Ischemic Stroke in Emergency Medicine Treatment & Management

  • Author: Salvador Cruz-Flores, MD, MPH; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Oct 19, 2011
 

Approach Considerations

Multiple factors contribute to delays in seeking care for symptoms of stroke. Many strokes occur while patients are sleeping (also known as "wake-up" stroke) and are not discovered until the patient wakes. Stroke can leave some patients too incapacitated to call for help. Occasionally, a stroke goes unrecognized by the patient or their caregivers. (See Diagnostic Considerations).[30, 49]

The median time from symptom onset to ED presentation ranges from 4-24 hours in the United States.[18] Prehospital care providers are essential to timely stroke care. Course curricula for prehospital care providers are beginning to include more information on stroke than ever before. Through certification and ACLS instruction, as well as continuing medical education classes, prehospital care providers can remain current on stroke and promote stroke awareness in their own communities.

Physician and nursing staff involved in the care of patients who have had a stroke, in the ED and in the hospital, should participate in scheduled stroke education. This will help them to maintain the skills required to treat stroke patients effectively and to remain current on medical advances for all stroke types.

Establishing the time at which stroke symptoms first occurred is of paramount importance when considering patients for possible thrombolytic therapy. An essential question is, "When was the patient last seen to be normal?" It is advisable for emergency clinicians to rapidly enlist the assistance of family members or relatives to establish time of symptom onset and to identify other pertinent components of the patient's presentation history.

The central goal of therapy in acute ischemic stroke is to preserve the area of oligemia in the ischemic penumbra. The area of oligemia can be preserved by limiting the severity of ischemic injury (ie, neuronal protection) or by reducing the duration of ischemia (ie, restoring blood flow to the compromised area).

Recanalization strategies, including IV recombinant tissue-type plasminogen activator (rt-PA) and intra-arterial approaches, attempt to establish revascularization so that cells in the penumbra can be rescued before irreversible injury occurs. Restoring blood flow can mitigate the effects of ischemia only if performed quickly. Neuroprotective strategies are intended to preserve the penumbral tissues and to extend the time window for revascularization techniques; however, at the present time, no neuroprotective agents are available and approved for use in ischemic stroke.

The ischemic cascade offers many points at which such interventions could be attempted. Multiple strategies and interventions for blocking this cascade are currently under investigation. The timing of the restoration of cerebral blood flow appears to be a critical factor. Time may also prove to be a key factor in neuronal protection. It is expected that neuroprotective agents, which block the earliest stages of the ischemic cascade (eg, glutamate receptor antagonists, calcium channel blockers), will be effective only in the proximal phases of presentation.

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Emergency Response and Transport

Recognition that a stroke may have occurred and rapid transport to the appropriate receiving facility are necessary after addressing the ABCs. Of patients with signs or symptoms of stroke, 29-65% utilize some facet of the emergency medical services (EMS) system.[50, 51] Furthermore, most patients who call EMS are those who present within 3 hours of symptom onset. EMS use is associated with shorter time periods from symptom onset to hospital arrival.[52, 53]

Stroke should be a priority dispatch with prompt EMS response. EMS responders should provide in as timely a manner as possible advance notice to their emergency department destination so as to allow preparation and marshaling of personnel and resources. There is now ongoing development of stroke center designation that would then become the preferred destination for patients with acute stroke symptoms utilizing EMS.

Data supporting the use of emergency air transport for patients with acute stroke symptoms are limited. Further evaluation of this transportation modality is necessary to minimize the potentially high number of stroke mimics and to maximize the appropriate use of transport resources. Telemedicine is also a technology that has the potential to provide timely expert advice to rural and underserved clinics and hospitals.[18]

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Acute Management of Stroke

The goal for the acute management of patients with stroke is to stabilize the patient and to complete initial evaluation and assessment, including imaging and laboratory studies within 60 minutes of patient arrival.[18] A Finnish study demonstrated that time to treatment with thrombolytics can be decreased with changes in EMS and ED coordination and in ED procedures for treating acute stroke patients.[54] Critical decisions focus on blood pressure control, the need for intubation, and determination of risk-to-benefit profile for thrombolytic intervention. Referral to a physician with a special interest in stroke is ideal. Stroke care units exist and improve outcomes with specially trained personnel.

Comorbid medical problems need to be addressed. Hypoglycemia and hyperglycemia need to be identified and treated early in the evaluation. Hyperthermia is infrequently associated with stroke but can increase morbidity. Administration of acetaminophen, by mouth or per rectum, is indicated in the presence of fever (temperature >100.4°F). Supplemental oxygen is recommended when the patient has a documented oxygen requirement. In the small proportion of patients with stroke who are relatively hypotensive, pharmacologically increasing blood pressure may improve flow through critical stenoses.

An area of continued interest in acute stroke is glucose management. A Cochrane review found that the use of intravenous insulin to maintain serum glucose within the first few hours of ischemic stroke did not improve functional outcome, death, or final neurological deficit and significantly increased the risk of hypoglycemia.[55]

The 2011 AHA/ASA statement on CVT notes that appropriate acute therapy should focus on preventing complications and anticoagulation therapy. The recommended tests were MRI and MR venography (MRV) because they are the most sensitive. Blood workup should be performed later based on the underlying causes.[40]

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Thrombolytic Therapy

Thrombolytics restore cerebral blood flow among some patients with acute ischemic stroke and may lead to improvement or resolution of neurologic deficits. Unfortunately, thrombolytics can also cause symptomatic intracranial hemorrhage, defined as radiographic evidence of hemorrhage combined with escalation of the NIHSS score by 4 or more points. Therefore, if the patient is a candidate for thrombolytic therapy, a thorough review of the inclusion and exclusion criteria must be performed. The exclusion criteria largely focus on identifying risk of hemorrhagic complication associated with thrombolytic use.

While streptokinase and rt-PA have been shown to benefit patients with acute MI, only alteplase (rt-PA) has been shown to benefit selected patients with acute ischemic stroke.

In May 2009, the American Heart Association/American Stroke Association (AHA/ASA) guidelines for the administration of rt-PA following acute stroke were revised to expand the window of treatment from 3 hours to 4.5 hours to provide more patients with an opportunity to receive benefit from this effective therapy.[4, 5, 56] Eligibility criteria for treatment in the 3-4.5 hours after acute stroke are similar to those for treatment at earlier time periods, with any 1 of the following additional exclusion criteria:

  • Patients older than 80 years
  • All patients taking oral anticoagulants are excluded regardless of the international normalized ratio (INR)
  • Patients with baseline NIHSS greater than 25
  • Patients with a history of stroke and diabetes

Caution should be exercised in the administration of rt-PA to patients with major deficits. Patients with evidence of low attenuation (edema or ischemia) involving more than a third of the distribution of the MCA on their initial NCCT scan are less likely to have favorable outcome after thrombolytic therapy and are thought to be at higher risk for hemorrhagic transformation of their ischemic stroke.[32] In addition to the risk of symptomatic intracranial hemorrhage (6.4% in the NINDS trial), other complications include potentially hemodynamically significant hemorrhage and angioedema or allergic reactions.[18]

Streptokinase has not been shown to benefit patients with acute ischemic stroke, but it has been shown to increase their risk of intracranial hemorrhage and death.

Researchers have studied the use of transcranial ultrasound as a means of assisting rt-PA in thrombolysis. By delivering mechanical pressure waves to the thrombus, ultrasound can theoretically expose more of its surface to the circulating thrombolytic agent. Further research is necessary to determine the exact role of transcranial Doppler ultrasound in assisting thrombolytics in acute ischemic stroke.

No human trials comparing the IV versus intra-arterial administration of thrombolytics exist. Theoretic advantages to intra-arterial delivery may include the possibility that higher local concentrations of thrombolytic would allow lower total doses of the agent (and theoretically less risk of systemic bleed) and a longer therapeutic window; however, the longer time to administration via the intra-arterial approach versus the IV approach may mitigate some of this advantage.

For more information, see Thrombolytic Therapy.

For more information, see Reperfusion Injury in Stroke.

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Antiplatelet Agents

The International Stroke Trial and the Chinese Acute Stroke Trial (CAST) demonstrated modest benefit from the use of aspirin in the setting of acute ischemic stroke. The International Stroke Trial randomized 20,000 patients within 48 hours of stroke onset to treatment with aspirin 325 mg, subcutaneous heparin in 2 different dose regimens, aspirin with heparin, and a placebo. The study found that aspirin therapy reduced the risk of early stroke recurrence.[57, 58]

CAST evaluated 21,106 patients and had a 4-week mortality reduction of 3.3% contrasted to 3.9%. A separate study also found that the combination of aspirin and low–molecular-weight heparin did not significantly improve outcomes.[57]

The early initiation of aspirin plus extended-release dipyridamole is likely to be as safe and effective in preventing disability as is later initiation after 7 days following stroke onset, according to a German study. The study’s authors attempted to assess the precise time to initiate dipyridamole following ischemic stroke or TIA.[59] Patients from 46 stroke units who presented with an NIHSS score of 20 or less were randomly assigned to receive aspirin 25 mg plus extended-release dipyridamole 200 mg bid (early dipyridamole regimen) (n=283) or aspirin monotherapy (100 mg once daily) for 7 days (n=260). Therapy in either group was initiated within 24 hours of stroke onset.

After 2 weeks, all patients received aspirin plus dipyridamole for up to 90 days. At day 90, 154 (56%) patients in the early dipyridamole group and 133 (52%) in the aspirin plus later dipyridamole group had no or mild disability (P = .45).

Other antiplatelet agents are also under evaluation for use in the acute presentation of ischemic stroke. In a preliminary pilot study, abciximab was given within 6 hours to establish a safety profile. A trend toward improved outcome at 3 months for the treatment versus the placebo group was noted.[60] Further clinical trials are necessary.

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Neuroprotective Agents

Despite very promising results in several animal studies, as of yet no single neuroprotective agent in ischemic stroke is supported by randomized, placebo-controlled human studies. Nevertheless, substantial research is underway evaluating different neuroprotective strategies, including hypothermia.

For more information, see Neuroprotective Agents in Stroke.

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Mechanical Thrombolysis

Studies have evaluated the efficacy of mechanical clot disruption in the setting of acute stroke. In most cases, these technologies were used in combination with thrombolysis. In an investigation by Berlis et al, mechanical disruption via an endovascular photoacoustic device was found to be more effective than thrombolysis alone in recanalization rates.[61]

There are currently 2 FDA-approved devices for the endovascular treatment of acute ischemic stroke: the Concentric Retriever, which is mainly a grasping device, and the Penumbra device, which employs an aspiration function to remove clots.[62, 63, 64] The Penumbra trial demonstrated 82% recanalization in patients when using the aspiration function of the Penumbra device.

Successful recanalization occurred in 12 of 28 patients in the Mechanical Embolus Retrieval in Cerebral Ischemia (MERCI) 1 pilot trial, a study of the Merci Retrieval System.[65]

In a second MERCI study, recanalization was achieved in 48% of those in which the device was deployed. Clot was successfully retrieved from all major cerebral arteries; however, the recanalization rate for the MCA was lowest. A further study of clot extraction, the Prolyse in Acute Cerebral Thromboembolism II (PROACT II) study, identified a recanalization rate of 66%.[66, 67]

The Multi MERCI trial used the newer generation Concentric retrieval device (L5). Recanalization was demonstrated in approximately 55% of patients who did not receive t-PA and in 68% of those for whom t-PA was given in a group of patients with acute ischemic stroke presenting within 8 hours of onset of symptoms. Seventy-three percent of patients who failed IV t-PA therapy had recanalization following mechanical embolectomy.[68] However, based on these results, the FDA has cleared the use of the MERCI device in patients who are either ineligible for or who have failed IV thrombolytics.

According to the 2011 AHA/ASA statement on CVT, evidence is insufficient to draw conclusions about the value of endovascular thrombolysis in patients with CVT. For that reason, the statement recommends this therapy only in patients with progressive neurological deterioration that persists despite medical treatment.[40]

For more information, see Mechanical Thrombolysis in Acute Stroke.

For more information, see Cerebral Revascularization.

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Fever Control

Antipyretics are indicated for febrile stroke patients, since hyperthermia accelerates ischemic neuronal injury. Substantial experimental evidence suggests that mild brain hypothermia is neuroprotective. The use of induced hypothermia is currently being evaluated in phase I clinical trials.[69, 70, 71]

High body temperature in the first 12-24 hours after stroke onset has been associated with poor functional outcome. Results from the Paracetamol (Acetaminophen) In Stroke (PAIS) trial did not support the routine use of high-dose acetaminophen in patients with acute stroke. The study assessed whether early treatment with paracetamol improves functional outcome in patients with acute stroke by reducing body temperature and preventing fever. Patients (n=1400) were randomly assigned to receive acetaminophen (6 g daily) or placebo within 12 hours of symptom onset. After 3 months, improvement on the modified Rankin scale was not beyond what was expected.[72]

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Cerebral Edema Control

Significant cerebral edema after ischemic stroke is thought to be somewhat rare (10-20%); maximum severity of edema is reached 72-96 hours after the onset of stroke.

Early indicators of ischemia on presentation and on NCCT scans are independent indicators of potential swelling and deterioration. Mannitol and other therapies to reduce ICP may be used in emergency situations, although their usefulness in swelling secondary to ischemic stroke is unknown. No evidence exists supporting the use of corticosteroids to decrease cerebral edema in acute ischemic stroke. Prompt neurosurgical assistance should be sought when indicated.[18]

Patient position, hyperventilation, hyperosmolar therapy, and, rarely, barbiturate coma may be used, as in patients with increased ICP secondary to closed head injury. Hemicraniectomy has shown to decrease mortality and disability among patients with large hemispheric infarctions associated with life-threatening edema.[73, 74, 75, 76]

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Seizure Control

Seizures occur in 2-23% of patients within the first days after stroke. Although seizure prophylaxis is not indicated, prevention of subsequent seizures with standard antiepileptic therapy is recommended.[18]

The 2011 AHA/ASA CVT statement notes a lack of clinical trials on the use of anticonvulsants to control seizures, which occur in 37% of adults, 48% of children, and 71% of newborns who present with CVT. Therefore, opinions on their use vary greatly. However, because seizures increase the risk of anoxic damage, anticonvulsant treatment after even a single seizure is reasonable.[40]

Post-ischemia strokes are usually focal, but they may be generalized. A fraction of patients who have experienced stroke develop chronic seizure disorders. Seizures secondary to ischemic stroke should be managed in the same manner as other seizure disorders that arise as a result of neurologic injury.[18]

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Acute Decompensation or Escalation

In the case of the rapidly decompensating patient or the patient with deteriorating neurologic status, reassessment of ABCs as well as hemodynamics and reimaging are indicated. Many patients who develop hemorrhagic transformation or progressive cerebral edema will demonstrate acute clinical decline. Rarely, a patient may have escalation of symptoms secondary to increased size of the ischemic penumbra. Some advocate resetting the time window to zero in this circumstance and encourage consideration of reperfusion strategies.

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Anticoagulation and Prophylaxis

Heparin is known to prolong the lytic state caused by t-PA. Currently, data are inadequate to justify the utilization of heparin or other anticoagulants in the acute management of patients with ischemic stroke. Patients with embolic stroke who have another indication for anticoagulation (eg, atrial fibrillation) may be placed on anticoagulation therapy with the goal of preventing further embolic disease; however, the potential beneficial effects from that decision must be weighted against the risk of hemorrhagic transformation.[18]

Immobilized stroke patients who are not receiving anticoagulants, such as IV heparin or an oral anticoagulant, may benefit from the administration of low-dose, subcutaneous unfractionated or low–molecular-weight heparin, which reduces the risk of deep venous thrombosis.[18]

For more information, see Stroke Anticoagulation and Prophylaxis.

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Induced Hypothermia

Hypothermia is fast becoming the standard of care for the ongoing treatment of patients surviving cardiac arrest due to ventricular tachycardia or ventricular fibrillation. However, no major clinical study has demonstrated a role for hypothermia in the early treatment of ischemic stroke.[18]

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Carotid Endarterectomy

Many surgical and endovascular techniques have been studied in the treatment of acute ischemic stroke. Carotid endarterectomy has been used with some success in the acute management of internal carotid artery occlusions, but no evidence supports its use in acute stroke.

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Stroke Prevention

Primary prevention refers to the treatment of individuals with no previous history of stroke. Measures may include the use of platelet antiaggregants; 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (ie, statins); and exercise. In February 2011, AHA/ASA guidelines for the primary prevention of stroke were published. The guideline emphasizes the importance of lifestyle changes to reduce well-documented modifiable risk factors, citing an 80% lower risk of a first stroke in people who follow a healthy lifestyle compared with those who do not.[77]

Secondary prevention refers to the treatment of individuals who have already had a stroke. Measures may include the use of platelet antiaggregants, antihypertensives, HMG-CoA reductase inhibitors (statins), and lifestyle interventions.

Smoking cessation, blood pressure control, diabetes control, a low-fat diet, weight loss, and regular exercise should be encouraged as strongly as the medications described above. Written prescriptions for exercise and medications for smoking cessation (nicotine patch, bupropion, varenicline) increase the likelihood of success with these interventions.

In addition to these well-documented factors, the 2011 AHA/ASA guidelines for primary stroke prevention indicate that it is reasonable to avoid exposure to environmental tobacco smoke despite a lack of stroke-specific data.

The use of aspirin for primary stroke prevention is not recommended for persons at low risk. Aspirin is recommended for this purpose only in persons with at least a 6-10% risk of cardiovascular events over 10 years.[77]

For patients with stroke risk due to asymptomatic carotid artery stenosis, the 2011 AHA/ASA primary prevention guidelines state that older studies that showed revascularization surgery as more beneficial than medical treatment may now be obsolete due to improvements in medical therapies. Therefore, individual patient comorbidities, life expectancy, and preferences should determine whether medical treatment alone or carotid revascularization is selected.[77]

Atrial fibrillation is a major risk factor for stroke. The 2011 ACC Foundation (ACCF)/AHA/Heart Rhythm Society (HRS) atrial fibrillation guideline update on dabigatran states that the new anticoagulant dabigatran is useful as an alternative to warfarin in patients with atrial fibrillation who do not have a prosthetic heart valve or hemodynamically significant valve disease.[78]

The 2011 AHA/ASA primary stroke prevention guideline recommends that EDs screen for AF and assess patients for anticoagulation therapy if AF is found.[77]

For patients with atrial fibrillation after stroke or TIA, the 2010 AHA/ASA secondary stroke prevention guideline is in accord with the standard recommendation of warfarin, with aspirin as an alternative for patients who cannot take oral anticoagulants. However, clopidogrel should not be used in combination with aspirin for such patients because the bleeding risk of the combination is comparable to that of warfarin. The guideline states that the benefit of warfarin after stroke or TIA in patients without atrial fibrillation has not been established.[79]

The 2011 AHA/ASA guideline recommends ED-based smoking cessation interventions, and considers it reasonable for EDs to screen patients for hypertension and drug abuse.[77]

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Specialized Stroke Centers

Given the multitude of factors that go into the care of a patient with acute stroke, the concept of the specialized stroke center has evolved. The Brain Attack Coalition provided recommendations for the establishment of 2 tiers of stroke centers: primary stroke centers (PSCs) and comprehensive stroke centers (CSCs).[18] The Joint Commission for the Accreditation of Hospital Organizations (JCAHO) now provides accreditation for PSC, and efforts to establish the requirements that distinguish CSC are currently ongoing.

The PSC is designed to maximize the timely provision of stroke-specific therapy, including the administration of rt-PA, and is also capable of providing care to patients with uncomplicated stroke. The CSC shares the commitment that the PSC has to acute delivery of rt-PA and also provides care to patients with hemorrhagic stroke and intracranial hemorrhage and all patients with stroke requiring ICU level of care.[18]

Once patients have been identified as potential stroke patients, their ED evaluation must be fast-tracked to allow for the completion of required laboratory tests and requisite noncontrast head CT scanning, as well as the notification and involvement of neurologic consultation. These requirements have led to the development of "stroke codes" or "stroke activations" in which EMS crews have been trained to identify possible stroke patients and arrange for their speedy, preferential transport to a PSC or CSC.

Additionally, Stroke Centers should have personnel versed at monitoring stroke vital signs, which include the following:

  • Blood pressure
  • Glucose levels
  • Temperature
  • Oxygenation
  • Change in neurologic status

Hospitals with specialized stroke teams have demonstrated significantly increased rates of thrombolytic administration and decreased mortality. Cumulatively, the center should identify performance measures and include mechanisms for evaluating the effectiveness of the system as well as its component parts. The acute care of the stroke patient is more than anything a systems-based team approach requiring the cooperation of the ED, radiology, pharmacy, neurology, and ICU staff.

A stroke system should ensure effective interaction and collaboration among the agencies, services, and people involved in providing prevention and the timely identification, transport, treatment, and rehabilitation of stroke patients.

For more information, see Stroke Team Creation and Primary Stroke Center Certification.

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Palliative Care

Palliative care is an important component of comprehensive stroke care. Some stroke patients will simply not recover, and others will be in a state of debilitation such that the most humane and appropriate therapeutic concern is the comfort of the patient. Some patients have advanced directives providing instructions for medical providers in the event of severe medical illness or injury.

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Consultations

Consultations are tailored to individual patient needs.

An experienced professional who is sufficiently familiar with stroke or a stroke team should be available within 15 minutes of the patient's arrival in the ED. Often, occupational therapy, physical therapy, speech therapy, and physical medicine and rehabilitation experts are consulted within the first day of hospitalization. Consultation of cardiology and vascular surgery or neurosurgery may be warranted based on the results of carotid duplex scanning , neuroimaging, transthoracic and transesophageal echocardiography, and clinical course. During hospitalization, additional useful consultations include the following:

  • Home health care coordinator
  • Rehabilitation coordinator
  • Social worker
  • Psychiatrist (commonly for depression)
  • Dietitian
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Contributor Information and Disclosures
Author

Salvador Cruz-Flores, MD, MPH  Professor of Neurology, Director of Souers Stroke Institute, Department of Neurology and Psychiatry, St Louis University School of Medicine; Director, Mid-America Stroke Network and Neuroscience Critical Care Unit, St Louis University Hospital

Salvador Cruz-Flores, MD, MPH is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Neurology, American College of Physicians, American Heart Association, American Society of Neuroimaging, American Stroke Association, National Stroke Association, Neurocritical Care Society, and Society of Critical Care Medicine

Disclosure: Axio inc Honoraria Review panel membership; Roche Honoraria Review panel membership; Lilly Honoraria Review panel membership

Coauthor(s)

Jeffrey L Arnold, MD, FACEP  Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose.

Joseph U Becker, MD  Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine

Joseph U Becker, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Everett C Hills, MD, MS  Vice Chair, Department of Physical Medicine and Rehabilitation, Medical Director for Outpatient Services, Penn State Hershey Rehabilitation Hospital; Assistant Professor of Physical Medicine and Rehabilitation, Assistant Professor of Orthopaedics and Rehabilitation, Penn State Milton S Hershey Medical Center and Pennsylvania State University College of Medicine

Everett C Hills, MD, MS is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Congress of Rehabilitation Medicine, American Medical Association, American Society of Neurorehabilitation, Association of Academic Physiatrists, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Edward C Jauch, MD, MS, FAHA, FACEP  Professor, Division of Emergency Medicine and Department of Neurosciences, Medical University of South Carolina

Edward C Jauch, MD, MS, FAHA, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Heart Association, American Medical Association, National Stroke Association, Society for Academic Emergency Medicine, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Thomas A Kent, MD  Professor and Director of Stroke Research and Education, Department of Neurology, Baylor College of Medicine; Chief of Neurology, Michael E DeBakey Veterans Affairs Medical Center

Thomas A Kent, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences, Royal Society of Medicine, Sigma Xi, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

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

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Brett Kissela, MD  MS, Professor, Co-Director of the Neurology Residency Program, Vice-Chair of Education and Clinical Services, Department of Neurology, University of Cincinnati

Brett Kissela, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, and Phi Beta Kappa

Disclosure: Allergan Consulting fee Consulting; Allergan Honoraria Speaking and teaching

Consuelo T Lorenzo, MD  Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health Immanuel Rehabilitation Center

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Richard Salcido, MD  Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Brian Silver, MD, FRCPC, FAHA  Director, Stroke Center, Rhode Island Hospital; Associate Professor of Neurology, The Warren Alpert Medical School of Brown University

Brian Silver, MD, FRCPC, FAHA is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, American Stroke Association, Massachusetts Medical Society, Michigan State Medical Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: eMedicine Free access to materials Writing; MedLink Free access to materials Writing; Medicolegal defense work Consulting fee Consulting; Oakstone Publishing Payment Audio reviews

Brian Stettler, MD  Assistant Professor, Program Director, Emergency Medicine Residency Program, Department of Emergency Medicine, and Faculty Greater Cincinnati/Northern Kentucky Stroke Team, University of Cincinnati

Disclosure: Nothing to disclose.

Charles R Wira, MD  Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale School of Medicine

Charles R Wira, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

J Stephen Huff, MD  Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

J Stephen Huff, MD  Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Helmi L Lutsep, MD  Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

References

  1. Shiber JR, Fontane E, Adewale A. Stroke registry: hemorrhagic vs ischemic strokes. Am J Emerg Med. Mar 2010;28(3):331-3. [Medline].

  2. Adams HP Jr, Davis PH, Leira EC, Chang KC, Bendixen BH, Clarke WR, et al. Baseline NIH Stroke Scale score strongly predicts outcome after stroke: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology. Jul 13 1999;53(1):126-31. [Medline].

  3. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med. Dec 14 1995;333(24):1581-7. [Medline].

  4. Hacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. Sep 25 2008;359(13):1317-29. [Medline].

  5. [Guideline] Del Zoppo GJ, Saver JL, Jauch EC, Adams HP Jr. Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator: a science advisory from the American Heart Association/American Stroke Association. Stroke. Aug 2009;40(8):2945-8. [Medline]. [Full Text].

  6. Donnan GA, Fisher M, Macleod M, Davis SM. Stroke. Lancet. May 10 2008;371(9624):1612-23. [Medline].

  7. Dirnagl U, Iadecola C, Moskowitz MA. Pathobiology of ischaemic stroke: an integrated view. Trends Neurosci. Sep 1999;22(9):391-7. [Medline].

  8. Yuan J, Yankner BA. Apoptosis in the nervous system. Nature. Oct 12 2000;407(6805):802-9. [Medline].

  9. Kasner SE, Grotta JC. Emergency identification and treatment of acute ischemic stroke. Ann Emerg Med. Nov 1997;30(5):642-53. [Medline].

  10. Gotoh O, Asano T, Koide T, Takakura K. Ischemic brain edema following occlusion of the middle cerebral artery in the rat. I: The time courses of the brain water, sodium and potassium contents and blood-brain barrier permeability to 125I-albumin. Stroke. Jan-Feb 1985;16(1):101-9. [Medline].

  11. Bell BA, Symon L, Branston NM. CBF and time thresholds for the formation of ischemic cerebral edema, and effect of reperfusion in baboons. J Neurosurg. Jan 1985;62(1):31-41. [Medline].

  12. Mullins ME, Lev MH, Schellingerhout D, Gonzalez RG, Schaefer PW. Intracranial hemorrhage complicating acute stroke: how common is hemorrhagic stroke on initial head CT scan and how often is initial clinical diagnosis of acute stroke eventually confirmed?. AJNR Am J Neuroradiol. Oct 2005;26(9):2207-12. [Medline].

  13. Lyden PD, Zivin JA. Hemorrhagic transformation after cerebral ischemia: mechanisms and incidence. Cerebrovasc Brain Metab Rev. Spring 1993;5(1):1-16. [Medline].

  14. Nighoghossian N, Hermier M, Adeleine P, Blanc-Lasserre K, Derex L, Honnorat J, et al. Old microbleeds are a potential risk factor for cerebral bleeding after ischemic stroke: a gradient-echo T2*-weighted brain MRI study. Stroke. Mar 2002;33(3):735-42. [Medline].

  15. González RG. Imaging-guided acute ischemic stroke therapy: From "time is brain" to "physiology is brain". AJNR Am J Neuroradiol. Apr 2006;27(4):728-35. [Medline].

  16. Albers GW, Amarenco P, Easton JD, Sacco RL, Teal P. Antithrombotic and thrombolytic therapy for ischemic stroke: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. Sep 2004;126(3 Suppl):483S-512S. [Medline].

  17. Dubey N, Bakshi R, Wasay M, Dmochowski J. Early computed tomography hypodensity predicts hemorrhage after intravenous tissue plasminogen activator in acute ischemic stroke. J Neuroimaging. Apr 2001;11(2):184-8. [Medline].

  18. [Guideline] Adams HP Jr, del Zoppo G, Alberts MJ, Bhatt DL, Brass L, Furlan A, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. May 2007;38(5):1655-711. [Medline].

  19. Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. Jun 2009;40(6):2276-93. [Medline].

  20. Tintinalli J, Kellen G, Stapczynski J. American College of Emergency Physicians. Emergency Medicine: A Comprehensive Study Guide. 6th. New York: McGraw Hill; 2004:1382-1390.

  21. Leira EC, Chang KC, Davis PH, Clarke WR, Woolson RF, Hansen MD, et al. Can we predict early recurrence in acute stroke?. Cerebrovasc Dis. 2004;18(2):139-44. [Medline].

  22. Witt BJ, Ballman KV, Brown RD Jr, Meverden RA, Jacobsen SJ, Roger VL. The incidence of stroke after myocardial infarction: a meta-analysis. Am J Med. Apr 2006;119(4):354.e1-9. [Medline].

  23. Wessels T, Wessels C, Ellsiepen A, Reuter I, Trittmacher S, Stolz E. Contribution of diffusion-weighted imaging in determination of stroke etiology. AJNR Am J Neuroradiol. Jan 2006;27(1):35-9. [Medline].

  24. Roh JK, Kang DW, Lee SH, Yoon BW, Chang KH. Significance of acute multiple brain infarction on diffusion-weighted imaging. Stroke. Mar 2000;31(3):688-94. [Medline].

  25. Adams H, Adams R, Del Zoppo G, Goldstein LB. Guidelines for the early management of patients with ischemic stroke: 2005 guidelines update a scientific statement from the Stroke Council of the American Heart Association/American Stroke Association. Stroke. Apr 2005;36(4):916-23. [Medline].

  26. Derdeyn CP, Khosla A, Videen TO, Fritsch SM, Carpenter DL, Grubb RL Jr. Severe hemodynamic impairment and border zone--region infarction. Radiology. Jul 2001;220(1):195-201. [Medline].

  27. Pollanen MS, Deck JH. Directed embolization is an alternate cause of cerebral watershed infarction. Arch Pathol Lab Med. Oct 1989;113(10):1139-41. [Medline].

  28. Waterston JA, Brown MM, Butler P, Swash M. Small deep cerebral infarcts associated with occlusive internal carotid artery disease. A hemodynamic phenomenon?. Arch Neurol. Sep 1990;47(9):953-7. [Medline].

  29. U.S. Centers for Disease Control and Prevention and the Heart Disease and Stroke Statistics - 2007 Update, published by the American Heart Association. Available at http://www.strokecenter.org/patients/stats.htm. Accessed September 2008.

  30. American Heart Association. 2002 Heart and Stroke Facts Statistical Update. Dallas: American Heart Association; 2001.

  31. Schneider AT, Kissela B, Woo D, Kleindorfer D, Alwell K, Miller R, et al. Ischemic stroke subtypes: a population-based study of incidence rates among blacks and whites. Stroke. Jul 2004;35(7):1552-6. [Medline].

  32. von Kummer R, Allen KL, Holle R, Bozzao L, Bastianello S, Manelfe C, et al. Acute stroke: usefulness of early CT findings before thrombolytic therapy. Radiology. Nov 1997;205(2):327-33. [Medline].

  33. Hacke W, Kaste M, Fieschi C, Toni D, Lesaffre E, von Kummer R, et al. Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. The European Cooperative Acute Stroke Study (ECASS). JAMA. Oct 4 1995;274(13):1017-25. [Medline].

  34. Bruno A, Levine SR, Frankel MR, Brott TG, Lin Y, Tilley BC, et al. Admission glucose level and clinical outcomes in the NINDS rt-PA Stroke Trial. Neurology. Sep 10 2002;59(5):669-74. [Medline].

  35. Bruno A, Biller J, Adams HP Jr, Clarke WR, Woolson RF, Williams LS, et al. Acute blood glucose level and outcome from ischemic stroke. Trial of ORG 10172 in Acute Stroke Treatment (TOAST) Investigators. Neurology. Jan 15 1999;52(2):280-4. [Medline].

  36. Baird TA, Parsons MW, Phanh T, Butcher KS, Desmond PM, Tress BM, et al. Persistent poststroke hyperglycemia is independently associated with infarct expansion and worse clinical outcome. Stroke. Sep 2003;34(9):2208-14. [Medline].

  37. National Institutes of Health Stroke Scale. Available at http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf. Accessed October 2008.

  38. Huff JS. Stroke mimics and chameleons. Emerg Med Clin North Am. Aug 2002;20(3):583-95. [Medline].

  39. Libman RB, Wirkowski E, Alvir J, Rao TH. Conditions that mimic stroke in the emergency department. Implications for acute stroke trials. Arch Neurol. Nov 1995;52(11):1119-22. [Medline].

  40. [Guideline] Saposnik G, Barinagarrementeria F, Brown RD Jr, Bushnell CD, Cucchiara B, Cushman M, et al. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Apr 2011;42(4):1158-92. [Medline].

  41. Sorensen AG, Buonanno FS, Gonzalez RG, Schwamm LH, Lev MH, Huang-Hellinger FR, et al. Hyperacute stroke: evaluation with combined multisection diffusion-weighted and hemodynamically weighted echo-planar MR imaging. Radiology. May 1996;199(2):391-401. [Medline].

  42. González RG, Schaefer PW, Buonanno FS, Schwamm LH, Budzik RF, Rordorf G, et al. Diffusion-weighted MR imaging: diagnostic accuracy in patients imaged within 6 hours of stroke symptom onset. Radiology. Jan 1999;210(1):155-62. [Medline].

  43. Schellinger PD, Bryan RN, Caplan LR, Detre JA, Edelman RR, Jaigobin C, et al. Evidence-based guideline: The role of diffusion and perfusion MRI for the diagnosis of acute ischemic stroke: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. Jul 13 2010;75(2):177-85. [Medline].

  44. Sorensen AG, Copen WA, Ostergaard L, Buonanno FS, Gonzalez RG, Rordorf G, et al. Hyperacute stroke: simultaneous measurement of relative cerebral blood volume, relative cerebral blood flow, and mean tissue transit time. Radiology. Feb 1999;210(2):519-27. [Medline].

  45. Molyneux AJ, Kerr RS, Yu LM, Clarke M, Sneade M, Yarnold JA, et al. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. Sep 3-9 2005;366(9488):809-17. [Medline].

  46. Byrne JV. The aneurysm "clip or coil" debate. Acta Neurochir (Wien). Feb 2006;148(2):115-20. [Medline].

  47. Camerlingo M, Casto L, Censori B, Ferraro B, Gazzaniga GC, Mamoli A. Transcranial Doppler in acute ischemic stroke of the middle cerebral artery territories. Acta Neurol Scand. Aug 1993;88(2):108-11. [Medline].

  48. Sagar G, Riley P, Vohrah A. Is admission chest radiography of any clinical value in acute stroke patients?. Clin Radiol. Jul 1996;51(7):499-502. [Medline].

  49. Mandelzweig L, Goldbourt U, Boyko V, Tanne D. Perceptual, social, and behavioral factors associated with delays in seeking medical care in patients with symptoms of acute stroke. Stroke. May 2006;37(5):1248-53. [Medline].

  50. Handschu R, Poppe R, Rauss J, Neundörfer B, Erbguth F. Emergency calls in acute stroke. Stroke. Apr 2003;34(4):1005-9. [Medline].

  51. Williams JE, Rosamond WD, Morris DL. Stroke symptom attribution and time to emergency department arrival: the delay in accessing stroke healthcare study. Acad Emerg Med. Jan 2000;7(1):93-6. [Medline].

  52. Zweifler RM, Mendizabal JE, Cunningham S, Shah AK, Rothrock JF. Hospital presentation after stroke in a community sample: the Mobile Stroke Project. South Med J. Nov 2002;95(11):1263-8. [Medline].

  53. Lacy CR, Suh DC, Bueno M, Kostis JB. Delay in presentation and evaluation for acute stroke: Stroke Time Registry for Outcomes Knowledge and Epidemiology (S.T.R.O.K.E.). Stroke. Jan 2001;32(1):63-9. [Medline].

  54. Puolakka T, Väyrynen T, Häppölä O, Soinne L, Kuisma M, Lindsberg PJ. Sequential analysis of pretreatment delays in stroke thrombolysis. Acad Emerg Med. Sep 2010;17(9):965-9. [Medline].

  55. Bellolio MF, Gilmore RM, Stead LG. Insulin for glycaemic control in acute ischaemic stroke. Cochrane Database Syst Rev. Sep 7 2011;9:CD005346. [Medline].

  56. Wahlgren N, Ahmed N, Dávalos A, Hacke W, Millán M, Muir K, et al. Thrombolysis with alteplase 3-4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. Oct 11 2008;372(9646):1303-9. [Medline].

  57. CAST: randomised placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke. CAST (Chinese Acute Stroke Trial) Collaborative Group. Lancet. Jun 7 1997;349(9066):1641-9. [Medline].

  58. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. International Stroke Trial Collaborative Group. Lancet. May 31 1997;349(9065):1569-81. [Medline].

  59. [Best Evidence] Dengler R, Diener HC, Schwartz A, Grond M, Schumacher H, Machnig T, et al. Early treatment with aspirin plus extended-release dipyridamole for transient ischaemic attack or ischaemic stroke within 24 h of symptom onset (EARLY trial): a randomised, open-label, blinded-endpoint trial. Lancet Neurol. Feb 2010;9(2):159-66. [Medline].

  60. Abciximab in acute ischemic stroke: a randomized, double-blind, placebo-controlled, dose-escalation study. The Abciximab in Ischemic Stroke Investigators. Stroke. Mar 2000;31(3):601-9. [Medline].

  61. Berlis A, Lutsep H, Barnwell S, Norbash A, Wechsler L, Jungreis CA, et al. Mechanical thrombolysis in acute ischemic stroke with endovascular photoacoustic recanalization. Stroke. May 2004;35(5):1112-6. [Medline].

  62. Smith WS, Sung G, Saver J, Budzik R, Duckwiler G, Liebeskind DS, et al. Mechanical thrombectomy for acute ischemic stroke: final results of the Multi MERCI trial. Stroke. Apr 2008;39(4):1205-12. [Medline].

  63. Bose A, Henkes H, Alfke K, Reith W, Mayer TE, Berlis A. The Penumbra System: a mechanical device for the treatment of acute stroke due to thromboembolism. AJNR Am J Neuroradiol. Aug 2008;29(7):1409-13. [Medline].

  64. Martin PJ, Enevoldson TP, Humphrey PR. Causes of ischaemic stroke in the young. Postgrad Med J. Jan 1997;73(855):8-16. [Medline]. [Full Text].

  65. Gobin YP, Starkman S, Duckwiler GR, Grobelny T, Kidwell CS, Jahan R, et al. MERCI 1: a phase 1 study of Mechanical Embolus Removal in Cerebral Ischemia. Stroke. Dec 2004;35(12):2848-54. [Medline].

  66. Smith WS, Sung G, Starkman S, Saver JL, Kidwell CS, Gobin YP, et al. Safety and efficacy of mechanical embolectomy in acute ischemic stroke: results of the MERCI trial. Stroke. Jul 2005;36(7):1432-8. [Medline].

  67. Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, Kase C, et al. 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].

  68. Marks MP, Olivot JM, Kemp S, Lansberg MG, Bammer R, Wechsler LR, et al. Patients with acute stroke treated with intravenous tPA 3-6 hours after stroke onset: correlations between MR angiography findings and perfusion- and diffusion-weighted imaging in the DEFUSE study. Radiology. Nov 2008;249(2):614-23. [Medline]. [Full Text].

  69. Marion DW. Controlled normothermia in neurologic intensive care. Crit Care Med. Feb 2004;32(2 Suppl):S43-5. [Medline].

  70. Olsen TS, Weber UJ, Kammersgaard LP. Therapeutic hypothermia for acute stroke. Lancet Neurol. Jul 2003;2(7):410-6. [Medline].

  71. Hemmen TM, Raman R, Guluma KZ, Meyer BC, Gomes JA, Cruz-Flores S, et al. Intravenous thrombolysis plus hypothermia for acute treatment of ischemic stroke (ICTuS-L): final results. Stroke. Oct 2010;41(10):2265-70. [Medline].

  72. [Best Evidence] den Hertog HM, van der Worp HB, van Gemert HM, Algra A, Kappelle LJ, van Gijn J, et al. The Paracetamol (Acetaminophen) In Stroke (PAIS) trial: a multicentre, randomised, placebo-controlled, phase III trial. Lancet Neurol. May 2009;8(5):434-40. [Medline].

  73. Hofmeijer J, Kappelle LJ, Algra A, Amelink GJ, van Gijn J, van der Worp HB. Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol. Apr 2009;8(4):326-33. [Medline].

  74. Jüttler E, Schwab S, Schmiedek P, Unterberg A, Hennerici M, Woitzik J, et al. Decompressive Surgery for the Treatment of Malignant Infarction of the Middle Cerebral Artery (DESTINY): a randomized, controlled trial. Stroke. Sep 2007;38(9):2518-25. [Medline].

  75. Vahedi K, Hofmeijer J, Juettler E, Vicaut E, George B, Algra A, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol. Mar 2007;6(3):215-22. [Medline].

  76. Vahedi K, Vicaut E, Mateo J, Kurtz A, Orabi M, Guichard JP, et al. Sequential-design, multicenter, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial). Stroke. Sep 2007;38(9):2506-17. [Medline].

  77. [Guideline] Goldstein LB, Bushnell CD, Adams RJ, Appel LJ, Braun LT, Chaturvedi S, et al. Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Feb 2011;42(2):517-84. [Medline]. [Full Text].

  78. [Guideline] Wann LS, Curtis AB, Ellenbogen KA, Estes NA 3rd, Ezekowitz MD, Jackman WM, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on Dabigatran): a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. Mar 15 2011;123(10):1144-50. [Medline]. [Full Text].

  79. [Guideline] Furie KL, Kasner SE, Adams RJ, Albers GW, Bush RL, Fagan SC, et al. Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for healthcare professionals from the american heart association/american stroke association. Stroke. Jan 2011;42(1):227-76. [Medline]. [Full Text].

  80. Delgado AL, Jahromi B, Müller N, et al. Endovascular therapy of cerebral vasospasm: two year experience with angioplasty and/or intraarterial administration of nicardipine and verapamil. Acta Neurochir Suppl. 2008;104:347-351.

  81. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet. Nov 16 1996;348(9038):1329-39. [Medline].

  82. Adams RJ, Chimowitz MI, Alpert JS, Awad IA, Cerqueria MD, Fayad P, et al. Coronary risk evaluation in patients with transient ischemic attack and ischemic stroke: a scientific statement for healthcare professionals from the Stroke Council and the Council on Clinical Cardiology of the American Heart Association/American Stroke Association. Stroke. Sep 2003;34(9):2310-22. [Medline].

  83. Albers GW, Clark WM, Madden KP, Hamilton SA. ATLANTIS trial: results for patients treated within 3 hours of stroke onset. Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke. Stroke. Feb 2002;33(2):493-5. [Medline].

  84. Alexandrov AV, Molina CA, Grotta JC, Garami Z, Ford SR, Alvarez-Sabin J, et al. Ultrasound-enhanced systemic thrombolysis for acute ischemic stroke. N Engl J Med. Nov 18 2004;351(21):2170-8. [Medline].

  85. [Best Evidence] Amarenco P, Bogousslavsky J, Callahan A 3rd, Goldstein LB, Hennerici M, Rudolph AE, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. Aug 10 2006;355(6):549-59. [Medline].

  86. American Heart Association. Cost to treat heart disease in United States will triple by 2030. Published January 24, 2011. Available at http://www.newsroom.heart.org/index.php?s=43&item=1241. Accessed February 23, 2011.

  87. American Heart Association. Textbook of Advanced Cardiac Life Support. American Heart Association;1997.

  88. Aso K, Ogasawara K, Sasaki M, Kobayashi M, Suga Y, Chida K. Preoperative cerebrovascular reactivity to acetazolamide measured by brain perfusion SPECT predicts development of cerebral ischemic lesions caused by microemboli during carotid endarterectomy. Eur J Nucl Med Mol Imaging. Feb 2009;36(2):294-301. [Medline].

  89. Baigent C, Blackwell L, Collins R, Emberson J, Godwin J, Peto R, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet. May 30 2009;373(9678):1849-60. [Medline]. [Full Text].

  90. Barber PA, Darby DG, Desmond PM, Gerraty RP, Yang Q, Li T, et al. Identification of major ischemic change. Diffusion-weighted imaging versus computed tomography. Stroke. Oct 1999;30(10):2059-65. [Medline].

  91. Becker H, Desch H, Hacker H, Pencz A. CT fogging effect with ischemic cerebral infarcts. Neuroradiology. Oct 31 1979;18(4):185-92. [Medline].

  92. Bennett CL, Connors JM, Carwile JM, Moake JL, Bell WR, Tarantolo SR, et al. Thrombotic thrombocytopenic purpura associated with clopidogrel. N Engl J Med. Jun 15 2000;342(24):1773-7. [Medline].

  93. Borisch I, Horn M, Butz B, Zorger N, Draganski B, Hoelscher T. Preoperative evaluation of carotid artery stenosis: comparison of contrast-enhanced MR angiography and duplex sonography with digital subtraction angiography. AJNR Am J Neuroradiol. Jun-Jul 2003;24(6):1117-22. [Medline].

  94. Bozzao L, Bastianello S, Fantozzi LM, Angeloni U, Argentino C, Fieschi C. Correlation of angiographic and sequential CT findings in patients with evolving cerebral infarction. AJNR Am J Neuroradiol. Nov-Dec 1989;10(6):1215-22. [Medline].

  95. Bozzao L, Fantozzi LM, Bastianello S, Bozzao A, Argentino C, Lenzi GL, et al. Ischaemic supratentorial stroke: angiographic findings in patients examined in the very early phase. J Neurol. Sep 1989;236(6):340-2. [Medline].

  96. Brott T, Adams HP Jr, Olinger CP, Marler JR, Barsan WG, Biller J, et al. Measurements of acute cerebral infarction: a clinical examination scale. Stroke. Jul 1989;20(7):864-70. [Medline].

  97. Brown PB, Zwiebel WJ, Call GK. Degree of cervical carotid artery stenosis and hemispheric stroke: duplex US findings. Radiology. Feb 1989;170(2):541-3. [Medline].

  98. [Best Evidence] Bruno A, Kent TA, Coull BM, Shankar RR, Saha C, Becker KJ, et al. Treatment of hyperglycemia in ischemic stroke (THIS): a randomized pilot trial. Stroke. Feb 2008;39(2):384-9. [Medline].

  99. Burdette JH, Ricci PE, Petitti N, Elster AD. Cerebral infarction: time course of signal intensity changes on diffusion-weighted MR images. AJR Am J Roentgenol. Sep 1998;171(3):791-5. [Medline].

  100. Carroll BA. Duplex sonography in patients with hemispheric symptoms. J Ultrasound Med. Oct 1989;8(10):535-40. [Medline].

  101. Castillo J, Leira R, García MM, Serena J, Blanco M, Dávalos A. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. Feb 2004;35(2):520-6. [Medline].

  102. Chalela JA, Katzan I, Liebeskind DS, Rasmussen P, Zaidat O, Suarez JI, et al. Safety of intra-arterial thrombolysis in the postoperative period. Stroke. Jun 2001;32(6):1365-9. [Medline].

  103. Chandra V, Panday R, Laxminarayan R, et al. Disease Control Priorities in Developing Countries. In: Jamison DT, et al. Neurologic Disorders. The World Bank: Oxford University Press; 2006:627-643.

  104. Chappell FM, Wardlaw JM, Young GR, Gillard JH, Roditi GH, Yip B. Carotid artery stenosis: accuracy of noninvasive tests--individual patient data meta-analysis. Radiology. May 2009;251(2):493-502. [Medline].

  105. Chimowitz MI, Lynn MJ, Howlett-Smith H, Stern BJ, Hertzberg VS, Frankel MR, et al. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med. Mar 31 2005;352(13):1305-16. [Medline].

  106. Collaborative overview of randomised trials of antiplatelet therapy--I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists' Collaboration. BMJ. Jan 8 1994;308(6921):81-106. [Medline]. [Full Text].

  107. [Best Evidence] Connolly S, Pogue J, Hart R, Pfeffer M, Hohnloser S, Chrolavicius S, et al. Clopidogrel plus aspirin versus oral anticoagulation for atrial fibrillation in the Atrial fibrillation Clopidogrel Trial with Irbesartan for prevention of Vascular Events (ACTIVE W): a randomised controlled trial. Lancet. Jun 10 2006;367(9526):1903-12. [Medline].

  108. Crowther MA, Ginsberg JS, Julian J, Denburg J, Hirsh J, Douketis J, et al. A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome. N Engl J Med. Sep 18 2003;349(12):1133-8. [Medline].

  109. Dahlöf B, Devereux RB, Kjeldsen SE, Julius S, Beevers G, de Faire U, et al. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet. Mar 23 2002;359(9311):995-1003. [Medline].

  110. de Virgilio C, Toosie K, Arnell T, Lewis RJ, Donayre CE, Baker JD, et al. Asymptomatic carotid artery stenosis screening in patients with lower extremity atherosclerosis: a prospective study. Ann Vasc Surg. Jul 1997;11(4):374-7. [Medline].

  111. Derex L, Tomsick TA, Brott TG, Lewandowski CA, Frankel MR, Clark W. Outcome of stroke patients without angiographically revealed arterial occlusion within four hours of symptom onset. AJNR Am J Neuroradiol. Apr 2001;22(4):685-90. [Medline].

  112. [Best Evidence] Diedler J, Ahmed N, Sykora M, Uyttenboogaart M, Overgaard K, Luijckx GJ, et al. Safety of intravenous thrombolysis for acute ischemic stroke in patients receiving antiplatelet therapy at stroke onset. Stroke. Feb 2010;41(2):288-94. [Medline].

  113. Diener HC, Bogousslavsky J, Brass LM, Cimminiello C, Csiba L, Kaste M, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet. Jul 24-30 2004;364(9431):331-7. [Medline].

  114. Diener HC, Cunha L, Forbes C, Sivenius J, Smets P, Lowenthal A. European Stroke Prevention Study. 2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke. J Neurol Sci. Nov 1996;143(1-2):1-13. [Medline].

  115. Donnan GA, Hommel M, Davis SM, McNeil JJ. Streptokinase in acute ischaemic stroke. Steering Committees of the ASK and MAST-E trials. Australian Streptokinase Trial. Lancet. Jul 1 1995;346(8966):56. [Medline].

  116. Ducrocq X, Bracard S, Taillandier L, Anxionnat R, Lacour JC, Guillemin F, et al. Comparison of intravenous and intra-arterial urokinase thrombolysis for acute ischaemic stroke. J Neuroradiol. Jan 2005;32(1):26-32. [Medline].

  117. Eastwood JD, Lev MH, Azhari T, Lee TY, Barboriak DP, Delong DM, et al. CT perfusion scanning with deconvolution analysis: pilot study in patients with acute middle cerebral artery stroke. Radiology. Jan 2002;222(1):227-36. [Medline].

  118. Elster AD, Moody DM. Early cerebral infarction: gadopentetate dimeglumine enhancement. Radiology. Dec 1990;177(3):627-32. [Medline].

  119. Final report on the aspirin component of the ongoing Physicians' Health Study. Steering Committee of the Physicians' Health Study Research Group. N Engl J Med. Jul 20 1989;321(3):129-35. [Medline].

  120. Fisher CM. Capsular infarcts: the underlying vascular lesions. Arch Neurol. Feb 1979;36(2):65-73. [Medline].

  121. Fisher CM. Lacunar strokes and infarcts: a review. Neurology. Aug 1982;32(8):871-6. [Medline].

  122. González RG, Schaefer PW, Buonanno FS, Schwamm LH, Budzik RF, Rordorf G, et al. Diffusion-weighted MR imaging: diagnostic accuracy in patients imaged within 6 hours of stroke symptom onset. Radiology. Jan 1999;210(1):155-62. [Medline].

  123. Graham GD. Tissue plasminogen activator for acute ischemic stroke in clinical practice: a meta-analysis of safety data. Stroke. Dec 2003;34(12):2847-50. [Medline].

  124. Grant EG, Benson CB, Moneta GL, Alexandrov AV, Baker JD, Bluth EI, et al. Carotid artery stenosis: gray-scale and Doppler US diagnosis--Society of Radiologists in Ultrasound Consensus Conference. Radiology. Nov 2003;229(2):340-6. [Medline].

  125. Grant EG, Duerinckx AJ, El Saden SM, Melany ML, Hathout GM, Zimmerman PT, et al. Ability to use duplex US to quantify internal carotid arterial stenoses: fact or fiction?. Radiology. Jan 2000;214(1):247-52. [Medline].

  126. Hacke W, Albers G, Al-Rawi Y, Bogousslavsky J, Davalos A, Eliasziw M, et al. The Desmoteplase in Acute Ischemic Stroke Trial (DIAS): a phase II MRI-based 9-hour window acute stroke thrombolysis trial with intravenous desmoteplase. Stroke. Jan 2005;36(1):66-73. [Medline].

  127. Hacke W, Kaste M, Fieschi C, von Kummer R, Davalos A, Meier D, et al. Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II). Second European-Australasian Acute Stroke Study Investigators. Lancet. Oct 17 1998;352(9136):1245-51. [Medline].

  128. [Best Evidence] Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A. Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial. Lancet. May 20 2006;367(9523):1665-73. [Medline].

  129. Hass WK, Easton JD, Adams HP Jr, Pryse-Phillips W, Molony BA, Anderson S, et al. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. Ticlopidine Aspirin Stroke Study Group. N Engl J Med. Aug 24 1989;321(8):501-7. [Medline].

  130. Homma S, Sacco RL, Di Tullio MR, Sciacca RR, Mohr JP. Effect of medical treatment in stroke patients with patent foramen ovale: patent foramen ovale in Cryptogenic Stroke Study. Circulation. Jun 4 2002;105(22):2625-31. [Medline].

  131. Horowitz DR, Tuhrim S, Weinberger JM, Rudolph SH. Mechanisms in lacunar infarction. Stroke. Mar 1992;23(3):325-7. [Medline].

  132. Ingall TJ, O'Fallon WM, Asplund K, Goldfrank LR, Hertzberg VS, Louis TA. Findings from the reanalysis of the NINDS tissue plasminogen activator for acute ischemic stroke treatment trial. Stroke. Oct 2004;35(10):2418-24. [Medline].

  133. Iso H, Hennekens CH, Stampfer MJ, Rexrode KM, Colditz GA, Speizer FE, et al. Prospective study of aspirin use and risk of stroke in women. Stroke. Sep 1999;30(9):1764-71. [Medline].

  134. Johnston KC, Mayer SA. Blood pressure reduction in ischemic stroke: a two-edged sword?. Neurology. Oct 28 2003;61(8):1030-1. [Medline].

  135. Karonen JO, Partanen PL, Vanninen RL, Vainio PA, Aronen HJ. Evolution of MR contrast enhancement patterns during the first week after acute ischemic stroke. AJNR Am J Neuroradiol. Jan 2001;22(1):103-11. [Medline].

  136. Klotz E, König M. Perfusion measurements of the brain: using dynamic CT for the quantitative assessment of cerebral ischemia in acute stroke. Eur J Radiol. Jun 1999;30(3):170-84. [Medline].

  137. Kolin A, Norris JW. Myocardial damage from acute cerebral lesions. Stroke. Nov-Dec 1984;15(6):990-3. [Medline].

  138. Krieger D, Hacke W. Stroke: Pathophysiology, Diagnosis and Management. In: The intensive care of the stroke patient. 3rd ed. New York, NY: Churchill Livingstone; 1998.

  139. Kucinski T, Väterlein O, Glauche V, Fiehler J, Klotz E, Eckert B, et al. Correlation of apparent diffusion coefficient and computed tomography density in acute ischemic stroke. Stroke. Jul 2002;33(7):1786-91. [Medline].

  140. Kurl S, Laukkanen JA, Rauramaa R, Lakka TA, Sivenius J, Salonen JT. Cardiorespiratory fitness and the risk for stroke in men. Arch Intern Med. Jul 28 2003;163(14):1682-8. [Medline].

  141. Lee LJ, Kidwell CS, Alger J, Starkman S, Saver JL. Impact on stroke subtype diagnosis of early diffusion-weighted magnetic resonance imaging and magnetic resonance angiography. Stroke. May 2000;31(5):1081-9. [Medline].

  142. Levine SR, Brey RL, Tilley BC, Thompson JL, Sacco RL, Sciacca RR, et al. Antiphospholipid antibodies and subsequent thrombo-occlusive events in patients with ischemic stroke. JAMA. Feb 4 2004;291(5):576-84. [Medline].

  143. Lövblad KO, Baird AE, Schlaug G, Benfield A, Siewert B, Voetsch B, et al. Ischemic lesion volumes in acute stroke by diffusion-weighted magnetic resonance imaging correlate with clinical outcome. Ann Neurol. Aug 1997;42(2):164-70. [Medline].

  144. Macleod MR, Davis SM, Mitchell PJ, Gerraty RP, Fitt G, Hankey GJ, et al. Results of a multicentre, randomised controlled trial of intra-arterial urokinase in the treatment of acute posterior circulation ischaemic stroke. Cerebrovasc Dis. 2005;20(1):12-7. [Medline].

  145. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. Dec 18 2002;288(23):2981-97. [Medline].

  146. Marks MP. CT in ischemic stroke. Neuroimaging Clin N Am. Aug 1998;8(3):515-23. [Medline].

  147. Marler JR, Jones PW, Emr M. Proceedings of a National Symposium on Rapid Identification and Treatment of Acute Stroke. In: Bethesda MD: The National Institute of Neurological Disorders and Stroke, National Institutes of Health;. August 1997.

  148. Mas JL, Arquizan C, Lamy C, Zuber M, Cabanes L, Derumeaux G, et al. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med. Dec 13 2001;345(24):1740-6. [Medline].

  149. Meerwaldt R, Slart RH, van Dam GM, Luijckx GJ, Tio RA, Zeebregts CJ. PET/SPECT imaging: from carotid vulnerability to brain viability. Eur J Radiol. Apr 2010;74(1):104-9. [Medline].

  150. Milhaud D, Popp J, Thouvenot E, Heroum C, Bonafé A. Mechanical ventilation in ischemic stroke. J Stroke Cerebrovasc Dis. Jul-Aug 2004;13(4):183-8. [Medline].

  151. Minematsu K, Li L, Fisher M, Sotak CH, Davis MA, Fiandaca MS. Diffusion-weighted magnetic resonance imaging: rapid and quantitative detection of focal brain ischemia. Neurology. Jan 1992;42(1):235-40. [Medline].

  152. Mohr JP, Thompson JL, Lazar RM, Levin B, Sacco RL, Furie KL, et al. A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke. N Engl J Med. Nov 15 2001;345(20):1444-51. [Medline].

  153. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. Jul 6 2002;360(9326):7-22. [Medline].

  154. Nabavi DG, Cenic A, Craen RA, Gelb AW, Bennett JD, Kozak R, et al. CT assessment of cerebral perfusion: experimental validation and initial clinical experience. Radiology. Oct 1999;213(1):141-9. [Medline].

  155. Neumann-Haefelin T, Wittsack HJ, Wenserski F, Siebler M, Seitz RJ, Mödder U, et al. Diffusion- and perfusion-weighted MRI. The DWI/PWI mismatch region in acute stroke. Stroke. Aug 1999;30(8):1591-7. [Medline].

  156. Noguchi K, Ogawa T, Inugami A, Fujita H, Hatazawa J, Shimosegawa E, et al. MRI of acute cerebral infarction: a comparison of FLAIR and T2-weighted fast spin-echo imaging. Neuroradiology. Jun 1997;39(6):406-10. [Medline].

  157. Oppenheim C, Logak M, Dormont D, Lehéricy S, Manaï R, Samson Y, et al. Diagnosis of acute ischaemic stroke with fluid-attenuated inversion recovery and diffusion-weighted sequences. Neuroradiology. Aug 2000;42(8):602-7. [Medline].

  158. Oppenheimer SM, Hachinski VC. The cardiac consequences of stroke. Neurol Clin. Feb 1992;10(1):167-76. [Medline].

  159. Padma V, Fisher M, Moonis M. Role of heparin and low-molecular-weight heparins in the management of acute ischemic stroke. Expert Rev Cardiovasc Ther. May 2006;4(3):405-15. [Medline].

  160. Paula WK. Heads down: flat positioning improves blood flow velocity in acute ischemic stroke. Neurology. Nov 8 2005;65(9):1514; author reply 1514. [Medline].

  161. Peto R, Gray R, Collins R, Wheatley K, Hennekens C, Jamrozik K, et al. Randomised trial of prophylactic daily aspirin in British male doctors. Br Med J (Clin Res Ed). Jan 30 1988;296(6618):313-6. [Medline]. [Full Text].

  162. Plehn JF, Davis BR, Sacks FM, Rouleau JL, Pfeffer MA, Bernstein V, et al. Reduction of stroke incidence after myocardial infarction with pravastatin: the Cholesterol and Recurrent Events (CARE) study. The Care Investigators. Circulation. Jan 19 1999;99(2):216-23. [Medline].

  163. Powers WJ, Grubb RL Jr, Darriet D, Raichle ME. Cerebral blood flow and cerebral metabolic rate of oxygen requirements for cerebral function and viability in humans. J Cereb Blood Flow Metab. Dec 1985;5(4):600-608. [Medline].

  164. Pressman BD, Tourje EJ, Thompson JR. An early CT sign of ischemic infarction: increased density in a cerebral artery. AJR Am J Roentgenol. Sep 1987;149(3):583-6. [Medline].

  165. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet. Sep 29 2001;358(9287):1033-41. [Medline].

  166. [Best Evidence] Ridker PM, Cook NR, Lee IM, Gordon D, Gaziano JM, Manson JE, et al. A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women. N Engl J Med. Mar 31 2005;352(13):1293-304. [Medline].

  167. Rouhl RP, Lodder J. ESPRIT: is aspirin plus dipyridamole superior to aspirin alone in TIA or minor stroke patients?. Expert Rev Neurother. Nov 2008;8(11):1661-5. [Medline].

  168. Rubin GD, Rofsky NM. Cerebral Arteries and Veins. In: CT and MR Angiography: Comprehensive Vascular Assessment. Lippincott Williams & Wilkins; 2009:381-441.

  169. Saur D, Kucinski T, Grzyska U, Eckert B, Eggers C, Niesen W. Sensitivity and interrater agreement of CT and diffusion-weighted MR imaging in hyperacute stroke. AJNR Am J Neuroradiol. May 2003;24(5):878-85. [Medline].

  170. Schaefer PW, Hassankhani A, Putman C, Sorensen AG, Schwamm L, Koroshetz W. Characterization and evolution of diffusion MR imaging abnormalities in stroke patients undergoing intra-arterial thrombolysis. AJNR Am J Neuroradiol. Jun-Jul 2004;25(6):951-7. [Medline].

  171. Schaefer PW, Roccatagliata L, Ledezma C, Hoh B, Schwamm LH, Koroshetz W. First-pass quantitative CT perfusion identifies thresholds for salvageable penumbra in acute stroke patients treated with intra-arterial therapy. AJNR Am J Neuroradiol. Jan 2006;27(1):20-5. [Medline].

  172. Schrader J, Lüders S, Kulschewski A, Hammersen F, Plate K, Berger J, et al. Morbidity and Mortality After Stroke, Eprosartan Compared with Nitrendipine for Secondary Prevention: principal results of a prospective randomized controlled study (MOSES). Stroke. Jun 2005;36(6):1218-26. [Medline].

  173. Schramm P, Schellinger PD, Klotz E, Kallenberg K, Fiebach JB, Külkens S, et al. Comparison of perfusion computed tomography and computed tomography angiography source images with perfusion-weighted imaging and diffusion-weighted imaging in patients with acute stroke of less than 6 hours' duration. Stroke. Jul 2004;35(7):1652-8. [Medline].

  174. Schuierer G, Huk W. The unilateral hyperdense middle cerebral artery: an early CT-sign of embolism or thrombosis. Neuroradiology. 1988;30(2):120-2. [Medline].

  175. Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, MacFarlane PW, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med. Nov 16 1995;333(20):1301-7. [Medline].

  176. Shetty SK, Lev MH. CT perfusion in acute stroke. Neuroimaging Clin N Am. Aug 2005;15(3):481-501, ix. [Medline].

  177. Sims JR, Rordorf G, Smith EE, Koroshetz WJ, Lev MH, Buonanno F, et al. Arterial occlusion revealed by CT angiography predicts NIH stroke score and acute outcomes after IV tPA treatment. AJNR Am J Neuroradiol. Feb 2005;26(2):246-51. [Medline].

  178. Singer DE, Albers GW, Dalen JE, Go AS, Halperin JL, Manning WJ. Antithrombotic therapy in atrial fibrillation: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. Sep 2004;126(3 Suppl):429S-456S. [Medline].

  179. Sirna S, Biller J, Skorton DJ, Seabold JE. Cardiac evaluation of the patient with stroke. Stroke. Jan 1990;21(1):14-23. [Medline].

  180. Skriver EB, Olsen TS. Transient disappearance of cerebral infarcts on CT scan, the so-called fogging effect. Neuroradiology. 1981;22(2):61-5. [Medline].

  181. Sterzi R, Candelise L, Gattinoni M, Bersano A, Micieli G. Stroke-unit care for patients with acute stroke. Lancet. Apr 14 2007;369(9569):1255. [Medline].

  182. Sunshine JL, Tarr RW, Lanzieri CF, Landis DM, Selman WR, Lewin JS. Hyperacute stroke: ultrafast MR imaging to triage patients prior to therapy. Radiology. Aug 1999;212(2):325-32. [Medline].

  183. Thrombolytic therapy with streptokinase in acute ischemic stroke. The Multicenter Acute Stroke Trial--Europe Study Group. N Engl J Med. Jul 18 1996;335(3):145-50. [Medline].

  184. Tijssen JG. Low-dose and high-dose acetylsalicylic acid, with and without dipyridamole: a review of clinical trial results. Neurology. Sep 1998;51(3 Suppl 3):S15-6. [Medline].

  185. Tomura N, Uemura K, Inugami A, Fujita H, Higano S, Shishido F. Early CT finding in cerebral infarction: obscuration of the lentiform nucleus. Radiology. Aug 1988;168(2):463-7. [Medline].

  186. Torres-Mozqueda F, He J, Yeh IB, Schwamm LH, Lev MH, Schaefer PW. An acute ischemic stroke classification instrument that includes CT or MR angiography: the Boston Acute Stroke Imaging Scale. AJNR Am J Neuroradiol. Jun 2008;29(6):1111-7. [Medline].

  187. Toyoda K, Ida M, Fukuda K. Fluid-attenuated inversion recovery intraarterial signal: an early sign of hyperacute cerebral ischemia. AJNR Am J Neuroradiol. Jun-Jul 2001;22(6):1021-9. [Medline].

  188. Truwit CL, Barkovich AJ, Gean-Marton A, Hibri N, Norman D. Loss of the insular ribbon: another early CT sign of acute middle cerebral artery infarction. Radiology. Sep 1990;176(3):801-6. [Medline].

  189. Tsivgoulis G, Eggers J, Ribo M, Perren F, Saqqur M, Rubiera M, et al. Safety and efficacy of ultrasound-enhanced thrombolysis: a comprehensive review and meta-analysis of randomized and nonrandomized studies. Stroke. Feb 2010;41(2):280-7. [Medline].

  190. Verro P, Tanenbaum LN, Borden NM, Sen S, Eshkar N. CT angiography in acute ischemic stroke: preliminary results. Stroke. Jan 2002;33(1):276-8. [Medline].

  191. von Kummer R, Meyding-Lamadé U, Forsting M, Rosin L, Rieke K, Hacke W. Sensitivity and prognostic value of early CT in occlusion of the middle cerebral artery trunk. AJNR Am J Neuroradiol. Jan 1994;15(1):9-15; discussion 16-8. [Medline].

  192. Wardlaw JM, Mielke O. Early signs of brain infarction at CT: observer reliability and outcome after thrombolytic treatment--systematic review. Radiology. May 2005;235(2):444-53. [Medline].

  193. Wildermuth S, Knauth M, Brandt T, Winter R, Sartor K, Hacke W. Role of CT angiography in patient selection for thrombolytic therapy in acute hemispheric stroke. Stroke. May 1998;29(5):935-8. [Medline].

  194. Williams LS, Yilmaz EY, Lopez-Yunez AM. Retrospective assessment of initial stroke severity with the NIH Stroke Scale. Stroke. Apr 2000;31(4):858-62. [Medline].

  195. Wintermark M, Maeder P, Thiran JP, Schnyder P, Meuli R. Quantitative assessment of regional cerebral blood flows by perfusion CT studies at low injection rates: a critical review of the underlying theoretical models. Eur Radiol. 2001;11(7):1220-30. [Medline].

  196. Wintermark M, Reichhart M, Thiran JP, Maeder P, Chalaron M, Schnyder P, et al. Prognostic accuracy of cerebral blood flow measurement by perfusion computed tomography, at the time of emergency room admission, in acute stroke patients. Ann Neurol. Apr 2002;51(4):417-32. [Medline].

  197. Woodcock RJ Jr, Short J, Do HM, Jensen ME, Kallmes DF. Imaging of acute subarachnoid hemorrhage with a fluid-attenuated inversion recovery sequence in an animal model: comparison with non-contrast-enhanced CT. AJNR Am J Neuroradiol. Oct 2001;22(9):1698-703. [Medline].

  198. Wright WL, Geocadin RG. Postresuscitative intensive care: neuroprotective strategies after cardiac arrest. Semin Neurol. Sep 2006;26(4):396-402. [Medline].

  199. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. Jan 20 2000;342(3):145-53. [Medline].

 
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Axial noncontrast computed tomography (NCCT) demonstrates diffuse hypodensity in the right lentiform nucleus with mass effect upon the frontal horn of the right lateral ventricle in this 70-year-old female with history of left-sided weakness for several hours duration.
Magnetic Resonance Imaging (MRI) was subsequently obtained in the same patient as in the above image. An axial T2 FLAIR image (left) demonstrates high signal in the lentiform nucleus with mass effect. The axial diffusion weighted image (middle) demonstrates high signal in the same area with corresponding low signal on the apparent diffusion coefficient (ADC) maps, consistent with true restricted diffusion and an acute infarction. Maximum intensity projection from a 3D time-of-flight magnetic resonance angiogram (MRA, right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).
MIP image from a CTA demonstrates a filling defect or high-grade stenosis at the branching point of the right MCA trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.
Cardioembolic stroke: Axial diffusion-weighted images demonstrate scattered foci of high signal in the subcortical and deep white matter bilaterally in a patient with a known cardiac source for embolization. An area of low signal in the left gangliocapsular region may be secondary to prior hemorrhage or subacute to chronic lacunar infarct. Recurrent strokes are most commonly secondary to cardioembolic phenomenon.
Axial noncontrast CT demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in this 60-year-old male with new onset of right-sided weakness. The lesion demonstrates high signal on the FLAIR sequence (middle image) and diffusion-weighted MRI (right image), with low signal on the ADC maps indicating an acute lacunar infarction. Lacunar infarcts are typically no more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata, brainstem and cerebellum.
MRI was obtained to evaluate this 62-year-old hypertensive and diabetic male with a history of transient episodes of right-sided weakness and aphasia. The FLAIR image (left) demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter, bilaterally. This configuration is typical for deep border-zone or watershed infarction, in this case the anterior and posterior MCA watershed areas. The left sided infarcts have corresponding low signal on the ADC map (right), signifying acuity. An old left posterior parietal infarct is noted as well.
This 48-year-old male presented with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference. Angiogram with selective injection of the right internal carotid artery demonstrates occlusion of the M1 segment of the right MCA and A2 segment of the right ACA (images courtesy of Concentric Medical).
Follow-up imaging in the same patient as in the above image after mechanical embolectomy demonstrates complete recanalization of the right middle cerebral artery and partial recanalization of the right A2 segment (images courtesy of Concentric Medical).
Cerebral angiogram demonstrates an occlusion of the distal basilar artery in this 31-year-old male approximately 4.5 hours after symptom onset (images courtesy of Concentric Medical).
Image on the left demonstrates deployment of a clot retrieval device in the same patient as in the above image. Follow up angiogram after embolectomy demonstrates recanalization of the distal basilar artery with filling of the superior cerebellar arteries and posterior cerebral arteries. The patient had complete resolution of symptoms following embolectomy (images courtesy of Concentric Medical).
Noncontrast CT in this 52-year-old male with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity and sulcal effacement involving the left anterior and middle cerebral artery territories consistent with acute infarction. There are scattered curvilinear areas of hyperdensity noted suggestive of developing petechial hemorrhage in this large area of infarction.
MRA in the same patient as in the above image (left) demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal MCA trunk and attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high signal confirmed to be true restricted diffusion on the ADC map consistent with acute infarction.
Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the ICA bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the MCA with the apex representing the Sylvian point.
Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SICA) arise distally from the basilar artery prior to its bifurcation into the posterior cerebral arteries.
Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The MCA can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches) and M4 (distal cortical branches on the lateral hemispheric convexities).
Regions of interest are selected for arterial and venous input (image on left) for dynamic susceptibility-weighted perfusion MRI. Signal-time curves (image on right) obtained from these ROI demonstrate transient signal drop following the administration of IV contrast. The information obtained from the dynamic parenchymal signal changes postcontrast is used to generate maps of different perfusion parameters.
Vascular distributions: MCA infarction. Noncontrast CT demonstrates a large acute infarction in the MCA territory involving the lateral surfaces of the left frontal, parietal, and temporal lobes, as well as the left insular and subinsular regions, with mass effect and rightward midline shift. There is sparing of the caudate head and at least part of the lentiform nucleus and internal capsule, which receive blood supply from the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of involvement of the medial frontal lobe (ACA territory), thalami and paramedian occipital lobe (PCA territory).
Vascular distributions: anterior choroidal artery infarction. The diffusion-weighted image (left) demonstrates high signal with associated signal dropout on the apparent diffusion coefficient (ADC) map involving the posterior limb of the internal capsule. This is the typical distribution of the anterior choroidal artery, the last branch of the internal carotid artery before bifurcating into the anterior and middle cerebral arteries. The anterior choroidal artery may also arise from the MCA.
Vascular distributions: ACA infarction. Diffusion-weighted image on the left demonstrates high signal in the paramedian frontal and high parietal regions. The opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger ACA infarction involving the left paramedian frontal and posterior parietal regions. There is also infarction of the lateral temporoparietal regions bilaterally (both MCA distributions), greater on the left indicating multivessel involvement suggesting emboli.
Vascular distributions: PCA infarction. The noncontrast CT images demonstrate PCA distribution infarction involving the right occipital and inferomedial temporal lobes. The image on the right demonstrates additional involvement of the thalamus, also part of the PCA territory.
The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The MCA (red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal and anterior temporal lobes, insula and basal ganglia. The ACA (blue) supplies the medial frontal and parietal lobes. The PCA (green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
Table 1. Vascular Supply to the Brain
VASCULAR TERRITORYStructures Supplied
Anterior Circulation (Carotid)
Anterior Cerebral ArteryCortical branches: medial frontal and parietal lobe



Medial lenticulostriate branches: caudate head, globus pallidus, anterior limb of internal capsule



Middle Cerebral ArteryCortical branches: lateral frontal and parietal lobes lateral and anterior temporal lobe



Lateral lenticulostriate branches: globus pallidus and putamen, internal capsule



Anterior Choroidal ArteryOptic tracts, medial temporal lobe, ventrolateral thalamus, corona radiata, posterior limb of the internal capsule
Posterior Circulation (Vertebrobasilar)
Posterior Cerebral ArteryCortical branches: occipital lobes, medial and posterior temporal and parietal lobes



Perforating branches: brainstem, posterior thalamus and midbrain



Posterior Inferior Cerebellar ArteryInferior vermis; posterior and inferior cerebellar hemispheres
Anterior Inferior Cerebellar ArteryAnterolateral cerebellum
Superior Cerebellar ArterySuperior vermis; superior cerebellum
Table 2. NIH Stroke Scale
CategoryDescriptionScore
1alevel of consciousness (LOC)Alert



Drowsy



Stuporous



Coma



0



1



2



3



1bLOC questions (month, age)Answers both correctly



Answers 1 correctly



Incorrect on both



0



1



2



1cAnswers both correctly Answers 1 correctly Incorrect on bothObeys both correctly



Obeys 1 correctly



Incorrect on both



0



1



2



2Best gaze (follow finger)Normal



Partial gaze palsy



Forced deviation



0



1



2



3Best visual (visual fields)No visual loss



Partial hemianopia



Complete hemianopia



Bilateral hemianopia



0



1



2



3



4Facial palsy (show teeth, raise brows, squeeze eyes shut)Normal Minor



Partial Complete



0



1



2



3



5Motor arm left* (raise 90°, hold 10 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



6Motor arm right* (raise 90°, hold 10 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



7Motor leg left* (raise 30°, hold 5 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



8Motor leg right* (raise 30°, hold 5 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



9Limb ataxia (finger-nose, heel-shin)Absent



Present in 1 limb



Present in 2 limbs



0



1



2



10Sensory (pinprick to face, arm, leg)Normal



Partial loss



Severe loss



0



1



2



11Extinction/neglect (double simultaneous testing)No neglect



Partial neglect



Complete neglect



0



1



2



12Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty")Normal articulation



Mild to moderate dysarthria



Near to unintelligible or worse



0



1



2



13Best language** (name items, describe pictures)No aphasia



Mild to moderate aphasia



Severe aphasia



Mute



0



1



2



3



Total-0-42
* For limbs with amputation, joint fusion, etc, score 9 and explain.



** For intubation or other physical barriers to speech, score 9 and explain. Do not add 9 to the total score. NIH Stroke Scale (PDF)



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