When I use a word . . . Facial blindness—prosopagnosia

Prosopagnosia is an impaired or absent ability to recognise faces. It has two forms: (a) developmental prosopagnosia, which is thought to have a genetic basis, reportedly associated with a mutation in the MCTP2 gene which encodes a calcium binding transmembrane protein, and occurs in the absence of brain damage, and (b) acquired prosopagnosia, which occurs as a result of different forms of brain damage, typically in the occipitotemporal region. It has been reported after right posterior cerebral artery infarction, Alzheimer’s disease, carbon monoxide poisoning, encephalitis, neoplasms, right temporal lobe atrophy, medial/anterior temporal lobe epilepsy, temporal lobectomy, and trauma. Acquired prosopagnosia is rare, but developmental prosopagnosia occurs in about 2.5% of the population and is associated with aphantasia. The condition was described at least as early as 1844 and several times thereafter, but it was not given a name until 1947, when Joachim Bodamer called it “Prosopagnosie” in German, which was translated into English in 1950 as “prosopagnosia.” The cardinal features are: lasting and irritating subjective uncertainty of face recognition; face recognition deficit especially in crowded places or out-of context encounters; false-negative and false-positive face recognition events; face recognition time longer than socially accepted; prolonged face learning time longer than socially accepted; onset in childhood; development of adaptive behaviour; no gaze contact necessary; use of explicit learning strategies for visual person recognition; and impaired visual recognition of objects and scenes. I recognise some of these features in myself.