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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

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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  • Prevent stroke: What you can do. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/prevention.htm#print. Accessed Sept. 13, 2023.
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  • Papadakis MA, et al., eds. Quick Medical Diagnosis & Treatment 2023. McGraw Hill; 2023. https://accessmedicine.mhmedical.com. Accessed Sept. 13, 2023.
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  • 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.
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Associated Procedures

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ORIGINAL RESEARCH article

Risk profile, clinical presentation, and determinants of stroke subtypes among patients with stroke admitted to public referral hospitals, northwest ethiopia in 2021: a cross-sectional study.

\nGashaw Walle Ayehu

  • 1 Department of Biomedical Sciences, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia
  • 2 School of Medicine, College of Medicine and Health Science, Bahir Dar University, Bahir Dar, Ethiopia
  • 3 School of Medicine, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia
  • 4 Department of Biomedical sciences, Goba Referral Hospital, Madda Walabu University, Bale-Goba, Ethiopia
  • 5 Department of Public Health, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia
  • 6 Department of Adult Health Nursing, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia

Background: Stroke is the second leading cause of death worldwide, with a significant increase in stroke burden over the last two and half decades, especially in developing countries. African countries are undergoing an epidemiological transition from being dominated by infectious diseases to being double-burdened by non-communicable diseases, with existing infectious diseases driven by sociodemographic and lifestyle changes and a weak healthcare system. Data on the risk profile, clinical presentation, and predictors of stroke subtypes are still limited. Therefore, the main aim of this study was to assess the risk profile, clinical presentation, and predictors of stroke in public referral hospitals of Northwest Ethiopia.

Methods: For this study, 554 patients with stroke admitted to three public referral hospitals were prospectively followed up. Data were collected using a pre-tested interviewer-administered questionnaire. STATA version 16 was used for data analyses. Candidate variables significant in bivariate analysis were selected for multivariate binary logistic regression, and statistical significance was set at a p < 0.05.

Results: Of the 554 patients with stroke, 60.3% had an ischemic stroke. The mean age of the participants was 61 ± 12.85 years, and more than half (53.25%) of them were women. The most common risk factor identified was hypertension (29.7%), followed by congestive heart failure. The most common clinical presentation was hemiparesis, which was reported by 57.7% of the patients, followed by loss of consciousness (20.7%) and aphasia (9%). Through multivariable logistic regression, age (AOR = 1.03, 95% CI:1.01–1.05), sedentary physical activity level (AOR = 6.78, 95% CI:1.97–23.32), absence of a family history of chronic illness (AOR = 3.79, 95% CI:2.21–6.48), hypertension (AOR=0.51, 95% CI:0.31–0.85), and past stroke (AOR = 3.54, 95% CI:0.93–13.49) were found to be independent determinants of the stroke subtype.

Conclusion: Age, the level of sedentary physical activity, absence of a family history of chronic illness, hypertension, and past stroke were independent determinants of stroke subtype.

Introduction

Stroke is the second leading cause of death worldwide, with a significant increase in stroke burden over the last two and half decades, especially in developing countries ( 1 ). African countries are undergoing an epidemiological transition from being dominated by infectious diseases to being double-burdened by non-communicable diseases, with existing infectious diseases driven by sociodemographic and lifestyle changes and poor healthcare system ( 2 , 3 ). In 2013, an estimated 535,000 new cases and 2.1 million survivors of stroke were found in Africa ( 4 ). Currently, stroke morbidity, mortality, and disability are increasing worldwide ( 4 , 5 ). Data from the Global Burden of Disease (GBD), Injuries, and Risk Factors study revealed that stroke is the leading cardiovascular disease (CVD) that causes mortality and disability in sub-Saharan Africa (SSA) and other low- and middle-income countries (LMICs) ( 6 ).

The prevalence of hemorrhagic stroke (HS) is higher in African countries than in Western countries. This disparity is usually ascribed to racial or genetic factors but may be due to differences in risk factor burden ( 7 ), which is largely driven by demographic changes and enhanced by an increasing magnitude of modifiable risk factors ( 8 ). Age, sex, family history, and ethnicity are non-modifiable risk factors, while hypertension, diabetes mellites, alcohol, smoking, diet, and physical inactivity are among some of the identified modifiable risk factors ( 9 – 13 ). Underdiagnosis or late diagnosis of hypertension and other risk factors like delayed presentation to the health institution, poor risk factor control, and failure to adhere to treatments are major challenges that need to be addressed ( 9 , 14 – 17 ).

The burden, factors, and outcome of stroke vary in Ethiopia between regions and over various time periods ( 18 – 22 ). Risk factors of stroke can be classified into modifiable and non-modifiable factors. Age, sex, family history, and race/ethnicity are non-modifiable risk factors, while renal dysfunction, hyperlipidemia, hypertension, alcohol drinking, smoking, diet, obesity, and physical inactivity are among some of the identified modifiable risk factors ( 13 , 22 – 24 ). Stroke can be prevented by lifestyle modification and controlling major risk factors.

Data on risk profiles, clinical presentations, and predictors of stroke subtypes are still limited. Therefore, the main aim of this study was to assess the risk profile, clinical presentation, and predictors of stroke subtypes in public referral hospitals of Northwest Ethiopia.

A cross-sectional study was conducted in three public referral hospitals located in Northwest Ethiopia: the University of Gondar Hospital located in Gondar, Tibebe Ghion Specialized Hospital, and Felege Hiwot Regional Referral Hospital located in Bahir Dar. The study was conducted from December to June 2020–2021. The study included 554 patients with stroke (age ≥ 18 years) admitted to and treated at the three public referral hospitals. The inclusion criterion was specified to include all patients with stroke whose diagnosis was confirmed by a CT scan. Patients who were dead before diagnosis confirmation by CT scan, whose initial assessment or diagnosis of stroke was later changed to another case (ruled out stroke) with further evaluation, and who were being treated by other health institutions and referred after treatment or due to complications were excluded.

Operational definitions

Diabetes mellitus.

Patients who were previously on oral hypoglycemic agents/insulin treatment, who had a diagnosis of any type of DM or an FBS level ≥126 mg/dl, or who had a documented RBS level ≥200 mg/dl or a glycosylated hemoglobin level ≥6.5% ( 25 ).

Dyslipidemia or hyperlipidemia

Patients with a history of hyperlipidemia or using lipid-lowering medication or a total cholesterol level ≥200 mg/dl, an LDL cholesterol level ≥100 mg/ dl, an HDL cholesterol level <40 mg/dl in case of men or <50 mg/dl in case of women, and/or a serum triglyceride level ≥150 mg/dl ( 26 – 28 ).

Hypertension

Patients receiving antihypertensive medication, who were previously diagnosed with hypertension, or with a blood pressure level ≥140/90 mm/Hg for two measurements ( 28 , 29 ).

Alcohol use

Patients consuming ≥2 drinks/day in the case of men and ≥1 drink in the case of women on average (previous drinker/ex-drinker for more than 1 year) ( 14 , 30 , 31 ).

Patients taking two cigarettes per day in the case of men and one per day in the case of women on average ( 9 , 30 , 31 ).

Former smoker

Patients who abstained from smoking for >1 year ( 9 , 30 , 31 ).

Current smoker

Patients currently smoking for 1 year ( 9 , 30 , 31 ).

Physical activity level

It is the measure of planned or incidental activity, including mode or type of activity, frequency of performing an activity, duration of performing an activity, and intensity of performing an activity ( 32 ).

Extremely inactive

It is a PAL < 1.40 (e.g., cerebral palsy) ( 16 , 33 ).

Patients with a PAL = 1.40–1.69 (e.g., an office worker with little or no exercise) ( 16 , 33 ).

Moderately active

Patients with a PAL = 1.70–1.99 (e.g., construction worker or a person running 1 h daily) ( 16 , 33 ).

Vigorously active

Patients with a PAL = 2–2.40 (e.g., agriculture worker non-mechanized or person swimming 2 h daily) ( 16 , 33 ).

Extremely active

Patients with a PAL > 2.40 (e.g., competitive cyclist) ( 16 , 33 ).

Data collection tool and procedure

Data collection was carried out by an (R-3) internal medicine resident in each hospital with training on the contents of the data collection tool. The data collection tool was developed based on previous research findings and the WHO STEPwise approach to stroke surveillance ( 34 ). All relevant data were retrieved from patients' charts, and interviews were conducted with the patients/caregivers using a prepared data extraction form and questionnaire. The patients' history used in the study was obtained from the patients and/or relatives in the language they understood (Amharic). The data collection form was used to collect data on the sociodemographic and behavioral characteristics and clinical characteristics of patients such as risk factors, clinical presentation, and subtypes of stroke.

Data management and analysis

The collected data were coded, manually checked, and entered into the data management system by using Epi-info version 7. The data were cleaned and edited by simple frequencies and cross-tabulations before analysis, and then, they were exported to STATA version 16 and checked for missing values. Descriptive statistics and numerical summary measures were presented using frequency distribution tables. During candidate selection, adequate significant variables were obtained at a P < 0.05, which was considered a cutoff point for multivariate logistic regression analysis using a backward stepwise approach to identify the independent predictors of stroke subtypes. The data were represented as odds ratios (ORs) and 95% confidence intervals.

The study population comprised 554 patients who were admitted during the study period to the three public referral hospitals, among whom 334 cases (60.29%) had an ischemic stroke and 220 (39.71%) had a hemorrhagic stroke. All the patients were evaluated for stroke using a CT scan.

The mean age of the participants was 61 ± 12.85 years, ranging from 28 to 89 years, and 33% were in the age category of 60–69 years. More than half (53.25%) of the participants were women, and the remaining 46.75% were men. The majority of the participants (68.4%) were rural residents, and 49.64% of patients were housewives. Regarding the educational status of the patients, 67.69% have no formal education. The majority of the patients (84.66%) were married. Regarding behavioral characteristics, 95.49%, 34.3%, and 4.33% consume fruits and vegetables <2 times per week, were former drinkers, and were former smokers, respectively ( Table 1 ).

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Table 1 . Characteristics and risk profile of patients with stroke admitted to public referral hospitals, Northwest Ethiopia, 2020–2021.

Risk factors for stroke

Table 1 shows the frequency of identified risk factors by stroke subtype. The presence of comorbidity was identified in 269 (48.5%) patients, with 104 patients (47.3%) with HS and 165 patients (49.4%) with IS. The most common comorbidity identified was hypertension, which was in 165 patients (29.7%), followed by CHF in 35 (6.3%), DM in 20 (3.6%), hyperlipidemia in 20 (3.6%), past stroke in 19 (3.4%), and AF in 5 (0.9%). Among patients with hypertension, 89 (40.45%) had a hemorrhagic stroke and 76 (22.6%) had an ischemic stroke.

About 60 (10.8%) patients had a family history of chronic illness, with hypertension being the major chronic illness in the family in 31 patients (5.6%). A total of 190 patients (34.3%) were identified as former drinkers, 59 as current drinkers (10.6%), and the remaining as non-drinkers. Regarding physical activity, a significant share of patients, 95 (17.1%), were sedentary, and 20 (3.6%) were extremely inactive. In total, 529 patients (95.5%) eat fruit and vegetables <2 times per week.

Clinical presentation of patients with stroke

The most common clinical presentation was hemiparesis as reported by 320 (57.7%) patients, followed by loss of consciousness by 115 patients (20.7%) and aphasia by 50 patients (9%). Most patients with hemorrhage presented with hemiparesis (47.7%), loss of consciousness (34.1%), vomiting (6.8%), and aphasia (6.8%). Similarly, the chief complaint among patients with ischemic stroke was hemiparesis (64.4%), followed by coma (12%), aphasia (10.5%), and slurred speech (6%). Overall, of 225 (40.6%) patients with stroke, 59.1% of patients with hemorrhagic stroke, and 28.4% of patients with ischemic stroke had complications during hospital presentation. Aspiration pneumonia (28.9%) was the most common medical complication, and brain edema (17.1%) was the most common neurologic complication ( Table 2 ).

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Table 2 . Clinical presentation of patients with stroke admitted to public referral public hospitals, Northwest Ethiopia, 2020–2021.

Determinants of stroke subtypes

Through binary logistic regression, age, cigarette smoking, physical activity level, family history of chronic illness, type of comorbidity, complication during admission, and clinical presentation were selected as candidate variables to be included in multivariate logistic regression with a p < 0.05. Through multivariate logistic regression, age (AOR = 1.03, 95% CI = 1.01–1.05), the level of sedentary physical activity (AOR = 6.78, 95% CI = 1.97–23.32), absence of a family history of chronic illness (AOR = 3.79, 95% CI = 2.21–6.48), and past stroke (AOR = 3.54, 95% CI = 0.93–13.49) were found to be independent determinants of hemorrhagic stroke subtypes, while hypertension (AOR = 0.51, 95% CI = 0.31–0.85) was independently and strongly associated with an ischemic stroke compared with a hemorrhagic stroke.

With a 1-year increase in patients' age, the odds of having a hemorrhagic stroke compared with ischemic stroke will increase by 3%. Patients with sedentary activity levels were seven times more likely to experience a hemorrhagic stroke than an ischemic stroke. The odds of hemorrhagic stroke vs. ischemic stroke were 3.79 times higher in patients with the absence of a family history of chronic illness than in their counterparts. Furthermore, patients with a history of stroke were 3.54 times more likely to experience a hemorrhagic stroke than an ischemic stroke. Meanwhile, patients with hypertension were 0.51 times less likely to experience a hemorrhagic stroke than an ischemic stroke ( Table 3 ).

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Table 3 . Determinants of stroke subtypes among patients with stroke admitted to public referral hospitals, Northwest Ethiopia, 2020/2021.

The study data were drawn from the large study on stroke conducted in public referral hospitals in Northwest Ethiopia. The findings of this study will lead to advances in and unique contributions to the previously published studies by exploring the risk factors, clinical presentations, and determinant subtypes of stroke.

The mean age of the participants was 61 ± 12.85 years, which was in line with studies conducted in other sub-Saharan African countries ( 19 , 22 , 35 – 37 ), but it was lower than that in studies conducted in developed countries ( 38 , 39 ). This disagreement may be due to the Ethiopian population's lifestyle modification, abuse of alcohol, physical inactivity, cigarette smoking, and poor health-seeking behavior, which could result in the early onset of stroke.

In contrast to other previous studies, the percentage of stroke was higher in female patients than in male counterparts ( 9 , 40 ). The possible reason for the higher percentage among female patients may be due to increased risk factors of stroke such as high use of contraception, pregnancy-related disorders, and migraine.

Almost half of the participants had comorbidity, which include both patients with an ischemic stroke and patients with a hemorrhagic stroke. Similar to other studies conducted in Ethiopia, Senegal, Nigeria, Iran, and China, hypertension was the most common comorbidity ( 9 , 17 , 22 , 30 , 41 – 43 ). This trend may reflect that there is still a limitation in screening for hypertension, underdiagnosis, poor blood pressure control in patients with hypertension, and a poor healthcare system.

Considering the habit of alcohol drinking and cigarette smoking, compared with previous studies conducted in Ethiopia, 34.3% former drinkers and 10.6% current drinkers, the habit was low in the current study, with 4.3% former smokers and no current smokers ( 9 , 19 ). This could be due to underreporting of cigarette smoking, which is seen as being forbidden in the community in the catchment area of our study, although it has high abusers of alcohol. Alcoholism and the risk factor of stroke are associated with aggravating the effects that cause cardioembolism and hypertension.

At hospital presentation, the most common chief complaint was hemiparesis, which was reported by 57.7% of patients, followed by loss of consciousness (20.7%) and slurred speech (4.5%). A similar finding was reported in studies conducted in Ethiopia, India, and Pakistan ( 8 , 35 , 41 , 44 , 45 ). This finding was unlike other studies from Ethiopia, where a headache was the most common clinical presentation ( 9 ). The difference could be because this study was carried out among patients admitted to hospitals, which may contain more severe cases and late hospital presentations, thus leading to disease severity either at onset or in the later stages and complications.

Multivariate logistic regression showed that age, the level of sedentary physical activity, absence of a family history of chronic illness, and past stroke were identified as independent determinants of a hemorrhagic stroke compared with an ischemic stroke, while hypertension was associated with an ischemic stroke compared with a hemorrhagic stroke.

The results of our study revealed that an increase in age is associated with the odds of having a hemorrhagic stroke compared with an ischemic stroke, which is in contrast to studies from Central Africa, Nigeria, and China ( 7 , 23 , 46 ), but supported by a study from Australia ( 15 ). However, advanced age with heavy alcohol consumption could predispose individuals to hypertensive intraparenchymal hemorrhage.

Patients with sedentary activity levels were seven times more likely to experience a hemorrhagic stroke than an ischemic stroke ( 16 , 47 ). The mechanistic basis of the effect of physical activity on stroke risk is likely to prevent obesity, hypertension, dyslipidemia, and the development of type 2 diabetes, all of which are implicated as risk factors of stroke.

The odds of hemorrhagic stroke vs. ischemic stroke were 3.79 times higher in patients with the absence of a family history of chronic illness than in their counterparts, which is supported by different studies ( 7 , 48 – 50 ). This could be explained by the fact that a family history of DM, hypertension, and obesity are risk factors for ischemic stroke, largely by their link to atherosclerosis, but the effect of a family history of chronic illness may require further stratification and investigation.

Contradicting a study conducted in Singapore, out study showed that patients with a history of stroke were more likely to experience hemorrhagic stroke than an ischemic stroke ( 51 ), which could, in part, be explained by differences in the study population, stroke subtypes, stroke severity, and first-ever or recurrent strokes.

Furthermore, we observed hypertension was independently and strongly associated with ischemic stroke compared with hemorrhagic stroke, which is supported by other studies ( 7 , 48 , 49 ), but this finding contradicts the result of a study conducted in 22 countries ( 48 ). A possible explanation may be that, while hypertension predisposes patients to both strokes, atherosclerotic plaque formation (which favors IS) and higher blood pressures may be required for microaneurysmal rupture compared with plaque accident. Finally, in our study, there was no specific clinical presentation significantly associated with the stroke subtypes.

Strengths and limitations of the study

This study attempted to identify risk factors, clinical presentations, and predictors of stroke subtypes via a prospective follow-up of CT scan-confirmed cases in multiple health facilities to ascertain the reliability of the outcome of the study. This may reduce the false-positive and false-negative associations between different variables of the study. The limitation of the study is the study type being a hospital-based study rather than a longitudinal community-based study. Thus, attention should be given to the generalization of the findings to a large community. In addition, we relied on patient reports for some risk factors and other patient-related histories, which may introduce a recall bias.

The majority of the patients were middle-aged, women, rural residents, and participants with no formal education. The early-onset stroke poses a significant challenge for the healthcare system and the economy of low-income countries. Hypertension was the most common risk factor identified in the current study. The most common clinical presentation was hemiparesis, followed by coma and slurred speech. In addition, the majority of patients with stroke presented with complications during admission.

Age, the level of sedentary physical activity, absence of a family history of chronic illness, hypertension, and past stroke were independent determinants of stroke subtypes. This study has an important clinical implication that uncontrolled hypertension or undiagnosed hypertension are still the targets of wrestling in Ethiopia. Although this strategy in addition to lifestyle modification, screening first-degree relatives for chronic disease and rehabilitation of patients with stroke can be used to reduce the burden of the disease.

Data availability statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

Ethics statement

The studies involving human participants were reviewed and approved by College of Health Science Ethical Review Committee, Debre Tabor University. The patients/participants provided their written informed consent to participate in this study.

Author contributions

GA, GY, EZ, ZE, ATA, BA, DA, AA, and MA contributed to the design of the study, analysis, interpretation, and wrote the manuscript. GA, GY, and ZE made the data analysis and interpretation of the data. YA, EZ, DA, AA, FA, and MA contributed to the design of the study, drafting, and edition of the manuscript. All authors critically revised the manuscript and have approved the final manuscript.

Acknowledgments

We would like to thank the participants of the study. We also thank and appreciate data collectors and staff of the University of Gondar Teaching Hospital, Tibebe Ghion Comprehensive Specialized Hospital, and Felege Hiwot Regional Referral Hospital.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher's note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Abbreviations

AF, atrial fibrillation; CHF, congestive heart failure; CVD, cardiovascular disease; DM, diabetes mellitus; DVT, deep venous thrombosis; FBS, fasting blood sugar; GBD, global burden of disease; HDL, high-density lipoprotein; HS, hemorrhagic stroke; ICP, intra-cranial pressure; IS, ischemic stroke; LDL, low-density lipoprotein; LMICs, low- and middle-income countries; PAL, physical activity level; RBS, random blood sugar; SSA, sub-Saharan Africa; UTI, urinary tract infection.

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Keywords: risk profile, clinical presentation, determinants, stroke subtype, Ethiopia

Citation: Ayehu GW, Yitbarek GY, Zewdie EA, Amsalu BT, Abie Y, Atlaw D, Agegnehu A, Admasu FT, Azanaw MM, Amare AT and Emiru ZA (2022) Risk profile, clinical presentation, and determinants of stroke subtypes among patients with stroke admitted to public referral hospitals, Northwest Ethiopia in 2021: A cross-sectional study. Front. Neurol. 13:988677. doi: 10.3389/fneur.2022.988677

Received: 07 July 2022; Accepted: 22 August 2022; Published: 25 October 2022.

Reviewed by:

Copyright © 2022 Ayehu, Yitbarek, Zewdie, Amsalu, Abie, Atlaw, Agegnehu, Admasu, Azanaw, Amare and Emiru. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Gashaw Walle Ayehu, gashawwalle01@gmail.com

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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clinical presentations of stroke

Acute Ischemic Stroke (AIS)

June 26, 2022 by Josh Farkas

  • Rapid Reference 🚀
  • Blood pressure control
  • Anticoagulation & antiplatelet therapy
  • Respiratory support
  • Seizure management
  • Dysphagia evaluation & nutritional support
  • Additional supportive measures
  • Neuroworsening in AIS
  • Thrombolytic-induced angioedema
  • Hemorrhagic transformation (including post-thrombolysis)
  • Malignant MCA syndrome
  • Cerebellar stroke & posterior fossa syndrome
  • Basilar artery thrombosis
  • Moyamoya disease
  • Goals of this chapter
  • Anterior Cerebral Artery (ACA)
  • Middle Cerebral Artery (MCA)
  • Anterior Choroidal Artery
  • Posterior Cerebral Artery (PCA)
  • Basilar Artery
  • Brainstem syndromes
  • Lacunar syndromes
  • Thalamic syndromes
  • Physiology: Core infarct vs. ischemic penumbra
  • Diagnosis: Stroke mimics
  • Exam & NIH stroke scale
  • Investigation of the cause of AIS
  • Noncontrast CT
  • CT angiography (CTA)
  • CT perfusion
  • Endovascular therapy
  • Questions & discussion

(back to contents)

thrombolysis/endovascular therapy

  • If potential candidate, activate a stroke code.

labs to consider

  • STAT fingerstick glucose.
  • Complete blood count.
  • Electrolytes including Ca/Mg/Phos.
  • Liver function tests.
  • Generally PT, PTT, fibrinogen.
  • Anti-Xa for patients on oral Xa inhibitors (e.g., api Xa ban).
  • Blood cultures x2 if concern for endocarditis (e.g., fever or history of IV drug use).
  • Pregnancy test as appropriate.

blood pressure control 📖

  • No intervention: permissive HTN (<220/<120).
  • Status post thrombolysis: <180/<105.
  • TICI 0-2a flow: SBP 120-180 mm.
  • TICI 2b-3 flow: SBP 120-160 mm.
  • May use labetalol boluses PRN, or clevidipine/nicardipine infusion.
  • Maintenance IV fluid may be considered for patients who are NPO with minimal fluid inputs, but I/O balance should be followed carefully with avoidance of volume overload.

antiplatelet therapy 📖

  • Antiplatelet therapy with aspirin (or clopidogrel, if aspirin allergy).
  • Start with a loading dose (325 mg aspirin, or 300 mg clopidogrel).
  • (1) Status post thrombolysis (generally delayed until 24 hours after thrombolysis and review of post-thrombolysis CT scan).
  • (2) Decompressive craniectomy is possible.

DVT prophylaxis 📖

  • Enoxaparin is preferred, if renal function allows (GFR >30 ml/min).
  • Hold chemical DVT prophylaxis for 24 hours following thrombolysis (use sequential compression devices).
  • If febrile (>38C), investigate for infection and start scheduled acetaminophen 💉 (e.g., 1 gram q6hrs for most patients).
  • Consider atorvastatin 80 mg daily (if no contraindication and stroke is thought to be atherosclerotic in origin).

management of hypertension

Bp for patients not receiving any intervention.

  • Systolic >220 mm .
  • Diastolic >120 mm .
  • Hypertensive emergency with target organ damage  caused by hypertension (e.g., myocardial ischemia, hypertensive nephropathy, pulmonary edema).  Hypertensive emergency is discussed further here 📖 .
  • If blood pressure reduction is needed, this should be gentle (e.g., ~15% reduction during the first 24 hours, unless there is target organ damage). ( 33512282 )

Bp for patients receiving thrombolysis

  • Before thrombolysis : Target Bp <185/<110. ( 31662037 )
  • After thrombolysis : Target Bp <180/<105 for 24 hours. ( 31662037 )

Bp control for patients receiving endovascular therapy

  • Peri-procedural period : For patients undergoing intubation prior to endovascular therapy, avoid hypotension. Even small blood pressure reductions (e.g., >10% decrease) may correlate with worse outcomes. A reasonable blood pressure target for most patients in the periprocedural period might be a systolic BP of ~140-180 mm. ( 31346678 )
  • Most guidelines recommend <180/105 (similar to post-thrombolysis patients). ( 31662037 )
  • TICI 0-2a flow: Target SBP 120-180 mm.
  • TICI 2b-3 flow: Target SBP 120-160 mm. ( 31346678 ; 35034076 , 36333037 )
  • The neurointerventionalist will often recommend an individualized blood pressure target.

preferred agents for lowering blood pressure

  • Nicardipine 💉 or clevidipine 💉 infusions are highly effective. 📖
  • PRN labetalol boluses may be used if the blood pressure is only slightly above target (the dosing and strategy for labetalol use are discussed further here 💉 ).

management of hypotension

  • Hypotension is potentially dangerous in this situation, since it may promote cerebral hypoperfusion.  Several studies have found an association between hypotension and worse neurological outcomes. ( 36333037 )
  • Evaluate for the etiology of hypotension and treat any causes (e.g., hypovolemia).
  • Discontinue any antihypertensives.
  • The use of vasopressors here is not evidence-based, but could be reasonable within specific patient scenarios (e.g., the perfusion-dependent patient whose neurological exam worsens due to hypotension, so vasopressors are started and this causes an improvement in the neurological exam).

volume management

  • Avoiding hypotension is important, as this could compromise perfusion of ischemic tissue.
  • A euvolemic state should be targeted.
  • (1) Hypotensive patients, especially if examination or clinical history suggests hypovolemia.
  • (2) Patients who are NPO for extended periods.
  • (3) Patients with widely labile blood pressure and evidence of hypovolemia (the combination of hypovolemia plus variable systemic vasoconstriction may cause wide blood pressure swings). 📖
  • Follow input/output balance and ensure that patients don't become hypervolemic .

anticoagulation for cardioembolic infarction in context of atrial fibrillation

  • (a) Anticoagulation may increase the risk of hemorrhagic conversion.
  • (b) Anticoagulation may decrease the risk of another stroke.
  • Warfarin may be preferable to a direct oral anticoagulant (DOAC), since warfarin can be rapidly reversed if hemorrhagic transformation occurs. Bridging with heparin is not generally beneficial.
  • For larger strokes with a higher risk of hemorrhagic transformation, it makes sense to delay anticoagulation initiation towards closer to the ~14 day mark.

antiplatelet therapy

  • Aspirin is one of the most strongly evidence-based therapies for acute stroke (demonstrated to reduce recurrence and mortality). ( 10835439 )
  • Start aspirin with a loading dose of 325 mg orally or 300 mg rectally, followed by 81 mg daily.
  • In patients with aspirin allergy: use clopidogrel instead (beginning with a 300-mg loading dose).
  • For patients treated with thrombolysis: delay initiation of antiplatelet therapy until after reviewing the CT scan performed ~24 hours after thrombolysis.

dual antiplatelet therapy

  • Dual antiplatelet therapy has shown benefit in acute ischemic stroke, but this has been studied only in high-risk TIA and minor stroke. As such, this data will not apply to most critically ill patients with acute ischemic stroke.
  • Dual antiplatelet therapy is not generally recommended for patients with moderate or large strokes.

DVT prophylaxis

  • Low-molecular-weight heparin is preferred for DVT prophylaxis. ( 17448820 )
  • Patients treated with thrombolysis or successful endovascular thrombectomy: delay chemical DVT prophylaxis for 24 hours.
  • Patients unable to receive chemical DVT prophylaxis should be managed with intermittent pneumatic compression. ( 26418530 )

management of hypoxemia

  • Guidelines recommend targeting an oxygen saturation >94%. ( 31662037 )
  • Supplemental oxygen is not recommended for patients who are not hypoxemic.
  • Ischemic stroke by itself shouldn't generally cause hypoxemia. Thus, hypoxemia should be investigated to determine an underlying cause (e.g., aspiration pneumonitis).

intubation & mechanical ventilation

  • Respiratory failure (especially hypercapnia that may be exacerbating elevated intracranial pressure).
  • Bulbar dysfunction with inability to protect the airway.
  • To facilitate procedural sedation (e.g., endovascular therapy).
  • Impaired consciousness with ongoing neuroworsening.
  • Anterior territory strokes usually don't impair airway protection, unless there is edema compressing other areas of the brain (i.e., malignant MCA syndrome). Thus, the need for airway protection in an anterior stroke should trigger consideration for whether a decompressive craniectomy is indicated (more on this below 📖 ).
  • Erratic breathing patterns may associate with certain strokes (discussed further here 📖 ).

epidemiology

  • Higher stroke severity.
  • Cortical involvement, especially involvement of multiple lobes.
  • Hemorrhagic conversion.
  • In the context of acute ischemic stroke, seizure may reflect hemorrhagic transformation .

possible indications for continuous EEG monitoring (LaRoche 2018)

  • Fluctuating neurologic deficits.
  • Unexplained coma or altered level of consciousness.
  • Following a seizure or status epilepticus, if the patient has a persistently abnormal mental status.
  • Seizures or status epilepticus that requires active therapy.
  • Treatment precludes reliable neurologic examination (e.g., paralysis).
  • Clinical suspicion of seizure (e.g., twitching).
  • Seizure prophylaxis is not recommended. ( 31662037 )
  • If seizures occur, they should be treated in the usual fashion. Ongoing use of a maintenance antiepileptic agent is generally continued to prevent recurrence (at least in the short term). 📖

dysphagia evaluation

  • Dysphagia is common following ischemic stroke.
  • All patients should receive a bedside dysphagia screening examination prior to initiation of a diet (e.g., supervised ability to drink a glass of water by a bedside nurse or speech and language therapist).
  • Patients who fail the bedside screening examination may require more comprehensive dysphagia evaluation.

early enteral nutritional support

  • Patients who are intubated should have enteral nutrition started within 24-48 hours, as is standard for any critically ill patient. 📖
  • Patients who are not intubated and have substantial dysphagia should have enteral nutrition started within <7 days. ( 31662037 ) Feeding may be provided via a small-bore, flexible feeding tube. 📖 A small-bore feeding tube is often adequate to provide nutritional support and enteral medication access for some weeks, during which the patient's ability to swallow would hopefully recover.
  • If patients have persistent dysphagia for >2-3 weeks, then the utility of a percutaneous gastrostomy tube (PEG tube) may be considered.
  • High-intensity statin (e.g., atorvastatin 80 mg) is often recommended based on the SPARCL trial. ( 16899775 )

fever investigation & treatment 📖

  • Elevated temperature (>38C) should be investigated and treated aggressively. ( 31662037 ) For example, this might include an infection workup 📖 followed by scheduled acetaminophen to suppress fever (e.g., 1 gram q6hr scheduled ). Simply providing individual doses of acetaminophen PRN for every fever spike is less likely to achieve consistent temperature control. If acetaminophen fails to achieve normothermia, physical cooling should be initiated (e.g., cooling blankets). ( 31346678 )
  • Note that the cutoff of an actionable temperature here (>38 C) is less than the usual definition of fever in the ICU (>38.3 C).
  • Unlike intracranial hemorrhage, ischemic stroke is unlikely to cause a neurogenic fever. 📖

glycemic control

  • Hyperglycemia correlates with worse outcomes in stroke, as is generally true within critical care. However, the risks-vs-benefits of lowering glucose remain unclear. Hypoglycemia is certainly quite detrimental to an injured brain.
  • The SHINE trial of tight glycemic control (targeting a glucose of 80-130 mg/dL) found that tight glycemic control actually caused harm (in terms of an increased risk of severe hypoglycemia). ( 31334795 )
  • The usual approach to glycemic control among critically ill patients may be reasonable for these patients. 📖

differential diagnosis: more common considerations

  • Hypoglycemia .
  • Infarct extension , reocclusion, or additional infarctions (e.g., due to additional embolic events).
  • Hemorrhagic transformation (may occur even without thrombolysis or endovascular therapy).
  • Edema (e.g., malignant MCA syndrome).
  • Elevated intracranial pressure (e.g., due to a cerebellar stroke that obstructs the cerebral aqueduct).
  • Hypertension causing PRES (posterior reversible encephalopathy syndrome).
  • Excessive drop in blood pressure causing brain malperfusion.
  • Medication effects (e.g., procedural sedation).
  • Seizure (including nonconvulsive seizures and postictal state).

approach: tests to consider

  • If relative hypotension causing brain malperfusion is suspected, may elevate the blood pressure using vasopressors and repeat the clinical examination. (Albin 2022)
  • STAT CT scan (evaluate for hemorrhage, edema, or elevated intracranial pressure).
  • EEG (especially consider for altered mental status that remains unexplained despite neuroimaging).

clinical presentations of stroke

  • Angioedema is a rare complication of thrombolysis that occurs with a frequency of ~2%. It usually begins 30-120 minutes after tPA infusion. (Louis 2021) This is a physiological class effect that results from augmenting plasmin activity, so it may result from the use of any thrombolytic (e.g., tPA or tenecteplase).
  • Thrombolytic-induced angioedema is a form of bradykinin-mediated angioedema , based on the mechanism shown above. ( 30215283 ) Clinically, bradykinin-mediated angioedema is often asymmetric angioedema that frequently involves the tongue or lips without involving other organ systems (e.g., absence of pruritus, hypotension, bronchospasm). 📖
  • The risk of angioedema is increased in patients taking ACE inhibitors or patients with C1-esterase deficiency (as expected, since these cause increased bradykinin levels). ( 26288671 )
  • There is no high-quality evidence on this topic.
  • If thrombolytic is still being infused, the infusion should be discontinued immediately. Discontinue any ACE inhibitors as well.
  • In many cases, angioedema may be mild and self-limited, so close observation may be all that is necessary. Given that thrombolytics have a short half-life, most cases may be expected to improve over time. However, if angioedema is rapidly enlarging and threatening the airway, then intubation may be necessary.
  • Tranexamic acid would theoretically be beneficial here, but lacks evidentiary support. Additionally, tranexamic acid could abrogate any therapeutic benefits of thrombolysis on the stroke.
  • Mechanistically, C1 inhibitor concentrate might be expected to be the best therapy here, with success reported in one case. ( 27174372 ) The use of icatibant for thrombolytic-induced angioedema has been described, but this medication is not widely available. ( 29653785 )
  • ⚠️ Patients with angioedema following thrombolysis that is clinically consistent with bradykinin-mediated angioedema are not expected to respond to treatments directed at histamine -mediated angioedema (e.g., epinephrine, steroid, and antihistamines).
  • Hemorrhagic transformation may result from the natural evolution of ischemic stroke, usually within the first week.
  • (#1) Petechial hemorrhages : Most hemorrhagic transformations are small , petechial hemorrhages of little clinical significance.
  • (#2) Asymptomatic hematomas : Small hematomas can occur within infarcted brain. If the hematoma is small and it occurs in a region of brain tissue which is already nonfunctional, this may not affect clinical outcome.
  • (#3) Symptomatic hematomas : Large hematomas may exert mass effect, cause vasogenic edema, and worsen clinical outcomes. Symptomatic hematoma formation occurs in ~2% of patients without thrombolysis, or up to ~6% of patients treated with thrombolysis. ( 32668115 )
  • Hemorrhagic infarct type 1 (HI-1) : Petechial hemorrhages at the margins.
  • Hemorrhagic infarct type 2 (HI-2) : Petechial hemorrhages throughout the infarct, no mass effect.
  • Parenchymal hematoma type 1 (PH-1) : Hemorrhage of <30% of the stroke volume with mild mass effect.
  • Parenchymal hematoma type 2 (PH-2) : Hemorrhage of >30% of the stroke volume with substantial mass effect, or hemorrhagic extension beyond the infarct.

risk factors for hemorrhagic transformation

  • Large infarct size (e.g., hypodensity in more than a third of the MCA territory).
  • Coagulopathy (e.g., therapeutic anticoagulation or thrombolysis).
  • Diabetes mellitus, hyperglycemia.
  • Uncontrolled hypertension. ( 32224752 )

clinical presentation of symptomatic hemorrhagic transformation

  • ⚠️ It may be very difficult to differentiate neurological deterioration due to progression of acute ischemic stroke versus superimposed hemorrhage. When in doubt, there should be a low threshold to obtain a CT scan.
  • Headache, nausea/vomiting.
  • Acute spike in blood pressure.

management of symptomatic hemorrhagic transformation

  • Immediately stop thrombolytic if this is still infusing. Discontinue any other anticoagulating medications.
  • Reverse any relevant coagulopathies. Especially if the patient recently received thrombolysis, this should be aggressively reversed. 📖
  • Measure coagulation labs as a baseline (INR, PTT, fibrinogen, complete blood count, type & cross-match). This shouldn't delay the administration of blood products to reverse known coagulopathies (e.g., thrombolysis), but it may help guide ongoing coagulation optimization. ( 33952393 )
  • Additional aspects of intracranial hemorrhage management here: 📖 .
  • Proximal MCA infarction may lead to marked edema causing herniation and death (e.g., malignant MCA syndrome). Edema usually peaks after 3-4 days, but reperfusion may accelerate this. (Shutter 2019)
  • Decompressive craniectomy may prevent herniation and death, by opening of a generous bone window.
  • Patients with malignant MCA syndrome can have a normal intracranial pressure (ICP). Deterioration results from tissue shifts, rather than having a globally elevated intracranial pressure. (Nelson, 2020)

risk factors for malignant MCA syndrome

  • Younger patients (who have less underlying atrophy and thus less space to accommodate edema).
  • Dense MCA sign indicates a proximal MCA infarction with a large territory at risk.
  • >50% of MCA territory shows hypodense edema on CT scan.
  • Involvement of multiple vascular territories (e.g., combined infarction of ACA plus MCA territories).
  • MRI diffusion weighted imaging (DWI) volume >82 ml if performed within six hours of stroke onset. ( 36333037 )
  • Mass effect is seen on imaging (e.g., midline shift, effacement of the ipsilateral sulci and lateral ventricles), especially if this occurs rapidly .
  • Frank hypodensity on CT scan within the first six hours. (Nelson, 2020)
  • Early development of encephalopathy. ( 36333037 )

initial management of MCA edema

  • AHA guidelines indicate that it's reasonable to use a decrease in level of consciousness attributed to brain swelling as a trigger for decompressive craniectomy. ( 31662037 )
  • Medical therapies for ICP elevation (e.g., hypertonic therapy) should be used to treat edema. Medical management alone will usually fail. However, medical therapies can be used as a temporizing measure, to help bridge the patient to craniectomy. 📖

craniectomy for MCA syndrome

  • For malignant MCA syndrome, craniectomy is undoubtedly a life-saving procedure. The thorny issue is what quality of life would patients subsequently be left with. Surviving patients are likely to be left with severe disability. (Nelson, 2020)
  • Younger age (<60 years old).
  • Earlier surgery (within <24-48 hours of stroke onset, and prior to any herniation symptoms). ( 36333037 )
  • Surgical intervention prior to irreversible secondary brain injury.
  • The value of decompressive craniectomy among patients >60 years old is questionable. The DESTINY-II trial involved 112 patients over 60 years old with large MCA infarctions (inclusion required involvement of more than two thirds of the MCA territory, reduced level of consciousness, and NIH Stroke Scale scores of >14 or >19 in nondominant or dominant infarctions, respectively). Regardless of whether patients were randomized to medical therapy or decompressive craniectomy, no patients in either group achieved functional independence (Modified Rankin Scale 0-2). There were no differences in the number of patients with moderate disability after a year (Modified Rankin Scale 3). Craniectomy prevented death by increasing the number of patients with moderately severe or severe disability. 🌊 ( 24645942 )
  • For a discussion of patient management status following craniectomy: 📖

potential danger

  • (#1) Noncommunicating hydrocephalus could result from compression of the cerebral aqueduct or the fourth ventricle.
  • (#2) If more severe, swelling could compress the adjacent brainstem .
  • Occlusion of the posterior inferior cerebellar artery (PICA) is the most worrisome, since it supplies the largest portion of the cerebellum. (Nelson, 2020)
  • Involvement of the cerebellar vermis is associated with increased likelihood of deterioration.
  • ⚠️ Note that among patients with noncommunicating hydrocephalus, treatment with an external ventricular drain alone (without suboccipital craniectomy) may lead to upward transtentorial herniation of the cerebellum.
  • Patients undergoing decompressive suboccipital craniectomy for cerebellar infarction tend to have better outcomes than patients undergoing decompressive craniectomy for MCA infarction, because the underlying stroke is smaller and involves less eloquent areas of the brain (with 35-40% of patients achieving functional independence). (Nelson, 2020)
  • For a discussion of patient management following posterior fossa surgery: 📖
  • Moyamoya disease is a chronic, progressive, idiopathic, occlusive disease involving the internal carotid artery, proximal ACA (anterior cerebral artery), and proximal MCA (middle cerebral artery). Disease may be bilateral or unilateral. Hypertrophied small collateral vessels generate a characteristic “puff of smoke” appearance on angiography.
  • Genetic diseases (Sickle cell disease, trisomy 21, pseudoxanthoma elasticum, glycogen storage disease type 1a, Fabry disease, neurofibromatosis type I, polycystic kidney disease, tissue plasminogen activator deficiency).
  • CNS infections (tuberculosis, EBV infection).
  • Inflammatory diseases (eosinophilic angiitis, Kawasaki syndrome, Sjogrens disease, lupus).
  • Postradiation vasculopathy.
  • Fibromuscular dysplasia.
  • Women of East Asian descent seem to be most often affected.
  • Among adults, the peak incidence occurs among patients in their 40s.

clinical manifestations include:

  • (1) Acute ischemic stroke: Moyamoya disease most often presents with an ischemic event.
  • About a third of patients present with an intracranial hemorrhage resulting from fragile collaterals and/or false aneurysms. ( 34618759 )
  • Hemorrhage is most commonly located in the basal ganglia.
  • Subarachnoid hemorrhage may occur.
  • (3) Recurrent headaches.
  • CT scan may show evidence of ischemic stroke and/or hemorrhage.
  • T2 may show collateral flow voids in the basal ganglia and basilar cistern.
  • FLAIR may show sulcal brightness, due to slow flow via pial collaterals.
  • Stenosis/occlusion of distal internal carotid artery or proximal arteries within the circle of Willis.
  • Hypertrophy of collateral capillaries occurs as a compensatory mechanism, which may resemble a “puff of smoke” on angiography.
  • (Going further: Momoya disease in Radiopaedia 🌊 )
  • Surgical revascularization may be indicated (e.g., bypass from the superficial temporal artery to the middle cerebral artery). Revascularization may run the risk of cerebral hyperperfusion syndrome , due to rapid restoration of blood flow.
  • Hypertrophied, fragile collateral arteries have a tendency to bleed. Therefore, some caution should be exercised with anticoagulation. Nonetheless, aspirin is commonly prescribed to patients with ischemic symptoms. (Louis 2021)

Acute ischemic stroke is an enormously broad topic, which alone is the subject of many textbooks. It would be impossible to provide detailed information about all aspects of ischemic stroke within a single chapter.

The intensivist's role in stroke care is a humble one – predominantly to assist with supportive management. Most strokes will already be diagnosed prior to ICU arrival. Likewise, major treatment decisions regarding thrombolysis and endovascular therapy have generally already been made (or will be determined by neurology and neuroradiology teams).

The goal of this chapter is to provide a foundation for understanding stroke care, with an emphasis on supportive therapies. Some aspects (e.g., when to pursue thrombolysis and/or endovascular therapy) are omitted since they are beyond the scope of practice of most intensivists. The stroke neurology team will typically focus on issues surrounding neuroimaging, thrombolysis, and endovascular therapy. Meanwhile, the ICU team may simultaneously focus on supportive care (e.g., airway assessment, blood pressure control, hemodynamic optimization, vascular access, electrolyte and glucose management). Dividing up the tasks with ongoing close communication may allow for rapid and comprehensive patient management.

anterior cerebral artery syndromes

  • Contralateral leg weakness and sensory loss.
  • Poor judgement, apraxia.
  • Flat affect, abulia = apathy and reduced speech.
  • Imitation behavior: automatic and involuntary imitation of the examiner's movements. (Louis 2021)
  • Incontinence.
  • “Alien hand sign” or hemiballism – one hand acts involuntarily.
  • Acute confusional state.
  • Contralateral hemineglect may occur (particularly when that is the left).
  • Transcortical motor aphasia (due to involvement of the supplementary motor area). This is similar to Broca's aphasia, but with preservation of repetition.

bilateral anterior cerebral artery occlusion

  • Some patients have an anatomic variant where the proximal anterior cerebral arteries share a common trunk (A1) (this variant is called an “Azygous ACA”).
  • Occlusion of this shared artery will cause bilateral anterior cerebral artery occlusion. The combination of bilateral leg weakness and incontinence may mimic a spinal cord lesion. Other clinical findings may include executive dysfunction with abulia (paucity of spontaneous behaviors) or even akinetic mutism (awake unresponsiveness). (Louis 2021)

clinical presentations of stroke

anatomy of the anterior cerebral artery (ACA)

  • The recurrent artery of Huebner comes off the proximal ACA, providing blood to parts of the internal capsule, globus pallidus, putamen, and caudate head (figure below). Infarction of this artery may cause contralateral hemiparesis and/or movement disorder, abulia, incontinence, and dysarthria. (Louis 2021)
  • A1 = ACA proximal to the anterior communicating artery.
  • A2 = ACA distal to the anterior communicating artery.

effects of superior MCA trunk occlusion

  • Contralateral hemiparesis of face and arm.
  • May have contralateral hemisensory loss involving face and arm.
  • Conjugate ipsilateral eye deviation.
  • Neglect of the contralateral side of space (including visual, auditory, and tactile stimuli).
  • Anosognosia (lack of insight into neurological deficits).
  • Broca's aphasia.
  • Bilateral apraxia (inability to perform purposeful movements such as brushing teeth).

effects of inferior MCA trunk occlusion

  • Contralateral superior quadrantanopia.
  • Anosognosia (unawareness of deficits).
  • Motor neglect (not moving left side, yet strength is intact – for example, may be able to withdraw from pain).
  • Sensory neglect.
  • Wernicke's aphasia.
  • ⚠️ Patients may appear confused or psychotic. Given intact sensation and motor function, this can be difficult to sort out from a primary psychiatric event or diffuse metabolic encephalopathy.

proximal MCA syndromes (occlusion near the base of M1)

  • Contralateral hemiplegia involving the face and arm > leg.
  • Contralateral hemisensory loss.
  • Contralateral hemianopia.
  • Ipsilateral conjugate eye deviation.
  • Hemispatial neglect (generally of the left side).
  • Anosognosia.
  • Drowsiness and eyelid-opening apraxia (less common).
  • Global aphasia.

occlusion of the deep territory (lenticulostriate arteries supplying the basal ganglia and internal capsule)

  • Primary effect: Contralateral hemiparesis (may mimic a lacunar syndrome).
  • Nondominant hemisphere: Mild hemineglect.
  • Dominant hemisphere: Dysarthria, with sparing of repetition (similar to transcortical aphasia).

anatomy of the MCA

  • M1 = Horizontal portion which gives off lenticulostriate arteries.
  • M2 occurs before the MCA splits into superior vs. inferior divisions.
  • M2 occlusions may be amenable to endovascular therapy.
  • M3 (inferior)= Cortical branches of the MCA that run along the temporal lobe. This supplies the lateral surface of the temporal lobe and the inferior parietal lobe.
  • M4 (superior) = Cortical branches of MCA that run along the parietal lobe. This supplies the frontal and superior parietal lobes.

clinical consequences of infarction may include:

  • Contralateral hemiparesis.
  • “Cortical signs” (e.g., hemineglect) may or may not be seen. An absence of cortical signs may point towards a choroidal infarction (as opposed to an MCA infarct).
  • The anterior choroidal artery originates directly from the internal carotid artery.
  • Posterior thalamus (including the lateral geniculate nucleus, which relays sensory information to the cortex).
  • Internal capsule (including descending motor and ascending thalamocortical pathways).

posterior cerebral artery syndromes

  • Hemianopia or superior quadrantanopia.
  • Thalamic involvement may cause contralateral sensory loss (ventroposterolateral nuclei) or reduced arousal.
  • Uncommonly, may cause contralateral hemiplegia (due to involvement of the internal capsule) .
  • Alexia without agraphia (patients are able to write but not read). This results from infarction of the splenium of the corpus callosum, thereby cutting off visual information from the language processing centers.
  • Difficulty naming objects (transcortical sensory aphasia).
  • Visual agnosia (inability to describe what an object is used for).
  • Inferomedial temporal lobe infarction may cause global amnesia or agitated delirium . (Louis 2021)
  • Thalamic aphasia (if the thalamus is involved).
  • Prosopagnosia (inability to recognize faces).
  • Anton syndrome: cortical blindness that is unrecognized by the patient, who may confabulate what they are seeing.
  • Charles Bonnet syndrome: release visual hallucinations.
  • Agitated delirium may occur. (Louis 2021)

anatomy of the posterior cerebral artery (PCA)

  • PCA supplies the posterior thalamus via small thalamoperforator arteries coming off the proximal PCA, as well as longer arteries (posterior choroidal artery and thalamogeniculate arteries).
  • Branches of the PCA supply the midbrain, inferomedial temporal lobe, and occipital lobe

The thalami are critical relay and processing centers involved in connections between the cortex, basal ganglia, midbrain, and cerebellum. The thalami consist of about two dozen nuclei that are closely packed together. The discussion below highlights some key clinical aspects of the more common thalamic infarctions.

clinical presentations of stroke

anterior thalamic infarct (12%)

  • Vascular supply: tuberothalamic arteries originate from the posterior communicating artery.
  • Clinical effects seem to result largely from impacts on the limbic system (dorsomedial nucleus). These may include disorientation, euphoria, apathy, lack of insight or spontaneity, anterograde memory impairment, and transcortical aphasia (for left-sided lesions; this involves halting speech with preserved repetition). ( 29460331 )

paramedian thalamic infarct (35%)

  • Differential diagnosis of disorders involving the bilateral thalami: 📖 .
  • Clinical effects include impaired arousal, which may last for hours to days. Chronic impairment may include mood and behavioral changes (e.g., agitation, aggression, disorientation, apathy).
  • Bilateral paramedian infarctions cause stupor/coma, amnesia with confabulation, mood changes (including irritability and apathy), and vertical gaze paresis. ( 29460331 )

inferolateral thalamic infarct (45%)

  • Vascular supply: thalamogeniculate arteries are 5-10 arteries arising from the P2 segment of the posterior cerebral artery.
  • Central pain syndrome (Dejerine-Roussy syndrome).
  • Hemibody sensory loss (potentially including all types of sensation). Small lacunar infarcts that involve the ventral posterior lateral nuclei can cause a pure sensory stroke.
  • Impaired extremity movement (especially ataxic hemiparesis). ( 29460331 )

posterior thalamic infarct (rare)

  • Vascular supply: posterior choroidal arteries arise from both the P2 segment of the posterior cerebral artery and also some branches from the posterior communicating artery.
  • Clinical effects may include homonymous quadrantanopia, hemisensory loss, transcortical aphasia, and memory disturbances. ( 29460331 )

proximal basilar artery syndrome (base of the basilar artery)

  • Impaired consciousness (somnolence ranging to coma).
  • Quadriplegia. May also have “crossed” paralysis (e.g., left face and right limbs).
  • Abnormal movements (e.g., twitching, jerking, tremor, or shivering).
  • Oculomotor abnormalities, which may include horizontal gaze palsy (bilateral or unilateral), internuclear ophthalmoplegia (unilateral or bilateral), one and a half syndrome, skew deviation, gaze paretic nystagmus, or bilateral ptosis.
  • Pinpoint pupils.
  • Bulbar symptoms, which may include: Facial weakness, dysphagia, dysarthria, palatal myoclonus.
  • Pseudobulbar affect.
  • Sensory loss to light touch.

mid basilar artery (Locked-in syndrome)

  • Quadriplegia and facial paralysis, with extensor plantar response.
  • Horizontal gaze palsy (vertical gaze and/or blinking may remain intact).
  • Anarthria and dysphagia.
  • Hearing loss can occur.

top of the basilar syndrome

  • This results in ischemia of the midbrain, thalamus, and occipital lobes (but not the pons). The cerebellum may also be involved via the superior cerebellar artery.
  • Pupillary abnormalities (may involve afferents to Edinger-Westphal nucleus, CN3 nucleus, or descending sympathetic system). Pupils may be dilated, mid-position, or small.
  • Vertical gaze impairment, internuclear ophthalmoplegia, or skew deviation.
  • Hemianopsia or complete cortical blindness.
  • Amnesia, agitation, and hallucinations (may involve colors and objects).
  • Ataxia, tremor, dysarthria (if the cerebellum is involved).
  • Homonymous hemianopsia.

management of basilar artery stroke

  • Biologically, basilar occlusion may often result from in situ atherosclerotic plaques with superimposed thrombosis. Clinically, this may result in a stuttering process as the clot grows and retracts.
  • The natural history of basilar artery occlusion without intervention is very poor.
  • Since the biology of basilar occlusions may involve fresher thrombus than most embolic strokes, these patients might be more amenable to thrombolysis than those with other stroke types.
  • Recent studies support the use of endovascular therapy for basilar strokes.

pure motor, dysarthria-clumsy hand, or ataxic hemiparesis

  • Pure motor: Isolated contralateral face/arm/leg weakness.
  • Dysarthria-clumsy hand: Dysarthria, facial weakness, slight weakness/clumsiness of the contralateral hand.
  • Ataxic hemiparesis: Ipsilateral hemibody weakness and limb ataxia (that is disproportionate to the weakness).
  • Corona radiata (small MCA branches).
  • Posterior limb of internal capsule (lenticulostriate arteries, anterior choroidal artery, or perforators from the posterior cerebral artery).
  • Cerebral peduncle (small proximal posterior cerebral artery branches).
  • Anterior pons (basilar perforators).

pure sensory stroke (thalamic lacune)

  • Symptoms: Hemibody sensory loss of all modalities.
  • Localization: Infarction of the ventral posterior lateral (VPL) and ventral medial nuclei (VPM), supplied by thalamoperforators from the posterior cerebral artery.

sensorimotor stroke (thalamocapsular lacune)

  • Symptoms: Combination of thalamic lacune plus pure motor hemiparesis.
  • Localization: Posterior limb of the internal capsule plus either thalamic VPL/VPM or thalamic somatosensory radiation. May result from infarction of the thalamoperforator branches of the posterior cerebral artery, or lenticulostriate arteries.

basal ganglia lacune

  • Usually asymptomatic, but may cause hemiballismus.
  • Localized to caudate, putamen, globus pallidus, or subthalamic nucleus. Due to infarction of lenticulostriate, anterior choroidal, or Heubner's arteries.

The concept of core infarct vs. ischemic penumbra is clinically most relevant for large vessel anterior circulation infarcts, where these can be well defined radiologically. However, the general concepts apply to any ischemic stroke.

core infarct

  • The infarct core refers to tissue which has already been irrevocably damaged. Even if the vessel could be immediately opened, the core infarct would not recover.
  • The radiological definition of core infarct is based on the development of cytotoxic edema , reflective of neuronal cells swelling. This cytotoxic edema causes a diffusion restriction on MRI, which is the reference standard for defining the core infarct. However, there are also CT techniques to identify the core infarct.
  • For anterior hemispheric infarctions, a core infarct volume over ~50-70 ml suggests a poor responsiveness to endovascular therapy. ( 31485117 )

ischemic penumbra

  • Ischemic penumbra is tissue which surrounds the core infarct. The ischemic penumbra is malperfused and nonfunctional, but the tissue is still potentially viable if blood supply can be restored. The ischemic penumbra is often maintained by a trickle of blood flow supplied via collateral circulation.
  • The entire purpose of revascularization (either with thrombolysis or endovascular therapy) is to resurrect the ischemic penumbra. Alternatively, if the ischemic penumbra is small , then there is little more tissue to salvage: the stroke has already completed.

rapid progressors versus slow progressors

  • The natural history of untreated stroke is for the ischemic penumbra to gradually necrose. Thus, over time, the ischemic penumbra will disappear while the core infarct expands.
  • The velocity with which the ischemic penumbra necroses varies widely between patients, depending on collateral circulation . Rapid progressors may quickly complete an infarction within hours, due to poor collateral flow. Alternatively, slow progressors may continue to have large ischemic penumbras for many hours (or even days). These slow progressors may remain good candidates for revascularization therapy well beyond traditional thrombolysis time windows (e.g., >>4.5 hours).

moving from time thresholds to tissue thresholds

  • The mantra of stroke neurology is that “time is brain.” However, this is only partially true, because different patients progress at different speeds over time. Thus, 4.5 hours could have an entirely different meaning for a slow progressor versus a rapid progressor .
  • Applying a rigid time threshold across all patients made sense in the 1990's, when that's all that we had. However, in the modern era of neuroimaging, it is increasingly possible to rapidly determine the amount of salvageable tissue.
  • Based on the perpetual evolution of CT and MRI technology, it's possible that tissue viability may largely replace time cutoffs when considering candidacy for interventions.

common stroke mimics

  • Migraine aura is usually marked by positive symptoms (e.g., bright/flashing lights, shimmering scotomas, tingling paresthesias). These positive visual symptoms aren't generally caused by an ischemic stroke. Alternatively, loss of function would be more suggestive of ischemic stroke.
  • Migraine headache can be helpful, but migraine aura can occur without headache.
  • Paralysis (Todd's paralysis) is most classic, but other deficits may occur as well.
  • Deficits should improve over minutes-hours. (Louis 2021)
  • May be triggered by various metabolic derangements (e.g., hypoglycemia, hypoxia, fever, hyponatremia, uremia, or hypercalcemia). ( 33896525 )
  • Patients often have a combination of diffuse encephalopathy plus a focal deficit(s).
  • Medication effect or intoxication .
  • Examples may include tumor, abscess, viral encephalitis, or autoimmune encephalitis.
  • Typically these pathologies may be distinguished on the basis of a more gradual symptom onset compared to ischemic stroke.
  • Presyncope or syncope .
  • PRES . 📖

transient ischemic attack (TIA)

  • Clinical syndrome with abrupt onset of focal neurological symptoms consistent with ischemia, which resolves within 24 hours (and usually much sooner than that, often lasting minutes).
  • No abnormality is detected on neuroimaging (e.g., lack of diffusion restriction on MRI scan).
  • With improved MRI scans, TIA is becoming less common (as these are often being reclassified as small ischemic strokes based on MRI abnormality). Patients who are unable to receive an MRI scan (e.g., due to a pacemaker) are more likely to be diagnosed with “TIA.”
  • Patients are at risk of a recurrent stroke and should receive immediate neurology consultation. Further management of TIA is beyond the scope of this book.
  • Last known normal time (which is not necessarily the same as when the symptoms were first noticed).
  • Anticoagulants and antiplatelet agents?
  • History of atrial fibrillation?
  • Risk factors for atherosclerotic disease (e.g., hypertension, diabetes, smoking, coronary artery disease, peripheral artery disease).
  • Recent medical history (e.g., recent surgery/procedure? recent head/neck trauma?).
  • Pattern of symptoms (stuttering? improving? worsening?).
  • Any evidence of seizure (e.g., incontinence, bruising, tongue biting).

NIH stroke scale overview

  • The score doesn't necessarily correlate with functional outcomes (e.g., severe aphasia yields two points, which is the same score as would result from bilateral subtle weakness of both arms – although severe aphasia would obviously be more debilitating).

calculating the NIH stroke scale

  • 1 = Drowsy.
  • 2 = Obtunded.
  • 3 = Unresponsive.
  • 0 = Correct.
  • 1 = 1 mistake -or- unable to speak, e.g. due to dysarthria.
  • 2 = 2 mistakes -or- aphasic.
  • 1 = 1 failure.
  • 2 = 2 failures.
  • 0 = Normal.
  • 1 = Partial gaze palsy.
  • 2 = Complete gaze palsy.
  • 1 = Partial hemianopia (e.g., quadrantanopia).
  • 2 = Complete hemianopia.
  • 3 = Bilateral hemianopia.
  • 1 = Minor paralysis (e.g., nasolabial flattening).
  • 2 = Partial paralysis (e.g., lower face).
  • 3 = Complete unilateral paralysis.
  • In arms: Score if arm drifts down before 10 seconds.
  • In legs: Score if leg drifts down before 5 seconds.
  • 2 = Some effort against gravity.
  • 3 = No effort against gravity.
  • 4 = No movement.
  • 1 = One limb.
  • 2 = Two or more limbs.
  • 1 = Mild-moderate sensory loss.
  • 2 = Severe sensory loss.
  • 0 = No aphasia.
  • 1 = Mild aphasia.
  • 2 = Severe aphasia.
  • 0 = Normal articulation.
  • 1 = Mild dysarthria.
  • 2 = Severe dysarthria (or completely mute).
  • 1 = Visual, tactile, auditory, spatial, or personal inattention.
  • 2 = Profound hemi-inattention or extinction to more than one modality.

ischemic stroke in elderly patient

  • Thrombosis due to local cerebral atherosclerosis.
  • Carotid artery atherosclerosis with embolization or occlusion.
  • Cardioembolic stroke due to atrial fibrillation, prosthetic valve thrombus, or ventricular thrombus (in severe left ventricular dysfunction).
  • Ultrasonography of carotid arteries.
  • Echocardiography.
  • Telemetry to evaluate for atrial fibrillation.

ischemic stroke in younger patient

  • Septic embolism from endocarditis .
  • Paradoxical embolization (DVT passes through a patent foramen ovale).
  • Cervical artery dissection .
  • Substance use (e.g., cocaine and other sympathomimetics).
  • Inflammatory vasculitis (e.g., lupus, primary CNS angiitis).
  • Meningovascular neurosyphilis. 📖
  • Tuberculosis.
  • Acquired thrombophilia (e.g., HITT or antiphospholipid antibody syndrome).
  • RCVS (reversible cerebrovascular vasoconstriction syndrome).
  • Echocardiography with bubble study, to evaluate for shunt.
  • Blood cultures , if endocarditis is possible.
  • Evaluation for cervical arterial dissection (e.g. MRA or CTA).
  • Evaluation for neurosyphilis (usually with serum VRDL or RPR). 📖
  • Inflammatory markers or coagulation studies, depending on clinical context.
  • Due to time constraints, CT imaging is generally used as a front-line imaging study.
  • ⚠️ Remember that contrast dye doesn't cause renal failure. 📖 Definitive imaging should not be delayed or omitted due to concerns regarding the possibility of “contrast nephropathy.”

(#1) any evidence of intracranial hemorrhage

  • Identifying intracranial hemorrhage is of paramount importance, since this changes management entirely. Subdural hematomas 📖 or subarachnoid hemorrhages 📖 may not be obvious on CT scan, so they should be carefully sought.
  • Hemorrhage may also represent secondary hemorrhagic transformation following an ischemic stroke. 📖 If a hemorrhage is surrounded by an unexpected amount of edema that conforms to an arterial vascular distribution, this may suggest a primary ischemic stroke with secondary hemorrhagic transformation.

(#2) hyperdense vessel sign due to an occluded artery

  • As blood clots, it becomes more dense and thus increasingly hyperdense on CT scan.
  • The dense MCA sign is encountered most often (with a sensitivity of ~33% and a specificity of 95% for MCA occlusion). ( 31589578 ) However, hyperdense vessel signs may also be seen in the anterior cerebral artery, posterior cerebral artery, or basilar arteries. If the thrombus involves the M2 segment of the MCA within the Sylvian fissure, this may cause a “hyperdense dot sign.”
  • Hyperdense vessels can be mimicked by atherosclerosis, contrasted CT scans, polycythemia, or streak artefact. It's essential to compare the vessel to other vessels seen on the scan (as well as prior CT scans, if available).
  • Dense vessels may be more easily detected using thin sections and/or using a maximal intensity projection (MIP) setting.
  • (1) This identifies large vessel occlusion , which may be amenable to endovascular therapy.
  • (2) Hyperdense MCA sign longer than 8 mm predicts poor recanalization after thrombolysis. ( 33896525 )
  • (3) Hyperdense MCA sign implies a risk of malignant MCA syndrome. 📖

(#3) signs of cerebral venous sinus thrombosis

  • CT signs of cerebral venous sinus thrombosis should be sought, especially in younger patients. (More on the imaging findings of cerebral venous sinus thrombosis 📖 )
  • (⚠️ If there is substantial concern regarding cerebral venous sinus thrombosis, a CT venogram is needed to exclude the diagnosis.)

(#4) loss of grey-white matter differentiation

clinical presentations of stroke

  • Loss of grey-white differentiation can be seen as soon as an hour after stroke. It is often considered to reflect irreversibly infarcted brain tissue. ( 32224753 ) The extent of grey-white differentiation loss provides an early indication of the extent of the infarction.
  • Disappearing basal ganglia sign (loss of grey-white differentiation along the edges of the basal ganglia).
  • Insular ribbon sign (loss of grey-white differentiation along the insular cortex).
  • Cortical ribbon sign (loss of grey-white differentiation along the cortex).
  • Comparison to the contralateral side can be helpful.
  • It may be more easily identified with narrow windowing of the CT scan, to accentuate differences between grey and white matter (e.g., a CT window width of 8-35 and a window level of 32-35 HU). ( 31589578 ; 32224753 )
  • ASPECTS score is a systematic approach to define the extent of an MCA or internal carotid artery infarction. A normal score is ten. Points are deducted for loss of grey-white differentiation within ten regions of the anterior circulation (so a score of zero would indicate a catastrophic hemispheric infarction).

(#5) vasogenic edema

  • Within ~3-6 hours , infarcted tissue often develops vasogenic edema and becomes hypodense . Frank hypodensity reflects irreversible infarction. ( 31589578 )
  • Edema may cause midline shift and compression of ventricles and cisterns (e.g., malignant MCA syndrome). Serial CT scan is essential for patients with large MCA infarctions, as edema may evolve over a period of 2-3 days. 📖

identification of large vessel occlusion & technical feasibility of endovascular therapy

  • With increased utilization of endovascular therapy, it's increasingly important to evaluate for the presence of large vessel occlusion . CT angiography is excellent for this.
  • Aside from identifying any large occlusions, CTA clarifies vascular anatomy (creating a map to guide IR intervention). In some situations, CTA may reveal patients who are not safe candidates for intervention (e.g., due to highly stenotic vessels or unstable aneurysmal disease).

evaluation of underlying vascular pathology that caused the stroke, e.g.:

  • These cause ~2.5% of all ischemic strokes, with a greater prevalence in younger patients.
  • History may include minor neck trauma (e.g. hyperextension or neck manipulation) and neck discomfort.
  • Dissection isn't a contraindication to endovascular therapy, but it may make it harder to gain access.
  • ~10% of strokes are due to carotid atherosclerosis, which carries a high risk of early recurrence.
  • Vascular surgery should be consulted to consider followup carotid endarterectomy.

CT perfusion is useful to evaluate for salvageable ischemic penumbra in the context of hemispheric (supratentorial) stroke. However, this isn't generally designed to evaluate posterior circulation strokes. Additionally, CT perfusion only represents a snapshot of blood flow at one point in time – so this may not accurately reflect the status of the brain parenchyma (which depends on an integration of fluctuating blood flow over time) . ( 32224753 )

sorting out infarct core versus ischemic penumbra using CT perfusion

clinical presentations of stroke

  • Several parameters can be used to sort out the core infarct versus the ischemic penumbra, as shown above. Different CT systems may use different parameters.
  • Core infarct is identified based on cerebral blood flow <30%.
  • Core infarct plus ischemic penumbra is identified based on elevated maximal transit time >6 seconds.
  • If the two images match up, then the volume of ischemic penumbra is small (completed infarct).
  • If the ischemic core is much smaller, then the volume of ischemic penumbra must be large (implying significant salvageable brain tissue).
  • The ischemic core volume ( <50-70 ml suggests a favorable prognosis following intervention).
  • The mismatch ratio of penumbra/core ( ratios >1.2-1.8 suggest benefit from endovascular therapy). ( 32947473 ) A mismatch ratio of >1.2 was used in EXTEND IA, whereas a mismatch ratio >1.8 was used in SWIFT PRIME.

clinical presentations of stroke

CT perfusion to reach a unique diagnosis

  • CT perfusion is typically applied to a patient with known or strongly suspected large ischemic stroke , to determine whether revascularization could be beneficial.
  • (1) Patients with seizure acting as a stroke mimic may have increased regional blood perfusion.
  • (2) Occasionally, CT perfusion may reveal a very small ischemic stroke (e.g., one which would have been missed via CT scan with CT angiography alone).

role of MRI

  • The use of MRI for hyperacute stroke imaging is often limited by logistic considerations.
  • MRI is superior to CT scan for brainstem strokes.

interpretation of various sequences

  • Restricted diffusion is the reference standard for assessment of infarct core (irreversibly damaged tissue at the center of the infarction). ( 31589578 )
  • Thus, the combination of hyperintensity on DWI without a corresponding FLAIR hyperintensity identifies a hyperacute stroke . ( 21978972 )
  • Absent or sluggish arterial blood flow may be seen as a diminution of normal black arterial flow voids on T2/FLAIR images.
  • GRE/SWI : The acute thrombus within an artery has a high concentration of deoxyhemoglobin, which may be visualized as a dark signal on these sequences. Any hemorrhagic transformation will also be detected with GRE/SWI.

endovascular therapy basics

  • Endovascular therapy involves mechanical clot removal from a proximal occlusion. Locations which might be amenable to endovascular therapy include the distal internal carotid, MCA (primarily the M1 segment, but possibly also the M2 segment), proximal ACA, or the basilar artery.
  • ⚠️ Patients may be eligible for endovascular therapy well beyond the usual 3-4.5 hour thrombolysis windows.
  • TICI Grade 0 : No perfusion.
  • TICI Grade 1 : Penetration with minimal perfusion.
  • TICI Grade 2A : Filling of <2/3 of the vascular territory.
  • TICI Grade 2B : Complete filling of vascular territory, at a slower rate than normal.
  • TICI Grade 3: Normal perfusion.

post-procedure patient management

  • (1) Blood pressure management is discussed here: 📖
  • More on the management of retroperitoneal hematoma status post femoral artery instrumentation here. 📖

clinical presentations of stroke

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  • Hydralazine should be avoided (may cause unpredictable changes in blood pressure).
  • For large hemispheric strokes, endovascular intervention may remain a viable therapy even beyond 3-4.5 hours after stroke initiation. Prompt consultation with neurology and/or neurointerventionalists should be obtained even in patients presenting relatively late.

Guide to emoji hyperlinks

  • 📄 = Link to open-access journal article.
  • AHA/ASA 2019 Guidelines for the early management of patients with acute ischemic stroke ( Powers WJ et al. ).

Review of seminal studies by The Bottom Line

  • DESTINY II trial (2014) – Decompressive hemicraniectomy for malignant MCA infarction in patients >60 years old did not improve the number of patients with good long-term functional outcomes.
  • 26288671 O'Carroll CB, Aguilar MI. Management of Postthrombolysis Hemorrhagic and Orolingual Angioedema Complications. Neurohospitalist. 2015 Jul;5(3):133-41. doi: 10.1177/1941874415587680 [ PubMed ]
  • Tang, Y., Mukherjee, S., & Wintermark, M. (2015). Emergency Neuroradiology: A Case-Based Approach (1st ed.). Cambridge University Press.
  • 27174372 Pahs L, Droege C, Kneale H, Pancioli A. A Novel Approach to the Treatment of Orolingual Angioedema After Tissue Plasminogen Activator Administration. Ann Emerg Med. 2016 Sep;68(3):345-8. doi: 10.1016/j.annemergmed.2016.02.019 [ PubMed ]
  • 27695601 Tipirneni A, Koch S, Romano JG, Malik AM. A 27-Year-Old Man With Right-Sided Hemiparesis and Dysarthria. Neurohospitalist. 2016 Oct;6(4):174-180. doi: 10.1177/1941874416648197 [ PubMed ]
  • 29460331 Li S, Kumar Y, Gupta N, Abdelbaki A, Sahwney H, Kumar A, Mangla M, Mangla R. Clinical and Neuroimaging Findings in Thalamic Territory Infarctions: A Review. J Neuroimaging. 2018 Jul;28(4):343-349. doi: 10.1111/jon.12503 [ PubMed ]
  • 29653785 Brown E, Campana C, Zimmerman J, Brooks S. Icatibant for the treatment of orolingual angioedema following the administration of tissue plasminogen activator. Am J Emerg Med. 2018 Jun;36(6):1125.e1-1125.e2. doi: 10.1016/j.ajem.2018.03.018 [ PubMed ]
  • 30215283 Bar B, Biller J. Select hyperacute complications of ischemic stroke: cerebral edema, hemorrhagic transformation, and orolingual angioedema secondary to intravenous Alteplase. Expert Rev Neurother. 2018 Oct;18(10):749-759. doi: 10.1080/14737175.2018.1521723 [ PubMed ]
  • LaRoche, S. M., & Haider, H. A. (2018). Handbook of ICU EEG Monitoring (2nd ed.). Demos Medical.
  • 31346678 Smith M, Reddy U, Robba C, Sharma D, Citerio G. Acute ischaemic stroke: challenges for the intensivist. Intensive Care Med. 2019 Sep;45(9):1177-1189. doi: 10.1007/s00134-019-05705-y [ PubMed ]
  • 31485117 Patra A, Janu A, Sahu A. MR Imaging in Neurocritical Care. Indian J Crit Care Med. 2019 Jun;23(Suppl 2):S104-S114. doi: 10.5005/jp-journals-10071-23186 [ PubMed ]
  • 31589578 Potter CA, Vagal AS, Goyal M, Nunez DB, Leslie-Mazwi TM, Lev MH. CT for Treatment Selection in Acute Ischemic Stroke: A Code Stroke Primer. Radiographics. 2019 Oct;39(6):1717-1738. doi: 10.1148/rg.2019190142 [ PubMed ]
  • 31662037 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. 2019 Dec;50(12):e344-e418. doi: 10.1161/STR.0000000000000211 [ PubMed ]
  • Shutter, L. A., Molyneaux, B. J. (2019). Neurocritical care. Oxford University press.
  • Wijdicks E.F.M., Findlay, J. Y., Freeman, W. D., Sen A. (2019). Mayo Clinic critical and Neurocritical Care Board Review. Oxford University Press.
  • 32054610 Phipps MS, Cronin CA. Management of acute ischemic stroke. BMJ. 2020 Feb 13;368:l6983. doi: 10.1136/bmj.l6983 [ PubMed ]
  • 32224752 Rabinstein AA. Update on Treatment of Acute Ischemic Stroke. Continuum (Minneap Minn). 2020 Apr;26(2):268-286. doi: 10.1212/CON.0000000000000840 [ PubMed ]
  • 32224753 Menon BK. Neuroimaging in Acute Stroke. Continuum (Minneap Minn). 2020 Apr;26(2):287-309. doi: 10.1212/CON.0000000000000839 [ PubMed ]
  • 32668115 Powers WJ. Acute Ischemic Stroke. N Engl J Med. 2020 Jul 16;383(3):252-260. doi: 10.1056/NEJMcp1917030 [ PubMed ]
  • 32947473 Herpich F, Rincon F. Management of Acute Ischemic Stroke. Crit Care Med. 2020 Nov;48(11):1654-1663. doi: 10.1097/CCM.0000000000004597 [ PubMed ]
  • Nelson, S. E., & Nyquist, P. A. (2020). Neurointensive Care Unit: Clinical Practice and Organization (Current Clinical Neurology) (1st ed. 2020 ed.). Springer.
  • 33512282 Mullhi RK, Singh N, Veenith T. Critical care management of the patient with an acute ischaemic stroke. Br J Hosp Med (Lond). 2021 Jan 2;82(1):1-9. doi: 10.12968/hmed.2020.0123 [ PubMed ]
  • 33896525 Zubair AS, Sheth KN. Emergency Care of Patients with Acute Ischemic Stroke. Neurol Clin. 2021 May;39(2):391-404. doi: 10.1016/j.ncl.2021.02.001 [ PubMed ]
  • 33947658 Bhalla A, Patel M, Birns J. An update on hyper-acute management of ischaemic stroke. Clin Med (Lond). 2021 May;21(3):215-221. doi: 10.7861/clinmed.2020-0998 [ PubMed ]
  • 33952393 O'Carroll CB, Brown BL, Freeman WD. Intracerebral Hemorrhage: A Common yet Disproportionately Deadly Stroke Subtype. Mayo Clin Proc. 2021 Jun;96(6):1639-1654. doi: 10.1016/j.mayocp.2020.10.034 [ PubMed ]
  • 34010530 Langezaal LCM, van der Hoeven EJRJ, Mont'Alverne FJA, et al.; BASICS Study Group. Endovascular Therapy for Stroke Due to Basilar-Artery Occlusion. N Engl J Med. 2021 May 20;384(20):1910-1920. doi: 10.1056/NEJMoa2030297 [ PubMed ]
  • 34680603 Hasan TF, Hasan H, Kelley RE. Overview of Acute Ischemic Stroke Evaluation and Management. Biomedicines. 2021 Oct 16;9(10):1486. doi: 10.3390/biomedicines9101486 [ PubMed ]
  • Louis ED, Mayer SA, Noble JM. (2021). Merritt’s Neurology (Fourteenth). LWW.
  • 34798968 Lyden S, Wold J. Acute Treatment of Ischemic Stroke. Neurol Clin. 2022 Feb;40(1):17-32. doi: 10.1016/j.ncl.2021.08.002 [ PubMed ]
  • 35034076 Sharma D, Smith M. The intensive care management of acute ischaemic stroke. Curr Opin Crit Care. 2022 Apr 1;28(2):157-165. doi: 10.1097/MCC.0000000000000912 [ PubMed ]
  • Albin, C. S. W., & Zafar, S. F. (2022). The Acute Neurology Survival Guide: A Practical Resource for Inpatient and ICU Neurology (1st ed. 2022 ed.). Springer.
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  • Research article
  • Open access
  • Published: 07 August 2019

Risk factors, clinical presentations and predictors of stroke among adult patients admitted to stroke unit of Jimma university medical center, south west Ethiopia: prospective observational study

  • Ginenus Fekadu 1 ,
  • Legese Chelkeba 2 &
  • Ayantu Kebede 3  

BMC Neurology volume  19 , Article number:  187 ( 2019 ) Cite this article

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Stroke is the second-leading global cause of death behind heart disease in 2013 and is a major cause of permanent disability. The burden of stroke in terms of mortality, morbidity and disability is increasing across the world. It is currently observed to be one of the commonest reasons of admission in many health care setups and becoming an alarming serious public health problem in our country Ethiopia. Despite the high burden of strokes globally, there is insufficient information on the current clinical profile of stroke in low and middle income countries (LMICs) including Ethiopia. So, this study was aimed to assess risk factors, clinical presentations and predictors of stroke subtypes among adult patients admitted to stroke unit of Jimma university medical center (JUMC).

Prospective observational study design was carried out at stroke unit (SU) of JUMC for 4 consecutive months from March 10–July 10, 2017. A standardized data extraction checklist and patient interview was used to collect data. Data was entered into Epi data version 3.1 and analyzed using SPSS version 20. Multivariable logistic regression was used to identify the predictors of stroke subtypes.

A total of 116 eligible stroke patients were recruited during the study period. The mean age of the patients was 55.1 ± 14.0 years and males comprised 62.9%. According to world health organization (WHO) criteria of stroke diagnosis, 51.7% of patients had ischemic while 48.3% had hemorrhagic stroke. The most common risk factor identified was hypertension (75.9%) followed by family history (33.6%), alcohol intake (22.4%), smoking (17.2%) and heart failure (17.2%). The most common clinical presentation was headache complained by 75.0% of the patients followed by aphasia 60.3% and hemiparesis 53.4%. Atrial fibrillation was the independent predictor of hemorrhagic stroke (AOR: 0.08, 95% CI: 0.01–0.68).

The clinical characteristics of stroke in this set up were similar to other low- and middle-resource countries. As stroke is a high priority chronic disease, large-scale public health campaign should be launched focusing on public education regarding stroke risk factors and necessary interventions.

Peer Review reports

Stroke is acute clinical event of focal or global neurological disturbance related to impairment of cerebral circulation, which lasts longer than 24 h resulting in death with no known cause other than vascular origin. Without blood to supply oxygen and to remove waste products, brain cells quickly begin to die [ 1 , 2 , 3 , 4 ]. Stroke is the second-leading global cause of death behind heart disease in 2013 and is a major cause of permanent disability [ 5 , 6 , 7 ]. Currently, the burden of stroke in terms of mortality, morbidity and disability is increasing across the world [ 8 , 9 ]. Additionally, data from Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) of 2010 revealed that stroke is the leading cardiovascular disease (CVD) which causes mortality and disability in sub-Saharan Africa (SSA) and other low and middle income countries (LMICs) [ 10 ].

Risk factors for stroke can be classified as modifiable and non-modifiable. Age, sex, family history and race/ethnicity are non-modifiable risk factors; while hypertension, smoking, diet, and physical inactivity are among some of identified modifiable risk factors [ 11 ]. Different risk factors apply to an African population in the development of stroke [ 12 ]. Africa might be increasingly affected by high burden of stroke and other vascular diseases due to health transitions in line with ever-changing social, economic and demographic patterns [ 13 ]. Additionally, the poor are increasingly affected by stroke, which can be attributable to the changing population exposures to risk factors and inability to afford the high cost of stroke care [ 14 ]. Yet, only little data about context-specific risk factors for prioritizing interventions to reduce the stroke burden in sub-Saharan Africa is available [ 15 , 16 ].

Compared to developed countries, the percentage of hemorrhagic stroke (HS) mortality rate was higher in SSA and other LMICs [ 10 , 17 , 18 ]. There have been variations in the prevalence of major risk factors among the stroke subtypes, demonstrating that knowledge of pathophysiology is crucial for the right management and care of the patients [ 19 ]. In addition to highest burden of stroke risk factors in LMICs, the racial or genetic factors also plays key roles in the pathogenesis of stroke. For example, hypertension and diabetes mellitus (DM) appear to be more prevalent among black races as compared to white races [ 17 ]. Currently even though several modifiable risk factors are becoming significant, hypertension is still the most common risk factor globally including our country [ 20 ].

Stroke is currently observed to be one of the commonest reasons of admission in many health care setups and becoming an alarming serious public health problem in our country Ethiopia [ 21 , 22 ]. Under-diagnosing of hypertension and other risk factors, delayed presentation to the hospital, poor risk factors control and failure to adhere to the treatments are some of the major challenges that needs to be addressed [ 21 , 23 ]. Etiologic investigation for stroke was infrequently performed due to lack of systematic cardiological examinations and brain imaging, most of the time for economic reasons and unavailability of the instruments [ 24 ]. The findings of the studies done in Ethiopia frequently changed from one another with respect to various demographic profiles, location and risk factors [ 21 ]. Most of the data’s regarding stroke that used in the management, follow-up and prevention of stroke come from studies in developed countries [ 22 ]. Thus, in our country we haven’t pooled data on prevalence, risk factors and outcome of the stroke.

The shortage of data specific to the Ethiopian setting limits the formulation of well-designed response and management of stroke [ 21 ]. So it is imperative that a lot has to be done to overcome the current challenges concerning the risk factors and clinical profile of stroke in Ethiopia [ 22 ]. Hence this study will generate evidences for improving the prevention strategy of stroke and guide health authorities to halt or reduce the devastating effects of stoke at different sectors of our community by having overview knowledge of clinical characteristics of stroke. This study data was part of huge study project done in stroke unit (SU) of Jimma university medical center (JUMC) with novel and extensive findings focusing on stroke. Hence, this study was aimed to assess risk factors, clinical presentation and predictors of stroke subtypes among adult patients admitted to SU of JUMC.

Since this data was part of study previously described by Fekadu etal [ 24 ], we have used similar methods. Additionally, the study participants in this finding share similarity with previously published articles of the same study project. Prospective observational study design was conducted at SU of JUMC located at south-west Ethiopia for 4 consecutive months from March 10–July 10, 2017. All adult patients (> 18 years) diagnosed to had stroke clinically or by brain imaging and admitted to SU of JUMC during the study period were included. Those not willing to give an informed consent, died before evaluation, changed diagnosis of stroke, transformed stroke and with hematomas were excluded [ 23 , 24 ].

Data collection tool and procedure

Data collection was carried out by two trained nurses and one internal medicine resident. Data collectors collect data using interviewer administered questionnaire and standardized data extraction form from the case records of the patients. Data collection tool (Additional file  1 ) was developed based on the previous study findings done at different sites and using the WHO step wise approach to stroke surveillance [ 25 ]. The necessary history used for the study was taken from the patient and/or caregivers by the language they understood. To ensure quality of data, the data abstraction tool was developed in English, translated to local language (Amharic and Afan Oromo) and back translated into English to check its consistency. The data collection form was used to collect data on the sociodemographic characteristics, clinical characteristics of patients such as risk factors, clinical presentation and subtypes of stroke.

Data processing and analysis

The data was entered to Epidata version 3.1 and analyzed using statistical package for the social sciences (SPSS) version 20. Descriptive statistics such as proportions, means, standard deviations, medians and Interquartile ranges were calculated to describe the independent variables. During candidate selection because of adequate significant variables were obtained at P  < 0.05, it was considered as cut off point for candidate selection for multivariable logistic regression analysis model with backward stepwise approach to identify the independent predictors of stroke subtypes. The data was summarized using odds ratio (OR) and 95% confidence interval. Confidence interval which doesn’t contain 1 and predictor variables with p value less than 0.05 was considered statistically significant.

Operational definition

Alcohol abuse/ consumption: on average ≥ 2 drinks/day for males and ≥ 1 drinks for females (previous drinker: ex drinker for more than 1 year) [ 26 ].

Diabetes mellitus: If the patient was previously on oral hypoglycemic agents/insulin treatment or had the diagnosis of any type of DM or FBS ≥ 126 mg/dl or had a documented RBS ≥ 200 mg/dl or glycosylated hemoglobin of ≥6.5% [ 7 , 27 , 28 , 29 ]

Dyslipidemia or hyperlipidemia: Previous had history of hyperlipidemia or using lipid lowering medication or total cholesterol ≥200 mg/dl, LDL cholesterol ≥100 mg/dl, and HDL-cholesterol < 40 mg/dl for men or < 50 mg/dl for women, and/or serum triglyceride level ≥ 150 mg/dl [ 27 , 30 ].

Hypertension: Previously receiving antihypertensive medication or when the patient was previously diagnosed with hypertension or detecting blood pressure of ≥ 140/90 mm/Hg for two measurements [ 7 , 27 , 28 , 29 ].

Obesity: According to the WHO, Body Mass Index (BMI) ≥ 30 kg/m 2 [ 28 ].

Central obesity: Waist circumference greater than 102 cm in men and 88 cm in women [ 28 ].

Smoker: On average 2 cigarettes per day in men and 1 per day in women

Former smoker: who abstained from smoking for greater than 1 years [ 31 ].

Current smoker: smoking within 1 year ago [ 31 ].

One hundred twenty five patients were admitted to SU of JUMC with suspected diagnosis of stroke and 9 patients were excluded from the study during the study period. From 116 study participants included in the study; history was obtained solely from 11 patients (9.5%), from the patient and caregiver in 50 cases (43.1%), and solely from caregivers in 55 cases (47.4%). According to WHO criteria 51.7% patients had ischemic type of stroke (IS) while 48.3% had hemorrhagic stroke (HS). Of the total 116 patients, 61 patients evaluated with CT scan of the brain and the rest 55 patients were evaluated clinically to have stroke [ 24 ].

Patient characteristics

The mean age of the patients was 55.1 ± 14.0 years and 65 (56.0%) were in age of group of 45–65 years. Males comprised of 73 (62.9%) with male: female ratio of 1.70:1. Majority of the participants (42.2%) had informal education and 85.3% of patients were independent at home during pre-stroke. Majority of the patients had normal mean body mass index (BMI) (63.8%) and 15.5% of the patients were overweight [ 23 ]. Regarding the food habit of the patients during the pre-stroke, 81.9% were mixed diet users ( Table  1 ).

Risk factors for stroke subtypes

Risk factors were identified in 114 (98.3%) patients; 59 (98.3%) of IS and 55 (98.2%) of HS patients. The most common risk factor identified was hypertension in 88 (75.9%) patients followed by family history in 39 (33.6%), alcohol intake 26 (22.4%) and smoking 20 (17.2%). Thirty six patients (83.7%) of IS and 34 (75.6%) of HS patients had a pre-stroke knowledge of being hypertensive. Twenty eight patients (24.1%) had no current and previous history of hypertension [17 (28.3%) of IS and 11(19.6%) of HS patients] ( Table  2 ).

About 18 (20.5%) of the patients had no prior knowledge of being hypertensive, but diagnosed in hospital during admission for stroke. From 46 patients with no previous history of hypertension including newly diagnosed, 19 (41.3%) were never had their blood pressure measured and the remaining measured but was in normal range.

Among the patients with recorded history of hypertension, the median duration of hypertension prior to stroke diagnosis was 3 years (ranged 0.04 to 25 years). Of 70 patients with pre-existing hypertension, 27 (38.6%) were on anti-hypertensive medications, 24 (34.3%) of the patients were discontinued their antihypertensive medication and 19 (27.1%) hadn’t started antihypertensive medication before stroke occurrence. From 51 patients previously started antihypertensive medication the median duration since the medication started was 3 years. From the 27 patients that were on antihypertensive medication during hospital arrival, 19 (70.4%) of the patients’ blood pressure was not controlled. The median month since discontinuation of their antihypertensive medications before onset of stroke was 2.5 months (ranged 0.5 to 48 months).

Diabetes Mellitus was identified as co-morbidity in 8 patients (4 of them previously diagnosed). It was more prevalent in males and in middle age group, but there was no statistically significant difference between stroke subtypes ( p  = 0.178). Among the patients with previous history of diabetes, the mean duration of diabetes prior to stroke was 5.3 years (ranged 3 to 9 years). Although all previously diagnosed patients were on anti-diabetics, only 1 patient’s blood glucose was controlled (RBS ≤ 200 mg/dl) during hospital arrival.

Physical inactivity/ sedentary life was detected in 13 (11.2%) patients, the remaining patients had habit of physical activity. Of those who had physical activity, 101 (98.1%) had work related aerobic physical activity and 2 (1.9%) had aerobic/planned physical activity. From nine patients (7.8%) who gave a history of previous stroke, eight of them were ischemic stroke patients. From those patients who had previous history of stroke, one patient had history of hypertension for 25 years.

Alcohol consumption and cigarette smoking was less prevalent in IS than HS patients, which was statistically significant among smokers ( p  = 0.038). Majority of the patients who used alcohol were former drinker before 1 year (84.6%), but no difference in smoking status of the patients between the current and previous smokers. Seventy stoke patients (83.6%) had two or more risk factors for stroke, while 17 (14.7%) had one identified risk factor. In addition 17 (14.7%) patients had more than five identified risk factors. With this, the average risk factor for the patient was 3.38 (ranged 0 to 9) risk factors.

C linical presentation of stroke patients

The most common clinical presentation was headache complained by 87 (75.0%) patients followed by aphasia 70 (60.3%) and hemiparesis 62 (53.4%). Most of ischemic stroke patients presented with headache (71.7%), aphasia (60.0%) and facial palsy (58.3%). Similarly, the common clinical presentations among hemorrhagic stroke patients was headache (78.6%) followed by aphasia (60.7%) and vomiting (57.1%) ( Table  3 ).

Hemorrhagic stroke patients were more likely to be presented with coma ( P  = 0.033), vomiting ( P  = 0.028) and neck stiffness ( p  = 0.015), but ischemic stroke patients were more likely presented with chest pain ( p  = 0.016). In other clinical presentations there was no statistical significant difference between stroke subtypes. The average clinical presentation per patient was 6 (ranged from 2 to 12).

Predictors of stroke subtypes

Using P  < 0.05 for candidate variable selection for predictors of stroke subtypes on binary logistic regression; atrial fibrillation, heart failure, previous stroke, coronary disease, smoking, migraine/headache and previous situation of hypertension management were selected to be included in multivariable logistic regression. Up on multivariable logistic regression only atrial fibrillation (AOR: 0.08; 95% CI: 0.01–0.68, P: 0.021) was the independent predictor for hemorrhagic stroke. Patients having atrial fibrillation were 0.08 times less likely experience hemorrhagic stroke than ischemic stroke ( Table  4 ).

This study data was drawn from the huge study project done on stroke in SU of JUMC. The study populations participated in this finding share similarity with previously published articles of the same project [ 23 , 24 ]. Even though this study shared similarity and textual overlap in the method and the socio-demographic part with previous findings, this finding provides advance and unique contribution over the previous published studies by exploring the risk factors and clinical presentation of stroke.

The mean age of the patients (55.1 ± 14.0 years), was in line with other studies carried out in developing countries including Ethiopia [ 29 , 32 , 33 , 34 , 35 , 36 ], but lower compared to studies by Tirschwell et al. and Sagui et al. [ 37 , 38 ]. In developing countries like Ethiopia, stroke occurs a few years earlier as compared to developed countries. This disagreement may be due to liability of hospital based studies to selection bias, demographic differences (differences in birth rates and survival into old age) and poor risk factor control. Thus community based studies are required to clearly find out and compare incidence as well as prevalence of stroke by age in our area. Young stroke (< 45 Years) comprised of more than one fifth (22.4%) of all patients similar to study in other part of Ethiopia [ 36 ], but higher than study in Gujarat, Nigeria and other parts of Ethiopia [ 21 , 22 , 32 , 39 ].

The higher percentage of stroke in male patients over females was in line with other previous studies [ 14 , 17 , 29 , 30 , 39 ]. The possible reason may be increased risk factors such as cigarette smoking and alcohol consumption among males. In addition, there is no vascular protection of endogenous estrogens in males. This was unlike to some studies where female patients were dominant [ 13 , 22 ]; may be due high use of contraception, pregnancy related disorders and migraine causing stroke among females in those studies. In our study finding majority of the patients were rural residents. Contrary to this, findings by Gebremariam et al. [ 21 ] and Greffie et al. [ 22 ] showed that majority of the patients were from urban areas. It is clear that hospital-based cohorts differ in the type of persons that come to the hospital. The location and catchment area of the hospital determines category of patients visiting the hospital. Additionally, cities and rural regions may differ in age constituencies. The high burden of stroke in rural population may also be due to reduced awareness and poor control of risk factors.

Majority of the patients were farmers (37.9%) and housewives (35.3%), which correlates with the study in Nigeria [ 40 ], but contrary to studies in Zambia and Vietnam [ 37 , 41 ]. Lack of information, ignorance of the risk factors and inability to manage such risk factors might be responsible to this effect. Even when the patients understand the risk factors, they may not accept them to be the cause for stroke nor be able to afford the cost of medications. Additionally, since managing risk factors of stroke require longer period or may be life time; most patients failed to adhere and follow it properly. The above causes might have contributed in many directions to the high prevalence of stroke among peoples with lower educational level including housewives and farmers.

In this study majority of the patients (63.8%) had normal BMI and only 15.5% of the patients were overweight. Majority of the patients in developing countries had low or normal BMI because of low economic status and have increased labor related physical activities. Compared to normal weight patients, obese and overweight patients are susceptible to develop a stroke. This may be associated with increased risk factors, insulin resistance, pro-thrombotic state, excessive secretion of free fatty acids, release of excitatory amino acids and sympathetic nervous system activation. This directly or indirectly related to thrombotic and coagulation adverse events thereby reducing the functional outcome and may result in catabolic imbalance. At the same time, immobilization in obese patients can impair the post stroke recovery and outcome.

The most common risk factor identified was hypertension in 75.9%, consistent with other findings as uncontrolled hypertension is the most important risk factor for stroke both in developing and developed countries [ 12 , 13 , 29 , 30 , 32 , 36 , 37 ]. This trend may reflect poor community awareness, health practices and access to healthcare including different patient related factors. Even when blacks are treated for hypertension, they are less likely than white races to be adhere with treatments given for them. This leads us to believe that hypertension is underdiagnosed and less treated in our study community due to lack of an active screening program, failure to take routine blood pressure measurements, poor medical history taking and poor follow up of the patients. Additionally, adherence with long-term treatment is a great challenge to achieve the optimum outcome as uncomplicated hypertension is usually asymptomatic and denial of the disease is common.

In this study, 79.5% of the hypertensive patients had a pre-stroke knowledge of being hypertensive and 27(38.6%) were on anti-hypertensive medication prior to the stroke occurrence. This was in line with study by Gebremariam et al. in which 20 (37.0%) of the patients had prescribed anti-hypertensive medication prior to the stroke occurrence [ 21 ]. But it was in contrary to study by Watila et al. [ 32 ] in which more than half of the patients had no prior knowledge of being hypertensive and only small proportion of patients had treatment for hypertension prior to having a stroke. The median duration of hypertension prior to stroke was 3 years, in line with previous study in Ethiopia by Gebremariam et al. [ 21 ].

From patients who were on antihypertensive medication during hospital arrival, in majority of the patients’ blood pressure was not controlled (≥ 140/90 mmHg). Poor control of blood pressure is associated with adherence problem, lack of frequent monitoring, cost issue for medications and transportation for follow up. The proportion of patients that never had their blood pressure measured was lower than finding by Walker etal [ 33 ]. Most patients discontinued their antihypertensive medications by convincing themselves as they were cured or improved, because hypertension is asymptomatic disease until organ damage is evident.

Diabetes mellitus is one of the major risk factor for the development of atherosclerosis and the excess risk of stroke. It was diagnosed as co-morbidity in 8 patients, without statistically significant difference between stroke subtypes. According to study by Alemayehu et al. infarction is the most common type of stroke events in diabetic individuals (57.7%) [ 13 ]. In our study the prevalence of DM was lower compared to study by Sarkar et al. (25.9%) [ 34 ], 46.8% by De Carvalho etal [ 42 ], 23.8% by Desalu etal [ 43 ], 19.5% by Owolabi etal [ 17 ] and 10.1% by Watila etal [ 32 ]. But was closely similar with study by Deresse et al. in Ethiopia which was identified in 7.8% of stroke patients [ 29 ]. This discrepancy could be due to our small sample size, referral bias and single hospital-based design of our study. We recommend well designed multi-centered studies to quantify the risk of diabetes in Ethiopian stroke patients. The mean duration of diabetes prior to stroke was 5.3 year, that was closely correlates with study by Gebremariam etal [ 21 ].

Habituation of alcohol (22.4%) and smoking (17.2%) was higher compared to other previous studies [ 14 , 17 , 32 , 39 , 43 ]. This was mostly associated with the community in catchment area of our hospital were highly abuser of social drugs. The majority of smokers develop stroke due to smoking may predispose blood vessels to thrombosis and facilitates platelets aggregation possibly by causing an imbalance between brain vascular coagulation and abnormal fibrinolysis. This might alter the function of blood brain barrier and disrupt normal endothelial cell function. The relation between alcoholism and risk factor of stroke is more susceptible to aggravating effect which causes cardio embolism and hypertension thereby increases the risk of ischemic stroke.

In this study 12.9% of patients were previous user of diet containing low fruit and vegetable. The relation between risk of stroke and diet may be associated with increased daily total fat intake that greatly increases risk of stroke. But vegetable foods have low saturated fat and are protective for our health and organ function. Similar to previous study by Tirschwell et al. [ 37 ] cardiac disease like atrial fibrillation, coronary disease and heart failure were commonly associated with ischemic stroke than hemorrhagic strokes. Atrial fibrillation which is great source of cardioembolic stroke was diagnosed in 16.4% that was consistent with study by De Carvalho etal 14.95% [ 42 ] and Sagui etal 14.7% [ 38 ].

Up on multivariate logistic regression, atrial fibrillation was the independent predictor for hemorrhagic stroke. Patients having atrial fibrillation were less likely experience hemorrhagic stroke than ischemic stroke. From the pathophysiology of the stroke, atrial fibrillation is the most common reason for cardioembolic stroke that occludes cerebral arteries which favors ischemic stroke over hemorrhagic stroke. This finding complies with study by Atadzhanov etal in Zambia [ 16 , 41 ].

At the onset of stroke, the most common clinical presentation was headache (75.0%) followed by aphasia (60.3%) and hemiparesis (53.4%), similar finding was reported on study by Walker et al. in Gambia [ 33 ]. This finding was unlike to other studies where motor symptoms (hemiplegia/hemiparesis) were the most common clinical presentation among stroke patients [ 13 , 14 , 22 , 35 , 39 , 42 ]. The difference could be due to two major reasons. Primarily we have collected data on motor symptoms separately; hemiparesis and hemiplegia. Thus if we had collected as one category the result complies with those other previous studies, as 82.6% of patients manifest either hemiplegia/hemiparesis. Secondly even though the severity varies in degrees due to the nature of the disease most patients may complain the headache as the study was prospective with face to face interview. Initial presentation of urinary incontinence was higher (37.9%) as compared to other study by Greffie et al. [ 22 ]. Aphasia was one common presentation in this study which was less presentation as compared to other previous studies [ 14 , 22 , 39 ]. Similar to our finding, study by Kuriakose etal [ 7 ] reported that vomiting favors hemorrhagic stroke. This may be one indicator of stroke diagnosis based on clinical where brain imaging is not available. In general average clinical presentation for the patient was 6, which was higher than study in India by Kuriakose et al. in which majority of the patients had 3–4 clinical manifestation during admission [ 7 ].

Strength and limitations of the study

This study attempted to identify different risk factors related to stroke with a prospective clinical follow-up that focused on the need of preventive strategy and improvement of patient care. To ensure a uniform data collection, we ascertained consistently ascertainable risk factor identification and obtained more or less reliable information to achieve the goals of our study. More generable case ascertainment than in earlier studies, in-person health care professional assessment to verify eligibility for inclusion was addressed.

The study was associated with some limitations and drawbacks. First, this study was a hospital-based study rather than longitudinal community based study. Hence it may be subjected to referral bias, as most of the acute stroke patients’ visit our hospital only from the south western part of Ethiopia. These referral bias as well as convenience sampling approach used might not reflect the true prevalence of the stroke in the community. Even though the study was hospital based, having only one referral center might probably reflect the actual magnitude of stroke in our country.

Secondly, about half of the patients were diagnosed clinically alone to have stroke based on clinical presentations, risk profiles, disease course and other supportive investigations. Clinical way of diagnosis based on clinician judgment rather than biological may distort accuracy and reliability of the data. This may cause unintended false positive and false negative association between different variables of the study. Thus caution should be taken for the generalization of the finding for large community.

Thirdly, in our study protocol, the risk factor status was not refined sufficiently enough especially for ischemic stroke patients with cardiac cases. Even simple and inexpensive diagnostic tests like electrocardiograms (ECG) were not routinely performed. Poor risk factor identification and diagnosis may underestimate or overestimates some factors. Finally, the sample size was small hampering the analysis of some prognostic indicators due to the short recruitment period. In addition, we counted on patient reports of some of their risk factors and other patient related histories, which may introduce recall bias.

Majority of the patients were males, middle aged, rural residents, uneducated and farmers with low socioeconomic status. The increasing burden of stroke in LMICs countries like Ethiopia poses a challenge to the health care system and the community as a whole. The most common risk factor identified was hypertension and the level of poor blood pressure control in hypertensive patients we observed in this study was alarming. The most common clinical presentation was headache and motor symptoms (hemiplegia/hemiparesis). Hemorrhagic stroke patients were more likely to have coma, vomiting and neck stiffness but ischemic stroke patients were more likely presented with chest pain.

As stroke is a high priority chronic global case, large-scale community health campaign should be launched focusing on community education regarding risk factors of stroke as well as recognition of stroke-related symptoms, prognosis and outcomes. The importance of early recognition and treatment may help to improve outcomes, facilitate consistent and continuous follow up as well as with available treatment options disability can be minimized. Educational programs for front-line health-care providers, focusing on simple supportive interventions, could improve outcomes in settings where advanced diagnostics and treatment of stroke remain limited.

In addition, there should be influential contribution from every social media and political level of the country with the goal of increasing the awareness of risk factors and making the community to understand the challenging effect of the stroke on human health and economy of the country. Thus, policy makers should put strategies for screening and management of common risk factors like hypertension.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Abbreviations

Atrial fibrillation

Body Mass Index

Diabetes Mellitus

Global Burden of Diseases

Hemorrhagic stroke

Ischemic heart Disease

Ischemic stroke

Jimma university medical center

Low and middle income countries

Sub Saharan Africa

Stroke unit

World Health Organization

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Acknowledgments

We thank Jimma University for supporting the study. We are grateful to staff members of stroke unit of JUMC, data collectors and study participants for their cooperation in the success of this study.

The only funder for the study was Jimma University . The funding body did not have any role in study design, data collection, data analysis, interpretation of data or in writing the manuscript.

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Ginenus Fekadu

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Legese Chelkeba

Department of Epidemiology, Institute of Health, Jimma University, Jimma, Ethiopia

Ayantu Kebede

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GF contributes in the design of the study, analysis, interpretation and write up of the manuscript. AK made the data analysis and interpretation of the data. LC contributed to the design of the study and edition of the manuscript. All authors critically revised the manuscript and have approved the final manuscript.

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Ethical clearance was obtained from the Institutional Review Board (IRB) of Jimma University, Institute of health with reference number of IHRPGC/107/207. Permission was obtained from responsible bodies of the JUMC and stroke unit prior to the interview and review of the patient data. At hospital written informed consent was obtained from the study participants. All patients got the right to opt out of the research. For patients who were not of sound mind to consent; those of altered level of consciousness or severe aphasias, one of the family members or caregivers was given the written consent. This was done by explaining the objective and importance of the study as it is beneficial for patient’s quality service delivery for future encounters. The data from the case records and interview was handled with strong confidentiality. Neither the case records nor the data extracted was used for any other purpose. The confidentiality and privacy of patients was assured throughout by removing identifiers from data collection tools using different codes [ 23 , 24 ].

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Fekadu, G., Chelkeba, L. & Kebede, A. Risk factors, clinical presentations and predictors of stroke among adult patients admitted to stroke unit of Jimma university medical center, south west Ethiopia: prospective observational study. BMC Neurol 19 , 187 (2019). https://doi.org/10.1186/s12883-019-1409-0

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Clinical Presentation and Diagnosis of Cerebrovascular Disease

Chapter 30 Clinical Presentation and Diagnosis of Cerebrovascular Disease Mark J. Alberts Stroke is a common and serious disorder. Each year stroke affects almost 800,000 people in the United States and about 16 million people throughout the world. 1 Associated high morbidity and mortality provide impetus for improving diagnosis, acute management, and prevention of strokes. A full understanding of how patients with stroke and cerebrovascular disease come to medical attention, along with a logical approach for defining the mechanism of stroke, are needed for safe and effective implementation of acute therapies and prevention strategies. This chapter will focus on clinical manifestations of all types of cerebrovascular disease and how clinicians can approach diagnostic evaluation. Overview of Clinical Stroke Stroke and cerebrovascular disease are caused by some disturbance of the cerebral vessels in almost all cases. In simple terms, we can divide stroke into two major types: ischemic and hemorrhagic. Ischemic stroke is the most common variety and is responsible for 80% to 85% of all strokes; hemorrhagic stroke accounts for the remainder. 2 On occasion, an ischemic stroke can undergo secondary hemorrhagic transformation; likewise, a cerebral hemorrhage (particularly a subarachnoid hemorrhage [SAH]) can cause a secondary ischemic stroke via vasospasm. Ischemic stroke occurs when a blood vessel in or around the brain becomes occluded or has a high-grade stenosis that reduces the perfusion of distal cerebral tissue. A variety of mechanisms and processes can lead to such occlusions and will be discussed later in more detail. On rare occasions, venous thrombosis can occlude a cerebral vein and lead to ischemic as well as hemorrhagic strokes (venous infarction). Hemorrhagic stroke (intracerebral hemorrhage [ICH] and SAH) occurs when a blood vessel in or around the brain ruptures or leaks blood into the brain parenchyma (ICH) or into the subarachnoid space (SAH). It is not uncommon for there to be some overlap, such as an ICH also causing some degree of SAH and/or an intraventricular hemorrhage. Likewise, an SAH can produce some elements of an ICH if the aneurysmal rupture directs blood into the brain parenchyma. As with ischemic stroke, a variety of processes and lesions can produce ICH and SAH, but most affect integrity of the vessel wall in some way. Clinical Manifestations of Stroke and Cerebrovascular Disease Stroke is similar to real estate in that much of its presentation and prognosis depend on size and location. The area of brain involved dictates presenting symptoms. Blood vessels that supply different parts of the brain are affected by different types of cerebrovascular disease and have different mechanisms (pathophysiology) for the stroke. This concept greatly influences and defines the approach a vascular neurologist or neurosurgeon uses when assessing patients with a stroke or cerebrovascular disease. 3, 4 For example, a patient with evidence of involvement of the left hemispheric cortex (e.g., aphasia, visual field defect, weakness of contralateral face and arm) is likely to have a process involving the left middle cerebral artery (MCA). If head computed tomography (CT) does not show evidence of a hemorrhage, likely etiologies would include an embolic event from the heart (e.g., atrial fibrillation) or an artery-to-artery embolism (as might be seen with a high-grade lesion at the carotid bifurcation in the neck). Another patient with a pure motor hemiparesis but no other deficits is likely to have a lesion affecting the motor pathways in the internal capsule, often due to occlusion of a small penetrating artery (lenticulostriate vessel) deep in the brain. Most ischemic strokes will respect the vascular territory of one or more arteries. 5 Indeed, lesions that do not respect typical arterial territories lead to concern for a nonvascular process (e.g., tumor, infection). Common ischemic stroke syndromes can be found in Tables 30-1 and 30-2 . Table 30-1 Common Large-Vessel Ischemic Stroke Syndromes Table 30-2 Common Lacunar Stroke Syndromes Evaluation of hemorrhagic stroke follows a similar logical assessment, but is further complicated by spread of the initial bleed, the effects of increased intracranial pressure, and other secondary effects that lead to neurological manifestations beyond the original injury. In this case, detailed cerebral imaging is vital for understanding the mechanism of the stroke and reasons for secondary worsening. The discussions that follow offer more detailed descriptions of common hemorrhagic stroke syndromes correlated with their likely anatomy and most likely pathophysiology. Besides location of the stroke, the tempo of onset and progression of symptoms often provide valuable information about stroke etiology and mechanism. Stroke symptoms that progress in a casual manner with gradual onset and worsening over many minutes or longer often suggest a thrombotic process or hypoperfusion due to occlusion or stenosis of a larger proximal vessel. Such a leisurely progression can also be seen with stroke mimics such as complicated migraines or partial seizures. The converse is a stroke syndrome with sudden onset of maximal symptoms that remain stable; this suggests an embolic process such as a cardioembolic stroke due to atrial fibrillation. Similar reasoning holds true for most cases of hemorrhagic stroke. Intracerebral hemorrhage often presents with abrupt onset of symptoms, but close questioning may reveal that symptoms actually progressed over 15 to 30 minutes as the hematoma grew and expanded. 6 Subarachnoid hemorrhage is often characterized by sudden onset of the worst headache of one’s life, with significant nausea, vomiting, and stiff neck in many cases. The phrase “worst headache of my life” is so characteristic of SAH that a patient who presents to the physician or emergency department with that symptom complex is assumed to have SAH until proven otherwise. 7 Transient Ischemic Attack A transient ischemic attack (TIA) is often a prodrome to an ischemic stroke. Symptoms of a TIA are identical to those of a stroke, but with resolution within 24 hours (according to the old definition of a TIA). In reality, most TIA syndromes last just a few minutes, not many hours. In fact, modern brain imaging using magnetic resonance imaging (MRI) with diffusion-weighted sequences has now shown that 25% to 30% of patients with a TIA lasting 30 min to 2 hours will have a new diffusion-weighted imaging (DWI) lesion on MRI indicating a stroke based on a tissue definition. 8 Transient ischemic attack symptoms lasting 6 hours or longer have a 50% likelihood of having a new stroke on MRI with DWI techniques. Therefore the perceived distinction between a TIA and a stroke should be viewed more as a continuum from minor transient neuronal dysfunction to permanent brain infarction. Although it was once thought that the risk of stroke after a TIA was low, new imaging studies as well as epidemiological studies have proven this is not the case. Based on purely clinical criteria (not MRI results), several recent studies have shown that after a TIA, 10% of patients will have a stroke within 3 months, and half those strokes (5%) will occur within 48 hours of the initial TIA. About 25% of patients with a TIA will have a stroke, myocardial infarction (MI), death, recurrent TIA, or be hospitalized within the next 3 months. 9 Based on these poor outcomes, recently published guidelines recommend hospital admission for patients with a recent TIA. 8 Further studies have attempted to better define those patients with a TIA who are at higher risk of having a stroke within the next 2 to 7 days. Several scoring systems have been developed ( Table 30-3 ) that may be useful for assessing such risks. Of course, any such assessment tool must be tempered by good clinical judgment and consideration of all clinical factors. Table 30-3 Transient Ischemic Attack Scoring Systems ABCD Age, blood pressure, clinical symptoms, duration ABCD2 Age, blood pressure, clinical symptoms, duration, diabetes ABCD2I Age, blood pressure, clinical symptoms, duration, infarction Age: 60 years or greater = 1 point Blood pressure: systolic 140 mmHg or greater = 1 point or diastolic 90 mmHg or greater = 1 point Clinical symptoms: unilateral weakness = 2 points; speech disturbance without weakness = 1 point Duration: 60 minutes or more = 2 points; 10-59 minutes = 1 point Diabetes: 1 point (on antidiabetic medications) Infarction: evidence for acute ischemic stroke on CT or MRI CT, computed tomography; MRI, magnetic resonance imaging. From Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al: Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 369:283–292, 2007. 50 Several types of TIAs deserve special mention because of their unique presentations. One is sudden blindness in one eye, which typically occurs as a “shade coming down” over the eye. Some patients report a graying out of vision in the eye, like looking through a gray haze or cloud. This type of TIA is often referred to as amaurosis fugax . This symptom complex typically resolves in a few minutes, although it can last for several hours. There is sometimes pain in or around the eye, but patients usually do not have any other focal neurological complaints. Some cases of amaurosis are due to emboli to the retinal circulation from an ulcerated plaque in or near the carotid bifurcation in the neck. Other cases can be due to local disease in the ophthalmic artery or in the posterior ciliary artery that supplies the optic nerve. 10 The other unique type of TIA is the limb-shaking TIA . This typically involves the arm or leg on one side of the body. Patients report uncontrollable shaking of a limb that can be precipitated by movement. These spells can last seconds to minutes. They are not epileptic in origin; electroencephalogram (EEG) is unremarkable. These TIAs are associated with severe stenosis of the contralateral internal or common carotid artery. 11 Once the carotid artery is opened (usually with an endarterectomy), the spells cease. Lastly is the topic of crescendo TIAs . This refers to a pattern where TIAs are recurrent, last longer, or are more severe in nature. This is a very worrisome type of TIA and is associated with a risk of stroke as high as 25% to 50% over the next few weeks. 12 Some hemorrhagic strokes may also have a TIA equivalent, namely the sentinel headache before a SAH. The sentinel headache present as an acute headache that is unusual in terms of its nature, severity, and onset. It typically lasts more than an hour but does not have other impressive focal neurological findings and resolves prior to the definitive SAH presentation. Sentinel headaches occur in 25% to 50% of patients with a subsequent aneurysmal SAH and typically antedate the SAH by days to weeks (average 2 weeks). 13, 14 It is thought that most of these headaches are due to either minor leakage from a fragile aneurysm or enlargement of the aneurysm, resulting in pressure on a nearby structure that produces pain. Ischemic Stroke Syndromes There are numerous manifestations of ischemic stroke, and they can be classified based on brain location involved, artery affected, or symptoms produced. Although advanced diagnostic techniques have altered some of the clinical rules of stroke symptoms and etiology, there are still some useful concepts that can guide us in terms of stroke location and mechanism. Tables 30-1 and 30-2 list some classic ischemic stroke syndromes with their major clinical manifestations, vascular territory, and underlying pathophysiology. 5 Broadly speaking, ischemic strokes typically involve one or more vessels or vascular territories and produce a clinical picture of focal neurological deficit. Typically, clinicians look for unilateral weakness or sensory deficits, unilateral visual field abnormalities, speech disturbance (aphasia or dysarthria), neglect syndromes, unilateral ataxia, ophthalmoplegias, or gaze abnormalities as clues of a stroke. Symptoms such as vague diffuse weakness alone, headaches alone, memory loss, abnormal behavior, or isolated dizziness are rarely caused by an ischemic stroke. The appearance of a lesion in a typical vascular territory (based on brain imaging) is a key feature of almost all stroke syndromes. 4 Presence of cortical deficits (aphasia, visual field cuts, neglect syndromes) often indicates involvement of a major cerebral vessel in the cerebral hemispheres. Presence of ataxia, bilateral motor or sensory deficits, Horner’s syndrome, ophthalmoplegias, and crossed sensory findings (one side of the face and the other side of the body) often indicates a stroke in the posterior (vertebral-basilar) territory. There are specific syndromes that indicate small-vessel involvement deep in the brain. These so-called lacunar strokes are due to occlusion of small penetrating arteries that arise directly from larger parent vessels. Favored locations include the deep basal ganglia structures, thalamus, and brainstem (pons). A listing of large-vessel and lacunar syndromes appears in Tables 30-1 and 30-2 . Atherothrombosis accounts for the majority of ischemic strokes. These lesions can occur anywhere in the cerebral vasculature, but they tend to have a preference for specific locations such as the bifurcation of the carotid artery in the neck, intracranial carotid siphons, proximal portion of the middle cerebral artery, mid-portion of the basilar artery, and aortic arch. An atherosclerotic plaque forms over many years, then ruptures causing formation of a superimposed thrombus. 15 This atherothrombotic lesion can totally occlude the vessel, produce severe narrowing (leading to watershed ischemia), or be a source of embolic material that embolizes to more distal parts of the cerebral vasculature (artery-to-artery emboli). Cardiac embolism accounts for 15% to 20% of all ischemic strokes. A variety of conditions such as atrial fibrillation, endocarditis, prior myocardial infarction, valvular disease, and cardiomyopathy often lead to formation of intracardiac thrombi that subsequently embolize to the brain (and other organs). 4, 16 Most lacunar strokes are due to either lipohyalinosis or microatheromata occluding a small penetrating artery. Special Cases Ischemic Stroke in Young Adults All clinicians see young adults (often defined as ≤ 45 years of age) with ischemic strokes. Such cases often entail a special evaluation because of the unique processes and conditions that can produce strokes in this age group. Many case series have examined the diseases leading to ischemic strokes in the young, and in general they fall into a few major categories: (1) premature atherosclerosis, (2) unusual vascular pathologies, (3) cardiac etiology, (4) coagulopathy, and (5) other diseases. 17 Premature atherosclerosis typically occurs in patients with risk factors for atherosclerosis; in some cases these have not been diagnosed or not properly treated. Examples include hypertension, hyperlipidemia, diabetes, smoking, and obesity. The types of uncommon vascular pathologies often seen in young adults with a stroke include dissection of a vessel (often not related to any obvious trauma), fibromuscular dysplasia, moyamoya disease, or a vasculitis related to an inflammatory condition or drug abuse. 17 Numerous cardiac processes can lead to strokes in the young, such as congenital heart disease, a patent foramen ovale (particularly with evidence of venous thrombi), valvular disease (infectious or inflammatory), cardiomyopathy, myxoma, papillary fibroelastoma, and many others. Myriad clotting disorders have been associated with strokes in young adults, the most common being lupus anticoagulants, anticardiolipin antibodies, and protein C and protein S deficiency. 18 In general, these coagulopathies are more likely to cause venous thrombosis than arterial thrombosis. Clotting disorders related to hematological malignancies can cause both ischemic and hemorrhagic strokes. 19 Various systemic diseases are also associated with hypercoagulable states such as inflammatory bowel disease, hemoglobinopathies, elevated homocysteine, and cancer. The “other” category covers a host of conditions, some rare and some common, that cause strokes in young adults. Migraine headaches and pregnancy are the most common of these. Patients with complex or complicated migraines, prolonged auras, or taking contraceptives have a higher risk of stroke. 20 Pregnancy, particularly in the third trimester and up to 3 months postpartum is associated with increased stroke risk, particularly venous thrombosis and cerebral hemorrhage. 21, 22 Drug abuse is another common cause of ischemic and hemorrhagic strokes in young adults. 23 Other rare conditions include CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke), isolated central nervous system (CNS) vasculitis, Sneddon syndrome (combination of a livedo reticular rash, antiphospholipid antibodies, and ischemic stroke), Marfan’s syndrome, and a host of others (especially connective tissue disorders) have been known to cause strokes in this population. Strokes Related to Systemic Disease Numerous systemic disorders are important and potent risk factors for stroke: hypertension, diabetes, hyperlipidemia, smoking, heart disease (atrial fibrillation, myocardial infarction, valvular disease, etc.), drug abuse, and others. These have been covered in other chapters of this book. Our focus here is on specific systemic disorders that lead to specific or unusual types of strokes. There are a number of unique systemic disorders that cause strokes in patients of any age. Autoimmune diseases, such as lupus, can produce strokes through a variety of mechanisms that include advanced or premature atherosclerosis, vasculitis, hypercoagulable states, and cardioembolic events. 24 Sickle cell disease (SCD) also leads to ischemic strokes and hemorrhagic strokes due to myriad processes including a large-vessel arteriopathy, small-vessel occlusion, rupture of moyamoya vessels (producing ICH and/or SAH), and accelerated atherosclerosis due to hypertension and renal failure. 25, 26 Drug abuse, particularly cocaine, can produce ischemic strokes via a number of processes including vasospasm, cardiac emboli (due to cardiomyopathy), hypertension, and endocarditis. 27 Drug abuse can produce an ICH or SAH due to extreme hypertension and necrotizing vasculitis. It is a fallacy to assume that drug abuse only occurs in young patients or those from certain demographic groups. All patients admitted with a stroke should be tested for drug abuse with urine toxicology screens, not excluding those older than 50 years and white-collar professionals. Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) is now recognized as increasing the risk of stroke. This is partially because patients with HIV/AIDS are living longer, and some are having strokes as a result of accelerated development of typical stroke risk factors. It is also clear that modern drug therapy for AIDS can increase the risk of stroke (particularly ischemic stroke). 28, 29 Systemic cancer is a commonly overlooked cause of strokes. Sometimes the stroke diagnosis precedes diagnosis of the underlying cancer. Mechanisms for strokes related to cancer include a hypercoagulable state and nonbacterial thrombotic endocarditis. Oftentimes these strokes are multiple, variable in size, and in different vascular territories. 30, 31 Such patients may also have deep venous thrombosis (DVT). Liver failure appears to increase risk of ischemic and hemorrhagic stroke. Intracerebral Hemorrhage In broad terms, ICH can be divided into traumatic and nontraumatic etiologies. This chapter will focus on nontraumatic ICH, since ICH related to trauma is not routinely considered a stroke. Intracerebral hemorrhage is typically caused by rupture of a blood vessel within the brain parenchyma. Patients typically develop a focal neurological deficit suddenly, but symptoms often evolve over 10 to 30 minutes as the hematoma gradually expands. Headache is commonly present, and the vast majority of patients have markedly elevated blood pressure (often in excess of 200 mmHg systolic) even without a prior history of hypertension. Nausea and vomiting can also occur, particularly with ICH that involves the brainstem and/or cerebellum. Chronic or acute hypertension is the most common etiology for nontraumatic ICH, and this type of bleed typically occurs in specific brain locations ( Table 30-4 ). As with ischemic stroke, location of the ICH is highly correlated with the type of symptoms produced. Recent studies using serial brain scans have shown that 30% to 40% of ICHs will expand over the first 24 hours after admission; such expansion is almost always associated with clinical worsening. 6, 32 High blood pressure may be a risk factor for ICH expansion, although this association has not been mechanistically proven. Table 30-4 Location and Symptoms for Common Types of Intracerebral Hemorrhage ICH Location Likely Etiology Common Symptoms Basal ganglia Hypertension Contralateral hemiparesis, speech changes, gaze deviation, altered mentation if large Lobar Hypertension, CAA Cortical syndromes, weakness, visual field lesions, altered mentation if large Thalamus Hypertension Altered mentation, sensory changes, gaze abnormalities Pons Hypertension Coma, gaze and pupil abnormalities, quadriparesis Cerebellum Hypertension, AVM Ipsilateral ataxia, dizziness, vertigo, nausea/vomiting Hemispheric cortex AVM, extreme hypertension, mycotic aneurysm Headaches, seizures, cortical syndromes AVM, arteriovenous malformation; CAA, cerebral amyloid angiopathy; ICH, intracerebral hemorrhage. Another increasingly common etiology for ICH is cerebral amyloid angiopathy (CAA), which typically affects patients older than 70 years of age. Cerebral amyloid angiopathy is caused by deposition of one or more amyloid proteins within the wall of cerebral small arterioles. A typical CAA bleed occurs in a lobar region (junction of gray matter and white matter), most commonly in the parietal, temporal, and occipital lobes. Intracerebral hemorrhages due to CAA can be multiple and recurrent. 33 – 35 There is a clear association between CAA, ICH, and Alzhemier’s disease. Sometimes an ischemic stroke can undergo hemorrhagic transformation and become an ICH. This occurs in up to 15% of cases of ischemic stroke and is associated with large strokes, cardioembolic strokes, and the use of anticoagulants and thrombolytic agents. A variety of vascular malformations can cause an ICH, particularly arteriovenous malformations (AVMs) and cavernous malformations (less commonly, capillary telangiectasias and developmental venous anomalies). Arteriovenous malformations are the most common and serious type of vascular malformation that cause an ICH, and recurrent ICHs, as well as producing seizures and local neurological deficits. 36 The characteristics and hemorrhagic risk of each of these lesions is shown in Table 30-5 . Table 30-5 Common Types of Central Nervous System Vascular Lesions That Lead to Cerebral Hemorrhage

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clinical presentations of stroke

Isolated Insular Stroke: Clinical Presentation

Affiliations.

  • 1 U.O.S.D. Stroke Unit, Department of Clinical and Experimental Medicine, AOU Policlinico G. Martino, University of Messina, Messina, Italy.
  • 2 U.O.S.D. Stroke Unit, Department of Clinical and Experimental Medicine, AOU Policlinico G. Martino, University of Messina, Messina, Italy, [email protected].
  • 3 Neuroradiology Unit, Department of Biomedical, Dental Science and Morphological and Functional Images, University of Messina, Messina, Italy.
  • PMID: 32023607
  • DOI: 10.1159/000504777

The symptoms related to insular ischemia have been the object of several studies in patients affected by stroke, although they are often accompanied by other ischemic alteration of adjacent brain structures supplied by the middle cerebral artery (MCA). The insula is vulnerable because of an ischemia due to thromboembolic vascular occlusion of the M1 MCA segment and the 2 main MCA branches (M2), mainly when they abruptly arise from the principal stem at a right angle. This topographical and anatomical peculiarity could enable an embolic formation, especially due to atrial fibrillation (AF), to occlude the transition pathway between M1 and M2, while the proximal origin of vascular supply protects the insula from ischemia due to hemodynamic factors. The aim of the study is to characterize the clinical aspects of acute ischemic strokes as a first event in the insular territory with specific attention to atypical manifestation. We have considered 233 patients with a first event stroke involving the insular territory and 13 cases of isolated insular stroke (IIS), from the stroke registry of the Policlinico "G.Martino", University of Messina, between the February 10, 2014 and the February 7, 2018. IIS patients showed CT/MRI lesions restricted to the insular region. Exclusion criteria were coexisting neurological diseases, structural brain lesions, extension to the subinsular area >50% of the total infarct volume. We identified 13 IIS patients (mean age 74 years), with an isolated symptom or a combination of typical and atypical aspects. Furthermore, we observed high frequency detection of cardiac disturbances. To our knowledge, just a few previous studies have described IIS; their incidence is still not well defined. IIS manifested with a combination of deficits including motor, somatosensory, speaking, coordination, autonomic and cognitive disturbances. After an ischemic stroke, AF manifestation could follow briefly the major event and its duration could be very short, as an autonomic dysfunction due to an insular infarction. This clinical condition requires a continuous cardiac monitoring for this dangerous occurrence.

Keywords: Autonomic activation after stroke; Insular stroke; Neurointensive care; Stroke diagnostics.

© 2020 S. Karger AG, Basel.

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Pivotal role of multiphase computed tomography angiography for collateral assessment in patients with acute ischemic stroke

  • Computed Tomography
  • Open access
  • Published: 23 June 2023
  • Volume 128 , pages 944–959, ( 2023 )

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  • Giorgio Busto   ORCID: orcid.org/0000-0002-7007-6030 1 , 6 ,
  • Andrea Morotti 2 ,
  • Edoardo Carlesi 1 ,
  • Alessandro Fiorenza 2 ,
  • Francesca Di Pasquale 3 ,
  • Sara Mancini 1 ,
  • Ivano Lombardo 1 ,
  • Elisa Scola 1 ,
  • Davide Gadda 1 ,
  • Marco Moretti 1 ,
  • Vittorio Miele 4 &
  • Enrico Fainardi 5  

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The cerebral collateral circulation is the main compensatory mechanism that maintains the ischemic penumbra viable, the tissue at risk for infarction that can be saved if blood flow is restored by reperfusion therapies. In clinical practice, the extent of collateral vessels recruited after vessel occlusion can be easily assessed with computed tomography angiography (CTA) using two different techniques: single-phase CTA (sCTA) and multi-phase CTA (mCTA). Both these methodologies have demonstrated a high prognostic predictive value for prognosis due to the strong association between the presence of good collaterals and favorable radiological and clinical outcomes in patients with acute ischemic stroke (AIS). However, mCTA seems to be superior to sCTA in the evaluation of collaterals and a promising tool for identifying AIS patients who can benefit from reperfusion therapies. In particular, it has recently been proposed the use of mCTA eligibility criteria has been recently proposed for the selection of AIS patients suitable for endovascular treatment instead of the current accepted criteria based on CT perfusion. In this review, we analyzed the characteristics, advantages and disadvantages of sCTA and mCTA to better understand their fields of application and the potential of mCTA in becoming the method of choice to assess collateral extent in AIS patients.

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Introduction

The collateral circulation consists of the opening of alternative vascular channels distal to an occluded intracranial artery resulting in a massive vasodilatation that improves blood flow in hypoperfused brain regions. In acute ischemic stroke (AIS), collaterals represent the more important compensatory mechanism maintaining viable the ischemic penumbra, the reversibly damaged brain tissue at risk for infarction surrounding the irreversibly injured infarct core. The ischemic penumbra is the target of reperfusion therapies since it is potentially salvageable [ 1 ]. The prognostic value of collaterals in AIS patients is now generally accepted. Poor collaterals are predictors of unsuccessful recanalization and unfavorable clinical outcomes, while robust collaterals are associated with high recanalization rate, tissue reperfusion, early clinical improvement, small Final Infarct Volume (FIV), low risk of hemorrhagic transformation (HT) and favorable clinical outcomes [ 2 , 3 ]. In addition, collaterals are associated with reduced ischemic core growth and allow the identification of patients showing rapid or delayed infarct expansion (namely fast or slow progressors) [ 4 ]. Therefore, collaterals could play a crucial role for the selection of patients candidates for intravenous thrombolysis (IVT) and endovascular treatment (EVT) in both early and late time windows [ 2 ]. Different imaging modalities are used for an appropriate evaluation of collateral extent that has become a major need in clinical practice [ 1 , 2 , 5 , 6 ]. Digital subtraction angiography (DSA) is still considered as the gold standard for accurate identification of occlusion site and measurement of collaterals due to its high temporal and spatial resolution. In this setting, the American Society of Interventional and Therapeutic Neuroradiology/Society of Interventional Radiology (ASITN/SIR) scale [ 7 , 8 ] and Careggi Collateral Score (CCS) [ 8 , 9 , 10 ] are some of the classifications used for collateral grading with DSA. However, DSA has many limitations since it is an invasive and time-consuming procedure, requires multiple acquisition to visualize both anterior and posterior collaterals and is at risk for thromboembolism. Information on collaterals can also be obtained with perfusion techniques, such as CTP and Magnetic Resonance Perfusion-Weighted Imaging (MR-PWI), using some multiparametric maps and, in particular, the Hypoperfusion Intensity Ratio (HIR) that is calculated on time-to-maximum of the tissue residue function (Tmax) maps as the quotient between the lesion volumes with Tmax > 10 s and > 6 s corresponding to the ratio between infarcted tissue and hypoperfused tissue, respectively. Nevertheless, although a strong correlation between HIR and collateral extent has been demonstrated, HIR does not allow a direct visualization of collaterals. Thus, based on these considerations, collateral assessment is currently performed with computed tomography angiography (CTA) that is a widely available, non-invasive, safe and therefore feasible method [ 2 , 5 , 6 ]. Single-phase CTA (sCTA) is able to identify the point of occlusion and collateral filling, but multi-phase CT angiography (mCTA) was recently proposed, consisting of a three-time points acquisition which provides a more detailed evaluation of collaterals and presents several advantages over sCTA. In fact, mCTA demonstrated a better correlation with FIV and functional outcome, and higher interrater reliability compared to sCTA. Moreover, several studies showed that mCTA is a useful tool for patient selection undergoing EVT, especially in the extended time window where the collateral assessment with mCTA could replace the current approach based on CT perfusion (CTP) parameters [ 6 ].

Functional anatomy of collateral circulation

The cerebral collateral circulation is a vascular system that regulates cerebral blood flow (CBF) in case of vessel occlusion and consists of a network of anastomoses belonging to both the arterial and venous circulation [ 1 , 2 , 11 , 12 , 13 ]. On the arterial side, three principal routes exist: (1) collaterals between the intracranial and the extracranial arteries provided by ophthalmic and superficial temporal arteries; (2) collaterals between the intracranial arteries based on the circle of Willis, a ring-shaped circuit of vessels in which the anterior communicating artery promotes interhemispheric blood flow and the posterior communicating arteries connecting the anterior and posterior circulation; (3) collaterals between the intracranial arteries provided by pial or leptomeningeal branches which generate a communication among the three large vessels of each hemisphere (anterior, middle and posterior cerebral arteries) supplying the cortical surface. At intracranial level, collaterals represented by the components of circle of Willis are indicated as primary, whereas pial (leptomeningeal) collaterals are considered as secondary because are usually recruited when primary collaterals fail. Of note, a variable anatomic configuration is typical of the circle of Willis since the anterior portion results to be complete in only 68%, the posterior portion in 47% and the entire circle in only 36% of individuals. In this regard, it has recently been suggested that the different structures of the circle of Wills could be implicated in defining fast progressors and could correlate with poor collateral score [ 14 ]. A high anatomic variability is also characteristic of venous collateral circulation collaterals that increases CBF drainage in case of occlusion of prominent pathways or venous hypertension and allows the exit of blood from the brain through multiple routes. Functionally, collateral activation is modulated by sympathetic system via intrinsic and extrinsic innervations which act on parenchymal vessels and vascular branches on the brain surface, respectively [ 12 ]. However, the two key events leading the opening of collaterals are the recruitment and the remodeling [ 1 , 2 , 11 , 12 ]. The collateral recruitment can occur early, immediately or in minutes, or can be delayed, as typically occurs in chronic obstructive disease but sometimes appears within a few hours also after acute vessel occlusion providing a potential explanation for spontaneous acute tissue reperfusion. This recruitment is due to the drop of perfusion pressure in vessels downstream the occlusion with formation of a pressure gradient favoring the diversion of blood flow into collaterals and the shear stress that induces vasodilatation. Nevertheless, collateral recruitment is impaired by several conditions including advanced age, chronic hypertension, cerebral small vessel disease [ 1 ]. A greater lumen expansion of collaterals associated with increase in tortuosity, vessel length and wall thickness represents the collateral remodeling that develops in days or weeks, mainly during conditions characterized by a chronic decreased in CBF such as stenosis or occlusion of the internal carotid artery.

CTA acquisition and collateral grading

Scta technique.

sCTA images are obtained on a standard CT scanner through a volumetric acquisition starting approximately 5–10 s after automatic injection of 50–70 mL of a contrast bolus at the rate of 4–5 mL/s into an antecubital vein. sCTA source images are then reformatted with maximum intensity projection (MIP), a 3D reconstruction algorithm that provides images with a good anatomic detail of cerebral vessels and allows an accurate visualization of collaterals [ 5 , 15 ]. Usually, sCTA covers from the aortic arch to vertex for the identification of occlusion site at the level of cervical and intracranial vessels (Fig.  1 ). Several grading scales have been proposed, but four collateral scores based on visual inspection of the degree of collateral filling are the most utilized grading systems in clinical practice (Table 1 ). The collateral grading system introduced by Miteff and coworkers [ 16 ] is a qualitative 3-point scale assigning 3 different grades of retrograde filling to the distal branches of middle cerebral artery (MCA) in the occluded territory that result in poor (grade 1), intermediate (grade 2) and good (grade 3) collaterals (Fig.  2 , Panel A). The collateral score suggested by Tan and colleagues [ 17 ] is a qualitative a 4-point scale that classifies collateral supply filling of occluded middle cerebral artery territory in 4 different grades corresponding to poor (scores 0–1) and good (scores 2–3) collaterals (Fig.  2 , Panel B). The collateral scoring system published by Mass and collaborators [ 18 ] is a qualitative 5-point scale that compares the opacification of sylvian and leptomeningeal vessels between occluded territory and contralateral normal side obtaining 5 different grades that represent poor (grade 1), intermediate (grade 2) and good (grades 3–5) collaterals (Fig.  2 , Panel C). The collateral score described by Menon et al. [ 19 ] is a semiquantitative 20-point score that divides the territories supplied by anterior cerebral artery (ACA) and MCA in 9 regions attributing 0, 2 or 4 points to sylvian scissure and 0, 1 or 2 points to remaining areas after comparison of opacification of pial and lenticulostriate vessels between the occluded territory and contralateral normal side. Collaterals are judged as poor, intermediate and good with a scoring of 0–10 points, 11–16 points and 17–20 points, respectively (Fig.  2 , Panel D). In all these collateral scores, except Tan grading, intermediate and good collaterals are considered as good. However, there is currently no consensus on the standard methodology to use for evaluating collateral extent since in prior publications, Menon scale performed better than Miteff score in predicting core and penumbra volumes likely because of its greater ability to estimate the delay rather than the backflow in the affected territory [ 20 ].

figure 1

Single-phase CT angiography covers from the aortic arch to vertex and maximum intensity projection reconstructions for the visualization of cervical and intracranial vessels. CTA of the cervical and intracranial vessels was performed as follows: 0.7 mL/kg contrast (maximum 90 mL), 5- to 10-s delay from injection to scanning, 120 kV, 270 mA, 1 s/rotation, 1.25-mm-thick slices, and table speed 3.75 mm/rotation. The axial images were reconstructed at 1-mm overlapping sections, and multiplanar reconstructions for axial, coronal, and sagittal images of the circle of Willis were performed with 3 mm thickness at 1-mm intervals. Thick-section axial maximum intensity projections at 24 mm thickness and 4-mm intervals were also reconstructed

figure 2

Single-phase CT angiography collateral scores. Green arrows indicate occlusion site or occluded hemisphere. M1, anterior MCA at ganglionic level; M2, lateral MCA at ganglionic level; M3, posterior MCA at ganglionic level; M4, anterior MCA at supraganglionic level; M5, lateral MCA at supraganglionic level; M6, posterior MCA at supraganglionic level; ACA, anterior cerebral artery; BG, basal ganglia

mCTA technique

mCTA is a three-phase acquisition offering time-resolved cerebral angiograms of brain vessels. The first phase replicates the only one phase of sCTA covering from aortic arch to vertex, whereas the following two phases are acquired from the skull base to vertex after table repositioning to the skull base for the visualization of intracranial vessels with a delay 8 s each (Fig.  3 ). There are no differences in the other characteristics of acquisition compared to sCTA. Therefore, the first phase corresponds to arterial phase, the second phase to equilibrium/venous or peak venous or phase and the third one to late venous phase [ 21 ]. mCTA can also be reconstructed from CTP peak of arterial phase obtaining three simulated mCTA phases [ 22 ]. In this case, however, the first phase includes only intracranial and not also cervical vessels as in the original mCTA acquisition. Using mCTA, collaterals are assessed with the grading system proposed by Menon and colleagues that is a qualitative 6-point scale (Table 2 ) in which collateral supply is categorized based on extent and prominence of vascular enhancement after comparison between the occluded territory and contralateral normal side and is identified as poor (grades 0–1), intermediate (grades 2–3) and good (grades 4–5) [ 21 ]. In contrast with sCTA classifications, mCTA Menon score defines intermediate profile as poor and not as good collaterals. Of note, while this classification was fully applied in several studies evaluating collaterals with mCTA [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ], in others collateral filling was measured with sCTA Menon score [ 17 , 20 , 29 ] or sCTA Tan grading [ 17 , 31 , 32 , 33 ] and intermediate pattern was included in good collaterals. Furthermore, grade 2 instead of grade 4, as stated in the original publication of Menon et al., was found to be the optimal threshold for identifying a good functional independence [ 27 ]. Thus, the more accurate score for calculating mCTA collateral extent has to be definitely validated.

figure 3

Multiphase CT angiography covering from the carotid bifurcation to vertex (first phase) and from the skull base to vertex (second and third phases) with maximum intensity projection (MIP) reconstructions for the visualization of cervical and intracranial vessels (first phase) and intracranial vessels only (second and third phases). Green arrow indicates occlusion site. CTA of the cervical and intracranial vessels was performed as follows: 0.7 mL/kg contrast (maximum 90 mL), 5- to 10-s delay from injection to scanning, 120 kV, 270 mA, 1 s/rotation, 0.625-mm-thick slices, and table speed 3.75 mm/rotation. The second phase was acquired after a delay of 8 s that allows for table repositioning to the skull base. Scanning duration for each additional phase was 3.4 s. Thus, the three phases were each 12 s apart. The axial images were reconstructed at 1-mm overlapping sections, and multiplanar reconstructions for axial, coronal, and sagittal images of the circle of Willis were performed with 3 mm thickness at 1-mm intervals. Thick-section axial maximum intensity projections at 24 mm thickness and 4-mm intervals were also reconstructed

Automated collateral detection

Several efforts have recently been made to obtain an automated assessment of collateral extent and provide a reliable quantitative collateral scoring, mainly based on artificial intelligence programs. For sCTA, a good agreement was found between visual grading scale proposed by Tan and an automated collateral score performed using in-house [ 34 , 35 ] or commercial software algorithms, such as Brainomix [ 36 ], StrokeViewer [ 37 ] and Canon [ 38 ]. In addition, a study analyzing patients from MR CLEAN database with in-house software showed that quantitative score was an independent predictor of functional outcome and FIV [ 34 ]. For mCTA, the most used automated method is provided by GE Healthcare FastStroke software generating time-variant color-coded maps which correlated well with conventional mCTA collateral score for the evaluation of collateral flow [ 38 , 39 ], improved the interpretation of collateral status [ 40 ] and enhanced the predictive value of collaterals for good outcome [ 41 ]. Another in-house software with a good performance for the measurement of collateral supply was more recently described using CTP-derived mCTA images [ 42 ]. However, a validation on a larger population of patients is needed before the introduction of these automated software in clinical practice.

CTA collateral assessment in AIS

A large number of previous studies demonstrated the high predictive value of good collaterals assessed by sCTA for favorable clinical outcome, small FIV and low rates of HT in AIS patients treated with IVT and EVT [ 43 , 44 , 45 ]. These findings were confirmed and expanded in a series of recent publications using both sCTA and mCTA techniques, mainly in patients that underwent EVT.

sCTA collaterals

A clear association between intermediate and good collaterals and favorable clinical outcome was found in a post hoc analysis of Interventional Management of Stroke (IMS) III trial evaluating sCTA collaterals with Maas and Tan scores in AIS patients treated with IVT within 3 h or combined IVT and EVT within 7 h from symptom onset [ 46 ]. The same correlation between good collaterals and functional independence was observed in two post hoc analyses of MR CLEAN (Multicenter Randomized Clinical Trial of Endovascular Treatment of Acute Ischemic Stroke in the Netherlands) [ 47 ] and DAWN (Triage of Wake-up and Late Presenting Strokes Undergoing Neurointervention With Trevo) [ 48 ] trials which measured sCTA collaterals using Tan score in patients receiving EVT at 6 h and at 6–24 h after stroke, respectively. However, benefit from EVT was also seen in patients with poor collaterals rated with Tan scale in an analysis of MR CLEAN Registry [ 49 ] and in HERMES (Highly Effective Reperfusion Evaluated in Multiple Endovascular Stroke Trials) meta-analysis including patients who underwent EVT with or without IVT from 4.5 to 12 h after symptom onset [ 50 ]. Conversely, in a post hoc analysis of DEFUSE 3 (Endovascular Therapy Following Imaging Evaluation for Ischemic Stroke) no association was reported between sCTA collaterals graded with Maas and Tan scores and clinical outcome in patients treated with EVT at 6–16 h from onset [ 51 ]. Next, some investigations showed that good collaterals classified on sCTA with Tan scale predicted successful recanalization after IVT within 4.5 h [ 52 ] and EVT up to 24 h [ 48 , 53 ] after onset, whereas the beneficial effect on clinical outcome of an earlier time to recanalization was independent of collaterals evaluated with Tan score in an analysis of MR CLEAN Registry [ 54 ] and detected only in patients with poor collaterals assessed by Miteff scale in a study based on a Korean Registry including patients treated with EVT within 6 h after onset [ 55 ]. Nevertheless, in a further analysis of the MR CLEAN Registry successful recanalization after EVT was not affected by sCTA collateral status graded by Tan score [ 56 ]. In addition, some studies revealed the predictive value of poor sCTA collaterals scored with Tan and Miteff scales for larger FIV as defined on non-contrast CT (NCCT) or Diffusion-Weighted Imaging (MR-DWI) [ 48 , 57 , 58 ] and increased HT rates [ 59 , 60 ] in patients treated with EVT up to 24 h from onset. A robust association of good sCTA collaterals with reduced core growth and slow infarct progression was then identified in several studies including untreated patients and patients undergoing EVT within 24 h after onset where Tan [ 51 , 61 , 62 , 63 , 64 ], Maas [ 65 ], Menon [ 66 ] and Miteff [ 67 ] were used as grading scores. In this setting, it is interesting to note that while poor collaterals were associated with penumbral salvage in a population of not treated patients [ 61 , 67 ], an analysis of Acute Stroke Registry and Analysis of Lausanne (ASTRAL) did not document any correlation between penumbra volume determined by CTP and sCTA collaterals assessed with Tan score in untreated and IVT and/or EVT-treated patients admitted within 24 h from onset, suggesting that the relationship between collaterals and tissue at risk for infarction remains to be completely clarified [ 68 ]. Overall, these data indicate that sCTA collateral assessment is an important tool for predicting radiological and clinical outcomes in AIS patients receiving IVT and/or EVT in early and late time windows. On the other hand, sCTA collaterals were also associated with clot characteristics as patients with good collateral score had longer thrombi [ 69 ] and elevated thrombus permeability [ 70 ], reflecting the presence of residual blood flow through the clot. Finally, a lower edema progression and a greater benefit from EVT in patients with large core have been reported in patients with good sCTA collateral filling [ 71 , 72 ].

mCTA collaterals

In the seminal work of Menon and associates the predictive value of mCTA collateral score for functional outcome was modest in AIS patients untreated or treated with IVT and EVT with or without IVT within 12 h of symptom onset [ 21 ]. This not excellent association of mCTA collateral assessment with prognosis was confirmed in two recent studies comparing the precision of different grading system applied to mCTA in identifying the degree of functional independence in patients receiving EVT in the same time window. In fact, no significant correlation with clinical outcome was seen for mCTA Menon and sCTA Miteff, Tan and Maas classifications in the first investigation [ 73 ], as well as for sCTA Menon and Tan scores in the HERMES analysis [ 74 ]. However, the evaluation of collateral filling with mCTA was successfully used as selection tool for AIS patients’ candidates for EVT within 12 h from stroke in the Endovascular Treatment for Small Core and Proximal Occlusion Ischemic Stroke (ESCAPE) trial [ 31 ] where patients with good collaterals undergoing EVT achieved more frequently a favorable outcome than controls treated with standard medical therapy. In agreement with these findings, data coming from subsequent studies documented the ability of mCTA scoring system in the prediction of functional outcome. A significant association between good mCTA collaterals and functional independency at 3 months was observed in patients treated within 4.5 after onset with EVT with or without IVT [ 25 ] and treated with standard medical therapy, IVT and/or EVT [ 24 ]. Next, recent publications showed that patients untreated or treated with EVT and/or IVT within 5 h [ 75 ], between 5 and 15 h [ 22 ] and within 24 h after ictus [ 28 ] who had a good mCTA collateral status at presentation achieved a favorable outcome. In addition, good mCTA collaterals were correlated with small FIV as delineated on NCCT or MR-DWI in patients receiving standard medical therapy, IVT and/or EVT within 4.5 [ 25 ], 12 [ 76 , 77 ] and 24 h of symptom onset [ 28 ]. Another association was found between good mCTA collaterals and small admission infarct core as estimated on NCCT Alberta Stroke Program Early Computed Tomography Score (ASPECTS) methodology or MR-DWI in patients untreated or treated with IVT and/or EVT within 8 [ 26 ] and 14 h after onset [ 30 ]. Finally, good collaterals on mCTA were also linked with slow infarct growth rate in patients treated with IVT and/or EVT within 6 h from symptom onset and achieving successful recanalization [ 33 ]. In addition, poor mCTA collaterals were independent markers of malignant infarction defined as development of a large space-occupying brain edema involving at least 2/3 of the MCA territory with ventricles’ compression or midline shift in patients not treated or treated with IVT and/or EVT within 4.5 h from onset [ 23 ].

Superiority of mCTA over sCTA

The main limitation of sCTA is the lack of temporal resolution since the acquisition based on a single time point can lead to an overestimation of collaterals when scans are obtained too late in the venous phase, due to a slow blood flow as a consequence of reduced cardiac output or cervical carotid artery stenosis, or an underestimation of collateral supply when scans are acquired too early in the arterial phase [ 2 , 6 , 15 ]. For the same reason, sCTA is unable to correctly visualize delayed collateral filling during the venous phase with the possibility of considering patients having good collaterals as patients with poor collaterals [ 6 ]. These misleading results can be overcome by mCTA that provides three time-resolved images allowing to explore collateral circulation not only in the arterial phase, but also in peak and late venous phases [ 6 , 21 ]. As a consequence, mCTA ensures a more accurate collateral assessment than sCTA, avoiding misclassification due to the appearance of delayed filling of collaterals in venous phases (Fig.  4 ). In addition, mCTA shows other advantages over sCTA such as higher interrater reliability and, more important, a superior accuracy in predicting functional outcome at 3 months as demonstrated in the original publication by Menon and associates [ 21 ]. Other studies repeatedly confirmed that mCTA is superior to sCTA as prognostic predictor in patients admitted at 4.5–15 h after symptom onset and treated with standard medical therapy and IVT and/or EVT [ 22 , 24 , 75 ]. In this regard, the stronger demonstration that mCTA improves outcome prediction compared to sCTA has been reported by Wang and collaborators [ 28 ] where mCTA resulted independently associated with functional outcome in patients untreated and treated with IVT and/or EVT within 24 h after onset, whereas sCTA did not. Intriguingly, mCTA outperforms sCTA also in the analysis of venous outflow at the level of cortical veins representing an indirect indicator of collateral extent and tissue perfusion. In fact, venous drainage reflects the ability of cortical venous system in containing the increased blood volume due to the opening of collaterals and then the effective blood flow traffic through cerebral microcirculation in the ischemic territory [ 1 , 11 , 78 , 79 , 80 ]. sCTA usually determines cortical venous filling according to the Cortical Vein Opacification Score (COVES) proposed by Jansen et al. in a post hoc analysis of MR CLEAN trial that is a qualitative 6-point scale in which the opacification of the superficial middle cerebral vein, the vein of Labbé and the sphenoparietal sinus is classified as complete absence (grade 0), moderate (grade 1) and full (grade 2) after comparison between occluded and unaffected territories. Grades 0–2 indicate poor venous outflow, whereas Grades 3–6 are considered good venous outflow [ 81 ]. Several publications reported a strong association of favorable venous outflow with good functional outcome, good collaterals, successful recanalization, lower risk for HT and lower edema progression in AIS patients receiving EVT with or without IVT between 6 and 16 h after symptom onset [ 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 ]. However, Singh and associates recently analyzed patients treated with IVT and/or EVT within 12 h from onset enrolled in Rapid Assessment of Collaterals Using Multi-Phase CTA in the Triage of Patients with Acute Ischemic Stroke for IV or IA Therapy (PRove-IT) multicenter cohort study [ 88 ]. They demonstrated that COVES also including the opacification of the vein of Trolard was more robust as outcome determinant than sCTA COVES. This novel classification, described as total venous score (TVS), is a qualitative 24-point scale in which the filling of the superficial middle cerebral vein, the vein of Labbé, the sphenoparietal sinus and the vein of Trolard is graded as no (grade 0), partial (grade 1) and full (grade 2) opacification in all three phases. The final score is generated by adding the opacification scores calculated in each mCTA phase. In particular, this study documented the relevance of venous opacification during mCTA second and third phases in the actual evaluation of venous filling, suggesting that venous outflow is a time-dependent phenomenon (Fig.  5 ). Based on these findings, although not without drawbacks as collateral filling could be reduced by flow-limiting proximal stenosis and poor cardiac function [ 6 , 21 ], mCTA is currently considered the method of choice for collateral assessment in early (0–6 h) and late (6–24 h) time windows for EVT [ 6 ].

figure 4

Multiphase CT angiography evaluates collaterals better than single-phase CT angiography. In the first arterial phase corresponding to single-phase CT angiography acquisition collaterals are erroneously judged as poor. On the contrary, the second peak venous phase reveals that collaterals are good. Green arrow shows occlusion site. Yellow arrows indicate collateral extent in the occluded hemisphere

figure 5

Opacification of sphenoparietal sinus (green arrows), superficial middle cerebral vein (yellow arrows) vein of Labbé (red arrows) and vein of Trolard (blue arrows) within the occluded territory in all three phases of multiphase CT angiography

Multi-phase CTA collateral-based selection for EVT

DEFUSE 3 [ 89 ] and DAWN [ 90 ] randomized controlled trials (RCTs) have recently demonstrated the utility of CTP in the identification of AIS patients suitable for EVT in late time window (6–24 h) and patients selected for EVT because of a favorable CTP profile achieved a good outcome more frequently than controls treated with standard care. In both trials, patients were treated if they satisfied specific optimal CTP-derived parameters, collectively named target mismatch, automatically calculated with a dedicated software (RAPID; Rapid Processing of Perfusion and Diffusion; iSchemaView, Menlo Park, CA) using prespecified CTP thresholds. More precisely, absolute time to the peak of the residual function (Tmax) values more than 6 s (Tmax > 6 s) was assumed to indicate critically hypoperfused tissue and relative cerebral blood flow (CBF) values less than 30% of normally perfused tissue (rCBF < 30%) were considered to delineate infarct core. However, despite the successful results of these RCTs, futile recanalization rates were of about 50% [ 91 ], suggesting that selection strategy should be improved. ESCAPE trial [ 31 ] showed that an mCTA-based selection for EVT could be a promising alternative. Therefore, some research groups have started to explore whether CTA was non-inferior to CTP in the identification of AIS patients who can benefit from EVT. mCTA was initially compared to CTP DEFUSE 3 and DAWN eligibility criteria for the selection of patients’ candidates for reperfusion therapies in two studies evaluating patients treated with EVT or standard medical therapy at 6–12 h after symptom onset from Prove-IT dataset [ 92 ] and at 6–24 h after stroke in a Korean single center [ 93 ]. In both studies, good collaterals and a good CTP profile were equivalent in predicting favorable outcome. A subsequent study reported that mCTA collaterals were not inferior to perfusion in determining outcome in patients treated with IVT and/or EVT within 24 h of onset [ 28 ]. Other two investigations substantially confirmed these findings. Functional outcome was comparable in patients receiving EVT selected with NCCT ASPECTS and mCTA at 6–12 h after onset in ESCAPE Na1 trial [ 94 ] and with CTP at 6–16 h and at 6–24 h from onset in DEFUSE 3 [ 89 ] and DAWN [ 90 ] trial, respectively. More recently, in a Selection Of Late-window Stroke for Thrombectomy by Imaging Collateral Extent (SOLSTICE) Consortium pooled analysis including patients overlapping DEFUSE 3 and DAWN trials as baseline characteristics treated with EVT, the selection with collateral and perfusion imaging showed a similar predictive value for clinical outcome [ 95 ]. However, the latest study of Tan et al. did not replicate these results and demonstrated that CTP selection criteria were superior than mCTA eligibility criteria in predicting outcome [ 96 ]. Therefore, the possibility that mCTA collateral guided can replace CTP-guided criteria in the selection of patients suitable for EVT in the late time window (6–24 h) still remains matter of debate. In this regard, the relationships between mCTA collateral-based and CTP-based selection criteria were well summarized by Ospel and colleagues which collected data from patients untreated and treated with IVT and/or EVT within 12 h of onset enrolled in Prove-IT study [ 97 ]. In this publication, infarct core was defined using three threshold values (rCBF < 30%, CBF < 7 mL/100 g/min, 10 and CBV < 2 mL/100 g) obtaining different results for CTP-guided selection according to the different CTP thresholds utilized. Patients considered eligible for EVT with combined CTP (small core + large penumbra) and mCTA (good collaterals) achieved favorable outcome in 62–87% of cases. In addition, mCTA eligibility criteria selected more patients (91%) than CTP eligibility criteria (7%-36%), but with lower good outcome rates (53–57%). Surprisingly, 51–62% of patients who were not eligible by either mCTA or CTP achieved a good outcome. Therefore, these findings suggest that, although the selection criteria are currently limited, the integration between mCTA collateral-based and CTP-based selection criteria could represent the best paradigm.

Future perspectives

In line with the observations emerged from the study of Ospel et al. [ 97 ], the recently proposed opportunity to generate CTP maps (delay maps) from mCTA could allow to combine mCTA and CTP data for EVT patient selection with the advantage of reducing acquisition time and radiation dose [ 98 , 99 ]. In the same way, it is now well-accepted that the fate of ischemic tissue depends not only on the amount of blood delivered by collaterals, but also on the blood volume flowing across the microcirculation and drained by venous system. Therefore, the simultaneous assessment of collateral extent by CTA with tissue-level collaterals by HIR and venous outflow by CTA, the so-called cerebral collateral cascade [ 100 , 101 ], may be a further option for improving our ability to identify AIS patients who actually benefit from reperfusion therapies.

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Winkelmeier L, Heit JJ, Adusumilli G, Geest V, Guenego A, Broocks G, Prüter J, Gloyer NO, Meyer L, Kniep H, Lansberg MG, Albers GW, Wintermark M, Fiehler J, Faizy TD (2023) Poor venous outflow profiles increase the risk of reperfusion hemorrhage after endovascular treatment. J Cereb Blood Flow Metab 43:72–83

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Goyal M, Menon BK, van Zwam WH, Dippel DW, Mitchell PJ, Demchuk AM, Dávalos A, Majoie CB, van der Lugt A, de Miquel MA, Donnan GA, Roos YB, Bonafe A, Jahan R, Diener HC, van den Berg LA, Levy EI, Berkhemer OA, Pereira VM, Rempel J, Millán M, Davis SM, Roy D, Thornton J, Román LS, Ribó M, Beumer D, Stouch B, Brown S, Campbell BC, van Oostenbrugge RJ, Saver JL, Hill MD, Jovin TG, HERMES collaborators (2016) Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet 387:1723–1731

Almekhlafi MA, Kunz WG, McTaggart RA, Jayaraman MV, Najm M, Ahn SH, Fainardi E, Rubiera M, Khaw AV, Zini A, Hill MD, Demchuk AM, Goyal M, Menon BK (2020) Imaging triage of patients with late-window (6–24 hours) acute ischemic stroke: a comparative study using multiphase CT angiography versus CT perfusion. AJNR Am J Neuroradiol 41:129–133

Kim B, Jung C, Nam HS, Kim BM, Kim YD, Heo JH, Kim DJ, Kim JH, Han K, Kim JH, Kim BJ (2019) Comparison between perfusion- and collateral-based triage for endovascular thrombectomy in a late time window. Stroke 50:3465–3470

Menon BK, Ospel JM, McTaggart RA, Nogueira RG, Demchuk AM, Poppe A, Rempel JL, Zerna C, Joshi M, Almekhlafi MA, Field TS, Dowlatshahi D, van Adel BA, Sauvageau E, Tarpley J, Moreira T, Bang OY, Heck D, Psychogios MN, Tymianski M, Hill MD, Goyal M, ESCAPE-NA1 investigators (2020) Imaging criteria across pivotal randomized controlled trials for late window thrombectomy patient selection. J NeuroInterv Surg 25, Online ahead of print

Almekhlafi MA, Thornton J, Casetta I, Goyal M, Nannoni S, Herlihy D, Fainardi E, Power S, Saia V, Hegarty A, Pracucci G, Demchuk A, Mangiafico S, Boyle K, Michel P, Bala F, Gill R, Kuczynski A, Ademola A, Hill MD, Toni D, Murphy S, Kim BJ, Menon BK, Selection Of Late-window Stroke for Thrombectomy by Imaging Collateral Extent (SOLSTICE) Consortium (2022) Stroke imaging prior to thrombectomy in the late window: results from a pooled multicentre analysis. J Neurol Neurosurg Psychiatry 93:468–474

Tan Z, Parsons M, Bivard A, Sharma G, Mitchell P, Dowling R, Bush S, Churilov L, Xu A, Yan B (2022) Comparison of computed tomography perfusion and multiphase computed tomography angiogram in predicting clinical outcomes in endovascular thrombectomy. Stroke 53:2926–2934

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Giorgio Busto, Edoardo Carlesi, Sara Mancini, Ivano Lombardo, Elisa Scola, Davide Gadda & Marco Moretti

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Busto, G., Morotti, A., Carlesi, E. et al. Pivotal role of multiphase computed tomography angiography for collateral assessment in patients with acute ischemic stroke. Radiol med 128 , 944–959 (2023). https://doi.org/10.1007/s11547-023-01668-9

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Clinical presentation and diagnosis of cerebrovascular disease.

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Chapter 30 Clinical Presentation and Diagnosis of Cerebrovascular Disease

Mark J. Alberts

Stroke is a common and serious disorder. Each year stroke affects almost 800,000 people in the United States and about 16 million people throughout the world. 1 Associated high morbidity and mortality provide impetus for improving diagnosis, acute management, and prevention of strokes. A full understanding of how patients with stroke and cerebrovascular disease come to medical attention, along with a logical approach for defining the mechanism of stroke, are needed for safe and effective implementation of acute therapies and prevention strategies. This chapter will focus on clinical manifestations of all types of cerebrovascular disease and how clinicians can approach diagnostic evaluation.

Overview of Clinical Stroke

Stroke and cerebrovascular disease are caused by some disturbance of the cerebral vessels in almost all cases. In simple terms, we can divide stroke into two major types: ischemic and hemorrhagic. Ischemic stroke is the most common variety and is responsible for 80% to 85% of all strokes; hemorrhagic stroke accounts for the remainder. 2 On occasion, an ischemic stroke can undergo secondary hemorrhagic transformation; likewise, a cerebral hemorrhage (particularly a subarachnoid hemorrhage [SAH]) can cause a secondary ischemic stroke via vasospasm.

Ischemic stroke occurs when a blood vessel in or around the brain becomes occluded or has a high-grade stenosis that reduces the perfusion of distal cerebral tissue. A variety of mechanisms and processes can lead to such occlusions and will be discussed later in more detail. On rare occasions, venous thrombosis can occlude a cerebral vein and lead to ischemic as well as hemorrhagic strokes (venous infarction).

Hemorrhagic stroke (intracerebral hemorrhage [ICH] and SAH) occurs when a blood vessel in or around the brain ruptures or leaks blood into the brain parenchyma (ICH) or into the subarachnoid space (SAH). It is not uncommon for there to be some overlap, such as an ICH also causing some degree of SAH and/or an intraventricular hemorrhage. Likewise, an SAH can produce some elements of an ICH if the aneurysmal rupture directs blood into the brain parenchyma. As with ischemic stroke, a variety of processes and lesions can produce ICH and SAH, but most affect integrity of the vessel wall in some way.

Clinical Manifestations of Stroke and Cerebrovascular Disease

Stroke is similar to real estate in that much of its presentation and prognosis depend on size and location. The area of brain involved dictates presenting symptoms. Blood vessels that supply different parts of the brain are affected by different types of cerebrovascular disease and have different mechanisms (pathophysiology) for the stroke. This concept greatly influences and defines the approach a vascular neurologist or neurosurgeon uses when assessing patients with a stroke or cerebrovascular disease. 3, 4

For example, a patient with evidence of involvement of the left hemispheric cortex (e.g., aphasia, visual field defect, weakness of contralateral face and arm) is likely to have a process involving the left middle cerebral artery (MCA). If head computed tomography (CT) does not show evidence of a hemorrhage, likely etiologies would include an embolic event from the heart (e.g., atrial fibrillation) or an artery-to-artery embolism (as might be seen with a high-grade lesion at the carotid bifurcation in the neck). Another patient with a pure motor hemiparesis but no other deficits is likely to have a lesion affecting the motor pathways in the internal capsule, often due to occlusion of a small penetrating artery (lenticulostriate vessel) deep in the brain. Most ischemic strokes will respect the vascular territory of one or more arteries. 5 Indeed, lesions that do not respect typical arterial territories lead to concern for a nonvascular process (e.g., tumor, infection). Common ischemic stroke syndromes can be found in Tables 30-1 and 30-2 .

Table 30-1 Common Large-Vessel Ischemic Stroke Syndromes

clinical presentations of stroke

Table 30-2 Common Lacunar Stroke Syndromes

clinical presentations of stroke

Evaluation of hemorrhagic stroke follows a similar logical assessment, but is further complicated by spread of the initial bleed, the effects of increased intracranial pressure, and other secondary effects that lead to neurological manifestations beyond the original injury. In this case, detailed cerebral imaging is vital for understanding the mechanism of the stroke and reasons for secondary worsening. The discussions that follow offer more detailed descriptions of common hemorrhagic stroke syndromes correlated with their likely anatomy and most likely pathophysiology.

Besides location of the stroke, the tempo of onset and progression of symptoms often provide valuable information about stroke etiology and mechanism. Stroke symptoms that progress in a casual manner with gradual onset and worsening over many minutes or longer often suggest a thrombotic process or hypoperfusion due to occlusion or stenosis of a larger proximal vessel. Such a leisurely progression can also be seen with stroke mimics such as complicated migraines or partial seizures. The converse is a stroke syndrome with sudden onset of maximal symptoms that remain stable; this suggests an embolic process such as a cardioembolic stroke due to atrial fibrillation.

Similar reasoning holds true for most cases of hemorrhagic stroke. Intracerebral hemorrhage often presents with abrupt onset of symptoms, but close questioning may reveal that symptoms actually progressed over 15 to 30 minutes as the hematoma grew and expanded. 6 Subarachnoid hemorrhage is often characterized by sudden onset of the worst headache of one’s life, with significant nausea, vomiting, and stiff neck in many cases. The phrase “worst headache of my life” is so characteristic of SAH that a patient who presents to the physician or emergency department with that symptom complex is assumed to have SAH until proven otherwise. 7

Transient Ischemic Attack

A transient ischemic attack (TIA) is often a prodrome to an ischemic stroke. Symptoms of a TIA are identical to those of a stroke, but with resolution within 24 hours (according to the old definition of a TIA). In reality, most TIA syndromes last just a few minutes, not many hours. In fact, modern brain imaging using magnetic resonance imaging (MRI) with diffusion-weighted sequences has now shown that 25% to 30% of patients with a TIA lasting 30 min to 2 hours will have a new diffusion-weighted imaging (DWI) lesion on MRI indicating a stroke based on a tissue definition. 8 Transient ischemic attack symptoms lasting 6 hours or longer have a 50% likelihood of having a new stroke on MRI with DWI techniques. Therefore the perceived distinction between a TIA and a stroke should be viewed more as a continuum from minor transient neuronal dysfunction to permanent brain infarction.

Although it was once thought that the risk of stroke after a TIA was low, new imaging studies as well as epidemiological studies have proven this is not the case. Based on purely clinical criteria (not MRI results), several recent studies have shown that after a TIA, 10% of patients will have a stroke within 3 months, and half those strokes (5%) will occur within 48 hours of the initial TIA. About 25% of patients with a TIA will have a stroke, myocardial infarction (MI), death, recurrent TIA, or be hospitalized within the next 3 months. 9 Based on these poor outcomes, recently published guidelines recommend hospital admission for patients with a recent TIA. 8

Further studies have attempted to better define those patients with a TIA who are at higher risk of having a stroke within the next 2 to 7 days. Several scoring systems have been developed ( Table 30-3 ) that may be useful for assessing such risks. Of course, any such assessment tool must be tempered by good clinical judgment and consideration of all clinical factors.

Table 30-3 Transient Ischemic Attack Scoring Systems

CT, computed tomography; MRI, magnetic resonance imaging.

From Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al: Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 369:283–292, 2007. 50

Several types of TIAs deserve special mention because of their unique presentations. One is sudden blindness in one eye, which typically occurs as a “shade coming down” over the eye. Some patients report a graying out of vision in the eye, like looking through a gray haze or cloud. This type of TIA is often referred to as amaurosis fugax . This symptom complex typically resolves in a few minutes, although it can last for several hours. There is sometimes pain in or around the eye, but patients usually do not have any other focal neurological complaints. Some cases of amaurosis are due to emboli to the retinal circulation from an ulcerated plaque in or near the carotid bifurcation in the neck. Other cases can be due to local disease in the ophthalmic artery or in the posterior ciliary artery that supplies the optic nerve. 10

The other unique type of TIA is the limb-shaking TIA . This typically involves the arm or leg on one side of the body. Patients report uncontrollable shaking of a limb that can be precipitated by movement. These spells can last seconds to minutes. They are not epileptic in origin; electroencephalogram (EEG) is unremarkable. These TIAs are associated with severe stenosis of the contralateral internal or common carotid artery. 11 Once the carotid artery is opened (usually with an endarterectomy), the spells cease.

Lastly is the topic of crescendo TIAs . This refers to a pattern where TIAs are recurrent, last longer, or are more severe in nature. This is a very worrisome type of TIA and is associated with a risk of stroke as high as 25% to 50% over the next few weeks. 12

Some hemorrhagic strokes may also have a TIA equivalent, namely the sentinel headache before a SAH. The sentinel headache present as an acute headache that is unusual in terms of its nature, severity, and onset. It typically lasts more than an hour but does not have other impressive focal neurological findings and resolves prior to the definitive SAH presentation. Sentinel headaches occur in 25% to 50% of patients with a subsequent aneurysmal SAH and typically antedate the SAH by days to weeks (average 2 weeks). 13, 14 It is thought that most of these headaches are due to either minor leakage from a fragile aneurysm or enlargement of the aneurysm, resulting in pressure on a nearby structure that produces pain.

Ischemic Stroke Syndromes

There are numerous manifestations of ischemic stroke, and they can be classified based on brain location involved, artery affected, or symptoms produced. Although advanced diagnostic techniques have altered some of the clinical rules of stroke symptoms and etiology, there are still some useful concepts that can guide us in terms of stroke location and mechanism. Tables 30-1 and 30-2 list some classic ischemic stroke syndromes with their major clinical manifestations, vascular territory, and underlying pathophysiology. 5

Broadly speaking, ischemic strokes typically involve one or more vessels or vascular territories and produce a clinical picture of focal neurological deficit. Typically, clinicians look for unilateral weakness or sensory deficits, unilateral visual field abnormalities, speech disturbance (aphasia or dysarthria), neglect syndromes, unilateral ataxia, ophthalmoplegias, or gaze abnormalities as clues of a stroke. Symptoms such as vague diffuse weakness alone, headaches alone, memory loss, abnormal behavior, or isolated dizziness are rarely caused by an ischemic stroke. The appearance of a lesion in a typical vascular territory (based on brain imaging) is a key feature of almost all stroke syndromes. 4

Presence of cortical deficits (aphasia, visual field cuts, neglect syndromes) often indicates involvement of a major cerebral vessel in the cerebral hemispheres. Presence of ataxia, bilateral motor or sensory deficits, Horner’s syndrome, ophthalmoplegias, and crossed sensory findings (one side of the face and the other side of the body) often indicates a stroke in the posterior (vertebral-basilar) territory. There are specific syndromes that indicate small-vessel involvement deep in the brain. These so-called lacunar strokes are due to occlusion of small penetrating arteries that arise directly from larger parent vessels. Favored locations include the deep basal ganglia structures, thalamus, and brainstem (pons). A listing of large-vessel and lacunar syndromes appears in Tables 30-1 and 30-2 .

Atherothrombosis accounts for the majority of ischemic strokes. These lesions can occur anywhere in the cerebral vasculature, but they tend to have a preference for specific locations such as the bifurcation of the carotid artery in the neck, intracranial carotid siphons, proximal portion of the middle cerebral artery, mid-portion of the basilar artery, and aortic arch. An atherosclerotic plaque forms over many years, then ruptures causing formation of a superimposed thrombus. 15 This atherothrombotic lesion can totally occlude the vessel, produce severe narrowing (leading to watershed ischemia), or be a source of embolic material that embolizes to more distal parts of the cerebral vasculature (artery-to-artery emboli).

Cardiac embolism accounts for 15% to 20% of all ischemic strokes. A variety of conditions such as atrial fibrillation, endocarditis, prior myocardial infarction, valvular disease, and cardiomyopathy often lead to formation of intracardiac thrombi that subsequently embolize to the brain (and other organs). 4, 16 Most lacunar strokes are due to either lipohyalinosis or microatheromata occluding a small penetrating artery.

Special Cases

Ischemic stroke in young adults.

All clinicians see young adults (often defined as ≤ 45 years of age) with ischemic strokes. Such cases often entail a special evaluation because of the unique processes and conditions that can produce strokes in this age group. Many case series have examined the diseases leading to ischemic strokes in the young, and in general they fall into a few major categories: (1) premature atherosclerosis, (2) unusual vascular pathologies, (3) cardiac etiology, (4) coagulopathy, and (5) other diseases. 17

Premature atherosclerosis typically occurs in patients with risk factors for atherosclerosis; in some cases these have not been diagnosed or not properly treated. Examples include hypertension, hyperlipidemia, diabetes, smoking, and obesity. The types of uncommon vascular pathologies often seen in young adults with a stroke include dissection of a vessel (often not related to any obvious trauma), fibromuscular dysplasia, moyamoya disease, or a vasculitis related to an inflammatory condition or drug abuse. 17 Numerous cardiac processes can lead to strokes in the young, such as congenital heart disease, a patent foramen ovale (particularly with evidence of venous thrombi), valvular disease (infectious or inflammatory), cardiomyopathy, myxoma, papillary fibroelastoma, and many others. Myriad clotting disorders have been associated with strokes in young adults, the most common being lupus anticoagulants, anticardiolipin antibodies, and protein C and protein S deficiency. 18 In general, these coagulopathies are more likely to cause venous thrombosis than arterial thrombosis. Clotting disorders related to hematological malignancies can cause both ischemic and hemorrhagic strokes. 19 Various systemic diseases are also associated with hypercoagulable states such as inflammatory bowel disease, hemoglobinopathies, elevated homocysteine, and cancer.

The “other” category covers a host of conditions, some rare and some common, that cause strokes in young adults. Migraine headaches and pregnancy are the most common of these. Patients with complex or complicated migraines, prolonged auras, or taking contraceptives have a higher risk of stroke. 20 Pregnancy, particularly in the third trimester and up to 3 months postpartum is associated with increased stroke risk, particularly venous thrombosis and cerebral hemorrhage. 21, 22 Drug abuse is another common cause of ischemic and hemorrhagic strokes in young adults. 23 Other rare conditions include CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke), isolated central nervous system (CNS) vasculitis, Sneddon syndrome (combination of a livedo reticular rash, antiphospholipid antibodies, and ischemic stroke), Marfan’s syndrome, and a host of others (especially connective tissue disorders) have been known to cause strokes in this population.

Strokes Related to Systemic Disease

Numerous systemic disorders are important and potent risk factors for stroke: hypertension, diabetes, hyperlipidemia, smoking, heart disease (atrial fibrillation, myocardial infarction, valvular disease, etc.), drug abuse, and others. These have been covered in other chapters of this book. Our focus here is on specific systemic disorders that lead to specific or unusual types of strokes.

There are a number of unique systemic disorders that cause strokes in patients of any age. Autoimmune diseases, such as lupus, can produce strokes through a variety of mechanisms that include advanced or premature atherosclerosis, vasculitis, hypercoagulable states, and cardioembolic events. 24 Sickle cell disease (SCD) also leads to ischemic strokes and hemorrhagic strokes due to myriad processes including a large-vessel arteriopathy, small-vessel occlusion, rupture of moyamoya vessels (producing ICH and/or SAH), and accelerated atherosclerosis due to hypertension and renal failure. 25, 26

Drug abuse, particularly cocaine, can produce ischemic strokes via a number of processes including vasospasm, cardiac emboli (due to cardiomyopathy), hypertension, and endocarditis. 27 Drug abuse can produce an ICH or SAH due to extreme hypertension and necrotizing vasculitis. It is a fallacy to assume that drug abuse only occurs in young patients or those from certain demographic groups. All patients admitted with a stroke should be tested for drug abuse with urine toxicology screens, not excluding those older than 50 years and white-collar professionals.

Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) is now recognized as increasing the risk of stroke. This is partially because patients with HIV/AIDS are living longer, and some are having strokes as a result of accelerated development of typical stroke risk factors. It is also clear that modern drug therapy for AIDS can increase the risk of stroke (particularly ischemic stroke). 28, 29

Systemic cancer is a commonly overlooked cause of strokes. Sometimes the stroke diagnosis precedes diagnosis of the underlying cancer. Mechanisms for strokes related to cancer include a hypercoagulable state and nonbacterial thrombotic endocarditis. Oftentimes these strokes are multiple, variable in size, and in different vascular territories. 30, 31 Such patients may also have deep venous thrombosis (DVT). Liver failure appears to increase risk of ischemic and hemorrhagic stroke.

Intracerebral Hemorrhage

In broad terms, ICH can be divided into traumatic and nontraumatic etiologies. This chapter will focus on nontraumatic ICH, since ICH related to trauma is not routinely considered a stroke. Intracerebral hemorrhage is typically caused by rupture of a blood vessel within the brain parenchyma. Patients typically develop a focal neurological deficit suddenly, but symptoms often evolve over 10 to 30 minutes as the hematoma gradually expands. Headache is commonly present, and the vast majority of patients have markedly elevated blood pressure (often in excess of 200 mmHg systolic) even without a prior history of hypertension. Nausea and vomiting can also occur, particularly with ICH that involves the brainstem and/or cerebellum.

Chronic or acute hypertension is the most common etiology for nontraumatic ICH, and this type of bleed typically occurs in specific brain locations ( Table 30-4

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Clinical presentation of vertebrobasilar stroke

Vanessa carvalho.

a Department of Neurology, Hospital Pedro Hispano/Unidade Local de Saúde de Matosinhos, Matosinhos

Vitor Tedim Cruz

b Epidemiologic Research Unit, Public Health Institute, University of Porto, Porto, Portugal.

Vertebrobasilar (VB) stroke is responsible for 20% of all strokes and transient ischemic attacks. Due to the vast cerebral territory it supplies, VB ischemia can present with a wide range of symptoms and signs, sometimes even overlapping with carotid circulation stroke. Furthermore, brain computed tomography, usually performed as initial imaging modality, has a suboptimal visualization of the posterior fossa, making VB stroke an even more challenging diagnosis to any physician. Hence, awareness of the vertebrobasilar anatomy and the clinical presentation of VB ischemia is crucial to promote early recognition of this disorder.

Introduction

It is estimated that nearly a fourth of all transient ischemic attacks (TIA) and strokes occur in the vertebrobasilar (VB) vascular territory. 1 Although traditionally VB stroke is regarded as having a more benign outcome when compared to anterior circulation stroke, data is still conflicting, with some studies showing a higher impairment in VB stroke patients, 2 with 21% of death or major disability at 3 months. 3

Furthermore, screening tools commonly used to assess patients likely to have an acute stroke, such as the Face Arm Speech Test, or to determine patients with TIA or minor stroke with high risk of recurrence (ABCD2 score) have been primarily evaluated in groups of unselected patients with ischemic events, most of them with anterior circulation strokes. Thus, both scales are less effective in the diagnosis and identification of high risk cases of posterior circulation ischemic events, 4 highlighting the importance of the recognition of the VB stroke presentation.

Our purpose is to review the anatomy and the clinical presentation of VB stroke.

The VB vascular system comprises the vertebral, basilar and posterior cerebral arteries and their branches. It feeds the posterior region of the brain, including the brainstem, the thalamus, the cerebellum and areas of the occipital and temporal lobes. 5

Starting with the vertebral artery, which arises from the subclavian artery on each side, it divides into 4 segments, 3 extracranial and 1 intracranial. The first segment (V1) follows the origin of artery until the entrance in the transverse process of the fifth or sixth cervical vertebrae. The second part (V2) courses within the intervertebral foramina, exiting behind the atlas, giving rise to the third portion (V3) that runs in the direction of the foramen magnum. After piercing the dura and arachnoid at the base of the skull, the fourth segment runs intracranially, and meets the contralateral artery at the midline, in the medullo-pontine junction, to form the basilar artery. This fourth segment gives rise to the posterior inferior cerebellar artery and to the anterior spinal artery (ASA). Of note, asymmetry in diameter is common in the vertebral arteries, and atresia can occur in 15% of the normal individuals. 6

Cranially, the basilar artery runs in the ventral surface of the pons and gives rise to several important branches, namely the pontine branches, both paramedian, short circumferential and long circumferential, the anterior inferior cerebellar artery and the superior cerebellar artery (SCA). At the interpeduncular fossa, after giving rise to the SCA, the basilar artery divides into the 2 posterior cerebral arteries (PCA). In most patients, the latter often receive contribution from the anterior circulation through the posterior communicating artery. Moreover, in 10% of individuals, PCA arises solely from the carotid artery, the “fetal variant” of the PCA. 7 The PCA is responsible for the vascular supply of the posterior temporal and occipital cortex, and also gives small branches to the midbrain, thalamus, hypothalamus and corpus callosum. 5 , 8

Caplan et al, further divided the vertebrobasilar system into proximal intracranial, middle intracranial and distal intracranial territories. Each one implies a different probability of stroke. 3 , 9

Clinical presentation

Regarding the clinical presentation of VB stroke, in a clinical series of 407 patients, the most common symptoms experienced by patients were dizziness (47%), unilateral limb weakness (41%), dysarthria (31%), headache (28%), vomiting and nausea (27%); as for clinical signs, the most frequent were unilateral limb weakness (38%), gait ataxia (31%), unilateral limb ataxia (30%), dysarthria (28%) and nystagmus (24%). 10 Hence patients with VB ischemia can present not only with symptoms and signs suggesting posterior circulation but also with symptoms that overlap with carotid system ischemia or with unspecific symptoms such as nausea, vomiting and headache. Signs and symptoms that should prompt us to suspect of VB ischemia are vertigo, ataxia or gait unsteadiness, bilateral sensorimotor deficit, respiratory disfunction, consciousness impairment, cranial nerve (CN) impairment and crossed deficits. 8 However, most patients do not present with a single symptom or sign but with a cluster of manifestations, mirroring the ischemic area. This syndrome can help us to localize the stroke and also to deduce the underlying mechanism: for instance, medial strokes in the brainstem are usually due to lesions of the paramedian branches of the basilar or vertebral artery, and hence due to small vessel disease, while lateral strokes are more likely indicative of disease of the larger circumferential vessel that supplies the region.

Before we discuss the posterior circulation syndromes (see Table ​ Table1), 1 ), we must understand the organization of the brainstem. The brain derives from the anterior end of the neural tube. The neural tube has a ventral portion (basal plate) and a dorsal portion (alar plate). The basal plate will contain the motor neurons and the alar plate will contain the sensory neurons. The development of the fourth ventricle will displace the alar plates laterally, hence the CN nuclei that are ventral and medial are motor and those that are dorsal and lateral are sensory. 11

Vertebrobasilar ischemic syndromes

AICA = anterior-inferior cerebellar artery, ASA = anterior spinal artery, ICP = inferior cerebellar peduncle, LGN = lateral geniculate nucleus, MCP = middle cerebellar peduncle, MGN = medial geniculate nucleus, MLF = Medial longitunal fasciculus, PCoA = posterior communicating artery, PICA = posterior-inferior cerebellar artery, PPRF = Paramedian pontine reticular formation, SCA = superior cerebellar artery, SCP = superior cerebellar peduncle, VA = vertebral artery. 15 , 19

Furthermore, we can localize the cranio-caudal level of the lesion using the impaired CN: if there is sign of dysfunction of the glossopharyngeal, vagus, accessory, or hypoglossal (IX–XII) nerves/fascicles, the lesion must lie in the medulla; if the abducens, the facial or the vestibulocochlear (VI–VIII) nerves are impaired, it localizes to the pons and, if there are signs of dysfunction to the oculomotor or the trochlear nerve (III and IV), the lesion is likely in the midbrain. Of note, the trigeminal complex has 3 nuclei that extend from the midbrain until the upper cervical cord, so isolated facial sensory impairment itself does not localize the lesion. Each section of the brainstem can be further divided into 3 longitudinally organized regions: the basis, more anteriorly, where the corticospinal and corticobulbar tracts lie, the tegmentum, in the middle, where we can find most structures, including the CN nuclei and the sensory pathways, and, lying more dorsally, the roof or tectum. 8 , 12

Medullary infarctions can be grossly divided into medial and lateral, the latter being far more frequent. 13 Medial medullary stroke (or Dejerine syndrome) is usually due to occlusion of the ASA or of median branches of the vertebral artery. The clinical presentation comprises contralateral hemiparesis (pyramidal tract), contralateral loss of vibration and postural sensation (medial lemniscus) and ipsilateral paresis of the tongue (hypoglossal nucleus/fascicle). 14 Lateral medullary infarct (or Wallenberg syndrome), is usually incomplete, and the classical triad includes ipsilateral Horner syndrome (descending sympathetic pathway), ipsilateral ataxia (inferior cerebellar peduncle) and contralateral hemisensory loss (ascending spinothalamic tract). 15 Patients can also present ipsilateral intention tremor (inferior cerebellar peduncle), ipsilateral facial sensory impairment (spinal tract and nucleus of the trigeminal nerve), saccadic lateropulsion (characterized by an undershoot of contralaterally directed saccades, overshoot of ipsilaterally directed saccades and ipsilateral deviation of vertical saccades), 16 vertigo, nausea and contralateral nystagmus (vestibular nuclei), dysgeusia (solitary nuclei) and paralysis of the ipsilateral palate, dysarthria and dysphonia (ambiguus nuclei). Other possible clinical symptoms from lateral medullary dysfunction are palatal myoclonus (inferior olive) and skew deviation and diplopia due to lesion to the vestibular nuclei. 17 When both medial and lateral medulla are afflicted, usually due to a VA occlusion, a hemimedullary syndrome (or Babinski syndrome) occurs, with simultaneous contralateral hemiparesis and hemisensory loss, ipsilateral ataxia, Horner syndrome, facial sensory loss, tongue weakness and dysarthria. 8 , 18

The pons can be divided into 4 groups, according to its vascular supply: the anterior (further divided into anteromedial and anterolateral), lateral and tegmental regions. Infarction in the anteromedial and anterolateral region are usually due to occlusion of paramedian and circumferential pontine branches of the basilar artery. Lesions in this region can damage the corticobulbar, corticopontocerebellar and corticospinal tracts, leading to contralateral hemiplegia or hemiparesis, facial palsy, ataxia, dysphagia, dysarthria and, less frequently loss of proprioception (medial lemniscus), ipsilateral peripheral facial palsy (facial nucleus/fascicle), ipsilateral lateral rectus palsy (abducens fascicle) and paresis of ipsilateral horizontal gaze (abducens nucleus). If the Medial longitunal fasciculus (MLF) is damaged, the patient can present with internuclear ophthalmoplegia (INO): the ipsilateral eye is unable to adduct, and the contralateral eye can abduct but has horizontal nystagmus when gaze is directed to the contralateral side. Convergence is usually preserved. The classical brainstem syndromes of Raymond and Millard-Gubler can occur due to ventromedial pontine infarctions and are further described in Table ​ Table1. 1 . Ventrolateral infarctions are rarer and contain the same structures as the ventromedial region so their presentation is usually similar. However, when a stroke is purely ventrolateral, due to the somatotopic organization of the pyramidal tract (face and arms more medial and the legs represented more laterally), there is a disproportionate impairment of the lower limbs. Dorsolateral pons stroke is characterized by ipsilateral ataxia (middle cerebellar peduncle, pontocerebellar fibbers), contralateral loss of pain and temperature of the limbs and trunk (lateral spinothalamic tract), ipsilateral tinnitus and reduced auditory acuity, ipsilateral peripheral facial palsy (facial nucleus/fascicle), loss of facial sensation (trigeminal principal nucleus), paresis of ipsilateral masticatory muscles (trigeminal motor nucleus), vertigo, nausea, vomiting (vestibular nuclei) and ipsilateral lateral rectus palsy. The syndromes of Marie-Foix and Foville and Raymon-Cestan can result of lateral pontine strokes and are described in Table ​ Table1. 1 . Tegmental lesions are very unusual and usually consist of consciousness impairment, ataxia, skew deviation, vertigo, Abducens nerve palsy and one and a half syndrome. Bilateral medial lesions of the pons cause “locked-in” syndrome: due to lesion of the cortico-bulbar and corticospinal fibers and of the abducens nucleus in a quadriplegic patient, unable to perform horizontal gaze movement, but conscious and able to communicate only through vertical eye movements and blinking. 8 , 10 , 18

Lesions in the basis of the mesencephalon, supplied by proximal branches of the PCA, cause the classical Weber syndrome, with palsy of the ipsilateral oculomotor nucleus (oculomotor fascicle) and contralateral hemiparesis (pyramidal tract). Lesions in the oculomotor nerve can be further divided into nuclear or infranuclear/fascicular. 19 Fascicular oculomotor lesions usually are characterized by ipsilateral involvement of all the oculomotor innervated muscles, sparing the contralateral eye but the degree of impairment of each subtype of ocular muscle palsy might vary, and hence produce a partial oculomotor palsy. 19 Conversely, in nuclear lesions there is unilateral palsy of the third CN associated with weakness of the ipsilateral and contralateral superior rectus muscle (due to crossed innervation of the medial subnucleus that innervate this muscle) and bilateral incomplete ptosis (since a single caudal subnucleus innervates both elevator palpebrae superioris). However, fascicular lesions are often accompanied by nuclear lesions because the paramedian branches of the top of the basilar artery often supply both structures. 20

A lesion in the tegmentum will additionally cause contralateral involuntary movements, such as chorea, tremor or athetosis due to lesion to red nucleus (Benedikt's syndrome) or ipsilateral ataxia when involves the superior cerebellar peduncle (Claude's syndrome). 18 Lesions to the tectum of the midbrain can cause Parinaud's syndrome, which is characterized by loss of vertical gaze (with upgaze more severely impaired), convergence-retraction nystagmus, convergence impairment, pupillary light-near dissociation and eyelid retraction (Collier's sign). 18 Similar to “locked-in-syndrome”, emboli can lodge in the distal BA and cause bilateral ischemia in the midbrain, thalamus, and temporal and occipital lobes. Patients present with combined symptoms of the ischemic regions, with vertical gaze palsy, pupillary abnormalities, consciousness fluctuation and delirium, vivid visual hallucinations (“peduncular hallucinosis”), visual field defects, and motor and sensory deficits. 21 , 22

Occipital infarction, usually due to ACP embolism, usually presents with visual field defects, either contralateral homonymous hemianopia or contralateral inferior or superior quadrantanopia, if the lesion is in the supra or infracalcarine sulcus, respectively. Bilateral lesions can cause cortical blindness or even Anton syndrome, in which the patient, although blind, denies the deficit and has visual hallucinations or confabulates. Bilateral watershed lesions in the parietooccipital junction can cause Balint syndrome, in which patients experience optic ataxia (inability to reach targets using visual guidance), oculomotor apraxia (inability to voluntarily direct gaze), and simultagnosia (described as the inability to synthesize objects within a visual field). 22

Finally, the VB circulation also supplies the thalamus trough branches from the first (P1) and second (P2) segments of the ACP. Thalamic strokes can have a wide range of clinical presentations, according to the affected nuclei groups. The most common presentation is hemisensory deficit in all the sensory modalities, frequently accompanied by motor deficit due to the proximity to the internal capsule, but thalamic aphasia and behavior abnormalities can occur if the anterior nuclei are involved, 23 as well as visual field defect, tremor or acute impaired consciousness, particularly in bilateral thalamic lesions. 24 Thalamic vascular syndromes are further explained in Schmahmann's “Vascular syndromes of the thalamus” 24 or in Powel and Hughes’ “A chamber of secrets—The neurology of the thalamus: lessons from acute stroke”. 25

The different posterior circulation syndromes are also described in Table ​ Table1 1 .

Diagnostic workup and ancillary tests

Brain computed tomography (CT), the most frequently available imaging technique in the emergency department, has a poor sensitivity for the posterior fossae. 26 Hence an MRI, in particular diffusion-weighted imaging (DWI), is a much-preferred imaging scan when a VB stroke is suspected. However, in a recent metanalysis, 6.8% of all acute ischemic events were negative, and posterior circulation stroke was 5-times more likely to be negative on DWI. 27 In fact, in another recent study, 13.7% of the clinically suspected strokes were DWI negative, and 30% of these were located in the brainstem, 28 highlighting the importance of the clinical diagnosis.

As for stroke etiology and subsequent etiological work-up, most frequent mechanisms are embolism, large artery thrombosis and lipohyalinosis. 3 ,29 If we divide the most frequent etiology by the different vascular territories (proximal, middle and distal), half of the proximal territory infarctions are caused by cardiac and artery-to-artery embolism (from the extracranial vertebral arteries), while the other half is explained by hypoperfusion due to intracranial vertebral occlusive disease. Middle territory stroke is usually due to occlusive lesions of the basilar artery or its branches and more distal territory lesions are attributable to embolism (both cardiogenic or artery-to-artery), the remainder being explained by small vessels disease. 9 Involvement of both distal and middle regions (either alone or in combination) are associated with a greater risk of death or major disability. 3

Therefore, a comprehensive etiology workup must be performed in all patients, including endovascular imaging, echocardiogram and cardiac rhythm monitorization. Also, one should never forget that some rarer causes of stroke or stroke mimics have some preference for the posterior circulation and should be considered in the proper context 5 —this include vertebral dissection, subclavian steal syndrome, giant cell arteritis, mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and posterior reversible encephalopathy syndrome (PRES) (see Table ​ Table2 2 ).

Rare causes of vertebrobasilar stroke

MELAS = mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, PRES = posterior reversible encephalopathy syndrome, VA = vertebral artery, Yo = years-old. 5

Vertebrobasilar stroke often presents as a clinical challenge to the emergency department physician. It is a non-neglectable cause of morbidity and mortality in stroke patients, which can be avoided or minimized with correct recognition and treatment.

The clinical presentation is wide, from mild unspecific symptoms to catastrophic presentations such as locked-in-syndrome or top of the basilar syndrome. Furthermore, the lower sensitivity of brain CT for the posterior fossae and the higher probability of a DWI-negative MRI in these patients, make a high level of suspicion crucial in these patients, in order to recognize and treat VB stroke.

Conflicts of interest

The authors declare no conflicts of interest.

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