Ischemic strokes occurring in the anterior circulation are the most common of all ischemic strokes, accounting for approximately 70% of all cases. They 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 middle cerebral artery (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 anterior cerebral artery (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 less 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.
Population differences
The patterns of arterial occlusion are different in African Americans and Asians than in whites.
Asians and African Americans have higher rates of intracranial arterial occlusive disease than whites. The intracranial arterial occlusive disease in these populations typically involves the main stem of the MCA or the ACA.
In whites, the arterial occlusive disease typically involves the extracranial carotid arteries, and lesions in the middle and anterior cerebral arteries are usually of embolic origin.
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, as shown in the image below.
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 MCA is the direct continuation of the artery, while the 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 major vessels of the anterior and posterior circulations.
The collateral circulation is an important potential source of blood supply in cases of internal carotid artery occlusive disease. The 2 primary sources of collateral flow via the circle of Willis are the anterior and the posterior communicating arteries. Blood may flow from the contralateral ICA via the A1 segment of the contralateral anterior cerebral artery through the anterior communicating artery to the ipsilateral ACA (appears as reversal of flow). Blood may come from the posterior circulation (posterior cerebral arteries) via the posterior communicating artery (reversal of flow).
Note that a high degree of variation exists in the normal vascular anatomy of the circle of Willis. For example, in as many as 20% of patients, the posterior cerebral arteries (ie, fetal variant) 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.
If the primary collateral circulation fails, secondary sources of collaterals may come from the branches of the ipsilateral external carotid artery. Branches from the maxillary artery anastomose with the ophthalmic artery leading to reversal of flow in the ophthalmic artery and into the occluded ICA. Leptomeningeal collaterals may also anastomose with distal MCA branches and lead to reversed flow in the MCA.
The acute ischemic process varies markedly from patient to patient. Patients with similar clinical syndromes may have markedly different pathophysiologic profiles. Many new pathophysiologic insights have been obtained from studies using functional brain imaging (eg, magnetic resonance imaging [MRI], positron emission tomography [PET] scanning, single-photon emission computed tomography [SPECT] scanning).
Several pathophysiologic 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.
The first pattern, perfusion-diffusion mismatch, 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. In many patients, an arterial occlusion is identified on MR angiography (MRA).
The second pattern is 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. In many patients, an arterial occlusion is identified on MRA.
The third pattern is the reperfusion pattern, in which a perfusion deficit no longer exists and the MRA is normal. This pattern occurs in approximately 10-15% of patients in the first 24 hours.
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.
Approximately 750,000 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 420,000 new cases of anterior circulation ischemic stroke per year are reported in the United States.
International stroke incidence
The risk of stroke is highest in Eastern Europe, followed by Western Europe, Asia, the rest of Europe, and North America.
Recurrence
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 a transient ischemic attack (TIA).
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, mortality rates after intracerebral hemorrhage are as high as 30% at 1 month.
Conversely, the ischemic 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 risk is highest in African Americans, being up to 4-fold higher than in whites. This may relate in part to higher rates of some vascular risk factors, such as hypertension and diabetes, in the black population. Stroke risks are also higher in Hispanics and Asians, relative to whites.
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 do 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.
Risk factors for anterior circulation stroke include those that are not modifiable and those that potentially are modifiable.
Risk factors for anterior circulation stroke include the following:
Age (risk rises exponentially with age)
Sex (more common in males at all ages)
Race (African American > Asian > Caucasian)
Geography (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 for anterior circulation stroke include the following:
Patients typically present with sudden onset of focal neurological symptoms. Specific features of the time course and evolution, focal neurologic symptoms, and global symptoms are listed below.
Time course and evolution of anterior circulation stroke can be characterized as follows:
Sudden or rapid onset
Maximal intensity reached within 24 hours
Gradual or stepwise worsening in as many as 30% of patients
Focal neurologic symptoms in this type of stroke include the following:
Cognitive impairment - Difficulty with speech
Weakness or incoordination - Unilateral
Numbness or loss of sensation - Typically unilateral
Dysarthria
Visual loss - Either in 1 eye or in 1 visual field
Global symptoms in anterior circulation stroke include the following:
Presentation related to the left hemisphere of the brain includes the following:
Right hemiparesis - Variable involvement of face and upper and lower extremity
Right-sided sensory loss in a pattern similar to that of the motor deficit - Usually involves all modalities, decreased stereognosis, and graphesthesia
Right homonymous hemianopia
Dysarthria
Aphasia, fluent and nonfluent
Alexia
Agraphia
Acalculia
Apraxia
Right hemisphere (ie, nondominant)
Presentation related to the right hemisphere of the brain includes the following:
Left hemiparesis - Same pattern as on right
Left-sided sensory loss - Similar pattern that of 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 cortical and subcortical localization can be seen in this clinical scenario.
Findings related to the ACA territory are as follows:
Crural paresis > arm paresis
Frontal signs (eg, abulia)
Findings related to the anterior choroidal artery territory are as follows:
Hemiparesis
Hemianesthesia
Homonymous hemianopia
Lacunar syndromes
Pure motor hemiparesis is characterized as follows:
Contralateral - Usually affects the face and upper and lower extremities equally
Also associated with dysarthria
No sensory or visual loss
No cognitive impairment
Pure sensory stroke is characterized as follows:
Contralateral loss of all sensory modalities - Equally affects the face and upper and lower extremities
No motor signs, dysarthria, visual loss, or cognitive impairment
Dysarthria-clumsy hand syndrome is characterized as follows:
Dysarthria
Dysphagia
Contralateral tongue and facial weakness and paresis
Clumsiness of the contralateral arm and hand
Homolateral ataxia and crural paresis are characterized as follows:
Paresis of the contralateral leg and side of the face
Prominent ataxia of the contralateral leg and arm
Isolated motor/sensory stroke is characterized as follows:
Paralysis and sensory loss of the contralateral leg, arm, and face
The following laboratory tests are indicated in the patient with stroke in order to assist in the individual’s 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)
Brain computed tomography scanning
Noncontrast computed tomography (CT) scanning 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.[2]
The Alberta Stroke Programme Early CT Score (ASPECTS) score may have prognostic utility (a favorable score is >7/10), but in a study it did not show utility in clinical decision-making for recombinant tissue plasminogen activator (rtPA) therapy.
Other advances in CT scanning include the advent of CT angiography and CT perfusion imaging.[3]
Magnetic resonance imaging
MRI sequences, such as diffusion-weighted imaging (DWI), allow detection of ischemic lesions within minutes of stroke onset.[4] Lesions appear as hyperintense and are easily distinguishable from the surrounding brain.[5] 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 MRA and MR perfusion imaging, MRI 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 little 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.
Cardiac echocardiography
Cardiac echocardiography helps to rule out a cardiac source of cerebral embolism and aids 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 to rule out a significant carotid artery stenosis as a cause of stroke that may require surgical intervention.
Image the neck with ultrasonography, MRA, or conventional digital subtraction angiography.
Hypercoagulability screen
This is performed in patients with cryptogenic stroke and the possibility of a hypercoagulable etiology.
Electrocardiogram
This is also indicated. One study suggests that patients presenting with cerebral ischemia without atrial fibrillation may benefit from prolongation of Holter monitoring (more than 7 days). Those patients who received the Holter monitor for up to 7 days had a higher detection rate of paroxysmal atrial fibrillation, which lead to a change in therapy. This prolonged use of the monitor should be considered for those patients with unexplained cerebral ischemia.[6]
The medical interventions that have been shown to improve outcomes after stroke are (1) treatment in a stroke unit, (2) intravenous rtPA therapy administered within 3-4.5 hours of onset to patients with ischemic stroke, (3) mechanical thrombectomy, and (4) antiplatelet therapy, including aspirin administered within the first 48 hours of stroke.
Thrombolysis
Intravenous thrombolysis beyond the first 3 hours is under investigation. One trial, the European Cooperative Acute Stroke Study (ECASS) 3, is investigating the efficacy and safety of IV tPA administration 3–4.5 hours after symptom onset. Small trials have suggested that patients may respond to tPA after 3 hours if a perfusion-diffusion mismatch pattern (believed to be indicative of the presence of potentially viable tissue) can be identified.
In May 2009, the American Heart Association/American Stroke Association (AHA/ASA) introduced revised guidelines that increased the tPA treatment window in acute ischemic stroke to 4.5 hours. However, this change has not yet been approved by the US Food and Drug Administration (FDA).
Intra-arterial thrombolysis may be considered in highly select patients with MCA occlusions who present within 6 hours of onset and who are not eligible for IV thrombolysis. Some highly select patients with basilar artery thrombosis may be considered for intra-arterial thrombolysis up to 24 hours after onset.
Mechanical thrombolysis
In 2004, mechanical clot disruption using the Concentric MERCI (Mechanical Embolus Removal in Cerebral Ischemia) Retrieval System for acute ischemic stroke treated within 8 hours of symptom onset received FDA clearance. Another mechanical device, the Penumbra System, received FDA clearance in 2007. Both devices may be used for patients with persistent clots after IV thrombolysis.
Additional treatment
Medical management of anterior circulation ischemic stroke also includes the intravenous administration of normal saline over the first 24 hours and administration of therapies aimed at secondary stroke prevention, usually antiplatelet agents or anticoagulants, depending on the etiology of the stroke.
The administration of aspirin (in doses ranging from 30 mg to 625 mg) within the first 48 hours of stroke is supported by pooled data from the Chinese Acute Stroke Trial (CAST) and the International Stroke Trial.[7, 8]
Antihypertensive therapy is typically deferred for 48 hours in order to prevent hypoperfusion in the ischemic penumbra. The regimen of indapamide and perindopril is supported by the results of the PROGRESS trial.[9] Evidence indicates that high-dose statins have utility for secondary stroke prevention and TIAs, including in patients without elevated cholesterol level or coronary heart disease.
In a clinical treatment trial, extracranial-intracranial bypass surgery plus medical therapy compared with medical therapy alone did not reduce the risk of recurrent ipsilateral ischemic stroke at 2 years in patients with recently symptomatic atherosclerotic internal carotid artery occlusion and hemodynamic cerebral ischemia.[10]
In patients presenting within 6 hours of stroke onset with a stroke affecting a proximal, anterior circulation vessel, endovascular thrombectomy may improve outcomes.[11]
Craniotomy and endarterectomy
Emergency decompression with craniotomy is performed in some centers in patients with malignant MCA syndrome. It is a matter of debate as to whether younger patients and those with right hemisphere syndromes are preferentially operated on (because of better potential for functional recovery). The timing of surgical intervention is also critical.
Carotid endarterectomy is recommended for the secondary prevention of stroke for patients with internal carotid artery stenosis of 70-99%, and for some patients with 50-69% stenosis.
The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) compared carotid stenting and carotid endarterectomy to better understand the short- and long-term outcomes of each procedure. The outcomes appeared to be similar, but during the periprocedural period, carotid stenting resulted in a higher risk of stroke, and carotid endarterectomy resulted in a higher risk of myocardial infarction.[12]
Additional treatment considerations
The following should also be considered in the treatment of patients with anterior circulation stroke:
Treatment and monitoring of comorbid diseases such as diabetes, heart disease, hypertension, and arthritis
Symptomatic treatment of confusion, agitation, headache, pain, nausea, and vomiting
After initial stroke treatment, there is an emphasis on secondary prevention. Two trials have shown some promise in reduction of recurrent events. The CHANCE trial showed that in patients with minor stroke (defined by NIHSS ≤ 3) or high-risk TIA (ABCD2 score ≥ 4), starting aspirin and clopidogrel within 24 hours of symptom onset led to a reduction of recurrent stroke at 90 days.[13] There were concerns with this study with regard to its generalizability as it was done using Chinese patients only, a population known to have differing rates of stroke and stroke risk factors/mechanisms. An updated trial, POINT, was published in 2018 in part to address these concerns.[14] This was an international trial and used the same NIHSS and ABCD2 scores to enroll patients in the trial. This trial showed that at 90 days, dual antiplatelet therapy with aspirin and clopidogrel started within 12 hours of symptom onset resulted in less stroke. However, there was an increase in the rate of bleeding with this study, but this may be due to the fact that loading doses of clopidogrel were double those used in the CHANCE trial.
From the CHANCE trial, guidelines from the AHA have been modified to reflect their findings: [15]
Administration of aspirin is recommended in patients with AIS within 24 to 48 hours after onset. For those treated with IV alteplase, aspirin administration is generally delayed until 24 hours later but might be considered in the presence of concomitant conditions for which such treatment given in the absence of IV alteplase is known to provide substantial benefit or withholding such treatment is known to cause substantial risk.
Aspirin is not recommended as a substitute for acute stroke treatment in patients who are otherwise eligible for IV alteplase or mechanical thrombectomy.
The efficacy of IV tirofiban and eptifibatide is not well established. Further clinical trials are needed.
The administration of other glycoprotein IIb/IIIa receptor antagonists, including abciximab, in the treatment of AIS is potentially harmful and should not be performed. Further research testing the safety and efficacy of these medications in patients with AIS is required.
In patients presenting with minor stroke, treatment for 21 days with dual antiplatelet therapy (aspirin and clopidogrel) begun within 24 hours can be beneficial for early secondary stroke prevention for a period of up to 90 days from symptom onset.
Ticagrelor is not recommended (over aspirin) in the acute treatment of patients with minor stroke.
Thrombectomy has emerged in recent years as a rapidly advancing treatment modality for acute stroke, with its maximal utility in anterior circulation stroke and more specifically middle cerebral artery stroke. This is both in isolation or in conjunction with IV thrombolysis which remains as standard of care.
Initial studies assessing the efficacy of endovascular therapy were negative;[16, 17, 18] however, this may have been due to the equipment and radiographic imaging available at the time — both have subsequently improved. With newer equipment and better imaging to confirm arterial occlusions, studies have shown strong evidence for benefit with this intervention.[19, 20, 21, 22, 23] The first of these studies to show benefit was the Dutch-led MR CLEAN trial[19] where intra-arterial tPA and mechanical thrombectomy showed superior mRS scores in patients at 90 days as compared to usual care. In both arms of this trial, approximately 90% of patients received intravenous tPA prior to randomization. Based on the data from this trial, an online calculator to predict outcomes with endovascular therapy has been created (MR PREDICTS), and subsequently validated.[24]
While the initial studies showed benefit of endovascular treatment up to 6 hours after the acute stroke, other trials have shown the utility of using tissue perfusion rather than discrete time windows to determine whether a patient is a candidate for endovascular therapy.[25, 26] These have resulted in changes to guidelines from the AHA[15] , which are as follows:
Patients should be considered for thrombectomy in under 6 hours after stroke onset if they meet this criterion and these other criteria:
Prestroke modified Rankin Scale (mRS) score of 0 to 1;
Causative occlusion of the internal carotid artery or middle cerebral artery segment 1 (M1);
Age over 18 years;
National Institutes of Health Stroke Scale score of 6 or greater; and
Alberta Stroke Program Early CT Score of 6 or greater.
All patients with stroke should be admitted to the hospital and treated in a comprehensive stroke unit with an interdisciplinary team. Treatment in a stroke unit has been shown to improve patient outcomes.
Eligible patients should be transferred by emergency services personnel to a primary stroke center for consideration for treatment with IV tPA, if it is possible to do so. In some rural areas, telemedicine is being used for the emergency evaluation and management of patients with stroke prior to transfer to larger medical centers.
The overall aims of inpatient care include reperfusion of ischemic brain tissue as quickly as possible and the prevention of acute, subacute, or chronic medical and neurologic complications.
Check vital signs and perform neurological assessments, and check oxygen saturation; administer supplemental oxygen if the patient is hypoxic.
Monitor cardiac function.
Administer anticoagulants or advise compression stockings to bedridden patients to avoid deep venous thrombosis.
Avoid an indwelling bladder catheter if possible, and control blood pressure optimally.
Generally, patients are allowed nothing by mouth for the first 24 hours, except for patients with very mild or rapidly resolving deficits. IV fluids should avoid dextrose and preferably involve isotonic saline.
Perform a bedside or fluoroscopic swallowing assessment; adjust the patient’s diet according to the results. If nutritional needs must be met, commence nasogastric feeding.
Assess for a future need by the patient for enteral feeding (typically via percutaneous gastrostomy tube).
Advise bed rest for the first 24 hours; the head of the bed should be below 30 degrees to avoid exacerbation of cerebral hypoperfusion in evolving infarcts (which sometimes can lead to neurologic 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. IV 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.
Educate patients and their families regarding stroke, its treatment, its complications, and plans for future care.
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. Provide referrals to stroke support groups.
Provide educational material from organizations such as the American Stroke Association and the National Stroke Association.
For patient education information, see eMedicineHealth's Stroke Center, as well as Stroke and Transient Ischemic Attack (TIA, Mini-stroke).
Draga Jichici, MD, FRCP, FAHA, Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada
Disclosure: Nothing to disclose.
Coauthor(s)
Arjun V Sharma, MBBS, MSc, Resident Physician, Department of Neurology, McMaster University School of Medicine, Canada
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Helmi L Lutsep, MD, Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center
Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Consultant, Abbott Vascular, Inc. .
Additional Contributors
Alison Elizabeth Baird, MBBS, PhD, MPH, FRACP, Professor of Neurology and Physiology/Pharmacology, Director of Division of Cerebrovascular Disease and Stroke, State University of New York Downstate Medical Center
Disclosure: Received consulting fee from National Institutes of Health for review panel membership; Received none from National Institutes of Health/DHHS for development of intellectual property; Received honoraria from Mount Sinai School of Medicine for speaking and teaching; Received consulting fee from Avanir Pharmaceuticals for consulting.
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