Lacunar infarcts are the “small strokes with big test-day impact”—they show up in vignettes as pure motor/pure sensory deficits with no cortical signs, and the question is usually asking you to recognize deep perforator vessel disease from chronic hypertension/diabetes.
The 10-second one-liner
Lacunar infarcts = small, deep ischemic strokes from lipohyalinosis (HTN/DM) of penetrating arteries → pure motor or pure sensory deficits without cortical findings (e.g., aphasia, neglect, visual field cuts).
Visual mnemonic: “LACUNAR = LACk of CoRtical signs”
If you see:
- Weakness and/or numbness
- But NO aphasia, neglect, gaze deviation, homonymous hemianopia, cortical sensory loss
→ think lacunar (subcortical/internal capsule/thalamus/pons).
Memory hook: “LACk of CoRtical signs” → LACUNAR
Step-by-step flowchart (how to answer USMLE-style)
Step 1: Is it ischemic stroke symptoms?
- Sudden focal neuro deficit (minutes to hours), vascular pattern
- Often in a patient with HTN, diabetes, smoking, hyperlipidemia
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Step 2: Are there cortical signs?
Cortical signs = big artery territory clues
- Aphasia (dominant hemisphere)
- Neglect (nondominant parietal)
- Homonymous hemianopia
- Gaze preference/deviation
- Cortical sensory loss
- Seizure at onset (often cortical irritation)
If YES → think large vessel (MCA/ACA/PCA) or embolic stroke (not lacunar).
If NO → go to Step 3.
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Step 3: Is the deficit “pure” and stereotyped?
Common lacunar syndromes (classic Step patterns):
- Pure motor hemiparesis (face/arm/leg)
- Pure sensory stroke
- Sensorimotor stroke
- Ataxic hemiparesis
- Dysarthria–clumsy hand syndrome
If it fits → go to Step 4.
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Step 4: Localize to deep structures (penetrating arteries)
High-yield locations and what they do:
- Internal capsule → pure motor
- Thalamus (VPL/VPM region) → pure sensory
- Pons (basis pontis) → motor/ataxia/dysarthria
- Basal ganglia (putamen/caudate) → variable motor findings
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Step 5: Name the pathology + vessel type
Most classic mechanism:
- Lipohyalinosis (chronic HTN/DM) of small penetrating arteries
Also: - Microatheroma of perforators
Result: small cavitary infarcts (“lacunes”), typically < 15–20 mm.
High-yield “don’t-miss” fact: Charcot-Bouchard vs lacunar infarct
These get paired in questions because both are HTN-related small-vessel diseases, but the outcomes differ.
| Entity | Vessel problem | Typical outcome | Classic location clues |
|---|---|---|---|
| Lacunar infarct | Lipohyalinosis / microatheroma of penetrating arteries | Small deep ischemic infarct → pure motor/sensory syndromes | Internal capsule, thalamus, pons, basal ganglia |
| Charcot-Bouchard microaneurysm | HTN-induced microaneurysms of small arteries | Intraparenchymal hemorrhage | Basal ganglia (putamen), thalamus, pons, cerebellum |
Rule of thumb:
- HTN + pure motor/sensory + no cortical signs → lacunar ischemic stroke
- HTN + sudden severe headache/LOC + bleed on CT → hypertensive hemorrhage (Charcot-Bouchard)
The “lacunar syndromes” cheat sheet
1) Pure motor hemiparesis
- Contralateral face/arm/leg weakness
- No sensory loss, no cortical deficits
- Lesion: posterior limb internal capsule (± basis pontis)
- Vessel: lenticulostriate arteries (MCA perforators) are common offenders
2) Pure sensory stroke
- Contralateral numbness/tingling of face/arm/leg
- Lesion: thalamus (VPL/VPM area)
- Vessel: thalamoperforators (often from PCA)
3) Sensorimotor stroke
- Weakness + sensory loss (still no cortical signs)
- Lesion: thalamocapsular region
4) Ataxic hemiparesis
- Ipsilateral ataxia + contralateral weakness pattern (subcortical coordination disruption)
- Lesion: pons or internal capsule
5) Dysarthria–clumsy hand syndrome
- Slurred speech + clumsy hand (fine motor trouble)
- Lesion: pons or internal capsule
Imaging + exam traps (what NBME likes)
- Noncontrast CT early may be normal in small ischemic strokes → don’t be fooled.
- MRI DWI is more sensitive early for small deep infarcts.
- Lacunar infarcts don’t produce cortical signs because cortex is spared.
- A patient with “stroke symptoms” plus aphasia or neglect is not a lacunar syndrome.
Why it happens: the path buzzwords
Risk factors (high yield)
- Chronic hypertension (most classic)
- Diabetes
- Smoking, dyslipidemia, age
Pathology terms to recognize
- Lipohyalinosis: hyaline thickening + narrowing of small penetrating arterioles (HTN/DM)
- Fibrinoid necrosis can be seen in severe HTN small-vessel injury (more bleed-prone contexts)
Rapid-fire vignette translator (practice)
- “Longstanding HTN, sudden contralateral arm/leg weakness, intact language/vision” → pure motor lacunar (internal capsule)
- “Sudden contralateral numbness, no weakness, no aphasia” → thalamic lacunar
- “Slurred speech + clumsy hand, no cortical deficits” → pontine/internal capsule lacunar
- “Stroke + aphasia + gaze deviation” → cortical MCA stroke, not lacunar
Bottom line (shareable takeaway)
Lacunar infarct = deep perforator ischemic stroke from HTN/DM small-vessel disease → pure motor/pure sensory syndromes with no cortical signs.