Executive Function in Comorbid Dyslexia-ADHD

The association between compromised EF and comorbid dyslexia-ADHD is more consistent than dyslexia alone, with most studies finding evidence of an impairment (McGee et al., 2004; Rucklidge & Tannock, 2002; Tiffin-Richards et al., 2008; Willcutt et al., 2001, 2005). Studies have found evidence for (Rucklidge & Tannock, 2002; Willcutt et al., 2005), and against a common EF (response inhibition) impairment (Bental & Tirosh, 2007);

for a working memory impairment (McGee et al., 2004; Rucklidge & Tannock, 2002; Tiffin-Richards et al., 2008; Willcutt et al., 2001); and, for (Tiffin-Tiffin-Richards et al., 2008) and against a switching impairment in comorbid dyslexia-ADHD (Bental & Tirosh, 2007).

Although there is debate surrounding which specific aspects of EF are compromised in comorbid dyslexia-ADHD, there are difficulties also in understanding the source of

impairments in the comorbid condition, such that some find deficits associated with each pure form of condition are additive in the comorbid condition (Willcutt et al., 2001) while others suggest that they are more severe (Rucklidge & Tannock, 2002).

Neale and Kendler (1995) proposed a number of explanations for comorbidity between behaviourally distinct conditions. These explanations suggest that comorbidity may be due to chance (artefact of chance), a single impairment manifesting differently at the

behavioural level (alternate forms), one condition increasing risk for the behavioural expression of another condition (multiform), each isolated condition and comorbid condition being separate (independent conditions) and each isolated condition having

shared impairments which result in the comorbid condition (correlated liabilities) (Neale &

Kendler, 1995). The alternate forms explanation of comorbidity proposes that isolated conditions may be characterised by a single shared underlying impairment which manifests differently at the behavioural level and results in comorbidity due to

environmental risk factors interacting with genetic risk factors. The multiform explanation of comorbidity proposes that one condition characterised by a single impairment

increases likelihood of the behavioural manifestation only of the other condition. The independent conditions explanation of comorbidity proposes that each isolated condition and the comorbid instance are independent. The correlated liabilities explanation

suggests that each isolated condition share some impairments which explain comorbidity.

A number of these explanations have been explored in comorbid dyslexia-ADHD.

Comorbidity between these conditions does not appear to be a product of chance, as both conditions co-occur at a greater than chance rate (American Psychiatric Association, 2013;

Gilger et al., 1992; Willcutt & Pennington, 2000). The phenocopy hypothesis (multiform) (Pennington, Groisser, & Welsh, 1993) suggests that comorbid dyslexia-ADHD is

characterised by the same underlying impairments as dyslexia alone and is only associated with symptoms of ADHD due to frustration with reading. The cognitive subtype hypothesis (independent conditions) (Rucklidge & Tannock, 2002) suggests that comorbid dyslexia-ADHD is a unique subtype as it appears to be associated with more severe and additional impairments than either isolated condition. While the multiple deficit hypothesis

(correlated liabilities) (McGrath et al., 2011; Willcutt et al., 2010) suggests that each isolated condition is underpinned by distinct impairments as well as shared impairments which result in comorbidity.

Pennington et al. (1993) proposed the phenocopy explanation of comorbid dyslexia-ADHD, employing a double dissociation design the found impaired phonological abilities in dyslexia, impaired EF abilities in ADHD and only impaired phonological abilities in

comorbid dyslexia-ADHD, suggesting that the comorbid group exhibited the same

underlying impairments of dyslexia alone yet expressed the symptoms of ADHD. However, subsequent studies failed to replicate these findings and instead suggested that the

comorbid group exhibit an additive combination of impairments from dyslexia and ADHD

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alone (Willcutt et al., 2001). Employing a similar design, Willcutt et al. (2001) found that comorbid dyslexia-ADHD expressed the impairments associated with dyslexia alone (phonological, working memory) and ADHD alone (response inhibition) in an additive manner. Further studies have replicated this additive effect, of phonological impairments associated with dyslexia and EF impairments associated with ADHD expressing in an additive manner in the comorbid condition (Gooch, Snowling, & Hulme, 2011). Findings of additivity and a failure to replicate the phenocopy explanation suggests that it is not a sufficient explanation of comorbidity between dyslexia and ADHD. However, double dissociation studies of dyslexia and ADHD suggest that dyslexia alone is associated with a single phonological deficit and ADHD alone is associated with a single EF deficit, which does not consider findings of impaired EF in dyslexia alone (see section 2.6).

Rucklidge and Tannock (2002) proposed the cognitive subtype hypothesis when they found that the comorbid group demonstrated an additive and more severe profile of impairments (speed, naming) than either dyslexia alone (verbal working memory) or ADHD alone (speed, naming, inhibition). Studies supporting this explanation of comorbid dyslexia-ADHD have found phonological impairments in dyslexia alone, executive

impairments in ADHD alone and additional rapid naming and working memory impairments in the comorbid condition (Bental & Tirosh, 2007). This strengthens the explanation of the comorbid condition as a unique cognitive subtype, although neither provide an explanation of findings of impaired EF in dyslexia alone (see section 2.6).

The multiple deficit/shared aetiology hypothesis (McGrath et al., 2011; Pennington, 2006;

Willcutt et al., 2010) suggests that complex neurodevelopmental conditions such as dyslexia and ADHD are unlikely to arise from a single deficit (e.g. phonological- dyslexia, EF- ADHD) rather each isolated condition is associated with multiple distinct and shared risk factors, and shared risk factors explain comorbidity. Pennington (2006) suggests that phonological impairments appear to be a specific risk for dyslexia, inhibition appears to be a specific risk for ADHD while processing speed appears to be a shared risk factor for both and therefore may explain comorbidity. However, studies differ with regard to the profile of impairments in each case, Willcutt et al. (2010) found that dyslexia, ADHD and

comorbid dyslexia-ADHD were impaired relative to control participants on working

memory, inhibition, processing speed, phonological awareness and verbal reasoning and that the comorbid group had more severe processing speed and response inhibition impairments, suggesting that each condition is associated with EF. However, at a predictive level processing speed appeared to be the only shared risk factor, as ADHD symptoms were predicted by speed and inhibition and dyslexia symptoms were predicted by working memory, phonological awareness, speed and verbal reasoning. Processing speed as a shared overlapping risk factor has been replicated by other studies suggesting that it may explain overlap (Shanahan et al., 2006; Willcutt et al., 2005). These studies determine overlap based on shared cognitive processes implicated in core

symptomatology but do not extend explanations to non-core symptomatology. These studies typically suggest that although EF is impaired it is not related to core symptoms in dyslexia, yet a number of studies suggest that EF impairments are associated with dyslexia (see section 2.6) and appear to be implicated in core reading symptoms (see section 2.8).

This suggests the importance of exploring the role of EF in dyslexia while systematically accounting for processing speed impairments.

For now, at the level of impairments it appears that both dyslexia and ADHD appear to be underpinned by multiple cognitive deficits including EF, and the multiple deficit hypothesis may provide the optimum explanation for comorbidity (Germanò et al., 2010).

2.8 EF Involvement in Core (Reading) and Non-Core (Socio-Emotional) Issues Associated