Varieties of Developmental Dyslexia - Assignment Example

Varieties of Developmental Dyslexia Introduction Dyslexia, also known as developmental reading disorder is the most common childhood learning disability manifesting in school going children. It is characterized by an unexpected difficulty in reading in otherwise intelligent children who are motivated and have ample opportunities to learn considered necessary for accurate and fluent reading (Fisher, 2001). Incidence and prevalence Dyslexia affects 80% of all individuals identified as learning disabled (Shaywitz, 2007). Its incidence is estimated to be about 8 to 15% (Earl, 2006). Though there is not enough evidence to conclude that the condition is more common in boys, boys are 3-4 times more likely to be referred for reading problems (Tynan, 2006). There are no racial differences in dyslexia. It occurs in all languages, races and religions. Morbidity and mortality Dyslexia is associated with a high level of social and psychological morbidity for the individual and their family. In approximately 40-50% of cases, the disability is persistent into adulthood (Schulte et al, 2007). Etiology and pathogenesis Reading is a process that synthesizes data from the highly developed visual perception system and transfers it to the highly developed language system via brain's network of nerve cells that connect centers of vision, language and memory. This transformation of data involves certain skills like recognizing specific visual symbols as letters, focusing and scanning across the page, recognizing sounds associated with letters and making that connection, understanding words and grammar, building ideas and images, comparing new ideas to what one already knows and storing ideas in memory (Earl, 2006). Dyslexia is a disorder related to the language system and involves deficient processing of individual linguistic units, called phonemes, which comprise all spoken and written words (Tynan, 2006). A child with dyslexia typically has problems with segmentation, the process of recognizing different phonemes that constitute words or with blending these sounds to make words (Tynan, 2006). The disability in dyslexia can involve any task in reading. While a significant number of children with dyslexia share an inability to distinguish or separate the sounds in spoken words, others may have trouble with rhyming games, such as rhyming cat with bat or cannot recall seeing a specific word previously and have poor "word confrontation" memory recognition (Earl, 2006). There is a broad spectrum of dyslexia related phenotypes like phonological decoding, phoneme awareness, orthographic processing, short-term memory, rapid naming and basic mathematical abilities. Many theories have been put forward to analyze the etiology dyslexia. Dyslexia is usually considered of constitutional origin, but its actual mechanisms are still mysterious and currently remain the subject of intense research endeavour in various neuroscientific areas and along several theoretical frameworks (Habib, 2000). Early studies drew attention towards a possible abnormality in specific stages of prenatal maturation of the cerebral cortex and suggested a role of atypical development of brain asymmetries (Habib, 2000). Neuropsychological studies have provided considerable evidence that the main mechanism leading to these children's learning difficulties is phonological in nature, namely a basic defect in segmenting and manipulating the phoneme constituents of speech (Habib, 2000). Since individuals with dyslexia have difficulties with phonological decoding of orthographic symbols (Leonard et al, 1993) and show deficits in phoneme processing (Ramus et al, 2003), it has been thought that pathology of some parts of the brain leading to defects in segmenting words in to their phonologic constituents is the cause for dyslexia. The parts of brain which are incriminated in the pathogenesis of dyslexia are Wernickes' area, angular gyrus, extrastriate and straite cortex and inferior frontal gyrus (Shaywitz, 1998). This is known as the phonological theory. It has been observed that children with dyslexia have delayed motor mile stones and characteristic clumsiness (Nicolson et al, 1995) and people with dyslexia have poor coordination, balance and time estimation (Fawcett et al, 1996). These changes have been attributed to changes in the cerebellum like greater ratio left: right grey matter and altered choline/noradrenaline and creatine/noradrenaline ratios (Rae et al, 1998). Also, since binocular control in dyslexics was poor and there is destabilization of binocular function leading to visual confusion and letters, impaired function of magnocellular pathway has been thought of (Stein & Walsh, 1997). Post mortem studies on those with dyslexia have revealed microscopic cortical malformations in the language areas, particularly in both inferior frontal gyrus and temporo-parietal areas of the brain (Galaburda et al, 1985). The inferior frontal gyrus is involved in speech perception, rapid auditory processing and phonological aspects of reading. The fact that dyslexia has a genetic etiology began to dawn when researchers started observing that dyslexia runs in families and amongst twins. A study by Rabin and colleagues (1993) mapped the gene to 1p34-1p36 on chromosome 1 and concluded that dyslexia was inherited in an autosomal dominant fashion with high degree of penetrance. Fagerheim and colleagues (1999) located the gene to locus 2p15-16 on chromosome 2. Nopolo and colleagues (2001) reported a dyslexia locus on 3p12-q13. This locus has been named DYX5. Smith and colleagues (1991) have converged the dyslexia locus to 6p21.3. This gene locus has been named DYX2. Londin and others (2003) have highlighted 5 genes that are highly expressed in the brains of those with reading disorders: P24, SSADH, GPLD1, KIAA0386, and KIAA0319. These are mapped to 6p22.3 near marker JA04. Fisher and colleagues (2002) identified and linked phonological processing and phoneme awareness to the locus 18p11.2 on chromosome 18. Another locus on Xq26 was detected on the X-chromosome by the same researchers, indicating towards higher incidence of dyslexia in males than in females. . Lubs and colleagues (1993) discovered translocation with centric fusion of chromosomes 13 and 14 in a few dyslexic families. In another study by (Froster et al, 1993), balanced translocation t (2; 15) (q11; q22) was reported. Other etiologies have also been thought of. It has also been reported that fetal testosterone levels during late pregnancy may play a critical role (Tonnessen, 1990). Dyslexia is sometimes associated with autoimmune diseases like Graves and Hashimotos's thyroiditis (Wood & Cooper, 1992). Clinical manifestations Children with dyslexia will have difficulty in any task of reading. While some may not be able to seperate sounds in spoken words, some others may have trouble with rhyming words. They often forget the learned aspects quickly. They usually take longer time to inculcate information into their long term memory. In tasks requiring new learning, they may have more difficulty than others despite good intelligent levels and may need instructions repeated several times. These difficulties may have an emotional impact on the students. When these problems creep into adulthood, other problems may emerge. Dyslexic adults develop low self esteem. They lack confidence in their abilities and feel isolated. Dyslexia appears to have a negative impact on working practices and career progression, but remains a poorly understood and often hidden disability (Morris & Turnbull, 2007). This could affect their work performance. Dyslexic persons also have some positive aspects. They are able to think holistically. They are good at creativity and imagination. They have good visualization skills, spatial ability and good problem solving skills. The subtypes of dyslexia are based on different patterns of underlying symptoms. According to Castles and Coltheart (1993), there are at least 2 prevalent and distinct varieties of developmental dyslexia, the first of which is characterized by a specific difficulty using the lexical procedure, and the second by a difficulty using the sublexical procedure. Comorbid conditions Comorbidity with attention deficit hyperactive disorder is very common association with dyslexia. Children with a reading disorder are twice as likely as other children to have ADHD; the rate of such dual incidence approaches 15% (Fletcher 1999). Other comorbid problems include social maladjustment and multiple learning disabilities. Prognosis The current data indicate that deficits in phonological coding continue to characterize dyslexic readers even in adolescence; performance on phonological processing measures contributes most to discriminating dyslexic and average readers, and average and superior readers as well (Shaywitz, 1999). Treatment Since dyslexia is a disability due to brain malfunction, it is difficult to cure the condition. Medications and counseling are not used to treat dyslexia. Hence the main form of treatment would be remedial education. This type of education is individualized and is based upon the results of psychological testing by the treatment providers. The most common method of treatment administered to children with dyslexia is known as the multisensory approach wherein techniques involving hearing, vision and touch are used to improve reading skills. This can be achieved by using educational tools. These children will need to be sent to either special education setting or special tutoring setting or both (Tynan 2006). The fundamental aim is to make children aware of correspondences between graphemes and phonemes and to relate these to reading and spelling. This can be done by phenomic processing instruction (Richardson, 1984). Recently, remarkable success is claimed for an exercise-based treatment that is designed to accelerate cerebellar development in patients with dyslexia, attention-deficit hyperactivity disorder, dyspraxia and Asperger's syndrome (Bishop 2007). However, there is no evidence to prove this and the physicians and parents must be aware of the fact that these treatments could be costly. In older children, adolescent and adults, management is most often based on accommodation. This allows them the time to decode each word and to apply their unimpaired higher-order cognitive and linguistic skills to the surrounding context to get at the meaning of words that they cannot entirely or rapidly decode. Other accomodations which may be useful are note-takers, taping classroom lectures, using recordings for the blind to access texts and other books they have difficulty reading, and the opportunity to take tests in alternate formats, such as short essays or even orally (Shaywitz 1998). Conclusion Dyslexia is the most common learning disability in children that can extend into adolescence and adulthood and cripple the education and employment perspectives of the individual. Multiple etiologies have been described, of which the genetic theory is the most widely applied. More research is warranted to look into the etiological and treatment aspects of the disease. References Castles, A., Coltheart, M. (1993). "Varieties of developmental dyslexia." Cognition, 47 (2): 149-80. Earl, D.(2006). Cognitive deficits. eMedicine from WebMD. Retrieved on 23rd November, 2007 from http://www.emedicine.com/ped/topic2762.htm [cited 6th October, 2007] Ehri, N., Willows, S., Yaghoub-Zadeh, S. (2001). Phonemic Awareness Instruction Helps Children Learn to Read: Evidence From the National Reading Panel's Meta-Analysis. Reading Research Quarterly, 36 (3): 250-287 Fagerheim, T., Raeymaekers, P., Tonnessen, F. E., Pedersen, M., Tranebjaerg, L. and Lubs, H. A. (1999). A new gene (DYX3) for dyslexia is located on chromosome 2. J. Med. Genet., 36: 664–669. Fawcett, A. J., Nicolson, R. R. and Dean, P. (1996). Impaired performance of children with dyslexia on a range of cerebellar tasks. Ann. Dyslexia, 46: 259–283. Fisher, S.E., Francks, C., Marlow, A.J, et al. (20010. Independent genome-wide scans identify a chromosome 18 quantitative-trait locus influencing dyslexia. Nature Genetics, 30: 86–91. Fisher, S. E. et al. (2002). Independent genome-wide scans identify chromosome 18 quantitative-trait locus influencing dyslexia. Nature Genet., 30, 86–91. Froster, U., Schulte-Korne, G., Hebebrand, J. and Remschmidt, H. (1993). Cosegregation of balanced translocation (1; 2) with retarded speech development and dyslexia. Lancet, 342: 178–179. Galaburda, A. M., Sherman, G. F., Rosen, G. D., Aboitiz, F., Geschwind, N. (1985). Developmental dyslexia: Four consecutive pa-tients with cortical anomalies. Ann. Neurol.,18: 222–233. Habib, M. (2000). The neurological basis of developmental dyslexia. An overview and working hypothesis. Brain, 123: 2373−2399 . Kaufmann, W. E. and Galaburda, A. M. (1989). Cerebrocortical micro-dysgenesis in neurologically normal subjects: A histopathologic study. Neurology, 39: 238–244. Leonard, C. M. et al. (19930. Anomalous cerebral structure in develop-mental dyslexia revealed with magnetic resonance imaging. Arch. Neurol., 50: 461–469. Londin, E. R., Meng, H. and Gruen, J. R. (20030. A transcription map the 6p22.3 reading disability locus identifying candidate genes. BMC Genomics, 4, 25–30. Lubs, H. A. et al.(1993). Familial dyslexia: Genetic and medical findings in eleven three-generation families. Ann. Dyslexia, 43, 44–60. Morris D & Turnbull P. (2007). A survey-based exploration of the impact of dyslexia on career progression of UK registered nurses. Journal of Nursing Management, 15(1): 97-106 Nicolson, R., Fawcett, A. J. and Dean, P. (1995). Time estimation deficits in developmental dyslexia: Evidence of cerebellum involvement. Proc. R. Soc. 259: 43–47 Nopola-Hemmi, J. et al. (2001). A dominant gene for developmental dyslexia on chromosome 3. J. Med. Genet., 38: 658–664. Rabin, M., Wen, X. L., Hepburn, M., Lubs, H. A., Feldman, E. and Duara, R. (19930. Suggestive linkage of developmental dyslexia to chromosome 1p34–p36. Lancet, 342: 178. Rae, C. et al. (1998). Metabolic abnormalities in developmental dyslexiadetected by magnetic resonance spectroscopy. Lancet, 351: 1849–1852. Ramus, F., Pidgeon, E. and Frith, U. 2003. The relationship between motor control and phonology in dyslexic children. J. Child Psychol. Psychiatry, 44: 712-722. Schulte-K et al. 2007. Interrelationship and Familiality of Dyslexia Related Quantitative Measures. Annals of Human Genetics, 71 (2): 160–175 Smith, S. D., Kimberling, W. J. and Pennington, B. F. 1991. Screening of multiple genes influencing dyslexia. Read. Writing: Interdiscip.J., 3, 285–298. Shaywitz, S. (1998). Current concepts: dyslexia. N Engl J Med., 338:307-312 Shaywitz, S.E., Gruen, J.R., Shaywitz, B.A. (2007). Management of dyslexia, its rationale, and underlying neurobiology. Pediatr Clin North Am., 54(3):609-23 Stein, J., Walsh, V. (1997). To see but not to read; the magnocellulartheory of dyslexia. TINS, 20: 147–152 Symtoms of dyslexia. Retrieved on 24th November, 2007 from: http://members.rediff.com/addbe/symptom.htm Tonnessen, F.E., 1990. Testesterone and dyslexia. Pediatr. Rehabil., 45: 417-426. Tynan, W.D. 2006. Learning disorder : Reading. Emedicine from WebMD. Retrieved on 24th November, 2007 from http://www.emedicine.com/ped/topic2792.htm Wood, L.C., Cooper, D.S. (19920. Autoimmune thyroid disease, left-handedness, and developmental dyslexia. Psychoneuroendocrinology, 17(1):95-9. Read More