Dyslexia and Sli: Atypical Psychology

Dyslexia and Specific language impairment (SLI) are two of the most commonly occurring learning disorders among children (Pennington and Bishop, 2009). SLI and dyslexia have similar a prevalence in modern day society and is estimated to affect 3 – 10% of children (Tomblin, 1997). Broadly speaking dyslexia has generally been viewed as a disorder that includes a deficit in printed word recognition whereas SLI is more to do with oral language deficits (Ramus, Marshall, Rosen and Van der Lely, 2010). Research investigating both of these disorders over many years has been vast but has traditionally been carried out by separate professionals and disciplines. Typically SLI research was conducted by speech/language pathologists and clinical linguists and dyslexia studies were mainly carried out by educational psychologists (Fraser, Goswami, and Ramsden, 2010). Although dyslexia and SLI have often been treated and classified as distinct disorders in the past, the recent reclassification of dyslexia in the 1970’s as a language disorder has bought attention to the striking similarities (Bishop and Snowling, 2004).

This has resulted in the general consensus regarding the nature of the relationship between these disorders as “…different manifestations of the same underlying problem differing only in severity or developmental stage” (Bishop and Snowling, 2004). However there are various research findings and theories that offer persuasive arguments and evidence suggesting opposing and conflicting views about the relationship of dyslexia and SLI. This essay aims to determine whether dyslexia can be considered as a mild form of SLI. This will be achieved by reviewing a range of factors on varying levels, firstly by comparing the definitions of each disorder drawing on any overlap or similarities that indicate supportive or opposing evidence. Secondly, evaluation of current literature and prominent findings that advocate and oppose the notion of dyslexia being a milder form of SLI will be carried out. Thirdly, causational aspects: etiology and neurobiology (biology and environment), cognition and behaviour of dyslexia and SLI will be investigated with consideration to commonalities and disparities.

Finally, this essay will review the most renowned models and hypotheses that pertain to the relationship between these two disorders. An argument will be made throughout the essay and a conclusion will be drawn from the evidence presented as to whether dyslexia can be considered as a milder form of SLI. Firstly, examining the definitions of dyslexia and SLI results in an inconclusive conclusion. Both dyslexia and SLI can be defined in various ways due to the varying levels of severity and subcategories of each disorder. For the purpose of this essay the definitions that will be used are the definitions that appeared most frequently cited among the literature reviewed. These definitions are specific yet broad enough to encompass the range of different levels and subcategories. Leonard (1998) describes SLI as oral language that is impaired and lagging behind other areas of development for no apparent reason. Snowling (2000) defines dyslexia as having poor literacy skills despite adequate intelligence and opportunity to learn.

The diagnosis criteria in both disorders are similar in that they both specify that no other impairment should be present that could account for these deficits (i.e. hearing problems) patients must display an otherwise normal IQ level and display no signs of any other handicaps or disadvantages that may affect the learning process (Newbury et al, 2011). Both dyslexia and SLI have similar aspects with diagnosis and overlapping exclusion criteria’s, however, the definitions are distinctly different in that they both specify impairments in different aspects of development, literacy skills in dyslexia and oral skills in SLI. It could be argued that due to the similarities and overlaps between the definitions there is supportive evidence that these disorders are related, however, the clear distinctions in the definitions firmly separate the two disorders providing supportive evidence to the notion that dyslexia should not be considered a milder form of SLI. Secondly, causations of dyslexia and SLI will be considered as research in this area attempts to determine the underlying problems and deficits of each disorder.

If the causations of dyslexia and SLI are the same in both cases then it stands to reason that the disorders should be classified as the same disorders (that may vary due to the severity). The first causation to be considered in is the behaviour characteristics that are typically exhibited. SLI behaviours are indicative of poor/below average vocabulary and grammar when comprehending and communicating orally (Joanisse & Seidenberg, 1998). Vast amounts of research has investigated causation factors of SLI and reveals that the underlying causes are often attributed to various aspects such as poor phonological awareness, inflicted morphology, impaired working memory span, analogical reasoning, visual imagery etc (Catts & Kamhi, 2005). In comparison, the research into dyslexic behaviours has predominantly been attributed to insufficient processes in the phonological processes (Fraser, Goswami, & Ramsden, 2010.) much like one of the behavioural aspects of SLI.

Overall the research into the causations of the behaviours certainly appear to overlap to a certain degree, especially when considering phonological deficits as it is an important contributing factor in both disorders (Bishop & Snowling, 2004), more so in dyslexia than SLI. SLI involves many more underlying processes and is a more complex disorder with various underlying factors. Therefore findings give supportive evidence to the notion that dyslexia is a milder form of SLI as its primary causation, is the same as one of the causation factors underlying SLI. Although dyslexia and SLI have this mutual causation in common it produces slightly different outcomes/behaviours (deficit in literacy and oral respectively). The second causation to be considered is the unique biological underpins of these disorders (specifically neurobiology and etiology). A review of the literature suggests that a complex genetic etiology which involves various interactions between genetic and environmental factors is a strong causational factor. Findings have consistently found that relatives of those with dyslexia and/or SLI have a 30 – 50 % chance of developing the disorder, giving supportive evidence of these disorders being hereditary (Newbury et al, 2011).

Genetic risk variants for dyslexia and SLI have been identified and current findings indicate shared genetic influences (Newbury et al, 2011). These genetic similarities imply a close biological relationship between dyslexia and SLI, but it is imperative to be aware that gene/environmental interaction should also be considered. Neurological research shows that dyslexia could be attributed to a reduction in the left hemisphere during language process (Newbury et al, 2011). Additionally neurological research has found that SLI appears to show evidence for atypical left-right planum temporal and perisylvian asymmetry (Newbury et al. 2011). These neurological findings suggest separate deficits in different parts of the brain being responsible for the causation of the disorders, opposing the notion of dyslexia being considered a milder form of SLI as they do not share unique neurological underpinnings. Further biological research has shown that birth disorders are associated with early abnormalities in neurological development resulting in dyslexia and/or SLI (Newbury et al. 2011). Overall, conflicting evidence has emerged regarding the relationship between dyslexia and SLI when looking at biological causations.

The final causation to be considered is the cognitive aspect. Cognition was briefly mentioned when discussing the causation of behaviour manifested in dyslexia and SLI. As already stated phonological awareness is attributed as the key underlying deficiency in dyslexia and SLI. However SLI appears to incorporate many more cognitive deficits such as low auditory level skills, phonological processing and phonological memory as well as syntax problems and semantic issues (Bailey & Snowling, 2002). This shows that SLI is a much more complex disorder than dyslexia involving more cognitive deficits and impairments, however, the cognitive causations in each disorder heavily overlap which gives supportive evidence arguing that dyslexia is a milder form of SLI. Investigating the causations of dyslexia and SLI highlights the complexities of both disorders and the many processes involved. Additionally the literature identifies and indicates that there is persuasive evidence linking both dyslexia and SLI.

While the causational research has provided a wealth of information regarding the underlying causes involved in dyslexia and SLI it is unspecified and unable to assess to what extent and how are they linked? Therefore causational explanations are limited when it comes to establishing the exact relationship between these disorders. In order to gain a further understanding of the relationship, and to investigate whether dyslexia can be considered as a milder form of SLI, consideration to models and hypotheses need to be reviewed. These models and hypotheses attempt to explain the nature of the relationship (if any) between dyslexia and SLI and to what extent they may be linked. Literature reviewed suggests that there are two main views regarding the relationship between these disorders. The first view suggests that both disorders are related and that they are qualitatively similar in that they both exhibit language impairments at an early age and reading problems at a school age (Tallal, Allard, Miller & Curtiss, 1997). Opposing this view is the notion that dyslexia and SLI should be classified as distinctly disorders, although both disorders share many behavioural similarities (Tallal et al. 1997).

There are currently 3 main models/interpretations of that attempt to explain the relationship between dyslexia and SLI. The first model to be considered is the “single source hypothesis”. This hypothesis holds 2 views, and attributes the cause of dyslexia and SLI to one single source; deficits in auditory processes or phonological difficulties. The first view of this model suggests that difficulties in both disorders are a result of deficits in the basic temporal processing. This interferes with auditory processing of rapidly changing acoustic features of speech. This in turn influences the acquisition of speech/learning of language, impacting linguistic representations (Tallal et al. 1997). The other view of the “‘single source hypothesis” suggests that difficulties in both disorders are due to phonological difficulties rather than auditory deficits (Bailey & Snowling, 2002). According to this model the relationship between the two disorders are the same but manifested by differing degrees of severity and is discernible by age (Bailey & Snowling, 2002). This gives supportive evidence arguing that dyslexia is a milder form of SLI as the same basic underlying problems are attributed to both disorders.

The second model looking at the relationship is the “comorbidity hypothesis”. This model advocates that dyslexia and SLI are distinct disorders but are typically found occurring together (comorbid). This hypothesis suggests that the underlying cause for dyslexia is poor phonological processing, whereas, SLI is the result of difficulties with syntax, semantics and discourse that effect oral language skills (Catts, Adlof, Hogan, & Ellis Weismer, 2005). According to this model phonological deficiencies are only seen in children with SLI if the SLI is accompanied by dyslexia (Bishop & Snowling, 2004). This model proposes that dyslexia and SLI have no relationship to one another as they involve different cognitive defects that result in different behavioural manifestations, therefore this model argues against the notion of dyslexia being a milder form of SLI. The last model to be considered is the “qualitative difference hypothesis”. This hypothesis sits between the “single source hypothesis”, which suggests that dyslexia and SLI are linked, and the “comorbidity hypothesis” which suggests that the two disorders are not linked.

The “qualitative difference hypothesis” suggests that dyslexia and SLI should be viewed as two distinct disorders but on the same continuum (Catts, et al. 2005). This model proposes that poor phonological processing underpins the deficiencies found in both disorders but result in different profiles. Phonological problems in dyslexia effects word reading abilities where as in SLI if effect oral language skills which results in various outcomes that interfere with literacy acquisition skills. These models incorporate the causational aspects considered at the beginning of this essay and have theorised about the relationship between dyslexia and SLI and to what extent they are linked, if at all. The models offer three very different views that conflict with one another. There doesn’t appear to be a clear cut answer to whether dyslexia can be considered a milder form of SLI. There is a wealth of literature that looks at the similarities and differences between these disorders; causations, relationships, definitions and many more aspects.

However, due to the complexities of understanding what exactly dyslexia and SLI is and the problems defining and identifying conclusively underlying causes it is difficult to determine whether dyslexia is a milder form of SLI. Using the evidence reviewed in this essay it appears that there is more research and literature providing a persuasive argument for the possibility of dyslexia being a milder form of SLI. This essay is not an exhaustive review of the research in this area as other factors need to be taken into consideration such as definitions, historical accounts and varying levels and sub categories of each disorder. However with the evidence reviewed it appears that there seems to be more support for the notion that dyslexia is a milder form of SLI. The causational aspects of these disorders showed that dyslexia shared underlying causes with SLI, however SLI generally incorporated more causations. It is important to determine the extent of the relationship of dyslexia and SLI and if they are of the same category just on differing levels as it affects the way the disorders are treated and identified. With a fuller understand of dyslexia and SLI it would be possible for early detection and administration of effective interventions. Word count: 2081

References

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