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Acute Stroke Management Resource:
Canadian Best Practice Recommendations for
Acute Stroke Management
2007
Objective
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Review the Canadian Best Practice Recommendations for
Stroke Care: 2006 related to Acute Stroke Management
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Stroke Unit Care
Brain Imaging
Blood Glucose
Acute Thrombolytic Treatment
Carotid Artery Imaging
Dysphagia Assessment
Acute Aspirin Therapy
Management of Subarachnoid and Intracerebral
Hemorrhage
Canadian Best Practice Recommendations
for Stroke Care: 2006
 Public Awareness and Responsiveness
 Patient and Caregiver Education
 Stroke Prevention
 Acute Stroke Management
 Stroke Rehabilitation and Community
Reintegration
 Follow-up and Community Reintegration after
Stroke
Canadian Best Practice Recommendations
for Acute Ischemic Stroke Management
 Acute Stroke Unit Care
 Brain Imaging
 Blood Glucose
 Acute Thrombolytic Treatment
 Carotid Artery Imaging
 Dysphagia Assessment
 Acute Aspirin Therapy
 Management of Subarachnoid and
Intracerebral Hemorrhage
Management of Patients with Acute
Ischemic Stroke
Objectives
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To review the goals of acute ischemic stroke
management
To review contributing factors to ischemic damage:
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Blood pressure
Blood Glucose
Body Temperature
Oxygen saturation
To review the Best Practice Recommendations related to
assessment:
 Brain Imaging
 Carotid Artery Imaging
 Dysphagia Assessment
Objectives
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To review the Best Practice Recommendations related to
interventions:
 Acute Aspirin Therapy
 Acute Thrombolytic Treatment
 Acute Stroke Unit
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To review the Best Practice Recommendations related to Mgt of
Subarachnoid and Intracerebral Hemorrhage:
To review acute complications of stroke:
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Increased intracranial pressure
Cerebral edema
Hemorrhagic transformation
Seizures
Shoulder pain assessment and treatment
Goals of Acute Ischemic Stroke Management
Reduce or minimize ischemic damage
 Reduce cerebral edema
 Prevent secondary complications
 Determine etiology of stroke
 Prevent recurrent stroke
 Facilitate access to rehabilitation and community
reintegration
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Contributing Factors to Ischemic Damage
Blood pressure
 Blood glucose
 Body temperature
 Oxygen saturation
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Contributing Factors to Ischemic Damage
Normal Brain Tissue
Dying Brain Tissue
Infarcted Brain Tissue
www.heartandstroke.ca/profed
Necrosis
Contributing Factors to Ischemic Damage:
Blood Pressure
Commonly seen in stroke patients
 Labile and may have spontaneous resolution
 May act as a compensatory mechanism to
maintain cerebral perfusion
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Contributing Factors to Ischemic Damage:
Blood Pressure
 Blood pressure reduction
 Unclear guidelines, address cautiously
 Measure accurately, continuous monitoring
 AHA/ASA Guidelines recommend:
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Initiate treatment if SBP>220mmHg or DBP>120mmHg
tPA candidates: Initiate treatment if SBP>185mmHG or
DBP>110mmHG
Lower blood pressure by 15-25% within 24 hours
Medication selection on case by case basis but consider
ability to lower blood pressure quickly but ability for rapid
reversal
Contributing Factors to Ischemic Damage:
Blood Pressure
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Timing of restarting blood pressure medications
and selection of medications dependant on
neuro status, stroke mechanism, swallowing
ability and presence of other diseases
Blood Glucose Recommendation
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All patients with suspected acute stroke should have
their blood glucose concentration checked immediately
Blood glucose measurement should be repeated if the
first value is abnormal or if the patient is known to have
diabetes
Hypoglycemia should be corrected immediately
Markedly elevated blood glucose concentrations should
be treated with glucose lowering agents (CSQCS,
Australian;Evidence Level B-C)
Contributing Factors to Ischemic Damage:
Blood Glucose
 Hyperglycemia
 Associated with worse stroke outcomes
 Independent adverse effect on prognosis
 Risk factor for hemorrhagic transformation
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Hypoglycemia
 Associated with focal neurological deficits
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Aphasia, hemiparesis, mental status changes
Contributing Factors to Ischemic Damage:
Body Temperature
 Hyperthermia
 Adverse effect on outcome
 May be secondary to a cause of stroke
 Reduction of fever may improve prognosis
Contributing Factors to Ischemic Damage:
Oxygen Saturation
 Hypoxia may exacerbate and worsen ischemic
damage
 Consider possible causes of respiratory
compromise
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Pneumonia
Partial airway obstruction
Hypoventilation
Atelectasis
Supplemental oxygen if pulse oximetry
<92%
Brain Imaging
Carotid Artery Imaging
Dysphagia Assessment
Brain Imaging Recommendation
All patients with suspected acute stroke should
undergo brain imaging immediately
 In most instances, the modality of choice is a
non-contrast CT scan
 If MRI is performed, the scan should include
diffusion-weighted sequences to detect
ischemia, and gradient echo and FLAIR
sequences for hemorrhage.
(CSQCS,RCP,NZ;Evidence Level B)
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Non-Contrast CT Scan: Acute Stroke
www.strokecenter.org
Diffusion Weighted MRI: Acute Stroke
Gladstone, 2005
Carotid Artery Imaging Recommendation
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Carotid artery imaging should be performed
within 24 hours of a carotid territory TIA or nondisabling ischemic stroke unless the patient is
not clearly a candidate for carotid
endarterectomy. (CSQCS,BPS-WG,SIGN
14;Evidence Level B)
Carotid Artery Doppler Ultra Sound
www.texasheartinstitute.org
www.pacificvascular.com
Dysphagia Assessment Recommendation
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All patients with stroke should have their swallow
screened prior to initiating oral intake of fluids or food
utilizing a simple valid reliable bedside testing protocol.
(CSQCS,SCORE,SIGN 78,NZ;Evidence Level B)
Patients with stroke presenting with features indicating
dysphagia or pulmonary aspiration should receive a full
clinical assessment of swallowing by an SLP or
appropriately trained specialist who should advise on
safe swallow and consistency of diet and fluids.
(RCP,CSQCS,SCORE,NZ;Evidence Level A)
Acute Aspirin Therapy
Acute Thrombolytic Therapy
Stroke Unit Care
Acute Aspirin Therapy
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After brain imaging has excluded intracranial
hemorrhage, all acute stroke patients should be given at
least 160mg of acetylsalicylic acid immediately as a one
time loading dose (RCP,NZ,SIGN13;Evidence Level A)
 In patients treated with tPA, ASA should be delayed until after
the 24 hour post thrombolysis scan has excluded intracranial
hemorrhage (RCP,NZ;Evidence Level A)
 ASA (50-325mg daily) should then be continued indefinitely or
until an alternative antithrombotic regime is started
(RCP;Evidence Level A)
 Dysphagic patients,may be given ASA by enteral feeding tube or
by rectal suppository (RCP;Evidence Level A)
Acute Thrombolytic Treatment
All acute ischemic stroke patients should be
evaluated to determine their eligibility for
treatment with intravenous tPA using the criteria
from the NINDS tPA Stroke Study
 Administration of tPA should follow the ASA
Guidelines (ASA, CSQCS,RCP;Evidence Level AB)
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 All eligible patients should receive tPA within one
hour of hospital arrival (CSQCS,RCP;Evidence
Level B-C)
Acute Thrombolytic Treatment
Medical Redirect and Repatriation
 Triage
 Eligibilty and exclusionary criteria
 Stroke team
 tPA orders
 Target times
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Acute Thrombolytic Treatment:
Medical Redirect and Repatriation
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Formal medical redirect and transfer agreements:
 Ensure identified eligible stroke patients access to tPA
 EMS/Paramedics trained to assess and identify possible eligible
candidates and activate Code Stroke
 Ambulance directed to Regional Stroke Centre
 Information needed: estimated time of arrival, patient
symptoms, established time of stroke onset
 Patients not meeting eligibility criteria are transported to nearest
emergency facility
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Repatriation agreements
 Facilitate patient care closer to home after stroke centre
care completed
Acute Thrombolytic Treatment:
Pre-Hospital Triage and Eligibility Criteria
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Pre-hospital triage
 Rapid assessment using an acute stroke protocol with eligibility
criteria
 Primary and secondary assessment
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Eligibility criteria
 Acute onset of new neurological deficits with reliably known time
of onset and consistent with cerebrovascular disease in the
cerebral hemispheres
 The deficit should be of a severity that would lead to decreased
quality of life
 Ability to complete all investigations within the 3 hour window
 Informed consent
Acute Thrombolytic Treatment: Triage
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Emergency department triage
 Canadian Triage and Acuity Scale (CTAS) Level ll
Emergent
 Triage of suspected stroke patients
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Airway, breathing, circulation (ABC)
Neurological: Level of consciousness, limb weakness, speech
impairment, visual disturbance
Quick history: Previous functional independence level
Time of onset: Confirmed <3 hours
Acute Thrombolytic Treatment:
Triage and Exclusion Criteria
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Exclusion criteria (ASA Guidelines 2007)
 Neurological signs that are clearing spontaneously
 Symptoms of stroke that are suggestive of subarachnoid
hemorrhage
 Onset of symptoms >3 hours
 Head trauma or prior stroke within previous 3 months
 Myocardial infarction within previous 3 months
 Gastrointestinal or urinary tract hemorrhage in previous 21 days
 Major surgery within the previous 14 days
 Arterial puncture at a noncompressible site in the previous 7
days
 History of previous intracranial hemorrhage
Acute Thrombolytic Treatment:
Triage and Exclusion Criteria
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Exclusion criteria for intravenous tPA (AHA 2007)
 Elevated blood pressure >185/110 mmHG that does not respond to
treatment
 Evidence of active bleeding or acute trauma (fracture) on examination
 Taking oral anticoagulant and INR >/=1.5 ( 1.7)
 Receiving heparin in previous 48 hours with abnormal aPTT
 Platelet count<100,000mm3
 Blood glucose <2.7 mmol/L or >22mmol/L
 Seizure with postictal residual neurological deficits
 CT evidence of multilobar infarction involving >1/3 cerebral hemisphere
or reveals cerebral hemorrhage
 The patient and family do not give consent for treatment
Optimal Stroke Management With tPA:
Stroke Team
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Benefits
 Reduces time to definitive treatment
 Early notification and mobilization further reduces time
 Critical to rapid diagnosis and treatment
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Composition
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Stage of care
Stroke expert, emergency or family physician
Medical, nursing staff, allied healthcare professionals
Stroke survivor, family, support network central to team
Optimal Stroke Management With tPA:
Stroke Orders
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Record stroke onset (last seen normal)
Vital signs including temperature, O2 saturation, neuro assessment
Capillary blood glucose
STAT blood: electrolytes, BUN, creatinine, glucose, CBC, PTT, INR,
pregnancy test
12-lead ECG
O2 at 2 L/minute by nasal cannula for oxygen saturation <92%
IV NS TKVO, Saline lok
Estimate patient’s weight (kg)
STAT noncontrast CT of head
Activate Code Stroke if <3 hours
Minimize invasive procedures, like catheterization
Optimal Stroke Management With tPA:
tPA Target Times
 Rapid coordinated emergency response
facilitates early diagnosis and treatment
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Door-to-triage
Door-to-stroke team notification
Door-to-CT scan
Door-to-needle
1 minute
15 minutes
25 minutes
60 minutes
Adverse Effects of tPA: Hemorrhage
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Superficial bleeding
 Observe potential bleeding sites: venous & arterial puncture,
lacerations, etc.
 Avoid invasive procedures during tPA and for 24 hours after
 Treat with compression
 Monitor all secretions for bleeding
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Intracranial hemorrhage
 Observe for deterioration of neuro status
 If suspected, stop tPA
 Obtain CT scan and coagulation workup
Adverse Effects of tPA: Angioedema
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Risk assessment
 Inquire if patient has had angioedema in past
 Take ACE inhibitor history
 Although angiotensin II (ATII) receptor antagonists
have not been implicated in the angioedema reaction,
caution is advised in patients reporting a history of
ATII antagonist use
Adverse Effects of tPA: Angioedema
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Monitoring
 Observe for facial, tongue,
and/or pharyngeal
angioedema 30 minutes, 45
minutes, 60 minutes and 75
minutes after initiation of IV
tPA infusion and periodically
for 24 hours afterwards
www.heartandstroke.ca/profed
Stroke Unit Care Recommendation
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Patients admitted to
hospital because of an
acute stroke should be
treated in an
interdisciplinary stroke
unit.
(CSQCS,SCORE,SIGN64;
Evidence Level A)
www.healthsystem.virginia.edu/internet/neurologytraining/images/fellowship_stroke/6C_conversation.jpg
Stroke Unit Care Recommendation
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Key components
 A stroke unit is a specialized, geographically defined
hospital unit dedicated to the management of stroke
patients (Australian,RCP;Evidence LevelA/1)
Stroke Unit Care Recommendation
The core interdisciplinary team should consist of
appropriate levels of medical, nursing, nutrition,
occupational therapy, physiotherapy, social work
and speech-language pathology staff
 Additional disciplines may include pharmacy,
(neuro)psychology and recreation therapy
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Stroke Unit Care Recommendation
The interdisciplinary team should assess patients
within 48 hours of admission and formulate a
management plan
 Clinicians should use standardized, valid
assessments to evaluate the patient’s stroke
related impairments and functional status
(RCP,BPS-WG;Evidence Level lll)
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Canadian Best Practice
Recommendations:
Management of Subarachnoid and
Intracerebral Hemorrhage
Management of Subarachnoid and
Intracerebral Hemorrhage
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Patients with suspected subarachnoid hemorrhage
should have an urgent neurosurgical consultation for
diagnosis and treatments (BPS-WG;Evidence Level B)
Patients with cerebellar hemorrhage should have an
urgent neurosurgical consultation for consideration of
craniotomy and evacuation of the hemorrhage (BPSWG;Evidence Level C)
Patients with supratentorial intracerebral hemorrhage
should be cared for on a stroke unit (BPS-WG;Evidence
Level B-C)
Management of Patients with Acute
Ischemic Stroke
Acute Stroke Complications
Increased Intracranial Pressure and
Cerebral Edema
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Typically occurs between 3 and 5 days
Common with patients who have occlusion of the stem of the MCA
Early swelling has been attributed to reperfusion edema and
possible effects of tPA (ASA,2007)
Malignant brain swelling: patients with large territorial infarct that
swells within 24 hours causing brain herniation.
Cerebellar infarcts: sudden apnea with brain stem compression and
cardiac arrhythmias
Anterior circulation strokes: low risk (10-20%) (Alexandrov &
Grotto,2002; del Zoppo et al, 1998)
Incidence of edema in posterior circulation strokes in unknown
Increased Intracranial Pressure and
Cerebral Edema
 Few signs predict clinical deterioration
 Multivariate analysis: history of hypertension,
heart failure, elevated white blood cell count,
presence of >50% MCA hypodensity and
involvement of additional vascular territory
(Kasner et al, 2001)
 Management goal: Prevention of further
deterioration
Increased Intracranial Pressure
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Signs and Symptoms-Early
LOC due to oxygen change and compression of RAS
Pupil dysfunction due to CN 111 compression
Motor weakness due to pyramidal tract pressure
Sensory deficit due to compression of ascending
tracts
 Cranial Nerve- extraoccular motor (3,4,6)
compression
 Headache
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Increased Intracranial Pressure
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Signs and Symptoms-Late
 LOC-coma
 Vomiting due to compression of 4th ventricle and
brainstem
 Pupil- largerfixed
 Hemiplegia
 Posturing-flexion (decorticate), extension
(decerebrate)
 Vital signs- widening PP,HR,RR changes
 Loss of corneal, gag reflexes
Cerebral Edema
P = pressure
www.heartandstroke.ca/profed
Increased Intracranial Pressure and
Cerebral Edema
 Management Strategies
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Assessment (Glasgow Coma Scale)
Fluid restriction
Treat hypoxia, hypercarbia and hyperthermia
Elevate HOB 30°
Avoid hypertensive agents that cause vasdilation
Late Stage: hyperventilation, osmotic diuretics,
drainage of cerebral spinal fluid, decompressive
surgery, hypothermia
Hemorrhagic Transformation
Many infarcts have some element of petechial
hemorrhage present
 More common in 2nd week after stroke and
larger strokes
 Location, size and cause of stroke
 Use of all antithrombotics, especially
anticoagulants and thrombolytics increase risk
 Management depends on amount of bleeding
and clinical presentation
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Seizures
Frequency in first few days: 2-23%
 Management is the same as neurological illness
 Prophylactic anticonvulsants not recommended
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Shoulder Pain Assessment and Treatment
Assessment should be conducted throughout the
continuum of care
 Factors that contribute to or exacerbate
shoulder pain should be identified and managed
appropriately
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 Staff and caregivers should be educated on correct
handling (RCP,SCORE;Evidence Level B)
 Consider use of supports for the arm
(RCP;Evidence Level A)
Shoulder Pain Assessment and Treatment
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Joint protection strategies should be instituted to
minimize joint trauma:
 The shoulder should not be passively moved past 90 degrees of
flexion and abduction unless the scapula is upwardly rotated and
the humerus is laterally rotated (SCORE;Evidence Level A)
 Overhead pulleys should not be used (Ottawa Panel;Evidence
Level A)
 The upper limb must be handled carefully during functional
activities (SCORE; Evidence Level B)
 Staff should position patients, whether lying or sitting, to
minimize the risk of complications such as shoulder pain
(RCP;Evidence B)
Shoulder Pain Assessment and Treatment
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Shoulder pain and limitations in range of motion
should be treated through gentle stretching and
mobilization techniques focusing especially on
external rotation and abduction
(SCORE;Evidence Level B)
Resources
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American Association of Neuroscience Nurses
www.aann.org
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American Stroke Association
www.strokeassociation.org
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Brain Attack Coalition
www.stroke-site.org
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Canadian Hypertension Education Program
www.hypertension.ca/chep/en/default.asp
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Canadian Stroke Strategy
www.canadianstrokestrategy.ca
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European Stroke Initiative
www.eusi-stroke.com
Resources
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Heart and Stroke Foundation Prof Ed
www.heartandstroke.ca/profed
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Heart and Stroke Foundation of Canada
www.heartandstroke.ca
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Internet Stroke Centre
www.strokecenter.org
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National Institute of Neurological Disorders and Stroke
www.ninds.nih.gov
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National Stroke Association
www.stroke.org/site/PageServer?pagename=HOME
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Scottish Intercollegiate Guidelines Network
www.sign.ac.uk
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StrokeEngine
www.medicine.mcgill.ca/strokengine