Cerebellar Hypoperfusion during Transient Global Amnesia: An MRI and Oculographic Study.
- Author:
Young Soon YANG
1
;
Ji Soo KIM
;
Sang Yun KIM
;
Yu Kyeong KIM
;
Yong Tae KWAK
;
Il Woo HAN
Author Information
- Publication Type:Original Article
- Keywords: transient global amnesia; MRI; SPECT; hippocampus; cerebellum; saccades; smooth pursuit
- MeSH: Amnesia, Retrograde; Amnesia, Transient Global; Brain; Cerebellar Ataxia; Cerebellar Diseases; Cerebellum; Eye Movements; Follow-Up Studies; Hippocampus; Humans; Ischemia; Magnetic Resonance Imaging; Pursuit, Smooth; Saccades; Tomography, Emission-Computed, Single-Photon
- From:Journal of Clinical Neurology 2009;5(2):74-80
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND AND PURPOSE: Transient global amnesia (TGA) is characterized by sudden anterograde and retrograde amnesia lasting for up to 24 hours. Diffusion-weighted magnetic resonance imaging (DWI) in cases of TGA and ischemia demonstrates a high frequency of high signal intensities restricted to the hippocampus, and this has been proposed as an etiology of TGA. The aims of this study were to characterize the DWI and single-photon-emission computed tomography (SPECT) findings during the acute and recovered phases of TGA and to correlate the findings with oculomotor abnormalities. METHODS: Five consecutive patients with a clinical diagnosis of TGA underwent DWI and SPECT of the brain within 24 hours after symptom onset and again 3 days later. Eye movements were also recorded using three-dimensional video-oculography. RESULTS: In all patients, DWI disclosed small punctuate (1-3 mm), high-signal lesions in the lateral portion of the hippocampus. The initial SPECT also revealed hypoperfusion in the cerebellar vermis, which had recovered by the follow-up examination. Three patients showed saccadic hypermetria or impaired smooth pursuit only during the acute phase. CONCLUSIONS: Our patients with TGA showed cerebellar vermian hypoperfusion in addition to ischemic insults to the lateral hippocampus. The oculomotor abnormalities observed in our patients support the occurrence of cerebellar dysfunction during the TGA attack.
