Comparison of the Phonological and Cerebellar Theories as Underpinnings of Dyslexia - Term Paper Example

In Focus: Comparison of the Phonological and Cerebellar Theories as Underpinnings of Dyslexia By definition, developmental dyslexia is a “discrepancybetween the reading ability and intelligence in children receiving adequate reading tuition” (Ramus et al, 2002). There has been substantial empirical evidence lending support to genetic causes of the condition. It is characterized as chronic, with deficiencies in reading being only one of the symptoms. While there has been progress in dyslexia research, there is still contention on the genetic and cognitive roots of dyslexia (Ramus et al, 2002). There is marked contention on the origins of dyslexia among psychologists. The distinguishing traits of the condition include reading and writing difficulties. It is surmised that it spawns from sensory dysfunctions, and these have been thoroughly backed up by empirical research. However, the definitive cause of the condition is yet to be determined (Coleman, 2002). The disorder has frequently been hypothesized to be the result of various sensory malfunctions. After years of research, it has been indicated that dyslexia also has visual and writing aspects, making it a learning disability that debilitates optimized performance (Francks et al, 2002). This essay aims to compare the two theories of dyslexia at the biological, cognitive and behavioral levels. However, before undertaking this comparison, it is important to lay down the different theories that explain this condition. These are the phonological, the magnocellular (auditory and visual) and the cerebellar theories (Ramus et al, 2002). I shall attempt to compare the phonological and cerebellar theories of dyslexia. Ramus et al (2002) undertook a multiple case study to evaluate the key theories explaining the origin of dyslexia. The sample of the study was composed of 16 university students for the control group. They were given various tests to gauge dyslexic traits. The outcomes suggest that majority of the respondents had a phonological deficit and that this was enough cause for them to have dyslexia. That is, in contrast with the cerebellar theory that has auditory and visual deficits as requisites to dyslexia, the study points out that the presence of a phonological deficit alone defines the condition. The presence of auditory deficits only worsens the condition, but are not necessarily required for having dyslexia. These deficits result in “literacy impairments.” Moreover, the study did not reinforce that motor deficiencies are rooted on the cerebellum (Ramus et al, 2002). At the biological and cognitive levels, the phonological deficit theory asserts that those afflicted with dyslexia are deficient in the “representation, storage, and retrieval of speech sounds.” (Ramus et al, 2002). The equivalence of the letters and sounds of speech is said to be a prerequisite of reading. If such a requirement is wanting, then the capacity for reading will not be normal (Snowling, 2001). Still at the cognitive level, the popular stance on dyslexia according to phonological theory asserts that the brain be able to match letters with speech sounds, and the failure to do so characterizes dyslexia (Ramus, 2001). Various authors, namely, Bradley & Bryant, Vellutino, Snowling, and Brady and Shankweiler concur that phonology is the central cause of dyslexia (Ramus et al, 2002). As such the phonological theory states that there is a strong association between cognitive deficiencies and behavioral difficulties (Ramus et al, 2002). In addition, at the cognitive level, the phonological deficit theory represents the condition as a deficiency in the coding of data. Later, this has been modified and explained as caused by “phonological processing difficulties (Vellutino et al in Snowling, 2001). Behaviorally, this results in the difficulty of the individual in reading alphabetic script. This has been asserted by Vellutino (1979 in Snowling, 2001) in his study involving juvenile dyslexics. And because they have difficulty in the storage and retrieval of data, this is manifested in the hardship of dyslexics in maintaining speech in short term memory and phoneme segmentation (Ramus, 2001). This theory is being critiqued, in lieu of the fact that those afflicted with the condition likewise have sensory deficiencies, which is advocated by the magnocellular theory. For instance, Ramus asserts that at the behavioral level, dyslexics are significantly less effective in the performance of auditory tasks necessitating the perception of fast speech and non-speech sounds (Tallal et al, 1993). Still at the behavioral level, there is empirical evidence pointing to the fact that they find it hard to perform visual tasks which entail motion perception, as attested to by the study of Stein & Walsh (1997). While the phonological deficit theory attributes dyslexia to the incapacity of the brain to represent, store and retrieve speech sounds, the magnocellular theory, in contrast demonstrates that dyslexics do have abnormalities in magnocellular pathways that are engaged in visual and auditory processing (Galaburda & Livingstone, 1993). Advocates of the magnocellular theory do not criticize the phonological theory, but instead state that phonological difficulties are caused by primary defects in hearing sounds. In addition, they say that visual difficulties may separately account for reading problems (Ramus, 2001). This is the biological aspect of the theory. One research, that of Paulesu et al (1996) demonstrated that the insula, a structure linking the Broca and Wernicke’s areas, was not functional among those with dyslexia. These brain regions are responsible for word processing tasks. This explains why dyslexic individuals have to exert a great deal of effort to convert sounds into images, and vice versa. Brain imaging research has also demonstrated the idea of a dysfunctional left perisylvia to which the phonological deficit is attributed (Shaywitz & Shaywitz, 2001). One other research pointing to the brain abnormalities as a cause is the one undertaken by Temple et al (2003) which investigated the brain scans of pediatric dyslexics. The normal subjects showed activation of frontal and tempoparietal areas; in contrast, dyslexics failed to activate the latter. Moreover a test on orthographic processing showed reduced activation of a region of the occipital cortex. Much of the empirical support for phonological theory stems from research demonstrating that those afflicted with the condition find it hard to perform phonological tasks (Ramus, 2001), which is the behavioral manifestation of the defect. A research conducted by Georgiewa et al (2002) undertook a study using 9 pediatric dyslexics and 8 controls who were subjected to functional magnetic resonance imaging (fMRI) during a reading task. The outcomes demonstrate that there are significant differences in the activation of the left inferior frontal gyrus, which were hyperactivated among dyslexics. These results lend further support to differences in phonological processing capacity between normal and dyslexic children. Simos et al (2002) has utilized magnetoencephalography (MEG) to examine 10 pediatric dyslexics and 8 control subjects on a visual reading task. The outcomes show that the left basal temporal cortex was fully activated in all subjects. However differences were detected in the activation of the tempoparietal regions which were mainly activated in the right hemisphere for dyslexics, in contrast with activated regions in the right hemisphere for normal subjects (Simon et al, 2002). A second theory on developmental dyslexia is the cerebellar theory. Biologically, the cerebellar theory posts that dyslexics’ cerebellum is not fully functional, causing their reading deficiencies (Ramus et al, 2002). This is placed in marked contrast with the biological basis of the phonological theory which is the incapacity of the brain to represent, store and retrieve information. Researches conducted by Nicolson & Fawcett (1999) illustrate that a substantial number of pediatric dyslexics (8 to 18 years old) conventionally demonstrated abnormalities in the cerebellum. These covers posture, tone of muscle, and abnormalities in limb motion. The cerebellum regulates motor control and thus has an effect on speech; such motor deficiencies would then lead to phonological difficulties. In addition, this also regulates carrying out tasks such as driving and reading which are largely automatic. This incapacity to automize makes dyslexics incapable of carrying out the sound-speech match. Empirical support for this theory is empirically anchored on findings that suggest that behaviorally learning difficulties are observed among dyslexics (Nicolson et al, 1999). Still on the biological aspect of the magnocellular theory, Nicolson, Fawcett, & Dean (2001) have found that the issues confronting pediatric dyslexics are not constrained only to reading and spelling difficulties. There is also marked deficiency in autoimmunization, which is a function controlled by the cerebellum. The authors have also made use of brain scans to illustrate that abnormalities in the cerebellum were present in 80% of the dyslexic subjects. Critique of the Two Theories One of the weaknesses of the phonological theory is its failure to explain the rationale behind the sensory and motor difficulties among those afflicted with the condition. Those who advocate the phonological theory reason out that these facets are not central to dyslexia (Ramus et al, 2002; Snowling, 2001). On the other hand, the cerebellar theory has its own share of criticisms, including its inability to explain sensory difficulties; however, its advocates are considering the possibility of different cerebellar and magnocellular dyslexia subtypes (Fawcett and Nicolson, 2001). Yet another criticism on the cerebellar theory is that its core explanation of the condition lies in a motor deficiency, which assumes that phonological representations are dependent on the ability to articulate sounds. This view has been disputed in lieu of the findings that phonological development was possible even with severe speech impairment (Liberman & Mattingly, 1985). There is also no definitive number as to dyslexics that exhibit motor difficulties, and a number of studies have only found a limited percentage of dyslexics who have exhibited such difficulties (Yap & Van der Leij, 1994). In fact, Denckla (1985), that there are only rare instances in which motor difficulties are present, particularly among children who are also afflicted with attention deficit hyperactivitiy disorder (ADHD). Overall, the weakness of the phonological theory lies in the lack of discussion on the causes of sensory and motor difficulties in a substantial percentage of dyslexics. On the other hand, the cerebellar theory cannot explain why certain dyslexics do not suffer from sensory and motor difficulties, in addition to its failure to the weakness of the phonological theory (Ramus et al, 2002). Until now, there is still contention on the biological and cognitive explanations of dyslexia, with the exclusive use of only one theory (Coleman, 2002). The lack of agreement on the core features of dyslexia may be one reason for the difficulty in defining inclusion criteria for research and its current variability. Some traits of dyslexic patients may affect heritability. For example, in a study by DeFries (in Grigorenko, 2000), it has been indicated that the “heritability of spelling deficits seemed to increase with age whereas that of reading difficulties declined.” Moreover, genetic influences are more critical as a root cause of reading impairment among children with high IQs than those with lower IQs. Such a distinction causes the definition of dyslexia to be variable, among those with particular reading disorders and high risk samples. References Coleman, M. (2002). A critical investigation of the etiology of developmental dyslexia. Retrieved on July 20, 2006 from http://serendip.brynmawr.edu/bb/neuro/neuro03/web1/mcoleman.html Denckla, M. B. (1985). Revised neurological examination for subtle signs. 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