Effects of Co-Morbid Conditions on Treating Children with Dyslexia - Essay Example

?It has been suggested that there is a high level of co-morbidity between dyslexia and other specific learning difficulties. Discuss this in the light of current research. Introduction Dyslexia is one of the most common learning difficulties found in the education system (Reid, 2009), and therefore it is imperative that educators fully understand the condition. Dyslexia is particularly important in the school system as it means that a person may have difficulties in comprehension of written language, and may be unable to compose their thoughts (Peer & Reid, 2012). There are various different proposed causes of dyslexia, including evolutionary theories and those revolving around difficulties in the cerebellum, as does dysgraphia (Nicholson & Fawcett, 2009). The fact that these causes seem to be mainly biological in nature supports the fact that dyslexia is often found to be co-morbid with other learning difficulties that place strain on the individual. These can include, but are not limited to, attention deficit/hyperactivity disorder (ADHD), anxiety, depression, and conduct disorders (Reid, 2009). The purpose of this paper is to explore the conditions that are so often found to be co-morbid with dyslexia in the literature, and how this may affect the dyslexic child. Additionally, the paper will go on to discuss how these co-morbid conditions may affect the treatment or guidance that educators need to give children with dyslexia. What is Dyslexia? Dyslexia is a specific learning difficulty that affects one main area of an individual’s progress in education. It is a difficulty in reading that is apparent regardless of the individual’s IQ or their previous instruction in reading (Reid, 2009). Many believe that dyslexia is not a single condition, but can be used to encompass a wide range of difficulties that individuals may have when it comes to reading (Reid, 2009). There are many signs of dyslexia that can be used to diagnose a child or recommend them for a referral to a specialist. One of the most common is a delay in speech (Caroll & Myers, 2010), which is common to a number of learning difficulties and therefore care must be taken to avoid confusion or misdiagnosis. Another is the use of mirror writing or reversing certain letters in a sentence so that it becomes illegible to the non-dyslexic reader (Caroll & Myers, 2010). Again, this can be a sign of other learning difficulties with a broader scope than reading or writing, so care must be taken when diagnosing and teaching these children. There is currently no cure for dyslexia, nor is there any overwhelming consensus about treatment or management (Reid, 2009). There are several programmes in place which are aimed at providing advice to educators who have contact with dyslexic individuals. One of the major important aspects for managing dyslexia is to remove the sources of stress and anxiety (Reid, 2009). These can include pressure from parents, teachers and peers to learn to read and write at the same pace as other children their age, which is evidently not possible for the dyslexic individual. Care must be taken not to add additional stress onto a child when attempting to educate them. Lyytinen et al (2008) suggest that educational styles that focus on visual learning are more effective than a simple focus on oral phonological training. It must be noted that many management styles for dyslexia differ in their effectiveness for the individual and this must be recognized by those working in close contact with dyslexic individuals. Another interesting factor of dyslexia is that it seems to be highly heritable and therefore must have a genetic component (Scerri & Schulte-Korne, 2010). This may be linked to the co-morbidity that it has with other SpLDs, which are also highly heritable (Scerri & Schulte-Korne, 2010). There are some genetic markers that have been associated with dyslexia, including ROBO1 and DCDC2 (Scerri & Schulte-Korne, 2010). Abnormal codes in these genes is a good predictor of reading disorder. Some studies of dyslexia from a biological perspective have focused on the functions that are disrupted in abnormal copies of the gene, which can be a predictor of the biological root of dyslexia and some of the other SpLDs (Scerri & Schulte-Korne, 2010). Uncovering a biological cause could have significant implications for the classroom, as it will allow teaching styles to be adapted for dyslexic individuals that are targeted around the lack of function that they have. Additionally, there are several theories which try to explain the biological function of those with dyslexia (explained below), which could be linked to the function of these implicated genes. Theories of Dyslexia There are several theories relating to the development of dyslexia, which may help to explain some of the other specific learning difficulties and conditions that are often co-morbid with dyslexia. The first of these is known as the cerebellar theory of dyslexia (Reid, 2009), and proposes that dyslexia is caused by a mild dysfunction in the cerebellar region of the brain. The cerebellum is a brain area which is associated with both language and movement (Reid, 2009), which gives evidence as to why so many believe that it has a role to play in dyslexia. It is suggested that the dyslexic cerebellum has difficulties in motor control during speech articulation, which in turn contributes to the phonological processing deficits associated with the condition (Reid, 2009). This theory is perhaps the most widely purported, and could definitely explain why conditions such as dyspraxia (discussed at a later stage) are so commonly co-morbid in dyslexic individuals. Another important theory of dyslexia is known as the phonological deficit hypothesis, which suggests that the dyslexic individual has a cognitive-level difficulty in understanding phonetic rules (Reid, 2009). This is based upon evidence that show that dyslexic individuals may show more difficulty than non-dyslexic individuals when attempting to “decode” nonsense words based upon these established rules (Peer & Reid, 2012). The theory suggests that the phonological deficit could stem from a deficit in the left hemisphere of the brain, which is strongly associated to language (Peer & Reid, 2012). Many argue that this theory does not truly explain dyslexia because it merely describes one of the symptoms (phonological deficit) without offering any truly defined ‘cause’. The final important theory of dyslexia is known as the magnocellular deficit, which incorporates elements of the cerebellar theory as well as the phonological deficit hypothesis. Magnocellular cells are found in the midbrain and have some association with visual processing and motor co-ordination, which allows them to incorporate two of the main deficits associated with dyslexia (Peer & Reid, 2012). Many of the studies that have been done on the magnocellular theory of dyslexia have been heavily criticized for failing to take into account the high possibility that the condition is comorbid with another (Peer & Reid, 2012), as well as the fact that many of these studies use extremely small sample sizes (Reid, 2009). Specific Learning Difficulties As suggested in the question, dyslexia can often be comorbid with specific learning difficulties (or SpLD). These are different from more general learning difficulties in that they affect motor coordination, memory and information processing (Reid, 2009). Interestingly, many children with SpLD can also show normal or even high attainment in the right educational environment (Peer & Reid, 2012), and have also been shown to have a wide range of IQ levels like that found in the population at large (Karande, Sawant, Kulkarni, Galvankar & Sholapurwala, 2005). Indeed, one of the most useful ways of diagnosing a SpLD is to compare an intelligence quotient score (IQ score) with the child’s achievement in school, as discrepancies can indicate a SpLD (Laasonen et al, 2010). There are five main difficulties which are grouped into the subheading of SpLD (and which are often found in dyslexic individuals as part of a range, rather than as distinct conditions): dysgraphia, dyspraxia, dyscalculia, attention deficit disorder (ADD) and forms of Asperger’s syndrome and autism. Dysgraphia is a more specific difficulty with the use of the written word. Individuals with dysgraphia will have difficulty using their motor skills to convey written language, and as a result may have illegible handwriting (Laasonen et al, 2010). The main difference between dysgraphia and dyslexia is that the ability to read is not necessarily impaired, although the conditions can commonly be co-morbid (Peer & Reid, 2012). The level of written communication will be far below the level that the individual achieves in general intelligence (Peer & Reid, 2012). As dysgraphia affects motor skills, it can often be found in individuals with dyspraxia, which affects all areas of motor coordination. Individuals with dyspraxia often have difficulties with hand-eye co-ordination, movement in general, balance, perception, and occasionally speech (Peer & Reid, 2012). These individuals will often be mislabelled as being ‘clumsy’, preventing them getting the appropriate help in the classroom (Laasonen et al, 2010). Dyscalculia is very similar to dyslexia except these individuals show normal ability for the written and spoken word but have extreme difficulties with using mathematic and arithmetic skills. For example, these individuals may show a difficulty with mental arithmetic, as well as written addition, subtraction and so on (Laasonen et al, 2010). Abstract mathematical concepts such as time, multiplication, and more complex functions will often pose a challenge to those with the difficulty (Reid, 2009). Attention deficit disorder and attention deficit hyperactivity disorder (ADD or ADHD) is a common diagnosis for those who show disruptive behaviours in classroom situations which are often not reflected in a psychiatric cause (Reid, 2009). These individuals will often have difficulty concentrating, and those with ADHD may also show extreme hyperactivity, which makes them often wrongly labelled as being simply ‘naughty’ or ‘mischevious’ (Reid, 2009). There are a huge number of factors that have been attributed to the cause of ADD and ADHD, including neurological, environmental and genetic (Peer & Reid, 2012), as opposed to the reliance on theories as outlined above with dyslexia. The final learning difficulty which can sometimes be grouped into the SpLD category is Asperger’s Syndome, as well as some other forms of high-functioning autism (Peer & Reid, 2012). Although the autistic spectrum is far too complex for the scope of this essay, autistic disorders are in essence developmental disabilities which cause impairments in behaviour and social skills (Zager, 1999). It is considered to be a spectrum disorder because many individuals fall somewhere on a spectrum and there are no clear lines between different ‘types’ or manifestations of autism in many individuals (Zager, 1999). Like ADD/ADHD, autistic spectrum disorders have a wide variety of causal agents including genetics and environment, which are generally considered to contribute in varying amounts to the difficulty (Zager, 1999). Additionally, it is commonly co-morbid with ADD/ADHD as well as some of the other SpLD, despite the fact that many individuals with forms of high functioning autism can show extremely high intelligence skills in some areas (Peer & Reid, 2012). It has also been shown that ADHD and dyslexia are commonly co-morbid with each other. There have been some suggestions that ADHD may be more common in dyslexic individuals as it can be difficult to concentrate in school when reading is impaired (Sperling, Lu, Manis & Seidenberg, 2006).Germano, Gagliano & Curatolo (2010) showed that this co-morbidity may be particularly problematic because it seems to have an additive effect: individuals with both ADHD and dyslexia have worse neuropsychological, academic and behavioural outcomes than those with either one of the disorders as a singular entity. This could have serious implications for the classroom, as special precautions and educational styles will need to recognize this additive effect to ensure education is appropriate for those with both SpLDs. Comorbidity One of the most striking findings of recent years is that these SpLD conditions as outlined above (as well as obsessive compulsive disorder [OCD] and Tourette’s syndrome) are so commonly comorbid that they could be considered to be different elements of an overarching developmental disease (Pollack, 2009). This could be seen as analogous to the autistic spectrum, which takes a wide variety of individuals with similar developmental and learning difficulties and places them at different points on a scale, rather than giving each individual condition a specific name. In one study of 100 individuals with these disorders, no single patient was found to have a disorder in isolation, and there was a comorbidity incidence of 95% (Pauc, 2005). It must be acknowledged that there are some issues with the study. Firstly, 100 individuals is quite a small sample size, which means that there may be difficulties generalizing this information to the population as a whole. Additionally, the authors recognize that there are some similarities between the SpLD group and therefore it can be difficult to quantify comorbidity and disorder isolation. Despite these issues, it seems evident that this is something to bear in mind during the following discussion of comorbidity in the SpLDs. Russell & Pavelka (2013) give a good overview of the recent statistics about the co-morbidity of dyslexia, ADD/ADHD and autistic spectrum disorders. Interestingly, the diagnosis of either ADD/ADHD or autism is an exclusion for dyslexia, but Russell & Pavelka (2013) suggest that there are significant behavioural and cognitive overlaps between the conditions. 14% of children with some form of autism show symptoms of a reading disorder. Whilst this may seem fairly minimal, it does suggest that co-morbidity between the two conditions does exist. Interestingly, Russell & Pavelka (2013) touch on some of the reasons why there may be this co-morbidity. Dyslexic individuals may often have difficulty understanding the meaning of spoken or written words, and therefore can show difficulty in comprehension. Those with Asperger’s or high-functioning autism will have normal intelligence but have difficulty in social situations, which may stem from a similar lack of comprehension of ‘normal’ language use and slang (Reid, 2009). Twin studies also show that there could be a genetic link between autism and dyslexia, as up to 40% of twin individuals co-morbid for both disorders will have a twin co-morbid for the same (Russell & Pavelka, 2013) (much higher than the general 14% figure for the autistic population as a whole). One of the most interesting combinations of SpLD that can often be comorbid is the dyslexia and dyscalculia combination. Landerl, Fussenegger, Moll & Willburger (2009) studied four different groups of 8-10 year olds, including a control, dyslexic-only, dyscalculic-only and dyslexic-dyscalculic comorbid. As previously mentioned, dyslexia affects primarily phonology, whereas dyscalculia affects number modules, and therefore it was expected (and found) that there are different cognitive profiles for the groups. Phonological deficits were found in those with dyslexia and dyscalculia, as expected, but were not found significantly in dyscalculic individuals. As with the ADHD and dyslexia combination examined above, the combination of dyslexia and dyscalculia was found to be additive in terms of cognitive and behavioural impairment. Landerl et al (2009) suggest that these findings could indicate that, whilst there are some similarities between the two SpLDs, they both need to be approached differently in the classroom. Additionally, they may be variants of the same disorder, but affecting different brain regions, hence the additive effect (Landerl et al, 2009). Comorbidity Theories Above, it was illustrated that there is a staggering amount of evidence that the comorbidity of SpLDs is extremely common, if not inevitable. This has led to a wide range of academics creating theories about the comorbidity of these conditions and where this could have stemmed from. One area that seems to be affected in all types of SpLD is the use of working memory. Working memory is a term that refers to the active use of memory to hold pieces of information in the brain that may be transitory in nature (Reid, 2009). Working memory is used in both verbal and non-verbal activity (Jarvis & Gathercole, 2003), and is often used to make information available to the rest of the brain for further processing (Peer & Reid, 2012). Jeffries & Everatt (2004) showed that working memory skills are reduced in children with dyslexia (and other SpLDs and emotional problems) when compared with control (non-SEN children) in a study of 66 individuals (Reid, 2009). As a result of this finding, Jeffries & Everatt (2004) concluded that this may be involved in the production of comorbidity, particularly as the reduction in working memory was found in those with ADD/ADHD-type disorders. Another theory, supported by clinical and experimental evidence, is that there may be a reduction in fatty acid availability or types of fatty acid imbalance in those with types of SpLD, including dyslexia and dyspraxia. Richardson (2004) provided preliminary evidence that fatty acid supplementation may help in the treatment or management of types of SpLD. Indeed, fatty acid supplementation is now being used as a recommendation in many areas (Bloch & Seidenberg, 2011). Schuchardt, Huss, Stauss-Grabo & Hahn (2010) studied the relationship between fatty acid and developmental disorders, finding that there may be differences in fatty acid requirements between individuals which may contribute to some incidences of dyslexia, dyspraxia and ADD/ADHD. Whilst this type of study is still preliminary, it does provide an interesting scientific background to the comorbidity of these disorders which could be useful when considering the education and management of these individuals. Pauc (2010) conducted an interesting study about visual fixation in one of the specific learning difficulties, ADD/ADHD. In a small study of 100 children, it was found that 57% of them had an insufficient ability to converge, or had convergence failure. Convergence is a biological term referring to the ability of eyes to fixate upon a single object, using both eyes to focus on one single area (Ade-Ojo, 2012). Whilst a lack in this ability may seem an obvious contributor to ADD (attention will necessarily be affected if eyes cannot keep focus on an object), it is interesting to consider, as Pauc (2010) does, the effect that this has on the other SpLDs. Dyspraxia, for example, may be worsened by poor visual fixation because it will affect balance, hand-eye co-ordination and motor co-ordination. Dyslexia also may have roots in poor convergence, as this would render reading words on a page difficult. Pauc (2010) suggests that the reason that these disorders may so often be co-morbid with each other could be because of a common root in some individuals: poor visual ability which renders ‘normal’ tasks such as reading and movement difficult. The theory that dyslexia and dyscalculia have similar cognitive patterns with different manifestations is reinforced by research by Sigmundsson, Anholt & Talcott (2010). The similarities between the two may be linked to a deficit in processing motion stimuli, part of visual temporal processing. It was found that those with non-clinical mathematical difficulties showed deficits in visual temporal processing of motion stimuli, which was similarly found in those with dyslexia-only. As with the other theories of comorbidity, this has implications in the classroom as it could indicate ways in which educating dyslexic individuals could be improved. Additionally, this information could be used to educate those with both dyslexia and dyscalculia and may go some way of offsetting the additive effect that having both SpLDs has (Landerl et al, 2009). Implications for the Classroom There are many implications that the co-morbidity of SpLDs has for the classroom. It means that those involved in the teaching of individuals with dyslexia need to be aware that there may be other SpLDs that are contributing to development, education and behaviour. It would be useful for those involved with dyslexic individuals to be aware of the current research aimed at improving the education of those with dyspraxia and other SpLDs. For example, Miyahara & Baxter (2011) surveyed parents at a dyspraxia conference and found that 25% of the children of these individuals were affected by (professionally diagnosed) both dyspraxia and another SpLD. 69% of the parents at this conference said that they sent their children to unconventional or non-traditional educational activities or facilities, and 53% of the parents said that they had seem some improvement in physical skills as a result of this type of education. Knowing this type of information, as well as understanding that there may be a common root cause of dyslexia and dyspraxia, could encourage educators and parents to try out some of the non-typical educational techniques identified, such as complementary and alternative medicines (CAM). Butterworth & Kovas (2012) wrote an interesting article about how understanding this type of developmental disorder from a neurological and psychological perspective can improve education for these individuals. As suggested by the article, SpLDs affect 10% of the population and with their high rate of co-morbidity as outlined above dyslexia or dyslexia-like difficulties are likely to be present in many of these individuals. Understanding dyslexia specifically and understanding the additive effect that comorbidity of conditions can have on individuals is important for optimizing the educational experience for these children, as teaching styles can be adapted to the current research and theories about what brain processes are affected in dyslexic children. Additionally, it is important to look beyond dyslexia as a simple reading disorder because there are a wide range of other symptoms which stem from the similarity or comorbidity that it shares with other SpLDs (including balance and motor problems) which can be overlooked in education (Ade-Ojo, 2012). Brookes, Tinkler, Nicolson & Fawcett (2010) also showed that procedural learning may be important for the education of those with dyslexia, particularly those with motor difficulties or dyspraxia as a comorbid condition. In a study of 87 individuals without comorbid ADHD, balance deficits were found for a significant amount of those with dyslexia. Some children with dyslexia may be encouraged in schools to shy away from activities based around reading (Shaywitz, 2008), which can be detrimental to their education as a whole. These activities may require balance or other co-ordination, and therefore it’s important for educators to understand that this is not a solution because of the high rates of co-morbidity. This encourages educators to find ways to deal with dyslexia directly rather than just encouraging children to move on from reading, which can unfortunately be the case in some situations. Perhaps one of the most challenging aspects of teaching dyslexic individuals is that it is often comorbid with things like conduct disorder, as well as ADD/ADHD. This can complicate the education of these individuals because they are not simply affected by a reading disorder but may have other demands on their psychological and cognitive skills that need to be recognized in the classroom (Reid, 2009).Thambirajah (2012) found that many clinicians may actually fail to diagnose dyslexia because the conduct disorder or ADD/ADHD takes precedence in the diagnosis. Learning to understand the symptoms of dyslexia despite these comorbid conditions could therefore be a useful skill for educators of SpLD indiviudals to have. Thambirajah (2012) even goes so far as to suggest that educators should liaise with clinicians to help ensure that educational needs for dyslexic individuals are being met whilst the psychiatric conditions of conduct disorder (for example) are being treated. Additionally, understanding that conduct disorder and ADD/ADHD are real comorbid conditions rather than a result of dyslexia is also important for educators to understand, as this could help in the treatment and development of these individuals (Peer & Reid, 2012). Williams (2012) suggested that mood may play a part in dyslexia education and other SpLD outcomes. It is widely understood that individuals with dyslexia often feel isolated and can also be treated as ‘stupid’ by some of their peers or even their teachers and parents (Peer & Reid, 2012). This leads to negative mood outcomes, which can affect dyslexia education severely. What Williams (2012) found is that certain educational methods are more effective in dealing with the mood issues of dyslexic teenagers. These methods are those that encourage the child to think outside of the box, rather than trying to fit their education into the normal curriculum. What is also interesting is that Williams (2012) found evidence that educational styles that targeted all aspects of a person’s development were more effective with respect to psychological well-being and therefore had more positive educational outcomes. What this means is that educators need to be aware of comorbid conditions or even symptoms of commonly comorbid SpLD which may be at a sub-clinical level and incorporate these into teaching styles. For example, this could involve encouraging active reading with the child to target dyslexic symptoms (Shaywitz, 2008), as well as frequently working on mathematical problems to target dyscalculia (Shaywitz, 2008). If this child has ADD/ADHD, for example, teaching styles could be used in combination with commonly prescribed medications. One final element that needs to be discussed is the role that educators can play in the longitudinal development of those with dyslexia and comorbid conditions. This is important because the role of the educator is to prepare the developing child with skills that they will need in later life, and understanding this can be of huge benefit to the individual (Reid, 2009). Using a longitudinal study design has often been used in psychology and education to show the benefit that a certain type of education is having on the individual over a period of time (Marshall, 2012). Marshall (2012) indicates that due to the hereditary nature of dyslexia, there are certain elements of a reading disorder that cannot ever be fully eradicated, but there are significant improvements that can be made in the right environment. This includes using techniques that target both dyslexic symptoms as well as those of comorbid conditions throughout education to continually improve on the development of the child throughout school. It is this type of long-term approach that really works in assisting the dyslexic child in education. Conclusions There are a number of conclusions that can be drawn from the current research being conducted on dyslexia and other specific learning difficulties. The majority of the research has implications for educational professionals, who benefit from understanding the aetiology of dyslexia and other learning difficulties. Firstly, it is important to note just how common the comorbidity of dyslexia and other SpLDs can be. There are suggestions that this could be linked to the similarities between many of the disorders. Evidence can be found for this from several medical and psychological studies, such as research into fatty acids, which incorporate results from comorbid individuals as well as those with a single SpLD. This type of information can be used to help educators work out strategies to help those with SpLDs (including dyslexia) that incorporate all of the symptoms, rather than simply focusing on dyslexia or ADD, for example. This may include looking into educational research for each SpLD as a single entity and then combining effective strategies for their management into a plan for a comorbid individual. This type of approach can also be used to target the additive effect found in most individuals who are cormorbid for these SpLDs. Works Cited Ade-Ojo, G. O. (2012). Practitioners’ perceptions of dyslexia and approaches towards teaching learners with dyslexia in adult literacy classes. International Journal of Lifelong Education, 31(5), 623–641. Bloch, M. H., & Qawasmi, A. (2011). Omega-3 fatty acid supplementation for the treatment of children with attention-deficit/hyperactivity disorder symptomatology: systematic review and meta-analysis. Journal of the American Academy of Child & Adolescent Psychiatry, 50(10), 991–1000. Brookes, R. L., Tinkler, S., Nicolson, R. I., & Fawcett, A. J. (2010). Striking the right balance: motor difficulties in children and adults with dyslexia. 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