger the infarct size. These regions are the caudate, putamen, internal capsule, insular cortex, M1, M2, M3, M4, M5, and M6. [55]   Basilar artery occlusion:  This particular type of rare stroke, with about 80% of patients ending up with poor outcomes. AHA guidelines recommend mechanical thrombectomy within 6 hours of onset. Two large trials published in 2022 demonstrate the benefits of endovascular treatment over conventional therapy. The ATTENTION trial showed the benefits within 12 hours. [56] The BAOCHE trial showed the benefits of thrombectomy 6 to 24 hours after strokes due to basilar artery occlusion. [57] In conclusion, thrombectomy should be considered in the treatment of these patients for up to 24 hours.

Acute Hospital Management  [38]

• Labetalol 10 to 20 mg IV; may repeat once
• Nicardipine 5 mg/hour IV. Increase 2.5 mg/hour every 5 to 15 minutes. The maximum dose is 15 mg/hour.
• Clevidipine 1 to 2 mg/hour IV. Double dose every 15 minutes. Maximum 21 mg/hour.
• Hydralazine and enalaprilat may be considered.
• Temperature:  Hyperthermia >38 °C should be avoided and treated appropriately. Antipyretics such as acetaminophen may be used. Common sources of infection, such as pneumonia and urinary tract infections, should be ruled out. There is insufficient data to support therapeutic hypothermia in acute ischemic strokes currently. A retrospective study recently demonstrated an association between a peak temperature >39 °C (100.4 °F) in the first 24 hours and an increased risk of in-hospital mortality.
• Glucose: Maintain glucose in the 140 to 180 mg/dL range in the first 24 hours. Healthcare providers should treat blood glucose <60 mg/dL to achieve normoglycemia. The brain is dependent on oxidative pathways that require glucose for metabolism, and the metabolic demand of the brain is high; therefore, hypoglycemic episodes can decrease the brain's ability to repair. However, hyperglycemia is hypothesized to decrease reperfusion due to the oxidation of nitric oxide-dependent mechanisms and subsequent loss of vascular tone. Moreover, increased acidosis also plays a part, possibly due to injury to lactic acid-sensing channels. Capes et al showed that hyperglycemia in ischemic stroke patients increases 30-day mortality and is an independent risk factor for hemorrhagic stroke conversion. [58]
• Nutrition: Early enteric feeding should be encouraged. For patients with dysphagia, use a nasogastric tube to promote enteric feeding. If there is concern that the patient may have swallowing difficulties for a prolonged period (more than 2 to 3 weeks), placing a percutaneous gastrostomy tube is recommended. Early feeding has been demonstrated to have an absolute reduction in the risk of death. [59]
• DVT prophylaxis:  Intermittent pneumatic compression is recommended for all immobile patients unless contraindications exist. The European Stroke Organization recommended acutely intermittent pneumatic compression for all immobile stroke patients. They also recommended low-dose heparin or low molecular weight heparin for DVT prophylaxis if the benefit outweighs the risk of bleeding. [60] [61]
• Depression screening:  Screening for depression should be considered after an acute ischemic stroke. Rates of post-stroke depression range from 18% to 33%. Risk factors are female sex, large strokes, a stroke affecting the frontal areas, and poor social support. Selective serotonin reuptake inhibitors are the best medications for post-stroke depression. [62] [63]
• Cerebellar/Cerebral edema:  Cerebral edema occurs with acute ischemic stroke, first due to cytotoxic edema with cell swelling, followed by vasogenic edema when the blood-brain barrier is lost. The degree and volume of cerebral edema correlate well with the size of the stroke. Cerebral edema is not significant clinically in lacunar infarction. However, cerebral edema may become symptomatic, resulting in worsening of the stroke symptoms and worse in impairment of consciousness due to herniation. Cerebral edema peaks in 3 to 5 days after an ischemic stroke. [64] Cerebellar edema complicates cerebellar infarctions, and clinicians must know that these patients can rapidly decompensate. The increased ICP can cause obstructing hydrocephalus on the fourth ventricle or cause transtentorial herniation of the superior vermis and downward cerebellar tonsillar herniation. Signs include change or worsening mental status, decreased level of consciousness, respiratory abnormalities, change in pupillary size, posturing, and death. Early recognition and diagnosis of intracranial hypertension due to cerebral edema are essential in caring for acute stroke patients to improve outcomes. Obtain neurosurgical consultation early. A ventriculostomy is indicated in the setting of obstructive hydrocephalus after cerebellar infarct. A decompressive suboccipital craniectomy is highly recommended in cerebellar edema with mass effect cases. [65] [66]
• Seizures:  Post-stroke seizures occur in about 10% of patients, mainly hemorrhagic strokes or cortical infarcts. If the patient experiences a seizure within the first 2 weeks, antiepileptic drugs are indicated for a short period, generally 1 month. Long-term anticonvulsant therapy will be indicated if the seizure occurs later, for weeks or months after a stroke. However, the routine prophylactic use of antiepileptic drugs is not recommended. [67] [68]
• Cardiac evaluation:  Cardiac monitoring for atrial fibrillation or other arrhythmias is recommended in the first 24 hours. The benefit of further monitoring after that is unclear. An initial troponin is recommended because there is an association between stroke and coronary artery disease.
• Antiplatelet treatment:  Aspirin is recommended within 24 to 48 hours of symptom onset. A Cochrane review concluded that aspirin given within 48 hours of symptom onset for ischemic strokes prevented the recurrence of ischemic strokes and improved long-term outcomes. In addition, there was no significant risk of early intracranial hemorrhage with aspirin. [69]
• Antithrombotic treatment: Full-dose anticoagulation is not recommended in acute stroke. The main exception is low-dose anticoagulation for DVT prophylaxis. In patients with atrial fibrillation, the guidelines state it is reasonable to initiate oral anticoagulation within 4 to 14 days after neurological symptoms onset. When to start anticoagulation in patients with atrial fibrillation after acute stroke is always a dilemma; initiation usually depends on factors like stroke size and other comorbidities. Usually, if the stroke size is small to moderate, anticoagulation is started in 7 to 14 days. [70] Sometimes, there are patients with small hemorrhagic transformation after acute stroke, and in this scenario, delay of anticoagulation is warranted. Delay of anticoagulation after hemorrhagic transformation is not associated with excessive stroke recurrence. [71]
• Statins:  High-intensity statins (atorvastatin 80 mg daily or rosuvastatin 20 mg daily) are recommended for patients younger than 75 years with clinical atherosclerotic cardiovascular disease. In addition, patients may be continued on statins if they were on them before the ischemic stroke. [72]
• Differential Diagnosis

The differential diagnosis of ischemic stroke includes the following:

• Complicated migraine
• Drug toxicity 
• Intracranial abscess
• Intracranial hemorrhage
• Intracranial tumor
• Hyperglycemia
• Hypoglycemia
• Hypertensive encephalopathy
• Metabolic abnormalities
• Movement disorders
• Multiple sclerosis
• Wernicke encephalopathy

Prognosis in stroke is pivotal in guiding treatment decisions and informing patients and caregivers about potential outcomes. The prognosis involves assessing various factors such as the type of stroke, its severity, the extent of neurological deficits, comorbidities, and response to treatment. Predictive tools, including clinical scales and imaging modalities, aid in predicting outcomes like functional impairment, mortality, and risk of recurrence (see Image. Encephalomalacia Following Ischemic Stroke). Early intervention and rehabilitation significantly influence prognosis, highlighting the importance of prompt medical attention and personalized care. While some individuals may achieve full recovery, others might experience long-term disabilities or complications. The prognosis in stroke emphasizes the need for multidisciplinary approaches, ongoing monitoring, and support to optimize outcomes and enhance the quality of life for affected individuals and their families. [73] [74]

• Complications

The complications of acute ischemic stroke are many and common. [75] These include but are not limited to the following:

• DVT and pulmonary embolism: DVT prophylaxis is indicated.                                                                            
• Aspiration and pneumonia: A swallowing evaluation before feeding is always indicated and is part of stroke center accreditation.
• Seizures                                                                                                                                                        
• Depression                                                                                                                                                     
• Cerebral edema and increased intracranial pressure
• Postoperative and Rehabilitation Care

Early rehabilitation for stroke patients is beneficial, although very early rehabilitation, within 24 hours, should be avoided. The AVERT trial randomized patients to receive very early rehabilitation within 24 hours of stroke compared to usual stroke-unit care, and early mobilization demonstrated less favorable outcomes using the modified Rankin score. [76]  

• Deterrence and Patient Education

Deterrence and prevention strategies play a vital role in reducing the incidence and impact of ischemic stroke. By addressing modifiable risk factors such as hypertension, diabetes, high cholesterol, and smoking through lifestyle modifications and pharmacological interventions, individuals can significantly decrease their likelihood of experiencing a stroke. Additionally, raising awareness about the warning signs of stroke and promoting timely access to medical care for symptoms such as sudden weakness, numbness, or difficulty speaking can expedite treatment and minimize damage. Community-based education campaigns emphasizing healthy behaviors, regular exercise, and balanced diets further contribute to stroke prevention efforts. Through comprehensive efforts targeting both individual behaviors and societal factors, it is possible to mitigate the burden of ischemic stroke and enhance overall public health.

• Pearls and Other Issues

Clinical pearls that offer valuable insights into the management and care of patients with ischemic stroke include the following:

• Have a low threshold for evaluation of stroke, especially in at-risk populations. TIME IS BRAIN!                                 
• Stroke symptoms depend on the ischemic area of the brain and, therefore, vary.                                                         
• Noncontrast head CT is the first imaging indicated for acute stroke, mainly to rule out hemorrhage.                                      
• Consider TPA or TNK if thrombotic CVA is identified within 4.5 hours of symptom onset.                                             
• When indicated, an early CT angiogram or MR angiogram with perfusion study should be obtained to look for LVO and initiate endovascular thrombectomy therapy within 6 to 24 hours.                                               
• Be aware of presenting blood pressure. Blood pressure management recommendations may include aggressive blood pressure management or permissive hypertension, depending on the type of stroke and whether IV fibrinolytic is indicated. 
• Start an antiplatelet agent within 24 hours of presentation.                                                                                     
• Consider other risk factor management, including addressing hyperlipidemia, hyperglycemia, and cardiac arrhythmias that may increase the risk of vascular disease or a thrombotic event.                                                       
• Consider early and aggressive physical and occupational therapy after the onset of CVA.
• Enhancing Healthcare Team Outcomes

The effective management of ischemic stroke demands a cohesive and interprofessional healthcare team dedicated to delivering patient-centered care, improving outcomes, and maximizing safety and team performance. This approach includes physicians, advanced care practitioners, nurses, pharmacists, neuroimaging technicians, rehabilitation therapists, and stroke specialists working together.

Prompt recognition and treatment of ischemic stroke is critical. Emergency medicine providers must be adept at identifying early stroke symptoms to initiate immediate care. Neuroimaging technicians and radiologists are essential for quickly obtaining and interpreting scans such as CTs and MRIs, which are vital for confirming the diagnosis of ischemic stroke. Neurointeventionalists may be needed to provide interventions such as thrombectomies. Pharmacists play a crucial role in ensuring the timely administration of thrombolytic agents when appropriate and in managing the patient's medication regimen to prevent complications and secondary strokes. Nurses monitor patients closely for changes in condition and manage care protocols. Rehabilitation therapists are vital to the patient's recovery process, starting in the acute phase and continuing through long-term rehabilitation.

The prognosis for patients treated with TPA is good, but the outcomes are guarded for those who do not receive thrombolytic medication. [77]  Effective communication among all team members is paramount for the rapid diagnosis, decision-making, and implementation of treatment plans. This collaboration facilitates a comprehensive approach to care, from acute management to rehabilitation and secondary prevention. All care decisions should be based on ethical considerations, including informed consent and respect for patient autonomy. The team prioritizes shared decision-making, respecting patient preferences while ensuring beneficence and non-maleficence.

An interprofessional healthcare team approach is essential for a timely and effective response, minimizing complications, and prioritizing patient safety and quality of care in managing ischemic stroke. Education and ongoing professional development are essential. They ensure the healthcare team remains knowledgeable about the latest evidence-based practices in stroke care, from acute management to prevention of recurrence. Through dedicated collaboration, the healthcare team will provide patient-centered care from emergency care to rehabilitation, ultimately enhancing outcomes and quality of life for affected patients.

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Axial Section on Noncontrast CT Head Shows Left PCA Ischemic Stroke and No Hemorrhage. Contributed by O Kuybu, MD

Cushing Reaction: CNS Ischemic Response StatPearls Publishing Illustration

Encephalomalacia Following Ischemic Stroke Contributed by S Munakomi, MD

Left MCA Territory Infarction Contributed by S Munakomi, MD

Right-Sided MCA "Cord Sign" Harbingering Acute Infarction Contributed by S Munakomi, MD

Disclosure: Channing Hui declares no relevant financial relationships with ineligible companies.

Disclosure: Prasanna Tadi declares no relevant financial relationships with ineligible companies.

Disclosure: Mahammed Khan Suheb declares no relevant financial relationships with ineligible companies.

Disclosure: Laryssa Patti declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Hui C, Tadi P, Khan Suheb MZ, et al. Ischemic Stroke. [Updated 2024 Apr 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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• Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. [Stroke. 1993] Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE 3rd. Stroke. 1993 Jan; 24(1):35-41.
• [Stroke etiology and long-term need of care in ischemic stroke patients]. [Fortschr Neurol Psychiatr. 2009] [Stroke etiology and long-term need of care in ischemic stroke patients]. Dietl M, Pohle R, Weingärtner M, Polgar R, Grässel E, Schwab S, Kolominsky-Rabas P. Fortschr Neurol Psychiatr. 2009 Dec; 77(12):714-9. Epub 2009 Nov 30.
• Stroke subtype classification to mechanism-specific and undetermined categories by TOAST, A-S-C-O, and causative classification system: direct comparison in the North Dublin population stroke study. [Stroke. 2010] Stroke subtype classification to mechanism-specific and undetermined categories by TOAST, A-S-C-O, and causative classification system: direct comparison in the North Dublin population stroke study. Marnane M, Duggan CA, Sheehan OC, Merwick A, Hannon N, Curtin D, Harris D, Williams EB, Horgan G, Kyne L, et al. Stroke. 2010 Aug; 41(8):1579-86. Epub 2010 Jul 1.
• Review Inflammation in ischemic stroke subtypes. [Curr Pharm Des. 2012] Review Inflammation in ischemic stroke subtypes. Tuttolomondo A, Di Raimondo D, Pecoraro R, Arnao V, Pinto A, Licata G. Curr Pharm Des. 2012; 18(28):4289-310.
• Review [Aetiological classification of ischaemic strokes: comparison of the new A-S-C-O classification and the classification by the Spanish Society of Neurology's Cerebrovascular Disease Study Group]. [Neurologia. 2013] Review [Aetiological classification of ischaemic strokes: comparison of the new A-S-C-O classification and the classification by the Spanish Society of Neurology's Cerebrovascular Disease Study Group]. Sobrino García P, García Pastor A, García Arratibel A, Vicente Peracho G, Rodriguez Cruz PM, Pérez Sánchez JR, Díaz Otero F, Vázquez Alén P, Villanueva Osorio JA, Gil Núñez A. Neurologia. 2013 Sep; 28(7):417-24. Epub 2012 Sep 19.

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Overview of Stroke

• Symptoms and Signs |
• Evaluation |
• Treatment |
• Prognosis |

Strokes are a heterogeneous group of disorders involving sudden, focal interruption of cerebral blood flow that causes neurologic deficit. Strokes can be

Ischemic (80%), typically resulting from thrombosis or embolism

Hemorrhagic (20%), resulting from vascular rupture (eg, subarachnoid hemorrhage , intracerebral hemorrhage )

Transient stroke symptoms (typically lasting < 1 hour) without evidence of acute cerebral infarction (based on diffusion-weighted MRI) are termed a transient ischemic attack (TIA).

In the US, stroke is the 5th most common cause of death and the most common cause of neurologic disability in adults.

Strokes involve the arteries of the brain (see figure Arteries of the brain ), either the anterior circulation (branches of the internal carotid artery) or the posterior circulation (branches of the vertebral and basilar arteries).

Arteries of the Brain

Risk factors.

The following are modifiable risk factors that contribute to increased risk of stroke:

Hypertension

Cigarette smoking

Dyslipidemia

Insulin resistance

Abdominal obesity

Obstructive sleep apnea

Excess alcohol consumption

Lack of physical activity

High-risk diet (eg, high in saturated fats, trans fats, and calories)

Psychosocial stress (eg, depression )

Heart disorders (particularly disorders that predispose to emboli, such as acute myocardial infarction , infective endocarditis , and atrial fibrillation )

Carotid artery stenosis

Hypercoagulability (thrombotic stroke only)

Intracranial aneurysms (subarachnoid hemorrhage only)

Anticoagulants and antiplatelet medications

Unmodifiable risk factors include the following:

Prior stroke

Family history of stroke

Race ethnicity

Genetic factors

Symptoms and Signs of Stroke

Initial symptoms of stroke occur suddenly. Symptoms depend on the location of infarction (see figure Areas of the brain by function ).

Thus, symptoms can include numbness, weakness of limbs or face; aphasia; confusion; visual disturbances in one or both eyes (eg, transient monocular blindness, diplopia ); dizziness or loss of balance and coordination; and headache.

Areas of the brain by function

Neurologic deficits are used to determine the location of stroke (see table Selected Stroke Syndromes ). Anterior circulation stroke typically causes unilateral symptoms. Posterior circulation stroke can cause unilateral or bilateral deficits and is more likely to affect consciousness, especially when the basilar artery is involved.

Selected Stroke Syndromes

Systemic or autonomic disturbances (eg, hypertension, fever) occasionally occur.

Other manifestations, rather than neurologic deficits, often suggest the type of stroke. For example,

Sudden, severe headache suggests subarachnoid hemorrhage .

Impaired consciousness or coma, often accompanied by headache, nausea, and vomiting, suggests increased intracranial pressure , which can occur 48 to 72 hours after large ischemic strokes and earlier in many hemorrhagic strokes; fatal brain herniation may result.

Complications

Stroke complications can include sleep problems, confusion, depression, incontinence, atelectasis, pneumonia, and swallowing dysfunction, which can lead to aspiration, dehydration, or undernutrition. Immobility can lead to thromboembolic disease, deconditioning, sarcopenia, urinary tract infections, pressure ulcers, and contractures.

Daily functioning (including the ability to walk, see, feel, remember, think, and speak) may be decreased.

Evaluation of Stroke

Evaluation aims to establish the following:

Whether stroke has occurred

Whether stroke is ischemic or hemorrhagic

Whether emergency treatment is required

What the best strategies for preventing subsequent strokes are

Whether and how to pursue rehabilitation

Stroke is suspected in patients with any of the following:

Sudden neurologic deficits compatible with brain damage in an arterial territory

A particularly sudden, severe headache

Sudden, unexplained coma

Sudden impairment of consciousness

When stroke is suspected, clinicians may use standardized criteria to grade severity and follow changes over time. This approach can be particularly useful as an outcome measure in efficacy studies. The National Institutes of Health Stroke Scale (NIHSS) is often used. It is a 15-item scale to evaluate the patient's level of consciousness and language function and to identify motor and sensory deficits by asking the patient to answer questions and to perform physical and mental tasks. It is also useful for choosing appropriate treatment and predicting outcome.

Glucose is measured at bedside to rule out hypoglycemia. Measurement of blood glucose is the only laboratory test needed for all patients before thrombolytics are given. However, if the patient is receiving an anticoagulant, platelet count, international normalized ratio (INR), and partial thromboplastin time are measured.

If stroke is still suspected, immediate neuroimaging is required to differentiate hemorrhagic from ischemic stroke and to detect signs of increased intracranial pressure. CT is sensitive for intracranial blood but may be normal or show only subtle changes during the first hours of symptoms after anterior circulation ischemic stroke. CT also misses some small posterior circulation strokes. MRI is sensitive for intracranial blood and may detect signs of ischemic stroke missed by CT, but CT can usually be done more rapidly. If CT does not confirm clinically suspected stroke, diffusion-weighted MRI can usually detect ischemic stroke.

This image shows low attenuation in the distribution of the right middle cerebral artery consistent with a subacute ischemic stroke with hemorrhage developing in areas of ischemia.

© 2017 Elliot K. Fishman, MD.

This MRI scan shows an area of restricted diffusion consistent with an acute ischemic stroke in the left insular and frontal lobes.

Image courtesy of Ji Y. Chong, MD.

This noncontrast head CT scan shows a hyperdense left middle cerebral artery. This finding indicates a focal clot in the left middle cerebral artery (arrow).

If consciousness is impaired and lateralizing signs are absent or equivocal, further testing is done to check for causes other than stroke(eg, postictal state, metabolic encephalopathies):

Arterial blood gases (ABGs)

Blood and urine culture and routine toxicology

Electrocardiography (ECG) to check for myocardial infarction and new arrhythmias

Chest x-ray to check for new lung disease that may affect brain oxygenation.

Imaging tests to check for masses, hemorrhage, edema, evidence of bone trauma, and hydrocephalus (first, noncontrast head CT, followed by MRI or contrast CT if needed for diagnosis)

Echocardiography to check the heart for blood clots, pumping or structural abnormalities, and valve disorders

Electroencephalography

After the stroke is identified as ischemic or hemorrhagic, tests are done to determine the cause. Patients are also evaluated for coexisting acute general disorders (eg, infection, dehydration, hypoxia, hyperglycemia, hypertension). Patients are asked about depression, which commonly occurs after stroke. A dysphagia team evaluates swallowing; sometimes a barium swallow study is necessary.

Treatment of Stroke

Stabilization

Reperfusion for some ischemic strokes

Supportive measures and treatment of complications

Strategies to prevent future strokes

Rehabilitation

Stabilization may need to precede complete evaluation. Comatose or obtunded patients (eg, Glasgow Coma Score ≤ 8) may require airway support . If increased intracranial pressure is suspected, intracranial pressure monitoring and measures to reduce cerebral edema may be necessary.

Specific acute treatments vary by type of stroke. They may include reperfusion (eg, IV thrombolysis, mechanical thrombectomy) for some ischemic strokes.

Providing supportive care, correcting coexisting abnormalities (eg, fever, hypoxia, dehydration, hyperglycemia, sometimes hypertension), and preventing and treating complications are vital during the acute phase and convalescence (see table Strategies to Prevent and Treat Stroke Complications ); these measures clearly improve clinical outcomes ( 1 ). During convalescence, measures to prevent aspiration , deep venous thrombosis , urinary tract infections , pressure ulcers , and undernutrition may be necessary. Passive exercises, particularly of paralyzed limbs, and breathing exercises are started early to prevent contractures, atelectasis, and pneumonia.

Strategies to Prevent and Treat Stroke Complications

After a stroke, most patients require rehabilitation (occupational and physical therapy) to maximize functional recovery. Some need additional therapies (eg, speech therapy , feeding restrictions). For rehabilitation, an interdisciplinary approach is best.

Depression after stroke may require antidepressants; many patients benefit from counseling.

Modifying risk factors through lifestyle changes (eg, stopping cigarette smoking) and medications (eg, for hypertension) can help delay or prevent subsequent strokes. Other stroke prevention strategies are chosen based on the patient's risk factors. For ischemic stroke prevention , strategies may include procedures (eg, carotid endarterectomy, stent placement), antiplatelet therapy, and anticoagulation.

Treatment reference

1. Powers WJ, Rabinstein AA, Ackerson T, et al :Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke . 50 (12):3331–3332, 2019. doi: 10.1161/STROKEAHA.119.027708 Epub 2019 Oct 30.

Prognosis for Stroke

The sooner a stroke is treated, the less severe brain damage is likely to be and the better the chances for recovery.

Certain factors suggest a poor outcome. Strokes that impair consciousness or that affect a large part of the left side of the brain may be particularly grave.

Usually, the more quickly patients improve during the days after stroke, the more they will ultimately improve. Improvement commonly continues for 6 to 12 months after the stroke. In adults who have had an ischemic stroke, problems that remain after 12 months are likely to be permanent, but children continue to improve slowly for many months. Older people fare less well than younger people. For people who already have other serious disorders (eg, dementia), recovery is more limited. Of all the different causes of strokes, lacunar strokes have the best prognosis.

If a hemorrhagic stroke is not massive and intracranial hypertension is absent the outcome is likely to be better than that after an ischemic stroke with similar symptoms. Blood (in a hemorrhagic stroke) does not damage brain tissue as much as ischemia does.

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• Understanding stroke...

Understanding stroke:Pathophysiology, presentation, and investigation

• Related content
• Peer review
• K A L Carroll , fifth year medical student 1 ,
• J Chataway , consultant neurologist 1
• 1 Imperial College, London
• 2 St Mary's Hospital, London

Every 45 seconds, someone in the United States has an attack of stroke. K A L Carroll and J Chataway discuss the pathology and clinical features of stroke, in the first of a two part series

Stroke is an acute neurological injury in which blood supply to a part of the brain is interrupted. Five and a half million survivors of stroke are living in the world today. 1 In the United States alone, half a million people have their first stroke each year, and 200 000 have a recurrent attack. 2 The World Health Organization esti mates that 15 million people have strokes each year worldwide, 5.5 mil lion of which are fatal. 1 In industri alised countries, stroke is the third most common single cause of death (after ischaemic heart disease and cancer). In the US, someone has an attack every 45 seconds, and there is a stroke related death every three minutes. 2

Even if age specific stroke incidence remains stable or falls slightly because more people live into old age, the annual incidence will continue to rise. This increases mortality, but, because of the direct cost of treatment and the indirect costs of lost productivity, the result is a loss - of $57.9bn (£30.4bn; €45.1bn) a year in the US. 2 A thorough understanding of stroke's pathophysiology, presentation, investigation, and current and future treatments is crucial.

Strokes may either be haemorrhagic or ischaemic. Eighty eight per cent of all strokes are ischaemic, 9% are due to intracerebral haemorrhage, and 3% are due to subarachnoid haemorrhage. 2

Haemorrhagic stroke

Intracranial haemorrhage may occur within the brain parenchyma (intracerebral haemorrhage) or within the surrounding meningeal spaces (including epidural haematoma, subdural haematoma, and subarachnoid haemorrhage).

In intracerebral haemorrhage, bleeding occurs directly into the brain parenchyma. In addition to the area of the brain injured by the haemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the haematoma. A general increase in intracranial pressure may occur.

Non-traumatic intracerebral haemorrhage is usually due to hypertensive damage to blood vessel walls. Chronic hypertension causes lipohyalinosis, fibrinoid necrosis, and the development of Charcot-Bouchard aneurysms in arteries throughout the brain, which may then rupture. Non-traumatic intracerebral haemorrhage may also be due to excessive cerebral blood flow (for example, haemorrhagic transformation of an ischaemic infarct); rupture of an aneurysm or an arteriovenous malformation; an arteriopathy (for example, cerebral amyloid angiopathy); a coagulopathy; a vasculitis; haemorrhagic necrosis (for example, due to tumour or infection); or venous outflow obstruction (for example, cerebral venous thrombosis).

Non-penetrating and penetrating cranial trauma are also common causes of intracerebral haemorrhage.

Strokes due to hypertension more commonly occur in sites such as the basal ganglia, thalamus, pons, cerebellum, and other brainstem sites, whereas those due to other causes more commonly occur in lobar regions (particularly the parietal and occipital lobes).

Subarachnoid haemorrhage usually occurs after rupture of a berry aneurysm in the circle of Willis. Other uncommon causes include trauma, hypertensive haemorrhage, vasculitides, tumours, and coagulopathies. This results in blood accumulating in the basal cisterns and around the brainstem.

Ischaemic stroke

An acute vascular occlusion results in ischaemia in the dependent area of the brain. About 80% of ischaemic strokes are due to thromboses and emboli. The most common sites of thrombotic occlusion are cerebral artery branch points, particularly in the distribution of the internal carotid artery. Arterial stenosis precipitated by turbulent blood flow, atherosclerosis, and platelet adherence cause blood clots to form. Less common causes of thromboses, particularly seen in younger stroke patients, include cervical artery dissection, essential thrombocythaemia, polycythemia, sickle cell anaemia, protein C deficiency, fibromuscular dysplasia of the cerebral arteries, and cocaine misuse. 3

Emboli may arise from the heart, the extracranial arteries, or, rarely, the right sided circulation (paradoxical emboli), and can occlude the vasculature. Furthermore, rarely infective causes of emboli, such as subacute bacterial endocarditis, may cause occlusion, as may emboli due to iatrogenic causes, such as a cardiac prosthesis.

Small vessel disease within the brain causes a further 20% of ischaemic strokes. These are usually in patients with generalised small vessel disease - for example, hypertensive and diabetic patients. Multiple small emboli or an in situ process called lipohyalinosis (in which multiple microatheromata occlude the vessels) are thought to be responsible.

A system of categories of subtypes of ischaemic stroke mainly based on cause has been developed for the “Trial of Org” 10 172 in acute stroke treatment (TOAST). 4 This classification denotes five subtypes of ischaemic stroke - large artery atherosclerosis, cardioembolism, small vessel occlusion, stroke of other determined cause, and stroke of undetermined cause.

In all cases, loss of perfusion to a part of the brain results in an “ischaemic cascade” ( fig 1 ). Conse- quently the initial ischaemic insult is locally amplified.

Ischaemic cascade

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The high intracellular calcium acti- vates various enzymes that cause the destruction of the cell. Free radicals, arachidonic acid, and nitric oxide are generated by this process leading to further neuronal damage. Within hours to days of a stroke occurring, specific genes are activated that cause the formation of cytokines and other factors that in turn cause further inflammation and microcirculatory compromise. The area of damage thus spreads rapidly after the initial ischaemic event.

Risk factors

Stroke has numerous risk factors, some of which (such as increasing age and systolic blood pressure) are risk factors for both ischaemic and haemorrhagic stroke, however, other factors are more specific for type of stroke. The table gives important risk factors and their relative risk.

Risk factors for stroke

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Clinical presentation

Stroke should be considered in any patient presenting with an acute neu- rological deficit (focal or global) or altered level of consciousness. Patients' symptoms vary depending on the area of the brain affected and the extent of the damage.

Because of the importance of get- ting people who have had a stroke into hospital as rapidly as possible, there has been extensive research into prehospital assessment by patients themselves, family members, and prehospital care personnel, such as emergency medical technicians. The Cincinnati prehospital stroke scale has been developed using the three most important items (facial paresis, arm drift, and abnormal speech) derived from the stroke scale of the National Institutes of Health. 16

The Los Angeles prehospital stroke screen assesses for a unilateral arm drift, handgrip strength, and facial paresis. 17 Regardless of the scale used, it is important to increase public awareness as to the presenta- tion of stroke to decrease the time from onset to presentation in hospi- tal. In the UK, a campaign is cur- rently being run by the Stroke Association called FAST (the face arm speech test), which guides the public to present at hospital immedi- ately in the case of facial weakness, arm weakness, or speech disturbance.

No features of the history can accurately distinguish between ischaemic and haemorrhagic stroke. But haemorrhagic stroke is perhaps more likely if the presentation includes features of raised intracranial pressure (such as nausea, vomiting, and headache). Seizures are also more common in hemor- rhagic stroke than in ischaemic stroke, occurring in up to 28% of hemorrhagic strokes. Meningism, the symptoms of meningeal irritation associated with acute febrile illness or dehydration without actual infection of the meninges, may also result from blood in the ventricles after a haem- orrhagic stroke.

Four important stroke syndromes are caused by disruption of particular cerebrovascular distributions.

Anterior cerebral artery - This prima- rily affects frontal lobe function, which results in altered mental status, con- tralateral lower limb weakness and hypoaesthesia, and gait disturbance.

Middle cerebral artery - This com- monly results in contralateral hemi- paresis, contralateral hypoaesthesia, ipsilateral hemianopia, and gaze preference toward the side of the lesion. Agnosia, a loss in ability to recognise objects, persons, sounds, shapes or smells, in the absence of a specific sensory deficit or memory loss, is common.

Receptive or expressive aphasia may result if the lesion occurs in the dominant (mainly left) hemisphere. Neglect (behaviour as if the contralateral sensory space does not exist) may result when the lesion occurs in the parietal cortex.

Posterior cerebral artery - This affects vision and thought, producing homonymous hemianopia, cortical blindness, visual agnosia, altered mental status, and impaired memory.

Vertebrobasilar artery - causes a wide variety of cranial nerve, cerebellar, and brainstem deficits. These include vertigo, nystagmus, diplopia, visual field deficits, dysphagia, dysarthria, facial hypoaesthesia, syncope, and ataxia. Loss of pain and temperature sensation occurs on the ipsilateral face and contralateral body.

Investigations

After the necessary basic blood tests (including full blood count, biochemistry, and coagulation studies) and cardiac monitoring with electrocardiogram, a non-contrast head computed tomography scan is essential for rapidly distinguishing ischaemic from haemorrhagic stroke and may be able to define the anatomic distribution of the stroke. This is crucial because treatments for each type of stroke differ.

Within six hours of the onset of ischaemic stroke, most patients will have a normal computed tomography scan. After 6-12 hours, sufficient oedema may collect into the area of the stroke so that a region of hypo- density may be seen on the scan.

Radiological clues before this include:

Insular ribbon sign (loss of definition of grey-white interface in the lateral margins of the insula due to oedema in the insular cortex; fig 2 ) 18

Hyperdense middle cerebral artery sign ( fig 3 ) 19

Hypoattenuation in the lentiform nucleus ( fig 4 )

Sulcal obliteration

Shifting due to oedema

Loss of grey-white matter differentiation. 20 21

Computed tomograph after ischaemic stroke, showing oedema in insular cortex, as shown by solid arrows (open arrows show normal side). Reproduced from Chokski et al 27 with permission of Anderson Publishing

(below left) Computed tomograph after ischaemic stroke, showing hyperdense middle cerebral artery sign. Reproduced from Chokski et al 27 with permission of Anderson Publishing

(below right) Computed tomograph after ischaemic stroke, showing hypoattenuation in the lentiform nucleus, as shown by solid arrows (open arrows show normal side). Reproduced from Chokski et al 27 with permission of Anderson Publishing

These are all due to an increasing level of oedema in the brain, however, they rely on a high level of expertise of the radiologist and are often not present. Computed tomography scans also may fail to show some parenchymal haemorrhages smaller than 1 cm as a result of low resolution.

Conventional magnetic resonance imaging is not as sensitive as computed tomography for detecting haemorrhage in the acute setting. But newer techniques, such as perfusion and diffusion weighted magnetic resonance examinations, are more sensitive imaging methods for diagnosis in acute settings. Ischaemic areas can be determined within minutes or hours. But use of these methods has been restricted because they are not generally available and are difficult to employ under emergency conditions, particularly as they involve a patient lying flat for 40 minutes when they may be agitated or have a level of cardiorespiratory compromise.

Perfusion brain computed tomography, conversely, is a new imaging method capable of providing information about ischaemic brain tissue, which can be used in emergency conditions. 22 23 Perfusion is measured by monitoring the passage of contrast material (non-ionic iodine) through the brain using computed tomography. Perfusion examination of the entire brain is not possible yet, and because only a few neighbouring sections can be imaged, the anatomical region must be clinically determined. Various studies have shown that computed tomography perfusion scans yield comparable information to diffusion weighted magnetic resonance imaging scans. 24 25 But the entire brain cannot be analysed using perfusion computed tomography scanning, which is the major drawback, and further research is required to obtain an ideal investigation. Both types of investigation used have a high detection rate for haemorrhagic stroke.

Further investigations may include carotid duplex scanning for patients in whom carotid artery stenosis or occlusion is suspected, and transcranial Doppler ultrasound for evaluating the more proximal vasculature, including the middle cerebral artery, intracranial carotid artery, and vertebrobasilar artery. Echocardiography may be used for patients in whom cardiogenic embolism is suspected, and trans- oesophageal echocardiography may be used to detect a suspected thoracic aortic dissection, or transthoracic echocardiography for suspected acute myocardial infarction.

Computed tomography angiography is useful for patients with acute ischaemic stroke in whom accurate analysis of the cerebrovascular anatomy is required, particularly preoperatively. 26

References 1 – 27 are on Student BMJ.com.

Originally published as: Student BMJ 2006;14:319

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Ischaemic stroke

• Overview  
• Theory  
• Diagnosis  
• Management  
• Follow up  
• Resources  

When viewing this topic in a different language, you may notice some differences in the way the content is structured, but it still reflects the latest evidence-based guidance.

Ischaemic stroke is a leading cause of morbidity and mortality. If you suspect stroke, work rapidly through the initial assessment and aim for quick access to computed tomographic (CT) scan. Early initiation of reperfusion strategies (intravenous thrombolysis or mechanical thrombectomy) within 4.5 hours from onset of symptoms, if not contraindicated, is associated with improved functional outcomes.

Use a validated tool to aid recognition: use ROSIER (Recognition of Stroke in the Emergency Room) in the emergency department; use FAST (Face Arm Speech Test) in the community.

Manage any airway, breathing, and circulatory insufficiencies requiring urgent treatment.

Admit everyone with suspected stroke directly to a hyperacute or acute stroke unit within 4 hours of presentation.

Request non-enhanced CT scan as soon as possible (at most within 1 hour of arrival at hospital). Ischaemic stroke is a clinical diagnosis based on signs and symptoms. A normal CT scan does not rule out a stroke but will rule out intracranial haemorrhage, which must be excluded before starting thrombolysis.

Intravenous alteplase should be given (if not contraindicated) if treatment is started as soon as possible within 4.5 hours of onset of symptoms AND intracranial haemorrhage has been excluded by imaging.

Tenecteplase may be considered as a safe and effective alternative to alteplase within 4.5 hours of ischaemic stroke, but is off-label for this indication in the UK.

Mechanical thrombectomy can be performed in selected patients within 6 to 24 hours of symptoms onset.

The World Health Organization defines stroke as “a clinical syndrome consisting of rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin”. [1] Aho K, Harmsen P, Hatano S, et al. Cerebrovascular disease in the community: results of a WHO collaborative study. Bull World Health Organ. 1980;58(1):113-30. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2395897 http://www.ncbi.nlm.nih.gov/pubmed/6966542?tool=bestpractice.com

Stroke can be further subdivided into ischaemic stroke (caused by vascular occlusion or stenosis) and haemorrhagic stroke (caused by vascular rupture, resulting in intraparenchymal and/or subarachnoid haemorrhage). Central venous sinus thrombosis is a rare form of stroke that occurs due to thrombosis of the dural venous sinuses. This topic focuses on the first 24 hours of acute care of patients with ischaemic stroke.

For information on other types of stroke, see Stroke due to spontaneous intracerebral haemorrhage ,  Subarachnoid haemorrhage , and Cavernous sinus thrombosis .

History and exam

Key diagnostic factors.

• unilateral weakness or paralysis in the face, arm or leg
• visual disturbance
• risk factors

Other diagnostic factors

• sensory loss (numbness)
• gaze paresis
• arrhythmias, murmurs, or pulmonary oedema
• nausea and/or vomiting
• neck or facial pain
• miosis, ptosis, and facial anhidrosis (hemilateral)
• decreased level of consciousness or coma

Risk factors

• family history of stroke
• history of ischaemic stroke or TIA
• hypertension
• diabetes mellitus
• atrial fibrillation
• comorbid cardiac conditions
• carotid artery stenosis
• sickle cell disease
• dyslipidaemia
• lower levels of education
• black or South Asian ethnic groups
• poor diet and nutrition
• physical inactivity
• alcohol abuse
• oestrogen-containing therapy
• obstructive sleep apnoea
• illicit drug use
• hyperhomocysteinaemia
• elevated lipoprotein(a)
• hypercoagulable states
• elevated C-reactive protein
• aortic arch plaques

Diagnostic investigations

1st investigations to order.

• non-contrast CT head
• serum glucose
• serum electrolytes
• serum urea and creatinine
• cardiac enzymes
• prothrombin time and PTT (with INR)

Investigations to consider

• serum toxicology screen
• CT angiography
• CT or MRI perfusion-weighted imaging
• carotid ultrasound
• echocardiogram

Treatment algorithm

Suspected ischaemic stroke, confirmed ischaemic stroke, contributors, expert advisers, matthew jones, md, frcp.

Consultant Neurologist

Manchester Centre for Clinical Neurosciences

Northern Care Alliance

Honorary Senior Lecturer

University of Manchester

Disclosures

MJ is the chair of the Association of British Neurologists Education Committee (unpaid position). MJ is a faculty member of an MRCP revision course.

Rachael Power, MBChB, MRCP

Neurology Registrar

RP has been sponsored by Novartis to attend the International Headache Conference.

Acknowledgements

BMJ Best Practice would like to gratefully acknowledge the previous expert contributor for this topic, whose work has been retained in parts of the content:

George Ntaios, MD, MSc (ESO Stroke Medicine), PhD, FESO

Assistant Professor of Internal Medicine

Medical School

University of Thessaly

GN is on the advisory boards for, and has received honoraria, speaker fees, and research support from: Amgen, Bayer, Boehringer-Ingelheim, BMS/Pfizer, Elpen, Galenica, Medtronic, Sanofi, and Winmedica.

Peer reviewers

Kayvan khadjooi, md, frcp, pgcertmeded.

Consultant in Stroke Medicine

Addenbrooke’s Hospital

Associate Lecturer

School of Clinical Medicine

University of Cambridge

KK has received travel grants for conferences/speaker honoraria from Bayer, Boehringer, Daiichi-Sankyo, Pfizer, and Shire.

Helena Delgado-Cohen

Section Editor, BMJ Best Practice

HDC declares that she has no competing interests.

Tannaz Aliabadi-Oglesby

Lead Section Editor, BMJ Best Practice

TAO declares that she has no competing interests.

Julie Costello

Comorbidities Editor, BMJ Best Practice

JC declares that she has no competing interests.

Adam Mitchell

Drug Editor, BMJ Best Practice

AM declares that he has no competing interests.

Differentials

• Intracerebral haemorrhage
• Transient ischaemic attack (TIA)
• Hypertensive encephalopathy
• National clinical guideline for stroke for the United Kingdom and Ireland
• Stroke and transient ischaemic attack in over 16s: diagnosis and initial management

Calculators

NIH Stroke Score

Glasgow Coma Scale

Tracheal intubation animated demonstration

Bag-valve-mask ventilation animated demonstration

Patient information

Preventing another stroke

Stroke: emergency treatment

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