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Prosopagnosia
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
The acquired type of prosopagnosia is rare and far more severe. Frequently, someone with acquired prosopagnosia also has other deficits in their vision—called “comorbid” symptoms. These frequently include partial colorblindness (see Achromatopsia), difficulties in navigating through space (see Topographical Disorientation), and visual field defects that make them partially blind, usually in the upper part of their vision (Barton, 2011). This is often because people with acquired prosopagnosia develop the disorder during a stroke, and that stroke also damages multiple parts of the brain that are located close together. Speaking of which, let's discuss the brain pathology of prosopagnosia.
Vision and Higher Cortical Function
Published in Andrei I. Holodny, Functional Neuroimaging, 2019
Sonia Gill, John Ulmer, Edgar A. DeYoe
The ventrally directed stream extends from the occipital lobe into inferotemporal cortex (Fig. 4). At mid-level stages of this stream, there is a complex of visual areas whose boundaries and homology with monkey areas have been controversial (22). The areas labeled here as V4/VO are associated with color and form processing and are located in the posterior fusiform gyrus or anterior lingual gyrus in humans (23,24). Damage to this region can cause cerebral achromatopsia characterized by a loss of color vision with sparing of visual acuity (23,24). Just anterior to V4/VO is the “fusiform face area.” Complex patterns, especially faces are analyzed here (25), and damage to this region can cause face agnosia (prosopagnosia). More generally, lesions near this same region, potentially involving the lateral occipital (LO) complex or other inferotemporal visual areas, produce visual object agnosias (26,27). Injury to this region in the dominant hemisphere can result in the inability to recognize words (alexia) (28,29), which is the written word analogue to visual object agnosia.
How to master MCQs
Published in Chung Nen Chua, Li Wern Voon, Siddhartha Goel, Ophthalmology Fact Fixer, 2017
GerstmaniYs syndrome results from a lesion in the dominant parietal lobe. It is characterised by acalculia, agraphia, finger agnosia and left-right confusion. Prosopagnosia is an inability to recognise familiar faces and usually results from bilateral occipitotemporal involvement. Achromatopsia is abnormal colour discrimination and can arise from bilateral parietal or occipital lobe abnormalities. Akinetopsia implies insensitivity to motion and can result from a lesion in the middle temporal gyrus. Anton's syndrome occurs in blind patients who deny they are blind. It is seen in bilateral occipital lesions.
OCT Imaging in Infants
Published in Seminars in Ophthalmology, 2022
Sushma Jayanna, Subhadra Jalali, Tapas R Padhi, Komal Agarwal, Jay Chhablani
Achromatopsia is inherited as an autosomal recessive pattern, with severe vision loss, photophobia with nystagmus present within infancy. Fundus looks normal with loss of normal foveal reflex. OCT shows foveal hypoplasia, disruption of an ellipsoid layer at the fovea, with eventual thinning of the retina. ERG shows extinguished cone response with normal rod response.1,55 It is classified based on OCT into 5 stages in older children and adults. stage 1 with intact outer retina, stage 2 with inner segment ellipsoid line disruption; stage 3 with presence of an optically empty space; stage 4 with optically empty space with partial retinal pigment epithelium disruption; and stage 5 with complete retinal pigment epithelium disruption and/or loss of the outer nuclear layer. Hyperreflectivity of ELM appears first and could be the early sign of cone degeneration in eyes with intact outer retina. The staging system may be used to guide therapeutic decisions. This can help in assessing the disease progression and patient selection for novel gene therapies.82
Identification of colorblindness among selected primary school children in Hararghe Region, Eastern Ethiopia
Published in Alexandria Journal of Medicine, 2018
Temesgen Tola Geletu, Manikandan Muthuswamy, Tamiru Oljira Raga
Colorblindness is hereditary defect and can be grouped as monochromacy, dichromacy and trichromacy. Monochromacy is the total colorblindness that is very rare and it is manifested when two or all three of the cone pigments are not functioning or missing. However, dichromacy includes protanopia which is caused as a result of the complete absence of red retinal color receptors, and deuteranopia which results from the absence of green retinal color receptors and tritanopia which occurs when blue retinal photoreceptors are completely absent. In abberant trichromacy one of the three retinal photoreceptors is altered in its spectral sensitivity and results in protanomaly, deuteranomaly and tritanomaly in which the spectral specificity of the red, green and blue or yellow receptors is not functioning well. Achromatopsia is the most severe and rarest type of color vision impairment which occurs when an individual is unable to see any color due to absence of all the three retinal photoreceptors.11 The most common type of CVD is termed as Red-green CVD, which is also known as Daltonism.10
Long-Term Follow-up of Spasmus Nutans
Published in Journal of Binocular Vision and Ocular Motility, 2018
Rupin N. Parikh, John W. Simon, Jitka L. Zobal-Ratner, Gerard P. Barry
On the other hand, our patients presented with findings similar to those reported by previous authors. When faced with a new patient displaying typical findings, the clinician may not have the luxury of repeated assessments and ready access to electroretinography, specialized eye movement recordings, or other tools. Our approach is to follow children with suspected spasmus nutans, watching for evidence of poor vision, retinal degeneration, or optic nerve disease. Our patients had a follow-up averaging over 5 years, with no others acquiring additional ophthalmologic or neurologic diagnoses. Specifically, none developed high myopia, photophobia, night blindness, optic atrophy, or specific retinal pathology. The one child with achromatopsia was the only one of our patients with a visual acuity of less than 20/80 in the better eye. Because of her visual failure and paradoxical pupils, she was referred for electroretinography under general anesthesia, testing unavailable in our area. We acknowledge, nonetheless, that retinal disease may have been under-recognized, since we did not have access to electroretinography for all children.