Category: Cognitive Psychology

What makes us fear? Fear is a cognitive, intellectual, emotional, and empirical cognition. Fear itself does not represent facts, but fear itself is the message that we subconsciously send to ourselves that we are at risk. Fear is what helps us survived in the past million years. Humans right now have technologies to help us survive but our ancestors in the past are at the bottom of the food chain, which is really weak. We know a human is very easy to get killed by animals. They need to be very careful about everything in order to survive.

In our cognition, if things I have experienced before that is awful, it would be hard to change the mindset because the first impression of anything is important and unforgettable. For example, I am afraid of dogs, I have experienced the feeling of being chased by dogs. So in my subconscious, the dog is equal to “being chased by a dog” and “may get bite by a dog.” Therefore, the dog becomes a danger for me. This deep level of cognition has created fear.

Equally important, public information is a huge thing for everyone too. If a child is not teached or has not experienced the danger either a dog or a lion. This cognition will get the child into danger. Even if the lion is in front of him and it will eat him in the next moment. He will not feel scared. This is how knowledge is important. It is worth mentioning that fear itself is different from the fact itself. So fears and facts are two different things. Whether a child has fear depends upon knowledge of the lion or on his cognition of the lion. Whether the lion is dangerous or not. However, whether or not the child has a sense of fear or whether the child will eventually be eaten by the lion or hurt is two different things. Thus, we can see that public information is super important in order to survive or being a ‘normal’ person.

Moreover, you may have procrastination, so don’t feel like to go to work or not ready for life. It may be because of your heart, you are afraid there is more work than what you have right now. You are afraid there are more complicated issues in life. “If I try my best, I still may not be able to finish it.” Then you will try your best to let yourself get out in the situation. In another way, you may be very respectful to your parents. It may be more than just love, or it may be because of the fear that your parents will leave you. You want to give them as much as possible, be filial in time. You may think you are lazy and it is very likely that fear is at your disposal. Many young people seem to be lazy, but they tend to play computer games overnight or indulge in their hobbies. “I have to pay countless efforts and time for this.” Is that really because of laziness? If it’s just laziness, why do you pay so many efforts for games and hobbies? Even if faced with more accusations and it will go as before. Since those things in life put pressure on us, so we want to get out of the fear. We really want to put full energy into what we are interested in.

In addition, fear sends a message to ourselves that we are in danger. For example, I can say that I do not believe in ghosts, but when I see a ghost in the middle of the night, a ghost with white clothes and black hair. This scene may provoke fear in my heart. Since I have absorbed a lot of invisible information in the brain, from the people around me, the ghost stories I have heard when I was a child or the images I saw in a horror movie. The ghost in a horror movie actually always kill and harm people. This cognition is stimulated. So I will be scared invisibly. My conscious mind does not experience so many thoughts, because this kind of thinking, the analogy of the calculation is arranged by my subconscious mind, and is transformed into a simpler message conveyed to me, fear. So I began to feel scared and started making choices to escape, which is running away from this danger. Fear is the system helps us human survive from the past million years since the origin of human to now.

Generally speaking, I think fear is rational. We would not have a mechanism that is totally useless for us. Fear is a mechanism or system that remains in our human evolution, a sense of self-protection, and there is fear in everyone’s inheritance. We are from ancestors who knows fear and use them as a protection system. Our ancestors who did not have this kind of protection mechanism were naturally eliminated by nature. Those who lack fear tend to challenge those who are more powerful and they will get into danger. So fear itself is not a bad protection and fear is not a function we should be abandoned. Fear is a kind of message sent to ourselves by the subconscious. It is a kind of a protection mechanism, which directly converts our large amount of cognition, experience, emotion, and calculation into a simple message, feeling.

Introduction

Developmental dyslexia is a common learning disability that influences the reading and writing proficiency of those affected. Despite nearly 10% of the population having a form of dyslexia there is no universally accepted neurological starting point. I will be reviewing materials on some of the leading theories of causes of dyslexia and how they attempt to explain the brain processes involved and if there are potential limitations. Personally, I work with dyslexic children and adults in a school setting and am keen to explore how recent brain and mind theories explain the behaviour I can see in the classroom, and what I can do to help positively influence the learners to create a better learning experience.

Phonological Deficit Theory

Learning to read is a multidisciplinary process that requires the reader to link the written letters (orthography) to the corresponding sound (phonology) to achieve the intended meaning (semantics) (Share, 1995). Theoretically, individuals with a phonological deficit have an impairment when it comes to how the sounds of words are represented, which can be evidenced in poor readers who were found to have more variability in brainstem responses when hearing a single word than good readers did CITATION Hor131 l 2057 (Hornickel. J., 2013) which indicates a poorer phoneme representation in the brain of dyslexics.

Matching words to sounds, or graphemes to phonemes, is a core element of reading that people with dyslexia struggle with, the phonological deficit theory provides a sound link between a cognitive deficit and the behaviour of dyslexics. There is no confirmed neurological starting point for Developmental Dyslexia but there may be tangible differences within the brain which are responsible for how the letters and sounds are stored and retrieved in order to generate the correct speech sound (Ramus, 2003). The arcuate fasciculus is the part of the brain which is responsible for the process of letter sounds and language, it is located in the Perisylvian language area and numerous studies have shown that this area of the brain can be smaller in dyslexic brains than in typically developed brains (G. Silani., 2005) (E. Paulesu., 2001)

In the above scan CITATION Joh13 l 2057 (Gabrieli, 2013) we can see the Arcuate fasciculus (AF) which links Broca’s and Wernicke’s Areas in the Perisylvian Cortex. In brief, Broca’s area is responsible for the production of language and Wernicke’s area is responsible for transforming graphemes into phonemes, both are key aspects of reading. Altogether, the arcuate fasciculus, Broca and Wernicke’s areas create the dorsal language stream which focusses on the phonological elements of language. Therefore, any abnormality in the arcuate fasciculus, such as the shrinkage found in dyslexic brains, may reduce the corticocortical connectivity and cause detrimental effects when matching graphemes to phonemes. This in turn makes the reading process more arduous resulting in longer reading times. It is not known for certain how we read, although experts in the field have been creating and testing theories (Coltheart, 2001) (Seidenberg, 2005) therefore it is possible that people with a phonological deficit read differently to those with a typically developed brain.

Magnocellular Deficit theory

The magnocellular theory stands apart from the others as it is the only theory that explains the multiple deficits that dyslexia can have on the brain, although this has been contested between experts. Aside from slow reading and writing speeds it is common for dyslexics to struggle with neurological conditions such as coordination, sequencing, and confusing left and right (Stein, 2001). The visual magnocellular stream goes from retina to posterior parietal cortex and is responsible for keeping the eyes on the target word in binocular vision, which is important when recognizing orthographic information, it then has to be matched to the phoneme and meaning in order to be understood. The Magnocellular theory highlights the fact that people with dyslexia have an impairment in the Magnocellular stream, as shown by post-mortem explorations where the neurons were shorter, coercing the dyslexic brain to process orthographic information differently when undergoing language tasks CITATION Gal91 l 2057 (Galaburda, 1991). An experiment to test visual motion on dyslexics was completed in 1996 by GF Eden and results were shared from an fMRI scan showing the differences in brain activation between dyslexics and typically developed brains.

The diagram shows that during the motion test the typically developed brain used the middle temporal area (V5MT) and the dyslexic brain did not. The middle temporal area receives input from the magnocellular stream to process motion, colour and form separately which suggests that dyslexics process all the information in the posterior parietal cortex (PPC). The PPC controls normal eye movement and visuospatial attention helping the eye to focus, deficits in this area, or the Magnocellular stream which supplies it with information, could explain why some dyslexics see letters move when reading, making reading a lot more challenging and shown by slower reading speeds.

A limiting factor is that this test only shows a neurological difference when processing motion, not a static pattern. As text is static, I feel it does not answer all the questions. However, when we read a word in English we read from left to right, so our eyes are moving, and the shorter neurons and amalgamated processing in the PPC could be the cause for the aforementioned symptoms of dyslexia. A similar experiment was conducted involving 22 participants, two men with dyslexia and 20 typically developed volunteers were asked to complete a number of language tasks and their brain activity was measured using an fMRI scanner CITATION Yam131 l 2057 (Yamamoto., 2013). The results also showed more activation in the PPC in the dyslexic brain supporting the theory that the magnocellular visual pathway impairment is responsible for behaviours in dyslexics.

This could blend in with Coltheart’s dual route cascaded model of reading. When we read a new word we sound it out phonetically from left to right, but once we have seen the word and stored the grapheme -phoneme set in the brain it may become a static pattern, which dyslexics process in the typical way. Adult illiterates who learnt to read have the same brain biology as readers who learnt in childhood, despite the processes being different. It is possible then that people with dyslexia learn to read by repeated exposure to new words and storing them as a static pattern, instead of processing them afresh each time.

Cerebellar Deficit Theory

We have now looked at the phonological deficit theory, which suggests that poor readers struggle to manipulate the spoken word into phonemes, and the Magnocellular deficit theory proposing that a reading disability is caused by impaired visual and auditorial processing. The rationale for the cerebellar deficit theory of dyslexia relates to the automatisation of skills, suggesting that this inability to make certain skills subconscious is what causes the behavioural effects of dyslexia. Nicolson and colleagues tested the cerebellum activation of dyslexic and non-dyslexic children and discovered that the cerebellum was less active in dyslexic subjects when learning a new sequence in a motor skills task. Prior to this, disparate tests pertaining to balance, phonetic segmentation and naming pictures were conducted to conclude that the dyslexic children have difficulties when automizing any skill, not just a literary one CITATION Nic01 l 2057 m Nic94(Nicolson R. F., 2001; Nicolson R. F., 1994). This supports the theory that when the dyslexic mind is learning a new task, or word, the decision areas of the brain used for storing visual information are less active, suggesting their focus is more concentrated on one aspect, and requiring more mental effort to unite visual, auditorial and semantic processes resulting in slower processing times.

The light areas in the MRI scan show difference in activation between dyslexic and typical subjects when learning a new sequence, with less activation in the cerebellar for dyslexic subjects.

The MRI scan revealed that overall dyslexics have less cerebellar activation in the right, ipsilateral, brain hemisphere than typically developed brains. A non-language PET experiment was carried out by Jenkins and colleagues to establish the impact of the cerebellum on typical participants whilst avoiding any difference relating to literacy performance to confirm the cerebellums involvement in all motor skills CITATION Jen94 l 2057 (Jenkins, 1994). Further studies have since been conducted which support these findings. Rae et al performed a study on 29 participants, 14 dyslexics and 15 typical, all male, which highlighted a chemical difference for the dyslexic subjects in the left temporo-parietal lobe (responsible for understanding spoken and written language) and the right cerebellum, which controls motor function. This discovery provided strong evidence that the cerebellum is involved in the dysfunctional behaviours of dyslexics CITATION Rae98 l 2057 (Rae, 1998).

However, despite these tests seeming like empirical evidence they have still been interpreted by the people who conducted the experiment and there is not a commitment to categorically confirm that this is the evidence needed to understand how dyslexic brains work. One theory, based on the PET scan results which could not scan the whole cerebellum, is that their male dyslexic participants have a smaller number of larger neurons in the left Perisylvian language regions, but this has not been explicitly proven in post-mortem examinations.

A Critical Look

All three theories have helped to further the understanding of the cognitive neuroscience of Literacy and Dyslexia. The studies pertaining to each theory have provided empirical evidence of cognitive processing differences in dyslexics using functional magnetic resonance imaging and provided reasonable explanations for their results, and they have been published in recognized scientific journals.

Looking more closely at Hornickel’s experiment on the auditory responses, this test was conducted on poor readers, not necessarily people with dyslexia, who may have other contributing deficits to inhibit their response time. The data was collected using two different systems which also may have affected the results. The test may have been more taxing for people with a reading disability as neurons in the auditory system nuclei may recover more slowly after firing, resulting in a delayed response CITATION Sch05 l 2057 (Schaette R, 2005) or it could be that the subjects were watching a movie to improve compliance and were distracted. This experiment did not prove that dyslexics were born with this impairment or if the phonological areas did not develop typically. Furthermore, some studies have suggested that dyslexics have more internal noise, hinting that they hear a wider variety of sounds which could be evidenced by the varied auditory brainstem responses. Further research could be conducted to see if Developmental Dyslexics are bad at matching phonemes to graphemes or if they are hearing multiple phonemes when typical brains only hear one

The aim of these studies is to understand how dyslexic brains process information so a more suitable learning framework could be implemented from an earlier age. This would help future dyslexics feel more included and build self confidence in their academic ability but may help or hinder the current participants who are either trail blazers or an object of study. There is still room to develop, as some of the tests included dyslexic participants who had other disorders, such as attention deficit hyperactivity disorder (which they would require different support) but it is not clearly stated in Rae et al’s or Nicholson’s experiment if the dyslexic participants have any other mental issues. The magnocellular tests and the cerebellar tests involved in this review used only male dyslexics, possibly because dyslexia is more prevalent in men, so to continue studies with more gender variety may be a step forward.

Conclusion

Recent experiments on the arcuate fasciculus show a reduction in size in the dyslexic brain which creates a deficit in the phonological language area and adequately supports the phonological deficit theory.

Further tests have aimed to prove dyslexics hear a wider range of phonemes when presented with a single sound, evidencing poor phoneme representation, which could be done more robustly without audio-visual distractions.

The magnocellular theory suggests shorter neurons in the magnocellular stream and the experiments highlighted that dyslexics process visual motion differently than in typical brains, this could be used to create new learning strategies.

The cerebellum experiment used fMRI scans to confirm the involvement of the cerebellum in a variety of tasks and provided evidence that dyslexics had less activation in the cerebellum during all tasks, giving empirical credence to the cerebellum theory

It has still not been universally agreed on what cognitive impairments cause behavioural differences in the dyslexic brain, but each neurocognitive experiment has provided empirical evidence to support each theory and has been published by a reputable source.

Bibliography

1. BIBLIOGRAPHY Coltheart, M. R. (2001). DRC: A dual route cascaded model of visual word recognition and reading aloud. Psychological Review, 204 – 256.
2. E. Paulesu., J.-F. D. (2001). Dyslexia: Cultural Diversity and Biological Unity. Science, Vol 291, 2165 – 2168.
3. G. Silani., U. F.-F. (2005). Brain abnormalities underlying altered activation in dyslexia: a voxel based morphometry study. Brain, Vol 128, 2453 – 2461.
4. Gabrieli, J. (2013, August 1). Brain scans may help diagnose dyslexia. (M. N. Anne Trafton, Interviewer)
5. Galaburda, A. (1991). Physiological and anatomical evidence for a magnocellular defect in developmental dyslexia . PNAS Vol 88, 7943 – 7947.
6. History, A. M. (Director). (2010). Sciene Bulletins: How does reading change the brain? [Motion Picture].
7. Hornickel. J., K. N. (2013). Unstable Representation of Sound: A Biological Marker of. The Journal of Neuroscience, 3500 –3504.
8. Jenkins, I. (1994). Motor sequence learning – a study with Positron EmissionTomography. Journal of Neuroscience, Vol. 14, 3775 -3790.
9. NHS. (2020, 1 10). Overview Dyslexia. Retrieved from National Health Service: https:www.nhs.ukconditionsdyslexia#:~:text=Dyslexia is a common learning,, intelligence isn’t affected.
10. Nicolson, R. F. ( 1994). Comparison of Deficits in Cognitive and Motor Skills among Children with Dyslexia. Annals of Dyslexia, 147–164.
11. Nicolson, R. F. (2001). Developmental Dyslexia: the cerebellar deficit hypothesis. TRENDS in Neurosciences Vol.24, 508 – 511.
12. Rae, C. L. (1998). Metabolic abnormalities indevelopmental dyslexia detected by magneticresonance spectroscopy. The Lancet, Vol 351, 1849–1852.
13. Ramus, F. R. (2003). Theories of developmental dyslexia: insights from a multiple case study of dyslexic adults. Brain, Vol 126, 841-865.
14. Schaette R, G. T. (2005). Spike-train variability of auditory neurons in vivo: dynamic responses follow predictions from constant stimuli. J Neurophysiol Vol 93, 3270 –3281.
15. Seidenberg, M. (2005). Connectionist Models of Word Reading. Sage Journals, 238-242.
16. Share, D. (1995). Phonological recoding and self-teaching: sine qua non of reading acquisition. Cognition, 151 – 218.
17. Yamamoto., H. K. (2013). Deficits in Magnocellular Pathway in Developmental Dyslexia: A Functional Magnetic Resonance Imaging-Electroencephalography Study. Journal of Behavioral and Brain Science, Vol. 3, 1-11.

Introduction

Developmental dyslexia is a common learning disability that influences the reading and writing proficiency of those affected. Despite nearly 10% of the population having a form of dyslexia there is no universally accepted neurological starting point. I will be reviewing materials on some of the leading theories of causes of dyslexia and how they attempt to explain the brain processes involved and if there are potential limitations. Personally, I work with dyslexic children and adults in a school setting and am keen to explore how recent brain and mind theories explain the behaviour I can see in the classroom, and what I can do to help positively influence the learners to create a better learning experience.

Phonological Deficit Theory

Learning to read is a multidisciplinary process that requires the reader to link the written letters (orthography) to the corresponding sound (phonology) to achieve the intended meaning (semantics) (Share, 1995). Theoretically, individuals with a phonological deficit have an impairment when it comes to how the sounds of words are represented, which can be evidenced in poor readers who were found to have more variability in brainstem responses when hearing a single word than good readers did CITATION Hor131 l 2057 (Hornickel. J., 2013) which indicates a poorer phoneme representation in the brain of dyslexics.

Matching words to sounds, or graphemes to phonemes, is a core element of reading that people with dyslexia struggle with, the phonological deficit theory provides a sound link between a cognitive deficit and the behaviour of dyslexics. There is no confirmed neurological starting point for Developmental Dyslexia but there may be tangible differences within the brain which are responsible for how the letters and sounds are stored and retrieved in order to generate the correct speech sound (Ramus, 2003). The arcuate fasciculus is the part of the brain which is responsible for the process of letter sounds and language, it is located in the Perisylvian language area and numerous studies have shown that this area of the brain can be smaller in dyslexic brains than in typically developed brains (G. Silani., 2005) (E. Paulesu., 2001)

In the above scan CITATION Joh13 l 2057 (Gabrieli, 2013) we can see the Arcuate fasciculus (AF) which links Broca’s and Wernicke’s Areas in the Perisylvian Cortex. In brief, Broca’s area is responsible for the production of language and Wernicke’s area is responsible for transforming graphemes into phonemes, both are key aspects of reading. Altogether, the arcuate fasciculus, Broca and Wernicke’s areas create the dorsal language stream which focusses on the phonological elements of language. Therefore, any abnormality in the arcuate fasciculus, such as the shrinkage found in dyslexic brains, may reduce the corticocortical connectivity and cause detrimental effects when matching graphemes to phonemes. This in turn makes the reading process more arduous resulting in longer reading times. It is not known for certain how we read, although experts in the field have been creating and testing theories (Coltheart, 2001) (Seidenberg, 2005) therefore it is possible that people with a phonological deficit read differently to those with a typically developed brain.

Magnocellular Deficit theory

The magnocellular theory stands apart from the others as it is the only theory that explains the multiple deficits that dyslexia can have on the brain, although this has been contested between experts. Aside from slow reading and writing speeds it is common for dyslexics to struggle with neurological conditions such as coordination, sequencing, and confusing left and right (Stein, 2001). The visual magnocellular stream goes from retina to posterior parietal cortex and is responsible for keeping the eyes on the target word in binocular vision, which is important when recognizing orthographic information, it then has to be matched to the phoneme and meaning in order to be understood. The Magnocellular theory highlights the fact that people with dyslexia have an impairment in the Magnocellular stream, as shown by post-mortem explorations where the neurons were shorter, coercing the dyslexic brain to process orthographic information differently when undergoing language tasks CITATION Gal91 l 2057 (Galaburda, 1991). An experiment to test visual motion on dyslexics was completed in 1996 by GF Eden and results were shared from an fMRI scan showing the differences in brain activation between dyslexics and typically developed brains.

The diagram shows that during the motion test the typically developed brain used the middle temporal area (V5MT) and the dyslexic brain did not. The middle temporal area receives input from the magnocellular stream to process motion, colour and form separately which suggests that dyslexics process all the information in the posterior parietal cortex (PPC). The PPC controls normal eye movement and visuospatial attention helping the eye to focus, deficits in this area, or the Magnocellular stream which supplies it with information, could explain why some dyslexics see letters move when reading, making reading a lot more challenging and shown by slower reading speeds.

A limiting factor is that this test only shows a neurological difference when processing motion, not a static pattern. As text is static, I feel it does not answer all the questions. However, when we read a word in English we read from left to right, so our eyes are moving, and the shorter neurons and amalgamated processing in the PPC could be the cause for the aforementioned symptoms of dyslexia. A similar experiment was conducted involving 22 participants, two men with dyslexia and 20 typically developed volunteers were asked to complete a number of language tasks and their brain activity was measured using an fMRI scanner CITATION Yam131 l 2057 (Yamamoto., 2013). The results also showed more activation in the PPC in the dyslexic brain supporting the theory that the magnocellular visual pathway impairment is responsible for behaviours in dyslexics.

This could blend in with Coltheart’s dual route cascaded model of reading. When we read a new word we sound it out phonetically from left to right, but once we have seen the word and stored the grapheme -phoneme set in the brain it may become a static pattern, which dyslexics process in the typical way. Adult illiterates who learnt to read have the same brain biology as readers who learnt in childhood, despite the processes being different. It is possible then that people with dyslexia learn to read by repeated exposure to new words and storing them as a static pattern, instead of processing them afresh each time.

Cerebellar Deficit Theory

We have now looked at the phonological deficit theory, which suggests that poor readers struggle to manipulate the spoken word into phonemes, and the Magnocellular deficit theory proposing that a reading disability is caused by impaired visual and auditorial processing. The rationale for the cerebellar deficit theory of dyslexia relates to the automatisation of skills, suggesting that this inability to make certain skills subconscious is what causes the behavioural effects of dyslexia. Nicolson and colleagues tested the cerebellum activation of dyslexic and non-dyslexic children and discovered that the cerebellum was less active in dyslexic subjects when learning a new sequence in a motor skills task. Prior to this, disparate tests pertaining to balance, phonetic segmentation and naming pictures were conducted to conclude that the dyslexic children have difficulties when automizing any skill, not just a literary one CITATION Nic01 l 2057 m Nic94(Nicolson R. F., 2001; Nicolson R. F., 1994). This supports the theory that when the dyslexic mind is learning a new task, or word, the decision areas of the brain used for storing visual information are less active, suggesting their focus is more concentrated on one aspect, and requiring more mental effort to unite visual, auditorial and semantic processes resulting in slower processing times.

The light areas in the MRI scan show difference in activation between dyslexic and typical subjects when learning a new sequence, with less activation in the cerebellar for dyslexic subjects.

The MRI scan revealed that overall dyslexics have less cerebellar activation in the right, ipsilateral, brain hemisphere than typically developed brains. A non-language PET experiment was carried out by Jenkins and colleagues to establish the impact of the cerebellum on typical participants whilst avoiding any difference relating to literacy performance to confirm the cerebellums involvement in all motor skills CITATION Jen94 l 2057 (Jenkins, 1994). Further studies have since been conducted which support these findings. Rae et al performed a study on 29 participants, 14 dyslexics and 15 typical, all male, which highlighted a chemical difference for the dyslexic subjects in the left temporo-parietal lobe (responsible for understanding spoken and written language) and the right cerebellum, which controls motor function. This discovery provided strong evidence that the cerebellum is involved in the dysfunctional behaviours of dyslexics CITATION Rae98 l 2057 (Rae, 1998).

However, despite these tests seeming like empirical evidence they have still been interpreted by the people who conducted the experiment and there is not a commitment to categorically confirm that this is the evidence needed to understand how dyslexic brains work. One theory, based on the PET scan results which could not scan the whole cerebellum, is that their male dyslexic participants have a smaller number of larger neurons in the left Perisylvian language regions, but this has not been explicitly proven in post-mortem examinations.

A Critical Look

All three theories have helped to further the understanding of the cognitive neuroscience of Literacy and Dyslexia. The studies pertaining to each theory have provided empirical evidence of cognitive processing differences in dyslexics using functional magnetic resonance imaging and provided reasonable explanations for their results, and they have been published in recognized scientific journals.

Looking more closely at Hornickel’s experiment on the auditory responses, this test was conducted on poor readers, not necessarily people with dyslexia, who may have other contributing deficits to inhibit their response time. The data was collected using two different systems which also may have affected the results. The test may have been more taxing for people with a reading disability as neurons in the auditory system nuclei may recover more slowly after firing, resulting in a delayed response CITATION Sch05 l 2057 (Schaette R, 2005) or it could be that the subjects were watching a movie to improve compliance and were distracted. This experiment did not prove that dyslexics were born with this impairment or if the phonological areas did not develop typically. Furthermore, some studies have suggested that dyslexics have more internal noise, hinting that they hear a wider variety of sounds which could be evidenced by the varied auditory brainstem responses. Further research could be conducted to see if Developmental Dyslexics are bad at matching phonemes to graphemes or if they are hearing multiple phonemes when typical brains only hear one

The aim of these studies is to understand how dyslexic brains process information so a more suitable learning framework could be implemented from an earlier age. This would help future dyslexics feel more included and build self confidence in their academic ability but may help or hinder the current participants who are either trail blazers or an object of study. There is still room to develop, as some of the tests included dyslexic participants who had other disorders, such as attention deficit hyperactivity disorder (which they would require different support) but it is not clearly stated in Rae et al’s or Nicholson’s experiment if the dyslexic participants have any other mental issues. The magnocellular tests and the cerebellar tests involved in this review used only male dyslexics, possibly because dyslexia is more prevalent in men, so to continue studies with more gender variety may be a step forward.

Conclusion

Recent experiments on the arcuate fasciculus show a reduction in size in the dyslexic brain which creates a deficit in the phonological language area and adequately supports the phonological deficit theory.

Further tests have aimed to prove dyslexics hear a wider range of phonemes when presented with a single sound, evidencing poor phoneme representation, which could be done more robustly without audio-visual distractions.

The magnocellular theory suggests shorter neurons in the magnocellular stream and the experiments highlighted that dyslexics process visual motion differently than in typical brains, this could be used to create new learning strategies.

The cerebellum experiment used fMRI scans to confirm the involvement of the cerebellum in a variety of tasks and provided evidence that dyslexics had less activation in the cerebellum during all tasks, giving empirical credence to the cerebellum theory

It has still not been universally agreed on what cognitive impairments cause behavioural differences in the dyslexic brain, but each neurocognitive experiment has provided empirical evidence to support each theory and has been published by a reputable source.

Bibliography

1. BIBLIOGRAPHY Coltheart, M. R. (2001). DRC: A dual route cascaded model of visual word recognition and reading aloud. Psychological Review, 204 – 256.
2. E. Paulesu., J.-F. D. (2001). Dyslexia: Cultural Diversity and Biological Unity. Science, Vol 291, 2165 – 2168.
3. G. Silani., U. F.-F. (2005). Brain abnormalities underlying altered activation in dyslexia: a voxel based morphometry study. Brain, Vol 128, 2453 – 2461.
4. Gabrieli, J. (2013, August 1). Brain scans may help diagnose dyslexia. (M. N. Anne Trafton, Interviewer)
5. Galaburda, A. (1991). Physiological and anatomical evidence for a magnocellular defect in developmental dyslexia . PNAS Vol 88, 7943 – 7947.
6. History, A. M. (Director). (2010). Sciene Bulletins: How does reading change the brain? [Motion Picture].
7. Hornickel. J., K. N. (2013). Unstable Representation of Sound: A Biological Marker of. The Journal of Neuroscience, 3500 –3504.
8. Jenkins, I. (1994). Motor sequence learning – a study with Positron EmissionTomography. Journal of Neuroscience, Vol. 14, 3775 -3790.
9. NHS. (2020, 1 10). Overview Dyslexia. Retrieved from National Health Service: https:www.nhs.ukconditionsdyslexia#:~:text=Dyslexia is a common learning,, intelligence isn’t affected.
10. Nicolson, R. F. ( 1994). Comparison of Deficits in Cognitive and Motor Skills among Children with Dyslexia. Annals of Dyslexia, 147–164.
11. Nicolson, R. F. (2001). Developmental Dyslexia: the cerebellar deficit hypothesis. TRENDS in Neurosciences Vol.24, 508 – 511.
12. Rae, C. L. (1998). Metabolic abnormalities indevelopmental dyslexia detected by magneticresonance spectroscopy. The Lancet, Vol 351, 1849–1852.
13. Ramus, F. R. (2003). Theories of developmental dyslexia: insights from a multiple case study of dyslexic adults. Brain, Vol 126, 841-865.
14. Schaette R, G. T. (2005). Spike-train variability of auditory neurons in vivo: dynamic responses follow predictions from constant stimuli. J Neurophysiol Vol 93, 3270 –3281.
15. Seidenberg, M. (2005). Connectionist Models of Word Reading. Sage Journals, 238-242.
16. Share, D. (1995). Phonological recoding and self-teaching: sine qua non of reading acquisition. Cognition, 151 – 218.
17. Yamamoto., H. K. (2013). Deficits in Magnocellular Pathway in Developmental Dyslexia: A Functional Magnetic Resonance Imaging-Electroencephalography Study. Journal of Behavioral and Brain Science, Vol. 3, 1-11.