Monthly Archive for March, 2008

Helmer Myklebust

Helmer R. Myklebust, one of the pioneering figures in Learning Disabilities, died 26 February 2008. Predicated on his work on differentiating among speech disorders, Professor Myklebust emphasized the language-based aspects of Learning Disabilities. He theorized that there were different types of Learning Disabilities and that these types required different treatments. Throughout his career, Professor Myklebust promoted empirical study of language disorders and Learning Disabilities.

Professor Myklebust came to the study of Learning Disabilities after extensive work in hearing and speech disorders. In the 1940s he studied deafness and in the 1950s he focused on aphasia. In 1967, with his collaborator Doris Johnson, Professor Myklebust published one of the first books focused on Learning Disabilities: Learning Disabilities: Educational Principles and Remedial Approaches and later he edited a series of volumes presenting research and theory about Learning Disabilities under the title Progress in Learning Disabilities.

Professor Myklebust sought to differentiate among different variants of Learning Disabilities. He thought that Learning Disabilities could be separated into disorders of auditory language (generalized auditory disorders, auditory receptive disorders, and auditory expressive disorders), disorders of written language (auditory dyslexia, visual dyslexia, and written expression), disorders of arithmetic, and disorders of a non-verbal type. Professor Myklebust proposed that the problems children experienced were a consequence of difficulties in “interneurosensory learning.”

Professor Myklebust, who was born 2 august 1910 in Lester (IA, US), was among a small group of educators and psychologists who generally credited with founding the study of Learning Disabilities. Along with Samuel Kirk, William Cruickshank, Marianne Frostig, Newell Kephart, and perhaps a few others, Myklebust pursued the recognition of the difficulties experienced by these children and their families.

He received a bachelors degree from Augustana College, a masters degrees from Gallaudet College and Temple University, and a doctoral degree from Rutgers University. He taught and conducted research at several institutions, including Northern Illinois University; Northwestern University, where he spent most of his career and where he founded the Children’s Hearing and Aphasia Clinic; University of Illinois, Chicago. Memorial services were held 8 March.

Johnson, D. J., & Myklebust, H. (1967). Learning disabilities: Educational principles and remedial approaches. NY: Grune & Stratton.

Myklebust, H. (1954). Auditory disorders in children: A manual for differential diagnosis. NY: Grune & Stratton.

Myklebust, H. (Ed.). (1968-1975). Progress in learning disabilities (vols. 1-5). NY: Grune & Stratton.

I am late in publishing this note; thanks to Hal McGrady for alerting me to the death of this giant figure in the history or LD.

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Differential drug effects in arithmetic

Professor Orly Rubinsten and colleagues found that methylphenidate affects the arithmetic performance of children in different ways, but its effects are not only on children with ADHD. When they received methylphenidate, the active ingredient in Ritalin, children had higher correct responding on problems requiring them to follow a series of steps than when they didn’t receive the drug; in contrast, there were no differences between drug and no-drug conditions on simpler tasks. The effects occurred for children with dyscalculia, less math problems, or no math problems.

Methylphenidate has Differential Effects on Numerical Abilities in ADHD Children with and without Co-Morbid Mathematical Difficulties
Authors: Orly Rubinsten, Anne-Claude Bedard, Rosemary Tannock
doi: 10.2174/1874350100801010011

Abstract:
Objective. To investigate effects of methylphenidate (MPH) on numerical performance in children with Attention- Deficit/Hyperactivity Disorder (ADHD) with and without concurrent math difficulties. Method. Data were analyzed from three groups of children with ADHD, who varied in arithmetic abilities. Groups were matched for IQ and reading abilities and classification was based on ICD-10 criteria, using scores on a standardized arithmetic achievement test. Thus, we identified one group with severe difficulties in arithmetic (ADHD+Developmental Dyscalculia; DD), second group with more general and less severe difficulties in arithmetic (ADHD+Mathematical Disabilities; MD), and a third group with good arithmetic abilities (ADHD). All children completed a 10-minute arithmetic task involving subtraction problems, during an acute, randomized, placebo-controlled cross-over trial with three dose levels of methylphenidate (10mg, 15mg, 20mg). Results. (1) Both ADHD+MD and ADHD+DD were impaired in using strategies that implicate working memory (i.e., borrowing). However, only the ADHD+DD were impaired in using implicit knowledge of quantities (i.e., doing simple subtractions). (2) MPH improved all children’s performance of arithmetic procedures (borrowing) that involves working memory, but had no effect on basic numerical skills that involves understanding of quantities. Conclusions. We show clear dissociation of MPH functions: it improves working memory functions but does not improve specific cognitive functions such as quantity manipulation. Moreover, MPH shows decreased efficacy for arithmetic performance in ADHD+DD, highlighting the need for additional intervention in this subgroup.

Keywords: Methylphenidate, developmental dyscalculia, ADHD
Affiliation: Neurosciences and Mental Health Research Program, Research Institute, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, Canada.

The study appeared in The Open Psychology Journal and the entire article is available for free via the Open Journal initiative.

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Brain Gym (Skeptic’s Dictionary)

Wheeeheee! Over on the Skeptic’s Dictionary, Robert T. Carroll has a take-down and pin of Brain Gym. The contemporary incarnation of some ideas that were thoroughly discredited in Learning Disabilities in the 1970s, Brain Gym is making something of a splash. Shoot, it even appeared in one of my Curry School colleague’s classes for a while, as I understand.

Professor Carroll’s indictment of Brain Gym presents a good opportunity to make an important point. The problem with Brain Gym and many of its siblings is not that the activities might not be worthwhile, it’s that the advocates over-reach so substantially. Shoot, I’m glad to advocate that we teach kids who might fit the clumsy category how to walk, move, dance, play basketball, and etc. I just don’t want people to be sold a bill of goods about how doing so will improve those children’s reading, etc.

Read Professor Carroll’s analysis. Need info on the research about the benefits of perceptual-motor training? Here’s a link to a meta-analysis.

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Dyscalculia day

Liz Ditz has a post noting today’s status as “International Dyscalculia Awareness Day, Today.” Read it here.

DYX1C1: How genetic variation affects proteins and thus dyslexia

Although the paper was published several years ago, it is worth noting. It may not be news, but it forms part of the fabric one has to consider in thinking about the nature of dyslexia. Read this in the context of other stories (e.g., this one) about genetic bases for dyslexia.

A candidate gene for developmental dyslexia encodes a nuclear tetratricopeptide repeat domain protein dynamically regulated in brain

Mikko Taipale, Nina Kaminen, Jaana Nopola-Hemmi, Tuomas Haltia, Birgitta Myllyluoma, Heikki Lyytinen, Kurt Muller, Minna Kaaranen, Perttu J. Lindsberg, Katariina Hannula-Jouppi, and Juha Kere

Communicated by Albert de la Chapelle, Ohio State University, Columbus, OH, June 24, 2003 (received for review December 23, 2002)

Approximately 3–10% of people have specific difficulties in reading, despite adequate intelligence, education, and social environment. We report here the characterization of a gene, DYX1C1 near the DYX1 locus in chromosome 15q21, that is disrupted by a translocation t(2;15)(q11;q21) segregating coincidentally with dyslexia. Two sequence changes in DYX1C1, one involving the translation initiation sequence and an Elk-1 transcription factor binding site (–3G A) and a codon (1249G T), introducing a premature stop codon and truncating the predicted protein by 4 aa, associate alone and in combination with dyslexia. DYX1C1 encodes a 420-aa protein with three tetratricopeptide repeat (TPR) domains, thought to be protein interaction modules, but otherwise with no homology to known proteins. The mouse Dyx1c1 protein is 78% identical to the human protein, and the nonhuman primates differ at 0.5–1.4% of residues. DYX1C1 is expressed in several tissues, including the brain, and the protein resides in the nucleus. In human brain, DYX1C1 protein localizes to a fraction of cortical neurons and white matter glial cells. We conclude that DYX1C1 should be regarded as a candidate gene for developmental dyslexia. Detailed study of its function may open a path to understanding a complex process of development and maturation of the human brain.

Link to the PNAS materials.

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