Imaging evolution of acute lacunar infarction: leukoariosis or lacune?

In acute lacunar infarction, MRI may overestimate eventual infarct size and the imaging evolution of acute lesions is not fully understood. Our objective was to examine eventual infarct size, the incidence of cavity formation, and factors associated with cavitation in patients presenting with acute lacunar infarction.

Patients with acute diffusion-weighted imaging (DWI) infarcts ≤25 mm in diameter, in the distribution of a penetrating artery, who had a follow-up MRI or CT at least 1 month or longer from stroke onset were retrospectively included. We measured baseline lesion size on DWI and T2/fluid-attenuated inversion recovery (FLAIR) and follow-up lesion size on T2/FLAIR and CT. Follow-up MRI and CT images were assessed for cavity formation. Predictors for cavitation were assessed in a multivariate model.

We identified 75 patients with lacunar infarction and follow-up CT or MRI, done 20.2 ± 16.6 and 21.2 ± 17.4 months after stroke, respectively. Mean baseline DWI size was 13.5 ± 5.7 and T2/FLAIR size was 13.1 ± 5.3 mm. Follow-up T2/FLAIR lesion size was 8.2 ± 3.4 mm and smaller than baseline DWI and T2/FLAIR (p = <0.001). Follow-up whole lesion size on CT scan was 7.1 ± 4.1 and smaller than baseline DWI and T2/FLAIR (p = 0.001). Cavitation occurred in 23/38 (61%) MRI and 50/70 (70%) CT scans. We identified periventricular white matter lesions as a predictor of cavity formation by MRI and CT.

Acute DWI significantly overestimates final infarct size. A third of lacunar infarcts do not develop a cavity.