Sample Healthcare Research Paper on Dyslexia

Dyslexia

Initially referred to as word blindness, dyslexia is a learning disability among people throughout the world where people struggle to break down words into their smallest basic parts, making the learning of language a challenging process. In the United States, dyslexia is prevalent among children, estimated to affect seven to twelve percent of the children population in the country (Schulte-Körne, 2010). In the long history of dyslexia, the condition was first recognized a hundred and fifty years ago and the medical community has debated the condition over time recognizing that it is a crucial and challenging area of research.

History of Dyslexia

Over the last century, since the discovery of dyslexia, the definition of the condition has taken an in-depth and more nuanced comprehension. The challenge faced by early experts on the distinction of the problem of word blindness was that they could not find any problems with their patients’ vision capabilities. Furthermore, early specialists struggled with isolating their patient’s challenges from other medical disorders or conditions, for example, lesions in or trauma to the brain. Dyslexia was first found in eighteen seventy-seven by Adolf Kussmaul, a German Neurologist, who watched the occurrence of word-blindness among individuals who battled with reading words and interpreting the text in the right order. About a decade later Rudolf Berlin, an ophthalmologist coined the name “dyslexia”. The term dyslexia is derived from the Greek word that means “difficulty with words.” Berlin utilized the term as a clarification for the medical case of a little boy who had serious impairments in writing and reading despite showing typical intellectual capabilities. Simultaneously, James Hinshelwood, James Kerr, and William Pringle Morgan analyzed word blindness past the isolated symptom however explicitly evaluated cases including children (India, 2019).

This work concerning children was a critical advance in the investigation of dyslexia since it evacuated other potential logical factors, for example, neglect or brain trauma. Since the early days of the condition’s initial findings, defining dyslexia has become increasingly specific as not all people with dyslexia have the same diagnosis. Consequently, the medical community has categorized dyslexia in several categories, each concerned with a specific issue related to the capability of reading and analyzing text.

Causes of Dyslexia

Although the exact cause of dyslexia is not entirely clear, brain and anatomical imagery have revealed differences in the way the brain of a dyslexic person functions and develops. As a result, there are various theories on the causes of dyslexia. One of the theories proposes that behavioral symptoms might be viewed as manifestations of the fundamental cause. The major symptom of dyslexia is poor reading abilities. Thus, for much of the research on dyslexia, the focal point of consideration is on reading-related manifestations, and as a result, dyslexia research has been more inclined to concentrate on pre-reading and reading skills. Behavior level theories could, along these lines, incorporate lack of ideas of print, lack of opportunity, lack of letter knowledge or lack of experience as causal factors of dyslexia (Fawcett & Nicolson, 2019).

However, to understand the underlying cause of poor reading, other symptoms have to be examined which in turn leads to a range of secondary causes, which coupled with the primary symptoms, permit a differential diagnosis of the underlying cause of the condition. Subsequently, another theory on the causes of dyslexia is that difficulties in reading can be attributed to challenges in phonological processing; that is, difficulties in breaking down a word to its fundamental sounds (Schulte-Körne, 2010). Such challenges lead to difficulties in sound segmentation as well as in word blending, elements which are critical for spelling and reading development.

Theories structured at the brain level generally attempt to explain the inability to break down a word to its constituent parts and sounds as caused by the structure of the brain. The advent and increasing advancement of brain imaging have revealed the involvement of the cerebellum in sensory processing and cognitive abilities as well as language; thus, providing a natural link to the various viewpoints on dyslexia (Fawcett & Nicolson, 2019). Additionally, a range of variables could be at play and affecting during the pre-reading years, and that these could lead to a wide variety of symptoms within and past abilities related to reading. The significant course of impairment is through phonological processing connected to weakness in speech production, with further difficulties emerging from limitations of working memory and automatization issues. These issues, in due time, lead to the difficulties of spelling, writing, and reading are the characteristic aspects of dyslexia.

Another known cause of dyslexia is genetics. There is clear research evidence that supports the genetic transmission of dyslexia. For example, a boy child with a sibling or parent that is dyslexic has a fifty percent chance of being dyslexic (Schumacher et al., 2007). There has been numerous wide-spread research on genetics in the past decade resulting in genetic theories identifying a variety of genes, most of which are engaged in neuronal migrations. Sadly, there has been a baffling absence of progress. A key problem is that genetic examinations can only perform as good as the physical manifestations or phenotype obtained, and given that difficulty in reading is too broad a symptom, a proper phenotype or endophenotype is reliant on the nature of the investigated theoretical framework. Ultimately, genetic examinations are most appropriate for giving converging proof related to current hypotheses, as opposed to coordinating the improvement of new theories (Mascheretti, et al., 2017).

Types of Dyslexia

There are no officially accepted types of dyslexia; however, experts have categorized dyslexia into various subtypes. Additionally, as genetics plays a significant role in the condition, various reading challenges can be linked to specific combination of genes. Also, a person’s learning experiences can affect how their brain gets organized for reading. As such, these factors aid in explaining why people with dyslexia are not exactly alike (Mascheretti, et al., 2017). Subtypes, unlike types, mean that dyslexic people do not fall into one particular subtype rather a dyslexic individual can present symptoms from different subtypes.

A key characteristic of dyslexia is significantly reduced reading speed whereby individuals take two or three times more time to read text than a normal person. Consequently, reduced reading speed leads to an inability to understand what has been read. Additionally, associating individual letters with their sounds is difficult and slow leading to more reading and spelling mistakes. However, the development of the ability to read and spell comes in stages. Initially, children learn to spell phonetically which takes about an year to learn all sound-letter connections. The subsequent stage involves orthographically correct writing which involves the correct use of prefixes, suffixes and capital and lower case letters. As challenges faced during these stages cannot be attributed to a specific set of causes, it is impossible to categorize types of dyslexia according to etiology, since there are not specific spelling and reading mistakes associated with a “type” of dyslexia. Rather, errors in spelling and reading can only be assigned to individual developmental stages and can thus be associated with various subtypes of dyslexia (India, 2019).

Some of the most widely known subtypes of dyslexia include phonological dyslexia, surface dyslexia, rapid naming deficit and double deficit dyslexia. Phonological dyslexia is the most common subtype and the one which most people associate with the condition. It is difficulty breaking down the sounds of language and coordinating those sounds with written symbols, which leads to problems with sounding out or decoding words. Specialists think phonological dyslexia, which is sometimes referred to as dysphonetic dyslexia, is the most widely recognized subtype (Schulte-Körne, 2010).

Another subtype of dyslexia is surface dyslexia. Most individuals with dyslexia battle to some extent with the sounds in words. Individuals with this subtype are often okay with sounding out new words but have trouble with recognizing common words by sight. It might take them longer to arrive at a point where they can instantly perceive a specific word without the need to sound it out. This is presumably because the brain finds it difficult to recall what a particular word looks like. Individuals with surface dyslexia may experience increased difficulty with words that do not sound how they are spelled; for instance, words like debt or weight, and need to be memorized. Surface dyslexia is also known as dyseidetic dyslexia or visual dyslexia (Fawcett & Nicolson, 2019). Numerous individuals have both surface and phonological dyslexia; reason being, challenges with decoding can prevent one from mastering sighting words. Readers who are struggling probably will not come across a word regularly enough to start to remember it at a glance.

Rapid naming deficit and double deficit dyslexia are other dyslexia subtypes. Numerous yet not all individuals with dyslexia experience difficulty quickly naming things like colors, numbers, and letters when they see them. They can pronounce the names; however, it takes them longer to name a large number of them in succession. Specialists hypothesize that this issue is linked with problems with reading speed and processing speed. On the other hand, in double deficit dyslexia, a double deficit implies an individual with dyslexia is struggling with two elements of reading. Consequently, double deficit dyslexia is regularly used to portray individuals who experience difficulty with naming speed and have difficulty in recognizing the sounds in words. Furthermore, multiple specialists accept rapid naming deficit and phonological dyslexia are independent difficulties; however, that they can occur simultaneously (Fawcett & Nicolson, 2019). Having both of these difficulties simultaneously will generally lead to a more serious type of dyslexia.

Treatment of Dyslexia

There is no cure for dyslexia; thus, it is a lifelong condition. However, with the appropriate assistance, individuals with the disorder can learn to spell, write and read well. Furthermore, early identification of the disorder and treatment is critical for assisting dyslexic individuals to strive in school and life. Consequently, before the start of any treatment, an assessment must be done to decide a child’s particular area of incapacity. While there are numerous speculations about effective treatment for dyslexia, there is no genuine cure for it. As a result, it is the school’s responsibility to come up with an arrangement with the parent to address the child’s issues and needs. The plan can be actualized in a specialized education setting or the conventional classroom environment. A proper treatment plan will concentrate on reinforcing the child’s shortcomings while using his or her strengths. A direct methodology can incorporate an orderly study of phonics. Strategies intended to enable all the senses to cooperate proficiently can likewise be utilized. Additionally, computers are great assets for dyslexic children and should be used however much as possible. The child should be shown coping and compensation abilities (Schulte-Körne, 2010). Also, attention should be provided to ideal learning conditions and alternate student performance avenues.

On top of what is being offered at school, there are other treatment alternatives accessible outside the school setting. Albeit alternative treatments are generally prescribed, there is restricted research supporting the viability of these treatments. Furthermore, a significant number of these treatments are exorbitant, and it can be easy for disappointed parents to be deceived by something that is costly and sounds appealing.

Ultimately, the most significant part of any plan of treatment is attitude. Children are often impacted by the perspectives of the grown-ups around them. Dyslexia should not turn into a reason for a child to shy away from work that is written. Since the learning demands on a dyslexic child can be significant, making the child tire easily, increments in work should be divided into appropriate sizes. Regular recess sessions should be incorporated with class and schoolwork time. Support should be provided for both achievements and efforts. Alternate options to conventional written tasks should be evaluated and used. Instructors are figuring out how to convey information to learners in various ways that are intriguing as well as accommodating to students who may learn best by various strategies (Schulte-Körne, 2010). Interactive technology is giving intriguing approaches to learners to get criticism on what they have learned, in contrast to conventional pencil-paper assignments.

 

 

 

 

 

References

Fawcett, A. J., & Nicolson, R. I. (2019). Development of dyslexia: The delayed neural commitment framework. Frontiers in behavioral neuroscience 13, 112.  https://doi.org/ 10.3389/fnbeh.2019.00112

India. (2019, May 3). Word Blindness to Dyslexia. Trinity College. https://commons.trincoll.edu/edreform/2019/05/word-blindness-to-dyslexia/

Mascheretti, S., De Luca, A., Trezzi, V., DPeruzzo, D., Nordio, A., Marino, C., & Arrigoni, F. (2017). Neurogenetics of developmental dyslexia: from genes to behavior through brain neuroimaging and cognitive and sensorial mechanisms. Translational psychiatry, 7(1), 987. https://doi.org/10.1038/tp.2016.240

Schulte-Körne, G. (2010). The Prevention, Diagnosis, and Treatment of Dyslexia. Deutsches Ärzteblatt International 107(41), 718–727. https://doi.org/10.3238/arztebl.2010.0718

Schumacher, J., Hoffmann, P., Schmal, C., Schulte-Korne, G., & Nothen, M. (2007). Genetics of dyslexia: the evolving landscape. Journal of medical genetics 44(5), 289-297. https://doi.org/10.1136/jmg.2006.046516