AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

The anterior circulation of the brain describes the areas of the brain supplied by the right and left internal carotid arteries and their branches. The internal carotid arteries supply the majority of both cerebral hemispheres, except the occipital and medial temporal lobes, which are supplied from the posterior circulation (see Image 1). Ischemic strokes occurring in the anterior circulation are the most common of all ischemic strokes, accounting for approximately 70% of all cases.

The internal carotid artery originates at the bifurcation of the common carotid artery at the level of the thyroid cartilage in the neck. The extracranial portion of the artery passes into the carotid canal of the temporal bone without giving off any branches. The intracranial portion of the artery consists of the petrosal, cavernous (ie, S-shaped carotid syphon), and supraclinoid portions. The major intracranial branches arise from the supraclinoid portion, the first being the ophthalmic artery that enters the orbit through the optic foramen to supply the retina and optic nerve. Next, the posterior communicating artery arises just distal to the ophthalmic artery and joins the posterior cerebral artery.

The anterior choroidal artery arises prior to the terminal bifurcation of the internal carotid artery into the middle cerebral and anterior cerebral arteries. The middle cerebral artery (MCA) is the direct continuation of the artery, while the anterior cerebral artery (ACA) branches medially at the level of the anterior clinoid process. The circle of Willis consists of a vascular communication of blood vessels at the base of the brain connecting the anterior and posterior circulations. The vessels of the anterior circulation are connected via the posterior communicating arteries to the posterior circulation.

A high degree of variation exists in the normal vascular anatomy. For example, in as many as 20% of patients, the posterior cerebral arteries (ie, fetal) arise from the internal carotid artery as normal vascular variants. Therefore, some variation exists in the exact parts of the brain supplied by the anterior circulation. For additional resources, visit Stroke/Cerebrovascular Disease.

Pathophysiology

Ischemic strokes in the anterior circulation are caused most commonly by occlusion of one of the major intracranial arteries or of the small single perforator (penetrator) arteries. The most common causes of arterial occlusion involving the major cerebral arteries are (1) emboli, most commonly arising from atherosclerotic arterial narrowing at the bifurcation of the common carotid artery, from cardiac sources, or from atheroma in the aortic arch and (2) a combination of atherosclerotic stenosis and superimposed thrombosis. Lacunar strokes are believed to be caused by lipohyalinotic intrinsic disease of the small penetrating vessels.

The most common sites of occlusion of the internal carotid artery are the proximal 2 cm of the origin of the artery and, intracranially, the carotid siphon. Factors that modify the extent of infarction include the speed of occlusion and systemic blood pressure. Occlusion of the internal carotid artery is not infrequently silent, because external orbital-internal carotid and willisian collaterals can open up if the occlusion has occurred gradually over a period of time. Mechanisms of ischemia resulting from internal carotid artery occlusion are, most commonly, artery-to-artery embolism or propagating thrombus and perfusion failure from distal insufficiency.

The MCA is the largest of the intracerebral vessels and supplies through its pial branches almost the entire convex surface of the brain, including the lateral frontal, parietal, and temporal lobes; insula; claustrum; and extreme capsule. The lenticulostriate branches of the MCA supply the basal ganglia, including the caput nuclei caudati, the putamen, the lateral parts of the internal and external capsules, and sometimes the extreme capsule. Occlusion of the MCA commonly occurs in either the main stem (M1) or in one of the terminal superior and inferior divisions (M2). Occlusion of the M1 segment of the MCA prior to the origin of the lenticulostriate arteries in the presence of a good collateral circulation can give rise to the large striatocapsular infarct.

Occlusion of the MCA or its branches is the most common type of anterior circulation infarct, accounting for approximately 90% of infarcts and two thirds of all first strokes. Of MCA territory infarcts, 33% involve the deep MCA territory, 10% involve superficial and deep MCA territories, and over 50% involve the superficial MCA territory.

The ACA supplies the whole of the medial surfaces of the frontal and parietal lobes, the anterior four fifths of the corpus callosum, the frontobasal cerebral cortex, the anterior diencephalon, and the deep structures. Occlusion of the ACA is uncommon, occurring in only 2% of cases, often through atheromatous deposits in the proximal segment of the ACA.

The anterior choroidal artery supplies the lateral thalamus and posterior limb of the internal capsule. Occlusion of the anterior choroidal artery occurs in fewer than 1% of anterior circulation strokes. Often, ischemia in the distribution of the ophthalmic artery is transient in the setting of symptomatic internal carotid artery occlusion (ie, transient monocular blindness, occurring in approximately 25% of patients), but central retinal artery ischemia is relatively uncommon, presumably because of the efficient collateral supply.

Occlusion of single penetrating branches of the middle and anterior cerebral arteries that supply the deep white and gray matter produce the lacunar type of stroke. These occlusions account for as many as 20% of ischemic strokes.

The acute ischemic process varies markedly from patient to patient. Patients with similar clinical syndromes may have markedly different pathophysiological profiles. Many new pathophysiological insights have been obtained from studies using functional brain imaging (eg, magnetic resonance imaging [MRI], positron emission tomography [PET], single-photon emission computed tomography [SPECT]). Several pathophysiological ischemic stroke syndromes can be identified on the basis of imaging parameters of perfusion and tissue injury that could be used to target stroke treatment. Using new MRI methods, the following 3 patterns have been identified:

• Perfusion-diffusion mismatch, which may represent a situation of viable but ischemic tissue that could be salvaged by timely reperfusion. In this pattern, a larger area of hypoperfusion surrounds a zone of ischemic injury on diffusion-weighted imaging. This pattern occurs in approximately 70% of patients in the first 24 hours.
• Complete ischemia, in which the perfusion and diffusion lesions are of equivalent size, likely representing a complete infarct. This pattern has been identified in approximately 10-20% of patients in the first 24 hours.
• Reperfusion pattern, in which a perfusion deficit no longer exists. This pattern occurs in approximately 10-15% of patients in the first 24 hours.

Efforts are now underway to incorporate MR angiography findings as well.

Reperfusion is an important part of the ischemic process, and by 24 hours, 20-40% of arterial occlusions have begun to clear, with recanalization rates of 70% by 1 week and 90% by 3 weeks. Early reperfusion (<24 h) may have significant prognostic benefits and is associated with improved outcome and smaller infarct size, but later reperfusion may not alter outcome significantly and may be associated with hemorrhagic conversion of the infarct and edema formation.

Frequency

United States

In a recent study, Broderick et al estimated that approximately 731,000 new and recurrent cases of stroke occur each year in the United States. Approximately 80% of these are ischemic strokes. Anterior circulation ischemic stroke accounts for approximately 70% of all ischemic strokes. Approximately 409,360 new cases of anterior circulation ischemic stroke per year are reported in the United States.

International

The risk of stroke is highest in Eastern Europe, followed by Western Europe, Asia, the rest of Europe, and North America.

Mortality/Morbidity

• Stroke is the third leading cause of death in the United States and the leading cause of adult disability. High rates of morbidity and mortality are associated with all types of ischemic strokes, but the prognosis varies among subtypes. For example, the lacunar syndromes (ie, caused by occlusion of a single small penetrating artery) quite often are associated with a good prognosis and have a better prognosis than MCA syndromes.
• Overall, at 6 months after a stroke, as many as 30% of patients have died, 20-30% are moderately to severely disabled, 20-30% have mild to moderate disability, and 20-30% are without deficits.
• Stroke recurs in as many as 10% of stroke survivors in the first 12 months after stroke, with an incidence of 4% per year thereafter. After transient ischemic attack, the risk of stroke is 10.5% over the next 3 months, with the highest risk in the 2 days following TIA.

Race

The patterns of arterial occlusion are different in African Americans and Asians than in Caucasians.

• Asians and African Americans have higher rates of intracranial arterial occlusive disease than Caucasians. The intracranial arterial occlusive disease in these populations typically involves the main stem of the MCA or the ACA.
• In Caucasians, the arterial occlusive disease typically involves the extracranial carotid arteries, and lesions in the middle and anterior cerebral arteries are usually of embolic origin.

Sex

Strokes at all ages are more likely to occur in men, but overall more strokes occur in women. This is because strokes occur more commonly at older ages and females have a longer life span than males (the native protective effect of estrogen is lost at menopause). This disparity may become greater in the future with the aging of the population.

Age

The incidence of stroke rises exponentially with age, particularly in individuals older than 55 years.

• However, 25% of all strokes occur in individuals younger than 65 years of age; so stroke is not just a condition of the elderly.
• Strokes can occur at any age.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

Patients typically present with sudden onset of focal neurological symptoms. Specific features of the time course and evolution, focal neurological symptoms, and global symptoms are listed below.

• Time course and evolution
• • Sudden or rapid onset
  • Reaches maximal intensity within 24 hours
  • Gradual or stepwise worsening in as many as 30% of patients
• Focal neurological symptoms
• • Cognitive impairment - Difficulty with speech
  • Weakness or incoordination - Unilateral
  • Numbness or loss of sensation, typically unilateral
  • Dysarthria
  • Visual loss, either in one eye or in one visual field
• Global symptoms
• • Headache
  • Altered mental status
  • Syncope
  • Seizure
  • Coma

Physical

• Left hemisphere (ie, dominant)
• • Right hemiparesis, variable involvement of face and upper and lower extremity
  • Right-sided sensory loss, in a similar pattern to the motor deficit; usually involves all modalities, decreased stereognosis, graphesthesia
  • Right homonymous hemianopia
  • Dysarthria
  • Aphasia, fluent and nonfluent
  • Alexia
  • Agraphia
  • Acalculia
  • Apraxia
• Right hemisphere (ie, nondominant)
• • Left hemiparesis (same pattern as on right)
  • Left-sided sensory loss (similar pattern as the motor deficit)
  • Left homonymous hemianopia (same pattern as on right)
  • Dysarthria
  • Neglect of the left side of environment
  • Anosognosia
  • Asomatognosia
  • Loss of prosody of speech
  • Flat affect
• Cortical and subcortical: Findings consistent with both cortical and subcortical localization can be seen in this clinical scenario.
• ACA territory
• • Crural paresis > arm paresis
  • Frontal signs (eg, abulia)
• Anterior choroidal artery territory
• • Hemiparesis
  • Hemianesthesia
  • Homonymous hemianopia
• Lacunar syndromes
• • Pure motor hemiparesis
    • Contralateral, usually affecting the face and upper and lower extremities equally
    • Also associated with dysarthria
    • No sensory or visual loss or cognitive impairment
  • Pure sensory stroke
    • Contralateral loss of all sensory modalities, equally affecting the face and upper and lower extremities
    • No motor signs, dysarthria, visual loss, or cognitive impairment
  • Dysarthria-clumsy hand syndrome - Dysarthria, dysphagia, contralateral tongue and facial weakness and paresis, and clumsiness of the contralateral arm and hand
  • Homolateral ataxia and crural paresis - Paresis of the contralateral leg and side of the face, prominent ataxia of the contralateral leg and arm—also called "ataxic hemiparesis," meaning ataxia and weakness on the same side.
  • Isolated motor/sensory stroke
    • Paralysis and sensory loss of the contralateral leg, arm, and face
    • No visual loss or cognitive impairment

Causes

Risk factors include epidemiologic risk factors (ie, not modifiable) and potentially modifiable risk factors.

• Epidemiologic risk factors
• • Age (risk rises exponentially with age)
  • Sex (more common in males at all ages)
  • Race (African American > Asian > Caucasian)
  • Geographic (Eastern Europe > Western Europe > Asia > rest of Europe or North America)
  • Genetic risk factors (stroke or heart disease in individuals younger than 60 y; some familial syndromes, eg, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL])
• Potentially modifiable risk factors
• • Hypertension (diastolic or isolated systolic)
  • Diabetes mellitus type 1 or 2
  • Atrial fibrillation
  • Smoking
  • Coronary artery disease
  • Hypercholesterolemia
  • Alcohol abuse
  • Drug abuse (eg, cocaine)
  • Oral contraceptive use
  • Pregnancy

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Other Problems to be Considered

Brain tumor
Hypoglycemia
Brain abscess
Carotid disease and stroke

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

• The following laboratory tests are indicated in the patient with stroke both to assist in their acute care and to uncover any underlying medical conditions that could complicate the clinical course.
• • Coagulation profile
  • Glucose level
  • Electrolytes levels
  • Liver function tests
  • Erythrocyte sedimentation rate (ESR)
  • Complete blood count (CBC)

Imaging Studies

• Brain CT scan
• • Noncontrast CT scan of the brain is required emergently to rule out cerebral hemorrhage, subdural hematoma, and other intracerebral pathology prior to the administration of thrombolytic therapy.
  • Early signs of infarction that can be detected with CT scan include loss of gray-white matter differentiation and cortical sulcal effacement. The hyperdense MCA sign is indicative of thrombus in the MCA. The Alberta Stroke Programme Early CT Score (ASPECTS) score may have prognostic utility (a favorable score is >7/10) but did not show utility in clinical decision-making for recombinant tissue plasminogen activator (rt-PA) therapy in a recent study.
  • Other advances in CT scan include the advent of CT angiography and CT perfusion imaging.
• MRI
• • New MR sequences such as diffusion-weighted imaging (DWI) allow detection of ischemic lesions within minutes of stroke onset. Lesions appear as hyperintense and are easily distinguishable from the surrounding brain.
  • Even very small lesions can be detected, and old lesions may be distinguished from new ones by measuring the apparent diffusion coefficient.
  • In combination with MR angiography (MRA) and MR perfusion imaging, this modality allows multiple aspects of the ischemic process to be identified in a scanning session of approximately 25 minutes. This is available in many tertiary referral centers. Contrast-enhanced MRA using a neurovascular array permits rapid imaging of the vasculature from the aortic arch to the circle of Willis in as short as 2 minutes. This method seems sensitive for the detection of extracranial vascular disease, including vertebral and internal carotid artery dissections.
• Transcranial Doppler ultrasonography
• • Transcranial Doppler ultrasonography is used for rapid and noninvasive identification of the site of major arterial occlusion in the MCA, internal carotid artery, and ACA.
  • It also is used to identify embolic load with emboli detection.
• Chest radiography - This is used to determine heart size and pulmonary status.

Other Tests

• Cardiac echocardiography
• • Cardiac echocardiography helps in ruling out a cardiac source of cerebral embolism and in identifying aortic arch atheroma.
  • Transesophageal echocardiography is the investigation of choice, as it has higher detection rates for lesions in the left atrium (eg, thrombus) and the aortic arch.
• Imaging of the neck vessels
• • Imaging of the neck vessels helps in ruling out a significant carotid artery stenosis as a cause of stroke that may require surgical intervention.
  • Perform imaging with ultrasound, MRA, or conventional digital subtraction angiography.
• Hypercoagulability screen - For patients with cryptogenic stroke and a possibility of a hypercoagulable etiology
• ECG

Procedures

• Intravenous thrombolysis is recommended for patients with ischemic stroke presenting within the first 3 hours.
• Intravenous thrombolysis beyond the first 3 hours is under investigation. Patients are eligible for trials if a perfusion-diffusion mismatch pattern can be identified (believed to be indicative of the presence of potentially viable tissue).
• Mechanical clot disruption using the MERCI clot retrieval device for acute ischemic stroke treated within 8 hours of symptom onset received clearance from the Food and Drug Administration (FDA) in 2004. A second-generation device and use of the device in patients with persistent clots after intravenous thrombolysis are still under investigation.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Medical Care

The aim is to prevent acute, subacute, or chronic medical and neurological complications.

• Check vital signs and perform neurological assessments.
• Check oxygen saturation; administer supplemental oxygen if hypoxic.
• Monitor cardiac function.
• Administer anticoagulants or advise compression stockings to bedridden patients to avoid deep venous thrombosis.
• Avoid indwelling bladder catheter if possible.
• Control blood pressure optimally.

Surgical Care

Emergency decompression with craniotomy is performed in some centers for patients with malignant MCA syndrome. It is performed most commonly for right hemisphere infarctions because of better potential for functional recovery than left hemisphere infarctions.

Consultations

The following consultations are made depending on the individual patient's needs. In some centers, specialists work as an integrated stroke team.

• Physical therapy - For assessment of difficulty in sitting, standing, or walking and the need for assistive devices to aid walking
• Speech therapy - For assessment of swallowing, language impairments, or dysarthria
• Occupational therapy - For patients with decreased cognitive or upper extremity function and need for adaptive equipment
• Social services - For discharge planning
• Rehabilitation physician - For assessment of rehabilitation needs
• Psychiatry - For assessment of psychiatric status

Diet

• Generally, patients are allowed nothing by mouth for the first 24 hours, except for patients with very mild or rapidly resolving deficits. Intravenous fluids should avoid dextrose and preferably involve isotonic saline.
• Perform bedside or fluoroscopic swallowing assessment. Adjust diet depending on results; if necessary to meet nutritional needs, commence nasogastric feeding.
• Assess for future need of enteral feeding (typically via percutaneous gastrostomy tube).

Activity

• Advise bed rest for the first 24 hours with the head of the bed below 30 degrees to avoid exacerbation of cerebral hypoperfusion in evolving infarcts, which sometimes can lead to neurological worsening. The focally ischemic brain has impaired autoregulatory capacity and so may not compensate for changes in blood pressure that are tolerated under nonischemic conditions. Intravenous normal saline is also administered.
• If the patient's condition is stable after 24 hours, graded ambulation with assistance may commence, depending on functional status.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Intravenous recombinant tissue plasminogen activator (rt-PA) administered within 3 hours of stroke onset is the only FDA-approved pharmaceutical therapy for the acute treatment of ischemic stroke. Other medical management of anterior circulation ischemic stroke consists of optimal blood pressure control and administration of therapies aimed at secondary stroke prevention, usually antiplatelet agents or anticoagulants, depending on the etiology of the stroke.

Drug Category: Thrombolytic agents

These agents lyse thromboemboli lodged in cerebral blood vessels and restore blood flow, salvage the ischemic brain tissue, and improve clinical outcome. They must be administered within 3 hours of onset of stroke symptoms; beyond this time, the risk of intracerebral hemorrhage outweighs treatment benefits.

Drug Category: Anticoagulants

Emergent heparin therapy may be given for specific indications, such as internal carotid artery dissection or cerebral venous thrombosis. Heparin therapy also may be commenced in conjunction with warfarin therapy for secondary prevention of high-risk cardioembolic stroke; it may be started either on admission (if not receiving rt-PA) or 3-5 days after stroke onset. Early use of IV heparin has not, however, been proven to be of benefit in clinical trials. For patients confined to bed who do not have excessive risk of hemorrhagic transformation, administer subcutaneous heparin to prevent deep venous thrombosis.

Drug Name	Warfarin (Coumadin)
Description	Inhibits synthesis of 6 vitamin K-dependent proteins involved in anticoagulation system (factors II, VII, IX, X; proteins C, S). Many other coumarin derivatives are used worldwide.
Adult Dose	Initial dose: 5 mg/d PO for 2-4 d (lower in very elderly patients) Subsequent doses determined by INR achieved and source of embolism (INR 2-3 for most cardiac sources)
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; active bleeding; heparin-induced thrombocytopenia; severe renal or hepatic disease; open wounds; gastric ulcer
Interactions	Extensive literature available regarding warfarin-drug interactions, with variable level of evidence; drugs that increase anticoagulant effects include co-trimoxazole, erythromycin, fluconazole, isoniazid, amiodarone, aspirin, simvastatin, sulfinpyrazone, phenylbutazone, alcohol, cimetidine, and omeprazole; drugs that inhibit anticoagulant effect include rifampin, nafcillin, cholestyramine, barbiturates, carbamazepine, sucralfate, and azathioprine; OTC NSAIDs (eg, Naprosyn, ibuprofen) and aspirin are associated with increased risk of upper GI bleeding when used with warfarin; high doses of acetaminophen can prolong INR
Pregnancy	X - Contraindicated in pregnancy
Precautions	Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Drug Category: Antiplatelet agents

These agents are used for secondary prevention of ischemic stroke caused by atherosclerotic disease of small or large arteries. Data also support aspirin use within 48 h of an acute stroke.

Drug Name	Aspirin plus slow-release dipyridamole (Aggrenox)
Description	Aspirin inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. Dipyridamole is platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity, leading to increased cyclic-3', 5'-adenosine monophosphate within platelets and formation of potent platelet activator thromboxane A2. European Stroke Prevention Trial 2 demonstrated that combination therapy was better than aspirin alone for prevention of recurrent stroke or transient ischemic attack.
Adult Dose	25 mg aspirin + 200 mg dipyridamole SR PO bid (1 tab bid)
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma Because of association with Reye syndrome, do not use in children ( <16 y) with flu
Interactions	Aspirin: Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease salicylate serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increase bleeding time; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs Dipyridamole: Theophylline may decrease hypotensive effects; antiplatelet activity may increase heparin toxicity
Pregnancy	D - Unsafe in pregnancy
Precautions	Aspirin may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants Caution in hypotension when using dipyridamole; dipyridamole has peripheral vasodilating effects

Drug Name	Clopidogrel (Plavix)
Description	Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.
Adult Dose	75 mg/d PO qd
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; active pathological bleeding, such as peptic ulcer; intracranial hemorrhage
Interactions	Naproxen associated with increased occult GI blood loss; safety of coadministration with warfarin not established
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions (eg, ulcers) with propensity to bleed; prolongs bleeding time

Drug Name	Ticlopidine (Ticlid)
Description	Reported to be 15% more effective than aspirin. However, is associated with risks of neutropenia and thrombocytopenia and requires regular blood testing; therefore, use in patients who do not respond to aspirin or are allergic to aspirin.
Adult Dose	250 mg PO bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; neutropenia or thrombocytopenia; liver damage; active bleeding disorders
Interactions	Corticosteroids and antacids may decrease effects; theophylline, cimetidine, aspirin, and NSAIDS increase toxicity
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Discontinue if absolute neutrophil count decreases to <1200/mm3 or if platelet count falls to <80,000/mm3

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Further Inpatient Care

• Treatment and monitoring of comorbid diseases such as diabetes, heart disease, hypertension, and arthritis
• Symptomatic treatment of confusion, agitation, headache, pain, nausea, and vomiting
• Referral for chest physiotherapy, if required

Complications

• Neurological complications include cerebral edema, hemorrhagic transformation of cerebral infarction, seizures, hydrocephalus, increased intracranial pressure, and depression.
• Respiratory complications include aspiration, pneumonia, airway obstruction, hypoventilation, and atelectasis.
• Urinary complications include incontinence and urinary tract infections.
• Cardiovascular complications include myocardial infarction, congestive heart failure, hypertension, orthostatic hypotension, deep venous thrombosis, and pulmonary embolism.
• Nutritional, metabolic, and gastrointestinal complications include stress ulcers, gastrointestinal bleeding, constipation, dehydration, electrolyte disturbances, malnutrition, and hyperglycemia.
• Orthopedic and dermatologic complications include pressure sores, contractures, adhesive capsulitis of the shoulder, and falls with fractures.

Prognosis

• At 6 months after a stroke, approximately 20-30% of patients have died, 20-30% are moderately to severely disabled, 20-30% have mild to moderate disability, and 20-30% are without deficit.
• Despite treatment for secondary prevention, stroke recurrence rate is significant.
• A significant percentage of patients (ie, as many as 50% in some studies) suffer from depression after stroke. Also, a significant rate of stress and depression exists among caregivers of patients disabled by stroke.

Patient Education

• Educate patients and their families regarding stroke, its treatment, its complications, and plans for future care.
• Refer to stroke support groups.
• Provide educational material from organizations such as the American Stroke Association and the National Stroke Association.
• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education articles Stroke and Transient Ischemic Attack (Mini-stroke).

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Media file 1:  Anterior circulation stroke. Vascular territories.
	View Full Size Image
Media type:  Image

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

• Baird AE, Warach S. Magnetic resonance imaging of acute stroke. J Cereb Blood Flow Metab. Jun 1998;18(6):583-609. [Medline].
• Bogousslavsky J. Topographic patterns of cerebral infarcts. Correlation with etiology. Cerebrovasc Dis. 1991;1 (suppl 1):61-68.
• Broderick J, Brott T, Kothari R. The Greater Cincinnati/Northern Kentucky Stroke Study: preliminary first-ever and total incidence rates of stroke among blacks. Stroke. Feb 1998;29(2):415-21. [Medline].
• Demchuk AM, Hill MD, Barber PA, et al. Importance of early ischemic computed tomography changes using ASPECTS in NINDSrtPA Stroke Study. Stroke. Oct 2005;36(10):2110-5. [Medline].
• Fisher CM. Lacunar infarcts. A review. Cerebrovasc Dis. 1991;1:311-320.
• Furlan A, Higashida R, Wechsler L. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA. Dec 1 1999;282(21):2003-11. [Medline].
• Greshem GE. Rehabilitation of the stroke survivor. In: Barnett H, et al, eds. Stroke: Pathophysiology, Diagnosis and Management. 2^nd ed. New York: Churchill Livingstone; 1992:1189-201.
• Helgason CM. A new view of anterior choroidal artery territory infarction. J Neurol. Sep 1988;235(7):387-91. [Medline].
• Johnston SC, Gress DR, Browner WS. Short-term prognosis after emergency department diagnosis of TIA. JAMA. Dec 13 2000;284(22):2901-6. [Medline].
• Koga M, Saku Y, Toyoda K. Reappraisal of early CT signs to predict the arterial occlusion site in acute embolic stroke. J Neurol Neurosurg Psychiatry. May 2003;74(5):649-53. [Medline].
• Libman RB, Kwiatkowski TG, Hansen MD. Differences between Anterior and Posterior Circulation Stroke in TOAST. Cerebrovasc Dis. 2001;11(4):311-6. [Medline].
• Mohr JP, Gautier JC, Pessin MS. Internal carotid artery disease. In: Barnett H, et al, eds. Stroke: Pathophysiology, Diagnosis and Management. 2^nd ed. New York: Churchill Livingstone; 1992:285-335.
• Rajamani K, Gorman M. Trancranial Doppler in stroke. Biomed Pharmacother. Jun 2001;55(5):247-57. [Medline].
• Smith WS, Sung G, Starkman S, et al. Safety and efficacy of mechanical embolectomy in acute ischemic stroke: resultsof the MERCI trial. Stroke. Jul 2005;36(7):1432-8. [Medline].
• The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study G. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. Dec 14 1995;333(24):1581-7. [Medline].
• Wright VL, Olan W, Dick B, et al. Assessment of CE-MRA for the rapid detection of supra-aortic vascular disease. Neurology. Jul 12 2005;65(1):27-32. [Medline].
• Zweifler RM. Management of acute stroke. South Med J. Apr 2003;96(4):380-5. [Medline].

Article Last Updated: Jan 3, 2006