Background and purpose: The 'lacunar hypothesis' has been challenged, since small (diameter <15 mm) subcortical infarcts can be produced by middle cerebral artery disease (MCAD) or cardioembolism (CE), while a larger infarct can occur without evidence of MCAD or CE. We sought to assess whether the lacunar hypothesis based on size is still valid.
Methods: We studied 118 patients who were admitted within 72 h after stroke onset and had acute deep subcortical MCA territory infarcts detected by diffusion-weighted MRI, and who had undergone angiography (mostly MR angiography). Stroke mechanisms were arbitrarily categorized regardless of lesion size: (1) MCAD when there was a corresponding MCA lesion; (2) internal carotid artery disease (ICAD) when there was a significant (>50%) ipsilateral ICAD; (3) CE when there was emboligenic heart disease without MCAD or ICAD, and (4) small vessel disease (SVD) when there was neither CE nor MCAD. SVD was further divided into definite SVD (dSVD, longest diameter <15 mm) or probable SVD (pSVD, longest diameter > or =15 mm).
Results: Seventy-three patients (62%) had SVD, of which 38 (32%) had pSVD and 35 (30%) dSVD. Thirty-three patients (28%) had MCAD, five (4%) CE, and seven (6%) ICAD. The infarct diameter in MCAD was not larger than in SVD (p = 0.35), and there was no difference in clinical features or risk factors between MCAD and SVD, or between pSVD and dSVD. CE was distinguished from SVD by its larger size and cortical symptoms.
Conclusions: There are no clinical and lesion-size differences between MCAD and SVD, suggesting that there seems to be no rationale for the 15 mm size criterion for lacunar or small-vessel infarction.
Copyright 2007 S. Karger AG, Basel.