Jin Nakamura, Yuki Hagiwara, Yoshihiro Furukawa, Kiyoshi Matsukura, Keiichi Hokkoku, Nao Tsutsui, Chiyoko Nagai, Hiroshi Oba, Shunsuke Kobayashi
A 37-year-old woman with a history of antiphospholipid syndrome (APS) developed a progressive visuospatial impairment, including difficulty tying shoelaces and inserting keys. A neuropsychological assessment revealed simultagnosia, optic ataxia, dressing apraxia, alexia, agraphia, and left hemispatial neglect, mimicking the symptoms of posterior cortical atrophy (PCA). Brain MRI revealed occipital-parietal atrophy and FLAIR hyperintensities in the watershed areas, suggestive of chronic ischemia. Cerebral blood flow SPECT revealed bilateral hypoperfusion in the same regions. We report that chronic ischemic injury associated with antiphospholipid syndrome can produce a posterior cortical atrophy phenotype.