| Autor: |
Shiio M; Department of Neurology, Omori Red Cross Hospital, Japan., Maeda N; Department of Neurology, Omori Red Cross Hospital, Japan., Iwata A; Department of Neurology, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Japan., Ishibashi K; Team for Neuroimaging Research, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Japan., Ishii K; Team for Neuroimaging Research, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Japan., Takuma H; Takuma Neurology Clinic, Japan., Ishizaka Y; Department of Health Care, Mitsui Memorial Hospital, Japan., Sakurai Y; Takuma Neurology Clinic, Japan.; Department of Health Care, Mitsui Memorial Hospital, Japan. |
| Abstrakt: |
A 73-year-old woman with posterior cortical atrophy (PCA) presented with progressive apperceptive visual agnosia, alexia, agraphia, ventral simultanagnosia, prosopagnosia, and allocentric (stimulus-centered) left-sided hemispatial neglect. All of these symptoms were attributed to damage to the bilateral occipito-temporal cortices, consistent with ventral variant PCA. While the Pittsburgh compound B uptake was extensively distributed throughout the occipito-parietal (dorsal) and occipito-temporal (ventral) areas, the THK5351 (ligand binding to tau aggregates/astrocyte gliosis) accumulation was limited to the ventral area. These findings suggest that local accumulation of tau proteins and/or astrocyte gliosis over the occipito-temporal cortices can result in ventral variant PCA. |
