ADHD and Dyslexia: The Possible Link Via Sluggish Cognitive Tempo

September 1, 2015
E. Mark Mahone, PhD
Volume 32, Issue 9

Researchers have identified a “multiple-deficit” model of the comorbidity between ADHD and dyslexia in which each disorder has multiple predictors-some specific and some shared.

BRIEF COMMUNICATION

Before DSM-IV, investigators identified a subset of symptoms termed “sluggish cognitive tempo” (SCT) that were thought to be distinct from the core features of ADHD.1 Features of SCT include daydreaming, difficulty in sustaining attention, decreased orientation, confusion, lethargy, drowsiness, and physical underactivity.2 Functionally, SCT manifests in reduced speed and efficiency of responses (ie, slow processing speed).

At the time of publication of DSM-IV, there was insufficient evidence to warrant a separate ADHD subtype to characterize SCT. More recent factor analytic investigations, however, have honed the definition of SCT to include 3 core symptoms-lethargy, underactivity, and slowness-that appear distinct from the inattention associated with ADHD and are hypothesized to be a function of earlier selective attention processes.3,4 Initially, proposed revisions for DSM-5 included a separate “restrictive inattentive” ADHD subtype that in many ways mimicked the SCT construct; however, upon publication of DSM-5, the restrictive inattentive subtype was not included, leading clinicians and researchers to continue their efforts to clarify the phenotype of SCT and to determine whether (or how) it overlaps with ADHD.

The answer may lie at the intersection between ADHD and dyslexia.

ADHD and dyslexia represent 2 common childhood disorders that co-occur more often than expected by chance.5 The most parsimonious explanation for the co-occurrence is that they partially share genetic risk factors, with a stronger genetic correlation between dyslexia and inattention than between dyslexia and hyperactivity.6 To this end, researchers have identified a “multiple-deficit” model of the comorbidity between ADHD and dyslexia in which each disorder has multiple predictors-some specific and some shared.7

The ADHD model includes one unique predictor (response inhibition) and one shared predictor (processing speed), while the dyslexia model includes 2 unique predictors (phonological awareness and naming speed) and one shared predictor (processing speed). Here, processing speed represents the speed with which a task is completed with reasonable accuracy. Children with ADHD commonly display slow processing speed.8 However, slow processing speed is also observed in children with dyslexia.9 Moreover, becoming a skilled reader involves adequate reading fluency, which is linked to efficient processing speed. Thus, while processing speed is separable from the core phonological deficit in dyslexia, it can influence reading fluency, even among individuals who can read single words accurately (ie, those without “classic” phonological dyslexia), and can affect the development of more complex academic skills such as reading comprehension.11

To this end, processing speed, a core feature of the SCT construct, may represent a promising candidate for a behavioral “polyphenotype” (ie, a phenotype constituting core deficits of more than one disorder), whose psychological makeup can account for comorbidity between neurodevelopmental conditions and those with genetic architecture that can account for the genetic correlations between these highly prevalent disorders.10

It is hypothesized that examination of the shared phenotypic variance between ADHD and dyslexia via the SCT construct will provide more specificity than examination of attentional factors alone. Researchers and clinicians are encouraged to consider the potential mediating influence of SCT in understanding outcomes in children with ADHD and/or dyslexia, and to consider treatments that attend to the potentially unique influence of SCT.11

Disclosures:

Dr Mahone is Director of Neuropsychology at the Kennedy Krieger Institute and Professor of Psychiatry and Behavioral Sciences at the Johns Hopkins University School of Medicine, Baltimore, Maryland. He reports that he has received support by the NIH/CTSA grant (UL10RR25005).

References:

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11. Grigorenko EL. Commentary: Translating quantitative genetics into molecular genetics: decoupling reading disorder and ADHD-reflections on Greven et al. and Rosenberg et al. J Child Psychol Psychiatry. 2012;53:252-253.