Attention deficit hyperactivity disorder and dyslexia: a history of overlap

Araújo, Alexandra Prüfer de Queiroz Campos

doi:10.1590/s0004-282x2012000200001

Cited by 7 publications

(6 citation statements)

References 7 publications

(5 reference statements)

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“…Interestingly, some recent evidence has suggested that these visual attention deficits and phonological deficits may be orthogonal to one another, and moreover, likely mediated by separate neural mechanisms [4, 78]. Additional support for the role of attention in reading comes from the high comorbidity between dyslexia and ADHD, and the observation that 40% of children diagnosed with ADHD also exhibit reading impairments (although note that this overlap may not be due to deficits in visuospatial attention specifically) [79-81]. In the current study, knocking down Dyx1c1 led to significant impairments in visual attention in male rodents.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of the Candidate Dyslexia Susceptibility Gene Homolog Dyx1c1 in Rodents: Effects on Auditory Processing, Visual Attention, and Cortical and Thalamic Anatomy

Szalkowski¹,

Booker

Truong³

et al. 2013

Dev Neurosci

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The current study investigated the behavioral and neuroanatomical effects of embryonic knockdown of the candidate dyslexia susceptibility gene (CDSG) homolog Dyx1c1 through RNA interference (RNAi) in rats. Specifically, we examined long-term effects on visual attention abilities in male rats, in addition to assessing rapid and complex auditory processing abilities in male and, for the first time, female rats. Our results replicated prior evidence of complex acoustic processing deficits in Dyx1c1 male rats and revealed new evidence of comparable deficits in Dyx1c1 female rats. Moreover, we found new evidence that knocking down Dyx1c1 produced orthogonal impairments in visual attention in the male subgroup. Stereological analyses of male brains from prior RNAi studies revealed that, despite consistent visible evidence of disruptions of neuronal migration (i.e., heterotopia), knockdown of Dyx1c1 did not significantly alter the cortical volume, hippocampal volume, or midsagittal area of the corpus callosum (measured in a separate cohort of like-treated Dyx1c1 male rats). Dyx1c1 transfection did, however, lead to significant changes in medial geniculate nucleus (MGN) anatomy, with a significant shift to smaller MGN neurons in Dyx1c1-transfected animals. Combined results provide important information about the impact of Dyx1c1 on behavioral functions that parallel domains known to be affected in language-impaired populations as well as information about widespread changes to the brain following early disruption of this CDSG.

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Section: Discussionmentioning

confidence: 99%

Knockdown of the Candidate Dyslexia Susceptibility Gene Homolog Dyx1c1 in Rodents: Effects on Auditory Processing, Visual Attention, and Cortical and Thalamic Anatomy

Szalkowski¹,

Booker

Truong³

et al. 2013

Dev Neurosci

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“…The first issue concerns the well-established comorbidity of developmental dyslexia and attention deficit disorders (ADD; Araujo, 2012;Boada, Willcutt, & Pennington, 2012). Because the Hebb learning task is very demanding on sustained and focused attention, a differential Hebb effect is not necessarily the result of a deficit in serial learning hut may be attributed to the possible comorbid attention problems of persons with dyslexia (see also Wimmer's analogous critique on the automatization deficit hy pothesis of Nicolson & Fawcett, 1990;Wimmer, Mayringer, & Raberger, 1999).…”

Section: Methodological Issues and Improvementsmentioning

confidence: 99%

No solid empirical evidence for the solid (serial order learning impairment) hypothesis of dyslexia.

Staels¹,

Broeck²

2015

Journal of Experimental Psychology: Learning, Memory, and Cogni

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This article reports on 2 studies that attempted to replicate the findings of a study by Szmalec, Loncke, Page, and Duyck (2011) on Hebb repetition learning in dyslexic individuals, from which these authors concluded that dyslexics suffer from a deficit in long-term learning of serial order information. In 2 experiments, 1 on adolescents (N = 59) and 1 on children (N = 57), no empirical evidence was obtained for impaired Hebb learning in dyslexics, whether the same data-analytical procedure as Szmalec et al. was used or whether some methodological improvements were applied (e.g., using a more sensitive index of Hebb learning, and equating groups on filler performance with state trace analysis). In an additional state trace analysis, aggregating data over participants, it was shown that performance on the repeated Hebb sequences was almost perfectly predictable from performance on the nonrepeated sequences (fillers). The implications of these findings are outlined for the current discussion on the mechanisms for encoding immediate serial recall and long-term sequence learning and for computational models attempting to simulate these mechanisms.

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“…The consequence of the overlap of risk factors is that developmental disorders produce a greater than expected co-occurrence. For example, the comorbidity between dyslexia and ADHD has been well established with 25–40% of children with one disorder meeting criteria for the other (Araujo, 2012; August & Garfinkel, 1990; Boada, Willcutt, & Pennington, 2012; Semrud-Clikeman et al, 1992; Willcutt & Pennington, 2000). Therefore, it is crucial that in studies where performances on tasks that are very demanding on attentional functioning are compared between groups researchers should control for attentional functioning.…”

Section: Implicit (Sequence) Learning In Dyslexiamentioning

confidence: 99%

A specific implicit sequence learning deficit as an underlying cause of dyslexia? Investigating the role of attention in implicit learning tasks.

Staels

Broeck

2017

Neuropsychology

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Dyslexic children do not suffer from a specific implicit sequence learning deficit. The slower RTs of the dyslexic children throughout the entire implicit sequence learning process are caused by their comorbid attention problems and overall slowness. A key finding of the present study is that, in contrast to what was assumed for a long time, implicit learning relies on attentional resources, perhaps even more than explicit learning does. (PsycINFO Database Record

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Attention deficit hyperactivity disorder and dyslexia: a history of overlap

Cited by 7 publications

References 7 publications

Knockdown of the Candidate Dyslexia Susceptibility Gene Homolog Dyx1c1 in Rodents: Effects on Auditory Processing, Visual Attention, and Cortical and Thalamic Anatomy

Knockdown of the Candidate Dyslexia Susceptibility Gene Homolog Dyx1c1 in Rodents: Effects on Auditory Processing, Visual Attention, and Cortical and Thalamic Anatomy

No solid empirical evidence for the solid (serial order learning impairment) hypothesis of dyslexia.

A specific implicit sequence learning deficit as an underlying cause of dyslexia? Investigating the role of attention in implicit learning tasks.

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