Validación del Diseño

The phonological deficit theory states that dyslexia is caused by a high-level phonological processing impairment (Snowling, 1998). This impairment can manifest as problems with:

(1) phonological awareness (knowledge of the sound structure of language), (2)

phonological recoding (converting letters into speech sounds), (3) holding speech sounds in working memory, (4) blending and segmenting different phonemes to sound out unfamiliar words, and (5) phonological representations in long term memory (Snowling, 1998; Snowling & Hulme, 1994; Snowling, 2001; Wagner & Torgesen, 1987). Such problems are argued to cause inefficient reading and spelling strategies (Wagner &

Torgesen, 1987), and this is how a general phonological impairment is argued to cause the reading and spelling problems characteristic of dyslexia (see Figure 4 for causal chain).

Figure 4 Snowling’s (1998) Causal phonological deficit theory of dyslexia Behavioural Evidence for the Phonological Deficit Theory

At the behavioural-level there is strong support for the phonological deficit theory due to:

(1) phonological impairments observed in dyslexia, (2) phonological ability predicting future reading ability, and (3) phonological training improving reading ability.

Phonological impairments are consistently found in dyslexia (Katz, 1986; Swan &

Goswami, 1997; Wimmer et al., 1998), and phonological awareness is found to be

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predictive of future reading ability (Mann, 1984, 1993; Mann & Liberman, 1984);

suggesting the phonological impairments may be at the core of dyslexia. Good readers demonstrate difficulties with phonetically confusable words compared to phonetically non-confusable words, whereas poor readers demonstrate no differences suggesting that poor readers do not employ phonological representations to aid in reading like non-impaired readers do (Mann, 1984). Phonological impairments also seem to be causally related to reading, as phoneme-based interventions result in reading and phonological improvements in children with and without dyslexia (Kozminsky & Kozminsky, 1995;

Lovett et al., 1994).

Although there is strong evidence that phonological impairments are central to dyslexia, careful consideration is needed as: (1) the phonological theory is not able to account for different descriptive (i.e. not part of DSM diagnostic criteria) expressions of dyslexia (surface V phonological) while attentional abilities can, (2) lower level auditory processing appear to predict reading ability, and (3) other high-level cognitive processes (executive function) interfere with performance on phonological tasks.

One problem with the phonological deficit theory is that it cannot account for different expressions of dyslexia (surface and phonological dyslexia), whereas attentional

impairments can (Facoetti et al., 2006; Valdois, Bosse, & Tainturier, 2004). Phonological dyslexia is characterised by phonological impairments, whereas surface dyslexia is not.

When compared with surface dyslexia and a control group, phonological dyslexia is associated with a lack of attentional inhibition in the right visual field when instructed to attend to left (Facoetti et al., 2006), suggesting that attention may play a role in

phonological reading. Both phonological and attentional impairments demonstrate independent predictive ability for reading impairments in dyslexia (Valdois et al., 2004).

Attentional abilities better explain surface-phonological dyslexia distinction, indicating that the phonological theory is limited as it does not account for the influence of other high-level factors (attention) on the reading impairments found in dyslexia.

Although there is strong evidence for phonological impairments predicting reading ability, there is also evidence that auditory processing impairments are predictive of reading

ability. A longitudinal study of reading development examined dyslexia and non-dyslexia (with and without a genetic risk for dyslexia) and found that those who later developed dyslexia had auditory processing impairments (frequency modulation, speech perception) as well as phonological impairments (Boets et al., 2011). Both phonological abilities and lower level auditory processing abilities predicted different stages of development in reading: kindergarten to first grade reading was predicted by auditory processing,

whereas third grade reading ability was predicted by phonological awareness (Boets et al., 2011). This suggests that non-phonological auditory processing impairments may also play a role in dyslexia.

Neural Evidence for the Phonological Deficit Theory

At the neural level, there is evidence of a disruption to the phonological brain system in dyslexia, with under-activation of Broca’s area and the insula found in dyslexia during phonological tasks (Paulesu et al., 1996). Phonological deficits in dyslexia may be caused by malfunctioning of the insula which results in disconnection to other phonological sites in the brain (Paulesu et al., 1996). Disruption of the left perisylvian cortex is also found in dyslexia and is argued to cause problems with phonological representations (Ramus, 2004).

However, higher level cognitive factors implicated in task performance complicate the interpretation of such findings. Several meta-analyses exploring the neural underpinnings of phonological impairments in dyslexia indicate that the phonological brain system may not be implicated until adulthood and more importantly that attentional problems may cause phonological impairments in childhood (Richlan, 2012; Richlan et al., 2010; Richlan, Kronbichler, & Wimmer, 2009, 2011). For instance, Richlan et al. (2009) found abnormal activation in left temporo-parietal and occipito-temporal regions supporting the

phonological deficit theory, however, when this analysis was split by age (child v adult dyslexia), left temporo-parietal and occipital-parietal abnormalities were observed in adult dyslexia, while children demonstrated a network of under activation in the inferior

parietal lobule and only limited under activation in occipito-temporal regions. This

suggests that abnormalities in the phonological brain system may only be associated with

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adult dyslexia and not childhood dyslexia, making it difficult to understand how

phonological impairments are causally implicated. Another meta-analysis, found under-activation in the left occipito-temporal region, inferior frontal gyrus and inferior parietal lobule in dyslexia during reading (Richlan et al., 2010). Richlan (2012) suggests that dyslexia could be caused by top down attentional mechanisms (due to the role of the inferior parietal lobule in attention) which influence the output of phonological

representations in the inferior frontal gyrus and phonological decoding in the occipito-temporal region. Indeed, other high-level cognitive factors have also been argued to be implicated in phonological measures due to multiple task demands tapping executive function and working memory systems (Ramus & Szenkovits, 2008), suggesting that phonological impairments may manifest also as a consequence of other higher level cognitive problems (e.g. executive function, attention).

High-level Cognitive Confounds of Evidence Supporting the Phonological Deficit Theory A central assumption of the phonological deficit theory is that phonological impairments manifest in dyslexia. Of interest is the observation that these impairments manifest more so with other higher level task demands (EF, working memory) (Ramus & Szenkovits, 2008). Those with dyslexia are not impaired on all tasks that measure phonological

processing, and impairments are found only in tasks that have executive demands such as storage, speedy retrieval, detection and manipulation of phonemes (Ramus & Szenkovits, 2008). This suggests that impairments on these measures may be more reflective of a disorder specific EF impairment in processing phoneme information. At the neural level, there is also evidence to suggests that impairments in the top down attentional control network may be implicated in poor phonological decoding (Richlan, 2012). Given that EF impairments are found in dyslexia (Brosnan et al., 2002), and, also that EF processing contributes to reading ability independently of phonological processing (Swanson, 1999), a disorder specific EF impairment in processing phoneme content may explain why those with dyslexia are impaired on some but not all phonological tasks (Ramus & Ahissar, 2012), and potentially why dyslexia and ADHD so frequently co-occur.

Conclusion

Although there is strong evidence for the phonological deficit theory of dyslexia, interpretation of this research is complicated due to: (1) phonological theory not

adequately explaining the difference between surface dyslexia and phonological dyslexia, (2) auditory processing also being predictive of dyslexia, (3) the role of high-level cognitive factors in task performance, and (4) top down control of the phonological brain system by the attentional brain system. The theory also provides no explanation for why dyslexia and ADHD so frequently co-occur.