Tag Archive for 'Causes'

Function-based interventions for LD?

Most readers are likely familiar with the idea that one can, by carefully assessing the antecedents and consequences of a problem behavior, essentially determine what is causing that problem behavior to occur. Given that at least some—many?—students with Learning Disabilities (LD) have some problem-some behaviors, wouldn’t it be cool if there was an evidence base about using functional analysis techniques to document development of procedures for addressing the problem behaviors of students with LD?

In “A Systematic Review of Function-Based Interventions for Students with Learning Disabilities,” Professor John McKenna and his colleagues examined the research literature in search of that very evidence base. They were able to locate only a few studies that met the most rigorous standards, but those studies allowed them to conclude that this idea is a promising one. Here’s the source and the abstract with a hot DOI. I think the publisher (Wiley) may be allowing public access to the entire article, so try clicking on the PDF to download it. (I can’t tell, ’cause I’m working from my office, which has free access anyway; drop a comment to let me know.)

McKenna, J. W., Flower, A., Kim, M. K., Ciullo, S., & Haring, C. (2015). A systematic review of function-based interventions for students with learning disabilities. Learning Disabilities Research & Practice, 30, 15-28. DOI:10.1111/ldrp.12049

Students with learning disabilities (LD) experience pervasive academic deficits requiring extensive academic intervention; however, they may also engage in problem behaviors that adversely affect teaching and learning, thus lessening the potential impact of specialized instruction and supports. The learning deficits of students with LD are prevalent in the extant research, but behavioral needs appear to receive less attention. The authors report the results of a systematic review investigating the evidence-base for function-based interventions for students with LD using the What Works Clearinghouse (WWC) criteria for evaluating single-case studies. Fourteen studies with 17 participants met inclusion criteria, with the majority occurring in elementary settings. Although interventions tended to be effective, few included maintenance and generalization measures. Because of the small number of studies (n = 4) that met WWC design and effectiveness standards, the authors conclude that function-based interventions, although promising, cannot currently be considered an evidence-based practice for students with LD. Implications for practice, areas for future research, and study limitations are reported.

Visual differences are a consequence, not a cause, of dyslexia

In an article to appear 10 July 2013 in Neuron, Olumide Olulade, Eileen Napoliello, and Guinevere Eden present a series of studies that greatly help educators, psychologists, neurologists, and others understand the relationship between visual deficits and dyslexia. Although most people interested in reading have understood that problems with phonological processes undergird dyslexia, personal accounts of those with dyslexia and some anomalous evidence about the visual cortex and the performance of individuals with dyslexia on certain visual tasks kept the possibility of a visual component open to debate. Professor Eden’s group devised studies and collected the data that shed light on these issues.

In a nutshell, in their first study, Eden’s team found the same results that others had found: When their participants with dyslexia were compared to similar aged children, they showed certain deficits in visual processing associated with a particular part of the brain shown by fMRI. However, when their participants were compared with younger children of like reading ability, there are no deficits in the visual performance; so, these children must not have had the visual problems all along. In their third study, the researchers provided even stronger evidence: The provided powerful remedial reading instruction to their participants and they observed not only improved reading outcomes, but they also found that the students had improved performance on the visual tasks as reflected in fMRI. (Click the accompanying image for a movie of Professors Eden and Olulade explaining the experiments.)

Here is the abstract:

Developmental dyslexia is a reading disorder, yet deficits also manifest in the magnocellular-domi- nated dorsal visual system. Uncertainty about whether visual deficits are causal or consequential to reading disability encumbers accurate identifica- tion and appropriate treatment of this common learning disability. Using fMRI, we demonstrate in typical readers a relationship between reading ability and activity in area V5/MT during visual motion pro- cessing and, as expected, also found lower V5/MT activity for dyslexic children compared to age- matched controls. However, when dyslexics were matched to younger controls on reading ability, no differences emerged, suggesting that weakness in V5/MT may not be causal to dyslexia. To further test for causality, dyslexics underwent a phonolog- ical-based reading intervention. Surprisingly, V5/MT activity increased along with intervention-driven reading gains, demonstrating that activity here is mobilized through reading. Our results provide strong evidence that visual magnocellular dysfunc- tion is not causal to dyslexia but may instead be consequential to impoverished reading.

Olulade, O. A., Napoliello, E. M., & Eden, G. F. (2013). Abnormal visual motion processing is not a cause of dyslexia. Neuron, 79, 1-11. doi:10.1016/j.neuron.2013.05.002

More on smoking and neuropsych disorders

New research shows that using nicotine during pregnancy affects genes involved in myelination and, consequently may help explain why the children of mothers who smoke during pregnancy are more likely to develop such psychiatric disorders as attention deficit hyperactivity disorder, depression, autism, and even drug abuse. In a paper presented at Neuroscience 2010, the annual meeting of the Society for Neuroscience, Professor Ming Li, Ph.D., of the University of Virginia (Charlottesville, VA, US) reported that when rats were given nicotine during pregnancy, their offspring manifested changes in myelin genes for the limbic system, especially the prefrontal cortex, a brain region important for decision-making.

“Our research shows that gestational treatment with nicotine significantly modifies myelin gene expression in specific brain regions that are involved in behavioral processes,” according to Professor Li, leader of the study. “Myelin deficits have been observed in adults with various psychiatric disorders. Our findings suggest that abnormal myelination may contribute to the psychiatric disorders associated with maternal smoking.”
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Preliminary evidence of link between maternal smoking and risk of child problems

Researchers from the University of Alabama at Birmingham (AL, US) presented a paper at Neuroscience 2010, the annual meeting of the Society for Neuroscience in which they reported that exposure to nicotine during pregnancy leads to a decrease in adult stem cells and a change in synaptic plasticity in the hippocampus of the offspring. The synaptic changes could have lifelong consequences for the offspring. According to Professor Robin Lester of the Department of Neurobiology and lead researcher on the project, “These problems could include various cognitive deficits, learning difficulties, [and] ADHD.”

These are very preliminary findings. They come from research conducted with rats and will require extensive additional work to make the connections to human learning. Note that the mother rats apparently were also ingesting nicotine while nursing (first 10 days after birth) as well as during pregnancy. My reporting here is based entirely on press releases from UAB and the Society for Neuroscience (with abstract).

Sources: http://www.newswise.com/articles/view/571417/ and http://www.sfn.org/index.aspx?pagename=news_111410b
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The gene DYX1C1 and reading and spelling

Paul Bates and colleagues have reported new findings about the gene DYX1C1, which has been a focal point for research on genetic contributions to dyslexia for at least six years. Writing for the journal Molecular Psychiatry, the research team revealed that their examination of the relationship between DYX1C1 and variations in reading ability points at certain variations in genes and reading ability. Specific differences in individual nucleotides (single nucleotide polymorphisms, or SNPs), different from those reported previously, appear to be associated with ability and disability in reading and spelling.

The status of DYX1C1 (C15q21.3) as a susceptibility gene for dyslexia is unclear. We report the association of this gene with reading and spelling ability in a sample of adolescent twins and their siblings. Family-based association analyses were carried out on 13 single-nucleotide polymorphisms (SNPs) in DYX1C1, typed in 790 families with up to 5 offspring and tested on 6 validated measures of lexical processing (irregular word) and grapheme–phoneme decoding (pseudo-word) reading- and spelling-based measures of dyslexia, as well as a short-term memory measure. Significant association was observed at the misssense mutation rs17819126 for all reading measures and for spelling of lexical processing words, and at rs3743204 for both irregular and nonword reading. Verbal short-term memory was associated with rs685935. Support for association was not found at rs3743205 and rs61761345 as previously reported by Taipale et al., but these SNPs had very low (0.002 for rs3743205) minor allele frequencies in this sample. These results suggest that DYX1C1 influences reading and spelling ability with additional effects on short-term information storage or rehearsal. Missense mutation rs17819126 is a potential functional basis for the association of DYX1C1 with dyslexia.

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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.