Specific Phonological Deficit - Essay Example

DEVELOPMENTAL DYSLEXIA: SPECIFIC PHONOLOGICAL DEFICIT OR GENERAL SENSORIMOTOR DYSFUNCTION It is very clear that a significant proportion of individuals with dyslexia present not only motor deficits but also sensory deficits (Park, 2009 & Marshall, 2004). But as this ‘sensorimotor syndrome’ is researched in great detail, it is also clear that the sensory and motor disorders ultimately play only limited roles in a casual explanation of particular disability in reading (Vinson, 2007). (Ward, 2009) Development dyslexia is failure to get reading skills affecting around 5% children despite the fact that adequate intelligence, social background and education (Benasich & Fitch, 2012). A wide consensus has been given stating a neurological disorder with an origin of the genetic nature. Yet, after research carried out for decades, it seems unbelievable that theorists still disagree over the cognitive and neurological basis of the disorder (Woliver 2009). The dyslexia currently occupies no less than four major theories that can be classified into two antagonistic frameworks. Moreover, each of the theories supports the whole empirical evidence of the body (Shoel, 1990) On one side, theorists contend to state that specific characteristics of reading retardation of dyslexia is exclusively and directly caused by a deficit in the cognitive that is very particular to the processing and representation of speech sounds: it is the phonological theory. At the brain’s level, this cognitive deficit arises from a congenital dysfunction of specific cortical areas engaged with reading and phonology (Shaywitz, 2003). On the side, researchers agree with ideas of a phonological deficit. However, they view it as a more secondary as basic auditory impairment and connected with a basic sensorimotor deficit. (MacCracken, 1986) Separate theories developed on an auditory deficit basis reveal a motor dysfunction or magnocellular visual dysfunction, but have been unified recently under a general magnocellular dyslexia theory. Also, there is an attention variant of the theory. According to the research, there are two main causes of reading retardation, visual and phonological deficits. The phonological deficit is traced back to a more basic auditory impairment that has the same origin in biology as visual impairment, more specifically, a dysfunction of magno-cells in pathways of the sensory system (Tod, 2000). The dysfunction in the magnocellullar is also seen in the tactile domain reaching the cerebellum through the posterior parietal cortex. As a result, it causes further impairments in the motor domain (Guth et al, 2001). Therefore, in this theory, dyslexia is generally a sensorimotor syndrome. The phonological theory has been in existence for about 20 years. More and more studies have gradually emerged providing evidence for visual, auditory and motor impairments in dyslexics giving support to the sensorimotor theories. The adaptive procedures of psychophysics show several measures each threshold routinely uses so that individual data is taken seriously. Most auditory studies taken support the view proving dyslexics’ auditory processing is specifically impaired on fast transitions and short sounds called ‘temporal’ or ‘rapid’ auditory processing deficit. Such auditory dysfunction characteristics are consistent with the magnocellular theory, as the magno-cells are specifically sensitive to very high temporal frequencies. However, a closer look shows major inconsistencies between the theory and the data. Some deficits found have tasks that do not tap into the rapid auditory processing such as frequency modulation detection or frequency discrimination at 2 Hz. On the other hand, the expected deficits of rapid processing are not often observed. In fact, when intervals in the inter-stimulus were manipulated in a manner so systematic, dyslexic’s auditory processing was not poorer at intervals but at long intervals. Sometimes, it is better. Finally, three separate researches investigating auditory processing of dyslexics on a large psychophysical array tests administered to similar subjects. They showed that a dyslexic’s subset has difficulties with particular tests, but the pattern of poor and god performance cannot be characterized as a problem with temporal or rapid processing. Moreover, the performance pattern widely varies across individuals. A dyslexic’s coherent characterization of auditory performance still remains elusive (Orton Dyslexia Society, 1982) Is it a casual connection? The question is asked when an auditory deficit in an individual with dyslexia is present, is it responsible for deficit in phonology and/or for disability in reading? Auditory processing theory has supporters that created a hypothesis that impaired perception of transitions and sounds would be specifically detrimental to perception of speech, therefore, undermining the child’s representation of phonology (Shin, 1998). Evidence against the hypothesis was put forward. Recent studies are now established stating there is no reliable relationship between discrimination and speech categorization and performance on rapid tasks of auditory processing. Neither is there a relationship reliable enough between general measures of reading ability or phonological skills and any auditory measures (non-speech or speech) even when longitudinally assessed. If anything, dyslexics with the worst auditory impairments seem to have also severely impaired reading and phonology, although the opposite is not necessarily true. (Stowe, 2000) Interestingly, auditory training programs exist that improve the reading skills and language of dyslexic and dysphasic children. Unfortunately, these programs do not protect themselves against Hawthorne and placebo effects through running randomized double blind controlled trials (Jordan, 1996) The Hawthorne effect is the positive results exclusively caused through being the trial subject. A few independent studies attempt to assess the effects of controversial programs based on a training to adapt to rapid auditory processing finding it no more effective than a more conventional intervention program. They have created a challenge for the role played by rapid auditory processing in the training (Sprod et al, 2004). The auditory disorders observed in people with dyslexia are not specifically ‘temporal’ or ‘rapid’ in nature. These disorders are prevented to a subset of the population of dyslexics and have very little influence on the phonology development and reading (Payne & Turner, 1999). Therefore, it seems the phonological deficit that characterizes dyslexia can arise in the absence of disorders in the auditory system with the most severe impairments in the system, nevertheless, acting as disturbing factors. A particular phonological deficit originating from the left peri-sylvian is postulated to be the main cause of problems caused by reading (Fyre, Liederman et al, 2010). Debate on visual dyslexia deficits is articulated around three commonly asked questions similar to the ones asked about auditory deficit. First, do disorders related to the vision cause difficulties in reading? Secondly, do those disorders have an origin of the magnocellular nature? And lastly, what dyslexia proportions are affected? Even after excluding the main ophthalmologic disorders, it is plausible for more subtle visual deficits to have a reading impact (Hayes, 2006) Perhaps the best example is visual stress whereby the condition provokes distortions on the visual ability, sometimes leading to impaired fluency in reading. The condition can be improved through using colored glasses or overlays. Other visual problems often mentioned of dyslexia include poor vergence control and instability of binocular fixation, slight visual-spatial attention deficits and increased visual crowding (Reid, 1998) Although these causes of impairment in reading are plausible, both their relationship to retardation in reading and their prevalence remain debatable especially because visual disorders are usually accompanied by a deficit of phonology (Thomson, 1998) whether a dysfunction of the magnocellular is the main cause of these visual related impairments is far from being clear. Several studies provide evidence those individuals with dyslexia have thresholds of elevated detection or abnormal visual caused potential for stimuli in the temporal and spatial ranges of the system of the magno-cells. But then again, it has been unclear as to whether some stimuli uniquely tap the system (Parker et al, 2002) A growing number of studies have reported inconsistent findings with visual deficit that is particular to the magnocellular system. These studies often find visual deficits present covering a whole range of temporal and spatial frequencies. Questions have also been asked whether group differences explained by memory or attention rather than sensory disorders. In addition, visual deficits are restricted to a dyslexic subset (Thomson, 1984). A general dysfunction of the magno-cell is hypothesized to engender motor and auditory deficits (Valett, 1980) the auditory deficit, therefore, causes a deficit of the phonological nature. As a result, it triggers the same flow of events as it was predicted in the phonological theory. The visual deficit in the magno-cell is viewed as another deficit caused by reading problems. In motor/visual cerebellar theory, the impairment in its motor system is also thought to contribute to reading and phonological problems on its own (Patterson et al, 2007). In conclusion, even though the phonological deficit is still in dire need of a complete neurological and cognitive characterization, the case around its casual etiology role of writing and reading disability of the greater majority of children with dyslexia is overwhelming. The most recent study shows that this phonological deficit is not accounted for by a deficit of auditory processing at a lower level, leave alone a deficit particular to temporal or rapid processing. More specifically, all the problems caused by the sensorimotor investigated in individuals with dyslexia has both limited effects on skills for reading and limited prevalence. However, it still remains possible that particular visual deficit, the likes of visual stress, may at times sufficiently disrupt ability to read leading to diagnosis of the condition of dyslexia. According to the current state of knowledge acquired, developmental dyslexia seems characterized, at best, as a particular phonological deficit, sometimes accompanied by a syndrome of the sensorimotor nature. A complete dyslexia theory must explain both the origin of the neurological deficit in phonology, as well as reasons as to why a syndrome of the sensorimotor takes place more often in individuals with dyslexia than in the general population (International Dyslexia Association et al, 2006) References Benasich, A., & Fitch, R. H. (2012). Developmental dyslexia: Early precursors, neurobehavioral markers and biological substrates. Baltimore: Paul H. Brookes Pub. Clarke, L. (1973). Cant read, cant write, cant takl [sic] too good either: How to recognize and overcome dyslexia in your child. 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