Explain stroke syndromes in great detail including images, tables, flowchart References - Tintinalli's 9th edition & Rosen's 10th edition

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Stroke Syndromes - Comprehensive Review

Sources: Tintinalli's Emergency Medicine, 9th Ed. (Chapter 167, Steven Go) & Rosen's Emergency Medicine, 10th Ed. (Chapter 87, Linda Papa & William J. Meurer)

1. Epidemiology & Overview

  • 795,000 strokes/year in the United States (one stroke every 40 seconds; one death every 4 minutes)
  • 77% are first-ever strokes; 23% recurrent
  • Ischemic strokes: 87% of all strokes
  • Intracerebral hemorrhage (ICH): 10%
  • Subarachnoid hemorrhage (SAH): 3%
  • Age-adjusted stroke death rate fell 28.7% from 2004-2014 with improved stroke units, thrombolysis, and thrombectomy
(Tintinalli's, Ch. 167)

2. Vascular Anatomy - The Essential Framework

Figure 167-1. Cerebral Hemisphere, Lateral Aspect - MCA branches and cortical localization:
Cerebral hemisphere lateral aspect - MCA distribution and cortical regions
Figure 167-2. Cerebral Hemisphere, Medial Aspect - ACA and PCA distribution:
Cerebral hemisphere medial aspect - ACA and PCA distribution

Table 1: Cerebrovascular Anatomy - Circulation, Arteries, and Brain Regions Supplied

CirculationMajor ArteriesMajor Regions Supplied
Anterior (Internal Carotid System)OphthalmicOptic nerve and retina
Anterior Cerebral (ACA)Frontal pole; Anteromedial cerebral cortex; Anterior corpus callosum
Middle Cerebral (MCA)Frontoparietal lobe; Anterotemporal lobe
Posterior (Vertebral System)VertebralBrainstem
PICA (Posteroinferior Cerebellar)Cerebellum, lateral medulla
BasilarThalamus, pons
Posterior Cerebral (PCA)Auditory/vestibular structures; Medial temporal lobe; Visual occipital cortex
(Tintinalli's, Table 167-1)

3. Stroke Classification

Table 2: Stroke Classification

TypeSubtypeFrequencyKey Mechanism
IschemicThrombotic (large vessel)~33% of all strokesAtherosclerotic plaque with clot at bifurcation
Thrombotic (lacunar/small vessel)~20%Lipohyalinosis of small penetrating vessels; HTN/DM
Cardioembolic~25%Mural thrombus (AF is most common); artery-to-artery emboli
Cryptogenic>33%No clear cause identified
HemorrhagicIntracerebral hemorrhage (ICH)10%Hypertensive vasculopathy; amyloid angiopathy
Subarachnoid hemorrhage (SAH)3%Ruptured aneurysm/AVM
(Tintinalli's Table 167-2; Rosen's Ch. 87)

4. ISCHEMIC STROKE SYNDROMES

Key principle (Rosen's): Anterior circulation strokes produce contralateral hemiparesis of face and body. Vertebrobasilar strokes produce ipsilateral cranial nerve deficits + contralateral hemiparesis ("crossed deficits").

4.1 Anterior Cerebral Artery (ACA) Infarction

Frequency: Uncommon - only 0.5% to 3% of all strokes
FeatureDetail
Motor/SensoryContralateral lower extremity weakness > upper extremity; sparing of hands and face (leg >> arm)
Frontal lobe featuresAltered mentation, impaired judgment and insight
Primitive reflexesGrasp reflex, suck reflex present
IncontinenceBowel and bladder incontinence
Language (left lesion)Akinetic mutism, transcortical motor aphasia
GaitApraxia or clumsiness
"Paralysis and hypoesthesia of the lower limb opposite the side of the lesion are characteristic. Leg weakness is more pronounced than arm weakness." - Rosen's Ch. 87

4.2 Middle Cerebral Artery (MCA) Infarction

Most commonly involved vessel in stroke. Clinical findings are highly variable depending on lesion location and hemisphere dominance (left hemisphere dominant in right-handed patients and ~80% of left-handers).
FeatureDetail
Motor/SensoryContralateral hemiparesis + sensory loss; face and arm > leg
HemianopsiaContralateral homonymous hemianopsia
Gaze preferenceToward the side of the infarct (disruption of cortical lateral gaze center)
Dominant hemisphere (usually left)Aphasia - expressive (Broca), receptive (Wernicke), or global
Non-dominant hemisphere (usually right)Inattention, hemispatial neglect, extinction on double-simultaneous stimulation, dysarthria without aphasia, constructional apraxia
Aphasia subtypes (MCA dominant hemisphere):
TypeAreaDeficit
Broca's (Expressive)Inferior frontal gyrus (Broca's area)Cannot communicate verbally; understanding intact
Wernicke's (Receptive)Posterior superior temporal gyrusCannot process/understand speech; fluent but meaningless speech
GlobalLarge MCA territoryBoth expression and comprehension lost
DysarthriaMotor deficitPoor articulation but intact word choice; not cortical
Aphasia localizes to the dominant cerebral cortex in MCA distribution. Dysarthria is a motor deficit. Dysphagia is difficulty swallowing - these three terms are commonly confused. - Rosen's Ch. 87

4.3 Posterior Cerebral Artery (PCA) Infarction - Distal Posterior Circulation

FeatureDetail
Visual fieldContralateral homonymous hemianopsia (most specific sign); cortical blindness
Visual agnosiaInability to recognize seen objects
Alexia without agraphiaCannot read; can write (unique to PCA)
Color anomiaInability to name colors
MemoryRecent memory loss (medial temporal involvement)
OculomotorUnilateral CN III palsy (ipsilateral)
HemiballismusThalamic involvement
MotorTypically minimal - patient may not realize stroke has occurred
SensoryLight-touch and pinprick deficits
"One of the more unique facets of this syndrome is that the patient may be unaware of any visual problem (visual neglect)." - Rosen's Ch. 87
PCA stroke: ipsilateral CN III palsy + contralateral homonymous hemianopsia - Rosen's Key Concepts

4.4 Basilar Artery Occlusion - Middle Posterior Circulation

FeatureDetail
Presenting symptomsUnilateral limb weakness, dizziness, dysarthria, diplopia, headache
Presenting signsUnilateral limb weakness, CN VII signs, dysarthria, Babinski sign, oculomotor signs
AssociatedDysphagia, nausea/vomiting, Horner's syndrome
Locked-in syndromeBilateral pyramidal tract lesions in ventral pons - complete paralysis except upward gaze and blinking
PrognosisHigh risk of death and poor outcomes

4.5 Vertebrobasilar Infarction - Proximal Posterior Circulation

FeatureDetail
SymptomsDizziness, nausea/vomiting, headache, dysphagia, unilateral limb weakness, CN V symptoms
SignsUnilateral limb ataxia, nystagmus, gait ataxia, CN V signs, limb sensory deficit, Horner's syndrome

4.6 Cerebellar Infarction

FeatureDetail
SymptomsDizziness ± vertigo, nausea/vomiting, gait instability, headache, limb ataxia, dysarthria, dysmetria, nystagmus, hearing loss, intractable hiccups
Mental statusAlert to comatose
CT sensitivityUp to 25% of noncontrasted head CTs can be normal - always get MRI-DWI if suspected
DangerRapid deterioration from cerebellar edema causing brainstem compression - watch for gaze palsy

4.7 Wallenberg Syndrome (Lateral Medullary Syndrome)

Caused by occlusion of the posterior inferior cerebellar artery (PICA) or vertebral artery
FeatureSideMechanism
Vertigo, nausea, vomiting, hiccups-Vestibular nucleus involvement
Horner syndrome (ptosis, miosis, anhidrosis)IpsilateralDescending sympathetic tract
Facial numbness + loss of corneal reflexIpsilateralCN V nucleus
Dysphagia + hoarsenessIpsilateralCN IX, X nucleus
Limb ataxiaIpsilateralCerebellum/inferior cerebellar peduncle
Pain + temperature loss (body)ContralateralSpinothalamic tract
MotorSparedCorticospinal tract not involved (no hemiplegia)
"Wallenberg syndrome causes vertigo, Horner syndrome, ipsilateral facial numbness, loss of corneal reflex, along with contralateral loss of pain and temperature." - Rosen's Key Concepts

4.8 Lacunar Infarction

  • Infarction of small penetrating arteries (terminal small vessels)
  • Strongly associated with chronic hypertension (80-90%) and diabetes
  • Size: few mm to 2 cm
  • Most common sites: basal ganglia, thalamus, pons, internal capsule
  • Mechanism: lipohyalinosis (hypertensive vasculopathy) or small emboli
Classic Lacunar Syndromes:
SyndromeLocationFeatures
Pure motor hemiplegiaInternal capsule (posterior limb) or ponsContralateral face, arm, leg weakness - NO sensory loss, NO cortical signs
Pure sensory strokeThalamus (VPL nucleus)Contralateral hemisensory loss - NO motor
Sensorimotor strokeThalamocapsular junctionCombined motor + sensory without cortical features
Ataxic hemiparesisPons or internal capsuleIpsilateral limb ataxia + contralateral hemiparesis
Dysarthria-clumsy handPons or genu of internal capsuleDysarthria + contralateral hand clumsiness
Prognosis generally more favorable than other stroke syndromes. - Tintinalli's Ch. 167

4.9 Stroke in Young Adults (15-45 years old)

  • 3-4% of all strokes occur in this age group
  • Average age of first stroke is becoming younger
CauseNotes
Cervical artery dissectionMost common determined cause in young adults
Oral contraceptives / pregnancyHypercoagulable state
Antiphospholipid antibodiesLupus anticoagulant, anticardiolipin Ab
Protein S/C deficiencyThrombophilia
Sickle cell anemiaSludging/thrombosis
Cocaine, amphetaminesVasoconstrictors - both ischemic and hemorrhagic
Migraine (rare)Prolonged vasoconstriction
Fibromuscular dysplasiaCerebrovascular
Infectious vasculopathyVaricella, fungal meningitis

4.10 Carotid & Vertebral Artery Dissection

  • Accounts for 2% of all strokes and up to 25% of strokes in young adults
  • Trauma (even minor: chiropractic manipulation, sneezing, sport) in ~40% of cases
Carotid Artery Dissection:
  • Headache: frontotemporal region; may mimic SAH ("thunderclap")
  • Partial Horner's syndrome (miosis + ptosis) in ~25%
  • Cranial nerve palsies in ~12%
  • Leads to anterior circulation symptoms
Vertebral Artery Dissection:
  • Dizziness/vertigo (58%), headache (51-65%), neck pain (46-66%)
  • Headache typically occipital
  • Symptoms: facial paresthesia, ataxia, limb weakness, dysarthria, hearing loss
  • Leads to posterior circulation symptoms / Wallenberg syndrome
TIAs preceding stroke in dissection patients are often misdiagnosed. - Rosen's Key Concepts

5. HEMORRHAGIC STROKE SYNDROMES

5.1 Intracerebral Hemorrhage (ICH)

  • 10-15% of all acute strokes; ~65,000 patients/year
  • 30-day mortality: up to 50% (half die in first 2 days)
  • Only 1 in 5 survivors are living independently at 6 months
Two major causes:
  1. Hypertensive vasculopathy - lipohyalinosis of deep penetrating arteries; deep locations
  2. Cerebral amyloid angiopathy - amyloid deposition in vessel walls; lobar, in elderly

Table 3: Common Sites of Hypertensive ICH (Box 87.1 - Rosen's)

LocationFrequencyTypical Presentation
Putamen44%Contralateral motor/sensory deficit
Other cortical areas25%Variable
Thalamus13%Limb pain, speech difficulty
Cerebellum9%Uncoordinated movements of trunk and limbs
Pons9%Numbness, weakness, ataxia, dizziness
Spontaneous ICH may be clinically indistinguishable from ischemic infarction. CT is mandatory to differentiate. - Tintinalli's Ch. 167
Distinguishing ICH clinically: Headache, nausea, and vomiting often precede the neurologic deficit, and the condition may rapidly deteriorate.

5.2 Subarachnoid Hemorrhage (SAH)

  • Characterized by sudden severe occipital or nuchal headache
  • "Thunderclap" headache - worst headache of life, maximal at onset
  • Associated with Valsalva activities (defecation, sex, weight lifting, coughing)
  • Preretinal hemorrhage on fundoscopy is a hallmark finding

6. Stroke Mimics

Table 4: Stroke Mimics and Distinguishing Features (Tintinalli's Table 167-5)

MimicDistinguishing Features
Todd's paralysis (post-ictal)Transient paralysis after seizure; disappears quickly
SyncopeNo persistent neurologic symptoms
Meningitis/EncephalitisFever; detected on lumbar puncture
Complicated migraineHistory of similar episodes, preceding aura
Brain tumor/AbscessFocal findings; detectable by imaging
Epidural/Subdural hematomaHistory of trauma, anticoagulant use
HypoglycemiaBedside glucose corrects deficits
HyponatremiaDiuretic use, excess free water intake
Hypertensive encephalopathyGlobal dysfunction; gradual onset; cerebral edema
Wernicke's encephalopathyAlcoholism/malnutrition; ataxia + ophthalmoplegia + confusion
LabyrinthitisPurely vestibular symptoms; no other focal findings
Bell's palsyIsolated peripheral CN VII (forehead involved)
Meniere's diseaseRecurrent episodes; tinnitus; deafness
Multiple sclerosisGradual onset; multifocal history
Conversion disorderNo CN findings; non-anatomic distribution; inconsistent exam
Drug toxicity (phenytoin, carbamazepine)Ataxia, vertigo, elevated blood levels

7. Clinical Features - Examination Approach

Anterior vs. Posterior Circulation Strokes

FeatureAnterior CirculationPosterior Circulation
ConsciousnessUsually preserved (unless bilateral or prior stroke)Can have loss of consciousness
Nausea/VomitingUncommonCommon (CTZ in brainstem)
Cranial nerve deficitsRare (CN VII central only)Common (CN III-XII)
Laterality of deficitsSame side of bodyCrossed (ipsilateral CN + contralateral motor/sensory)
Visual symptomsMonocular visual loss (ophthalmic a.)Bilateral field defects, diplopia, nystagmus
ProgressionProgresses in first 24 hrsMay progress up to 3 days
NIHSS weightingWeighted toward detectionUnder-detected (CN deficits score fewer points)
(Tintinalli's Ch. 167; Rosen's Ch. 87)

Key Physical Examination Points (Rosen's)

  • Gaze preference - suggests cortical or brainstem involvement (toward the lesion in cortical strokes)
  • Central vs. peripheral CN VII weakness - peripheral lesion: cannot wrinkle forehead; central: forehead spared
  • Pronator drift - sensitive sign of contralateral motor weakness
  • Double simultaneous extinction - tests sensory neglect; patient feels each side alone but not both together
  • Graphesthesia - number scratched on forearm; tests parietal lobe cortical sensation
  • Gait testing - critical but commonly omitted; detects subtle ataxia and focal cerebellar lesions

8. Anterior vs. Posterior Circulation: Summary Comparison

Table 5: Clinical Features by Vascular Territory

ArteryTerritoryClassic DeficitsKey Distinguishing Feature
ACAFrontal/medialContralateral leg > arm weakness; frontal signs; incontinenceLeg weakness > arm
MCALateral cortexContralateral face + arm > leg; aphasia (dominant); neglect (non-dominant)Face + arm > leg; aphasia vs. neglect
PCAOccipital/temporalContralateral homonymous hemianopsia; CN III palsy; visual agnosia; alexiaVisual field loss; minimal motor
BasilarPons/midbrainBilateral long tract signs; CN deficits; coma; locked-in syndromeBilateral + CN + LOC
PICA/Vertebral (Wallenberg)Lateral medullaIpsilateral: Horner, facial numbness, ataxia; Contralateral: pain/temp loss; No hemiplegiaCROSSED deficits; NO hemiplegia
LacunarDeep (BG, thalamus, capsule, pons)Pure motor or pure sensory; no cortical signsPure deficits; no cortical features
CerebellarCerebellumAtaxia, dysmetria, nystagmus, vertigo; CT often normalCT unreliable - use MRI-DWI

9. Stroke Progression Patterns

PatternTimingMechanism
Stroke in evolutionMinutes to hours~20% anterior; ~40% posterior circulation strokes progress
Anterior progressionUp to 24 hoursThrombus propagation
Posterior progressionUp to 3 daysThrombus propagation in vertebrobasilar system
Complete strokeDeficit maximal at onsetEmbolic typically
TIAComplete resolution; no infarction on DWITransient ischemia without tissue infarction

10. Stroke Diagnostic Flowchart

SUSPECTED STROKE
      │
      ▼
ABC + Vital Signs + Bedside glucose
(Treat hypoglycemia immediately)
      │
      ▼
Activate Stroke Team (immediately upon arrival)
      │
      ▼
Focused History: Last known well time, symptom onset, 
medications (anticoagulants), recent procedures/trauma
      │
      ▼
Neurological Exam: NIHSS score
      │
      ├─── Posterior signs (CN deficits, ataxia, 
      │    crossed findings, vertigo, diplopia)?
      │         └── Consider vertebrobasilar syndrome
      │              → MRI-DWI preferred over CT
      │
      ▼
Non-contrast CT Head (within 20 min of arrival)
      │
      ├── Hemorrhage on CT?
      │         YES → Hemorrhagic Stroke
      │               ├── ICH: BP control, reverse anticoagulation
      │               │   (PCC > FFP for warfarin; Vit K)
      │               └── SAH: Neurosurgical consult
      │
      └── No hemorrhage on CT?
                │
                ▼
           Ischemic Stroke
                │
                ▼
      Within 4.5 hours of symptom onset?
          AND eligible for tPA?
                │
           YES  │  NO
                │    └── General supportive care
                │        Antiplatelet therapy
                │        BP permissive unless >220/120
                ▼
      IV Alteplase (tPA)
      0.9 mg/kg (max 10 mg IV bolus + 90% over 60 min)
      Door-to-needle: ≤60 min (target ≤45 min)
                │
                ▼
      Emergent Large Vessel Occlusion (LVO)?
      CT Angiography
                │
                ▼
      Mechanical Thrombectomy (if LVO confirmed)
      Up to 24 hrs in selected patients (DAWN/DEFUSE3)
                │
                ▼
      Admit to Stroke Unit / ICU
(Tintinalli's Table 167-8; Rosen's Ch. 87)

11. Key Time Targets (AHA/ASA - Tintinalli's Table 167-8)

InterventionTime Goal from ED Arrival
Activation of stroke teamImmediately upon arrival
Start of brain imaging≤ 20 minutes
Administration of IV thrombolytics≤ 60 minutes (secondary goal ≤ 45 minutes)

12. NIHSS - National Institutes of Health Stroke Scale

  • Score range: 0-42 (0 = normal; higher = more severe)
  • Rapid (5-10 minutes); high interrater reliability
  • Important caveat: Weighted toward anterior circulation strokes - posterior strokes (CN deficits, ataxia) receive fewer points; ataxia scored as absent if weakness is present
  • Also has a bias toward detecting left hemisphere strokes

13. Prognosis & Complications

Factors worsening acute stroke prognosis (Rosen's):

  • Fever
  • Hypotension
  • Hypoxia
  • Hypoglycemia or Hyperglycemia

ICH-specific risks (Rosen's):

  • IV tPA: symptomatic intracranial hemorrhage in 2-7%; asymptomatic hemorrhage in 30-45% (>10 cerebral microbleeds)
  • Risk lowest with: low NIHSS, no hypertension, no diabetes, age < 70 years

Quick Reference: Wallenberg Syndrome Summary

SideFinding
IpsilateralHorner's syndrome (ptosis, miosis, anhidrosis)
IpsilateralFacial numbness + loss of corneal reflex (CN V nucleus)
IpsilateralDysphagia + hoarseness (CN IX, X)
IpsilateralLimb ataxia (cerebellar peduncle)
ContralateralLoss of pain and temperature on body (spinothalamic tract)
BothVertigo, nausea, vomiting, hiccups
AbsentHemiplegia (corticospinal tract spared)

Key Concepts Summary (Rosen's Chapter 87)

  1. Anterior circulation strokes → contralateral hemiparesis of face and body
  2. Vertebrobasilar strokes → ipsilateral CN deficits + contralateral hemiparesis (crossed deficits)
  3. PCA stroke → ipsilateral CN III palsy + contralateral homonymous hemianopsia
  4. Wallenberg syndrome → vertigo + Horner's + ipsilateral facial numbness + corneal reflex loss + contralateral pain/temperature loss
  5. Cervical artery dissection is the leading determined cause of stroke in young patients; TIAs often misdiagnosed
  6. IV tPA dose: 0.9 mg/kg (10% bolus + 90% over 1 hour); window = 4.5 hours
  7. Avoid overly aggressive BP management in acute ischemic stroke
  8. ICH reversal: prefer PCC over FFP (faster INR correction, lower infection risk, lower volume)
  9. Fever, hypotension, hypoxia, and glucose abnormalities worsen prognosis

References: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th Edition, Chapter 167 (Steven Go). Rosen's Emergency Medicine: Concepts and Clinical Practice, 10th Edition, Chapter 87 (Linda Papa & William J. Meurer).

Explain full chapter Stroke syndromes in Great detail including images, tables, flowchart, management, trials References - Tintinalli's 9th edition & Rosen's 10th edition

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STROKE SYNDROMES

Complete Chapter Review

References: Tintinalli's Emergency Medicine, 9th Ed. (Chapter 167 - Steven Go) | Rosen's Emergency Medicine, 10th Ed. (Chapter 87 - Linda Papa & William J. Meurer)

SECTION 1: EPIDEMIOLOGY

  • 795,000 strokes/year in the United States - one stroke every 40 seconds; one death every 4 minutes
  • 77% are first-ever strokes; 23% recurrent events
  • Estimated cost: $33.9 billion in total expenditures (2012-2013)
  • Age-adjusted stroke death rate fell 28.7% from 2004-2014 due to stroke units, thrombolysis, and endovascular thrombectomy
  • About 240,000 TIAs/year in the United States
Stroke Type Distribution:
  • Ischemic: 87% of all strokes
  • ICH: 10%
  • SAH: 3%
(Tintinalli's Ch. 167)

SECTION 2: PATHOPHYSIOLOGY & ANATOMY

Stroke = any disease process that interrupts blood flow to the brain. Injury is from:
  1. Loss of oxygen and glucose - failure of high-energy phosphate production
  2. Mediators of secondary cellular injury - glutamate excitotoxicity, free radicals
  3. Edema and mass effect - exacerbate initial insult
Neurons die within minutes of complete cessation of perfusion - this is why rapid reperfusion is the treatment cornerstone.

The Ischemic Penumbra

The area of irreversible infarct (core) is surrounded by ischemic tissue (penumbra) that may be salvageable. CT perfusion and DWI-MRI/FLAIR are used to measure the penumbra, especially for patients outside standard time windows.

Vascular Anatomy

Fig. 167-1: Cerebral Hemisphere, Lateral Aspect - MCA Distribution
Cerebral hemisphere lateral aspect showing MCA branches - Broca's area, sensory cortex, motor cortex, Wernicke's area, visual cortex
Fig. 167-2: Cerebral Hemisphere, Medial Aspect - ACA and PCA Distribution
Cerebral hemisphere medial aspect showing ACA, PCA, calcarine artery, hippocampal artery, visual cortex

Table 1: Cerebrovascular Anatomy - Circulation, Arteries & Brain Regions

CirculationMajor ArteryBrain Regions Supplied
Anterior (Internal Carotid System)OphthalmicOptic nerve, retina
Anterior Cerebral (ACA)Frontal pole; Anteromedial cortex; Anterior corpus callosum
Middle Cerebral (MCA)Frontoparietal lobe; Anterotemporal lobe; Deep white matter via lenticulostriate branches
Posterior (Vertebral-Basilar System)VertebralLateral medulla, cerebellum
PICADorsolateral medulla, inferior cerebellum
BasilarPons, midbrain, superior cerebellum
Posterior Cerebral (PCA)Thalamus; Medial temporal lobe; Occipital lobe; Visual cortex
(Tintinalli's Table 167-1)

SECTION 3: STROKE CLASSIFICATION

Table 2: Complete Stroke Classification (Tintinalli's Table 167-2)

TypeMechanismMajor CausesClinical Notes
ThromboticNarrowing/clot at damaged arterial lumenAtherosclerosis; Vasculitis; Arterial dissection; Polycythemia; Hypercoagulable states; Infections (HIV, syphilis, TB, aspergillosis)Gradual onset; wax and wane; common cause of TIA
EmbolicNormal lumen obstructed by remote materialValvular vegetations; Mural thrombi (AF); Paradoxical emboli; Cardiac tumors (myxoma); Artery-to-artery; Fat emboli; IV drug use; Septic emboliTypically sudden onset; 20% of ischemic strokes
HypoperfusionLow-flow state, watershed hypoperfusionCardiac failure with systemic hypotensionWatershed/border-zone pattern; wax and wane with hemodynamics
ICHIntraparenchymal bleed from weakened arteriolesHTN; Amyloid angiopathy; AVM; Cocaine; Anticoagulants; Tumor; Venous sinus thrombosis10% of all strokes; highest morbidity/mortality
SAHSubarachnoid space bleedingRuptured saccular aneurysm; Trauma; AVM3% of all strokes; thunderclap headache

SECTION 4: CLINICAL FEATURES

History - Key Distinguishing Features

PresentationSuggested Type
Sudden onset at maximal severityEmbolic or hemorrhagic
Stuttering or waxing and waning deficitThrombotic or hypoperfusion
Thunderclap headache + Valsalva activityRuptured aneurysm / SAH
Recent neck trauma or manipulationCervical artery dissection
AF, valvular replacement, recent MICardioembolic
Same vascular distribution TIAThrombotic vascular disease
TIAs in different distributionsEmbolic source
Hypertension + diabetes onsetLacunar or ICH

Table 3: Stroke Symptoms - Traditional vs. Non-Traditional (Tintinalli's Table 167-4)

Traditional SymptomsNon-Traditional Symptoms
Sudden numbness or weakness (face, arm, leg) - usually unilateralImpaired consciousness or syncope
Sudden aphasiaGeneralized weakness
Sudden dysarthriaAltered mental status
Sudden memory deficit / spatial disorientationDysphagia
Sudden visual deficit or diplopiaShortness of breath
Sudden dizziness, gait disturbance, ataxiaSudden pain in face, chest, arms, legs
Sudden severe headache with no known causeSeizure; Falls; Sudden hiccups; Nausea; Fatigue; Palpitations
Women tend to report more severe but diffuse nontraditional symptoms compared to men. - Tintinalli's Ch. 167

SECTION 5: ISCHEMIC STROKE SYNDROMES

Fundamental rule: Anterior circulation = contralateral hemiparesis face + body. Vertebrobasilar = ipsilateral CN deficits + contralateral motor/sensory (crossed deficits).

5.1 Anterior Cerebral Artery (ACA) Infarction

Frequency: 0.5%-3% of all strokes
FeatureDetail
Motor/SensoryContralateral leg > arm; sparing of face and hand
Frontal lobe featuresAltered mentation, impaired judgment and insight
Primitive reflexesGrasp reflex, suck reflex
IncontinenceBowel and bladder
Language (left lesion)Akinetic mutism; transcortical motor aphasia
GaitApraxia; clumsiness

5.2 Middle Cerebral Artery (MCA) Infarction

Most commonly involved vessel in stroke. Dominance: left hemisphere in right-handers and ~80% of left-handers.
FeatureDetail
Motor/SensoryContralateral hemiparesis + hemisensory loss; face + arm > leg
VisualContralateral homonymous hemianopsia
Gaze preferenceToward the side of infarct (disruption of cortical lateral gaze center)
Dominant hemisphere (left)Aphasia - Broca, Wernicke, or global
Non-dominant hemisphere (right)Inattention; hemispatial neglect; extinction on double simultaneous stimulation; constructional apraxia
Aphasia in Detail (MCA / Dominant Hemisphere):
TypeLocationProductionComprehensionRepetition
Broca's (expressive)Inferior frontal gyrusNon-fluent; effortfulRelatively intactImpaired
Wernicke's (receptive)Posterior superior temporalFluent but meaninglessSeverely impairedImpaired
GlobalLarge MCA territoryNon-fluentSeverely impairedImpaired
Dysarthria (not cortical)Motor mouth/tonguePoor articulation; intact word choiceNormalIntact
Aphasia localizes to the dominant cerebral cortex in MCA distribution. Dysarthria is a purely motor speech deficit. Dysphagia is difficulty swallowing - all three are frequently confused. - Rosen's Ch. 87

5.3 Posterior Cerebral Artery (PCA) Infarction

(Distal Posterior Circulation)
FeatureDetail
Visual fieldContralateral homonymous hemianopsia (most specific sign); cortical blindness
Visual agnosiaInability to recognize seen objects
Alexia without agraphiaCannot read; CAN write (unique PCA finding)
Color anomiaInability to name colors
MemoryRecent memory loss (medial temporal involvement)
OculomotorIpsilateral CN III palsy
HemiballismusThalamic involvement
MotorMinimal - patient may not realize a stroke has occurred
NeglectPatient may be unaware of visual problem (visual neglect)
PCA stroke: ipsilateral CN III palsy + contralateral homonymous hemianopsia. - Rosen's Key Concepts

5.4 Basilar Artery Occlusion

(Middle Posterior Circulation)
FeatureDetail
Presenting symptomsUnilateral limb weakness, dizziness, dysarthria, diplopia, headache
Presenting signsCN VII signs, Babinski sign, oculomotor signs, dysarthria
AssociatedDysphagia, nausea/vomiting, Horner's syndrome
Rare - Locked-in SyndromeBilateral pyramidal tract lesions in ventral pons; complete paralysis except upward gaze + blinking
PrognosisHigh mortality; among the worst prognosis of any stroke

5.5 Vertebrobasilar Infarction

(Proximal Posterior Circulation)
FeatureDetail
SymptomsDizziness, nausea/vomiting, headache, dysphagia, unilateral limb weakness, CN V symptoms
SignsUnilateral limb ataxia, nystagmus, gait ataxia, Horner's syndrome, CN V signs, limb sensory deficit

5.6 Wallenberg Syndrome (Lateral Medullary Syndrome)

Vessel: PICA occlusion or vertebral artery occlusion. Classic example of crossed deficit.
SideFindingTract/Structure
IpsilateralHorner's syndrome (ptosis + miosis + anhidrosis)Descending hypothalamo-spinal sympathetic tract
IpsilateralFacial numbness + loss of corneal reflexNucleus + spinal tract of CN V
IpsilateralDysphagia + hoarsenessNucleus ambiguus (CN IX, X)
IpsilateralLimb ataxiaInferior cerebellar peduncle / cerebellum
ContralateralLoss of pain + temperature on bodySpinothalamic tract
BilateralVertigo, nausea, vomiting, hiccupsVestibular nuclei; CTZ in brainstem
AbsentHemiplegiaCorticospinal tract is SPARED
"Wallenberg syndrome causes vertigo, Horner syndrome, ipsilateral facial numbness, loss of corneal reflex, along with contralateral loss of pain and temperature." - Rosen's Key Concepts

5.7 Cerebellar Infarction

FeatureDetail
SymptomsDizziness ± vertigo, nausea/vomiting, gait instability, headache, limb ataxia, dysarthria, dysmetria, nystagmus, hearing loss, intractable hiccups
Mental statusAlert to comatose
CT caveatUp to 25% of noncontrasted CTs are normal - always get MRI-DWI if suspected
DangerCerebellar edema → brainstem compression → rapid deterioration; watch for gaze palsy

5.8 Lacunar Infarction

Mechanism: Infarction of small penetrating arteries (terminal vessels 80-900 µm). Associated with chronic hypertension (80-90% of patients) and diabetes. Lipohyalinosis is the primary process. Size: few mm to 2 cm.
Common locations: Basal ganglia, thalamus, pons, internal capsule.
Classic Lacunar Syndromes:
SyndromeLocationKey Features
Pure Motor HemiplegiaPosterior limb internal capsule or ponsContralateral face + arm + leg weakness; NO sensory loss, NO cortical signs
Pure Sensory StrokeThalamus (VPL)Contralateral hemisensory loss only
Sensorimotor StrokeThalamocapsular junctionMotor + sensory, no cortical features
Ataxic HemiparesisPons or internal capsuleIpsilateral limb ataxia + contralateral hemiparesis
Dysarthria-Clumsy HandPons or genu of internal capsuleDysarthria + contralateral hand clumsiness
Prognosis generally more favorable than other stroke syndromes. - Tintinalli's Ch. 167

5.9 Stroke in Young Adults (15-45 years)

  • 3%-4% of all strokes; average age of first stroke getting younger
  • Must search for less common, often reversible, causes
CauseNotes
Cervical artery dissectionLeading determined cause in young adults; 20% of strokes in this group
Oral contraceptives / PregnancyHypercoagulable / prothrombotic state
Antiphospholipid antibodiesLupus anticoagulant, anticardiolipin antibodies
Protein S or C deficiencyHereditary thrombophilia
Sickle cell disease, polycythemiaSludging and thrombosis
Mitral valve prolapse, RHDCardioembolic - young adults
Cocaine, amphetamines, heroinVasoconstrictors; both ischemic + hemorrhagic
Migrainous strokeInfarction during typical migraine
HIV (CD4 <200)Rate ratio 2.5 for ischemic stroke
Fibromuscular dysplasiaCerebrovascular dysplasia
Cancer historyHypercoagulable; direct invasion

5.10 Carotid and Vertebral Artery Dissection

  • 2% of all strokes; up to 20-25% of strokes in young adults
  • Neck trauma in ~40% (often minor: chiropractic manipulation, sneezing, sports)
  • First symptom: unilateral headache (68%), neck pain (39%), face pain (10%)
  • Median delay from neck pain to neurologic symptoms: 4 days; from headache: 15 hours
Carotid Artery Dissection:
  • Frontotemporal headache; may mimic SAH (thunderclap quality)
  • Partial Horner's syndrome (miosis + ptosis) in ~25%; rarely, full Horner's
  • Cranial nerve palsies in ~12%
  • Anterior circulation symptoms; can lead to retinal infarction
Vertebral Artery Dissection:
  • Occipital headache (51-65%); neck pain (46-66%); dizziness/vertigo (58%)
  • Posterior circulation symptoms: facial paresthesia, ataxia, limb weakness, hearing loss
  • May cause Wallenberg syndrome
Diagnosis: CT/CTA or MRI/MRA have similar performance; choice by availability/stability.
TIAs preceding stroke in cervical dissection are often misdiagnosed. - Rosen's Key Concepts

SECTION 6: HEMORRHAGIC STROKE SYNDROMES

6.1 Intracerebral Hemorrhage (ICH)

  • 10%-15% of all strokes; ~65,000 patients/year
  • 30-day mortality: up to 50%; half die in first 2 days
  • Only 1 in 5 survivors are living independently at 6 months
  • ~40% show significant hemorrhage expansion in the first few hours
Two primary causes:
  1. Hypertensive vasculopathy - lipohyalinosis of deep penetrating vessels; deep ICH
  2. Cerebral amyloid angiopathy - amyloid in vessel walls; lobar ICH; elderly patients

Table 4: Sites of Hypertensive ICH and Presentations (Rosen's Box 87.1)

LocationFrequencyTypical Presentation
Putamen44%Contralateral motor + sensory deficit
Other cortical areas25%Variable (lobar)
Thalamus13%Limb pain, speech difficulty
Cerebellum9%Uncoordinated movements of trunk and limbs
Pons9%Numbness, weakness, ataxia, dizziness
ICH may be clinically indistinguishable from ischemic stroke. CT is mandatory to differentiate the two. - Tintinalli's Ch. 167
Clinical features suggesting ICH: Headache, nausea, and vomiting preceding the neurologic deficit; rapid deterioration.

ICH Score (Prognostic Tool) - Rosen's Table 87.3

ComponentScore
GCS 3-4+2
GCS 5-12+1
GCS 13-150
ICH volume ≥30 mL+1
Infratentorial origin+1
Age ≥80 years+1
Intraventricular hemorrhage+1
Higher score = higher 30-day mortality.

6.2 Subarachnoid Hemorrhage (SAH)

  • Thunderclap headache: "worst headache of my life," maximal at onset
  • Often associated with Valsalva activities: defecation, sexual activity, weight lifting, coughing
  • Severe occipital or nuchal headache that is sudden
  • Preretinal (subhyaloid) hemorrhage on fundoscopy is pathognomonic
  • Meningismus may develop within hours

SECTION 7: STROKE MIMICS

Table 5: Stroke Mimics and Distinguishing Features (Tintinalli's Table 167-5)

MimicKey Distinguishing Features
Todd's paralysis (post-ictal)Transient paralysis after seizure; disappears quickly; seizure may be caused by CVA
SyncopeNo persistent neurologic symptoms
Meningitis/EncephalitisFever; CSF changes on LP
Complicated migraineHistory of similar episodes; preceding aura; headache
Brain tumor/AbscessFocal neurologic findings; detectable by imaging; fever for abscess
Epidural/Subdural hematomaTrauma history; anticoagulant use; bleeding disorder
SAHThunderclap headache (note: SAH is itself a hemorrhagic stroke)
HypoglycemiaBedside glucose; diabetes history; corrects with dextrose
HyponatremiaDiuretic use; excessive free water; labs
Hypertensive encephalopathyGradual onset; global dysfunction; cerebral edema; improves with BP control
Hyperosmolar comaExtremely high glucose; diabetes history
Wernicke's encephalopathyAlcoholism/malnutrition; classic triad: ataxia + ophthalmoplegia + confusion
LabyrinthitisPurely vestibular symptoms; no other focal findings
Bell's palsyIsolated peripheral CN VII (forehead INVOLVED - cannot wrinkle)
Meniere's diseaseRecurrent episodes; tinnitus; progressive deafness
Multiple sclerosisGradual onset; multifocal history; young patient
Conversion disorderNo CN findings; non-anatomic distribution; inconsistent exam
Drug toxicity (phenytoin, carbamazepine, lithium)Toxidromes; elevated drug levels; ataxia/vertigo
CVSTHeadache, seizures, papilledema; venous phase on CTA or MRV

SECTION 8: PREHOSPITAL STROKE SCALES

Table 6: Prehospital Stroke Scales (Tintinalli's Table 167-3)

ScaleComponentsPositive if...
Cincinnati Prehospital Stroke Scale (CPSS)Facial droop; Arm drift; Speech abnormalityAny 1 of 3 present: sensitivity 59%, specificity 89%
Los Angeles Prehospital Stroke Screen (LAPSS)Age >45; No prior seizure; Not wheelchair-bound; BG 50-400; Asymmetric face/grip/arm strengthAll screening items + 1 neurologic finding
Melbourne Ambulance Stroke Screen (MASS)Age ≥45; No seizure; Not bedridden; BG 50-400; + facial droop/grip weakness/arm drift/abnormal speechAll 4 criteria + any 1 neurologic sign: sensitivity 90%

SECTION 9: NIHSS - National Institutes of Health Stroke Scale

  • Score range: 0-42 (0 = normal; higher = more severe)
  • Duration: 5-10 minutes; high interrater reliability
  • 15-item, 11-category neurologic evaluation
  • Caveat 1: Weighted toward anterior circulation strokes - posterior strokes (CN deficits, ataxia) get fewer points; ataxia scored absent if weakness present
  • Caveat 2: Bias toward detecting left hemisphere strokes
NIHSS Score RangeStroke Severity
0Normal
1-4Minor
5-15Moderate
16-20Moderate-severe
21-42Severe

SECTION 10: DIAGNOSTIC EVALUATION

Neuroimaging

Non-contrast CT (NCCT) Head:
  • First-line imaging; must be done within 20 minutes of ED arrival
  • Differentiates ischemic stroke from ICH and mass lesions
  • Ischemic stroke: gross changes NOT seen for 6-12 hours
  • Subtle early ischemic changes seen in up to 67% within first 3 hours:
    • Hyperdense artery sign (acute thrombus in vessel)
    • Sulcal effacement
    • Loss of insular ribbon
    • Loss of gray-white interface
    • Mass effect; acute hypodensity
CT Angiography (CTA):
  • High-quality images of large vessels; detects LVO (large vessel occlusion)
  • Identifies secondary causes of ICH: aneurysm, AVM, fistula
  • Spot sign on CTA = contrast extravasation in ICH → high risk of hemorrhage expansion
MRI:
  • DWI (Diffusion-Weighted Imaging): Detects ischemia within minutes of onset
  • FLAIR: Detects parenchymal edema; typically becomes positive 4-6 hours after onset
  • DWI-FLAIR mismatch = ischemia on DWI but FLAIR negative = suggests stroke onset within 4.5 hours (useful for wake-up strokes)
DWI and FLAIR Images - Wake-Up Stroke Identification (Rosen's Fig. 87.5):
DWI and FLAIR MRI images showing excluded scans on left and FLAIR-negative DWI-FLAIR mismatch
FLAIR-negative (DWI-FLAIR mismatch) = lesion on DWI but not FLAIR = stroke likely within 4.5 hours; FLAIR-positive = lesion on both = stroke likely older than 4.5 hours
MRI sensitivity: Detects posterior fossa strokes that CT misses; essential for suspected cerebellar infarction.

ASPECTS Score (Alberta Stroke Program Early CT Score)

  • 10-point scale assessing early ischemic changes in MCA territory on NCCT
  • Score ≥6 = relatively preserved brain tissue = favorable for intervention
  • Score <6 = extensive early ischemic changes = less benefit from thrombectomy

Laboratory Studies

Required before thrombolytics: bedside glucose only (do not delay tPA for other labs unless anticoagulant use suspected or thrombocytopenia history)
  • CBC, BMP, coagulation studies, type and screen
  • ECG (AF, MI, arrhythmias)
  • If ICH: drug screen (cocaine), look for coagulopathy

SECTION 11: TIME TARGETS

Table 7: NINDS Stroke Evaluation Targets (Rosen's Table 87.4 / Tintinalli's Table 167-8)

Management ComponentTarget Time Frame
Door to doctor10 min
Door to stroke team notification15 min
Door to CT scan initiation25 min
Door to CT scan interpretation45 min
Door to IV tPA administration≤60 min (goal ≤45 min)
Door to monitored bed3 hours
Access to neurosurgery2 hours

SECTION 12: MANAGEMENT

12.1 General Supportive Care (All Stroke Patients)

Table 8: Core ED Interventions for Suspected Acute Stroke (Tintinalli's Table 167-7)

InterventionRationale
ABC assessmentImmediate life threats first; active airway management if needed
IV accessRequired for possible thrombolytics; do NOT delay imaging for access
Pulse oximetryDetect hypoxia
Oxygen: only if SpO₂ <94%Routine O₂ not indicated; hyperbaric O₂ no benefit
Cardiac monitoringAF (most common cardioembolic cause); arrhythmias predict mortality
Bedside glucoseRule out hypoglycemia immediately; treat BG <60 with IV dextrose
Swallowing assessmentWithhold oral meds/fluids/food until assessed; aspiration risk
Avoid dextrose-containing IVFHyperglycemia worsens ischemic deficit
Correct dehydrationIncreases blood viscosity; but do NOT over-hydrate
Fever: identify cause + treatFever associated with ↑ morbidity/mortality; treat source + acetaminophen
Stroke unit admissionAssociated with decreased complications, length of stay, improved function
Glycemic control: Target blood glucose 140-180 mg/dL. Treat hypoglycemia (<60 mg/dL) with IV dextrose. Tight control (<140) not proven beneficial and risks hypoglycemia.

12.2 Blood Pressure Management

A. Acute Ischemic Stroke - NOT receiving tPA:
  • Do NOT treat unless SBP >220 mmHg or DBP >120 mmHg
  • The elevated BP is a compensatory response (Cushing's) maintaining cerebral perfusion
  • Exception: Treat if concurrent AMI, aortic dissection, hypertensive encephalopathy, severe CHF
B. Eligible for IV tPA (pre-treatment):
  • Must achieve SBP <185 mmHg AND DBP <110 mmHg before giving tPA
  • If BP does not decline to this level → DO NOT administer rtPA

Table 9: BP Management Algorithms (Tintinalli's Tables 167-9 & 167-10 / Rosen's Box 87.2)

ScenarioBP ThresholdAgents
Pre-tPA (to reach <185/110)SBP >185 or DBP >110Labetalol 10-20 mg IV x 1-2; OR Nicardipine 5 mg/h, titrate to 15 mg/h; OR Clevidipine 1-2 mg/h, double q2-5 min (max 21 mg/h)
During tPA (SBP 180-230 or DBP 105-120)SBP 180-230 or DBP 105-120Labetalol 10 mg IV q10-20 min (max 300 mg) OR infusion 2-8 mg/min
During tPA (refractory/severe)SBP >230 or DBP >140Nicardipine infusion OR sodium nitroprusside (0.5-10 mcg/kg/min); monitor arterially
BP monitoring after tPAEvery 15 min x 2h → every 30 min x 6h → every 60 min x 16h

12.3 Reperfusion Therapy - IV Thrombolytics

Key Trials for IV Alteplase

Table 10: Major Clinical Trials for IV tPA in Acute Ischemic Stroke

TrialYearnTime WindowKey Finding
NINDS19956240-3htPA 0.9 mg/kg vs. placebo: 13% absolute improvement in functional outcome at 3 months; sICH 6.4% vs. 0.6%; NO difference in mortality at 3 months. BASIS for FDA approval.
ECASS I19956200-6htPA 1.1 mg/kg; primary endpoint not met; ↑ parenchymal hemorrhage rate
ECASS II19988000-6htPA 0.9 mg/kg; no significant benefit; parenchymal hemorrhage 8.8% vs. 3.4%
ECASS III20088213-4.5htPA vs. placebo: mRS 0-1 at 90 days 52.4% vs. 45.2% (OR 1.34; P=0.04); sICH 2.4% vs. 0.2%; expanded window to 3-4.5 hours
IST-3201230350-6hLargest RCT; 72% received tPA after 3h; NO significant difference in primary outcome at 6 months; favorable secondary ordinal shift in disability; sICH 7% vs. 1%
WAKE-UP2018~503Unknown onsetMRI-guided (DWI-FLAIR mismatch); tPA vs. placebo in wake-up stroke; favorable outcome 53.3% vs. 41.8% (OR 1.61; P=0.02); sICH 2% vs. 0.4%; stopped early due to funding
ENCHANTED201633000-4.5hLow-dose alteplase (0.6 mg/kg) non-inferior to standard dose (0.9 mg/kg) for death/disability at 90 days; significantly fewer sICH; (63% Asian population; low dose is standard in Japan but NOT current AHA guideline)
Cochrane Meta-analysis201410,1870-6hTreated patients less likely to be dead or dependent; benefit regardless of ↑ sICH and early deaths; early treatment better than late

Alteplase Dosing

  • Dose: 0.9 mg/kg IV (maximum 90 mg total)
  • Administration: 10% of total dose as IV bolus over 1 minute; remaining 90% infused over 60 minutes
  • Do NOT use abbreviations (rtPA, tPA); use full name "alteplase" to avoid medication errors

Tenecteplase (TNK)

  • Single IV bolus (0.25 mg/kg; max 25 mg)
  • EXTEND-IA TNK trial and others: similar functional outcome, sICH, and mortality vs. alteplase at 90 days
  • Higher reperfusion rates before thrombectomy vs. alteplase in LVO patients
  • Moderate-to-high quality evidence supports use; AHA/ASA now recommends as alternative

AHA/ASA Inclusion Criteria for IV Alteplase (Tintinalli Table 167-11 / Rosen's Table 87.5)

Within 3 hours - INCLUSION:
  • Age ≥18 (no upper age limit)
  • Diagnosis of acute ischemic stroke with measurable neurologic deficit
  • Time of onset clearly established <3h (or last known well time)
3-4.5 hours - ADDITIONAL RESTRICTIONS:
  • Age ≤80 (per older criteria; see Note below)
  • No history of BOTH diabetes mellitus AND prior stroke
  • NIHSS ≤25
  • No oral anticoagulants
  • No imaging evidence of ischemia >1/3 of MCA territory
EXCLUSION CRITERIA:
  • Last known well >4.5 hours (or unknown onset without imaging selection)
  • Acute intracranial hemorrhage or history of prior ICH
  • Evidence of SAH
  • Recent brain imaging showing extensive clear hypodensity (obvious early ischemia)
  • Recent ischemic stroke or severe head trauma within 3 months
  • Acute posttraumatic brain infarction
  • Intracranial or intraspinal surgery within 21 days
  • GI or GU bleeding within 3 months
  • Active arterial puncture at non-compressible site within 7 days
  • SBP persistently >185 mmHg or DBP >110 mmHg despite treatment
  • Platelet count <100,000/mm³
  • INR >1.7 or aPTT >40s or PT >15s
  • Blood glucose <50 mg/dL (normalize first)
  • Current use of GP IIb/IIIa inhibitors
  • Known or suspected aortic arch dissection
  • Intra-axial or extra-axial neoplasm (some exceptions)
SELECTED SPECIAL SCENARIOS:
ConditionGuidance
Recent MINot a contraindication; STEMI involving left anterior, right, or inferior myocardium - can still give tPA
PregnancyMay be considered for moderate-to-severe stroke
Seizure at onsetNot a contraindication IF residual deficit is from stroke, not postictal
Unruptured aneurysm <10 mmNot a contraindication
Antiplatelet therapyGive tPA - benefit outweighs small ↑ sICH risk
Direct oral anticoagulants (DOAC)Do NOT give tPA unless appropriate coag labs normal OR last dose >48h (with normal renal function)
LMWHDo NOT give tPA if full treatment dose given within 24h

Post-tPA Complications

  • Symptomatic ICH: 2%-7%; greatest risk with most severe strokes
  • Asymptomatic ICH: 30%-45% (>10 cerebral microbleeds)
  • Cerebral microbleeds (CMBs): If >10 on prior MRI, risk of sICH = 30%-47%; benefits of tPA uncertain
  • PH2 hemorrhage (>30% of infarcted tissue + mass effect): ~50% mortality
Risk factors for sICH after tPA: Older age, high NIHSS, hypertension, hyperglycemia, diabetes, CHF, renal impairment, AF, antiplatelet use, leukoaraiosis, visible infarct on imaging

12.4 Endovascular Therapy - Mechanical Thrombectomy

AHA/ASA Indications for Stent Retriever Thrombectomy (0-6 hours) - Tintinalli Table 167-13

ALL 7 criteria must be met:
  1. Prestroke mRS 0-1 (no significant prior disability)
  2. Acute ischemic stroke receiving IV rtPA within 4.5h OR not eligible for rtPA
  3. Causative occlusion of ICA or proximal MCA (M1)
  4. Age ≥18
  5. NIHSS ≥6
  6. ASPECTS ≥6
  7. Treatment (groin puncture) initiable within 6 hours of symptom onset

Positive Thrombectomy Trials (0-6 hours)

TrialYearKey Finding
MR CLEAN2015Thrombectomy vs. standard; absolute difference in functional independence 13.5%; first positive modern thrombectomy RCT
ESCAPE2015Stopped early; 90-day mRS 0-2: 53% vs. 29%; mortality 10% vs. 19%
EXTEND-IA2015Stopped early; 90-day functional independence 71% vs. 40%
SWIFT PRIME2015Stopped early; 90-day mRS 0-2: 60% vs. 35%
REVASCAT2015mRS 0-2 at 90 days: 43.7% vs. 28.2%
THRACE2016mRS 0-2: 53% vs. 42%; reinforced 0-5h window
These 6 trials together represent a practice-changing moment in stroke treatment.

Extended Window Thrombectomy Trials (6-24 hours)

TrialWindownKey Finding
DAWN6-24h206Thrombectomy vs. standard; 90-day mRS 0-2: 49% vs. 13% (adjusted difference 33%); posterior probability >0.999; stopped early
DEFUSE 36-16h182Thrombectomy vs. standard; 90-day mRS 0-2: 45% vs. 17%; OR 2.77; stopped early
Both DAWN and DEFUSE 3 used perfusion imaging to identify salvageable tissue (penumbra mismatch). AHA/ASA recommends extended window thrombectomy ONLY if strict inclusion/exclusion criteria of DAWN or DEFUSE 3 are met.
Timing effects: Each 1-hour delay to reperfusion → less functional independence; benefit becomes nonsignificant after 7 hours in pooled analysis.
Combined tPA + Thrombectomy: Dual therapy (tPA + thrombectomy) → higher 3-month functional independence + lower mortality vs. thrombectomy alone. Thrombectomy should NOT be delayed to assess tPA response.

12.5 Antiplatelet Therapy

Aspirin (160-300 mg oral or rectal):
  • Recommended within 24-48 hours of ischemic stroke onset
  • Combined International Stroke Trial (IST, n=19,435) + Chinese Acute Stroke Trial (CAST, n=20,665): significant reduction in mortality and morbidity at 4 weeks and 6 months
  • DO NOT give within 24 hours of tPA
Dual Antiplatelet (Aspirin + Clopidogrel):
  • POINT trial and CHANCE trial: for minor stroke or high-risk TIA, dual antiplatelet for 21 days reduces early recurrent stroke but ↑ bleeding risk
  • NOT for moderate-severe stroke; most benefit in lacunar or minor stroke
ABCD2 Score for TIA Risk Stratification:
  • Previously recommended by guidelines; current ACEP 2016 policy states ABCD2 should NOT be used alone to identify TIA patients safe for discharge (inadequate LR+ and LR-)

12.6 Anticoagulation

  • Acute anticoagulation (heparin) in acute ischemic stroke: NOT recommended routinely
  • Benefits do NOT outweigh risk of symptomatic ICH in acute stroke
  • Exception: specific situations (stroke with concurrent AMI, dissection) - consult stroke specialist

12.7 Other Ischemic Stroke Management

Temperature control:
  • Fever (>38°C) significantly worsens outcome
  • Identify and treat source; acetaminophen for antipyresis
  • Avoid ibuprofen (no temperature lowering + bleeding risk)
  • Physical cooling is second-line only
  • Hypothermia induction: no benefit; increased infection risk
Carotid Endarterectomy:
  • For high-grade ICA lesions after TIA: best performed within 2 weeks of TIA (surgical benefit greatest)
  • CREST trial: Carotid stenting vs. endarterectomy - similar functional outcomes up to 10 years
  • Stenting preferred in: age <70, high surgical risk

SECTION 13: HEMORRHAGIC STROKE MANAGEMENT

13.1 ICH Management Principles

Initial goals:
  1. Prevent hemorrhage expansion (~20%-30% expand in first hours)
  2. Prevent secondary brain injury: airway + breathing + circulation
  3. Airway management: balance between aspiration prevention vs. loss of serial neurological exam

13.2 Blood Pressure in ICH

INTERACT2 Trial (2013): n=2839; SBP 150-220 mmHg; randomized to intensive target (SBP <140 mmHg within 1 hour) vs. standard (SBP <180 mmHg):
  • Intensive lowering did NOT significantly reduce death or severe disability
  • BUT improved functional outcomes at 90 days
ATACH 2 Trial: IV nicardipine within 3 hours; SBP 110-139 vs. 140-179 mmHg target:
  • No difference in death/disability
  • ↑ Renal adverse events in intensive group (9.0% vs. 4.0%)
Current recommendation: Target SBP <140-160 mmHg (AHA/ASA); agents: IV labetalol, nicardipine, clevidipine.

13.3 Anticoagulation Reversal

Table 11: Anticoagulation Reversal in ICH

AgentReversal
WarfarinVitamin K (phytonadione) IV + PCC (Prothrombin Complex Concentrate) preferred over FFP; PCC: faster INR correction, lower infection risk, lower volume
Warfarin (if PCC unavailable)FFP + Vitamin K
Dabigatran (direct thrombin inhibitor)Idarucizumab (Praxbind) - specific reversal
Rivaroxaban, Apixaban (Factor Xa inhibitors)Andexanet alfa - specific reversal; or 4-factor PCC
HeparinProtamine sulfate
LMWHProtamine sulfate (partial reversal)
Aspirin/ADP inhibitorsConsider desmopressin (ddAVP) 0.4 mcg/kg IV if proceeding to neurosurgery; platelet transfusion for neurosurgical procedures
PCC preferred over FFP: faster INR correction, lower infection risk, lower administered volume. - Rosen's Key Concepts
Tranexamic acid (TICH2 trial, n=2325): 2g IV within 8 hours - no improvement in 90-day functional status vs. placebo; some reduction in hematoma expansion and early death.

13.4 ICP Management in ICH

  • Indications for ICP monitoring: GCS ≤8; clinical transtentorial herniation; intraventricular hemorrhage or hydrocephalus
  • External ventricular drain: for hydrocephalus, especially IVH blocking 3rd/4th ventricles
  • Target CPP: 50-70 mmHg
  • Medical therapy:
    • Mannitol (0.25-1 g/kg IV): osmotic agent; safe but limited outcome improvement
    • Hypertonic saline (HTS) 3% or 23.4%: more effective than mannitol (meta-analysis); 23.4% HTS for herniation reversal
    • Elevate head of bed 30°; maintain normothermia; avoid hypotonic fluids
CLEAR III Trial: Alteplase irrigation of external ventricular drain vs. saline in IVH - NO improvement in functional outcomes at mRS 3 cutoff.

13.5 Seizures in ICH

  • Up to 16% risk of clinical seizures within 1 week (majority at onset)
  • No prophylactic antiseizure medication recommended
  • Treat clinical seizures with anticonvulsants
  • Continuous EEG monitoring for ICH patients with mental status out of proportion to brain injury
  • Levetiracetam 1000-1500 mg IV for electrographic seizures

13.6 Surgical Management of ICH

General rule: Standard open craniotomy for spontaneous ICH has NOT been proven to improve outcomes.
STICH I (2005): Early surgical hematoma evacuation vs. conservative management - no benefit for routine surgery; subgroup trend for benefit in superficial lobar hemorrhage
STICH II (2013): Superficial lobar ICH (within 1 cm of cortex); surgery vs. conservative - no significant benefit in primary outcome
ENRICH Trial (ongoing/early results): Minimally invasive parafascicular surgery (MIPS) within 24h; early results: 52% functional independence at follow-up; no mortality in 39-patient cohort
Cerebellar hemorrhage: If >3 cm OR with brainstem compression OR hydrocephalus → NEUROSURGICAL CONSULTATION; posterior fossa decompression may be lifesaving
Decompressive craniectomy (SWITCH trial, ongoing): For basal ganglia/thalamic ICH with GCS 8-13, NIHSS 10-30, hematoma 30-100 mL
Early DNR orders: Current AHA/ASA guidelines recommend aggressive early care and to postpone new DNR orders until at least day 2 of treatment (early DNR associated with self-fulfilling prophecy)

SECTION 14: TIA MANAGEMENT

Updated Definition (AHA): "A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction" - tissue-based, NOT time-based.
  • ~240,000 TIAs/year; ~10% stroke risk within 3 months; 50% of those in first 2 days
  • Patients with DWI-negative TIA have much lower recurrence risk
Dual Antiplatelet for Minor Stroke/High-Risk TIA:
  • Aspirin + Clopidogrel for 21 days (POINT trial, CHANCE trial)
  • Then transition to single antiplatelet
ABCD2 Score: Age, BP, Clinical features, Duration, Diabetes - NOT sufficient alone to risk-stratify for safe discharge (ACEP 2016 Clinical Policy).
Disposition: Most TIA patients without contraindications should be hospitalized or in an expedited 24-hour TIA clinic pathway.

SECTION 15: CEREBELLAR/BRAINSTEM STROKE TREATMENT

Special management considerations:
  • MRI-DWI mandatory (CT has up to 25% false-negative rate for posterior fossa)
  • Close monitoring for rapid deterioration from edema and brainstem compression
  • Serial exams: watch for gaze palsy, worsening ataxia, deteriorating consciousness
  • Neurosurgical consultation if cerebellar hemorrhage or large cerebellar infarct
  • Posterior fossa decompression may be lifesaving for large cerebellar stroke with edema

SECTION 16: STROKE IN SPECIAL POPULATIONS

Stroke with Concurrent AMI

  • Aspirin appropriate for both; consult cardiology before tPA
  • Recent STEMI involving left anterior, right, or inferior myocardium is NOT a contraindication to tPA

Stroke with Coagulopathy

  • Consult hematology + stroke neurology
  • Admit to comprehensive stroke center

Young Adults (18-50 years)

  • Younger victims have MORE FAVORABLE morbidity/mortality after IV thrombolysis, thrombectomy, and decompressive surgery for large MCA strokes
  • Treat aggressively
  • Increasing incidence linked to: ↑ hyperlipidemia, diabetes, obesity, recreational drug use

MASTER FLOWCHART: ACUTE STROKE MANAGEMENT IN THE ED

PATIENT ARRIVES WITH SUSPECTED STROKE
              │
              ▼
    ┌─────────────────────────────────────┐
    │  IMMEDIATE ACTIONS (0-5 min)        │
    │  • ABC + Vital Signs                │
    │  • Bedside glucose (treat <60 dextrose)│
    │  • IV access + cardiac monitor + SpO₂│
    │  • ACTIVATE STROKE TEAM NOW         │
    │  • Last known well TIME documented  │
    └─────────────────────────────────────┘
              │
              ▼
    ┌─────────────────────────────────────┐
    │  HISTORY & EXAM (5-15 min)          │
    │  • Time of onset (last known well)  │
    │  • Medications (anticoagulants?)    │
    │  • NIHSS score                      │
    │  • Posterior vs. anterior signs?    │
    └─────────────────────────────────────┘
              │
              ▼
    ┌─────────────────────────────────────┐
    │  NCCT HEAD (within 20 min)          │
    └─────────────────────────────────────┘
              │
    ┌─────────────┴──────────────┐
    │                            │
    ▼                            ▼
HEMORRHAGE                 NO HEMORRHAGE
    │                            │
    │                            ▼
    │                 ISCHEMIC STROKE
    │                            │
    │              ┌─────────────┴───────────────┐
    │              │                             │
    │              ▼                             ▼
    │     Within 4.5 hours?             Beyond 4.5 hours
    │       AND eligible?                 OR unknown onset
    │              │                             │
    │         YES  │  NO                         │
    │              │   └──────────────────┐      │
    │              │         BP <185/110? │      │
    │              │              YES     │      │
    │              ▼                      │      │
    │     IV ALTEPLASE                    │      │
    │     0.9 mg/kg (max 90mg)            │      │
    │     Bolus 10% over 1 min            │      │
    │     + infusion 90% over 60 min      │      │
    │              │                      │      │
    │              └──────────┬───────────┘      │
    │                         │                  │
    │              CTA HEAD/NECK                 │
    │              (LVO screen)                  │
    │                         │                  │
    │              LVO present? (ICA or M1)      │
    │           NIHSS ≥6, ASPECTS ≥6             │
    │                         │                  │
    │                YES       │   NO             │
    │                ▼         │    ▼             │
    │         MECHANICAL       │  SUPPORTIVE      │
    │         THROMBECTOMY     │  CARE            │
    │         (0-6h standard   │  + Aspirin       │
    │          6-24h if DAWN/  │  in 24-48h       │
    │          DEFUSE3 criteria│                  │
    │          met)            │                  │
    │                          │                  │
    │              PERFUSION IMAGING:             │
    │              DWI-FLAIR mismatch?            │
    │              → May extend tPA window        │
    │              for wake-up stroke             │
    │                                             │
    ▼
HEMORRHAGIC STROKE
    │
    ├── ICH
    │    • Reverse anticoagulation
    │    │  (Warfarin: PCC + Vit K; DOAC: specific reversal)
    │    • BP: target SBP <140-160 mmHg
    │    │  (Nicardipine or Labetalol IV)
    │    • ICP management if indicated
    │    │  (HOB 30°; Mannitol or HTS 3%)
    │    • Seizure treatment (no prophylaxis)
    │    • Cerebellar hemorrhage >3cm
    │    │  or brainstem compression → Neurosurgery
    │    • NO early DNR (wait ≥day 2)
    │    • Admit ICU / Stroke Unit
    │
    └── SAH
         • Neurosurgical consultation STAT
         • Nimodipine (vasospasm prevention)
         • Avoid anticoagulants/antiplatelets
         • BP control; aneurysm securing

MASTER COMPARISON TABLE: All Major Stroke Syndromes

Table 12: Comprehensive Stroke Syndrome Summary

ArteryTerritoryClassic DeficitsIpsilateral FindingsContralateral FindingsDistinguishing Feature
ACAFrontal/medial cortexFrontal syndromeLeg weakness > arm; leg sensory lossLeg >> arm
MCALateral cortexHemiparesis + sensoryFace + arm > leg; hemianopsiaAphasia (dominant) or Neglect (non-dominant)
PCAOccipital + thalamusVisual + memoryCN III palsyHomonymous hemianopsiaMinimal motor; alexia without agraphia
BasilarPons + midbrainBilateralMultiple CN palsiesBilateral motorLocked-in syndrome; coma
PICA/Vertebral (Wallenberg)Lateral medullaCrossed deficitsHorner's; facial numbness; ataxia; dysphoniaPain + temperature loss on bodyNO hemiplegia
LacunarBG/thalamus/pons/capsulePure motor or sensoryNoneContralateral pure deficitNo cortical signs
CerebellarCerebellumIpsilateral ataxiaIpsilateral dysmetria; ataxiaCT often normal; MRI required

PROGNOSTIC FACTORS

Factors Worsening Acute Stroke Prognosis (Rosen's Key Concepts)

FactorWhy It Worsens Outcome
Fever↑ Inflammatory response; ↑ metabolic demand; free radical production
HypotensionReduces cerebral perfusion; expands penumbra
HypoxiaDirectly extends ischemic injury
HypoglycemiaStarves neurons; worsens ischemic injury
HyperglycemiaAssociated with worse outcomes; mechanisms include ↑ lactic acidosis

Factors Worsening sICH Risk After tPA

Risk FactorEvidence Level
Older ageStrong
Higher NIHSS (severe stroke)Strong
HypertensionStrong
HyperglycemiaModerate
Diabetes mellitusModerate
Atrial fibrillationModerate
Prior antiplatelet useModerate
Leukoaraiosis on imagingModerate
Cerebral microbleeds >10Strong (30-47% sICH risk)

ANTERIOR vs. POSTERIOR CIRCULATION: FINAL COMPARISON

FeatureAnterior CirculationPosterior Circulation
ConsciousnessUsually preservedCan be lost (reticular activating system)
Nausea/vomitingUncommonCommon (CTZ in brainstem)
Cranial nerve deficitsRare (CN VII central)Very common (CN III-XII)
Deficit lateralitySame side of bodyCrossed (ipsilateral CN + contralateral body)
Visual symptomsMonocular loss (ophthalmic a.)Bilateral field defects; diplopia; nystagmus
ProgressionUp to 24 hoursUp to 3 days
NIHSS detectionWell detectedUnder-detected
CT reliabilityHigh sensitivityUp to 25% false-negative (posterior fossa)

Sources: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th Ed., Chapter 167 (Steven Go, pp. 1159-1178). Rosen's Emergency Medicine: Concepts and Clinical Practice, 10th Ed., Chapter 87 (Linda Papa & William J. Meurer, pp. 1424-1443).
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