Hemispheric Asymmetry of White Matter Hyperintensity in Association With Lacunar Infarction.

Background White matter hyperintensities ( WMHs ) are commonly asymmetric between hemispheres but for unknown reasons. We investigated asymmetric WMHs associated with lacunar infarcts. Methods and Results A total of 267 consecutive patients with small first-ever supratentorial infarcts (≤20 mm) were included. None had a relevant vascular stenosis. WMH asymmetry was measured based on the hemispheric difference of a modified Scheltens scale score (≥3 defined as asymmetric). We analyzed the association of the hemispheric WMH asymmetry with old silent lacunar infarcts or acute lacunar infarcts. We compared lesion frequency maps between groups and generated t-statistics maps. The mean age of patients was 64 years, and 63% were men. Asymmetric WMH was more than 3-fold as frequent ( P<0.001) in the group with old silent lacunar infarcts (42%, 43/102) than in the group without old silent lacunar infarcts (15%, 24/165). In patients with left hemispheric dominance of WMHs , an acute lacunar infarct was more likely to be located in the left (versus right) hemisphere (74% versus 26%, P<0.001). In patients with right hemispheric dominance of WMHs , an acute lacunar infarct was more likely to be located on the right (versus left) hemisphere (81% versus 19%, P<0.001). Mapping studies showed that the side of hemispheric dominance of WMHs was associated with acute and silent lacunes on the same side. Conclusions These are the first data to show that asymmetric WMH s are associated with both old silent lacunar infarcts and acute lacunar infarcts ipsilateral to the greatest WMH burden. This suggests that the hemisphere with relatively large WMHs is more vulnerable to ischemia.

Two Cases of Crossed Cerebellar Diaschisis with or without Thalamic Lesion on Brain MRI in Status Epilepticus.

We report two cases of status epilepticus who showed crossed cerebellar diaschisis (CCD) with or without pulvinar high signal intensity (HSI) on brain magnetic resonance imaging (MRI). The first patient had CCD with pulvinar HSI on MRI and periodic lateralized epileptiform discharges (PLEDs) on electroencephalography. MRI of the second patient revealed CCD without pulvinar HSI. And electroencephalography (EEG) of this patient did not show PLEDs. The authors suggest that the pulvinar lesion might be related to the generation of PLEDs in Status epilepticus.