Lacunar Infarct Reporting

STRIVE-2 terminology for small deep infarcts

Preferred framework. Avoid using “lacunar infarct” as the default label for every small deep lesion. STRIVE-2 distinguishes a recent infarct from its chronic cavitated sequela and favors morphology-based language that avoids overstatement of mechanism.

The preferred terms are recent small subcortical infarct and lacune of presumed vascular origin.

Recent / Acute Lesion

Use recent small subcortical infarct for a small deep infarct with appropriate DWI/ADC evolution, generally in the territory of a single perforating arteriole.

This is preferred to “acute lacunar infarct,” because lacune in STRIVE terminology denotes a chronic cavity rather than an acute lesion.

Chronic Cavitated Lesion

Use lacune of presumed vascular origin for a small round or ovoid subcortical CSF-signal cavity in deep gray matter, deep white matter, or brainstem.

A surrounding FLAIR-hyperintense gliotic rim supports this interpretation.

Noncavitated Chronic Lesion

For a small chronic T2/FLAIR-hyperintense focus without CSF-like cavitation, use:

Chronic small subcortical infarct, or
Small chronic subcortical lesion, likely vascular, if attribution is less secure.

Do not automatically call a noncavitated lesion a lacune. A recent small subcortical infarct does not necessarily evolve into one.

Copy-Ready Report Wording

Acute MRI

Small focus of restricted diffusion in the [right/left] [corona radiata/posterior limb of the internal capsule/thalamus/pons], compatible with a recent small subcortical infarct. No hemorrhagic transformation or mass effect.

Chronic cavitated lesion

Chronic lacune of presumed vascular origin in the [location], characterized by CSF-like signal with a surrounding FLAIR hyperintense gliotic rim.

Multiple chronic lesions

Multiple chronic lacunes of presumed vascular origin in the bilateral basal ganglia and thalami, with accompanying [mild/moderate/severe] white matter hyperintensities of presumed vascular origin.

When distinction from PVS is uncertain

Small CSF-signal focus in the [location], favored enlarged perivascular space / lacune of presumed vascular origin, depending on [absence/presence] of a surrounding FLAIR hyperintense gliotic rim and lesion morphology.

Acute Basal-Ganglia Lesions

A basal-ganglia lesion is compatible with a recent small subcortical infarct when it demonstrates recent infarction in a single perforator territory, such as a lenticulostriate distribution.

Preferred wording

Acute/recent small subcortical infarct involving the [right/left] [putamen/globus pallidus/caudate body/anterior limb or posterior limb of the internal capsule], with restricted diffusion. No hemorrhagic transformation or significant mass effect.

Clinical Compromise Wording

Small acute/recent lacunar-type infarct in the [location], likely involving a lenticulostriate perforator territory.

The formal version is most consistent with STRIVE-2. This alternative preserves familiar clinical language while avoiding use of lacune for an acute lesion.

Lacune Versus Enlarged Perivascular Space

Feature	Lacune of presumed vascular origin	Enlarged perivascular space
Morphology	Usually round or ovoid	Often linear or tubular
Signal	CSF-like on all sequences	CSF-like on all sequences
Typical setting	Chronic sequela of prior small subcortical infarction, small hemorrhage, or other small-vessel injury	Perivascular-space variant
FLAIR rim	Often has a surrounding gliotic hyperintense rim	Usually lacks a convincing gliotic rim
Location	Deep gray nuclei, deep white matter, brainstem	Basal ganglia and centrum semiovale; follows expected vessel course
Reporting implication	Supports prior tissue injury	Do not overcall as prior infarction

A lacune is a cavitated CSF-signal lesion. Avoid labeling every basal-ganglia CSF-signal focus as an “old lacunar infarct.”

Broader SVD Reporting

Report associated markers separately:

White matter hyperintensities of presumed vascular origin
Lacunes of presumed vascular origin
Enlarged perivascular spaces
Cerebral microbleeds
Cerebral atrophy, when relevant

This frames lacunes within the overall small-vessel-disease phenotype rather than as isolated findings.

Reporting Reminders

For a recent small subcortical infarct, state laterality, exact location, number, and DWI/ADC findings.
For a lacune, state location, approximate size, multiplicity, and whether a gliotic rim is present.
Be cautious assigning a single-perforator mechanism when a lesion is large, crosses expected perforator territories, is cortical, or implies multiple lenticulostriate branches.
A basal-ganglia/internal-capsule lesion larger than a single perforator territory may represent a striatocapsular infarct.

References

Wardlaw JM, et al. Neuroimaging standards for research into small vessel disease—advances since 2013. The Lancet Neurology. 2023;22(7):602–618.
Wardlaw JM, et al. Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. The Lancet Neurology. 2013;12(8):822–838.
STRIVE-2 terminology reference.
Striatocapsular infarction reference.