Lacunar stroke syndromes: pure motor, pure sensory and more
A small deep infarct can cause a dense deficit with no cortical signs. Learn the five classic lacunar stroke syndromes and match each one to its small vessel and site.
Chapters (9)
Recognise the classic lacunar syndromes (pure motor, pure sensory, sensorimotor, dysarthria–clumsy hand, ataxic hemiparesis) and relate each to its small-vessel location (internal capsule, thalamus, pons).
The short version
- A lacune is a small, deep infarct, roughly 1–15 mm across, from blockage of one small penetrating artery, classically in chronic hypertension.
- The clue is what is missing: no aphasia, no neglect, no visual field loss, so no cortical signs.
- Pure motor means posterior limb of the internal capsule (or basis pontis); pure sensory means lateral thalamus.
- Dysarthria–clumsy hand is usually pontine; sensorimotor is thalamus plus the adjacent capsule; ataxic hemiparesis is capsule or pons.
- Place the lesion on the side opposite the deficit; for weakness, this is because motor fibres cross at the pyramids.
The puzzle: a tiny infarct with a dense deficit
A 64-year-old man wakes with his right face, arm and leg all weak. He speaks normally, understands everything, sees normally and feels a pinprick everywhere. His scan shows one infarct, 9 mm across.
A tiny lesion, a dense deficit and no cortical signs. How? The answer is the lacunar stroke syndromes, and the key is to know where the small vessels sit.
Why small deep arteries cause lacunes
The deep structures, the internal capsule, the thalamus and the pons, are fed by small penetrating arteries that dive straight in from the big vessels.[1]
Each is nearly an end artery with very little collateral flow, so one blocked vessel infarcts its whole small territory.[1]
That infarct is a lacune: a small, deep infarct, roughly 1–15 mm across.[1]
The cause of a lacune and the clue: no cortical signs
The classic cause is chronic hypertension, often with diabetes. It thickens the artery wall with fibrous, fatty material called lipohyalinosis and narrows the lumen. Plaque at the mouth of the artery can block it too.[1][6]
The clue is what is missing. There is no aphasia, no neglect and no visual field loss: no cortical signs.[2]
The five classic lacunar syndromes and their sites
Five lacunar syndromes are classic.[2][3]
| Syndrome | What the patient has | Usual site |
|---|---|---|
| Pure motor | Weakness of face, arm and leg on one side, no sensory loss | Posterior limb of the internal capsule; basis of the pons is another |
| Pure sensory | Numbness of face, arm and leg on one side, no weakness | Lateral thalamus, ventral posterior nucleus (lateral part for the body, medial part for the face) |
| Sensorimotor | Weakness and numbness together | Thalamus and the capsule beside it |
| Dysarthria–clumsy hand | Slurred speech and a clumsy hand, often noticed when writing | Usually the pons |
| Ataxic hemiparesis | Weakness and ataxia together on one side, opposite the lesion, leg more than arm | Posterior limb of the capsule or the pons |
The pure sensory pattern comes from the lateral thalamus, the ventral posterior nucleus: the lateral part serves the body and the medial part serves the face.[3][4] The pure motor pattern is the capsule or the pons.[3][6]
The method: place the lesion in three steps
- Look for no cortical signsNo aphasia, neglect or visual field loss fits a lacunar syndrome.
- Ask which pathway is missingMotor, sensory or both.
- Place the lesionMotor: capsule or pons. Sensory: thalamus. Both: thalamus and the capsule beside it. Clumsy hand: pons.
Worked localisation: back to our man
- Face, arm and leg weak together on the right
- Sensation, language and vision are normal, so no sensory loss and no cortical signs
- That is pure motor
- Motor fibres cross lower down, at the pyramids, so right-sided weakness means a left-sided lesion
- Where the fibres run tightly together, in the left posterior limb of the internal capsule, one small infarct takes out face, arm and leg at once
Pure motor, then, means the capsule or the pons, and here the side of the weakness tells you the lesion is in the opposite posterior limb.[3][5][6]
Practice question
Original · USMLE styleA 54-year-old woman with hypertension and type 2 diabetes mellitus wakes with numbness of her left face, arm and leg. Strength, speech, language comprehension, vision and attention are normal. Blood pressure is 152/94 mmHg. Diffusion-weighted MRI shows a 7-mm acute infarct.
Common questions
What is a lacunar stroke?
A lacunar stroke is a small, deep infarct, roughly 1–15 mm across, caused by blockage of a single small penetrating artery. The classic cause is chronic hypertension, often with diabetes.
What are the five lacunar stroke syndromes?
Pure motor, pure sensory, sensorimotor, dysarthria–clumsy hand and ataxic hemiparesis.
Why are there no cortical signs in a lacunar stroke?
The infarct sits in deep structures such as the internal capsule, thalamus or pons, so there is no aphasia, neglect or visual field loss.
Where is the lesion in pure motor stroke?
The usual site is the posterior limb of the internal capsule. The basis of the pons is another. Motor fibres cross at the pyramids, so the weakness is on the side opposite the lesion.
Transcript
Read the full narration, by chapter630 words
0:00The puzzle: a tiny infarct, a dense deficit
A 64-year-old man wakes with his right face, arm and leg all weak. He speaks normally, understands everything, sees normally, and feels a pinprick everywhere. His scan shows one infarct, nine millimetres across. A tiny lesion, a dense deficit, and no cortical signs. How? Today: recognise the classic lacunar syndromes, and match each one to where the small vessel sits.
0:28Deep structures and their small end arteries
Deep structures, the internal capsule, the thalamus and the pons, are fed by small penetrating arteries that dive straight in from the big vessels. Each is nearly an end artery, with very little collateral flow, so one blocked vessel infarcts its whole small territory. That infarct is a lacune: a small, deep infarct, roughly one to 15 millimetres across.
0:54The cause and the clue: lipohyalinosis, plaque, no cortical signs
The classic cause is chronic hypertension, often with diabetes, which thickens the artery wall with fibrous, fatty material called lipohyalinosis and narrows the lumen. Plaque at the mouth of the artery can block it too. The clue is what is missing. No aphasia, no neglect, no visual field loss: no cortical signs.
1:18The five classic lacunar syndromes
Five syndromes are classic. Pure motor: weakness of the face, arm and leg on one side, with no sensory loss. The usual site is the posterior limb of the internal capsule; the basis of the pons is another. Pure sensory: numbness on the opposite side of the body, from the lateral thalamus, the ventral posterior nucleus: the lateral part for the body, the medial part for the face. Sensorimotor: weakness and numbness together, from the thalamus and the capsule beside it. Dysarthria and clumsy hand: slurred speech and a clumsy hand, often noticed when writing, usually from the pons. Ataxic hemiparesis: weakness and ataxia together on one side of the body, opposite the lesion, the leg more than the arm, from the posterior limb of the capsule or the pons.
2:13The method: place the lesion
The method: look for no cortical signs, ask which pathway is missing, motor, sensory or both, then place the lesion.
2:23Back to our man: pure motor
Back to our man. Weak face, arm and leg together, normal sensation, normal language and vision. That is pure motor. Motor fibres cross lower down, at the pyramids, so right-sided weakness means a lesion in the left posterior limb of the internal capsule, where the fibres run tightly together, so one small infarct takes out face, arm and leg at once. Your turn.
2:52Practice question
A 54-year-old woman with hypertension and type two diabetes wakes with numbness of her left face, arm and leg. Her strength, speech, language, vision and attention are normal. Blood pressure is 152 over 94 millimetres of mercury. Diffusion MRI shows a seven-millimetre infarct. Which of the following is the most likely site of the lesion? A, right basis pontis. B, right posterior limb of the internal capsule. C, right ventral posterior nucleus of the thalamus. D, left ventral posterior nucleus of the thalamus. E, right postcentral gyrus. Pause here and decide.
3:41The answer, option by option
A is out: pontine lacunes usually cause weakness, a clumsy hand or ataxia, and only rarely isolated numbness. B is out: the posterior limb mainly carries motor fibres, so a lesion there usually causes weakness, and she is not weak. D is out: wrong side. Her numbness is on the left, so the lesion lies in the right thalamus. E is out: a cortical infarct would bring cortical signs such as neglect, aphasia or a field defect, and she has none. So the answer is C. Isolated numbness without cortical signs is a pure sensory lacunar syndrome, from the ventral posterior nucleus of the thalamus on the opposite side.
4:28Recap and next lesson
Three things to keep. One: a lacune is a small deep infarct of a penetrating artery, usually from hypertension. Two: no cortical signs. Three: pure motor means capsule or pons, pure sensory means thalamus, clumsy hand means pons. Next, the visual pathway and its field defects.
Sources
Numbers in the text, e.g. [1], point here- Caplan LR. Lacunar infarction and small vessel disease: pathology and pathophysiology. J Stroke 2015. europepmc.org/article/PMC/PMC4325635
- European Stroke Organisation guideline on cerebral small vessel disease, part 2. Eur Stroke J 2024. europepmc.org/article/PMC/PMC10916806
- Stroke: causes and clinical features. europepmc.org/article/PMC/PMC7409792
- Lacunar infarct in the paramedian pons presenting as contralateral hemisensory loss. europepmc.org/article/PMC/PMC12798871
- Corticospinal vs Rubrospinal Revisited. Front Neurosci 2021. europepmc.org/article/PMC/PMC8226017
- Lacunar stroke. Wikipedia (secondary). en.wikipedia.org/wiki/Lacunar_stroke
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Image credits. Coronal brain section (Gray717) and corticospinal tract (Gray764): Gray's Anatomy (1918), Henry Gray / H. V. Carter, public domain, via Wikimedia Commons, recoloured and outlined. Illustrations: Servier Medical Art (smart.servier.com), CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/), adapted (cropped, recoloured, outlined): "Arterial wall", "Eye view". All other diagrams (vessels, glows, icons, tables, the question card) are original and drawn in code; the vessels on the brain plate are schematic. No AI-generated images.
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-NEURO-012.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01Upper vs lower motor neuron lesions: signs and localisation5:08
- EP 02Dorsal column vs spinothalamic tract: where each pathway crosses5:01
- EP 03Spinal cord syndromes compared: rebuild each from three tracts5:06
- EP 04Cranial nerve nuclei: a brainstem map by level and position5:10
- EP 05Brainstem crossed findings: the localisation rule4:50
- EP 06Medial vs lateral medullary syndrome: artery, structures and signs5:30
- EP 07Facial nerve palsy: why the forehead tells you the lesion4:59
- EP 08Stroke syndromes by artery: ACA, MCA and PCA4:41
- EP 09Lacunar stroke syndromes: pure motor, pure sensory and more4:54
- EP 10Visual pathway lesions and field defects4:42
- EP 11Basal ganglia direct and indirect pathways: D1, D2 and movement5:19
- EP 12Cerebellar lesion localisation: vermis vs hemisphere4:42
- EP 13Brain herniation syndromes: what is squeezed, and where4:56
- EP 14CSF flow and hydrocephalus: where the flow fails5:12
- EP 15Corticospinal tract: from cortex to anterior horn4:59
- EP 16Hypothalamic nuclei and their functions5:24