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Dyslexia, Research Paper Example

Pages: 20

Words: 5572

Research Paper

Introduction

Dyslexia is a controversial and ambiguous neurodevelopmental disorder causing much debate regarding its form, assessment, and the very existence of the issue as a real neurophysiological and neuropsychological problem. By a broad definition, it is “characterized by difficulties in learning to read despite conventional instruction, adequate intelligence, and a balanced socio-cultural background” (Wajuihian & Naidoo, 2012). However, as Smythe (2011) indicated, dyslexic individuals perceive their difficulties as real and serious, which usually spreads beyond plain reading and writing difficulties, and is manifested in a wider range of cognitive and developmental challenges.

Dyslexia as a particular type of a disorder is known since 1887 when the German physician Berlin published his monograph Dyslexia Eine besondere Art der Wortblindheit, coining the term “dyslexia” as a synonym to “word blindness”; this idea was proposed by Kussmaul in 1877 to denote the acquired loss of words (Smythe, 2011; Wajuihian & Naidoo, 2012). The term “dyslexia” is now used as a synonym to “developmental dyslexia” to denote a specific reading disability indicating that the development of a person is normal in all other aspects except reading (Wajuihian & Naidoo, 2012). The origin of the term is Greek: the word “dys” means a difficulty, and “lexicos” – means something pertaining to words – thus, the conceptual meaning of dyslexia is having some generic problem with words.

Besides accepting the very fact of dyslexia’s existence, there is a problem with defining the disorder. According to Smythe (2011), one of the most comprehensive definition was given by the Health Council of the Netherlands: “dyslexia is present when the automatization of word identification (reading) and/or spelling does not develop or does so very incompletely or with great difficulty” (p. 39). The Oxford Handbook of Psychiatry now defines dyslexia as “inability to read at the level of one’s age or intelligence level” (Macdonald, 2009, p. 272). However, the British Medical Association proposed to expand the effect of dyslexia on all aspects of human literacy indicating that the latter disorder affects “reading, spelling, writing”, and influences the “short-term memory” and “phonological awareness” of the individual (Macdonald, 2009, p. 272).

One of the most extended definitions has been provided by the British Dyslexia Association:

“Dyslexia is a combination of abilities and difficulties that affect the learning process in one or more of reading, spelling and writing. Accompanying weaknesses may be identified in areas of speed of processing, short-term memory, organization, sequencing, spoken language and motor skills. There may be difficulties with auditory and/or visual perception. Dyslexia can occur despite normal intellectual ability and education opportunity. It is constitutional in origin, part of one’s make-up and independent of socio-economic status” (Wajuihian & Naidoo, 2012, p. 25).

The present definition presupposes that dyslexia is a serious and multi-aspect developmental disorder that produces a certain range of impacts on the neurological, neurophysiological, and neuroanatomical features of an individual affected by it. Moreover, dyslexia has a potential of affecting the behavioral and psychological aspects of human functioning. Its manifestations are different at various stages of its course; hence, one has to understand the whole complex of dyslexia’s features and influence on an individual to be able to compose a workable and full profile of the disorder.

Neurological, Neurobehavioral, Neurophysiological, and Neuroanatomical Correlates, Etiologies, and Theories of Dyslexia

During the history of dyslexia research, a wide range of theories, correlates, and etiologies relating to the nature of dyslexia as a developmental disorder, and the nature of its impact on the individuals’ cognitive abilities have been in the focus of researchers. Smythe (2011) mentioned that Frith (1999) was one of the first researchers to comprehensively map out the causal theories of dyslexia: biological, cognitive, behavioral, and environmental influences on individuals. As for considering structural differences among people with and without dyslexia, one has to consider cerebellar and magnocellular theories as well (Smythe, 2011). However, there is no doubt that the root causes of dyslexia, and the nature of dyslexi’a impact on the human activity is in the human brain: “areas implicated include the anterior superior temporal gyrus, planum temporal or Heschl sulcus, superior temporal sulcus and fusiform gyrus” (Smythe, 2011, p. 40).

Punt, de Jong, de Groot, and Hadders-Angra (2010) also agreed that the primary problem causing dyslexia is in the human brain. The authors indicated that the postmortem research, as well as structural and functional neuroimaging, helped to single out the parts of brain potentially involved in the development of dyslexia in children. The most commonly mentioned part is the cerebral cortex; abnormalities of the cerebral cortex include focal dysplasia and neuronal ectopias found in the perisylvian areas responsible for language processing in the parietal lobe (Punt et al., 2010). Ectopias reflect the failure of neurons to complete their traditional function of reaching the part of the brain with a stimulus (Wajuihian & Naidoo, 2012). The abnormalities in the magnocellular visual pathway functioning as the route for visual motion processing projected to the parietal cortex are also considered the cause of dyslexia (Punt et al., 2010).

Wajuihian (2012) gave a more precise overview o the neuroanatomy of language-relevant structures in the brain potentially responsible for the formation of dyslexia. The author noted that the cerebral cortex (the layer of the brain referred to as the gray matter of the brain) covers the outer portion of cerebrum and cerebellum; the areas called the Sylvian fissure (separating the temporal lobe from the frontal and parietal lobes) is called the perisylvian region – it is located on the surface of the brain, and is the storage of the major part of language tissue (Wajuihian, 2012). Generally, the cortex area is considered the neural base of language in all human beings. However, some other important brain parts also take part in the language formation and processing activities; for instance, the angular gyrus is the part of the brain in the parietal lobe, and is involved in a number of language-related and cognitive processes (Wajuihian, 2012).

However, in addition to the purely neurobiological perspective on the formation of dyslexia in children, Wajuihian and Naidoo (2012) formulated a range of additional factors that can also contribute to the development of this disorder. Genetic factors are highly significant in the issue of dyslexia, since it is a heritable disorder, and 23-65% of children whose parents had a history of having dyslexia acquired the same disorder. The environmental factors are also meaningful for this type of the disorder, including the peri-natal factors (those disrupting the normal cortical growth, such as problems with the mother’s immune system, autoimmune diseases’ history in the family, etc.), substance use during pregnancy (cocaine, alcohol, etc.), and nutrition. Hence, all factors have to be kept in mind when trying to mitigate the risk of a child’s acquisition of dyslexia, as well as researching the causes thereof.

Flowers (1993) also commented on the brain-related causes of dyslexia formation. The author noted that the prior research detected “widespread cytoarchitectonic anomalies in some of the same autopsy material, especially in the left-hemisphere language areas” (p. 575-6). The present finding supports the previously cited evidence for the role of language-related parts’ of the brain functioning in predetermining the risk of dyslexia emergence. Some other observations of Flowers (1993) include seeing the possible relationship between dyslexia and stimuli processing mechanisms in any sensory modality. This problem, as seen by the researcher, can be easily overcome by means of slowing down the rate of stimulus presentation to facilitate stimuli processing mechanisms in the affected brain.

Another observation shared by Flowers (1993) and Wajuihian (2012) is the role of the planum temporale, or temporal planum (PT), in the development of dyslexia. PT is the “area on the surface of the temporal lobe posterior to the primary auditory cortex… symmetrical across the hemispheres of the subjects with dyslexia, whereas in the general population this region is usually larger on the left than on the right” (Flowers, 1993, p. 578). The reason for which people with a symmetric PT are at a higher risk of being dyslexic is that their left hemispheres appear not adapted to language the way a normal brain is (Wajuihian, 2012).

Wajuihian and Naidoo (2012) provided a comprehensive overview of theories of dyslexia; the authors discussed the phonological, cerebellar, auditory theories, and the theory of visual deficit. According to their opinion, the core assumption guiding the emergence of these theories is that dyslexia is caused by certain abnormalities in the human brain. The phonological theory of dyslexia states that reading difficulties in children emerge “in fragment spoken words down into their constituent sound unit (or phonemes), and affected individuals are unable to develop the association between letters (grapheme) and sound (phoneme), a function, which has been considered a major cause of reading and spelling impairment in most cases of developmental dyslexia” (Wajuihian & Naidoo, 2012, p. 29).

The present inference is in compliance with the observation that the majority of individuals experiencing dyslexia have problems with phoneme processing. Therefore, the majority of educational programs directed at mitigating the impact of dyslexia are targeted at the phonological competencies of individuals.

As for the cerebellar theory, it is also called the automaticity theory; it states that the role of cerebellum in the automatization of cognitive processes is essential, and works improperly in the brains of the dyslexic individuals. Cerebellum has been found out to be responsible for such cognitive processes as motor control and speech articulation. Hence, a dysfunction in cerebellum is now seen as a possible cause of dyslexia (Wajuihian & Naidoo, 2012).

The visual deficit, or magnocellular, theory refers to the dysfunctions in the neuroanatomy and neurophysiology of the magnocellular system as the possible cause of dyslexia (Wajuihian & Naidoo, 2012). The basis for this theory is the subdivision of the visual system into two sub-systems, the magnocellular (transient) and parvocellular (sustained) ones. Both of them carry information to the visual cortex; however, the magnocellular system is considered crucial in the timing of visual stimuli, motion perception, and eye response controls to visual targets (Wajuihian & Naidoo, 2012). Hence, in case the magnocellular system of the human brain works improperly, it can cause “destabilization of binocular fixation, resulting in visual confusion and mis-sequencing of letters in a word” (Wajuihian & Naidoo, 2012, p. 29).

Finally, the auditory theory of dyslexia refers the problem of dyslexia’s emergence to the individuals’ inability to distinguish speech sounds, which results in the deficit of neural systems processing rapidly presented auditory stimuli (Wajuihian & Naidoo, 2012). The present malfunction of the human brain presupposes its inability to “detect and process the dynamic acoustic patterns of speech, leading to impaired phonological processing with a resultant difficulty in reading” (Wajuihian & Naidoo, 2012, p. 29).

All these theories have found support from the clinical studies, so they all have the equal rights for existence at present. Much clinical research is now undertaken in the field of identifying the causes of dyslexia, and many studies are dedicated to understanding the brain function and the specificity of dysfunctions (including co-morbidities) in the dyslexic brain. For instance, Punt et al. (2010) conducted clinical research on the neurological and perceptual deficits in children with severe dyslexia. Their research findings indicated that 44 children with severe dyslexia (without psychiatric co-morbidity) had dyslexia as a unique diagnosis, while 60 children had that diagnosis combined with psychiatric co-morbidities (Punt et al., 2010). The co-morbid disorders commonly detected in the research included disturbance of emotions specific to childhood, adjustment disorders, hyperkinetic disorder, autism spectrum disorder, etc. (Punt et al., 2010). The present findings suggest that for many children, having dyslexia is associated with a wide spectrum of associated dysfunctions occurring in the complex supraspinal circuitries stemming from cortical structures’ dysfunctions (Punt et al., 2010). Such dysfunctions refer primarily to mild coordination problems (presupposing the cerebellar dysfunction), and presuppose the abnormalities in the perisylvian area, parietal lobes, and corpus callosum (Punt et al., 2010). The overall research recommendations of authors indicate that “the high prevalence of fine manipulative disability and dysregulation in posture and muscle tone emphasizes the need to pay attention to motor impairments in children with dyslexia” (Punt et al., 2010, p. 1131).

The clinical study conducted by Taroyan, Nicolson, and Buckley (2011) aimed at testing the coherent motion perceptions in dyslexic individuals; the study findings revealed that the behavioral performance of participants was good, with only 10-20% of errors made in perceptually difficult coherent and incoherent conditions. The authors also concluded that the “increased P3 amplitude in the tightly (40%) coherent motion condition in the right compared with the left hemisphere across both groups replicates the results from previous studies showing increased brain activation with higher coherence levels of motion” (Taroyan et al., 2011, p. 286). These results are consistent with the data provided above regarding the brain specificity of dyslexic individuals, and prove that “literacy problems and decreased performance sensitivity in perceptually difficult 10% coherent motion condition are associated with attenuated brain activation” (Taroyan et al., 2011, p. 286).

Neuropsychological, Psychological, and Behavioral Correlates, Etiologies, and Theories of Dyslexia

In addition to a variety of neuroanatomical and neurophysiological abnormalities observed in the individuals with dyslexia, one has to note that the disorder also imposes a set of neuropsychological and behavioral manifestations distinguishing the life, skills, and behaviors of dyslexic and non-dyslexic individuals. One of illustrative studies of the perceived behavioral correlates of dyslexic individuals indicated that people suffering from this disorder reported “restricted literacy skills which started in childhood and prevailed through to adulthood” (Macdonald, 2009, p. 274). However, the majority of respondents indicated much more discomfort with writing rather than reading activities. The nature of dyslexia’s effect on respondents’ life was characterized as follows:

“Literacy restrictions predominantly affected employment opportunities of participants and were central to the group’s life narratives. Literacy problems, caused by dyslexia, prevented five unemployed participants from considering applying for employment. This was either because of anxiety about completing application forms, or due to anxieties about undertaking literacy exercises during the interview procedures. Five participants had at least one bad experience during an interview” (Macdonald, 2009, pp. 274-5).

Some features of dyslexic individuals have been outlined by Ewing and Parvez (2012) who researched the influence of pathologies upon sensory perception and sensory coordination in children with developmental dyslexia and learning disorders. The researchers noted that developmental dyslexia develops in the pre-pubescent child, and sense perception and coordination of dyslexic individuals can be altered by pathologies (Ewing & Parvez, 2012). The authors also underlined that many dyslexic children have excellent speech, hearing, and visual perception, and a fairly high IQ. Moreover, people with dyslexia may have excellent memory and balance; dyslexic individuals can be very good with numbers, and can advance from their creativity, motivation, and active life (Ewing & Parvez, 2012).

Flowers (1993) supported this evidence 16 years before by indicating that students with dyslexia learn worse than their peers do, even in case they are provided with multiple opportunities for that, and are objectively assessed as neurologically, emotionally, and intellectually healthy people. The majority of dyslexia cases show that individuals can read to a certain extent, but to accomplish even a poor level of reading abilities, they have to work hard, and to have enormous motivation, accuracy, and attention. As it comes from the neuroanatomical evidence regarding dyslexia, the role of the brain in the reading potential is significant; hence, Flowers (1993) investigated the behavioral correlates of regional cerebral blood flow (rCBF) of dyslexic individuals, and found the positive correlations thereof involving left temporal flow – “single-word and paragraph reading, spelling, nonword reading, and rapid alternating naming” (p. 579). As for the angular gyrus, only oral and silent reading comprehension was positively correlated with the single-word and paragraph reading activities (Flowers, 1993).

Dyslexia is the disorder manifested mainly in reading challenges; hence, it is necessary to look for behavioral and neurophysiological correlates of dyslexia in behaviors related to reading. As Wajuihian and Naidoo (2012) estimated, dyslexic children often perform “word reversals, skipping of words, re-reads lines, points to words, word substitution, diplopia, poor comprehension in oral reading, might see text appearing to jump around on page, unable to tell difference between letters that look similar in shape such as “o” and “e”, unable to tell difference between letters with similar shape but different orientation such as “b” and “p” and, letters might look all jumped up and out of order” (p. 27).

Among other symptoms, one should note seeing words as reversed backwards, for instance, for a dyslexic person, the word “bird” appears to look like “drib”; dyslexia is often closely related to dysgraphia, i.e. the omission of beginning or ending letters, better spelling than reading, etc. (Wajuihian & Naidoo, 2012). Numeric association difficulties may also be met in dyslexic children – they are called dyscalculia. There are also difficulties associated exclusively with reading: “difficulty learning to read, difficulty identifying and generating rhyming words, or counting syllables in words, difficulty with manipulating sounds in words, difficulty distinguishing different sounds in words”, etc. (Wajuihian & Naidoo, 2012, p. 27).

In addition to problems limited almost exclusively to the reading and writing competencies, some researchers admit a much wider spectrum of effects that dyslexia may have on the children, for instance, lowered self-esteem, school dropout, juvenile delinquency, and the development of psychopathology in childhood and adolescence (Punt et al., 2010). The disorders detected as comorbid ones are “anxiety disorders, conduct and oppositional disorders, attention-deficit-hyperactivity disorder (ADHD), and deficits in attention, motor control, and perception (Punt et al., 2010, p. 1128).

The majority of researchers and clinicians find the common ground for considering dyslexia from the perspective of reading. As Wajuihian and Naidoo (2012) agreed, children’s learning to read is coordinated by a complicated brain-regulated system of skills, which includes a particular set of behaviors such as letter naming, letter perception, word recognition and comprehension, etc., which involve differing parts of the human brain in the process. However, regardless of other systems involved in the process, one has to note that dyslexia is commonly perceived as a language-based disorder characterized by difficulties in reading, spelling, and writing; the reading difficulty is mainly expressed in the low phonological processing abilities within the language system (Wajuihian & Naidoo, 2011). The researchers also note that the key problems of dyslexic individuals may be detected in their coding abilities – decoding, which means determining which sound or symbol is meant by the written language symbol, and encoding, which denotes identification of letters that would transform a spoken word into the written one (Wajuihian & Naidoo, 2011).

Wajuihian and Naidoo (2011) also stimulated that dyslexic individuals may usually not reveal any explicit problems with the spoken language, which cannot be said about the written language challenges. The difference in easiness of dealing with spoken language is usually explained by that fact that it involves hearing, while dealing with the written language involves vision; hence, dyslexia is traditionally associated with the brain problems in the vision areas. However, at the same time, Wejuihian and Naidoo (2011) admit that dyslexia is not a problem of defective vision, though a certain vision deficit is commonly associated with the reading problems in general, mainly because of its potential to complicate the educational interventions for dyslexic individuals. It is notable that not only impaired vision characterizes dyslexic people, since this disorder is also commonly associated with some other neurodevelopmental disorders – language impairments such as the oral communication disorder, and attention deficit hyperactivity disorder (Wejuihian & Naidoo, 2011).

Even in cases clear visual images are presented to dyslexic individuals, they may have problems with reading those images, and making the meaning of the images they see, which indicates the problems at the lower-order reading skills’ acquisition process affecting the higher-order processes of comprehending visual messages. Another key observation about behavioral correlates of dyslexic individuals is that they often involve in optometric practices and by making many letter reversal errors, transposing letters in words when reading or writing them, or confusing the right and left (Wejuihian & Naidoo, 2011). However, in general, dyslexia is a heterogeneous disorder by its nature, and it has a realm of other symptoms and manifestations that help to diagnose it.

There are certain exercises that can potentially improve reading skills in dyslexic individuals; some of them involve rapid naming (found specifically helpful for school-age children); the improvement of reading skills in adults was also obtained by means of practicing rapid naming, and was not correlated with the verbal IQ or any other measures used to assess the verbal linguistic performance (Flowers, 1993). Exercise is also commonly associated with the improvement of the dyslexic individuals’ state of health and educational achievement, since it “improves the neural blood flow and stimulates the biochemistries which support neuron and synapse formation” (Ewing & Parvez, 2012, p. 112). Keeping to a specific diet to deliver the proper amount of necessary corresponding substances to the brain is also an essential measure for dyslexic individuals: acidic and alcoholic drinks affect the natural metabolic processes in the organism; prevailing pH influences the level of bioavailability of minerals (such as sodium, potassium, magnesium, etc.) to facilitate the flow of ions in the neuronal membranes; low levels of iron affects the capability of blood to deliver oxygen to neural tissues (which affects attention and concentration); high levels of glucose (resulting from the low level of magnesium in the diet) cause sleepiness, lower attention, and lower immune function (Ewing & Parvez, 2012). Moreover, it is essential to admit that the dietary protein facilitates the fixation of memories (Ewing & Parvez, 2012).

Assessment Models and Measures to Assess the Neuropsychological Factors of Dyslexia

There are a number of studies developed for the sake of producing an assessment of dyslexia’s neurophysiological factors. The oldest method of assessment is an autopsy study; according to Wajuihian (2012), autopsy studies investigate the brains of dead dyslexics. The cause of death should be illness or accident. The first autopsy that revealed the neuropsychological basis of dyslexia was conducted by Drake in 1968 – the researcher reported his finding about the 12-year-old child’s brain containing a massive “hemorrhage in the inferior vermis of the cerebellum, an abnormal convulated pattern bilaterally in the parietal lobes, a thinned corpus callosum, and ectopic neurons deep in the white matter” (Wajuihian, 2012, p. 122). During his life, the child was noted to have problems with reading comprehension, arithmetic, was poor at spelling, and suffered from recurring frontal headaches, which allows suggesting dyslexia (Wajuihian, 2012).

Neuro-imaging techniques have become a more advanced and precise method of diagnosing and studying dyslexia; they are divided into structural and functioning techniques (Wajuihian & Naidoo, 2012). Structural imaging techniques include such procedures as magnetic resonance imaging (MRI) and computed tomography (CT) to generate the images of organ anatomy including the shape and size of the researched brain. Functional imaging techniques are used to visualize and map various parts of the human brain during exercising a certain task by the subject under research. This type of imaging techniques involves the use of positron emission tomography (PET), functional magnetic resonance imaging (fMRI), regional cerebral blood flow (rCBF), magnetoencephalography (MEG), and single photon emission computed tomography (SPECT) (Wajuihian & Naidoo, 2012).

Flowers (1993) also indicated the use of electrophysiological studies for researching dyslexia; the results of these studies indicate the longer latencies and reduced amplitude of the visual waveform components of children with dyslexia. Moreover, the results of many researchers in this type of assessment indicated the “replicable physiological deficits in children with reading disability, specifically in the midlatency (240 ms) component measures over the left hemisphere and believed to reflect temporal processes” (Flowers, 1993, p. 578). These findings suggest that the EP waveform associated with dyslexia in children was not affected by the reading improvement, which presupposes the need to create an “enduring brain profile” that can presuppose the early reading challenges (Flowers, 1993, p. 578).

Smythe (2011) noted that the solution to dyslexia is educational, not medical, since there is no treatment for this disorder. Hence, the author insisted that the diagnosis should also be conducted in the educational perspective. The most visible solution to the issue of diagnosing dyslexia may be seen in the identification of difficulties and needs of the individual with dyslexia, which can be done with the help of specific cognitive tests by an educational psychologist, a speech therapist, or a language therapist. Nevertheless, only the in-depth knowledge of dyslexia and its manifestations is the key to diagnosis.  The testing protocol should include various cognitive tests that would ensure phonological manipulation tasks and working memory testing. Moreover, non-word spelling is an efficient tool for assessment of dyslexia severity; unfamiliar words should be presented in it (Smythe, 2011).

Though dyslexia management lies mainly within the educational sphere, there is a common agreement that medical doctors may be the first specialists to identify the problem. These cases can be observed when medical examinations are held for children with high levels of stress and anxiety, which stem directly from their literacy challenges (Smythe, 2011). Some other medical problems detected in individuals with dyslexia are bed wetting and even “phantom illnesses” arising from the unconscious desire to escape testing. When diagnosing dyslexia, specialists should be aware of the fact that the disorder often has a genetic basis, so it is essential to identify whether parents of the child have similar problems. Finally, the comorbidity is a path to identifying dyslexia; this disorder often co-occurs with other developmental disorders such as executive functioning problems (expressed in the essay writing and affecting motor planning), or hyperactivity (Smythe, 2011).

Neuropsychological Profile Expected at Various Stages of the Disease

Dyslexia is commonly divided into three types of intensity: mild, moderate, and severe forms thereof. However, the division is also ambiguous, since a comparatively mild deficit can cause severe effects on the individual’s competencies. At the same time, some people with severe phonological deficit are known to have developed strong compensatory strategies to tackle the effect of dyslexia (Jamieson, 2007). Looking at the example cited by Ott (1997), a 10-year-old child with IQ 120 having a mild form of dyslexia will read at the equivalent of a child of 10.6 years, and to spell – of 8.6 years. The same child with a moderate form of dyslexia will read at the level of 8.3 years, and spell – at the level of 7.4 years. In case of a severe form of dyslexia, the indicators will be 6.3 years for reading, and 6.4 years for spelling (Ott, 1997).

To identify the severity of dyslexia in a child, the following tests should be accomplished:

  • Digit span
  • Coding
  • Auditory sequential memory
  • Rapid naming
  • Phonological awareness
  • Laterality
  • Arithmetic
  • Creative writing (Ott, 1997, p. 13).

The scores cited above, and the scores received as a result of taking these tests are not perceived in isolation, but are linked to numerous dyslexia sensitive factors to create the dyslexia profile of the child, and to identify the degree of the disorder (Ott, 1997).

In identifying the features characteristic to dyslexics, Ott (1997) also cited the research of Vail (1990) who divided individuals with dyslexia into the middle and the low group. According to the researcher’s idea, the middle group may even avoid the diagnosis of dyslexia, since their intelligence serves as a powerful instrument for concealing dyslexia’s presence. However, the threat to this group is that dyslexia is still present in their neurophysiological and neuropsychological profile, which causes certain internal worries and strain, resulting in stress and anxiety (Ott, 1997). The low group was characterized as the group with severe difficulties, even in the mechanics of reading, writing, spelling, and simplest arithmetic. However, some other researchers pointed out that a borderline dyslexic group also exists; this group is characterized by the incomplete cases of dyslexia. Such cases may include late reading, poor spelling, and the inability to communicate one’s thoughts easily on paper (Ott, 1997). These symptoms of the borderline dyslexia may not occur together, which complicates making the diagnosis, and lets referral to such cases as “dyslexia variants” (Ott, 1997, p. 13).

Ott (2006) revealed a more detailed account of features characteristic for all detected types of dyslexia:

  • Severe dyslexia – dyslexia can be considered severe in cases when a child has a high IQ and excellent verbal skills, but fails to communicate his or her ideas because of specific reading difficulties. The spelling skills are very poor, and handwriting is not understandable. The child with a sever form of dyslexia can even forget specific personal details such as the date of birth, or home address (Ott, 2006)
  • Moderate – in cases of a moderate dyslexia, children are assessed by specialists, and are provided with individual assistance. However, even under these conditions, they have problems with reading texts because of being poor decoders. Children with a moderate form of dyslexia are struggling writers, but can accomplish the task in case additional time is provided for them (Ott, 2006)
  • Mild – children with a mild form of dyslexia might have had problems during the process of learning to read. At present, they are equal readers with children of their age, but they are slow and inaccurate decoders. In writing, such children have many errors, mainly in the cases of using homophones, irregularly spelled words, and in the use of punctuation (Ott, 2006)
  • Borderline – the child with residual difficulties who have dyslexia tendencies regarding short-term memory, who experience certain difficulties with taking notes during the lecture because of poor processing skills, and sometimes have a problem with finding proper words in speech. Such children also have problems with essay writing because of challenging sequencing and organization activities (Ott, 2006).

It is notable that both children and adults may have dyslexia, since it is an incurable disorder, and once it has been diagnosed, a person has to live with it. However, the manifestation of dyslexia in children and adults is at times different. For instance, as Riccio, Sullivan, and Cohen (2010) noted, both children and adults “have been found to have smaller regions in language areas” of the brain (p. 19). However, children were distinguished from adults in the sense of revealing a positive correlation between performance of working memory tasks and the activation of prefrontal zones. Preschool children were a notable group of dyslexic individuals as well, since children with lower pre-reading skills were found to activate multiple regions of the brain (Riccio et al., 2010).

Conclusion

As it is notable from the present research, dyslexia is a complex neurodevelopmental disorder the origins of which can be found in various brain dysfunctions, heredity, and the complex of environmental factors leading to the creation of conditions favorable for dyslexia development. Though it is still the subject of debate regarding its existence and legitimacy as a realistic medical condition, dyslexia represents a serious neurological, neurophysiological, and neuropsychological disorder affecting not only the condition of a person regarding cognitive abilities, reading and writing competencies, and processing stimuli of audio-visual nature. It is the problem manifested in a wider range of social problems, such as low self-esteem, educational and employment challenges, problems in communication and establishment of social connections, etc. Therefore, there is a need for further research on the causes and consequences of dyslexia, which may provide the research and practitioner community with effective intervention models to mitigate the effect of dyslexia on the lives of individuals affected by it.

The core neurobiological causes of dyslexia are identified in the malfunctions of the perisylvian zone of the brain, the dysfunction of the planum temporale (PT). There are a number of theories generated to explain the roots of dyslexia, and each of the theories has the right for existence, mainly because the nature of dyslexia is not fully understood yet. However, there is a common understanding that dyslexia is a problem that should be targeted not medically but educationally; individuals with dyslexia have various symptoms at different stages of their lives, and the severity of dyslexia may vary. Hence, it is vital to work on the creation of optimal and workable interventions to help people with dyslexia acquire a normal quality of life, and to learn to communicate through all cognitive paths, thus living a full and healthy life, especially taking into account that people with dyslexia are usually characterized with the absence of any other cognitive impairments, have a high IQ, are creative and functional.

References

Ewing, G. W., & Parvez, S. H. (2012). The influence of pathologies upon sensory perception and sensory coordination in children with developmental dyslexia and learning disorders: A unified theory of developmental dyslexia. North American Journal of Medical Sciences, 4(3), pp. 109-115.

Flowers, D. L. (1993). Brain basis for dyslexia: A summary of work in progress. Journal of Learning Disabilities, 26(9), pp. 575-582.

Jamieson, C. (2007). Managing dyslexia at university: A resource for students, academic and support staff. New York, NY: Routledge.

Macdonald, S. J. (2009). Towards a social reality of dyslexia. British Journal of Learning Disabilities, 38, pp. 271-279.

Ott, P. (1997). How to detect and manage dyslexia: A reference and resource manual. Oxford, UK: Heinemann.

Ott, P. (2006). Teaching children with dyslexia: A practical guide. New York, NY: Routledge.

Punt, M., de Jong, M., de Groot, E., & Hadders-Algra, M. (2010). Minor neurological dysfunction in children with dyslexia. Developmental Medicine and Child Neurology, 52, pp. 1127-1132.

Riccio, C. A., Sullivan, J. R., & Cohen, M. J. (2010). Neuropsychological assessment and intervention for childhood and adolescent disorders. Hoboken, NJ: John Wiley & Sons.

Smythe, I., (2011). Dyslexia. British Journal of Hospital Medicine, 72(1), pp. 39-44.

Taroyan, N. A., Nicolson, R. I., & Buckley, D. (2011). Neurophysiological and behavioral correlates of coherent motion perception in dyslexia. Dyslexia, 17, pp. 282-289.

Wajuihian, S. (2012). Neurobiology of developmental dyslexia Part 1: A review of evidence from autopsy and structural neuro-imaging studies. Optometry and Vision Development, 43(3), pp. 120-131.

Wajuihian, S., & Naidoo, K. S. (2011). Dyslexia: An overview. Optometry and Vision Development, 43(1), pp. 24-33.

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