Lacunar infarcts (LACI) are small infarcts in the distal distribution of deep penetrating vessels. Acutely, they result from occlusion of a small penetrating end artery. They have traditionally been attributed to fibrinoid degeneration, microatheroma, and lipohyalinosis, although embolism may account for a minority.
The collective term “lacunar infarcts” is vague and discouraged by Standards for Reporting Vascular Changes on Neuroimaging 2 (STRIVE-2); preferred terminology distinguishes recent infarction, incidental DWI-positive lesions, and chronic lacunes.
STRIVE-2 Terminology
Recent small subcortical infarct (RSSI)
Recent infarction in the territory of one perforating artery, axial diameter ≤20 mm, with compatible imaging and symptoms within the preceding few weeks. It may or may not progress to a lacune; this corresponds to a symptomatic acute lacunar infarct.
Incidental subcortical DWI-positive lesion
Incidentally detected, asymptomatic subcortical DWI-hyperintense lesion ≤20 mm that may or may not progress to a lacune. This is preferred to “covert brain infarct,” “silent stroke,” or “silent infarct.”
Lacune
Round or ovoid subcortical CSF-like cavity ≤15 mm, typically 3–15 mm, of presumed vascular origin. “Chronic lacunar infarct” is discouraged unless prior small-vessel infarction is certain because prior subcortical hemorrhage can also cavitate.
Cortical cerebral microinfarct
Distinct from the above: an acute infarct <4 mm limited to cortical gray matter. “Lobar lacune” is not endorsed by STRIVE-2.
Epidemiology and Clinical Features
- Approximately 20–35% of ischemic strokes.
- Annual incidence: 13–33 per 100,000.
- Slight male predominance.
- Risk rises with age, especially after 55.
- Risk factors mirror nonlacunar ischemic stroke; atrial fibrillation and cardioembolic sources are less common.
Symptomatic patients may present with one of five lacunar stroke syndromes. Acute lesions may also be clinically silent, but accumulating burden increases vascular-dementia risk.
Vessels and Pathogenesis
Acute lesions arise from occlusion of penetrating end arteries, including:
Most result from in-situ microatheroma or lipohyalinosis. Disease at the perforator origin is termed branch atheromatous disease. Because embolism remains possible, an embolic evaluation may still be appropriate.
Evolution
As an acute infarct evolves, it may:
- Disappear or resolve
- Cavitate partially or completely, forming a lacune
- Develop a partial or complete hemosiderin rim
- Persist as chronic white- or gray-matter hyperintensity
- Leave only a small hemosiderin “smudge”
Pathologically, lacunes are small cavities of encephalomalacia traversed by a cobweb-like mesh of fibrous strands.
Imaging
MRI is the modality of choice.
| Modality / sequence | Acute lacunar infarct | Chronic lacune |
|---|
| CT | Ill-defined hypodensity; subtle focal CT-perfusion abnormality may occur. | CSF-density hypodense focus. |
| T1 | Slightly hypointense. | CSF signal. |
| T2 / FLAIR | Hyperintense. | CSF signal, sometimes with a peripheral hyperintense rim of marginal gliosis. |
| DWI | Restricted diffusion; may reveal lesions occult on other sequences. | No acute restriction. |
| SWI / T2* | Usually no change. | Possible partial or complete hypointense hemosiderin rim. |
| Postcontrast T1 | May enhance when acute or early subacute. | No expected enhancement. |
Management and Prognosis
Management follows standard ischemic-stroke care. Lacunar stroke is associated with recurrent ischemic or hemorrhagic stroke and with overall mortality.
The term was coined by Canadian neurologist Charles Miller Fisher (1913–2012), who described postmortem “lacunes” (Latin: lake) of empty fluid in the brains of stroke victims.
Differential Diagnosis
Source text last revised by Rohit Sharma on 6 December 2025.