Abstract
This study examines the neurological and neuropathological conditions, and clinical, imaging, and demographic traits linked to prosopagnosia. Out of 475 potential cases, 327 met criteria for probable or definite prosopagnosia. One patient had Niemann-Pick type C and another had a forkhead box G1 gene mutation; ten patients (80% male) had developmental prosopagnosia. Of 317 with acquired prosopagnosia, 228 had degenerative causes, primarily primary prosopagnosia syndrome, Alzheimer's disease dementia, posterior cortical atrophy, and semantic dementia. Non-degenerative cases often involved ischemic and hemorrhagic infarcts. Transient non-degenerative prosopagnosia, linked to hypoxic encephalopathy and migraines, improved over time. Degenerative prosopagnosia patients often showed temporal lobe involvement on PET scans, while non-degenerative patients had right temporal and occipital lobe lesions on MRI. Pathological findings included Alzheimer's, Lewy body disease, and frontotemporal lobar degeneration. Facial recognition loss spans various neurological illnesses.
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