ArticleInternal medicine (Tokyo, Japan)2018
Relationship between Cytotoxicity in the Hippocampus and an Abnormal High Intensity Area on the Diffusion-weighted Images of Three Patients with Transient Global Amnesia.
Article in Internal medicine (Tokyo, Japan), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 9 citations in OpenAlex.
- Mapping the transcriptomic changes of endothelial compartment in human hippocampus across aging and mild cognitive impairment.Biology open · 2021Article
- Stereological Changes in Microvascular Parameters in Hippocampus of a Transgenic Rat Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2021Article
- Transient Global Amnesia: An Electrophysiological Disorder Based on Cortical Spreading Depression-Transient Global Amnesia Model.Frontiers in human neuroscience · 2020Article
- Simultaneous transient global amnesia and Takotsubo syndrome after death of a relative: a case report.Journal of medical case reports · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Objective An abnormal high intensity area (HIA) on diffusion-weighted imaging (DWI) indicates the presence of cytotoxic edema and has been reported to be observed in the hippocampus of patients with transient global amnesia (TGA). The appearance of an HIA on DWI is usually delayed after the onset of patients with amnesia in TGA; thus, the significance of the HIA was evaluated in patients with TGA. Methods Three adult TGA patients who had a unilateral HIA on DWI (right, n=2; left, n=1) were enrolled. These patients were hospitalized due to acute-onset amnesia. Amnesia subsided within 24 hours of hospitalization in all three patients. Results The HIA was confined to the upper lateral zone of the body in the unilateral hippocampus where the CA1 region exists. The lesions were confirmed after the improvement of amnesia in the three patients. The location of the lesions corresponded to the watershed area where the upper and lower hippocampal arteries were anastomosed. Conclusion Cytotoxicity caused by glutamate-mediated calcium influx in the neurons of the CA1 region was recently reported in the pathogenesis of TGA. Based on the pathogenesis, the cytotoxicity was considered to have been caused by calcium overload throughout the entire CA1 region, and amnesia occurred due to this cytotoxicity. The cytotoxicity was more marked in the lesions because of the lower blood flow in the watershed area and was prolonged after the function of the CA1 region (excluding the watershed area) improved, which led to cytotoxic edema in the lesions.
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