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1
Clinical Aspects of Stroke
Pierre Fayad, MDReynolds Centennial Professor & Chairman,
Department of Neurological Sciences
University of Nebraska Medical Center, Omaha, NE
2
“Stroke”
• APOPLEXY from Greek “Apo Plexe” meaning “a stroke”.
• Anyone seized by sudden disability was thought to be “struck down” by the Gods.
Haubrich WS. Medical Meanings: A Glossary of Word Origins. Publisher: American College of Physicians 2003
3
Steps in Neurologic Evaluation
Gather information– Chief complaint– Symptoms, evolution– Physical examination
Analysis– Localization– Pattern of disease– Comparison to clinical database
Gather information– Diagnostic tests
Diagnosis & Treatment
4
Steps in Stroke EvaluationGather information
– Chief complaint– Symptoms and history: risk factors, chronologic
evolution– Physical examination: vascular and neurologic
Analysis– Localization: CNS level, large vessel, branch, …– Pattern of disease: tempo, risk factors– Comparison to clinical datatbase
Gather information– Diagnostic tests: location, size, type, mechanism
Diagnosis & Treatment
7
What Is A “STROKE”?
CLINICAL DEFINITION of focal neurologic deficit, of vascular etiology, lasting > 24 HOURS.
Diagnosis is dependent on neurologic deficit and NOT imaging.
“Generic term for a clinical syndrome that includes infarction, hemorrhage, and SAH.”
NINDS Classification of CVD III. Stroke 1990, 20:627-680
8
Types of Stroke
• Ischemic Stroke– Brain damage from lack of blood flow– Occlusion of blood vessel– Thrombosis, embolism
• Hemorrhagic stroke– Rupture of blood vessel– Brain damage from blood invasion
9
Stroke Subtypes: Stroke Data Bank
Lacunar19%
SAH13%
ICH13%
Other3%
Cardioembolic14%
Atherosclerotic6%
Undetermined32%
Stroke Data Bank, Foulkes et al, Stroke 1988;19:547
10
Definition of Transient Ischemic Attack• Classic definition
– A sudden, focal neurologic deficit lasting less than 24 hours, presumed to be of vascular origin, and confined to an area of the brain or eye perfused by a specific artery
• Proposed definition– A brief episode of neurologic dysfunction caused by
focal brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of acute infarction
Albers GW et al. N Engl J Med. 2002;347:1713-1716.
11
Short-term Prognosis after Emergency Department Diagnosis of TIA
Johnston SC, et al. JAMA 2000;284:2901-2906.
Inclusion criteria:
Objective:
Outcome measures:
Total events:
TIA by ED physicians
Short-term risk of strokeafter ED diagnosis
Risk of stroke and otherevents during the 90 daysafter index TIA
25.1%
Outcome events
10.5%
12.7%
2.6% 2.6%
Stroke RecurrentTIA
CV event Death
0 %
5 %
10 %
15 %
Within90 days
Within48 hr
5.3%
12
US Stroke Facts 2003• Incidence
– 700,000 new or recurrent stroke yearly– One stroke every 45 seconds
• Mortality– 168,000 Stroke-related death yearly (1 of 14 deaths)– Third leading cause of death after heart and cancer– One stroke-related death every 3 minutes– Of every 5 stroke deaths: 2 men, 3 women
• Costs– $51 billion in 2003 for stroke related medical costs and
disability
American Stroke Association
13
Stroke Risk Factors
Medical Conditions Hypertension Cardiac disease Atrial fibrillation Hyperlipidemia Diabetes mellitus Carotid stenosis Prior TIA or stroke
Non-Modifiable
Age, Gender, Race, Heredity
Behaviors Cigarette smoking Heavy alcohol use Physical inactivity
Modifiable
14
Goals For Acute Stroke Care• Rapid triage and identification of stroke
• Stroke type: Ischemic vs Hemorrhagic• Eligibility for “acute stroke therapy”• Determine size, location, & vascular territory• Establish plans for efficient Management &
discharge• Stabilization & prevention of complications• Determine etiology & mechanism• Initiate secondary stroke prevention strategies• Initiate rehabilitation assessment and therapy
15
Intracerebral Hemorrhage
16
Hypertensive ICH: Post-Mortem
17
Clinical Features Suggestive Of ICH
• Severe headache
• Depressed consciousness
• Nausea and vomiting
• Horizontal diplopia
• Papilledema and pre-retinal hemorrhages.
18
ICHSx
19
CAUSES OF INTRACRANIAL HEMORRHAGE
HTNHTN50%50%Amyloid angiopathyAmyloid angiopathy12%12%AnticoagulantsAnticoagulants10%10%TumorsTumors 8%8%Prescription and street drugsPrescription and street drugs 6%6%AVMs and aneurysmsAVMs and aneurysms 5%5%MiscellaneousMiscellaneous 9%9%
20
Charcot-Bouchard Microaneurysms
21
Intracranial Vascular Malformations
22
ICH - General Management
• Nutrition• DVT prophylaxis• Hydration and electrolytes• Acute arterial hypertension• Intracranial hypertension• Hydrocephalus• Seizure prophylaxis and treatment• Surgery and decompression
AHA Special Writing Group, Stroke 1999;30:905-915AHA Special Writing Group, Stroke 1999;30:905-915
23
Dose-Ranging Study: rFVIIa in Preventing Early Hematoma Growth in Acute ICH
• Multicenter, international, Phase II study, 400 patients, CT < 3 hrs from Sx, Rx < 60 min CT.
• Arms: Placebo, 40, 80, 160 mcg/kg• Significantly reduces
– 45-62% RR Dose-dependent hematoma growth– 38% RR Mortality
• Significantly improves– Global functional outcome (mRS and BI) at 90 days
• Small increase in the risk of acute thromboembolic events
Mayer SA et al. N Engl J Med. 2005;352:777-785.
24
Subarachnoid Hemorrhage
25
Subarachnoid Hemorrhage: Schematic
26
Berry Aneurysm Rupture
27
Location of Berry Aneurysms
28
SAH Symptoms
& Diagnosis
29
IntracranialAneurysms Sx
31Johnston SC, et al. Ann Neurol. 2000;48:11-19.
Aneurysm Coiling or Clipping
32
SAH - Delayed Vasospasm• Facts
– A leading cause of death and disability
– Starts 3-5 d after SAH, and maximal at 3-14 d.
– 20-30% delayed neurologic ischemic deficits.
• Diagnosis – TCD, angiography.
• Treatment– Nimodipine
– Hypertensive, hypervolemic, hyperosmolar Rx (HHH)
– Local IA papaverine -> transluminal angioplasty
33
Ischemic Stroke
34
Stroke Mimics• Metabolic
–Hyper/hypoglycemia, Hyponatremia, Hypo/hyperthyroidism, Hepatic encephalopathy
• Seizures• Subdural hematoma• Infections
–Brain abscess, encephalitis, meningitis
• Neoplasm• Drug overdose (also a cause of stroke).• Hypertensive encephalopathy• Psychogenic• Migraine
35
Vascular Localization
36
!!!Learn Neurology Stroke-By-Stroke!!!
37
Brain Picture
38
What The Brain Does
39
Cortical Functional Localization
40
Homunculus
41
Localizing Stroke
• Stroke affects three main areas of the brain
–Left hemisphere
–Right hemisphere
–Brainstem/cerebellum
• Neurologic deficits patterned in syndromes according to brain part affected and location
42
Cerebral Circulation
43
Cerebral Vascular Territories
44
Left (Dominant) Cerebral Hemisphere Syndrome
• Aphasia.
• Left gaze preference.
• Right visual field cut.
• Right hemiparesis.
• RIght hemisensory loss.
45
Right (Non-dominant) Cerebral Hemispheric Syndrome
• Neglect (left hemi-inattention)
• Right gaze preference.
• Left visual field deficit.
• Left hemiparesis.
• Left hemisensory loss.
47
Syndromes of Carotid Branch Occlusions
Location
Frontal Lobe
Parietal lobe
Temporal lobe
Occipital lobe
Artery
ACA
MCA: ant division
MCA: post division
MCA: post division
PCA
Dominant Non-dominant
Contralat LE weaknessAbulia
Contralat LE weaknessAbulia
Expressive aphasiaContralat hemiparesisIpsilat gaze deviation
AprosodiaContralat hemiparesisIpsilat gaze deviation
Conduction aphasiaGerstman’s synd, HH Contral hypoesthesia
Anosognosia, Apraxia, Contralateral neglect, Hypoesthesia, HH
Receptive aphasia, Contralateral HH
Contralateral Hemianopia
Alexia without agraphiaContralateral HH
Contralateral Hemianopia
48
Brainstem Syndrome
• Crossed signs.
• Hemiparesis or quadraparesis.
• Hemisensory loss or sensory loss in all four limbs.
• Eye movement abnormalities.
• Oropharyngeal weakness.
• Decreased consciousness.
• Hiccups or abnormal respirations.
49
Cerebellar Syndrome
• Gait or limb ataxia
• Vertigo, tinnitus
• Nausea, vomiting.
• Decreased Consciousness.
50
Acute Stroke Therapy
51
Platelets in Acute Vascular Events
AtheroscleroticVessel
PlaqueRupture
PlateletAdhesion,
Recruitment,Activation,
andAggregation
ThrombusFormation
ThromboticOcclusion
MI
Stroke
Acute Peripheral Arterial Occlusion
CollagenPlaquePlatelets Thrombus
52
Cerebral Ischemia: Basic Mechanisms
•Perfusion failure•Energy failure•Loss of membrane function•Edema•Cell death
53
Ischemic Cascade
QuickTime™ and aPhoto - JPEG decompressor
are needed to see this picture.
Brott T et al, NEJM 2000,343:710-721
54
ISCHEMIC PENUMBRA
55
Acute Ischemic Stroke: Large MCA, CT
56Time is Brain
58
Supportive Acute Stroke Care
• Monitor for potential worsening
• Stabilize vital signs
• Maintain adequate hydration
• Optimize nutrition: early, PO, NG feeds, PEG
• Prevent aspiration: screen for those at risk
• Treat fever aggressively: any elevations
• Mobilize early: within 24 hours
59
Therapies for Acute Cerebral Ischemia
• Antithrombotic therapy– Antiplatelet medications
– Aspirin, Clopidogrel, ASA/ER-DP– IV GP IIb IIIa antagonists (Abciximab)
– Anticoagulants – Hypofibrinogenemic (Ancrod)
• Reperfusion and perfusion enhancement– Thrombolytic therapy: Intravenous, intra-Arterial– Mechanical clot dissolution/removal
• Neuroprotective Therapies– Non-specific cellular protection– Specific neuronal protection
60
Acute Antiplatelet Therapy for Stroke
• Aspirin 160 mg daily, started within 48 hours, decreases risk of stroke and death at one month.
• Other antiplatelet agents not tested acutely.
• As a rule early AP Rx start recommended.
• Preferable to start same AP agent as OP.
CAST Collaborative Group, Lancet 1997;349:1641-1649
61
Acute Anticoagulation For Stroke: Conclusions
• Acute anticoagulation DOES NOT…– Does not improve overall outcome, prevent neurologic deterioration or
prevent recurrence
• Indications– SQ anticoagulation for DVT prophylaxis in immobilized patients or
paralyzed leg
– Sinus venous thrombosis
• Risks– Risk of cerebral hemorrhage and systemic bleed substantially
increased.
• Untested– Acute anticoagulation < 12 hours
62
NINDS IV tPA
Primary Outcomes
NEJM 1995;333:1581-1587
63
Acute Stroke: Intra-Arterial Lysis
Brott T et al, NEJM 2000,343:710-721
64
Merci Clot Retriever Concentric Medical Inc.
Gobain YP. Stroke 2004;35:2848-2854
65
MERCI-1: Example of Clots Retrieved
Gobain YP. Stroke 2004;35:2848-2854
66
Stroke Prevention Strategies
• Identify stroke subtype and mechanism
• Risk Factors and Lifestyle modification
• Non-Anti-thrombotic Treatments
• Oral Anticoagulation
• Antiplatelet Medications
• Surgery and interventions
67
Stroke Mechanism Determination
CT/MRI
Hemorrhagic StrokeHemorrhagic Stroke
Ischemic StrokeIschemic Stroke
Large Artery StrokeLarge Artery Stroke
Cardioembolic Stroke Cardioembolic Stroke
Lacunar syndrome, YesRisk Factors
No Lacunar small vessel Lacunar small vessel
stroke stroke
Other defined etiologies, YesNo
Infarct undetermined Infarct undetermined causecause
other
TIA or Stroke normal or infarct
Specific work-up
Tandem pathology, YesNo
TTE/TEE, ECGcardiac source, Yes
No
Infarction Determined Infarction Determined EtiologyEtiology
Duplex, TCD, MRA, angiogram
blood
Adapted Fayad PB; J. Cardiovascular Diagn & Proc 1994;12 (1):35-42.
68
Carotid Bifurcation Athero-Thrombo-Embolism
69
MCA Embolism
70
Common Cardioembolic
Sources
71
Intracranial Atherothrombosis
72
Lenticulostriate Arteries
73
Classic Lacunar SyndromesClinical features Common locationsLacunar Syndrome
Hemiparesis (arm, leg, face equally)
Post limb IC, Ant limb IC, Corona radiata
Sensory loss, dysesthesia (face, arm, leg)
Thalamus, centrum semiovale
Combined hemi motor and sensory deficits
Thalamus, putamen, corona radiata
Homolateral ataxia with crural paresis
Corona radiata, posterior limb IC, thalamus
Combined dysarthria, upper limb ataxia
Anterior limb IC, genu, pons hemorrhage
Pure motor hemiparesis
Pure sensory stroke
Sensory-motor stroke
Ataxic hemiparesis
Dysarthria-clumsy hand syndrome
Fayad et al. Curr. Rev CVD 1996, Current Medicine: 81-92
74
CarotidPathologies
75
Non Anti-Thrombotic Treatments
76
Non-Anti-Thrombotic Medical Therapies For Stroke Prevention-1: Lipid Lowering
• Clear benefit for statins in primary stroke prevention (20-30%) in patients with CAD and even average level of LDL cholesterol.
• No demonstration yet of statin benefit in secondary stroke risk reduction. (Exception HSP, SPARCL pending).
77
Non-Anti-Thrombotic Medical Therapies For Stroke Prevention-2: Anti-HTN
• Significant stroke risk reduction (20%-30% RRR ischemic, >50% RRR hemorrhagic) in treating hypertension, systolic or diastolic. (more evidence for systolic)
• Anti-HTN: Significant primary & stroke risk reduction, even in non-hypertensives.
• Superiority of Anti-HTN drug classes in stroke prevention undetermined yet.
78
Non-Anti-Thrombotic Medical Therapies For Stroke Prevention-3: Miscellaneous
• No benefit (but clear harm) from hormonal replacement in post-menopausal women.
• No benefit from Vitamin B supplementation in hyperhomocystinemia in patients with stroke or TIA.
79
Antiplatelet (AP) Therapy in Stroke Prevention: Summary
• Aspirin (ASA) not indicated for primary stroke prevention.
• Low-dose ASA recommended for secondary stroke prevention.
• No single AP agent more effective than aspirin.• To Date, ASA-ER DP only AP combination
effective and safe (> ASA) in secondary stroke prevention
• In patients at risk for stroke, the combination of Clopidogrel and aspirin significantly increase the risk of ICH, life-threatening and major bleeding.
80
AsymptomaticICA/CCA stenosis
Risk factormodification
Warfarin
Asymptomatic and healthywithout risk factors
AntiplateletAnti-HTN?Statins?
Men> 60
Women post-menopausal
Estrogen
Asymptomatic butwith risk factors
NVAFCardioembolic
source/pathology
Endarterectomy
Evaluate CAD
No other pathology
Primary Prevention Of Ischemic Stroke
Adapted From Fayad PB; J. Cardiovascular Diagn & Proc 1994;12 (1):35-42.
AMI
Statins
High riskLow risk
X
81
Secondary Prevention of Ischemic Stroke
Adapted From Fayad PB; J. Cardiovascular Diagn & Proc 1994;12 (1):35-42.
Extracranialcarotid stenosis
70-99%
TIA or STROKE
Cardiogenic embolism
Small VesselLacunar
Undeterminedetiology
CEA
50-69% < 50%
Intra/extra-cranialstenosis/occlusion
Large Vessel Athero
Documentedsource/pathology
AF
Antiplatelet, EstrogenAnti-HTN? Statins?
WarfarinXXXX
82
Carotid Stenting
Reimers B, et al. Circulation. 2001;104:12-15.
83
ACCULINK & ACCUNET Stent System (Guidant): ARCHER & CREST
ACCULINK ACCUNET
85
Cerebral Circulation
86
72-year-old right-handed African-American woman
admitted with weakness and speech difficulty
Stroke Case
87
Stroke Case:
• Sudden onset of right arm and leg weakness• Speech difficulty• Hospital admission ~6 h after symptom onset
72-year-old woman
Presentation
• Hypertension• Dyslipidemia• Diabetes• Nonsmoker• Rarely drinks alcohol
History
88
CT scan at 10 days
Stroke Case:72-year-old woman
Should this patient have had a follow-up scan earlier than 10 days post-admission?
Would an MRI have been better?