{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T21:10:03Z","timestamp":1792789803338,"version":"4.5.0"},"reference-count":14,"publisher":"BMJ","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["BMJ Case Reports"],"accepted":{"date-parts":[[2018,5,18]]},"abstract":"<jats:p>A 68-year-old lawyer developed insidious disturbances in topographic orientation and apraxia. He underwent a geriatric evaluation, only documenting slight cognitive disturbances, and a 18F-fluorodeoxyglucose positron emission tomography (FDG-PET), showing mild right-lateralised frontoparietal hypometabolism. After 1\u2009year, because of worsening in spatial orientation and the onset of dressing apraxia, he was referred to our memory clinic. The neuropsychological evaluation documented proeminent visuospatial, praxis deficits and dysgraphia. Cerebrospinal fluid biomarker analysis showed mild increase of total-\u03c4, with normal A\u03b21\u201342, ruling out Alzheimer\u2019s disease. Progression of the right parietal hypometabolism at FDG-PET and right superior longitudinal fasciculus damage at high-field MRI revealed a probable neurodegenerative aetiology. The neurological examination disclosed then Gerstmann\u2019s and Balint\u2019s syndromes, and extrapyramidal signs later appeared, suggesting the diagnosis of posterior cortical atrophy associated with corticobasal syndrome. Genetic analysis for mutations inmicrotubule-associated protein tau <jats:italic>(MAPT)<\/jats:italic>, <jats:italic>C9orf72<\/jats:italic> and <jats:italic>GRN<\/jats:italic> genes was negative. A 1-year follow-up documented significant worsening of the cognitive and functional impairment, revealing a frank dementia.<\/jats:p>","DOI":"10.1136\/bcr-2018-224312","type":"journal-article","created":{"date-parts":[[2018,6,18]],"date-time":"2018-06-18T00:55:18Z","timestamp":1529283318000},"page":"bcr-2018-224312","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":4,"title":["Case of posterior cortical atrophy (PCA) evolved to PCA-CBS"],"prefix":"10.1136","volume":"2018","author":[{"given":"Nicola","family":"Salvadori","sequence":"first","affiliation":[{"name":"Department of Medicine, Centre for Memory Disturbances, Laboratory of Neurochemistry, Section of Neurology, Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mirella","family":"Russo","sequence":"additional","affiliation":[{"name":"Department of Medicine, Centre for Memory Disturbances, Laboratory of Neurochemistry, Section of Neurology, 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