Retinal Thickness and P-ERG Changes in Adult Patients With Anisometropic and Strabismic Amblyopia

Objective To investigate the changes of retinal thickness and P-ERG signals in adult patients with anisometropic and strabismic amblyopia. Methods Sixty patients with monocular adult amblyopia, including 30 anisometropic amblyopes (AA group) and 30 strabismic amblyopes (SA group), were enrolled in our study at the outpatient clinic of The Hefei First People’s Hospital Hospital of Anhui medical University from June 2019 to November 2020. Retinal nerve fiber layer (RNFL) thickness was measured within 3.4 mm diameter range surrounding the optic nerve, and ganglion cell complex (GCC) layer thickness within 6 mm diameter range surrounding the fovea by an Optovue RTVue OCT in both amblyopic and fellow eyes. The amplitude and latency of P50 and N95 in P-ERG were recorded by a Roland electrophysiology instrument under two stimulation conditions with different temporal and spatial frequencies that were designed to bias the parvocellular and magnocellular pathways respectively. Data between amblyopic and fellow eyes was statistically analyzed by paired t test. The correlation between axial length and parameters of OCT and P-ERG was examined by Pearson correlation test. Results (1) Changes in RNFL thickness: In the AA group, RNFL thickness in temporal sector was significantly thinner (p = 0.033), while that in the nasal, superior and inferior sectors increased (p < 0.05) compared with fellow eyes. In SA group, no significant difference (each sector p > 0.05) was found between amblyopic eyes and fellow eyes. (2) Changes in GCC thickness: Compared with fellow eyes, in the AA group, GCC layer thickness of amblyopic eyes was significantly increased (p = 0.039), whereas in the SA group, we did not find a significant difference between amblyopic eyes and fellow eyes (p > 0.05). (3) P-ERG stimulated mode biased the parvocellular pathway: When compared with fellow eyes (n = 15), in the AA group, the amplitudes of P50 (p = 0.004) and N95 (p = 0.038) were significantly decreased in amblyopic eyes, but no significant latent time difference (p > 0.05) was found. In the same stimulus pattern, no statistically significant difference (n = 15, p > 0.05) between amblyopic eyes and fellow eyes was found in the amplitude and latency of P50 and N95 in the SA group. (4) P-ERG stimulated mode biased the magnocellular pathway: The amplitude and latency of P50 and N95 showed no statistically significant difference (p > 0.05) in either the AA group or the SA group. (5) We found no significant correlation between axial length and OCT, P-ERG parameters (p > 0.05) in either group. Conclusion Our results showed that the alterations in structure and function of retina that could be seen in adult anisometropic amblyopia were not found in adult strabismic amblyopia group. The functional loss in anisometropic amblyopia was found to bias to a damage of partial ganglion cells by the parvocellular pathway. These findings indicated that the pathological mechanisms were different between anisometropic and strabismic amblyopia.

Using perceptual tasks to selectively measure magnocellular and parvocellular performance: Rationale and a user’s guide

The visual system uses parallel pathways to process information. However, an ongoing debate centers on the extent to which the pathways from the retina, via the Lateral Geniculate nucleus to the visual cortex, process distinct aspects of the visual scene and, if they do, can stimuli in the laboratory be used to selectively drive them. These questions are important for a number of reasons, including that some pathologies are thought to be associated with impaired functioning of one of these pathways and certain cognitive functions have been preferentially linked to specific pathways. Here we examine the two main pathways that have been the focus of this debate: the magnocellular and parvocellular pathways. Specifically, we review the results of electrophysiological and lesion studies that have investigated their properties and conclude that while there is substantial overlap in the type of information that they process, it is possible to identify aspects of visual information that are predominantly processed by either the magnocellular or parvocellular pathway. We then discuss the types of visual stimuli that can be used to preferentially drive these pathways.

Layer-specific Loss and Compensation of Parvocellular Response in Subcortical Pathways of Adult Human Amblyopia

Abnormal visual experience in critical period causes amblyopia or lazy eye, reducing visual abilities even with corrected optics. A long-standing question is where in the human visual system does the amblyopic deficit arise. In particular, whether amblyopia induces selective deficits of the magnocellular (M) or the parvocellular (P) geniculostriate pathways, and whether the more ancient retinotectal pathway is also affected. Technical limitations to non-invasively measure layer-specific activity in human lateral geniculate nucleus (LGN) and superior colliculus (SC) hampered efforts in addressing these questions. In the current study, using lamina-resolved 3T and 7T fMRI and visual stimuli selectively activating the M and P pathways, we investigated layer-specific response properties of the LGN and the SC of amblyopia patients and normal controls. With stimuli presented to the amblyopic eye, there was a stronger response loss in the P layers than in the M layers of the LGN. Compared to normal controls, amblyopic eye’s response to the P stimulus was selectively reduced in the superficial SC, while the fellow eye’s response was robustly increased in the deep SC. Selective P response deficits of amblyopia were also observed in the visual pulvinar, early visual cortex, and ventral but not dorsal visual streams. These results provide strong in vivo evidence in adult amblyopic patients for selective deficits of parvocellular functions in the visual thalamus, and additionally reveal response deficits to the amblyopic eye and neural compensation to the fellow eye in the retinotectal pathway.HighlightsParvocellular response loss in the LGN P layers, visual pulvinar and ventral visual streamSelective amblyopic deficits of the parvocellular pathwayAmblyopic eye’s response decreased in the superficial SCFellow eye’s response increased in the deep SCAmblyopic deficits and neural compensation in the retinotectal pathway

The Functional Field of View of Older Adults is Associated With Contrast Discrimination in the Magnocellular not Parvocellular Pathway

Objectives As we age, the functional field of view (FFOV) declines and these declines predict falls and motor vehicle accidents in older adults (Owsley, C. (2013). Visual processing speed. Vision Research, 90, 52–56. doi:10.1016/j.visres.2012.11.014). To increase understanding of possible causes of this decline, the current study explored whether the FFOV in older adults is associated with the sensitivity of the magnocellular and parvocellular sub-cortical pathways. Method Forty-four younger (M = 27.18, SD = 5.40 years) and 44 older (M = 72.18, SD = 5.82 years) adults completed an FFOV test and the steady- and pulsed-pedestal paradigms of Pokorny and Smith (Pokorny, J., & Smith, V. C. (1997). Psychophysical signatures associated with magnocellular and parvocellular pathway contrast gain. Journal of the Optical Society of America. A, Optics, Image Science, and Vision, 14, 2477–2486. doi:10.1364/josaa.14.002477) as measures of magnocellular and parvocellular pathways, respectively. Results Older adults made more FFOV errors and had higher contrast discrimination thresholds in both the steady- and pulsed-pedestal paradigms, than younger adults. FFOV errors in the younger group were not related to contrast discrimination thresholds. In multiple regression, older group FFOV errors showed a strong unique association with contrast discrimination thresholds mediated via the magnocellular, but not the parvocellular pathway. Discussion We infer that reduced magnocellular pathway contrast sensitivity may contribute to reduced functional vision in older adults.

A Neuronal Network Model of the Primate Visual System: Color Mechanisms in the Retina, LGN and V1

Color plays a key role in human vision but the neural machinery that underlies the transformation from stimulus to perception is not well understood. Here, we implemented a two-dimensional network model of the first stages in the primate parvocellular pathway (retina, lateral geniculate nucleus and layer 4C[Formula: see text] in V1) consisting of conductance-based point neurons. Model parameters were tuned based on physiological and anatomical data from the primate foveal and parafoveal vision, the most relevant visual field areas for color vision. We exhaustively benchmarked the model against well-established chromatic and achromatic visual stimuli, showing spatial and temporal responses of the model to disk- and ring-shaped light flashes, spatially uniform squares and sine-wave gratings of varying spatial frequency. The spatiotemporal patterns of parvocellular cells and cortical cells are consistent with their classification into chromatically single-opponent and double-opponent groups, and nonopponent cells selective for luminance stimuli. The model was implemented in the widely used neural simulation tool NEST and released as open source software. The aim of our modeling is to provide a biologically realistic framework within which a broad range of neuronal interactions can be examined at several different levels, with a focus on understanding how color information is processed.

Spatial summation of individual cones in human color vision

The human retina contains three classes of cone photoreceptors each sensitive to different portions of the visual spectrum: long (L), medium (M) and short (S) wavelengths. Color information is computed by downstream neurons that compare relative activity across the three cone types. How cone signals are combined at a cellular scale has been more difficult to resolve. This is especially true near the fovea, where spectrally-opponent neurons in the parvocellular pathway draw excitatory input from a single cone and thus even the smallest stimulus will engage multiple color-signaling neurons. We used an adaptive optics microstimulator to target individual and pairs of cones with light. Consistent with prior work, we found that color percepts elicited from individual cones were predicted by their spectral sensitivity, although there was considerable variability even between cones within the same spectral class. The appearance of spots targeted at two cones were predicted by an average of their individual activations. However, two cones of the same subclass elicited percepts that were systematically more saturated than predicted by an average. Together, these observations suggest both spectral opponency and prior experience influence the appearance of small spots.

Response to short-term deprivation of the human adult visual cortex measured with 7T BOLD

Sensory deprivation during the post-natal ‘critical period’ leads to structural reorganization of the developing visual cortex. In adulthood, the visual cortex retains some flexibility and adapts to sensory deprivation. Here we show that short-term (2 hr) monocular deprivation in adult humans boosts the BOLD response to the deprived eye, changing ocular dominance of V1 vertices, consistent with homeostatic plasticity. The boost is strongest in V1, present in V2, V3 and V4 but absent in V3a and hMT+. Assessment of spatial frequency tuning in V1 by a population Receptive-Field technique shows that deprivation primarily boosts high spatial frequencies, consistent with a primary involvement of the parvocellular pathway. Crucially, the V1 deprivation effect correlates across participants with the perceptual increase of the deprived eye dominance assessed with binocular rivalry, suggesting a common origin. Our results demonstrate that visual cortex, particularly the ventral pathway, retains a high potential for homeostatic plasticity in the human adult.

Short-term plasticity of the human adult visual cortex measured with 7T BOLD

Visual cortex, particularly V1, is considered to be resilient to plastic changes in adults. In particular, ocular dominance is assumed to be hard-wired after the end of the critical period. We show that short-term (2h) monocular deprivation in adult humans boosts the BOLD response to the deprived eye, changing ocular dominance of V1 vertices, consistently with homeostatic plasticity. The boost is strongest in V1, present in V2, V3 & V4 but absent in V3a and MT. Assessment of spatial frequency tuning in V1 by a population Receptive-Field technique shows that deprivation primarily boosts high spatial frequencies, consistent with a primary involvement of the parvocellular pathway. Crucially, the V1 deprivation effect correlates across participants with the perceptual increase of the deprived eye dominance assessed with binocular rivalry, suggesting a common origin. Our results demonstrate that visual cortex, particularly the ventral pathway, retains a high potential for homeostatic plasticity in the human adult.