China
Africa
Explore chapters and articles related to this topic
Cortical Visual Loss
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
The lateral geniculate nucleus is the terminus of the optic tract, whose fibers synapse in this nucleus with the neurons that give rise to the optic radiations. This nucleus is located in the ventro-postero-lateral thalamus. It has a retinotopic organization: the macula is represented in a dorsal wedge and the far periphery is ventral, while the inferior quadrant is medial and the superior is lateral. Two arteries supply it. The lateral choroidal artery, a branch of the posterior cerebral artery, supplies the middle zone (20) while the anterior choroidal artery, a branch of the internal carotid artery, supplies its medial and lateral aspects (21, 22). This blood supply is reflected in the classic hemifield defects from partial destruction of the lateral geniculate nucleus. A lateral posterior choroidal artery stroke causes a sectoranopia (Figure 20.3a), a wedge-shaped defect emanating from the central field that straddles the horizontal meridian (20). An anterior choroidal artery stroke produces an inverse sectoranopia (Figure 20.3b), defects adjacent to the vertical meridian in the upper and lower field that spare the zone around the horizontal meridian (21–23). Ultimately, the patient will develop a subtle partial optic atrophy, but the pupil light reflexes are normal.
Disruptions in physical substrates of vision following traumatic brain injury
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
The diencephalon is the brain region above the brain stem, and it sits deep in the midline between the cerebral hemispheres. It has two major components: the thalamus and the hypothalamus. The thalamus gates sensory input to the cerebral hemispheres and is vital for processing of the attentional system. Pertinent visually related subcortical nuclei located in the thalamus are the pulvinar and the lateral geniculate body (LGN). The pulvinar occupies 40% of the thalamic volume, is located in the posterior portion, and is considered an association nucleus involved in complex visual function. The lateral pulvinar is linked with the posterior parietal, superior temporal, and medial and dorsolateral extrastriate cortices8 as well as the superior colliculus.9 It plays a role in orientation and processing visual information in the dorsal stream. The inferior pulvinar is linked with temporal lobe areas concerned with visual feature discrimination and extrastriate areas concerned with higher analysis of vision. It also receives visual input from the superior colliculus9 in addition to direct input from the retinal ganglion cells.8 The LGN is the other thalamic visually related nucleus that is part of the afferent system. The LGN also receives projections back from cortical-related visual areas, indicating that higher cortical processing can influence visual perception at an earlier level.
Plasticity of Visual Cortex in Adult Primates
Published in Jon H. Kaas, Christine E. Collins, The Primate Visual System, 2003
Christine E. Collins, Jon H. Kaas
of each of the lateral geniculate nucleus layers that receive input from that eye. In cats, this would involve one of the two “A” layers, and one or more of the “C” layers, while in monkeys a monocular lesion would involve one of the two complete parvocellular layers (and its sublayers), one of the two magnocellular layers, and zones of koniocellular inputs. For simplicity, these layers for each eye are depicted in Figure 7.1 as a single layer, and the single layers for each eye are shown as adjacent rather than stacked, as they are in the lateral geniculate nucleus (LGN). The two layers (e.g., sets of layers) then project in matching patterns to primary visual cortex, V1. A monocular lesion obviously deprives each set of monocular LGN layers of all visual activation in a portion of the retinotopic map corresponding to the lesion, while the equivalent part of V1 is deprived of activation from only one eye. Obviously, the converging inputs from undeprived geniculate layers can compensate for the missing inputs. Matching lesions of both retinas, however, totally deprive both portions of LGN layers and a portion of V1. The basic experimental question addressed in the studies in cats and monkeys is what happens to the deprived neurons in the LGN and V1 after retinal lesions?
Can pattern electroretinography be a relevant diagnostic aid in amblyopia? – A systematic review
Published in Seminars in Ophthalmology, 2022
Andresa Fernandes, Nuno Pinto, Ana Rita Tuna, Francisco Miguel Brardo, Maria Vaz Pato
In animal studies, Yin ZQ et al.34 showed that changes in the visual cortex of amblyopic cats were physiologically related to changes in retinal cells. Heravian et al., de Souza Lima et al. and Parisi et al.8,9,32 justify the changes observed in PERG responses with changes in the functionality of neurotransmitters that occur in amblyopic eyes. According to these authors, the cells of the lateral geniculate nucleus that receive signals from the amblyopic eye are smaller and weaker when compared to the same cells of the normal eye. Allen B. et al. and Szigeti A. et al.35,36 also believe that the weaker signal produced by retinal cells may be associated with microstructural abnormalities that may depend on the depth of amblyopia. The functional loss of the LGN cells can be due to a weaker stimulus coming from the cells present in the retinal area, during the critical phase of the development of the visual system.10
Impact of Alzheimer’s Disease in Ocular Motility and Visual Perception: A Narrative Review
Published in Seminars in Ophthalmology, 2022
Visual fields can be also affected in AD. Specifically, a loss of visual field related to damage to lateral geniculate nucleus in the upper quadrant of the corresponding retina, as well as to the accumulation of amyloid-Aℬ substances has been described.26,43 This type of visual loss mainly affects the lower quadrant of the visual field,26,65 although it also involves the central field.65 Likewise, significant reductions in global sensitivity have also been described.43,65 Most of the AD patients exhibit a progression of the visual field loss during the course of the disease, and consequently patients with more severe dementia show greater reductions in visual sensitivity.65 Other more complex visual field defects have been reported in some cases of AD, but they are less common and associated with degenerative changes in the primary visual cortex.51 One example of this is the presence of hemispatial neglect and homonymous hemianopsia with macular sparing51 or constriction of peripheral visual fields with depressed flicker fusion frequencies.71
The Effect of Congenital and Acquired Bilateral Anophthalmia on Brain Structure
Published in Neuro-Ophthalmology, 2021
Holly Bridge, Gaelle S. L. Coullon, Rupal Morjaria, Rebecca Trossman, Catherine E Warnaby, Brian Leatherbarrow, Russell G. Foster, Susan M. Downes
Structural brain changes due to both congenital and acquired blindness have been described in grey and white matter. Grey matter atrophy (up to 20–25%) has been noted in primary ‘visual’ areas1,2 and extra-striate regions2 in early blind individuals compared with sighted controls. Reduced white matter volume and fractional anisotropy (FA) were found in the optic chiasm, optic nerves, and optic radiations, as well as regions of the occipital lobe and corpus callosum1,2 in congenital and early-onset blindness, although the global organisation of the splenium remains unchanged.3 While there is considerable variability in the patterns of structural brain changes in blindness, some features are consistently present. This has been investigated in a large group (n > 50) of blind participants with different underlying causes, who showed consistent reduction in lateral geniculate nucleus (LGN) and V1 volume and increase in V1 cortical thickness. Furthermore, white matter microstructure within the optic radiation also showed abnormalities across the blind participants.4 However, although these differences are consistent across congenital and acquired blindness, they are likely to result from different plastic processes; altered development in the former case and degeneration in the latter.