STEPTRACKERNERVOUS SYSTEM | PATHOLOGY + ANATOMY + PHARMACOLOGY | HIGH-YIELD REVIEW

Stroke

Ischemic stroke by mechanism and by territory, the tissue changes over time, transient attacks, and treatment within the window.

FOCUS ON
Ischemic stroke (~85%): thrombotic (atherosclerosis), embolic (AF, carotid), lacunar (hypertensive lipohyalinosis), watershed (hypotension). Territory: MCA = face/arm + aphasia or neglect; ACA = leg; PCA = vision. Brain infarct → liquefactive necrosis: red neurons at 12–24 h → neutrophils → macrophages → gliosis → cyst. Noncontrast CT first, then tPA within 4.5 h.
TYPE · TERRITORY
MECHANISM · CAUSE
DEFICITS · FEATURES
CLUE
Thrombotic stroke
Atherosclerotic plaque rupture + thrombus at bifurcations (carotid, MCA, basilar)
Stepwise or stuttering onset, often during sleep; prior TIAs
Pale (anemic) infarct
Embolic stroke
Atrial fibrillation, mural thrombus after MI, endocarditis, carotid plaque, paradoxical (PFO)
Sudden maximal deficit; often MCA; multiple territories
Hemorrhagic transformation after reperfusion
Lacunar infarct
Hypertensive lipohyalinosis / hyaline arteriolosclerosis of small penetrating arteries (lenticulostriate)
Pure motor (internal capsule), pure sensory (thalamus), ataxic hemiparesis, dysarthria-clumsy hand; no cortical signs
Hypertension, diabetes
Watershed infarct
Global hypoperfusion (cardiac arrest, shock) → border zones (ACA-MCA, MCA-PCA)
Bilateral proximal arm and thigh weakness ("man in a barrel"), cortical vision loss
Also hippocampus (CA1), Purkinje cells
MCA territory
Lateral cortex: motor/sensory face and arm, language, parietal
Contralateral face and arm > leg weakness and sensory loss; aphasia (dominant) or neglect (nondominant); gaze toward lesion; hemianopia
Most common territory
ACA territory
Medial frontal and parietal cortex
Contralateral leg > arm weakness and sensory loss; urinary incontinence; abulia
Leg cortex is medial
PCA territory
Occipital cortex, thalamus, medial temporal lobe
Contralateral homonymous hemianopia with macular sparing; alexia without agraphia (dominant); thalamic pain
Vision without weakness
Transient ischemic attack
Brief ischemia without infarction
Focal deficit resolving within 24 h (usually < 1 h); amaurosis fugax (retinal emboli from carotid); normal DWI MRI
High short-term stroke risk
Imaging & acute treatment
Exclude hemorrhage, restore flow
Noncontrast CT (normal early in ischemia); MRI DWI positive in minutes; alteplase ≤ 4.5 h; thrombectomy for large-vessel occlusion
Aspirin after hemorrhage excluded
Secondary prevention
Lower recurrence
Antiplatelet, statin, BP control; anticoagulate AF (DOAC/warfarin); carotid endarterectomy for symptomatic stenosis ≥ 70%
PFO closure in selected young patients
Stroke in the young
Non-atherosclerotic causes
Arterial dissection (neck pain + Horner), PFO, antiphospholipid syndrome, cocaine, vasculitis, sickle cell, moyamoya, CADASIL (NOTCH3)
Neck manipulation → vertebral dissection

Mechanism — the ischemic cascade

↓ Blood flow
→
↓ ATPNa⁺/K⁺ pump fails
→
DepolarizationGlutamate release
→
NMDA → Ca²⁺ influxExcitotoxicity
→
Liquefactive necrosis

The core dies within minutes; the surrounding penumbra is salvageable — the reason for time-limited reperfusion. Most sensitive neurons: hippocampal CA1, Purkinje cells, neocortex (layers 3, 5, 6).

Infarct timeline

TIME
HISTOLOGY
12–24 h
Red neurons: eosinophilic cytoplasm, pyknotic nuclei
24–72 h
Neutrophils infiltrate
3–5 days
Microglia/macrophages engulf lipid (gitter cells)
1–2 weeks
Reactive gliosis + vascular proliferation around necrosis
> 2 weeks
Glial scar; cystic cavity surrounded by astrocytes

How it's tested

COMMON CONFUSIONMCA strokes weaken face and arm more than leg; ACA strokes weaken leg more than arm. Homunculus: leg is medial, face and hand lateral.
THE TRAPA normal noncontrast CT in the first hours does not rule out ischemic stroke — it rules out hemorrhage so thrombolysis can start.
YOUR APPROACHOnset (sudden vs stepwise) + deficit pattern → territory → mechanism (AF, carotid, HTN, hypotension) → time window → acute and preventive treatment.

If you see… think…

AF patient with sudden right face/arm weakness and aphasia → left MCA embolic stroke
Right leg weakness and urinary incontinence → left ACA stroke
Left homonymous hemianopia with macular sparing → right PCA stroke
Hypertensive with pure motor hemiparesis, no cortical signs → lacunar infarct (internal capsule)
Bilateral shoulder and hip weakness after cardiac arrest → watershed infarcts
Transient monocular "curtain" vision loss → amaurosis fugax (carotid emboli)
Eosinophilic shrunken neurons a day after stroke → red neurons (irreversible injury)
Old infarct seen as a fluid-filled cavity → liquefactive necrosis
Young man with neck pain, Horner, then stroke → carotid dissection
Migraines, subcortical infarcts, early dementia, NOTCH3 → CADASIL