A Defective Visual Pathway in Children with Reading Disability

Lehmkuhle, Stephen; Garzia, Ralph P.; Turner, Linda; Hash, Tina; Baro, John A.

doi:10.1056/nejm199304083281402

Cited by 151 publications

(91 citation statements)

References 26 publications

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“…However, the transient system theory has some empirical support (Breitmeyer, 1989;Badcock & Lovegrove, 1981;Lehmkuhle, Garzia, Turner, Hash, & Baro, 1993;Lovegrove et al, 1986;Lovegrove, Garzia, & Nicholson, 1990;Martin & Lovegrove, 1984), as does the motion perception theory (Eden et al, 1996). Thus, both warrant further comment.…”

Section: Visual Deficitsmentioning

confidence: 94%

“…Yet, it might be a correlate of the disorder, and perhaps even a biological marker. This possibility is given some Specific reading disability (dyslexia) support by anatomical and electrophysiological studies demonstrating structural and functional anomalies in the magnocellular pathways of a small number of those with dyslexia studied (Lehmkuhle et al, 1993;Livingstone, Rosen, Drislane, & Galaburda, 1991). However, a recent review of the literature by Skottun and Parke (1999) presented evidence from several studies of saccadic suppression that strongly suggests that it is the magnocellular system that is suppressed during saccadic movements of the eyes, not the parvocellular system.…”

Section: Visual Deficitsmentioning

confidence: 99%

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Specific reading disability (dyslexia): what have we learned in the past four decades?

Vellutino

Fletcher

Snowling

et al. 2004

Child Psychology Psychiatry

2,024

1,591

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We summarize some of the most important findings from research evaluating the hypothesized causes of specific reading disability (ÔdyslexiaÕ) over the past four decades. After outlining components of reading ability, we discuss manifest causes of reading difficulties, in terms of deficiencies in component reading skills that might lead to such difficulties. The evidence suggests that inadequate facility in word identification due, in most cases, to more basic deficits in alphabetic coding is the basic cause of difficulties in learning to read. We next discuss hypothesized deficiencies in readingrelated cognitive abilities as underlying causes of deficiencies in component reading skills. The evidence in these areas suggests that, in most cases, phonological skills deficiencies associated with phonological coding deficits are the probable causes of the disorder rather than visual, semantic, or syntactic deficits, although reading difficulties in some children may be associated with general language deficits. Hypothesized deficits in general learning abilities (e.g., attention, association learning, cross-modal transfer etc.) and low-level sensory deficits have weak validity as causal factors in specific reading disability. These inferences are, by and large, supported by research evaluating the biological foundations of dyslexia. Finally, evidence is presented in support of the idea that many poor readers are impaired because of inadequate instruction or other experiential factors. This does not mean that biological factors are not relevant, because the brain and environment interact to produce the neural networks that support reading acquisition. We conclude with a discussion of the clinical implications of the research findings, focusing on the need for enhanced instruction.

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Section: Visual Deficitsmentioning

confidence: 94%

Section: Visual Deficitsmentioning

confidence: 99%

Specific reading disability (dyslexia): what have we learned in the past four decades?

Vellutino

Fletcher

Snowling

et al. 2004

Child Psychology Psychiatry

2,024

1,591

View full text Add to dashboard Cite

show abstract

“…Specific reading disability in a small subset of patients with dyslexia has been attributed to a deficit in the magnocellular visual system. [183][184][185][186][187] In 1983, Breitmeyer 183 proposed that reading disability is an expression of the disruptive effects of a temporal processing deficit in the magnocellular system. Stein and Walsh 184,187 suggested that this deficit in the inhibitory function of the magnocellular system produces a visual trace of abnormal longevity that creates masking effects along with visual acuity problems when reading connected text.…”

Section: Magnocellular Deficit Theorymentioning

confidence: 99%

“…Also in opposition to Livingstone et al, May et al 189 found that the latency periods were shortened under low spatial frequency conditions. In 1993, Lehmkuhle et al 185 noted the lack of change in the latency of the visual evoked potential in reading-disabled children compared with the increased latency noted in children without a reading disability by using low spatial frequency target and high-frequency flicker fields. Their conclusion was that it is possible that a defect in the magnocellular pathway creates a timing disorder that precludes rapid and smooth integration of detailed visual information necessary for efficient reading.…”

Section: Magnocellular Deficit Theorymentioning

confidence: 99%

“…[183][184][185][186][187] The studies supporting this theory are outnumbered by studies that have found no loss of contrastsensitivity and other studies that have found contrast-sensitivity reductions or other findings inconsistent with a magnocellular deficit. [188][189][190][191][192][193][194][195][196][197][198][199][200][201] Thus, the evidence in support of the magnocellular theory is equivocal at best.…”

Section: Magnocellular Deficit Theorymentioning

confidence: 99%

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Learning Disabilities, Dyslexia, and Vision

Handler¹,

Fierson²

2011

Pediatrics

154

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Learning disabilities constitute a diverse group of disorders in which children who generally possess at least average intelligence have problems processing information or generating output. Their etiologies are multifactorial and reflect genetic influences and dysfunction of brain systems. Reading disability, or dyslexia, is the most common learning disability. It is a receptive language-based learning disability that is characterized by difficulties with decoding, fluent word recognition, rapid automatic naming, and/or reading-comprehension skills. These difficulties typically result from a deficit in the phonologic component of language that makes it difficult to use the alphabetic code to decode the written word. Early recognition and referral to qualified professionals for evidence-based evaluations and treatments are necessary to achieve the best possible outcome. Because dyslexia is a language-based disorder, treatment should be directed at this etiology. Remedial programs should include specific instruction in decoding, fluency training, vocabulary, and comprehension. Most programs include daily intensive individualized instruction that explicitly teaches phonemic awareness and the application of phonics. Vision problems can interfere with the process of reading, but children with dyslexia or related learning disabilities have the same visual function and ocular health as children without such conditions. Currently, there is inadequate scientific evidence to support the view that subtle eye or visual problems cause or increase the severity of learning disabilities. Because they are difficult for the public to understand and for educators to treat, learning disabilities have spawned a wide variety of scientifically unsupported vision-based diagnostic and treatment procedures. Scientific evidence does not support the claims that visual training, muscle exercises, ocular pursuit-and-tracking exercises, behavioral/perceptual vision therapy, “training” glasses, prisms, and colored lenses and filters are effective direct or indirect treatments for learning disabilities. There is no valid evidence that children who participate in vision therapy are more responsive to educational instruction than children who do not participate.

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Scholarly communication in developmental dyslexia: Influence of network structure on change in a hybrid problem area

Perry

Rice

1998

J. Am. Soc. Inf. Sci.

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Based on Mulkay's and Kuhn's models of change in sci entific structure, a scientific communication model of the emergence of a hybrid research area was developed and tested in the field of developmental dyslexia. Data included co-citation data on 74 dyslexia researchers at three points in time, who-to-whom communication net work data, survey responses, resumes, association and biographical sources, online reference and citation databases , publications, grant databases, and telephone in terviews. Researchers were partitioned into ''blocks'' of similar scientists on the basis of co-citation and commu nication relations, compared on selected network-level and individual-level characteristics in order to validate block labels, and situated historically in the politics and advances surrounding the problem area. Results show support for Mulkay's model of branching instead of Kuhn's model of scientific revolution. Evidence points to divergence rather than convergence among the related research areas, but suggests the need for longitudinal follow-up in order to rule out the impact of the inertia of aggregate co-citation data. Implications for theory, methodology, and research are discussed.

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A Defective Visual Pathway in Children with Reading Disability

Cited by 151 publications

References 26 publications

Specific reading disability (dyslexia): what have we learned in the past four decades?

Specific reading disability (dyslexia): what have we learned in the past four decades?

Learning Disabilities, Dyslexia, and Vision

Scholarly communication in developmental dyslexia: Influence of network structure on change in a hybrid problem area

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