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Gordon, Gael E.; McCulloch, Daphne L.

doi:10.1023/a:1002171011644

Cited by 42 publications

(8 citation statements)

References 19 publications

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“…However, since no information is available for 1–8 years of age, it is possible that these processes mature at an earlier stage. CS for lower-SF stimuli becomes mature later in life, between 8 (not adult-like) and 11 (adult-like) years of age (Gordon and McCulloch, 1999). To our knowledge, no studies investigated CS for lower and higher SFs at intermediate ages.…”

Section: Development Of Visual Mechanisms Underlying Form Processingmentioning

confidence: 99%

Keep Your Eyes on Development: The Behavioral and Neurophysiological Development of Visual Mechanisms Underlying Form Processing

Boomen¹,

Smagt²,

Kemner³

2012

Front. Psychiatry

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Visual form perception is essential for correct interpretation of, and interaction with, our environment. Form perception depends on visual acuity and processing of specific form characteristics, such as luminance contrast, spatial frequency, color, orientation, depth, and even motion information. As other cognitive processes, form perception matures with age. This paper aims at providing a concise overview of our current understanding of the typical development, from birth to adulthood, of form-characteristic processing, as measured both behaviorally and neurophysiologically. Two main conclusions can be drawn. First, the current literature conveys that for most reviewed characteristics a developmental pattern is apparent. These trajectories are discussed in relation to the organization of the visual system. The second conclusion is that significant gaps in the literature exist for several age-ranges. To complete our understanding of the typical and, by consequence, atypical development of visual mechanisms underlying form processing, future research should uncover these missing segments.

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Section: Development Of Visual Mechanisms Underlying Form Processingmentioning

confidence: 99%

Keep Your Eyes on Development: The Behavioral and Neurophysiological Development of Visual Mechanisms Underlying Form Processing

Boomen¹,

Smagt²,

Kemner³

2012

Front. Psychiatry

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“…Crewther et al [10] studied low-contrast flicker sensitivity in school-age children and concluded that the development of the magnocellular pathway was delayed. Gordon and McCulloch [11] found evidence for ongoing parvocellular maturation as late as 11 years of age. Klaver et al [12] provided imaging evidence for the delayed development of the M-pathway in the dorsal stream including the parietal lobule.…”

Section: Introductionmentioning

confidence: 99%

The Development and Aging of the Magnocellular and Parvocellular Visual Pathways as Indicated by VEP Recordings between 5 and 84 Years of Age

Benedek

Horváth

Kéri

et al. 2016

Vision

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It is well known that pattern reversal visual evoked potentials (VEPs) are age-sensitive. Through the use of this technique, it is possible to assess both of the major visual pathways (i.e., the magnocellular and parvocellular ones) in terms of function and development. What developmental path these pathways follow, and if they develop/age in parallel across the human lifespan is a matter of ongoing debate, yet, only a few VEP studies have dealt with this issue. This cross-sectional study examined a sample of 115 healthy volunteers aged 5 to 84 years. Beyond the standard checkerboard pattern reversal stimulation at 97% contrast, we recorded pattern-reversal VEPs at 6% contrast to selectively stimulate the M pathway and isoluminant red and green checkerboard stimulation was also used to selectively stimulate the P pathway. Our results do not support the developmental advantage of any of the pathways. The development of both pathways appear to take a remarkably long time (well into the 30s), and the signs of aging become marked over 50 years of age, especially in the case of the magnocellular pathway.

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“…Correlation of RNFL thickness with stage of MS, brain atrophy, degree of disability and disease duration found in a number of cross-sectional studies incited considerable interest in using assessment of the anterior visual pathway as a structural marker of CNS neurodegeneration in MS [1]–[8] and was even suggested as a possible outcome for future neuroprotection trials. [4], [9], [10] Recently, however, loss of RGC has also been demonstrated in non-optic neuritis (NON) eyes. A meta-analyses published by Petzold et al [11] showed significant thinning of RGC axons (so called retinal nerve fiber layer-RNFL) in MS-NON eyes.…”

Section: Introductionmentioning

confidence: 99%

Relationship between Optical Coherence Tomography and Electrophysiology of the Visual Pathway in Non-Optic Neuritis Eyes of Multiple Sclerosis Patients

et al. 2014

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PurposeLoss of retinal ganglion cells in in non-optic neuritis eyes of Multiple Sclerosis patients (MS-NON) has recently been demonstrated. However, the pathological basis of this loss at present is not clear. Therefore, the aim of the current study was to investigate associations of clinical (high and low contrast visual acuity) and electrophysiological (electroretinogram and multifocal Visual Evoked Potentials) measures of the visual pathway with neuronal and axonal loss of RGC in order to better understand the nature of this loss.MethodsSixty-two patients with relapsing remitting multiple sclerosis with no previous history of optic neuritis in at least one eye were enrolled. All patients underwent a detailed ophthalmological examination in addition to low contrast visual acuity, Optical Coherence Tomography, full field electroretinogram (ERG) and multifocal visual evoked potentials (mfVEP).ResultsThere was significant reduction of ganglion cell layer thickness, and total and temporal retinal nerve fibre layer (RNFL) thickness (p<0.0001, 0.002 and 0.0002 respectively). Multifocal VEP also demonstrated significant amplitude reduction and latency delay (p<0.0001 for both). Ganglion cell layer thickness, total and temporal RNFL thickness inversely correlated with mfVEP latency (r = −0.48, p<0.0001 respectively; r = −0.53, p<0.0001 and r = −0.59, p<0.0001 respectively). Ganglion cell layer thickness, total and temporal RNFL thickness also inversely correlated with the photopic b-wave latency (r = −0.35, p = 0.01; r = −0.33, p = 0.025; r = −0.36, p = 0.008 respectively). Multivariate linear regression model demonstrated that while both factors were significantly associated with RGC axonal and neuronal loss, the estimated predictive power of the posterior visual pathway damage was considerably larger compare to retinal dysfunction.ConclusionThe results of our study demonstrated significant association of RGC axonal and neuronal loss in NON-eyes of MS patients with both retinal dysfunction and post-chiasmal damage of the visual pathway.

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Cited by 42 publications

References 19 publications

Keep Your Eyes on Development: The Behavioral and Neurophysiological Development of Visual Mechanisms Underlying Form Processing

Keep Your Eyes on Development: The Behavioral and Neurophysiological Development of Visual Mechanisms Underlying Form Processing

The Development and Aging of the Magnocellular and Parvocellular Visual Pathways as Indicated by VEP Recordings between 5 and 84 Years of Age

Relationship between Optical Coherence Tomography and Electrophysiology of the Visual Pathway in Non-Optic Neuritis Eyes of Multiple Sclerosis Patients

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