# Lacunar Strokes and Small Vessel Disease

> Lacunar strokes and small vessel disease for NEET-PG Medicine cover pure motor, pure sensory, ataxic hemiparesis and dysarthria-clumsy hand syndromes.

- Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/lacunar-strokes-and-small-vessel-disease
- Exam / course: NEET-PG · Subject: Medicine
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-15
- Last updated: 2026-10-15
- Reference basis: Adams and Victor's Principles of Neurology; Harrison's Principles of Internal Medicine
- How to cite: "Lacunar Strokes and Small Vessel Disease", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/lacunar-strokes-and-small-vessel-disease

## Direct answer

Lacunar strokes are small subcortical infarcts, usually under 15 mm, caused by occlusion of penetrating arterioles and most often seen in hypertensive patients. They produce pure motor, pure sensory, ataxic hemiparesis or dysarthria-clumsy hand syndromes without cortical signs. Management centres on blood pressure control, antiplatelet therapy and statins rather than on large-artery procedures.

## What you must remember

- **Lacune size:** a small deep infarct, typically 3 to 15 mm, in a penetrating branch such as the lenticulostriate, thalamoperforating or pontine perforating artery.
- **Mechanism:** lipohyalinosis of small penetrating arteries, linked to chronic hypertension and diabetes, rather than large-artery atherosclerosis or cardiac embolism.
- **No cortical signs:** aphasia, neglect, hemianopia and apraxia are absent, and their presence argues against a lacune.
- **Pure motor hemiparesis:** the commonest lacunar syndrome, with equal weakness of face, arm and leg from the posterior limb of the internal capsule or pons.
- **Pure sensory stroke:** numbness of one half of the body without weakness, typically from a thalamic lesion.
- **Ataxic hemiparesis:** weakness with ipsilateral limb ataxia, from a pontine or internal capsule lesion.
- **Dysarthria-clumsy hand:** dysarthria with a clumsy hand, from a lesion in the base of the pons.
- **Secondary prevention:** antiplatelet therapy, a statin and blood pressure control, with long-term dual antiplatelet therapy not routine because bleeding risk rises.

## A syndrome-to-site map

A 60-year-old hypertensive man has sudden weakness of the left face, arm and leg, with no speech problem, neglect or visual field loss. The absence of cortical signs points towards a small deep infarct rather than a cortical lesion.

| Syndrome | Typical site | Key features | Exam clue |
|---|---|---|---|
| Pure motor hemiparesis | Internal capsule or pons | Equal face, arm and leg weakness | No sensory loss |
| Pure sensory stroke | Thalamus | Hemisensory loss without weakness | Numbness only |
| Ataxic hemiparesis | Pons or internal capsule | Weakness with ipsilateral ataxia | Limb incoordination |
| Dysarthria-clumsy hand | Base of pons | Dysarthria with clumsy hand | Speech and hand together |

Each lacunar syndrome is recognised by its combination of motor, sensory and speech features, not by any single sign. Lacunar syndromes are the diagnosis of exclusion once cortical, visual and large-artery features are ruled out. Diffusion-weighted MRI confirms the small lesion when CT is unclear.

Silent lacunes are common on MRI in older hypertensive adults, so an imaging finding alone does not make a stroke. The clinical syndrome that matches the lesion is what the exam expects you to name.

## Where the exam tries to catch you

Most lost marks come from calling a cortical stroke lacunar, or from misusing antiplatelet therapy.

- **Trap:** Calling a stroke lacunar when the patient has a visual field defect or aphasia. — **Correct:** Cortical and visual signs exclude a lacune, which points to a cortical or large-artery event.
- **Trap:** Assuming pure motor hemiparesis is always cortical because the weakness is complete. — **Correct:** Complete hemiparesis with no cortical signs fits an internal capsule or pontine lacune.
- **Trap:** Prescribing dual antiplatelet therapy indefinitely after a lacunar stroke. — **Correct:** Long-term dual therapy is not routine because bleeding risk rises, so single agent therapy is the standard long-term choice.
- **Trap:** Ignoring blood pressure when treating small vessel disease. — **Correct:** Chronic hypertension drives lipohyalinosis, so blood pressure control is a central part of prevention.

## Frequently asked questions

### What are the four classic lacunar syndromes?

The four classic lacunar syndromes are pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis and dysarthria-clumsy hand syndrome. Each arises from a small deep infarct and is generally not accompanied by aphasia, neglect or hemianopia.

### Why does a lacunar stroke not produce cortical signs?

A lacune occurs in a small penetrating artery supplying deep structures such as the internal capsule, thalamus and pons, not the cerebral cortex. The absence of cortical signs is therefore a diagnostic clue for a lacunar stroke.

### What is the usual mechanism of a lacunar infarct?

Lacunar infarcts are most often caused by lipohyalinosis of penetrating arterioles, a process strongly linked to chronic hypertension and diabetes. Large-artery atherosclerosis and cardiac embolism are less common sources and fall outside the lacunar pattern.

### Which MRI features indicate cerebral small vessel disease?

White matter hyperintensities, lacunes and cerebral microbleeds on MRI indicate cerebral small vessel disease. Microbleeds on susceptibility-weighted imaging also raise the risk of haemorrhage when antithrombotic drugs are considered.

### What is Binswanger disease?

Binswanger disease is subcortical arteriosclerotic encephalopathy, a chronic small vessel disease with extensive white matter change. It typically causes progressive cognitive decline and gait disturbance, often in a patient with long-standing hypertension.