E-ISSN: 1305-3612
Transient global amnesia: a study with Tc-99m ECD SPECT shortly after symptom onset and after recovery
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Nuclear Medicine and Molecular Imaging - Original Article
VOLUME: 22 ISSUE: 5
P: 476-480
September 2016

Transient global amnesia: a study with Tc-99m ECD SPECT shortly after symptom onset and after recovery

Diagn Interv Radiol 2016;22(5):476-480
DOI: 10.5152/dir.2016.15487
Bom Sahn Kim 1
Sang Soo Cho 2
Joon Young Choi 2
Young Hwan Kim 3
1. Department of Nuclear Medicine, Ewha Womans University School of Medicine, Seoul, Korea
2. Department of Nuclear Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea
3. Department of Nuclear Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea; Department of Nuclear Medicine, Hanyang University Guri Hospital, Kyeonggi, Korea
No information available.
No information available
Received Date: 20.10.2015
Accepted Date: 14.03.2016
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ABSTRACT

PURPOSE:

Transient global amnesia (TGA) is characterized by sudden loss of memory of recent events, transient inability to retain new information, and retrograde amnesia. We investigated the changes of regional cerebral blood flow in patients with TGA shortly after symptom onset and after recovery using Tc-99m-ethyl cysteinate dimer single-photon emission computed tomography (Tc-99m ECD SPECT) and statistical parametric mapping (SPM) analysis.

METHODS:

Six right-handed patients with TGA were studied using Tc-99m ECD SPECT shortly after symptom onset and after recovery. As a control group, six healthy individuals were also studied. Images were analyzed using SPM8 using voxel-based analysis to estimate the differences between TGA patients and controls.

RESULTS:

There was significant hypoperfusion in the left hippocampus, left thalamus, and bilateral cerebellum. In the follow-up SPECT scan, hypoperfusion in hippocampus and thalamus were restored, while hypoperfusion was noted in the temporoparietal region.

CONCLUSION:

Our results suggest that the underlying mechanism of TGA may be temporary ischemia in the hippocampus and thalamus. There was significant restoration of perfusion in the hippocampus and thalamus after recovery from TGA.