Structural changes to primary visual cortex in the congenital absence of cone input in achromatopsia
•Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM).•Reduction in cortical surface area in foveal, parafoveal and paracentral representations of V1 in those with ACHM.•In ACHM a localized thickening in the area of V1 that repres...
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| Published in: | NeuroImage clinical Vol. 33; p. 102925 |
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| Language: | English |
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| ISSN: | 2213-1582, 2213-1582 |
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| Abstract | •Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM).•Reduction in cortical surface area in foveal, parafoveal and paracentral representations of V1 in those with ACHM.•In ACHM a localized thickening in the area of V1 that represents the region of retina occupied solely by cones.•V1 changes in ACHM may limit its ability to take on normal properties if retinal function were to be restored.•Early intervention, before the development plastic period is over, may offer better restoration of vision in ACHM.
Autosomal recessive Achromatopsia (ACHM) is a rare inherited disorder associated with dysfunctional cone photoreceptors resulting in a congenital absence of cone input to visual cortex. This might lead to distinct changes in cortical architecture with a negative impact on the success of gene augmentation therapies. To investigate the status of the visual cortex in these patients, we performed a multi-centre study focusing on the cortical structure of regions that normally receive predominantly cone input. Using high-resolution T1-weighted MRI scans and surface-based morphometry, we compared cortical thickness, surface area and grey matter volume in foveal, parafoveal and paracentral representations of primary visual cortex in 15 individuals with ACHM and 42 normally sighted, healthy controls (HC). In ACHM, surface area was reduced in all tested representations, while thickening of the cortex was found highly localized to the most central representation. These results were comparable to more widespread changes in brain structure reported in congenitally blind individuals, suggesting similar developmental processes, i.e., irrespective of the underlying cause and extent of vision loss. The cortical differences we report here could limit the success of treatment of ACHM in adulthood. Interventions earlier in life when cortical structure is not different from normal would likely offer better visual outcomes for those with ACHM. |
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| AbstractList | Autosomal recessive Achromatopsia (ACHM) is a rare inherited disorder associated with dysfunctional cone photoreceptors resulting in a congenital absence of cone input to visual cortex. This might lead to distinct changes in cortical architecture with a negative impact on the success of gene augmentation therapies. To investigate the status of the visual cortex in these patients, we performed a multi-centre study focusing on the cortical structure of regions that normally receive predominantly cone input. Using high-resolution T1-weighted MRI scans and surface-based morphometry, we compared cortical thickness, surface area and grey matter volume in foveal, parafoveal and paracentral representations of primary visual cortex in 15 individuals with ACHM and 42 normally sighted, healthy controls (HC). In ACHM, surface area was reduced in all tested representations, while thickening of the cortex was found highly localized to the most central representation. These results were comparable to more widespread changes in brain structure reported in congenitally blind individuals, suggesting similar developmental processes, i.e., irrespective of the underlying cause and extent of vision loss. The cortical differences we report here could limit the success of treatment of ACHM in adulthood. Interventions earlier in life when cortical structure is not different from normal would likely offer better visual outcomes for those with ACHM. •Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM).•Reduction in cortical surface area in foveal, parafoveal and paracentral representations of V1 in those with ACHM.•In ACHM a localized thickening in the area of V1 that represents the region of retina occupied solely by cones.•V1 changes in ACHM may limit its ability to take on normal properties if retinal function were to be restored.•Early intervention, before the development plastic period is over, may offer better restoration of vision in ACHM. Autosomal recessive Achromatopsia (ACHM) is a rare inherited disorder associated with dysfunctional cone photoreceptors resulting in a congenital absence of cone input to visual cortex. This might lead to distinct changes in cortical architecture with a negative impact on the success of gene augmentation therapies. To investigate the status of the visual cortex in these patients, we performed a multi-centre study focusing on the cortical structure of regions that normally receive predominantly cone input. Using high-resolution T1-weighted MRI scans and surface-based morphometry, we compared cortical thickness, surface area and grey matter volume in foveal, parafoveal and paracentral representations of primary visual cortex in 15 individuals with ACHM and 42 normally sighted, healthy controls (HC). In ACHM, surface area was reduced in all tested representations, while thickening of the cortex was found highly localized to the most central representation. These results were comparable to more widespread changes in brain structure reported in congenitally blind individuals, suggesting similar developmental processes, i.e., irrespective of the underlying cause and extent of vision loss. The cortical differences we report here could limit the success of treatment of ACHM in adulthood. Interventions earlier in life when cortical structure is not different from normal would likely offer better visual outcomes for those with ACHM. Autosomal recessive Achromatopsia (ACHM) is a rare inherited disorder associated with dysfunctional cone photoreceptors resulting in a congenital absence of cone input to visual cortex. This might lead to distinct changes in cortical architecture with a negative impact on the success of gene augmentation therapies. To investigate the status of the visual cortex in these patients, we performed a multi-centre study focusing on the cortical structure of regions that normally receive predominantly cone input. Using high-resolution T1-weighted MRI scans and surface-based morphometry, we compared cortical thickness, surface area and grey matter volume in foveal, parafoveal and paracentral representations of primary visual cortex in 15 individuals with ACHM and 42 normally sighted, healthy controls (HC). In ACHM, surface area was reduced in all tested representations, while thickening of the cortex was found highly localized to the most central representation. These results were comparable to more widespread changes in brain structure reported in congenitally blind individuals, suggesting similar developmental processes, i.e., irrespective of the underlying cause and extent of vision loss. The cortical differences we report here could limit the success of treatment of ACHM in adulthood. Interventions earlier in life when cortical structure is not different from normal would likely offer better visual outcomes for those with ACHM.Autosomal recessive Achromatopsia (ACHM) is a rare inherited disorder associated with dysfunctional cone photoreceptors resulting in a congenital absence of cone input to visual cortex. This might lead to distinct changes in cortical architecture with a negative impact on the success of gene augmentation therapies. To investigate the status of the visual cortex in these patients, we performed a multi-centre study focusing on the cortical structure of regions that normally receive predominantly cone input. Using high-resolution T1-weighted MRI scans and surface-based morphometry, we compared cortical thickness, surface area and grey matter volume in foveal, parafoveal and paracentral representations of primary visual cortex in 15 individuals with ACHM and 42 normally sighted, healthy controls (HC). In ACHM, surface area was reduced in all tested representations, while thickening of the cortex was found highly localized to the most central representation. These results were comparable to more widespread changes in brain structure reported in congenitally blind individuals, suggesting similar developmental processes, i.e., irrespective of the underlying cause and extent of vision loss. The cortical differences we report here could limit the success of treatment of ACHM in adulthood. Interventions earlier in life when cortical structure is not different from normal would likely offer better visual outcomes for those with ACHM. Highlights•Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM). •Reduction in cortical surface area in foveal, parafoveal and paracentral representations of V1 in those with ACHM. •In ACHM a localized thickening in the area of V1 that represents the region of retina occupied solely by cones. •V1 changes in ACHM may limit its ability to take on normal properties if retinal function were to be restored. •Early intervention, before the development plastic period is over, may offer better restoration of vision in ACHM. • Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM). • Reduction in cortical surface area in foveal, parafoveal and paracentral representations of V1 in those with ACHM. • In ACHM a localized thickening in the area of V1 that represents the region of retina occupied solely by cones. • V1 changes in ACHM may limit its ability to take on normal properties if retinal function were to be restored. • Early intervention, before the development plastic period is over, may offer better restoration of vision in ACHM. Autosomal recessive Achromatopsia (ACHM) is a rare inherited disorder associated with dysfunctional cone photoreceptors resulting in a congenital absence of cone input to visual cortex. This might lead to distinct changes in cortical architecture with a negative impact on the success of gene augmentation therapies. To investigate the status of the visual cortex in these patients, we performed a multi-centre study focusing on the cortical structure of regions that normally receive predominantly cone input. Using high-resolution T1-weighted MRI scans and surface-based morphometry, we compared cortical thickness, surface area and grey matter volume in foveal, parafoveal and paracentral representations of primary visual cortex in 15 individuals with ACHM and 42 normally sighted, healthy controls (HC). In ACHM, surface area was reduced in all tested representations, while thickening of the cortex was found highly localized to the most central representation. These results were comparable to more widespread changes in brain structure reported in congenitally blind individuals, suggesting similar developmental processes, i.e., irrespective of the underlying cause and extent of vision loss. The cortical differences we report here could limit the success of treatment of ACHM in adulthood. Interventions earlier in life when cortical structure is not different from normal would likely offer better visual outcomes for those with ACHM. |
| ArticleNumber | 102925 |
| Author | Herbik, Anne Hoffmann, Michael B. Morland, Antony B. Käsmann-Kellner, Barbara Raz, Noa Gouws, Andre D. McLean, Rebecca J. Maguire, John Ahmadi, Khazar de Best, Pieter B. Baseler, Heidi A. Choritz, Lars Molz, Barbara Wieland, Ilse Banin, Eyal Lowndes, Rebecca Levin, Netta Vernon, Richard W. Kohl, Susanne Kanowski, Martin Gottlob, Irene |
| Author_xml | – sequence: 1 givenname: Barbara surname: Molz fullname: Molz, Barbara organization: Department of Psychology, University of York, Heslington, YO10 5DD York, United Kingdom – sequence: 2 givenname: Anne surname: Herbik fullname: Herbik, Anne organization: Department of Ophthalmology, University Hospital, Otto-von-Guericke University, 39120 Magdeburg, Germany – sequence: 3 givenname: Heidi A. surname: Baseler fullname: Baseler, Heidi A. organization: Department of Psychology, University of York, Heslington, YO10 5DD York, United Kingdom – sequence: 4 givenname: Pieter B. surname: de Best fullname: de Best, Pieter B. organization: MRI Unit, Department of Neurology, Hadassah Medical Center, 91120 Jerusalem, Israel – sequence: 5 givenname: Richard W. surname: Vernon fullname: Vernon, Richard W. organization: Department of Psychology, University of York, Heslington, YO10 5DD York, United Kingdom – sequence: 6 givenname: Noa surname: Raz fullname: Raz, Noa organization: MRI Unit, Department of Neurology, Hadassah Medical Center, 91120 Jerusalem, Israel – sequence: 7 givenname: Andre D. surname: Gouws fullname: Gouws, Andre D. organization: York Neuroimaging Centre, Department of Psychology, University of York, YO10 5NY York, United Kingdom – sequence: 8 givenname: Khazar surname: Ahmadi fullname: Ahmadi, Khazar organization: Department of Ophthalmology, University Hospital, Otto-von-Guericke University, 39120 Magdeburg, Germany – sequence: 9 givenname: Rebecca surname: Lowndes fullname: Lowndes, Rebecca organization: York Neuroimaging Centre, Department of Psychology, University of York, YO10 5NY York, United Kingdom – sequence: 10 givenname: Rebecca J. surname: McLean fullname: McLean, Rebecca J. organization: University of Leicester Ulverscroft Eye Unit, University of Leicester, Leicester Royal Infirmary, LE2 7LX Leicester, United Kingdom – sequence: 11 givenname: Irene surname: Gottlob fullname: Gottlob, Irene organization: University of Leicester Ulverscroft Eye Unit, University of Leicester, Leicester Royal Infirmary, LE2 7LX Leicester, United Kingdom – sequence: 12 givenname: Susanne surname: Kohl fullname: Kohl, Susanne organization: Molecular Genetics Laboratory, Institute for Ophthalmic Research, Centre for Ophthalmology, University Clinics Tübingen, 72076 Tübingen, Germany – sequence: 13 givenname: Lars surname: Choritz fullname: Choritz, Lars organization: Department of Ophthalmology, University Hospital, Otto-von-Guericke University, 39120 Magdeburg, Germany – sequence: 14 givenname: John surname: Maguire fullname: Maguire, John organization: School of Optometry and Vision Sciences, University of Bradford, BD7 1DP Bradford, United Kingdom – sequence: 15 givenname: Martin surname: Kanowski fullname: Kanowski, Martin organization: Department of Neurology, University Hospital, Otto-von-Guericke University, 39120 Magdeburg, Germany – sequence: 16 givenname: Barbara surname: Käsmann-Kellner fullname: Käsmann-Kellner, Barbara organization: Department of Ophthalmology, Saarland University Hospital and Medical Faculty of the Saarland University, 66421 Homburg, Germany – sequence: 17 givenname: Ilse surname: Wieland fullname: Wieland, Ilse organization: Department for Molecular Genetics, Institute for Human Genetics, University Hospital, Otto-von-Guericke University, 39120 Magdeburg, Germany – sequence: 18 givenname: Eyal surname: Banin fullname: Banin, Eyal organization: Degenerative Diseases of the Retina Unit, Department of Ophthalmology, Hadassah Medical Center, 91120 Jerusalem, Israel – sequence: 19 givenname: Netta surname: Levin fullname: Levin, Netta organization: MRI Unit, Department of Neurology, Hadassah Medical Center, 91120 Jerusalem, Israel – sequence: 20 givenname: Michael B. surname: Hoffmann fullname: Hoffmann, Michael B. organization: Department of Ophthalmology, University Hospital, Otto-von-Guericke University, 39120 Magdeburg, Germany – sequence: 21 givenname: Antony B. surname: Morland fullname: Morland, Antony B. email: antony.morland@york.ac.uk organization: Department of Psychology, University of York, Heslington, YO10 5DD York, United Kingdom |
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| Keywords | Primary visual cortex Surface-based morphology sMRI Achromatopsia Plasticity |
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| Snippet | •Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM).•Reduction in cortical surface area... Highlights•Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM). •Reduction in cortical... Autosomal recessive Achromatopsia (ACHM) is a rare inherited disorder associated with dysfunctional cone photoreceptors resulting in a congenital absence of... • Anatomy of primary visual cortex (V1) assessed with surface-based morphmetry in those with congenital achromatopsia (ACHM). • Reduction in cortical surface... |
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| SubjectTerms | Achromatopsia Adult Color Vision Defects - congenital Color Vision Defects - diagnostic imaging Color Vision Defects - genetics Fovea Centralis Humans Plasticity Primary Visual Cortex Radiology Regular Retinal Cone Photoreceptor Cells sMRI Surface-based morphology Visual Cortex - diagnostic imaging |
| Title | Structural changes to primary visual cortex in the congenital absence of cone input in achromatopsia |
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