Developmental Dyslexia Disease
Developmental dyslexia can have a profound effect on a child’s life, while he/she is trying to learn to read and spell (Lyon, Shaywitz, & Shaywitz, 2006). Dyslexia occurs in different developmental stages and difficulties that may exist in one stage may not be evident in another (Wajuihian & Naidoo, 2012). Eighty percent of those identified as having a learning disability are affected by dyslexia, making it the most prevalent learning disability. The estimated prevalence of dyslexia in school-aged children located in the United States is around five to seventeen percent (Wajuihian & Naidoo, 2012). Even though research is predominant in this area and with the prevalence rates so high there are still many misconceptions regarding dyslexia. The most common one is that writing words and letters backwards are symptoms of dyslexia. Commonly though, as an average child or dyslexic child is learning to read and write that he/she will reverse words or letters (Hudson, High, & Otaiba, 2007).
Another misconception is that dyslexia is a visual perception problem. Studies have shown that dyslexia pertains to the language processing center (Wajuihian & Naidoo, 2012). A person can be considered dyslexic when their reading is more than two standard deviations behind the level that they are expected to read at, which is based on their IQ, along with other features such as missequencing, confusing left and right, and incoordination (Lyon, Shaywitz, & Shaywitz, 2006; Wajuihian & Naidoo, 2012; Hudson, High, & Otaiba, 2007). Also, the individual’s difficulties must not be better explained by other issues such as developmental, sensory, neurological, or motor disorders and it is must significantly interfere with school, job-related performance, or activities of daily living (APA, 2013).
How it works
Children with dyslexia will typically show two obvious difficulties when they are asked to read at their grade level. Firstly, a child will not be able to read as many words of a text by sight as an average reader; they will stumble on words guess at them or try to sound them out. Secondly, they have difficulties deciphering or decoding a word. Which means they have trouble identifying unknown words and have poor skills in using letter to sound relationships (Hudson, High, & Otaiba, 2007). While there are visual cues as to what dyslexia causes, research is also being conducted to find the underlying biological reasoning of why people have difficulties reading and writing (Flowers, 1993). Specifically, the structure of the brain, genetics, and the neural pathways used to connect the various segments (Shaywitz, Mody, & Shaywitz, 2006; Flowers, 1993). In order to understand the interaction between dyslexia and the brain, this paper will investigate current and past research articles, thereby exploring various theories and the cause and effect of the brain structure on reading and writing. The Dyslexic Brain
The dyslexic brain appears to be fundamentally different than in people without dyslexia (Waldie et al., 2013; Shaywitz et al., 2002; Hudson, High, & Otaiba, 2007; Flowers, 1993; Pugh & Mencl, 2000; Galaburda, 2005). There are three subsections in the brain that are linked to reading and phonological analysis, which include the left temporoparietal region, the left occipitotemporal region and the inferior frontal gyrus (Waldie et al., 2013). The primary cognitive discrepancy in dyslexia can be tracked back to poor phonological coding, which impairs the way that speech sounds are represented, stored and retrieved (Flowers, 1993; Pugh & Mencl, 2000; Galaburda, 2005; Waldie et al., 2013). There are structural differences in the brain that differ between a person with dyslexia and without. The left hemisphere of the brain is mainly responsible for the ability to read, in people who have dyslexia; it has been shown that their left posterior language system showed decreased activation (Waldie et al., 2013; Shaywitz et al., 2002; Hudson, High, & Otaiba, 2007; Flowers, 1993; Pugh & Mencl, 2000; Galaburda, 2005, Odegard et al., 2007). Dyslexic people show regions of the brain that were under engaged; which included Wernicke’s area in the superior temporal gyrus, angular gyrus in the inferior parietal lobe, and striate and extra-striate regions of the occipital lobe (Pugh & Mencl, 2000; Zhang, Whitfield-Gabrieli, Christodoulou, & Gabrirli, 2013; Stein, 2001).
With the limited activation of the occipital lobe and the hyper-activation of the right hemisphere (discussed later) in dyslexia, this could be the cause that both attentional visual processes and sensory processes may be altered, reflecting separate deficits in each (Zhang et al., 2013). Research has been found that dyslexics have increased right hemisphere activation in temporoparietal regions during phonological processing, which is a pattern that is opposite of that observed in typical readers (Waldie et al., 2013; Shaywitz et al., 2002; Grigorenko, 2001; Stein, 2001). It is very likely that the extra activity in the right hemisphere, seen in both children and dyslexic adults, is a compensatory mechanism because of the extra cognitive effort and attention need required during the phonological process (Waldie et al., 2013; Galaburda, LeMay, Kemper, & Geschwind, 1978; Galaburda, 2005). Another difference in a dyslexic’s brain is the neural tissue present in the temporal planum (TP). This is a region on the surface of the temporal lobe, posterior to the primary auditory cortex, and is responsible for the speech and language area of the brain located in the Sylvian fissure. The TP region in the general population is typically larger on the left when compared to the right, whereas in a dyslexic brain both hemispheres were symmetrical (Flowers, 1993; Wajuihian & Naidoo, 2012; Grigorenko, 2001).
It is believed that the greater symmetry of the TP across the hemispheres, is possibly due to a larger number of cells in the right temporal planum. This idea was purposed on the bases of the reduced neuronal functioning in the left hemisphere (Flowers, 1993). An additional hypothesis of dyslexia was the result of discovering thick distributions of ectopias, or misplaced nerve cells, that were located all over the cerebral cortex. In particular, they were located in the perisylvian language areas, which therefore resulted in the alteration of brain organization. The nerve cells plant themselves in various locations on the cortex during a process call neuronal migration. Neuronal migration is a process that occurs during brain development, when new neurons migrate in search of their final locations in the brain. The neurons are formed from neural stem cells, usually a long way from the areas that these cells will be working (Galaburda, 2005). The ectopias that form demonstrate the failure of neurons to reach their normal targets during development (Wajuihian & Naidoo, 2012; Galaburda, 2005; Stein, 2001). Lastly, recent evidence has found that a disturbance in the occipitotemporal region of the brain, an area charged with reading words and naming the pictures of the words. May be linked to the underlying cause of reading and naming deficits witnessed in developmental dyslexia (McCrory, Mechelli, Frith, & Price, 2005; Shaywitz, Mody, & Shaywitz, 2006). The neurons located in this lobe are responsible for pulling out linguistic information from sequences of letters so that, within 250 milliseconds of being seen, they can be incorporated and perceived as words. This process results in the rapid, easy recognition of familiar words (Shaywitz, Mody, & Shaywitz, 2006).
Two Theories behind Dyslexia
After years of research and a consensus that dyslexia is a neurobiological disorder, there are two central theories that try to explain what causes dyslexia. The two theories are the phonological deficit theory and the magnocellular deficit theory, and both of them approach dyslexia from a different view point. The phonologic theory is based on a cognitive factor, where the magnocellular theory is based on a perceptual impairment. Each of these theories has their own empirical research to support their reasoning (Ramus et al., 2003). This section will discuss each theory and related it to the difficulties dyslexic people had when trying to read.
Phonological Deficit Theory:
The phonological deficit theory, which is a cognitive based theory, states that reading difficulties dyslexics suffer from is due to complications in breaking down of spoken words into their basic sound parts, also known as phonemes. The phonological theory, takes into account that unlike speech that will be picked up naturally, reading has to be taught, in which a student must learn the associations between letters and sounds (Shaywitz, Mody, and Shaywitz, 2006). People affected by dyslexia are not able to develop these associations between graphemes (letters) and phonemes (sounds). The inability to form these associations between the two is believed to be a major cause of reading and spelling deficiencies in developmental dyslexia (McLean, Stuart, Coltheart, & Castles, 2011; Wajuihian & Naidoo, 2012; Ramus et al., 2003; Shaywitz, Mody, Shaywitz, 2006). A dyslexia person will have difficulties with interpreting unfamiliar, or nonsense words, but deficiencies are also apparent in language based phonological processing, which measures both the explicit ability to change phonological depictions as well as the implicit understanding of phonological structure(McLean, Stuart, Coltheart, & Castles, 2011; Wajuihian & Naidoo, 2012; Ramus et al., 2003). Within the phonological theory there are two other major problems a dyslexic can face which are, the inability to rapidly name objects, pictures, colors, letters, or numbers; and suffering from verbal short term memory, though there has been a major debate on whether or not these are independent of the phonological theory (Ramus et al., 2003). Despite the trial and trivializations the phonologic theory has faced it still remains the most consistent, because most dyslexics show deficits in phoneme processing, and therefore it is the predominant theory (Wajuihian & Naidoo, 2012; Ramus et al., 2003).
Magnocellular Deficit Theory:
The magnocellular deficit theory is a perceptual based theory, which means it is dependent on how the environment is taken in and processed in the brain. The general magnocellular theory includes three different deficits which are: auditory deficit, a magnocellular visual dysfunction, or a cerebellar/motor dysfunction (Wajuihian & Naidoo, 2012; Ramus et al., 2003; Stein, 2001; McLean et al., 2011). More specifically, there are two causes that are directly linked to defective reading capabilities: visual deficits and phonological deficits. The visual deficits, which this section will mainly focus on, are linked to the dysfunction of the magnocells in the sensory pathways (McLean et al., 2011; Wajuihian & Naidoo, 2012; Ramus et al., 2003; Zhang et al., 2013; Stein, 2001). The phonological impairment can be linked to a more general auditory deficiency (Ramus et al., 2003). Within the visual system there are two subsections; they are the magnocellular (dorsal) pathway, which this theory suggests that it is defective, and the parvocellular (ventral) pathway (Wajuihian & Naidoo, 2012; Ramus at al., 2003; Stein, 2001; Zhang et al., 2013; McLean et al., 2011). Each of these pathways starts from the midget and parasol ganglion cell located in the retina. They leave the retina, as the optic nerve, traveling through the lateral geniculate nucleus (LGN) to each of their perceptive lobes (McLean, Stuart, Coltheart, & Castles, 2011).
The visual system not only feeds the visual cortex in the occipital lobe it also feeds into the language system for reading thru visual pathway lead from the posterior parietal (a magnocellular termination point) and from the temporal cortex. This is why on imaging studies they will consistently show activation in those areas when reading (Stein, 2001). The magnocellular pathway and its neurons are made for detecting visual motion and are responsible for timing visual event when reading; they are also in charge of controlling eye and limb movements (Wajuihian &Naidoo, 2012; Ramus et al., 2003; Stein, 2001).
The magnocellular deficit theory postulates that a percentage of individuals with dyslexia have some form of magnocellular pathway deficit, but a completely functioning parvocellular pathway, and that the magnocellular deficit may play a role in reading impairment (McLean et al., 2011; Stein, 2001; Ramus et al., 2003). In dyslexics the impaired functioning of the magnocellular pathway along with the atypical magnocellular layers within the LGN, can cause disruption of the binocular fixation, leading to visual confusion and sequencing the letters wrong within a word (Wajuihian &Naidoo, 2012; Stein, 2001). Studies have shown that, in brains of known dyslexics, the layers in the LGN, specifically to the magnocellular area were disordered and that the neurons were between twenty percent and thirty percent smaller than the areas in a normal reader’s brain (Wajuihian &Naidoo, 2012; Ramus et al., 2003; Stein, 2001).
Mentioned earlier, magnocellular cells are responsible for visual motion, and at first glance, when magnocellular cells are defective, the reduced sensitivity to visual motion might seem like it would have nothing to do with reading, nevertheless, it indicates reduced sensitivity of the visual magnocellular system (McLean et al., 2011; Wajuihian &Naidoo, 2012; Stein, 2001). Testing sensitivity to visual motion has established a way of consistently showing whether or not there is a magnocellular deficit. This is because the motion of the stimuli only engages the magnocellular cells within the visual cortex (Stein, 2001; McLean et al., 2011). Many dyslexics were found to have poorer motion sensitivity when compared with the controls that were matched for age and IQ (Stein, 2001). Contradicting Evidence The magnocellular deficit theory and the parvocellular theory are highly debated and is a controversial issue (Wajuihian & Naidoo, 2012; Ramus et al., 2003; Stein, 2001; McLean et al., 2011). Each theory has gaps and wholes that cannot be explained with current knowledge. In the magnocellular pathway specifically, the sensorimotor problems, auditory deficits, magnocellular deficits, and cerebellar deficits, are believed to have limited effects on reading abilities. Although it is still possible, some visual deficits could disrupt reading enough that it could potentially lead to a dyslexic diagnosis, but it is not evidence of magnocellular deficit (Wajuihian & Naidoo, 2012; Ramus et al., 2003).
It has been found that when visual deficits are present they tend to span a whole range of spatial and temporal frequencies (Ramus, 2003). Also, Ramus stated that letters and words are typically motionless when they are being read, therefore there is still uncertainty about whether there really is a magnocellular deficit or if it does exist would it affect reading abilities (2003). With current research and knowledge, many researchers currently believe that dyslexia is best labeled as a specific phonological deficit, which may be accompanied by a magnocellular deficit (Ramus, 2003; Wajuihian & Naidoo, 2012).
Implications of Research on Dyslexia
Working with students that have dyslexia can be challenging, thus understanding what dyslexia is and how affects the brain is high beneficial in helping the teacher cater to their needs. Working to improve a student’s phonics has proven to be the most successful (Allen, 2010; Odegard et al., 2007; Hudson, High, & Otaiba, 2007; Wai, Chan, & Zhang, 2014; Jacob, Wadlington, & Bailey, 1998; Snowling, 2013). The magnocellular deficit has shown to be much harder to work on in a classroom setting, due to skills of the teachers and resources required and many research articles and structured school lessons resemble this (Allen, 2010; Odegard et al., 2007; Hudson, High, & Otaiba, 2007; Snowling, 2013; Wai, Chan, & Zhang, 2014; Jacob, Wadlington, & Bailey, 1998). Research has shown that the most effective way to help dyslexic people read at a higher level is to incorporate systematics and syntax, multisensory, successive phonics-based program with clear directions in phonological awareness, sound-symbol association, syllables, and morphology (Allen, 2010; Odegard et al., 2007; Hudson, High, & Otaiba, 2007; Wai, Chan, & Zhang, 2014; Jacob, Wadlington, & Bailey, 1998).
It is highly stressed that dyslexic students should learn how to pronounce a specific word before trying to join the sound and letters and also before learning the morphological features of that word (Wai, Chan, & Zhang, 2014; Hudson, High, & Otaiba, 2007). It has also been found beneficial to combine both phonological and orthographical (spelling) strategies. Therefore a student is learning letter-sound relationships and how to go from a word’s orthographic representation to the word’s sound and meaning (Wai, Chan, & Zhang, 2014; Snowling, 2013; Allen, 2010; Jacob, Wadlington, & Bailey, 1998). It takes people with dyslexia a long time and a lot of work to improve their ability to read and spell, therefore research needs to continue exploring the causes of dyslexia in order to improve remediation techniques.