Clinical lacunar syndromes as predictors of lacunar infarctsA comparison of acute clinical lacunar syndromes and findingson diffusion-weighted MRI

Abstract

Almost all patients with acute ischemic lacunar syndromes have acute lesions on echo-planar diffusion-weighted MRI within 3 days after stroke onset. These lesions are mostly small and subcortical, compatible with lacunar infarcts caused by single penetrating artery occlusion, but in a minor proportion of patients (2 of 23 in our study) a cortical involvement is found.

Examining the Lacunar Hypothesis With Diffusion and Perfusion Magnetic Resonance Imaging

“…This is likely to be one of the factors giving rise to the milder strokes in these patients; the striatocapsular patients must at some point before assessment have had MCA embolic occlusion, but spontaneous recanalization has spared them from large territorial infarction and even from large striatocapsular infarction. 23 The average lacune volume was 0.57ϫ10 3 mm 3 , as has been found by others, 9 and this indicates an average infarct diameter of Ϸ10 mm. Fisher 2 said that it may be pointless to set an absolute limit for the size of a lacune, but emphasized that those Ͼ10 mm in diameter were unusually large.…”

“…[25][26][27] This series of lacunar syndrome patients may not be representative of patients encountered routinely in an emergency department, given the small sample taken from Ͼ800 stroke admissions, but the percentage of lacunar presentations within this larger MRI series (18%) is consistent with many prospective registries of stroke subtype. One previous series has described cortical infarcts in 2 of 23 patients presenting with lacunar syndromes, 9 but another group found only 1 cortical infarct in 43 patients with lacunar syndromes. 15 The early clinical assessment in our study may have accounted for missing subtle signs of dysfunction of cortical modalities, but although there is good evidence that stroke subtype definition within 12 hours is less accurate than at a later time point, 28 -30 the very small cortical infarcts seen on DWI in the 4 patients with combined cortical and subcortical infarcts were not likely to be clinically detectable.…”

“…Two other recent DWI studies suggest this. 9,15 With the possibility of occult cardiac embolism due to intermittent atrial fibrillation, and with the emergence of other proximal pathologies as significant potential sources of embolism, 36,37 decisions about further investigation should not necessarily be based solely on clinical bedside examination for cortical signs. Further prospective studies of patients with lacunar syndromes are needed to assess the routine clinical implications of this study, but for patients with lacunar syndromes acute diffusion and perhaps perfusion MRI may be an important modality for obtaining an early accurate diagnosis of the infarct type and mechanism.…”

“…Furthermore, it is known that acute DWI lesions with PWI deficits expand in the first 72 hours, 18,24 whereas lacunes have been shown to shrink slightly on outcome T2 follow-up, 1 to 5 months later. 9 …”

“…Recent studies using diffusion-weighted MRI (DWI) have shown that some patients with suspected subcortical infarcts have cortical lesions, 9 and multiple small subcortical infarcts on DWI indicate an embolic source of cerebral ischemia. 10 -13 In contrast to multiple DWI abnormalities, the stroke etiology in patients with solitary small DWI lesions is more difficult to determine.…”