BACKGROUND AND PURPOSE: A hypoxic-ischemic origin of transient global amnesia (TGA) has been suggested on the basis of the observation of infarctlike diffusion-weighted imaging (DWI) abnormalities in some affected individuals. We tested this hypothesis by comparing vascular risk factors, magnetic resonance imaging (MRI) markers of cerebral small-vessel disease, and other evidence of a cerebrovascular disorder between TGA patients with (DWI+) and without (DWI-) DWI lesions and normal community-based controls. METHODS: We retrospectively identified 86 patients hospitalized for TGA (mean+/-SD age, 65.9+/-10.9 years; 62% female). Brain MRI at 1.5 T was assessed for DWI lesions exhibiting restricted diffusion (ie, DWI+), white-matter hyperintensities, lacunes, and chronic infarcts (median time lag to clinical onset, 66.6+/-54.6 hours). Vascular risk factors and findings from duplex sonography, ECG, and echocardiography were recorded. A 1:2 age- and sex-matched sample of 172 elderly subjects (mean+/-SD age, 65.6+/-9.3 years; 62% female) free of neuropsychiatric disease served for comparison. RESULTS: DWI lesions were observed in 10 patients with TGA (11.5%; mean+/-SD age, 68.3+/-5.4 years; 8 women). They were all small and located in the mesiotemporal region (9 left hemisphere, 5 right hemisphere). The vascular risk profile of TGA patients and concomitant changes on brain MRI were comparable with those of healthy controls and did not show significant differences between DWI+ and DWI- subjects. A comprehensive diagnostic workup also provided no evidence for a higher rate of cerebrovascular disorder-related abnormalities in either the total group of TGA patients or TGA DWI+ patients. CONCLUSIONS: These findings do not support a cerebrovascular etiology of TGA, even in those individuals showing acute DWI lesions. Other pathophysiologic mechanisms need to be explored.
BACKGROUND AND PURPOSE: A hypoxic-ischemic origin of transient global amnesia (TGA) has been suggested on the basis of the observation of infarctlike diffusion-weighted imaging (DWI) abnormalities in some affected individuals. We tested this hypothesis by comparing vascular risk factors, magnetic resonance imaging (MRI) markers of cerebral small-vessel disease, and other evidence of a cerebrovascular disorder between TGA patients with (DWI+) and without (DWI-) DWI lesions and normal community-based controls. METHODS: We retrospectively identified 86 patients hospitalized for TGA (mean+/-SD age, 65.9+/-10.9 years; 62% female). Brain MRI at 1.5 T was assessed for DWI lesions exhibiting restricted diffusion (ie, DWI+), white-matter hyperintensities, lacunes, and chronic infarcts (median time lag to clinical onset, 66.6+/-54.6 hours). Vascular risk factors and findings from duplex sonography, ECG, and echocardiography were recorded. A 1:2 age- and sex-matched sample of 172 elderly subjects (mean+/-SD age, 65.6+/-9.3 years; 62% female) free of neuropsychiatric disease served for comparison. RESULTS: DWI lesions were observed in 10 patients with TGA (11.5%; mean+/-SD age, 68.3+/-5.4 years; 8 women). They were all small and located in the mesiotemporal region (9 left hemisphere, 5 right hemisphere). The vascular risk profile of TGA patients and concomitant changes on brain MRI were comparable with those of healthy controls and did not show significant differences between DWI+ and DWI- subjects. A comprehensive diagnostic workup also provided no evidence for a higher rate of cerebrovascular disorder-related abnormalities in either the total group of TGA patients or TGA DWI+ patients. CONCLUSIONS: These findings do not support a cerebrovascular etiology of TGA, even in those individuals showing acute DWI lesions. Other pathophysiologic mechanisms need to be explored.
Authors: Carlo Augusto Mallio; Giovanni Assenza; Filomena Occhicone; Yuri Errante; Bruno Beomonte Zobel; Carlo Cosimo Quattrocchi Journal: BMJ Case Rep Date: 2013-06-10