Cerebrovascular Accident/Transient lschemic Attack Case File

Cerebrovascular Accident/Transient lschemic Attack Case File

Eugene C. Toy MD, Donald Briscoe, MD, FA  AFP, Bruce Britton, MD, Joel J. Heidelbaugh, MD, FA  AFP, FACG

Case 44

A 60-year-old man is brought to the emergency room by ambulance because of slurred speech and left-sided weakness. His wife states the patient went to bed at approximately 11 PM the night before and was well. At 5 AM, the time they usually get up, she noticed that he had some difficulties talking and moving his left arm and leg. They arrived at the emergency department (ED) at 6 AM. He has history of long-standing hypertension (HTN), a heart attack 10 years ago, high cholesterol, and obesity. He is taking baby aspirin, an angiotensin-converting enzyme (ACE) inhibitor, and a statin on a daily basis. He consumed alcohol heavily in the past, but stopped drinking completely after the heart attack. He has smoked a half pack of cigarettes daily since his teenage years. His wife remembers that about 3 months ago he complained of mild bilateral leg pain during their morning walk and had to stop after 15 minutes. Also, she remembers that 1 month ago he had a "slight right eye blackout" for 5 minutes.

On presentation to the ED his blood pressure is 195/118 mm Hg, his pulse is 106 beats/min, his respiratory rate is 18 breaths/min, his temperature is 99.8°F (37.6°C), and his oxygen saturation is 97% on room air. Although his pupils are equally round and reactive and the ocular movements are intact, he is unable to turn his eyes voluntarily toward the left side. His neck is supple, there is no jugular venous distension, and there are no bruits. His lungs are clear, heart sounds regular without murmurs, and abdomen is nontender and unremarkable. His extremities are warm, but distal pulses in his feet are difficult to palpate. The neurologic examination reveals that he is awake, alert, and oriented, although he does not recognize that he is ill. He is right-handed, and shows loss of awareness and attention with respect to objects or stimuli on his left side. He has mild dysarthria, but his speech is fluent and he understands and follows commands appropriately. There is mild weakness on the left side of the face and left-sided homonymous hemianopsia, but there is no nystagmus or ptosis, and no tongue or uvula deviation. He is not able to move his left arm and leg, has hyperreflexia, and his left great toe is upgoing on Babinski test.

⯈ What is the most likely diagnosis?

⯈ What is your next diagnostic step?

⯈ What is your next step in therapy?

ANSWER TO CASE 44

Cerebrovascular Accident/Transient lschemic Attack

Summary: The patient is a 60-year-old, right-handed man with history of coronary artery disease, hypertension, and hypercholesterolemia, who presents to the emergency room with a 5-hour history of slurred speech and an inability to move his left arm and leg. He had an episode of amaurosis fugax (fleeting, painless, transient monocular vision loss) in his right eye 1 month prior to presentation of these symptoms. On physical examination, although he is alert and oriented, he has no awareness of his disability (anosognosia) and exhibits left-sided neglect, as well as significant hypertension, dysarthria, and left hemiparesis. He also has left-sided homonymous hemianopsia, conjugate rightward gaze deviation, left hemifacial weakness, and left hyperreflexia.

• Mostlikely diagnosis: Cerebrovascular accident (CVA).
• First diagnostic step: Obtain a STAT computed tomography (CT) scan of the brain without contrast.
• Next step in therapy: Determine advisability for acute treatment with thrombolytic agents.

ANALYSIS

Objectives

1. Recognize the significance of a correct diagnosis and evaluation of transient ischemic attacks (TIAs) and CVAs based on risk factors.
2. Recognize the conditions that can mimic a TIA or a stroke.
3. Understand that the clinical evaluation gives the most important clues about diagnosis of TIA or stroke.
4. Be familiar with the accepted approach for the early management of patients with ischemic stroke.
5. Be familiar with the current strategies for prevention of ischemic stroke and TIA.

Considerations

This 60-year-old patient has developed focal neurologic deficits, which is the common presentation of a patient with a stroke. Considering that he has a history of uncontrolled hypertension, hypercholesterolemia, and vascular manifestations of atherosclerosis such as coronary artery disease and peripheral vascular disease (lower extremity claudication), ischemic stroke is the most worrisome and probable diagnosis. Furthermore, he had a TIA (amaurosis fugax) 30 days prior to presentation, which places him at an even greater risk for an ischemic stroke. His neurologic deficits are compatible with an ischemic stroke in the territory of the right middle cerebral artery, which is his nondominant hemisphere, and the reason why he is not aphasic.

Of immediate importance, after securing ABCs (airway, breathing circulation), the clinician should confirm that the neurologic impairments are secondary to an ischemic stroke and not other conditions, specifically an intracranial hemorrhage. A brain CT without contrast should be obtained as soon as possible to exclude hemorrhage, tumor, abscess, and mass effect. Serum glucose, urine toxicology screen, coagulation studies, serum electrolytes, renal function tests, lipid profile, and a complete blood count (CBC) are also indicated. A 12-lead ECG should be obtained to exclude acute myocardial infarction or arrhythmia such as atrial fibrillation, and the patient should be placed on telemetry.

Since it has been more than 3 hours from the onset of symptoms, this patient is not a candidate for thrombolytic therapy. Although this patient's blood pressure is markedly elevated, in the setting of an acute ischemic CVA, blood pressure management should be cautious, as compensatory hypertension can be permitted to avoid increasing risk of ischemic injury from hypoperfusion.

This patient should be admitted to the hospital for further evaluation and management, preferably to a dedicated stroke unit if available. Aspirin should be given within 48 hours of the onset of stroke, and deep venous thrombosis (DVT) prophylaxis should be started with low-molecular-weight or unfractionated heparin. However, anticoagulation with heparin or warfarin for treatment of the infarction itself has a poor risk-benefit ratio and is not indicated. An evaluation of the patient's speech and swallowing function and an early physiotherapy consultation should be obtained. Further imaging with brain magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), or CT angiography can help to clarify the etiology of the stroke and guide treatment. In this patient, carotid duplex ultrasonography is indicated because he had an episode of amaurosis fugax, caused by a blockage of the ophthalmic artery which branches from the internal carotid artery.

Management of this patient's chronic medical conditions, to reduce his risk of subsequent strokes, is critical. In this patient, these measures include tight control of his hypertension and hypercholesterolemia, along with immediate smoking cessation. Since this patient had a stroke while taking daily aspirin, an alternative antiplatelet agent should be considered to prevent another stroke.

Approach To:

CVA/TIA

DEFINITIONS

TRANSIENT ISCHEMIC ATTACK: A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. There is no time cutoff that reliably distinguishes whether a symptomatic ischemic event will result in ischemic infarction.

TRANSIENT SYMPTOMS WITH INFARCTION (TSI): A transient episode of neurologic dysfunction associated with irreversible ischemic brain injury as evident by imaging changes even after resolution of symptoms.

ISCHEMIC STROKE: An infarction of the central nervous system with resultant neurologic deficit that persists beyond 24 hours or is interrupted by death within 24 hours.

HEMORRHAGIC STROKE: Central nervous system (CNS) damage secondary to intracerebral or subarachnoid hemorrhage. This is the etiology of 13% to 20% of strokes in the United States.

CLINICAL APPROACH

There are over a million people who suffer a stroke in the United States each year, and the incidence of TIA approaches 500,000 per year. Strokes remain the third leading cause of death in North America and are a major cause of disability. TIA is defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. Most TIAs last for less than 1 hour. A stroke is presumed to have occurred if the symptoms persist for more than 24 hours. However, there is an unreliable correlation of symptom duration with actual infarction. Patients with a TIA are at increased risk of a subsequent stroke. The reported occurrence of a stroke after a TIA is as high as 5.3% within 2 days and 10.5% within 90 days. Patients with a TIA often require hospital admission, further evaluation, and the same long-term management as stroke patients. An assessment called the ABCD2 score (Age, Blood pressure, Clinical features, Duration of symptoms, and Diabetes) can be used to identify patients at high risk of ischemic stroke in the first 7 days after TIA.

    The ABCD2 score is as follows:

Age ( > 60 years= 1 point)

Blood pressure elevation when first assessed after TIA (systolic >140 mm Hg or

diastolic > 90 mm Hg = 1 point)

Clinical features (unilateral weakness = 2 points; isolated speech disturbance = 1 point; 

other = 0 points)

Duration of neurologic symptoms ( > 60 minutes = 2 points; 10 to 59 minutes= 1 point;

<10 minutes= 0 points)

Diabetes (present = 1 point)

    Estimated 2-day stroke risk determined by the ABCD2 score are as follows:

Score 0 to 3: Low stroke risk (1%)

Score 4 to 5: Moderate risk ( 4%)

Score 6 to 7: High risk (8%)

Hypertension is the single most important risk factor for stroke, and the incidence of stroke in the United States has decreased partly as a result of better efforts to control hypertension in the past few decades. Other risk factors include diabetes mellitus, older age, male sex, family history, dyslipidemia, tobacco abuse, alcohol abuse, cocaine abuse, and prothrombotic disorders. Many cardiovascular conditions also predispose people to stroke, usually through formation of an embolic

clot. These conditions include atrial fibrillation, myocardial infarction, endocarditis, carotid stenosis, rheumatic heart disease, presence of a mechanical valve, advanced dilated cardiomyopathy, and a patent foramen ovale or atrial septal defect which can expose the systemic arterial system to a paradoxical embolus from a venous source. Sickle cell disease is also a risk factor for stroke and patients with this condition commonly experience their strokes as children.

Ischemic strokes are generally classified as being of thrombotic or embolic origin. Strokes that affect the small branches of the main arteries of the brain are termed lacunar infarcts or small-vessel strokes. These strokes often forewarn a larger, more debilitating stroke. The causes of the emboli are usually of cardiovascular origin and include the previously mentioned conditions as well as dissection of various vessels. While most emboli result from blood clots, emboli can also occur from vegetations from infective endocarditis, sterile vegetations from Libman-Sacks endocarditis (which occurs in systemic lupus erythematosus), and marantic endocarditis (which occurs with cancer).

DIAGNOSIS AND EVALUATION

Sudden onset of focal neurologic deficits is the usual presentation of stroke patients, although some patients can have a gradual worsening of symptoms. Unless there is a hemispheric infarction, basilar artery occlusion, or cerebellar stroke with edema, nearly all of the patients are alert. If the middle cerebral artery territory is affected, the patient will generally experience aphasia (when the dominant hemisphere is involved), contralateral hemiparesis, sensory loss, spatial neglect, and contralateral impaired conjugate gaze. When the territory of the anterior cerebral artery is affected, lower extremity deficits are more frequent than upper extremity deficits. These patients often have associated cognitive and personality changes. Vertebrobasilar stroke symptoms and signs include motor or sensory loss in all four extremities, crossed signs, disconjugate gaze, nystagmus, dysarthria, and dysphagia. If the cerebellum is affected by ischemic stroke, then ipsilateral limb and gait ataxia are commonly present.

    What risk factors for stroke are not modifiable?

• Age
• Family history
• Gender
• Ethnicity
• Prior stroke, TIA, or heart attack

    What risk factors for stroke are modifiable?

• Hypertension, including compliance with medications
• Cigarette smoking
• Diabetes mellitus
• Carotid or other artery disease
• Peripheral artery disease
• Atrial fibrillation
• Coronary heart disease
• Congestive heart failure
• Sickle cell disease
• Hyperlipidemia
• Poor diet
• Physical inactivity
• Obesity

Assessment of vital signs is important in the initial examination. Severe high blood pressure can be suggestive of hypertensive encephalopathy or intracranial hemorrhage. A fever may lead to consideration of an infectious cause. A rapid or irregularly irregular pulse may suggest atrial fibrillation as a potential cause of the stroke. A timely general physical examination and comprehensive neurologic examination should follow, as well as subsequent interval evaluations.

The differential diagnosis of acute neurologic signs and symptoms is broad. Along with CVAs, such symptoms can be caused by seizures, acute confusional states, delirium, syncope, metabolic and toxic encephalopathy ( eg, hypoglycemia, poisoning), brain tumors, CNS infections, migraines, multiple sclerosis, and subdural hematoma. Migraines with neurologic symptoms can be especially difficult to differentiate from stroke since migraines do not have to be accompanied by a headache. However, the symptoms of stroke are usually of a much more rapid onset than those of a migraine. Stroke victims are also usually alert and aware of what is happening to them, unlike people suffering from delirium or various types of encephalopathies. When it is determined that a stroke is the cause of the presentation, it is crucial to differentiate between ischemic and hemorrhagic stroke because of the implications on further treatment.

The initial assessment should establish if the patient is eligible for thrombolytic treatment; establishing the time of symptom onset is the most important factor. The onset of symptoms is assumed to be the time that the patient was last known to be free of symptoms, such as when they went to bed.

Brain Imaging

A CT scan of the brain without contrast is the initial imaging test of choice in the evaluation of acute stroke. A CT scan of the brain may not show evidence of an ischemic stroke for up to 72 hours, but can immediately exclude most cases of intracranial hemorrhage, tumors, or abscesses. CT is also more readily available, cost-effective, and takes less time than MRI and can also be used to detect a hemorrhagic transformation of an infarct in a patient with an ischemic stroke whose symptoms deteriorate. If neurologic symptoms have resolved, MRI evaluation within 24 hours is the preferred imaging study due to its increased sensitivity for differentiating between a TIA and a TSI stroke.

Further imaging studies may be indicated to clarify the etiology of the stroke and to detect intracranial or extracranial arterial occlusions, which may affect treatment decisions. Evaluation of the cerebrovascular system can be accomplished with magnetic resonance angiography (MRA), CT angiography, catheter angiography, or transcranial Doppler ultrasonography.

Other Tests

A 12-lead ECG should be performed in all stroke patients to detect or rule out acute myocardial infarctions, which can either cause a stroke or result from a stroke. An ECG will also aid in the diagnosis of atrial fibrillation or other arrhythmia that may cause a stroke. Echocardiography may also be necessary to assess the structure of the heart. Transesophageal echocardiography is particularly useful in detecting cardiac sources of embolism, such as thrombus caused by myocardial infarction, endocarditis, rheumatic heart disease, valvular prostheses, and atrial septa! defects. A carotid duplex ultrasonography evaluation is also recommended to evaluate for carotid plaques or stenosis.

Serum glucose, electrolytes, renal function tests, and urine toxicology screening are important to exclude hypoglycemia as well as metabolic and toxic encephalopathy. If the patient is on anticoagulant therapy, the prothrombin time, partial thromboplastin time, and platelet count should be measured and are required before considering thrombolytic therapy. A lipid panel, erythrocyte sedimentation rate, antinuclear antibodies (ANA), complete blood count, and serologic tests for syphilis are also often indicated. In young patients without an identifiable cause for a stroke, a workup for coagulation disorders or antiphospholipid syndrome may be indicated. A lumbar puncture is contraindicated if subarachnoid or intracranial hemorrhage is suspected.

TREATMENT

As in every critical patient, the initial survey should assess the ABCs. If hypoxia is detected, supplemental oxygen should be administered to maintain oxygen saturation above 92% and the cause of the hypoxia investigated (eg, partial airway obstruction, aspiration pneumonia, and atelectasis ). An endotracheal tube should be placed if the airway is threatened. A cardiac monitor should be placed to detect atrial fibrillation or any other arrhythmias.

Unless a hypertensive encephalopathy, aortic dissection, acute renal failure, or pulmonary edema is present, the treatment of arterial hypertension should be cautious. Prior to intravenous thrombolytic treatment, blood pressure should be lowered if systolic blood pressure is greater than 185 mm Hg or 110 mm Hg. After thrombolytic treatment, systolic blood pressure should be kept less than 180 mm Hg and diastolic blood pressure less than 105 mm Hg. Pharmacologic treatments for hypertension in patients with acute ischemic stroke include intravenous labetalol, nicardipine, and sodium nitroprusside.

Fever and elevated serum glucose after a stroke are often associated with less favorable outcomes and should be controlled during the poststroke period. An infectious source for the fever should be investigated.

Except when thrombolytic therapy is given, most patients with a nonhemorrhagic stroke should receive aspirin within the first 48 hours. Urgent anticoagulation is not recommended.

Judiciously selected patients can benefit from intravenous administration of recombinant tissue-type plasminogen activator (rtPA) if they can be treated within 3 hours of the onset of ischemic stroke. The risk of hemorrhage associated with rtPA treatment is approximately 5% and there are numerous contraindications to the use of thrombolytic therapy, including recent surgery, trauma, gastrointestinal bleeding, myocardial infarction, use of certain anticoagulant medications, and uncontrolled hypertension. Depending on availability, some hospitals have the capability of direct intra-arterial thrombolysis in which the thrombolytic agent is delivered directly to the clot via canalization or even mechanical retrieval of thrombus. These modes of treatment may be considered in centers with experimental protocols or extensive experience.

Poststroke cerebral edema can be a serious complication and can lead to herniation of the brain stem resulting in death. Cerebral edema should be treated with mannitol or decompression neurosurgery, although there is insufficient evidence to show significant benefit for these treatments in improving outcomes.

Acute treatment in a dedicated stroke unit results in better outcomes and decreased mortality. Early poststroke treatment care includes mobilization once the patient is stable and evaluations of the patient's ability to speak and swallow. After a stroke, the patient is often immobile and needs intensive medical care in order to avoid malnutrition, skin breakdown, and infection. A patient's neurologic deficits commonly improve after a stroke and may continue to improve for up to 6 months to a year. Prior strokes also predispose patients to seizures, and some patients may initially present with a seizure as the first symptom of stroke. When thrombolytic therapy is not used, DVT prophylaxis should be provided. Family support and treatment of depression should also be initiated when appropriate.

PREVENTION OF STROKE IN PATIENTS WITH PREVIOUS 

ISCHEMIC STROKE OR TIA

A history of a previous TIA or CVA confers a high risk for future events. Aggressive risk factor control should be undertaken in these patients. All patients should be counseled to quit smoking and to reduce alcohol intake. Hypertensive patients should be treated per Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, 8th report (JNC 8) guidelines (see Case 30). Elevated serum cholesterol should be treated with high-intensity lipidlowering (statin) therapy. Tight diabetic control should aim for a hemoglobin A1c level less than 8%. Antiplatelet agents such as aspirin (81-325 mg/d), the combination of aspirin and extended-release dipyridamole (Aggrenox), or clopidogrel (Plavix) should be started in patients with a history of noncardioembolic ischemic stroke or TIA.

Carotid endarterectomy (CEA) can reduce the risk of stroke in a patient with a history of previous TIA or CVA and symptomatic carotid artery stenosis of greater than 60% to 70%, and is typically not indicated when stenosis is less than 50%.

Noninvasive carotid balloon angioplasty and stenting is an alternative to CEA in select patients.

Anticoagulation with warfarin reduces the risk of stroke and stroke recurrence in patients with appropriate risk factors. It is indicated to reduce the risk of embolic strokes for patients with persistent or paroxysmal atrial fibrillation or advanced congestive heart failure. It is also indicated for patients with an ischemic stroke caused by a myocardial infarction and existence of a left ventricular thrombus, as well as for patients with rheumatic heart disease or a mechanical heart valve.

CASE CORRELATION

• See also Cases 32 (Dementia) and 34 (Migraine Headache).

COMPREHENSION QUESTIONS

44.1 A 72-year-old man is brought to the emergency department because of weakness

and numbness of the right arm. The evaluating medical student asks

the attending doctor about the diagnosis and management of transient ischemic

attacks. Which of the following would be most commonly expected in

a patient with a TIA?

A. Resolution of symptoms within 1 hour

B. Stroke within 90 days in less than 1 % of patients

C. CT evidence of infarction

D. CT evidence of ischemia

E. MRI evidence of infarction

44.2 An 84-year-old African-American woman was found by her daughter-in-law walking down the street a few blocks from her house. The daughter-in-law noticed that she did not appear to know where she was and did not recognize her. Upon prompting, she seemed confused and would not speak. The patient experienced a CVA 1 year previously and had mild residual deficits on her left side. She takes medications for hypertension, hyperlipidemia, constipation, and gout. In the emergency room, the patient has a blood pressure of 195/106 mm Hg, pulse of 86 beats/min, respiratory rate of 18 breaths/min, and temperature of 97.9°F (36.6°C). She does not follow commands and is oriented only to person. She complains of headache, yet a CT of the brain does not show evidence of an acute hemorrhage. Which of the following is the most appropriate next step in management?

A. Lumbar puncture

B. Chest x-ray

C. IV labetalol

D. MRI of the brain

E. IV mannitol

44.3 An 82-year-old man with a suspected stroke is transferred to a major medical stroke center from an outside rural hospital. Four hours have elapsed since initial presentation. His blood pressure is 164/92 and he is awake, alert, oriented, and moving all four extremities. Which of the following should be considered in the management of this patient?

A. Avoidance of acetaminophen

B. Aggressive blood pressure management

C. Thrombolysis

D. Early mobilization and therapy

E. A swallowing evaluation

44.4 A 65-year-old man was hospitalized due to sudden weakness of the right arm, which was diagnosed as an ischemic stroke. Carotid duplex ultrasonography revealed a 40% to 59% bilateral stenosis. Total cholesterol is 188 mg/dL and low-density lipoprotein (LDL) cholesterol is 98 mg/ dL. Which of the following is the best strategy regarding prevention of future strokes in this patient?

A. Warfarin

B. Carotid endarterectomy

C. Clopidogrel

D. Long-acting nitrates

E. Statin

44.5 A man is brought to the emergency room by ambulance. Coworkers at his office stated that he was acting normally until approximately 1 hour ago when he became confused and had trouble walking. One coworker thought that his right leg seemed especially weak. His vitals are temperature 97.4°F (36.3°C), pulse 118 beats/min, and blood pressure 90/65 mm Hg. The patient is arousable, but does not follow commands and is not oriented. He has a medical alert bracelet on his arm indicating that he is a diabetic and allergic to penicillin. A serum glucose level obtained at the bedside is 50 mg/ dL. Which of the following should be your immediate first step in management?

A. Immediately give the patient intravenous D50 or glucagon.

B. Immediately obtain a CT scan to assess possibility for giving rtPA.

C. Immediately perform a lumbar puncture to assess for subarachnoid hemorrhage.

D. Immediately give the patient mannitol.

E. Immediately start cardiopulmonary resuscitation (CPR) with chest compressions.

ANSWERS

44.1 A. TIA is a brief neurologic episode, typically less than 1 hour in duration that does not cause infarction. The occurrence of stroke after TIA is as high as 5.3% within 2 days and 10.5% within 90 days. Warfarin is indicated in specific circumstances, such as the presence of atrial fibrillation, but is not routinely used following a TIA.

44.2 C. IV labetalol should be started to achieve appropriate blood pressure control. Routine chest x-rays affect the clinical management in few patients with stroke, and are not recommended as routine initial workup. CT of the brain without contrast can exclude most cases of intracranial hemorrhage, tumors, or abscesses, and is the initial test of choice in the workup of suspected stroke but it can miss up to 15% of subarachnoid hemorrhages. When a subarachnoid hemorrhage is suspected but not seen on CT, a lumbar puncture is indicated for diagnosis.

44.3 D. Early mobilization of stroke patients should be started when they are considered medically stable. In the setting of an acute stroke, management of high blood pressure should be cautious. Thrombolytic therapy can be beneficial in selected patients, but carries significant risks and has numerous contraindications. Fever should be treated and a workup performed to determine its etiology, as it carries an increased risk of morbidity and mortality. At this point, 4 hours after symptoms, when the patient is speaking without difficulty, a swallowing evaluation is not immediately warranted.

44.4 C. Patients with stroke but no detected sources of embolism benefit from antiplatelet agents not anticoagulants. Aspirin, clopidogrel, or a combination of aspirin and dipyridamole are acceptable regimens. For patients with recent TIA or ischemic stroke and ipsilateral severe ( > 70%) carotid artery stenosis, carotid endarterectomy is recommended. When the degree of stenosis is less than 50%, there is no indication for CEA. Patients with a history of symptomatic cerebrovascular disease should be treated with high-intensity statin therapy.

44.5 A. The patient has severe hypoglycemia and needs to be treated immediately with intravenous glucose or glucagon. If the patient does not recover with glucose or glucagon infusion, then other tests, such as a CT scan, may be warranted. Be aware that hypoglycemia can mimic many of the symptoms of a stroke, including focal weakness. Mannitol is used in cases of cerebral edema and not for raising blood sugar. The patient is tachycardic, likely from hypoglycemia, and does not require CPR.

CLINICAL PEARLS

⯈ Hypertension is the single most important modifiable risk factor for stroke.

⯈ Although most strokes are cerebral infarctions, it is crucial to differentiate between ischemic and hemorrhagic stroke because of the implications on further treatment.

⯈ Judiciously selected patients can benefit from intravenous administration of rtPA.

⯈ CT of the brain without contrast is the initial imaging test of choice in most suspected strokes.

⯈ Unless a hypertensive encephalopathy, aortic dissection, acute renal failure, or pulmonary edema is present, the treatment of arterial hypertension should be cautious.

REFERENCES

Adams H, Adams R, Del Zoppo G, Goldstein LB. Guidelines for the early management of patients with ischemic stroke: 2007 guidelines update. A scientific statement from the Stroke Council of the American Heart Association/ American Stroke Association. Stroke. 2007; 38:1655-1711. 

Aiyagari V, Gorelick PB. Management of blood pressure for acute and recurrent stroke. Stroke. 2009; 40:2251-2256. 

Donnan G, Fisher M, Macleod M, Davis S. Stroke. Lancet. 2008; 371(9624):1612-1623. 

James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8).JAMA. 2014; 311(5):507-520. 

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. 2007; 369(9558):283. 

NASCET Steering Committee. North American Symptomatic Carotid Endarterectomy Trial. Stroke. 1991; 22(6):711-720. 

Simmons BB, Cirignano B, Gadegbeku AB. Transient ischemic attack: part I. Diagnosis and evaluation. Am Fam Physician. 2012; 86(6):521-526. 

Simmons BB, Gadegbeku AB, Cirignano B. Transient ischemic attack: part II. Risk factor modification and treatment. Am Fam Physician. 2012; 86(6):527-532. 

Smith WS,Johnston S, Hemphill], III. Cerebrovascular diseases. In: Kasper D, Fauci A, Hauser S, et al., eds. Harrison's Principles of Internal Medicine.19th ed. New York, NY: McGraw-Hill Education; 2015. Available at: http://accessmedicine.mhmedical.com. Accessed May 25, 2015. 

van der Work HB, van GijnJ. Acute ischemic stroke. New Engl] Med. 2007; 357(6):572-579.

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