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Background: Experimental studies of transient focal ischemia indicate biphasic detectability of lesions by diffusion-weighted imaging (DWI); poorly detectable phase exists at 1-12 hours after reperfusion. The present study aimed to clarify whether poorly detectable phase also exists in DWI of transient ischemic attack (TIA) patients., Methods: A retrospective study was conducted in 144 consecutive TIA patients who underwent magnetic resonance imaging (MRI) within 2 weeks after carotid TIA. Patients were classified into 9 groups according to time from disappearance of TIA symptoms to DWI: intraischemic period, 0-1 hour, 1-12 hours, 12-24 hours, 1-2 days, 2-3 days, 3-7 days, 7-10 days, and 10-14 days after the end of TIA., Results: Lesions were detected in 33 of 144 patients (22.9%). The frequency of positive lesions was 20% in the intraischemic period and 30.8% at 0-1 hour after the end of TIA; it markedly decreased to 8.7% at 1-12 hours after end of TIA. Thereafter, it increased to 21.7%, 30.8%, 36.4%, 37.0%, 38.5%, and 30% at 12-24 hours, 1-2 days, 2-3 days, 3-7 days, 7-10 days, and 10-14 days after the end of TIA, respectively. In 7 patients, MRI was repeated twice, at 1-12 hours and then at 5-13 days after the end of TIA. Lesions were never detected on the first MRI but were clearly demonstrated in 4 of 7 patients on the second MRI., Conclusions: The detectability of ischemic lesions may be biphasic after TIA as indicated by experimental studies., (Copyright © 2015 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Background/aims: The aim of this study is to clarify the relationship between lesion detectability by diffusion-weighted magnetic resonance imaging (DWI) and the etiology of transient ischemic attacks (TIAs)., Methods: A retrospective study was performed on 72 patients with carotid TIAs who underwent DWI studies within 2 weeks after the last episode., Results: Lesions were detected in 24 of 72 patients (33%). The detectability of lesions was 12% (3/25) in the large-artery atherosclerosis (LA) group, 57% (8/14) in the cardioembolism (CE) group, 8% (1/13) in the small-artery occlusion (SA) group, and 60% (12/20) in the other etiology or undetermined etiology (UD) group. Detectabilities in the CE group and the UD group were higher than those in the LA and SA groups. Of 24 patients with DWI-positive lesions, 17 (71%) had embolic sources in the heart; 9 were classified in the UD group because they had embolic sources both in the heart and large artery., Conclusion: Ischemic DWI lesions in TIAs are most likely caused by a cardioembolic mechanism. In TIA patients showing lesions on DWI, heart disease should be surveyed as the possible embolic source., ((c) 2007 S. Karger AG, Basel)

We report serial magnetic resonance imaging findings in a case of anoxic encephalopathy (AE). Diffusion-weighted images clearly showed early development of lesions in the cerebellum, cerebral cortex, and caudate putamen, along with delayed manifestation of lesions in the hippocampus, corpus callosum, and white matter. The present case is the first to demonstrate delayed development of postischemic changes in the hippocampus and deep white matter after AE on neuroimaging.

Background: The clinical relevance of the microembolic signals (MES) detected by transcranial Doppler sonography (TCD) in acute stroke remains unclear. In a prospective study the authors analyzed the relationship between MES and the findings on diffusion-weighted magnetic resonance imaging (DWI) in acute stroke patients., Methods: We performed TCD for a period of 30 min to detect MES in patients within 24 h of stroke onset, and DWI was done within the initial 7 days. MES were assessed from Doppler waves obtained from the middle cerebral artery contralateral to the side of the neurological deficits. The acute ischemic lesions observed on DWI were classified by their diameter (small, medium or large) and by their site (cortical, superficial perforator territory, internal borderzone or deep perforator territory)., Results: We obtained Doppler waves from 39 vessels in 37 patients; 2 patients had bilateral deficits. MES were detected in 12 vessels (MES-positive group) and not detected in 27 vessels (MES-negative group). No significant differences in clinical features were observed between the 2 groups. The number of small lesions was significantly higher in the MES-positive group than in the MES-negative group (p = 0.02). The numbers of cortical and superficial perforator infarcts were significantly higher in the MES-positive group than in the MES-negative group (p = 0.002 and 0.02, respectively)., Conclusion: In acute ischemic stroke, MES detected by TCD in the acute phase may produce small cortical and subcortical lesions found on DWI., ((c) 2007 S. Karger AG, Basel.)

Background and Purpose: Multiple acute brain infarctions in both cerebral hemispheres usually suggest an embolic mechanism, particularly one of aortic or cardiac origin. The purpose of this study was to clarify the etiologic mechanisms and topographic features of bihemispheric infarctions depicted on diffusion-weighted imaging (DWI)., Methods: Among 411 consecutive patients with ischemic stroke who underwent MR imaging in the acute phase, DWI showed bilateral infarctions in 19 (4.6%). In these patients, we analyzed the presence of carotid, aortic or cardiac embolic sources by using ultrasonography, cerebral angiography, and/or transesophageal echocardiography and evaluated the size and topographic distribution of the lesions. We assessed intracranial cross-flow through the anterior communicating artery, mainly on the basis of the anatomic information obtained from angiography or MR angiography., Results: Bilateral lesions were derived from cardiac and/or aortic embolic sources in 16 (84%) of 19 patients and appeared to originate from unilateral carotid diseases in three (16%). In nine (82%) of 11 patients with cardiac embolic sources, at least one large territorial or subcortical lesion was found in either hemisphere, whereas in all eight patients without a cardiac embolic source, the lesions were small and disseminated bilaterally., Conclusion: Unilateral carotid lesions can cause bihemispheric infarctions through cross-flow in the anterior communicating artery. On DWI, small bihemispheric, disseminated lesions strongly suggest an artery-to-artery embolism. In such cases, aortic and carotid lesions should be assessed as potential embolic sources.

Background: Various mechanisms can be considered in ischemic stroke with internal carotid artery (ICA) occlusive diseases. We clarified the etiologic mechanisms from lesion patterns on diffusion-weighted imaging (DWI). Methods: One hundred and twenty consecutive ischemic stroke patients with ipsilateral ICA occlusive diseases were enrolled and classified into 3 groups according to the size of DWI lesions: group A, massive; group B, moderate-to-large; and group C, small. Group C was divided into 3 subgroups according to the number of lesions: C1, 1-3; C2, 4-9; and C3, 10 or more. The relationship between the DWI findings and stroke subtypes according to the TOAST classification was investigated. Results: Cardioembolism was significantly more common in groups A and B than in group C, while large-artery atherosclerosis (LAA) was more frequent in group C than in groups A and B. In group A, cardioembolism accounted for 32%, while LAA was not observed. Statistical analyses showed trends toward a higher frequency of LAA in groups C2 and C3 than in group C1. Conclusions: Mechanisms of acute stroke in ICA diseases can be simply assessed from the lesion size and number, which may be useful in considering acute therapeutic strategies. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]