Archive for the 'Causes' Category

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Sigh–new content

Despite getting virtually no recommendations about future content (3 votes!), I’m starting to post some new content. The new content is, in my obviously biased view (else, why would I post it?), pretty important stuff. It’s about research, practice, knowledge, and all that sort of stuff as it connects to Learning Disabilities. In this page, I discuss big-idea concepts that recur in Learning Disabilities. These are the themes that one sees when one reads a diverse array of literature on the topic of LD.

I recommend it. What’s more, you won’t have to find this post each time you want to refer to the page; it will always be directly accessible under the “special content” link in the top navigation bar.

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More genetics and dyslexia

Professor Silvia Paracchini and colleagues have correlated the levels of one of the genes associated with chromosome 6p22, KIAA0319, with reading performance among the general population.

Association of the KIAA0319 Dyslexia Susceptibility Gene With Reading Skills in the General Population

Silvia Paracchini, D.Phil., Colin D. Steer, M.Sc., Lyn-Louise Buckingham, B.Sc., Andrew P. Morris, Ph.D., Susan Ring, Ph.D., Thomas Scerri, D.Phil., John Stein, F.R.C.P., Marcus E. Pembrey, M.D., Jiannis Ragoussis, Ph.D., Jean Golding, Ph.D., and Anthony P. Monaco, Ph.D.

Continue reading ‘More genetics and dyslexia’

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Irlen Kool-Aid consumed again

Yet another reporter has covered the benefits of providing colored lenses or overlays for improving reading performance. Based on subjective reports from a child and her father, Morgan Bond of television station KPVI in Pocatello (ID, US) described Irlen’s Syndrome as the cause and blue-tinted glasses as the solution to Noel Chapman’s reading problems.
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Relaxing to learn?

An anonymous post on the Hattiesburg (MS, US) American caught my attention. The poster applauded a facility called the “Dynamic Dyslexia Design School.” This is the school about which Liz Ditz posted a note a couple of months ago. The school is accredited by the International Multisensory Structured Language Education Council, which is probably a good thing. However, that didn’t prevent it’s director from providing a not-too-thoughtful explanation for reading problems:

The education is delivered in a way the dyslexic students can understand, said director Cena Holifield.

“They don’t feel the stress of everyone around them being able to do something they can’t. When they feel safe and secure, the pathways to the brain open and makes it easier to learn,” she said.

I’d hazard an alternative explanation: If the students seem more relaxed, it’s likely the result of succeeding, not the other way around.

Link to the full statement. Link to the school’s Web site. Link to Liz’s earlier post. More about the International Multisensory Structured Language Education Council.

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How genes may affect dyslexia

Writing in the Journal of the Federation of American Societies for Experimental Biology under the title “The Complex of TFII-I, PARP1, and SFPQ Proteins Regulates the DYX1C1 Gene Implicated in Neuronal Migration and Dyslexia,” Isabel Tapia-Páez and colleagues revealed that they have discovered a group of proteins that apparently act together to control the transcription of DNA (deoxyribonucleic acid that forms genetic material) code into RNA (ribonucleic acid which controls synthesis of proteins) code. Although the gene DYX1C1 has been implicated in only a small proportion of cases of dyslexia, it is important in general because the finding moves researchers closer to understanding how genes can influence behavior as complex as reading.
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Hey, teacher, my child can’t read

Dean Geyer, who is a parent of a child who had difficulty learning to read, has launched a blog entitled “Hey, Teacher, My Child Can’t Read.” His daughter’s experience is, in part, a success story; after five years of special education in Delaware (US), he reports that she is on the honor roll and no longer eligible for special education.

In his entries, Mr. Geyer frequently refers to “auditory processing disorder.” Although I am very glad to learn that Mr. Geyer’s daughter is succeeding, I am wary of attributing much to the diagnosis of auditory processing disorder. I’ve been hearing about this disorder for most of my career, but I have as yet not found a satisfactorily rigorous or substantiated account of it.

If someone could point me to a definitive resource on this disorder, we could examine it systematically. I fear, however, that a close examination of the resource will reveal that it is simply hypothesizing some hidden process that can’t be precisely tested and is pretty readily reduced to not having learned some pretty specific skills.

Here are some of the questions one should ask:

  1. How does one distinguish a child with auditory processing disorder from another child who doesn’t have the disorder?
  2. How trustworthy (psychometrically sound) are any instruments used in making the diagnosis of auditory processing disorder?
  3. What specific tasks would a child with auditory processing disorder fail? If the child was taught how to pass those tasks, would she still have auditory processing disorder?

By the way, I think there’s a similar case to be made for “non-verbal learning disability.”

Regardless of the outcomes of an investigation of auditory processing disorder, it’s still quite wonderful to know that Mr. Geyer’s daughter is succeeding. I encourage readers to jump over to Hey, Teacher, My Child Can’t Read and read his posts. I’m adding his site to LD Blog’s blog roll.

Update: It seems this domain name is no longer being maintained. More when I can get in touch with Mr. Geyer. 11 September 2009.

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RC > WR

A team of researchers who study reading and neuropsychology has reported results from a study that show what parts of the brain are involved in sentence comprehension other than those used for recognizing the words in the sentences. In a study entitled “Functional MRI of Sentence Comprehension in Children with Dyslexia: Beyond Word Recognition” that will appear soon in Cerebral Cortex, S. L. Rimrodt and colleagues (including Ken Pugh and Laurie Cutting, whom I know) compared the fMRI data from groups of children with and without dyslexia on tasks involving word reading and sentence comprehension. They found that the children with dyslexia had disproportional activation of areas of the brain usually employed in processing linguistic information, attending, and selecting responses.
Continue reading ‘RC > WR’

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Preschool language factors affecting reading achievement

Although perceptual explanations for reading problems were common in the early discussions of Learning Disabilities, educators now mostly agree that the language factors have far greater influence on reading problems. A recent study by Nicole Halaar and colleagues underscores this idea and, especially importantly, points to the importance of early childhood language development in later reading competence. In fact, although genetic factors play a role in later reading competence, environmental exert substantial influence.

Of course, given the extensive work on them over the past 20 years, educators understand the importance of phonemic awareness and decoding in reading. But these factors do not completely explain the variation in outcomes for children learning to read. The contributions of semantic and syntactic factors must be included to move closer to explaining why children differ in their reading outcomes, especially when the outcome of concern is facility in comprehending what one has read.
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Language development: Speechome Project

Here’s an interesting research project: Equip a house with a host of highly sensitive audio-video recording devices that pipe the data into cluster of high-powered computers which have an array of very capacious storage devices. Using this system, document the language environment in which a child is raised and record the child’s language development. Pretty nifty, hunh? A petabyte of developmental data!

This is, in fact, what a couple of parents—Deb Roy (Massachusetts Institute of Technology; Cambridge, MA, US) and Rupal Patel (Northwestern; Boston, MA, US)—have been doing for the past few years.

The high-powered academic couple—he directs of the Cognitive Machines Group at the Massachusetts Institute of Technology (MIT) Media Lab, and she directs the Communication Analysis and Design Laboratory at Northeastern University—scrambled to convert their suburban Boston home into a state-of-the-art research center that would host the most ambitious study ever conducted on how children acquire language. They named the linguistic data-mining odyssey the Human Speechome Project (HSP), a marriage between “Speech” and “Home.”

Why’s this relevant for LD Blog? Well, other research (especially Hart and Risley’s excellent work as summarized in Meaningful Differences, but note that there are many related studies in the research literature) has shown that differences in language environments have substantial effects on children’s language (e.g., vocabulary). Many Learning Disabilities are associated with problems in language (e.g., low phonological awareness, atypical syntax, problems in morphology, poor pragmatics). Understanding the language environment in which children develop their language skills might help explain some of the problems we see among children with Learning Disabilities.

Am I blaming parents? Nope. Language experiences that some children have may actually have protective effects. But, some experiences apparently are predictive of later outcomes. It would be good to know.

Am I saying that Learning Disabilities are environmental, that they have no biological components? Nope. I’m not saying that they do or do not have biological features. But, imagine that there are biological predispositions and that some language environments prevent or mitigate the manifestation of disability. That would be worth knowing, I’d say.

To complete a project examining the contribution of language environments to Learning Disabilities would require a prospective longitudinal study of substantial size. Supposing that Learning Disabilities appear in 5% of the population, then to get a enough children with Learning Disabilities to make the study reasonably sensitive, one would need 2000 families; at 5 per 100, that would yield about 100 children with Learning Disabilities. Now, if one were clever, she would look for families where there were siblings so that one could also examine the shared and non-shared environments, and start to factor in the contribution of genetic factors.

Imagine the financial cost of such a study….

If you could have a switch that would stop the recording at any time, would you agree to have such a system record your interactions with your newborn all the way through toddlerhood?

Meanwhile, to learn more about the Human Speechome Project, check these resources:

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ADHD in families

Dr. M. Romanos and colleagues examined the genetic make-up of several families and found that there are common elements that appear to be associated with ADHD. Although these findings point toward a genetic contribution to ADHD, it is important to note the caveat implied by the final sentence of the abstract: So many factors contribute to ADHD, that these results should not be construed as identifying the precise cause of the disorder. In the full article, the authors are circumspect about this: “The identification [in this study] of several novel linkage regions as well as replication of previously reported loci provides further evidence for the highly heterogeneous genetic etiology of ADHD.”

Genome-wide linkage analysis of ADHD using high-density SNP arrays: Novel loci at 5q13.1 and 14q12

M Romanos, C. Freitag, C. Jacob, D. W Craig, A. Dempfle, T. T. Nguyen, R. Halperin, S. Walitza, T. J Renner, C. Seitz, J. Romanos, H. Palmason, A. Reif, M. Heine, C. Windemuth-Kieselbach, C. Vogler, J. Sigmund, A. Warnke, H. Schäfer, J. Meyer, D. A. Stephan, & K. P. Lesch

Molecular Psychiatry (2008) 13, 522–530; doi:10.1038/mp.2008.12; published online 26 February 2008

Abstract

Previous genome-wide linkage studies applied the affected sib-pair design; one investigated extended pedigrees of a. genetic isolate. Here, results of a. genome-wide high-density linkage scan of attention-deficit/hyperactivity disorder (ADHD) using an array-based genotyping of approx ~50 K. single nucleotide polymorphism (SNPs) markers are presented. We investigated eight extended pedigrees of German origin that were non-related, not part of a. genetic isolate and ascertained on the basis of clinical referral. Two parametric analyses maximizing LOD scores (MOD) and a. non-parametric analysis for both a. broad and a. narrow phenotype approach were conducted. Novel linkage loci across all families were detected at 2q35, 5q13.1, 6q22-23 and 14q12, within individual families at 18q11.2-12.3. Further linkage regions at 7q21.11, 9q22 and 16q24.1 in all families, and at 1q25.1, 1q25.3, 9q31.1-33.1, 9q33, 12p13.33, 15q11.2-13.3 and 16p12.3-12.2 in individual families replicate previous findings. High-resolution linkage mapping points to several novel candidate genes characterized by dense expression in the brain and potential impact on disorder-relevant synaptic transmission. Our study provides further evidence for common gene effects throughout different populations despite the complex multifactorial etiology of ADHD.

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