Cognitive Neuroscience Research PDF

02 February 2024 21:51 Source Notes Is the Cortical Deficit in Amblyopia Due to Reduced Cortical Magnification, Loss of Neural Resolution, or Neural Disorganization? 1. Cortical Magnification in Amblyopic Monocular Elevation (AME) Representation: The study finds no support for the view that cortical...

02 February 2024 21:51 Source Notes Is the Cortical Deficit in Amblyopia Due to Reduced Cortical Magnification, Loss of Neural Resolution, or Neural Disorganization? 1. Cortical Magnification in Amblyopic Monocular Elevation (AME) Representation: The study finds no support for the view that cortical magnification is reduced in AME’s representation, challenging a current explanation for reduced spatial positional sensitivity in amblyopia. Contrary to some views, reduced resolution, vernier acuity, and increased positional uncertainty in amblyopia cannot be solely attributed to the AME driving fewer cells, especially in the foveal representation of early cortical areas. (Clavagnier et al., 2015) 2. Loss of Spatial Resolution of Cells and Receptive Field Size: The study shows that Population Receptive Field (pRF) sizes are generally enlarged for the AME representation in areas V1, V2, and V3. This enlargement is not consistent across all amblyopes, and there's no strong correlation between the extent of foveal receptive field enlargement and the behavioral acuity deficit. Potential explanations for enlarged pRFs include unsteady eye movements in the AME (ruled out in this study), increased positional scatter of receptive fields contributing to the pRF, and a reduced contribution from smaller receptive fields for AME input. The study also notes that fewer voxels survived the thresholding criterion for the AME, indicating possible reasons like fewer neurons contributing to the fMRI signal or more neurons with a lower signal-to-noise ratio. 3. Topological Cortical Map Disordering in AME Projection: The study supports the view that there is more variability in the positions of pRFs in the AME. This positional anomaly extends beyond area V1 into areas V2 and V3. The study challenges the idea that amblyopia can be explained solely in terms of V1 processing, indicating that extrastriate processing is also affected, leading to additional processing anomalies in areas V2 and V3. Results suggest that anomalies found in V1 are not merely reflected in later areas, and additional processing deficits occur in V2 and V3. 4. Methodological Considerations: The study relied on a single Gaussian model for the pRF, biased towards excitatory feedforward processing. Attempts to model data with a Difference-of-Gaussian (DoG) model for estimating surround inhibitory effects were not optimal due to the focus on foveal processing and restricted field size. Future studies are suggested to use conditions more conducive to deriving estimates of surround inhibition for better evaluation of feedback processing. 5. Summary: Comparing projections from amblyopic and fellow normal eyes of amblyopes with those of normal observers, the study concludes that the projection from the AME has a normal Cortical Magnification Factor (CMF) in all early visual areas, enlarged pRF sizes in striate and extrastriate cortex, and more topographic disorder in extrastriate areas. These findings are consistent with an explanation based on a normal complement of cells whose spatial resolution is reduced and whose topographical map is disordered. Results 1. pRF Sizes in the AME: ○ The study found significant differences in pRF sizes between the AME and FFE in areas V1 and V2, but not in V3. ○ In V1, pRF sizes were estimated to be larger in AME compared to FFE, indicating a notable difference in the receptive field size. 2. Variability in Eye Movements: ○ No significant correlation was found between the variability of eye positions and the size of the pRFs, suggesting that the enlarged pRF sizes in the AME cannot be attributed to poorer fixation capacity. 3. Cortical Magnification Factor (CMF): ○ The study found that CMF decreases with visual field eccentricity, but there was no significant difference in the CMF between the fellow eye and the AME in amblyopes. This suggests that the CMF is normal in the AME. 4. pRF Sizes in Extrastriate Areas (V2 and V3): ○ The differences found in V2 and V3 in the AME-derived and FFE-derived models suggest that later visual areas cannot simply derive their visual representation from early visual areas (V1). This implies additional processing anomalies in these areas. 5. Intra-Areal Cortical Topography: ○ The study observed high topological correspondence of pRF positions between fixing and AME within area V1. However, there was more variability in the amblyopes, particularly in V2 and V3, indicating a discrepancy in the topological fidelity of the maps. 6. Feedforward and Feedback Processing: ○ The study’s reliance on a single Gaussian model for the pRF indicates a bias toward excitatory feedforward processing. The study acknowledges the limitations in assessing feedback processing, suggesting that future studies should focus on conditions conducive to estimating surround inhibition. 6. Summary and Conclusions: The study concludes that the projection from the AME exhibits normal CMF, enlarged pRF sizes in striate and extrastriate cortex, and more topographic disorder in extrastriate areas. These findings support the idea of a normal complement of cells in amblyopia but with reduced spatial resolution and disordered topographical mapping. 7. Critical Analysis - Methodological Considerations: The study's methodology, particularly the use of a single Gaussian model for pRF, might have limited its ability to fully capture the complexities of neural processing in amblyopia, such as inhibitory interactions and feedback mechanisms. 8. Critical Analysis - Implications for Amblyopia Understanding: This research provides valuable insights into the neural underpinnings of amblyopia, challenging some traditional views and suggesting a more complex involvement of both striate and extrastriate visual areas. 9. Critical Analysis - Future Directions: The findings pave the way for future research to explore the precise mechanisms behind the enlarged pRFs and the topographic disorganization, as well as to develop more targeted treatments that consider these neural anomalies. Steady-State Contrast Response Functions Provide a Sensitive and Objective Index of Amblyopic Deficits (Baker et al., 2015) Background/Introduction 1. Amblyopia Definition: Loss of visual sensitivity in one eye, primarily neural, affecting visual acuity and contrast sensitivi ty. 2. New Treatment Methods: Recent methods go beyond traditional patching, including perceptual learning and game -based methods. 3. Need for Objective Measures: Current evaluations mostly rely on psychophysical tasks, which may be biased. Objective measures like fMRI are expensive and not widely available. 4. Electroencephalography (EEG) as an Alternative: EEG provides an affordable, objective measure of neural activity. 5. Steady-State Visual Evoked Potentials (SSVEPs): SSVEPs measure responses to flickering stimuli and offer a comprehensive picture of amblyopic deficits. Methods 6. Participants: Study involved 10 amblyopic and 5 control observers. 7. Stimuli: Static white noise patches with varying contrasts presented via virtual reality goggles. 8. SSVEP Measurement: EEG signals recorded to measure SSVEPs. 9. Procedure: Participants viewed targets at different contrasts, with or without a dichoptic mask. 10. Data Normalization and Analysis: EEG data normalized and analyzed for amplitude and phase variance. Results 11. Contrast Response Functions: In amblyopic eyes, responses were much weaker and shallower in slope. 12. Effect of Dichoptic Masking: Less suppression observed in amblyopes compared to controls. 13. Neural and Visual Acuity Correlation: Strong correlation between EEG amplitude ratios and visual acuity ratios. 14. Model Verification: Results partially confirmed the model's predictions about amblyopia. 15. Phase Variance: Increased phase variance in amblyopic stimulation, indicating less coherent neural responses. Discussion and Critical Analysis 16. Model Predictions and Results: Amblyopic eye showed reduced responses, confirming model predictions, but suppression effects from dichoptic masks were not as expected. 17. Implications for Amblyopia Understanding: Findings suggest more complex interocular interactions than previously thought, cha llenging assumptions about strong suppression from the fellow eye. 18. Potential Causes of Signal Reduction: Could be due to reduced synchronization of neural firing in the amblyopic eye. 19. Importance of EEG in Clinical Context: Offers a less expensive, more accessible method for monitoring amblyopia and its treat ment. 20. Study Limitations: Dichoptic masking effects were weaker than expected; future studies may explore this further. Summary Baker et al. (2015) provide a comprehensive analysis of amblyopic deficits using SSVEPs, revealing significant insights into the neural basis of amblyopia. Their findings challenge some traditional views, particularly regarding interocular suppression. The study underscores the potential of EEG as an objective, accessible tool for monitoring amblyopia and evaluating treatment efficacy. Neuroimaging of amblyopia and binocular vision: a review (Joly & Frankó) Background/Introduction: 1. Amblyopia Definition: A visual impairment stemming from abnormal visual experiences like strabismus or anisometropia. 2. Visual Acuity and Amblyopia: Characterized by a significant reduction in best -corrected visual acuity, not attributed to structural eye abnormalities. 3. Types of Amblyopia: Strabismic amblyopia leads to moderate acuity loss and increased contrast sensitivity at low spatial freq uency; anisometropic amblyopia causes moderate acuity loss and decreased contrast sensitivity. 4. Binocular Function in Amblyopia: The visual acuity loss in amblyopia is linked to a compromise in binocular vision due to the suppression of information from one eye. 5. Binocular Vision Development: The ability to extract depth information from 2D retinal images, critical for depth perception and motor tasks, develops early in life but reaches adult levels only between 6 and 9 years of age. Neural Mechanisms: 6. Cortical Network and Depth Processing: Neuroimaging studies show deficits in higher visual pathways, particularly in areas pr ocessing depth information from binocular cues. 7. Non-human Primates as Models: Studies in monkeys have contributed significantly to our understanding of human binocular vision an d its disorders. 8. Primary Visual Cortex (V1) in Binocular Disparity: V1 encodes absolute disparity but not relative disparity, which is critica l for depth perception. 9. Disparity Selective Neurons in Extrastriate Areas: Neurons selective to disparity found in areas like V2, V3, MT, and in the inferior temporal cortex, highlighting complex binocular processing beyond V1. 10. Functional MRI in Monkeys and Humans: fMRI studies confirm electrophysiological findings, showing activations in response to disparity stimuli in areas like V3A and V7, and differences in the role of dorsal and ventral areas in processing different types of disparities. Amblyopia's Neural Correlates: 11. Retinal Normalcy in Amblyopia: Studies show that the retina is typically normal in amblyopic eyes, with significant neural de ficits emerging at higher levels of visual processing. 12. Cortical Alterations: Amblyopia leads to reduced binocularly driven neurons in V1, and decreased coordination of responses, p articularly in cases of strabismic amblyopia. 13. Higher Visual Area Involvement: Studies indicate deficits in higher visual areas like the fusiform gyrus during amblyopic eye stimulation, suggesting broader cortical involvement. 14. Dorsal Pathway and Motion Processing: The dorsal visual pathway, including areas like MT+, shows reduced activity in amblyopi c patients, affecting global motion perception and vision-to-movement translation. Binocular Treatment: 15. Shift from Monocular to Binocular Treatment: Recent approaches focus on restoring binocular vision, as amblyopia is increasin gly viewed as a binocular disorder. 16. Innovative Treatment Methods: Techniques like dichoptic coherence motion discrimination tasks and adapted video games (like T etris) have shown effectiveness in improving visual acuity and binocular summation in adults. 17. Brain Stimulation Techniques: Methods like repetitive transcranial magnetic stimulation (rTMS) and anodal transcranial direct current stimulation have shown promise in treating adult amblyopia. Critical Analysis: 18. Complexity of Amblyopia: The review emphasizes amblyopia's complexity, involving both monocular and binocular deficits and co rtical processing beyond the primary visual cortex. 19. Importance of Binocular Approaches: The shift to binocular treatment methods marks a significant paradigm change, aligning tr eatment with the latest understanding of amblyopia's neural basis. 20. Role of Neuroimaging: Advanced neuroimaging techniques like fMRI play a crucial role in uncovering the neural mechanisms unde rlying amblyopia and evaluating the effectiveness of new treatments. 21. Potential for Adult Treatment: New treatment methods, including brain stimulation and binocular vision therapies, open possib ilities for effectively treating PSYC0031 Cognitive Neuroscience Page 1 Extra 21. Potential for Adult Treatment: New treatment methods, including brain stimulation and binocular vision therapies, open possib ilities for effectively treating adults, a group traditionally considered beyond the critical period for treatment. 22. Future Research Directions: Continued research is needed to fully understand the neural mechanisms of amblyopia, the effectiv eness of binocular treatments, and the role of higher visual areas in the condition. PSYC0031 Cognitive Neuroscience Page 2