Daniel Moroz1, Sherryse L Corrow2, Jeffrey C Corrow3, Alistair R S Barton4, Brad Duchaine5, Jason J S Barton6. 1. Human Vision and Eye Movement Laboratory, Departments of Medicine (Neurology), Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, Canada; University of Calgary, Calgary, Canada. Electronic address: daniel.moroz@ucalgary.ca. 2. Human Vision and Eye Movement Laboratory, Departments of Medicine (Neurology), Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, Canada. Electronic address: sherryse.corrow@icloud.com. 3. Human Vision and Eye Movement Laboratory, Departments of Medicine (Neurology), Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, Canada. Electronic address: corrowje@gmail.com. 4. Department of Physics, McGill University, Montréal, Canada. Electronic address: alistair.barton@mail.mcgill.ca. 5. Psychological and Brain Sciences, Dartmouth College, Dartmouth, USA. Electronic address: bradley.c.duchaine@dartmouth.edu. 6. Human Vision and Eye Movement Laboratory, Departments of Medicine (Neurology), Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, Canada. Electronic address: jasonbarton@shaw.ca.
Abstract
OBJECTIVE: Cerebral dyschromatopsia is sometimes associated with acquired prosopagnosia. Given the variability in structural lesions that cause acquired prosopagnosia, this study aimed to investigate the structural correlates of prosopagnosia-associated dyschromatopsia, and to determine if such colour processing deficits could also accompany developmental prosopagnosia. In addition, we studied whether cerebral dyschromatopsia is typified by a consistent pattern of hue impairments. METHODS: We investigated hue discrimination in a cohort of 12 subjects with acquired prosopagnosia and 9 with developmental prosopagnosia, along with 42 matched controls, using the Farnsworth-Munsell 100-hue test. RESULTS: We found impaired hue discrimination in six subjects with acquired prosopagnosia, five with bilateral and one with a unilateral occipitotemporal lesion. Structural MRI analysis showed maximum overlap of lesions in the right and left lingual and fusiform gyri. Fourier analysis of their error scores showed tritanopic-like deficits and blue-green impairments, similar to tendencies displayed by the healthy controls. Three subjects also showed a novel fourth Fourier component, indicating additional peak deficits in purple and green-yellow regions. No subject with developmental prosopagnosia had impaired hue discrimination. CONCLUSIONS: In our subjects with prosopagnosia, dyschromatopsia occurred in those with acquired lesions of the fusiform gyri, usually bilateral but sometimes unilateral. The dyschromatopsic deficit shows mainly an accentuation of normal tritatanopic-like tendencies. These are sometimes accompanied by additional deficits, although these could represent artifacts of the testing procedure.
OBJECTIVE:Cerebral dyschromatopsia is sometimes associated with acquired prosopagnosia. Given the variability in structural lesions that cause acquired prosopagnosia, this study aimed to investigate the structural correlates of prosopagnosia-associated dyschromatopsia, and to determine if such colour processing deficits could also accompany developmental prosopagnosia. In addition, we studied whether cerebral dyschromatopsia is typified by a consistent pattern of hue impairments. METHODS: We investigated hue discrimination in a cohort of 12 subjects with acquired prosopagnosia and 9 with developmental prosopagnosia, along with 42 matched controls, using the Farnsworth-Munsell 100-hue test. RESULTS: We found impaired hue discrimination in six subjects with acquired prosopagnosia, five with bilateral and one with a unilateral occipitotemporal lesion. Structural MRI analysis showed maximum overlap of lesions in the right and left lingual and fusiform gyri. Fourier analysis of their error scores showed tritanopic-like deficits and blue-green impairments, similar to tendencies displayed by the healthy controls. Three subjects also showed a novel fourth Fourier component, indicating additional peak deficits in purple and green-yellow regions. No subject with developmental prosopagnosia had impaired hue discrimination. CONCLUSIONS: In our subjects with prosopagnosia, dyschromatopsia occurred in those with acquired lesions of the fusiform gyri, usually bilateral but sometimes unilateral. The dyschromatopsic deficit shows mainly an accentuation of normal tritatanopic-like tendencies. These are sometimes accompanied by additional deficits, although these could represent artifacts of the testing procedure.
Authors: K Sakai; E Watanabe; Y Onodera; I Uchida; H Kato; E Yamamoto; H Koizumi; Y Miyashita Journal: Proc Biol Sci Date: 1995-07-22 Impact factor: 5.349