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There are conflicting reports concerning signal intensity changes in transient global amnesia (TGA) using diffusion weighted imaging (DWI).We prospectively an alysed DWI signal intensity changes in TIA and TGA patients, and compared the clinical ch aracteristics and risk factors of both groups. Using DWI and conventional T1 and T2 weighted turbo spin echo sequences, 28 patients with acute TGA (13 men, mean age 61.5years) and 74 TIA patients (47 men, mean age 62.4 years) were studied w ithin 48 hours after symptom onset. Every patient underwent an intensive diagnos tic investigation. In 10/28 (36%) of the TGA patients and 21/74 (28%) of the T IA patients, DWI signal intensity changes occurred. The time to DWI and the dura tion of symptoms were comparable in TIA and TGA patients.Overall, TIA patients s howed an increased prevalence of vascular risk factors compared with TGA patient s. In the TGA group, patients with abnormal DWI showed carotid atherosclerosis s ignificantly more frequently. Based on our data,we suggest that the aetiology of TGA could be explained by an ischaemic event; due to arterial thrombembolic isc haemia in one subgroup, particularly in those patients with increased vascular r isk factors, and due to venous ischaemia in another subgroup with valsalva-like activities before symptom onset.
There are conflicting reports concerning signal intensity changes in transient global amnesia (TGA) using Diffusion weighted imaging (DWI). We prospectively anlyzed DWI signal intensity changes in TIA and TGA patients, and compared the clinical chracteristics and risk factors of both groups. Using DWI and conventional T1 and T2 weighted turbo spin echo sequences, 28 patients with acute TGA (13 men, mean age 61.5 years) and 74 TIA patients (47 men, mean age 62.4 years) were studied w ithin 48 hours after symptom onset. Every patient underwent an intensive diagnostic investigation. In 10/28 (36%) of the TGA patients and 21/74 (28%) of the T IA patients, DWI signal intensity changes occurred. The time to DWI and the dura tion of symptoms were comparable in TIA and TGA patients. Overall, TIA patients s howed an increased prevalence of vascular risk factors compared with TGA patient s. In the TGA group, patients with abnormal DWI showed carotid atherosclerosis s ignificantly more frequent ly based on our data, we suggest that the aetiology of TGA could be explained by an ischaemic event; due to arterial thrombembolic isc haemia in one subgroup, particularly in those patients with increased vascular r isk factors, and due to venous ischaemia in another subgroup with valsalva-like activities before symptom onset