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Causal Explanations of Dyslexia

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Published: Wed, 04 Apr 2018

Introduction

Poor decoding and spelling abilities along with difficulties in precise and fluent recognition of words characterise the learning disability of dyslexia (International Dyslexia Association, 2001). Despite the extensive scientific attention that dyslexia has received there is still much debate about its causal explanation. Recently, Stoodly and Stein (2012) have pointed out that reading is only incidentally affected by this highly heritable neurobiological syndrome with multi-factorial aetiology. For example, it has been found that dyslexics exhibit various difficulties even in motor skills (Ramus, Pidgeon & Frith, 2003; Fawcett & Nicolson, 1995b;), mathematics (Ackerman & Dykman, 1995), balance (Yap & van der Leij, 1994), rapid processing (Nicolson & Fawcett, 1994a) and working memory (Ramus et al., 2003; Nicolson, Fawcett & Dean, 2001). Hence, the essay’s intention is to provide a brief overview of the most established causal explanations, before ultimately focus to the cerebellar deficit hypothesis.

Phonological deficit hypothesis – (PDH)

The majority of dyslexia’s research was dominated by the phonological and magnocellular deficit hypotheses. According to Castles and Friedman (2014), the PDH refers to a wide range of disabilities that derive from the production, perception, manipulation or retention of speech sounds. More specifically, the PDH states that the breaking of the spoken words into phonemes or syllables is the main cause of dyslexics’ reading problems (Nicolson & Fawcett, 2001). The theory’s most compelling arguments are its direct relationship with the way that humans learn how to read, as the phonological module is the language’s most basic level (Shaywitz, Morris, & Shaywitz, 2008), and the fact that almost all dyslexic children exhibit some kind of phonological deficiency (Stanovich, 1988a). However, the last view is highly debatable with Dehaene (2009) to be one of its strongest advocates and Ramus et al. (2003) and White et al. (2006) to reject it after discovering that some of their dyslectic participants exhibited only visual and no phonological deficiencies. Furthermore, PDH fails to explain dyslexia’s several secondary deficits, such as balance, memory, visual processing, mild motor coordination, etc. (Nicolson, Fawcett, Brookes & Needle, 2010).

Double deficit hypothesis – (DDH)

This theory emerged due to growing evidence that some dyslexic children with poor comprehension and sufficient decoding skills could not be diagnosed as dyslexic, because their symptoms could not be identified as phonological processing deficiencies (Vukovic & Siegel, 2006). Thus, Wolf and Bowers (1999) in order to address this problem proposed that readers should be classified according to their adequacy or inadequacy in the cognitive skills of speed naming and phonological processing, with those showing deficiencies in both (DDH) to exhibit the most reading difficulties. This theory was further supported by Turkeltaubetal, Gareau, Flowers, Zeffiro and Eden (2003) who proved that rapid automatising naming-RAN and phonological awareness-PA activated different brain regions. However, Vukovits and Siegel (2006) pointed out that some studies, including theirs, have failed to prove that RAN has a connection with reading development, thus providing limited support to the DDH. Nonetheless, a recent study provided neuroimaging evidence of the involvement of separated brain systems in the processing of the PA and RAN skills, strengthening even more the DDH (Norton et al., 2014). Despite the inconsistent data DDH provides a good explanation about dyslexia’s core symptoms, but fails to take into account the whole spectrum of its various subtypes.

Magnocellular deficit hypothesis – (MDH)

The MDH postulates that dyslexics’ reading problems emerge from their atypical visual or auditory magnocellular pathway-MP, which leads to sensory processing problems (Eden, 1996) due to its underdeveloped large neurones (Stein & Talcott, 1999). The hypothesis’ most supportive data came from a post-mortem study in the brains of dyslexics, demonstrating that in the lateral geniculate nucleus the neurones in the MP were misplaced and shrunk by 30% than the controls’ (Galaburda and Livingstone, 1993). This theory has long been confirmed by Lovegrove, Martin, Blackwood, and Badcock, (1980), who proved that dyslexics not only shown lower contrast sensitivity at high temporal frequencies, but at low spatial as well. They also proved that dyslexics’ contrast sensitivity at the high spatial frequencies was enhanced, a finding also confirmed by Mason, Cornelissen, Fowler and Stein (1993). However, despite the above findings, inconsistent data from subsequent studies gave rise to controversies about the MDH’s validity (see Scottum, 2000), as it became clear that the impairment was mild and not present in all the dyslexics (Stein, Talcott, & Walsh, 2000). Additionally, studies with small number of participants have failed to replicate Lovegrove’s et al. (1980) findings, probably due to the usage of inappropriate tests (not sensitive) or participants.

Cerebellar deficit hypothesis – (CDH)

Even though the MDH is adequately explaining some of dyslexia’s core manifestations it does not address the common problems of clumsiness, dysgraphia, automating skills, balance, fluency etc. The Automatization deficit hypothesis-ADH (Nicolson & Fawcett, 1990) emerged to explain some of the above difficulties, but was not able to specify the underlying brain structure (Fawcett & Nicolson, 2004). Hence, the CDH came to address this shortcoming and merged ADH’s cognitive level explanation with its neurological. Thus, one of the CDH’s strengths was its ability to explicate these non literacy problems, which were pointing out the cerebellum and led to its identification as dyslexia’s underlying neurological structure. One of the reasons that the cerebellum was not associated with dyslexia earlier was the notion that it had no relationship with the language. However, Fullbright et al. (1999), proved that reading did involved the cerebellum, a finding also supported by Scott et al. (2001), who discovered that tumours in the cerebellum were often associated with reading problems. After the emergence of the CDH a number of studies came into sight and provided further support. Specifically, anatomical cerebellar differences were revealed in dyslexics’ grey matter, as it was considerably reduced in both sides of their cerebellar nuclei (Brambati et al., 2004), a discovery recently reconfirmed by Stoodley (2014). However, cerebellar irregularities could not be identified either by Hoeft et al. (2007) or Silani et al. (2005), but this might was due to the selection criteria or dyslexics’ wide heterogeneity of symptoms. Concerning dyslexics’ balance difficulties-BD it was found that they were linked to the cerebellum and served as a by-product of dyslexia (Moe-Nilssen, Helbostad, Talcott & Toennessen, 2003), a view also acknowledge by Needle, Fawcett and Nicolson (2007), but not accepted by Loras, Sigmundsson, Stensdotter, and Talcott (2014). Their experiments demonstrated a lack in significant statistical connection between reading and balance in healthy subjects and thus they suggested that when reading problems exist BD could not be accounted as a reliable measurement for the assessment of dyslexia risk (Loras et al., 2014). Although, this in contrast with Viholainen et al. (2011), who did found a correlation and suggested that balance and reading seemed to share a genetic mechanism. This inconsistency maybe explained due to the possibility that this relationship only lies in individuals with some kind of disorder or is just the result of disorder comorbidity. Additionally, studies have revealed that compared to the control group, dyslexics’ volume of the right anterior lobe was significantly smaller (Eckert et al., 2003) and their cerebellum was particularly symmetrical (Rae et al, 2002). On the other hand, CDH generated significant controversy as some of its critics claimed that the cerebellum is just an “innocent bystander” and not dyslexia’s causal factor, because it might receives compromised input from other cortical or sensory brain areas (Zeffiro & Eden, 2001). Even though that this argument seems quite logical, there are not enough data to either support or reject it and only future research will shed further light. After all, in neuroscience research there are not only black and white findings. Furthermore, it is being claimed that cerebellar dysfunction cannot elucidate the whole range of dyslexia’s cases (Stoodley & Stein, 2011) and neither is only specific to dyslexia as it also appears to other deficits, such as Attention Deficit Hyperactivity Disorder or developmental coordination disorder (Rabeger & Wimmer, 2003; Ramus et al., 2003a). According to Stoodley and Stein (2011), there is also the criticism that the cerebellum is not involved in reading and is only responsible for motor skills, but it seems that this has already been refuted with several studies highlighting cerebellum’s involvement in reading (Turkeltaub, Eden, Jones, & Zeffiro, 2002), in modulating and refining language (Murdoch and Whelan, 2007), and even in rhyming (Booth, Wood, Lu, Houk & Bitanet, 2007), but no consensus has yet been established. With no doubt there is some truth in each of these criticisms, but more and more data provide a stronger support to the CDH.

Conclusion

It is undeniable that each hypothesis adds a little bit to the general picture and explains dyslexia’s causality from a different angle, by overlapping and complementing each another. Future research should focus more on imaging studies in order to identify each underlying neural mechanism related to dyslexia and aim to a unified deficit theory, possibly with many subtypes, so children with dyslexia could be taught and treated properly. This would also provide the opportunity to master the learning mechanisms and contribute to the cure/management of other learning disabilities as well.


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