Cognition, Language, and Brain: Dyslexia - Term Paper Example

 Cognition, language, and brain Dyslexia is a language-based learning disability as demonstrated by speech impediments in decoding of words, normally the result of inadequate abilities in the phonological process. This neurological disorder, which affects more then five percent of the population, has no correlation to intelligence but its fundamental causes are the subject of much debate. Its origins are genetic in nature and/or because of undesirable prenatal events, however, this explanation is not conclusive. The brain continues developing throughout childhood with respect to an individual’s particular environmental stimulus. As the brain develops, language skills are modified to a significant degree depending on particular outside influences. Therefore, “both genetic and environmental influences may contribute in varying degrees to the final shaping of the dyslexic brain” (Lishman, 2003). Dyslexia cannot be diagnosed or understood as a specific disorder which has led to misunderstandings within the scientific community and the public regarding the condition which this discussion attempts to clarify. An example of the non-specific nature of dyslexia centers on an argument regarding which part of the brain most affects the condition. Though it is widely accepted that the left hemisphere of the brain controls verbal functions and positron emission tomography scans have confirmed this assessment, others, such as Price et al (1998) hypothesize that “reading aloud involves a large number of cognitive processes including, at a minimum, visual and orthographic analysis, phonological retrieval, articulation, and hearing the sound of the spoken word” (Price et al, 1998, p. 305). Price went on to say deficits associated with dyslexia “might be the hallmarks of exclusive reliance on a right-hemisphere…the reading of dyslexics rely exclusively on a right-hemisphere” (Price et al, 1998, p. 305). Some type of right-hemisphere mechanism involving reading comprehension is necessary to be able to read aloud if any one of the left-sided functions such as processing stages, orthographic, semantic or phonological functions is not capable of operating normally. That the emotional and creative side of the brain plays some type of role in reading comprehension can hardly be disputed. For example, if a child is upset or they prefer to draw animal figures from letters instead of pronouncing them, the ability to read coherently may be slowed somewhat as compared to classmates. Dyslexia concerns many facets of brain function. However, it is not associated with emotional outbursts or an abundance/lack of creativity; it is a neurological disorder. The three most recognised theories that explain the source of dyslexia all originate from left-brained based functions. Dyslexic’s have difficulty matching sounds to letters according to the phonological theory which identifies the condition as essentially a left-hemisphere deficiency. The brain impediment makes difficult the association of visual symbols with fragments of sounds so that language cannot be processed in its correct progression (Snowling, 1996). The magnocellular theory describes another left-brain function, an inability to focus on and retain sounds and sights that change rapidly, an eye-tracking issue combined with problems detecting quick modifications in voice pitch (Stein & Talcott, 1999). The third theory describing left-brain responsibility is the cerebellar. This theory cites a malfunction in the cerebellum, the part of the brain that controls automatic actions and learned tasks (Nicolson et al, 1999). A number of studies conclude phonological processing impediments underlie dyslexia, found in everyone afflicted with the condition. Others acknowledge the phonological theory but view brain structure as the cause which is not related to phonological deficits which are simply the symptom. While temporal processing deficits can be detected in most dyslexics, this problem is not present in all cases. According to this logic, the presence of temporal processing deficiencies is not necessarily the cause of reading and language disorders. What remains unanswered is if temporal processing deficits are sufficient to bring about dyslexia. The phonological theory is limited in that it does not explain how motor and sensory disorders occur in dyslexics. Those who support the phonological theory generally disregard these disorders as not being one of the main elements of dyslexia. They are not the cause of the condition but may be an indicator of a reading deficit. Likewise, the cerebellar theory does not give an explanation for sensory disorders. However, advocates of the theory contemplate the idea of distinctive magnocellular and cerebellar dyslexia sub-types (Fawcett & Nicolson, 2001). Also, the cerebellar theory is built upon an obsolete analysis on the importance speech motor skills plays, that phonological training is reliant on articulation of speech. The position that phonology and articulation are expressively linked has been long discarded. Additionally, there remains an uncertainty regarding just what percentage of dyslexics are actually afflicted by motor skills deficiencies. The body of research dedicated to this area has not found associated motor problems except for dyslexics who also have ‘attention-deficit hyperactivity disorder’ (Wimmer et al, 1999). The magnocellular theory, though it uniquely accounts for a combination of the other theories, has problems of its own in that it fails to produce conclusions regarding auditory abnormalities in dyslexics (Heath et al, 1999). Another critique of the theory centers on outcomes “inconsistent with the idea that the auditory deficit lies in rapid auditory processing and therefore with magnocellular function” (Lorenzi et al, 2000). A further disparagement includes the fact that auditory disorders “do not predict phonological deficits and are restricted to those dyslexic individuals who also have additional language impairments” (Heath et al, 1999). Assessments on the visual aspects of the magnocellular theory have discovered “failures to replicate findings of a visual deficit and on inconsistencies between predictions and empirical results; most notably, visual impairments, when found, seem to be observed across the whole range of spatial frequencies, not just that characteristic of the magnocellular system” (Farrag et al, 2002). The phonological theory does not provide definitive answers because its does not rationalize the presence of motor and sensory disorders in a substantial percentage of dyslexics. The magnocellular theory is insufficient as well because if its inability to give an explanation for the deficiency of sensory and motor disorders in a substantial percentage of dyslexics. The cerebellar theory is especially insufficient as it is simply out-dated and burdened with each of the other theories credibility issues. There is the possibility that these three theories could be accurate when discussing the case of different people. For example, three subtypes of dyslexia could partially overlap one another each contributing to the phonological, magnocellular (auditory/visual) and cerebellar difficulties. Conversely, just one theory could explain all cases of dyslexia and the other symptoms do not cause but are caused by dyslexia. In order to more clearly define the causations of the condition, the percentage of dyslexics who have a particular deficit must be known in addition to discerning methodical links between particular deficiencies. The current collective bodies of work are unable to answer these questions. For dyslexics, reading tasks require additional concentration and repetition as they do not recognize letters and numbers that have been previously learned as readily as those without the condition. Because of this hindrance, dyslexics can experience an overload of their thought processes when performing reading tasks for the first time or those of a complex nature. Because they have difficulty with ‘automatic’ recognition of words, they require much more practice and patience from the instructor when attempting any reading skill before they can retrieve it automatically. The term ‘working memory’ describes the cognitive process that stores recent information in the brain for a short amount of time before this information is either discarded or conveyed into ‘long-term memory’ storage banks. A number of researchers consider the ineffectiveness of working memory the main fundamental aspect of dyslexia. Deficits related to dyslexia have been the focus of much research. It could be “more beneficial to refer to cognitive differences, as opposed to deficits, as some of these differences may enable dyslexic individuals to have particular strengths, such as good conceptual and creative higher-order thinking skills” (Department for Education and Skills, 2006). Dyslexics might not be capable of effectively processing sensory stimulus which may give understanding to their visual impediments and erratic visual fixations when reading. This visual impediment can result in letter order confusion which, in turn, results in reduced memory of the words visual appearance. This, as stated previously, could be an indication of an underlying source. “Phonological, visual or motor difficulties may all be indicative of an underlying temporal or timing difficulty, rather than alternative explanations for dyslexia. These timing difficulties may also have their origin in brain structure” (Department for Education and Skills, 2006). The prevailing view among researchers and scholars is that phonological processing impediments are present to varying degrees among all people afflicted with dyslexia although various opinions can be found regarding its fundamental source. A phonological deficit is not necessarily the causation of dyslexia because of the potential, albeit slight, that other unrelated factors are causing the reading impairment. However, an overwhelming amount of research has concluded that phonological deficits, which can occur separately from any motor or sensory impairment, are an adequate cause for the condition. Given this assertion, it should also be noted that a large percentage of dyslexics experience visual, auditory, or motor impediments. Deficits in auditory function exacerbate phonological deficits leading to reading difficulties for dyslexics. “The nature of the auditory deficits observed is not particularly consistent with the hypothesis of a rapid processing deficit related to a magnocellular dysfunction (and) neither is the nature of motor/timing impairments particularly consistent with the hypothesis of an automaticity deficit or a cerebellar dysfunction” (Ramus et al, 2003). At present, the specific nature of auditory processing problems and its relationship to the phonological deficit has not been scientifically established. The reason the motor and sensory impediments are commonly linked to phonological deficits as well as further developmental disorders is not yet clear. The phonological deficit theory proposes that dyslexics have difficulty with phonemic representation, storage, mentally recording sounds into letters in the brain and with recall. This theory offers a reliable explanation for reading impairments experienced by dyslexics. Learning to read and to speak the alphabet necessitates a connection between sounds and letters. In the case of dyslexics, sounds correspond inadequately to symbols with regard to storage and retrieval thereby hindering the grapheme-phoneme association which is the basis for understanding the alphabetic (Bradley & Bryant, 1978). The cerebellum theory of dyslexia claims that the condition is caused by a biological dysfunction of the cerebellum causing difficulties in the cognitive process. The cerebellum is the part of the brain that controls motor functions therefore plays a role in the articulation of language. The theory proposes that articulation impediments act to produce deficits in phonological interpretations. The cerebellum also plays a significant role in the retention of automatic tasks such as typing, driving and reading comprehension. A dyslexic’s inability to retain automatic functions affects the ability to learn grapheme-phoneme connections. Research that has involved brain imaging has shown metabolic, activation and anatomical discrepancies in the cerebellum of those afflicted with dyslexia. “Support for the cerebellar theory comes from evidence of poor dyslexic performance in a large number of motor tasks in dual tasks demonstrating impaired automatisation of balance and in time estimation, a non-motor cerebellar task” (Department for Education and Skills, 2006). The magnocellular theory expands on the cerebellum theory coalescing it to the known symptoms of dyslexic phonological dysfunction. “As the cerebellum receives massive input from various magnocellular systems in the brain, it is also predicted to be affected by the general magnocellular defect” (Stein et al, 2001). The cerebellum processes information received from the magnocellular area of the brain from which some language functions are affected. Deficiencies in just one of these areas most probably explain the various types of dyslexia symptoms and to what degree it afflicts an individual. Proficient language skills may be impeded as a consequence of the under-developed or an otherwise weakened structure of magnocells (large neurons) which controls motor functions and sensory events. “The visual demands of reading draw on the visual magnocellular system and any weakness can lead to visual confusion of letter order and poor visual memory for the written word” (Stein et al, 2001). Regarded as a generalisation of the visual theory, the magnocellular theory suggests that “the magnocellular dysfunction is not restricted to the visual pathways, but generalised to all modalities (visual, auditory, as well as tactile)” (Stein et al, 2001). The magnocellular theory identifies a deficiency in an area of the brain that causes auditory, visual, motor and tactile functions, and as a result, phonological difficulties, the sum total symptoms of dyslexia. The magnocellular theory has brought new scientific evidence into the study regarding the origin of dyslexia going beyond previous theories because of recent brain imaging technologies. These techniques have allowed researchers to more clearly identify abnormal structures in the brain and further study its active processes thus giving the theory added credibility but by no means provides definitive answers. Examining dyslexia from a neurological viewpoint, most all researchers agree that the source of the language impediment is an inherited malady generated by the left-hemisphere of the brain which is responsible for fundamental verbal functions and phonological visualizations. Though varying theorists provide varying opinions regarding the physical and physiological makeup of phonological difficulties, all concur with the central, underlying role that phonology plays in dyslexia. Therefore, the phonological theory is the most viable in terms of understanding and treating the condition as it put forward a direct association between cognitive deficits and the symptoms associated with dyslexia. References Bradley, L. & Bryant, P.E. (1978). “Difficulties in Auditory Organisation as a Possible Cause of Reading Backwardness.” Nature. Vol. 271, pp. 746-747. Department for Education and Skills. (2006). “A Framework for Understanding Dyslexia.” Theories of Dyslexia. Crown Copyright. Retrieved 3 August 2006 from < http://www.dfes.gov.uk/readwriteplus/understandingdyslexia/theoriesofdyslexia/cognitivetheories/> Farrag, A.F.; Khedr, E.M.; & Abel-Naser, W. (2002). “Impaired Parvocellular Pathway in Dyslexic Children.” European Journal of Neurology. Vol. 9, pp. 359-63. Fawcett, A.J. & Nicolson, R.I. (2001). “Dyslexia: The Role of the Cerebellum.” Dyslexia: Theory and Good Practice. A.J. Fawcett (Ed.). London: Whurr Publishers, pp. 89-105. Heath, S.M., Hogben, J.H. & Clark, C.D. (1999). “Auditory Temporal Processing in Disabled Readers With and Without Oral Language Delay.” Journal of Child Psychology & Psychiatry. Vol. 40, 637-47. Lishman, W. A. (2003). “Developmental Dyslexia.” Journal of Neurology Neurosurgery and Psychiatry. Vol 74, pp. 1603-1605. Lorenzi, C.; Dumont, A.; Füllgrabe, C. (2000). “Use of Temporal Envelope Cues by Children with Developmental Dyslexia.” Journal of Speech, Language and Hearing Research. Vol. 43, pp. 1367-1379. Nicolson , R.I.; Fawcett, A.J.; Berry, E.L.; Jenkins, I.H.; Dean, P. & Brooks, D.J. (1999). “Association of Abnormal Cerebellar Activation with Motor Learning Difficulties in Dyslexic Adults.” The Lancet. Vol. 353, pp 1662-1667. Price, C. J.; Howard, D.; Patterson, K.; Warburton, E. A.; Friston, K.; & Frackowiak, R. S. J. (1998). “A Functional Neuro-imaging Description of Two Deep Dyslexic Patients.” Journal of Cognitive Neuroscience. Vol. 10, pp. 303–315. Ramus, F.; Rosen, S.; Dakin, S.C.; Day, B.L.; Castellote, J.M.; White, S. & Frith, U. (2003). “Theories of Developmental Dyslexia: Insights from a Multiple Case Study of Dyslexic Adults.” Brain. Vol. 126, pp. 841-865. Snowling, M.J. (1996). “Developmental Dyslexia: An Introduction and Theoretical Overview.” Dyslexia, Speech and Language: A Practitioner’s Handbook. M.J. Snowling & J. Stackhouse (Eds.). London: Whurr Publishers, pp. 1-11. Stein, J. & Talcott, J. (1999). “Impaired Neuronal Timing in Developmental Dyslexia – The Magnocellular Hypothesis.” Dyslexia. Vol. 5, pp. 59-77. Stein, J.; Talcott, J.; & Witton, C. (2001). “The Sensorimotor Basis of Developmental Dyslexia.” Dyslexia: Theory and Good Practice. A.J. Fawcett (Ed.). London: Whurr Publishers, pp. 65-88. Wimmer, H.; Mayringer, H.; Raberger, T. (1999). “Reading and Dual-Task Balancing: Evidence Against the Automatization Deficit Explanation of Developmental Dyslexia.” Journal of Learning Disabilities. Vol. 32, pp. 473-478. Read More