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12 notes available
1 Last Minute Review 2 Cerebrovascular Anatomy 3 Stroke Syndromes 4 Acute Stroke Management 5 Stroke Workup 6 Secondary Prevention 7 Intracerebral Hemorrhage 8 SAH & Aneurysms 9 SDH & EDH 10 Venous Thrombosis 11 Vascular Malformations 12 Special Vascular Topics
Clinical › Vascular

Stroke Syndromes

Ischemic Stroke: Pathophysiology & Clinical Syndromes

What You'll Learn

  • Definitions of ischemic stroke, CNS infarction, and TIA (tissue-based vs. time-based)
  • Cerebral blood flow thresholds, ischemic penumbra, and the ischemic cascade
  • Modifiable and non-modifiable stroke risk factors
  • CHA2DS2-VASc scoring and anticoagulation indications
  • TOAST classification and ischemic stroke subtypes
  • Clinical stroke syndromes by vascular territory (ICA, MCA, ACA, PCA)
  • Aphasia types, localization, and distinguishing features
  • Classic lacunar syndromes and their anatomical correlates
  • Brainstem stroke syndromes (medullary, pontine, midbrain)
  • TIA risk stratification and the ABCD2 score
HighYield Pearls
  • Wallenberg (lateral medullary, PICA/vertebral): ipsilateral face pain/temp loss (CN V) + ipsilateral Horner + ipsilateral ataxia + ipsilateral palatal/pharyngeal weakness (CN IX/X — hoarse, dysphagia) + vertigo/nystagmus + CONTRALATERAL body pain/temp loss; NO motor weakness, NO tongue involvement (distinguishes from medial medullary)
  • Medial medullary / Dejerine (anterior spinal off vertebral): contralateral hemiparesis (pyramid) + contralateral lemniscal sensory loss + ipsilateral tongue weakness (CN XII — tongue deviates toward lesion)
  • Midbrain trio — all share ipsilateral CN III (down & out, dilated): Weber = + contralateral hemiparesis (cerebral peduncle); Claude = + contralateral ataxia/tremor (midbrain tegmentum, red nucleus / SCP); Benedikt = + contralateral involuntary movements / tremor / ataxia from red nucleus involvement (hemiparesis is less defining than in Weber)
  • Pontine eponyms — CN VI + CN VII LMN + contralateral hemiparesis: Millard-Gubler (ventrocaudal pons); Foville adds ipsilateral horizontal gaze palsy (PPRF); Locked-in (ventral pons / basilar) = quadriplegia + anarthria + horizontal gaze palsy with PRESERVED CONSCIOUSNESS and vertical eye/blink only — do NOT mistake for coma
  • Top-of-basilar syndrome: bilateral PCA + thalami + midbrain → cortical blindness, amnesia, agitated delirium, oculomotor abnormalities; rule out tip-of-basilar embolus — window for thrombectomy
  • MCA divisions: M1 = face/arm > leg hemiplegia + hemisensory loss + HH + cortical signs (aphasia if dominant, neglect if non-dominant) + eye deviation TOWARD lesion; Superior division = Broca + face/arm weakness, no field cut; Inferior division = Wernicke + contralateral superior quadrantanopia, minimal weakness
  • ACA vs PCA: ACA = contralateral leg > arm + abulia/akinetic mutism (bilateral) + transcortical motor aphasia + urinary incontinence + frontal release signs; PCA = contralateral HH (often macular sparing) + alexia without agraphia (dominant) + visual agnosia/prosopagnosia; thalamic PCA → Dejerine-Roussy (delayed contralateral burning pain)
  • AICA vs PICA (sort by hearing): AICA = lateral pontine — adds ipsilateral hearing loss + CN VII LMN; PICA = Wallenberg + cerebellar dysmetria; SCA = ipsilateral cerebellar ataxia + ipsilateral Horner ± contralateral pain/temp
  • Lacunar syndromes (NO cortical signs): Pure motor (PLIC/basis pontis), Pure sensory (VPL thalamus), Sensorimotor (thalamocapsular), Ataxic hemiparesis (PLIC or upper pons), Dysarthria-clumsy hand (genu of IC or pons); capsular warning syndrome (stuttering hemiparesis) = impending PLIC infarct
  • Watershed / border-zone strokes — mechanism can be hemodynamic, embolic, or mixed: ACA-MCA (parasagittal “man-in-a-barrel,” proximal arm sparing face/legs) and MCA-PCA (parieto-occipital → Balint); the internal MCA-LSA border-zone “rosary bead” pattern in the corona radiata is strongly associated with hemodynamic compromise / critical carotid stenosis and carries the worst recurrence.
  • Stroke chameleons: in young/pediatric stroke pursue CADASIL, MELAS, dissection, MoyaMoya, hypercoagulable workup; secondary prevention must be etiology-driven
🔍 Quick ReferenceBrainstem / cerebellar · Hemispheric / cortical · Lacunar / small-vessel
Brainstem / cerebellar syndromes
  • Wallenberg → lateral medullary (PICA/vertebral) — ipsilateral V + Horner + ataxia + hoarseness, contralateral body pain/temp
  • Dejerine → medial medullary (anterior spinal/vertebral) — contralateral hemiparesis + ipsilateral tongue (CN XII)
  • Weber → medial midbrain (cerebral peduncle) — ipsilateral CN III + contralateral hemiparesis
  • Claude → dorsomedial midbrain tegmentum — ipsilateral CN III + contralateral ataxia (red nucleus)
  • Benedikt → midbrain tegmentum (red nucleus) — ipsilateral CN III + contralateral involuntary movements / tremor / ataxia (hemiparesis less defining than in Weber)
  • Millard-Gubler → ventrocaudal pons — ipsilateral CN VI + CN VII LMN + contralateral hemiparesis
  • Foville → caudal pons — CN VI + CN VII + ipsilateral horizontal gaze palsy (PPRF) + contralateral hemiparesis
  • Locked-in → ventral pons (basilar) — quadriplegia + preserved consciousness + vertical gaze/blink only
  • AICA → lateral pontine — ipsilateral hearing loss + CN VII LMN + Horner + ataxia + contralateral pain/temp
  • PICA → Wallenberg + inferior cerebellum (dysmetria)
  • SCA → superior cerebellum — ipsilateral ataxia + Horner ± contralateral pain/temp
  • Top-of-basilar → bilateral PCA + thalami + midbrain — cortical blindness, amnesia, agitated delirium
Hemispheric / cortical signs
  • Eye deviation TOWARD lesion → cortical (MCA) — vs AWAY in pontine destructive
  • Face/arm > leg + aphasia/neglect → MCA territory
  • Leg > arm + abulia + urinary incontinence → ACA territory
  • Cortical blindness + macula-spared HH + alexia without agraphia → PCA territory (dominant + splenium)
  • Gerstmann (finger agnosia + acalculia + agraphia + L/R confusion) → dominant angular gyrus (MCA inferior division)
  • Anton syndrome (cortical blindness with denial) → bilateral occipital (PCA)
  • Balint (simultanagnosia + optic ataxia + ocular apraxia) → bilateral parieto-occipital MCA-PCA watershed
  • “Man in a barrel” (proximal arm > distal, face/legs spared) → parasagittal ACA-MCA watershed (post-arrest, hypotension)
  • Pure dysarthria + emotional incontinence (pseudobulbar) → bilateral corticobulbar tracts
  • Ipsilateral monocular vision loss + contralateral hemiparesis → ICA territory
Lacunar / small-vessel signs
  • Pure motor hemiparesis → posterior limb internal capsule (PLIC) or basis pontis
  • Pure sensory stroke → VPL thalamus (thalamoperforators)
  • Sensorimotor stroke → thalamocapsular junction
  • Ataxic hemiparesis → PLIC or upper pons basis
  • Dysarthria-clumsy hand → genu of internal capsule or pons
  • Dejerine-Roussy (delayed contralateral burning pain) → thalamic perforators (VPL)
  • Striatocapsular infarct → deep MCA lenticulostriate (LSA) territory
  • Capsular warning syndrome (stuttering hemiparesis) → impending PLIC lacunar infarct
Definitions
  • Ischemic stroke: Episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction
  • CNS infarction: Cell death attributable to ischemia, based on pathological/imaging evidence of focal ischemic injury in a defined vascular distribution, OR clinical evidence persisting ≥24 hours
  • TIA: Transient neurological dysfunction from focal ischemia without acute infarction on imaging
💎 Board Pearl

Up to 1/3 of patients with symptoms <24 hours have infarction on imaging. Modern TIA definition is tissue-based (no infarction), NOT time-based. DWI-positive = stroke, even if symptoms resolved.

Epidemiology
  • ~795,000 new or recurrent strokes per year in the US
  • 5th leading cause of death and leading cause of long-term disability
  • 87% ischemic, 13% hemorrhagic (10% ICH, 3% SAH)

Ischemic Stroke Subtypes by Frequency

  • Cardioembolism: 30% (most common ischemic subtype)
  • Large-vessel atherosclerosis: 20%
  • Small-vessel disease (lacunar): 20%
  • Cryptogenic: ~27%
  • Other determined: 3%
Pathophysiology of Ischemic Stroke

Cerebral Blood Flow Thresholds

  • Normal CBF: 50 cc/100g/min
  • ~20 cc/100g/min: EEG changes; neurons still viable
  • <10 cc/100g/min: Irreversible neuronal death

The Ischemic Penumbra

  • Core (CBF <10): Irreversible infarction within minutes
  • Penumbra (CBF 10–20): Electrically silent but structurally intact — SALVAGEABLE tissue — target of reperfusion therapy
  • Without reperfusion, penumbra progressively converts to core over hours

Ischemic Cascade

  • 30 seconds: Metabolism altered → 1 minute: Neuronal function ceases → 5 minutes: Chain of events leading to infarction
  • Energy failure → loss of ion homeostasis → glutamate excitotoxicity (NMDA/AMPA) → Ca2+ overload → free radicals → apoptosis/necrosis

Pathological Evolution of Infarction

  • 6–24 hours: Coagulation necrosis — “red neurons” (eosinophilic neuronal shrinkage), polymorphonucleocytes around vessels
  • 3–4 days: Edematous swelling, red cell extravasation
  • 72–96 hours: Liquefaction — macrophage invasion; “glitter cells” (lipid-laden macrophages)
  • Weeks–months: Astrocyte hypertrophy then hyperplasia; macrophages clear debris at ~1 cc/month
💎 Board Pearl

Penumbra (CBF 10–20) = target of reperfusion. “Time is brain” — ~1.9 million neurons die per minute during LVO. “Red neurons” = hallmark of acute ischemic injury on pathology.

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