Manifestations of Dyslexia Is Considered

Manifestations of Dyslexia

Dyslexia is considered to be an hereditary and genetic neurobiological disorder (Dyslexia, fluency, and the brain, 1999) whose symptoms frequently include, but are not limited to, difficulties with learning to read, write, spell, and to master various other tasks associated with auditory processing and the learning and usage of (particularly written) language (What is Dyslexia (2005); Dyslexia symptoms and Dyslexia signs (2005); The nature of Dyslexia (2005).

According to the International Dyslexia Association (2002):

Dyslexia... is a specific language-based disorder of constitutional origin characterized by difficulties in single word decoding, usually reflecting insufficient phonological processing abilities. These difficulties in single word decoding are often unexpected in relation to age and other cognitive and academic abilities; they are not the result of generalized developmental disability or sensory impairment. Dyslexia is manifest by variable difficulty with different forms of language, often including, in addition to problems reading, a conspicuous problem with acquiring proficiency in writing and spelling.

The term "dyslexic" comes from the Greek root "dys" (difficult) combined with the Greek noun "lesicos" (pertaining to words)(Dyslexia 2005). According to the International Dyslexia Association (2002), Dyslexia is a specific learning disability that is neurological in origin. It is characterized by difficulties with accurate and/or fluent word recognition and by poor spelling and decoding abilities.

The word "dyslexia" itself, used to describe a specific medical condition, however, was first introduced by Berlin in 1887 to describe extreme difficulty in reading and spelling words (The nature of dyslexia). According to the World Federation of Neurology (1968; cited in Critchley 1970):

Specific developmental dyslexia is a disorder manifested by difficulty learning to read

Despite conventional instruction, adequate intelligence, and adequate sociocultural opportunity. It is dependent upon fundamental cognitive disabilities which are frequently of constitutional origin.

Further, according to Frith (1986) use of the term "developmental," within that neurological definition of the word "dyslexia," implies a disorder of suspected congenital or hereditary [emphasis added] origin, in contrast to acquired Dyslexia, a disorder resulting from brain injury after the onset of reading (cited in The nature of dyslexia, 2005). Individuals with Dyslexia typically experience difficulties with various components of the processing and use of language. These typically include, but are not limited to, skills children typically are required to learn in school, such as reading, writing, and spelling (What is dyslexia?, 2005).

Critical Evaluation of the Available Literature

According to the available literature, Dyslexia most often manifests itself as a severe reading disability, and is, unfortunately, not a condition that a child can look forward to "outgrowing." (What is Dyslexia (2005) Moreover, "Dyslexic adults... tend to continue to have difficulty with language skills throughout their lives (Dyslexia, 2005).Still, with proper diagnosis, treatment, and support in childhood and adolescence, "a dyslexia diagnosis is no barrier to success" (Dyslexia). In fact, Individuals who have been helped to manage their dyslexia in childhood will almost always have easier, less problematic adulthoods than will those left to fend for themselves in a predominantly non-dyslexic world (Frith, (1991); Stein & Walsh (1997); Stein & Talcott (1999); Gorman (2003); Dyslexia teacher (2005); ("Dyslexia Project - Interim Report (summary)," (2003). Conversely, however, children who are not helped early on to manage their Dyslexia will almost always find it more difficult to live with the disorder as adults. It has been estimated that one in 10 children is dyslexic (Gorman, 2003).

Specific signs and symptoms of Dyslexia in childhood. According to available literature, indications of possible dyslexia first appear most clearly in the first two or three grades of primary school (Dyslexia-How to help, 2005), that is, when a child initially begins the formal, systematic processes of learning to read and write. Up to that point, signs of dyslexia, though they may have already have been present, are not as easily or definitively identified or diagnosed. This is because many typical signs of dyslexia (e.g., directional confusion; sequencing difficulties, and late talking or immature speech) are present during normal pre-school-age child development.

Additional childhood symptoms of Dyslexia may include, but are not limited to, difficulties with learning to read (often characterized by confusion between letters like "b"; "d"; "p," and "q") (What is Dyslexia (2005); bizarre reading and spelling (Dyslexia symptoms and Dyslexia signs (2005); poor eye-hand coordination; and poor handwriting (The nature of Dyslexia 2005). Other difficulties may include kinetic clumsiness; directional confusion; sequencing difficulties; handwriting difficulties (such as poor-quality handwriting and/or the mixing of printed and cursive letters); and poor motor coordination (The nature of Dyslexia; Dyslexia symptoms and dyslexia signs). Moreover, children with Dyslexia symptoms can be, and often are, badly misunderstood, and underestimated at school, by their teachers and their peers alike. This is why it is important to understand that Dyslexia is not so much a disability or a handicap (although its symptoms can easily lead to the perception, among Dyslexic individuals themselves, and others, that it is exactly that) as it is "a kind of mind. Very often it is a gifted mind, but it is a mind that is physiologically different. This brain difference is not a defect, but it makes learning language excessively hard" (What is dyslexia? 2005).

According to Dyslexia (2005):

Dyslexic learns at his/her own level and pace, and typically excels in one or more

Other area. Some of their experiences include difficulties with concentration, perception, memory, verbal skills, abstract reasoning, eye-hand coordination, social adjustment (low self-esteem is commonly observed behavioral characteristic), poor grades, and underachievement. Often, people with dyslexia are considered to be lazy, rebellious, class clowns, unmotivated, misfits, or of low intelligence. These misconceptions, without understanding dyslexia's [sic] effect on the person's life, lead to rejection, isolation, feelings of inferiority, discouragement, and low self-esteem.

Treatments for dyslexic children. Based on the literature, treatments for dyslexic children, particularly those also showing signs of Irlen Syndrome (IS) may include: use of a dark patch over one eye in order to help focus vision in the other eye; prescription of glasses with coloured lenses; glasses, and use of coloured overlays for reading (Stein & Walsh, 1997). Another treatment plan for dyslexic children is "an exercise-based treatment" (Young, 2002):

The treatment regime involves physical exercises designed to improve functioning of the cerebellum, a part of the brain involved in co-coordinating movement. It has been taken up by 10,000 people at Dyslexia, Dyspraxia and attention Treatment (DDAT)

Centres in the UK, U.S., and Australia.

Potential hazards of untreated childhood Dyslexia. The literature points out that children with Dyslexia, especially when the condition remains undiagnosed and untreated, statistically seem to have a greater than average chance, according to some research ("Dyslexia Project - Interim Report (summary), (2003); Poverty and social issues (21 July 2000), pp. 6; 11; 12-13; 14) of becoming troubled adolescents and adults (though that outcome is certainly not inevitable). Dyslexia is overrepresented, for example, within prison populations. According to Poverty and social issues (21 July 2000):

survey of young prisoners has found that one in two is dyslexic... An estimated 4-10 per cent of Scots are dyslexic, but a study at Edinburgh

University by Jane Kirk, a dyslexia adviser, and Gavin Reid, a senior lecturer, found that in a random sample of 50 young offenders at Polmont Institute, half were affected. Their report warns that undiagnosed dyslexics "might very well feel devalued at school and turn to deviant behaviour as a way of responding to a sense of low esteem - and as a way of achieving recognition from peers.

A pattern of maladjusted behaviour at school might well lead to more serious forms of deviant behaviour and then to imprisonment. (p. 14)

Specific problems of adults with Dyslexia. According to the literature, adults with Dyslexia who have received the help they need, in their early years, with their managing Dyslexia symptoms, usually have learned how to make successful compensations for the disorder by adulthood. Such adults typically lead normal, productive, and sometimes even extremely successful lives. Well-known adults with dyslexia have included Pablo Picasso; Tom Cruise; Richard Branson; Leonardo da Vinci; Thomas Edison; Jay Leno, and Whoopi Goldberg (Dyslexia, 2005; Dyslexic? You're not alone..., (2003).

Among adult dyslexics, however, symptoms will persist throughout life. Such lingering symptoms of Dyslexia in adulthood may include, but are not limited to: difficulties with following detailed discussions; slower-than-average reading speed and comprehension; difficulties with mentally working out sums (e.g., simple addition, subtraction, or multiplication); poor spelling; mixing up the order of syllables in long words; filling out forms; reversing numbers (e.g., 85 and 58); misdialing the telephone, or mixing up dates and times and [consequently] missing appointments (Dyslexia in adults, 2005).

Treatments for dyslexic adults. Available literature on the subject of treatments for dyslexic adults (Dyslexia treatments 2004; NSRI, 2005 EasiReader, 2005) indicates that treatments for dyslexic adults are controversial, and evidence of their efficacy remains anecdotal. One treatment for adults is through the DORE Achievement Centers (), a privately funded company in the United States, based in Louisville, Colorado. DORE individualized treatment "involves exercises aimed at minimizing or eliminating Cerebellular Developmental Delay (CDD), the likely cause of many learning disabilities such as dyslexia" (Dyslexia treatments). Specifically, treatment consists of "customized exercises that specifically concentrate on stimulating the cerebellum to improve functioning and help speed up the rate information is received and processed" (Dyslexia treatments).

The theory that Cerebellar Developmental Delay (CDD) is responsible for the reading and other, related, difficulties typically experienced by dyslexics. Symptoms of Dyslexia spring from "an under-functioning cerebellum, the part of the brain which plays a key role in cognitive skills, concentration, and balance"(Dyslexia treatments). According to the Dore Achievement Center the individualized exercises offered by the center to stimulate and enhance cerebellar function have also resulted, among successfully treated patients, in "improved reading, comprehension, memory, and general mental processing." The DORE Achievement Centers also report a greater degree of self-confidence; higher self-esteem, and a more positive mental attitude and outlook, overall, among the adult dyslexics that the center has successfully treated. Another treatment available for dyslexic adults, through the National Reading Styles Institute, Inc., involves the use of colored overlays:

Nothing cures dyslexia absolutely, but... Colored overlays have made a tremendous difference in the lives of dyslexics. For some people, looking at black letters on white paper causes headaches and eye fatigue, or words may seem to shake, move, or reverse. The correct colored overlay often dramatically reduces visual distortions or discomfort, and improves reading and learning ability.

According to NSRI (2005), colored overlays may help dyslexic adults (and children) with eliminating, or at least lessening: letter or word reversals; eye strain; headaches; problems with tracking words or numbers on a page; problems with copying; difficulties with reading for long periods of time; reading speed slowness, and reading comprehension difficulties.

Additionally, according to the literature, various other theories currently exist about how to best treat and educate dyslexic individuals, both children and adults. Most of these recommend various method(s) of exercising, stimulating, or otherwise strengthening areas of the brain responsible for processing auditory messages. A few others (these mostly for Irlen Syndrome (IS), a condition often co-existing with Dyslexia, in which written letters and symbols appear blurred or otherwise distorted) use eye patches; coloured overlays; specially designed and coloured computer screen backgrounds (EasiReader, 2005), or coloured or tinted glasses or contact lenses.

Additional available descriptive; informational; diagnostic, and academic literature. Much descriptive and diagnostic literature on various aspects of Dyslexia is available online from university; research based, and other websites. Much of that is informational, e.g., articles or links like "What is Dyslexia" or "The Nature of Dyslexia." Other available online information is self-diagnostic, e.g., "How Do I Know If I Have Dyslexia."

Available research findings on Dyslexia include work of top theorists John Stein and Uta Frith. Available articles by Stein, the pioneer of magnocellular theory, and some other magnocellular theorists, include The physiological basis of perceptual confusion in dyslexic children (Steinlab 2005); Neurophysiological bases of Dyslexia (Oxford Dyslexia unit, 2002); To see but not to read; the magnocellular theory of Dyslexia (Stein & Walsh, 1997); Impaired neuronal timing in Developmental Dyslexia -- the magnocellular hypothesis (Stein & Talcott, 1999); and Visual magnocellular impairment in adult developmental dyslexics (Talcott et al., 1998).

Uta Frith, Professor of Cognitive Neuroscience at University College, London, has extensively researched multiple causes of Dyslexia and connections between Dyslexia and other neurobiological disorders, including Autism; Attention Deficit Disorder (ADD), and Asperger's Syndrome. In Paradoxes in the definition of dyslexia (1999), suggests that Dyslexia is a complicated syndrome, springing from an intricate mixture of co-existing biological; cognitive; behavioural, and environmental factors. Therefore, Frith suggests, the syndrome of Dyslexia cannot, nor should it, be pidgeon-holed into one or the other theory, such as magnocellular, cerebellar, double-defict, etc. Rather, the root cause of Dyslexia is more likely to be a combination of those factors, plus environmental factors and other (often elusive) variables. These factors and variables are different in the case of every dyslexic, as well as across languages and cultures. Other, related articles by Frith and others include: Beneath the surface of developmental dyslexia (1985), and Why specific developmental disorders are not specific -- online and developmental effects in autism and dyslexia (Frith & Happe, 1998).

Other articles by Bradford (2005); Frith (1999); Stein (1999); Stein & Walsh (1997); Young (2002); Tallal (1980); Gorman (2003), suggest that among dyslexics, it is currently believed that there is an actual neurobiological difference in the "wiring" of the brain, one that in fact makes auditory-phonetic connections especially difficult to make, thus the (often severe) reading, writing, spelling, and other language learning and retention problems found typically among dyslexics). Within the available literature, it has been currently estimated that approximately one in 10 children is born with Dyslexia (Gorman, 2003). Males with Dyslexia are believed by some including to outnumber females with the disorder by a 4:1 ratio (Stein & Walsh (1997); New research finds that boys really do have more reading difficulties than girls (2005). Other current available research, however, suggests that boys and girls may actually have Dyslexia in more or less equal numbers, but that Dyslexia in boys is more likely to be noticed by teachers, due to boys' typically more boisterous, verbal, or disruptive behaviour in class; Dyslexic girls tend to be quieter and less apt to "act out" as a result of their reading, spelling, and other difficulties, and try to privately compensate for them (Gorman 2003).

Additional articles by Butterworth (2004); Randerson (2001), and Gorman (2003) point out that European nations, including Great Britain; France, and Germany, are just now catching up to the United States in realizing that Dyslexia is indeed a specific neurobiological syndrome that causes learning disabilities, not simply a manifestation of slowness, laziness, or, (perhaps most dangerous, since the child then may not receive help for the condition) a phase of childhood (Gorman, 2003). Moreover, according to another articles ("Dyslexia Poses Bigger Challenge for English Speakers" (2005) and processes of learning to read and write in certain phonetically complex languages (like English), numerous silent letters and words not spelled as they sound (e.g., "island' "colonel"), like English, may actually produce more dyslexic symptoms than other, phonetically simpler, languages, like Italian. Similarly, (Paulescu et al., (1996), suggests that symptoms typical of Dyslexia, i.e., difficulties with reading, writing, spelling, and other uses of (particularly written) language, spring from a combination of biological and cultural factors.

Four Main Theories of Dyslexia

Numerous theories have long co-existed about the root causes of Dyslexia; the four best-known among these are: (1) the phonological deficit theory; (2) the magnocellular theory; (3) the cerebellar theory; and (4) the double deficit theory. Other theories suggest combination causes, including the juxtaposition of, and interplay between, various biological, cognitive, environmental, and other (sometimes shifting) variables (Frith, 1999).

Phonological deficit theory

The phonological deficit theory of Dyslexia is the oldest and most longstanding of the key theories to be found within Dyslexia research. It was pioneered by Pringle-Morgan, who is considered the "father of Dyslexia research," in 1893 (Coleman, 2003). This theory holds that dyslexic readers, due to "phonological deficits" (Coleman, p. 1), have difficulties with "phonemic representation" (Coleman), that is, "mapping sounds into letters in the brain, and with phonemic recall" (pp. 1-2).

In other words, translating auditory sounds (speech) into phonemic representations (the small units of which all written language consists) in order to read the language fluently presents enormous difficulties for individuals with Dyslexia. The phonological deficit theory of Dyslexia is the cornerstone theory, upon which all other, later, theories of Dyslexia causes (e.g., magnocellular; cerebellar; double deficit, and others) have been formulated. This theory was responsible for suggesting that from which all other, more recent, Dyslexia theories derive: that dyslexic individuals have great difficulties with learning to read, and with reading comprehension due to the phonetic nature of language, as opposed to the non-phonetic nature of speech. Learning to speak is a 30,000-year-old evolutionary process. However, reading and writing have only existed for about the last 5,000 years. Therefore, according to some (Frith (1999); Stein, (1999); Gorman (2003);

And under phonological deficit theory in general, there is a "disconnect" between the learning of the speaking, reading, and writing processes of dyslexic, based on phonological deficits. Further, the International Dyslexia Association (2002) concurs, that a glitch indeed exists within the brain wiring of dyslexics, which makes language acquisition and usages, especially as it relates to reading, particularly difficult.

Magnocellular theory

The magnocellular theory of Dyslexia was pioneered by physiologist John Stein at the University of Oxford. Stein, a leading researcher, for over twenty-five years, of the causes and manifestations of Dyslexia, pioneered the theory of magnocellular deficits within the brain as the major cause of Dyslexia, and (by association) Irlen Syndrome (IS) (Professor John Stein, 2005). A fellow of Magdalen College, Stein explains:

I am... interested in the auditory and visual impairments suffered by dyslexic children... responsible for their auditory/phonological and visual/orthographic reading problems. My work... suggests... dyslexic children have impaired auditory and visual temporal processing which explains why they have difficulty acquiring the phonological and orthographic skills required for reading. Understanding these mechanisms has helped to explain why such seemingly bizarre treatments such as occluding one eye, wearing coloured spectacles, playing music into the right ear, and eating fish oils, may help some dyslexic children to overcome their problems.

Magnocellular theory suggests a collision of pathways (so-to-speak), the Magnocellular (M) and the Parvocellular (P), within the brain of the typical dyslexic individual, resulting in symptoms including letter reversals and blurring of words and letters (Stein & Walsh, 1999; Stein & Walsh, 1997). The reading-related impediments, caused by Magnocellular deficits are why, as Stein & Walsh explain:

Developmental dyslexics often complain that small letters appear to blur and move around when they are trying to read. Anatomical, electrophysiological, psychophysical and brain-imaging studies have all contributed to elucidating the functional organization of these and other visual confusions. They emerge not from damage to a single visual relay but from abnormalities of the magnocellular component of the visual system, which is specialized for processing fast temporal information. The m-stream culminates in the posterior parietal cortex, which plays an important role in guiding visual attention. The evidence is consistent with an increasingly sophisticated account of dyslexia that does not single out either phonological, or visual or motor deficits. Rather, temporal processing in all three systems seems to be impaired.

Dyslexics may be unable to process fast incoming sensory information adequately in any domain. (p. 147)

As Stein and others (Stein & Walsh (1999); Stein & Walsh (1997); Talcott et al. (1998)), suggest, the magnocellular theory of Dyslexia takes into account, and possibly explains combination symptoms like word reversal and blurred images common to Irlen Syndrome (IS).

Magnocellular deficits and Irlen Syndrome (IS). Stein (1999) and others, including Demb, Boynton, Best & Heeger (1998) and Boden and Brodeur (1999) have further suggested that interferences often experienced by dyslexics who also suffer from Irlen Syndrome (IS) symptoms, may actually be caused by magnocellular visual neurological pathway deficits (Stein 1999), that is, a crossover-effect of sorts, caused by the particular "wiring" of the dyslexic individual's brain, that thus interferes with the clear pathway transmissions, within that brain, of the magnocellular (M) pathway and the parvocellular (P) pathway (Stein). Both of these pathways are serve specific, independent functions in reading: the M. pathway guides eye movements, while the P. pathway provides the reader with detailed information along the way, at each focus point or fixation (Stein & Walsh, 19997).

Cerebellar theory

The magnocellular theory, although it is more specific, in terms of its descriptive nature, than the earlier phonological deficit theory, still does not account for all Dyslexia indications not direct results of magnocellular (M) or parvocellular (P) pathway abnormalities as described by Stein and others (Coleman 2003) For example, difficulties with handwriting, clumsiness, directional and sequencing confusion, and other motor skills-related weaknesses are among the key symptoms of 90% or more of dyslexics (Coleman). (Under the cerebellar theory, however, those types of symptoms are, according to Nicolson, Fawcett, & Dean 2001), due to cerebellar irregularities that impinge upon the fine motor skills and sense of balance. In 2001, Nicolson, Fawcett, & Dean found that deficits in reading, writing, and spelling, as well as in overall motor coordination, might be caused by an abnormally- functioning cerebellum in dyslexics.

In addition, such deficits in cerebellar function arguably explain both phonological and magnocellular deficits. Nicolson, Fawcett, & Dean's findings (2001) implied, then, that individual dyslexics could have either magnocellular or cerebellar deficits, or both. Either, however, could be the underlying reason for the phonological deficits, and accompanying reading, writing, and spelling difficulties, experienced by dyslexics.

In light of the current research of the double deficit and cebellar deficit theories, it is necessary that the traditional theories of dyslexia be revisited. Though both the phonological and magnocellular deficit theories provide key components which are helpful in the long standing investigation of dyslexia, they both are lacking in major ways. Using the both the double deficit and cerebellar theories in conjunction with these dominant theoretical models, however, may be useful in obtaining a more holistic understanding of the true nature of the disorder. Accounting for the major phonological deficits with the phonological theory, the disorders neurological origin through the use of both the magnocellular and cerebellar theories, and assessing the various subtypes of dyslexia through the double deficit theory would be the ideal strategy for efficient investigation of the etiology of dyslexia. In conclusion, a model which works to incorporate these four facets of investigation could potential advance the research and treatment of dyslexia, by broadening the current diagnostic spectrum of dyslexics and evoking varying styles of intervention which work to target the multitude a dyslexic symptoms and subtypes.