INTRODUCTION: Transient global amnesia (TGA) is a neurological disorder that consists in a sudden loss of anterograd memory and temporospatial disorientation during less than 24 hours. Several precipitating factors have been reported. Conventional neuroimaging scans usually are negative. Different etiopathogenic theories have been postulated but the vascular etiology is the most commonly accepted. CASE REPORTS: Three patients with a typical presentation of TGA are studied. In all of them two brain blood flow HMPAO SPECT were performed, within the first 48 hours from the onset and three months after as an evolutive control. The first patient showed a left temporal perfusion defect and temporoparietal hypoperfusion. The second showed frontotemporal hypoperfusion, temporal mesial defect and hypoperfusion in basal ganglia, all in the left side. The third patient showed thalamic hyperperfusion and cerebellum hypoperfusion, both in the left. In all of them, control SPECT normalized. CONCLUSION: Three etiopatogenic theories about TGA have been reported: epilepsy, migraine and blood flow impairment. In TGA neuroanatomic image and neurophysiologic studies usually do not show significative alterations. Conversely, functional studies as brain blood flow HMPAO SPECT, do show changes being the most common bilateral temporobasal hypoperfusion, although this is not the only pattern described. Causes of this variable behaviour remain unclear but can be related to different clinic expressions and, over all, to time of evolution from onset. The three cases in this study show three different perfusion patterns reported in TGA and all of them withhold the vascular etiopathogenic theory.
INTRODUCTION: Transient global amnesia (TGA) is a neurological disorder that consists in a sudden loss of anterograd memory and temporospatial disorientation during less than 24 hours. Several precipitating factors have been reported. Conventional neuroimaging scans usually are negative. Different etiopathogenic theories have been postulated but the vascular etiology is the most commonly accepted. CASE REPORTS: Three patients with a typical presentation of TGA are studied. In all of them two brain blood flow HMPAO SPECT were performed, within the first 48 hours from the onset and three months after as an evolutive control. The first patient showed a left temporal perfusion defect and temporoparietal hypoperfusion. The second showed frontotemporal hypoperfusion, temporal mesial defect and hypoperfusion in basal ganglia, all in the left side. The third patient showed thalamic hyperperfusion and cerebellum hypoperfusion, both in the left. In all of them, control SPECT normalized. CONCLUSION: Three etiopatogenic theories about TGA have been reported: epilepsy, migraine and blood flow impairment. In TGA neuroanatomic image and neurophysiologic studies usually do not show significative alterations. Conversely, functional studies as brain blood flow HMPAO SPECT, do show changes being the most common bilateral temporobasal hypoperfusion, although this is not the only pattern described. Causes of this variable behaviour remain unclear but can be related to different clinic expressions and, over all, to time of evolution from onset. The three cases in this study show three different perfusion patterns reported in TGA and all of them withhold the vascular etiopathogenic theory.