Lenticulostriate Strokes

Small vessel. Massive deficits. Zero cortical signs. Know the 5 syndromes cold.

Big-vessel stroke syndromes · Aphasia map

Clinical Vignette · clinical medicine Opener

A 62-year-old man with 20 years of untreated hypertension wakes up unable to move his right arm or leg. Face is equally weak. No aphasia. No confusion. No visual changes. Head CT is negative.

Pure motor hemiparesis is the classic lacunar syndrome. The giveaway is what is absent: no aphasia, no neglect, no hemianopia. That rules out MCA cortex. The posterior limb of the internal capsule (PLIC) carries all corticospinal fibers for face, arm, and leg through one tight bundle. One lenticulostriate artery blocked by HTN lipohyalinosis, and everything drops at once.

Interactive Anatomy

Where These Strokes Hit

Click any zone on the left hemisphere to see what goes wrong.

PLIC

VPL Thalamus

Putamen / BG

Pons

← Click a region to see which syndrome it produces

Traced Anatomy

Lacunar Syndrome Map

Tap any structure. Each one, when hit by a lacune, has a signature syndrome. 🔑Striatum = caudate + putamen (gets the inputs). Lentiform = putamen + globus pallidus (the visible lens shape). Putamen is in both umbrellas, that is why it is the most commonly hurt structure in HTN.

Striatum · Caudate + Putamen Lentiform · Putamen + Globus Pallidus

Coronal · Front View

Axial · Top Down

Tap a structure on either view, or pick a chip below. Each one has a signature lacunar syndrome.

Caudate Putamen GPe GPi Thalamus IC posterior limb Subthalamic Substantia nigra

Visual Library

Imaging & Anatomy

Tap any image to expand. Real radiology, real anatomy.

MRI · lacunar infarct

Progressive Reveal

What Are Lenticulostriate Arteries?

One concept per screen. Tap when ready.

Step-Through

How HTN Causes Lacunar Infarcts

The domino chain, one step at a time.

Full Pathway

Two Outcomes, One Vessel

Charcot-Bouchard + Lacunar Mechanism

Same penetrating artery. Same HTN. Two completely different catastrophes. 🔑The lipohyalinotic vessel can clog (lacunar infarct) OR balloon then burst (Charcot-Bouchard microaneurysm rupture). clinical medicine loves the second pathway in putaminal hemorrhage.

Causes · HTN (most common) + Diabetes

The setup: Years of pounding pressure infiltrate the wall of a deep penetrating artery with fat and hyaline (lipohyalinosis) and patchy small plaques (microatheromas). The wall becomes brittle, narrow, and prone to two opposite failures.

Path 1 · Occlusion

Lumen clogs shut

The narrowed lumen finally thromboses. No collaterals rescue the territory. The tissue dies and is reabsorbed over weeks, leaving a fluid-filled liquefactive necrosis cavity (a lacune). → lacunar infarct.

Path 2 · Aneurysm + Rupture

Wall balloons, then bursts

The weakened wall pouches outward into a tiny Charcot-Bouchard microaneurysm (<300µm). Under chronic HTN it eventually ruptures. → intracerebral hemorrhage.

Where they hide: Charcot-Bouchard microaneurysms cluster on penetrating arteries (lenticulostriates, thalamoperforators, basilar perforators). Same address as lacunes; same vessel, different verdict.

clinical medicine trap: Hypertensive intracerebral hemorrhage in a 60+ year-old with chronic HTN, classically in the basal ganglia / putamen (most common location, around 35 to 50 percent of cases), then thalamus, cerebellum, pons, lobar. The mechanism asked in clinical practice is rupture of a Charcot-Bouchard microaneurysm: not amyloid angiopathy, not AVM, not aneurysm of the Circle of Willis. Lipohyalinosis is the unifier of lacune AND hemorrhage in the same patient.

Syndrome Navigator

The 5 Classic Lacunar Syndromes

clinical medicine loves all 5. Use the arrows to cycle through. 🔑The 5 classic lacunar syndromes: pure motor · pure sensory · sensorimotor · ataxic hemiparesis · dysarthria-clumsy hand. Memorize the list cold. Every lacunar question in clinical practice is one of these five.

1 / 5

Battle Tabs

Pure Motor vs Pure Sensory

Two lacunes, two locations, zero overlap. Tap to switch.

Pure Motor Hemiparesis

Posterior Limb of Internal Capsule (PLIC)

Deficit Pattern

Face + arm + leg weakness, all equally severe on one side. Dense, complete hemiplegia.

What is Absent

No sensory loss. No aphasia. No visual field cut. No neglect. Cortex is intact.

Why PLIC

All corticospinal fibers for face + arm + leg pass through one narrow band the size of a thumbnail. One lenticulostriate occlusion drops every motor channel at once.

clinical medicine Move

Equal weakness across face, arm, AND leg points subcortical. MCA cortical strokes give arm > leg (homunculus spacing). Equal = PLIC lacune until proven otherwise.

Pure Sensory Stroke

VPL Nucleus of Thalamus

Deficit Pattern

Hemisensory loss across face, arm, and leg in ALL modalities (light touch, pinprick, vibration, proprioception). May present with burning dysesthesia (Dejerine-Roussy).

What is Absent

No motor weakness. No aphasia. No cortical signs. Strength is preserved on every channel.

Why VPL Thalamus

VPL is the panmodal sensory relay for the entire contralateral body. One thalamogeniculate branch occlusion blacks out the whole switchboard at once.

clinical medicine Move

Numbness across the whole side with normal strength is thalamic until proven otherwise. Cortical sensory loss is graphesthesia or stereognosis loss, not raw panmodal numbness.

Decision Tree

Stroke Localization in 3 Questions

Walk a stroke patient through the tree. Tap the right answer at each step.

Q1Are cortical signs present? (aphasia, neglect, hemianopia)

Q2No cortical signs. What is the dominant deficit pattern?

Localization

The One Rule

NO Cortical Signs

This is the only rule that matters for differentiating lacunar from cortical stroke.

clinical medicine Trap · Always Tested

Lacunar infarcts NEVER produce cortical signs

No aphasia · No neglect · No hemianopia · No cortical sensory loss · No seizures

The Trap: Dense hemiplegia with NO aphasia, neglect, or visual field cut = subcortical (PLIC lacunar). The same dense hemiplegia WITH aphasia or neglect = cortical (MCA). The absence of cortical signs IS the clue.

📈

Vessel Type

Small penetrating arteries (lenticulostriate, basilar perforators) vs. large named vessels (MCA, ACA, PCA)

🌍

Territory

Subcortical structures: basal ganglia, internal capsule, thalamus, brainstem vs. cortex + adjacent white matter

⛔

The Key Difference

Lacunar: no cortical signs. Cortical: cortical signs present (aphasia, neglect, hemianopia)

❌

Aphasia

Never. Language cortex is not in the lenticulostriate territory.

❌

Hemianopia

Never. Visual cortex (occipital lobe) is not involved.

❌

Neglect / Anosognosia

Never. Right parietal cortex is not hit by these vessels.

✔

Motor / Sensory

Yes, often pure. All fibers converge in the PLIC. One tiny infarct = total loss of face + arm + leg equally.

🗣

Aphasia

Yes, if dominant hemisphere MCA territory (Broca's or Wernicke's area)

👁

Hemianopia

Yes, if optic radiations or occipital cortex involved

🧠

Neglect

Yes, if right parietal lobe involved (non-dominant hemisphere)

📊

Motor Pattern

Often unequal: arm > leg in MCA territory; leg > arm in ACA territory. The cortical homunculus spreads these apart.