The Brain: Developmental Dyslexia

Question: What is Dyslexia?

Answer: A Genetically Inheritable Neurodevelopmental Disorder.

Developmental Dyslexia is a genetically inheritable a neurodevelopmental disorder that results in language-based learning differences which can inhibit language acquisition and development despite adequate cognitive function, motivation and educational instruction (International Dyslexia Association, 2015). Typically the symptoms of Developmental Dyslexia include difficulties with “both oral and written language skills”, such as spelling, decoding, reading and writing (International Dyslexia Association, 2015). Though the severity of these symptoms can vary significantly; there is some evidence that these variances are representative of different subcategories of dyslexia, such as dyseidetic and dysphonetic dyslexia, which possibly arise from their own distinct neurological deficits which can co-occur with other deficits or exist independently on their own (Ramus, F…et al, 2003). 

Question: How Common is Dyslexia

Answer: Very Common.

Dyslexia is considered the most common neurodevelopmental disorder to date (Caylac, 2011). However, because the statistics vary depending on how you define dyslexia the actual number of dyslexic persons is still unknown. While some studies indicate that the prevalence of dyslexia may be as high as 33% in some populations, most would agree that perhaps as many as 5-10% of any population could be affected (World Heritage Encyclopedia, 2015). Dyslexia is this common because it runs in families and has almost a 50% chance of being passed from child to parent.  

Question: What causes Dyslexia?

Answer: Impaired Perceptual Processing

Dyslexia symptoms were previously understood as a “deficit in the phonological component of the language” (Christmann, Lachmann, & Steinbrink, 2015). Though currently it is questioned whether the phonological deficit(s) observed are the cause of Developmental Dyslexia (i.e. symptoms) or whether the phonological deficit(s) observed are a secondary symptom as well (Christmann, Lachmann, & Steinbrink, 2015). Currently, it is believed that, at the core, Developmental Dyslexics suffer from a discrepancy in phonemic awareness as a consequence of a deficit in auditory processing that results in the inhibited “ temporal analysis of speech at the phoneme level” (Schulte-Körne, & Bruder, 2010). 

The most recent evidence indicates that the discrepancy in auditory processing impairs the auditory coding of “rapid changes in amplitude and frequency” that are essential for “phonological analysis” (Caylac, 2011). Purportedly this then creates the apparent cognitive phonological deficit observed in developmental dyslexia by inhibiting the appropriate phonological analysis of speech sounds, including phenome memory integration, “identifying the separate speech sounds within a word” and/or “learning how letters represent those sounds” (Caylac, 2011). Finally, this a deficit in phonological analysis cascades into secondary consequences that we recognize as symptoms of dyslexia, such as “difficulties in reading comprehension reduced the reading experience and inhibited vocabulary development” (Caylac, 2011).

Etiology (cont): Affected Perceptual Processing

Question: What types of perceptual processing are affected?   

Answer: The temporal analysis of speech at the phoneme level

Specifically, regarding the types of perceptual processing effect, those with Developmental Dyslexia have a harder time “perceiving rapidly changing auditory signals” and “differences in the pitch between two sounds” (Schulte-Körne, & Bruder, 2010).

For example: if one phenome comes in too fast upon the next phenome or they are too close together in pitch than a person with dyslexia is likely not integrating the first sound into memory. Instead, it will seem to blend into the second speech sound (Schulte-Körne, & Bruder, 2010).

The observed deficit in the perception of phonemes then results in an inability to process short rhythmic patterns, as seen in Developmental Dyslexia (Schulte-Körne, & Bruder, 2010).

Etiology (cont.): Sensory System Affected

Question: What causes impaired perceptual processing?

Answer: Idiopathic Auditory Processing Deficit  

It follows, that since the ability “integrate sounds temporally” is necessary to perceive an accurate representation of rhythmic patterns today leading research has turned to the brain in the hunt for the origin of the processing deficit (Schulte-Körne, & Bruder, 2010).

However, the mechanisms for speech are not controlled by anyone specialized structure in the brain and the exact physical origin of the observed auditory processing deficits seen in developmental dyslexia is still an evolving mystery (International Dyslexia Association, 2015).

Some research has uncovered brain-based differences between those who have dyslexia and those who do not, including a lack of the usual “left-greater-than-right asymmetry” as well as differences in the amount “gray and white volume matters in the temporoparietal and inferior frontal cortices” (International Dyslexia Association, 2015).

These differences are of particular interest to researchers because the left hemisphere is associated with speech development (International Dyslexia Association, 2015). And even more compelling, the temporoparietal and inferior frontal cortices are used in the phonological and semantic processing of words, and the inferior frontal cortices are used in the formation of speech sounds (International Dyslexia Association, 2015). 

However, without further research, it is still unclear if these differences are the cause or the consequence of dyslexia (Christmann, Lachmann, & Steinbrink, 2015).  For example: Did these brain areas not develop properly because some initial faulty mechanisms did not allow for them to be used, strengthened, and become well established [as they are in the control]? Or do the symptoms of underdevelopment result from these areas being genetically prone to underdevelopment? Either way, to compensate Dyslexics must use more of their right brain for language acquisition skills than non-dyslexics who use typically use their left (Community Psychiatric Centers, 2015). 

Bottom-Up or Top-Down?

Question: Is the Top-Down or Bottom-Up Approach More Applicable To Understanding Development Dyslexia?

Answer: Both are needed

Both the Bottom-Up and Top-Down theories are needed to explain the observed differences seen in the dyslexic language acquisition. The Bottom-Up approach explains the difficulties that are seen in perception and learning (i.e. integrating into memory) specific phonemic knowledge, despite the normal capability, to hear them or see them. But, the Top The down approach explains how the auditory processing deficit interferes with the cognitive processing of language concepts flowing down, such as the accurate reproduction of words one has heard said before or is reading from a book.

In the Bottom-Up Example:

Concerning speech sounds, the speed at which the sound is voiced makes the difference between hearing one sound or the other (i.e. “pa” or ‘ba). In theory, someone with auditory processing, related dyslexia might process these sounds too fast and result in not processing the first phenome in the brain. This results inability to integrate these speech sounds into memory and a discrepancy in memory with certain phenomes of speech (a phonological deficit).

In the Top DownExample: 

Because the auditory processing deficit has failed to integrate the speech sounds into memory and left the person a discrepancy in memory within certain phenomes of speech sounds (a phonological deficit), when a person with dyslexia tries to say, read or even spell a word it fails to be able to accurately reproduce the speech sounds needed purely from recall.

This cognitive failure results in difficulties reproducing and manipulating some of the speech sound needed for language tasks, such as reading, speaking, and writing.

Related & Co-Occurring Disorders

o   Dysgraphia

o   Developmental Coordination Disorder

o   Auditory Processing Disorder

o   Attention Deficit Hyperactive Disorder

(World Heritage Encyclopedia, 2015)

Although it is not uncommon for dyslexia to present in a child with no other conditions, Developmental Dyslexia can co-occur with other conditions that can aggravate the symptoms of dyslexia, or worse, further hinder learning.  Some of these conditions include Dysgraphia, Developmental Coordination Disorder, Auditory Processing Disorder, and ADHD. One study indicated that depending on the definition of ADHD- as many as 30-70% of the children with a dyslexia diagnosis could also be defined as having ADHD (World Heritage Encyclopedia, 2015). When left untreated a co-occurring condition can make the acquisition of early language skills even more challenging (World Heritage Encyclopedia, 2015). Ensuring your child has an accurate diagnosis clearly identifies the parameters of help needed and help ensure he or she gets the correct treatment early.

The Psychological Impact

• ·       Impaired Self Judgement
• ·       Lack of Self Confidence

(Community Psychiatric Centers, 2015)

Children with dyslexia suffer from a fundamental deficit in phonological and/or phonemic awareness that can impair reading, their desire to read and affect their self-confidence in their ability to learn to read. Even with intervention children with dyslexia will often still struggle with basic reading and writing skills, however they can overcome their differences and become good readers and proficient writers (Community Psychiatric Centers, 2015). The psychological impact of this struggle can include impaired self-perception and lack of self-confidence in personal ability, which can extend beyond academia (Community Psychiatric Centers, 2015). This often because the children with dyslexia are faced with learning challenges everyday experiences with their unchallenged peers. Consequent to social referencing, albeit unfair, children with dyslexia are at risk for feeling inadequate with their personal abilities and anxiety (Community Psychiatric Centers, 2015). Unfortunately, a lack of self-confidence can trickle into other social problems, like avoidance or withdrawal from activities.

Coping strategies and Treatment Methods

• o   Teach Phonemic Awareness Using Games or Activities
• o   Utilize a Multisensory Approach for Teaching
• o   Follow the Golden Rule When Reading
• o   Recognize Individuality and Achievement

Although dyslexia can present a lifelong learning challenge for those affected, children with dyslexia can be very successful, especially when they are given the right support in childhood. Various coping strategies are used with children who have dyslexia to reduce the impact that having a learning differences can have on them.

Teach Phonemic Awareness with

• ·       Games
• ·       Activities

Because these children struggle with phonemic awareness one helpful strategy is engaging children with dyslexia in games and activities that enhance phonemic awareness. Using games makes the activity fun and engaging, thereby taking the struggle out of learning while still teaching valuable lessons. Many games are interactive, such as the matching game “I spy something that begins with the “sh” sound…” (Community Psychiatric Centers, 2015). But, there are also various types of print out sheets available on the web that can teach phonemic awareness for older age groups, who may not be interested in a game of “I spy” with mom or dad (Community Psychiatric Centers, 2015).

Using a Multisensory Approach

• ·       Audio
• ·       Visual
• ·       Touch
• ·       Movement

The recommended strategy for helping children overcome their difficulties learning is to use a multisensory approach to teaching (Community Psychiatric Centers, 2015). As we reviewed, children with dyslexia can struggle to accurately perceive both visual and auditory stimuli concerning speech, non-speech, and some nonlinguistic stimuli as well. This makes processing information given only through visual and auditory methods more c1`hallenging for them (Community Psychiatric Centers, 2015). To encourage enhanced memory integration of the learning material covered children with dyslexia can benefit from a multisensory approach that utilizes sight, hearing, touch, and movement (Community Psychiatric Centers, 2015). 

One example might include, saying the sound, such as “sh”. Then, using clay, having them roll shapes to make an S and H. Once they have made the clay letters you can both say each letter sounds individual. Finally, you can then put them together to say their combined sound a few times as well.

Follow the Golden Rule

• ·       Practice Reading Often
• ·       Help Whenever Needed

Spend time listening to children with dyslexia read out loud and/or stay close during their silent reading time (Community Psychiatric Centers, 2015). This ensures you can help them with words they don’t know immediately. Following this “Golden Rule” of assisting with words immediately can eliminate the struggle of reading and enhance confidence in reading ability (Community Psychiatric Centers, 2015). This, in turn, reinforces that reading is a fun and rewarding experience we enjoy, rather than something that is difficult and should be avoided.

Recognize Individuality and Achievement

o   Give Praise

o   Emphasize Strengths

Give praise for a job well done and emphasize their strengths (Community Psychiatric Centers, 2015). As previously mentioned, children with dyslexia can suffer from confidence issues related to their learning differences that extend beyond their academic skills. It is important to emphasize their individual strengths to ensure they develop an awareness of them and positive self-identification with natural abilities (Community Psychiatric Centers, 2015). Ensuring adequate praise for a job well done will encourage their future participation in more challenging activities.

References

Caylak, E. (2011). The Auditory Temporal Processing Deficit Theory in Children with Developmental Dyslexia. Journal of Pediatric Neurology Vol .9 Issue .2, p. 151-168. Retrieved from http://search.proquest.com.libproxy.edmc.edu/docview/1314798978?pq-origsite=summon&http://search.proquest.com/healthcomplete/

Christmann, C.  Lachmann, T & Steinbrink, S. (2015). Evidence for a General Auditory Processing Deficit in Developmental Dyslexia From a Discrimination Paradigm Using Speech Versus Nonspeech Sounds Matched in Complexity. Journal of Speech-Language and Hearing Research (Impact Factor: 2.07). 12/2014; 58(1). DOI: 10.1044/2014_JSLHR-L-14-0174. Retrieved from https://www.sowi.uni-kl.de/fileadmin/frueh/publications/pub2015/Christmann_et__al___2015__in_JSLHR.pdf

Community Psychiatric Centers. (2015). Strategies to Treat Dyslexia and Related Learning Difficulties. Community Psychiatric Centers.  Retrieved from http://www.cpcwecare.com/pdf/Dyslexia_Strategies.pdf

International Dyslexia Association. (2015). Dyslexia and the Brain. International Dyslexia Association. Retrieved from http://eida.org/dyslexia-and-the-brain-fact-sheet

World Heritage Encyclopedia. (2015) Developmental Dyslexia. Project Gutenberg Self-Publishing Press & the World Public Library Association. Retrieved from http://www.gutenberg.us/articles/Developmental_dyslexia#cite_note-Huc-Chabrolle-26

Schulte-Körne, G., & Bruder. J. (2010). Clinical neurophysiology of visual and auditory processing in dyslexia: A review. Department of Child and Adolescent Psychiatry and Psychotherapy, University Hospital Munich, Munich, Germany. Retrieved from   http://www.sciencedirect.com.libproxy.edmc.edu/science/article/pii/S1388245710003810

Ramus, F., Rosen, S., Dakin, S., C., Day, B. L., Castellote, J. M., White, S., Frith, U. (2003). Theories of developmental dyslexia: insights from a multiple case study of dyslexic adults. Brain: A Journal of Neurology. Retrieved from http://brain.oxfordjournals.org/content/126/4/841

The Brain: Stress Response Activation and Managing Symptoms

James-Lange Theory of Emotions proposes that emotions are the brain’s interpretation of physiological responses to emotionally provocative stimuli. Darwin proposed that emotions played a significant role in the survival of the species and resulted from similar evolutionary processes as other behaviors and psychological functions did. For example, Emotions like fear invoke actions that either could attempt to overcome the source of fear through fight or run from the source through the flight. In this way, emotions help us process and respond to danger cues that aid in our survival. However, prolonged stress exposure and the constant activation of the Fight or Flight responses are associated with negative effects as well. 

Fight or Flight Response is provided by activity from the sympathetic branch of the autonomic nervous system. Fight or Flight Response is responsible for this biological process that prepares us for action in emergencies including producing stress hormones epinephrine, norepinephrine, and cortisol. In the anticipation of a sudden demand for energy needed to escape danger, a release of epinephrine induces glucose metabolism which in turn starts to metabolize nutrients stored within muscles to become accessible to provide energy. Norepinephrine is also released and increases blood flow to muscles by increasing the flow of blood from the heart (Carlson, 2009, p. 601).       

Norepinephrine is not just a stress hormone released in the body as it is also found secreted in the brain as a neurotransmitter (Carlson, 2009, p. 601). The amygdala is fundamental to emotional processes, especially those relating to fear. The amygdala is a structure located in the interior of temporal lobes (Argosy Online Universities Lecture, 2013). When exposed to stressors a stress response is activated in a pathway from the “central nucleus of the amygdala to the locus coeruleus”, provoking the release of norepinephrine from the brain. It is within the nucleus of the brain stem that the norepinephrine-secreting neurons are located (Carlson, 2009, p. 602). Corticotropin-releasing hormone activates the secretion of ACTH by the anterior pituitary gland in the brain, where it in turn also contributes to some of the emotional responses typically seen in stressful situations (Carlson, 2009, p. 611).

Cortisol, also called glucocorticoids, is a steroid secreted by the adrenal cortex, especially during experiences of stress, and is vital to survival (Carlson, 2009, p. 602). Cortisol is vital in the metabolism of protein and carbohydrates (Carlson, 2009, p. 602). Glucocorticoids have a specific function of helping with the endogenous decomposition of protein and converting it to glucose. This makes fats available for “energy, increase blood flow, and stimulates behavioral responsiveness by affecting the brain” (Carlson, 2009, p. 602). Glucocorticoids also affect the ability of the gonads to sense luteinizing hormone (LH) causing less endogenous production of sex steroid hormones (Carlson, 2009, p. 602). Long-term exposure to stress-induced glucocorticoids has been demonstrated to destroy neurons located in hippocampal formation which is largely associated with cognitive functions such as learning and memory (Carlson, 2009, p. 604). This cell death is caused by the decreases in the uptake of glucose and decreasing the reuptake of glutamate, causing extracellular glutamate which permits calcium to pass through NMDA receptors and kill neurons (Carlson, 2009, p. 604). While Glucocorticoids aid in vital functions prolonged exposure to stress-induced Glucocorticoids is associated with damage to “muscle tissue, steroid diabetes, infertility, inhibition of growth, inhibition of the inflammatory responses and acts to suppress the immune system” (Carlson, 2009).

Prolonged exposure to glucocorticoids works to suppress the immune system (Carlson, 2009, p. 610). Immune suppression from stress can put one at risk for upper respiratory infection and colds (Carlson, 2009, p. 610). Studies indicate that increases in the number of undesirable events and a decreases the number of desirable events in one's life lead to medical illness through immune’s suppression of the immunoglobulin, IgA, in mucous membranes of the nose, mouth, throat, and lungs (Carlson, 2009, p. 610). Immunoglobulin, IgA, is the primary defense against infectious microorganisms that enter the nose or mouth and is affected by mood (Carlson, 2009, p. 610-611). This risk would naturally be increased if one's immune system was already suppressed either by medication, illness, or age.

A stimulus that causes us psychological distress causes the emotions and feelings associated through increases in stress hormones from activation of the “Fight or Flight Response” (Carlson, 2009).  The stress response produces an increase in epinephrine and cortisol which will assist in our escape, but escape from certain life events is not always possible. This leaves the person who is suffering from prolonged exposure to stress at risk for a variety of psychological symptoms, physical illnesses, and brain damage from stress hormone toxicity. Prolonged stress is also associated with increased blood pressure from the increases in stress hormones Norepinephrine and Epinephrine. Over time contributes to cardiovascular disease and a variety of other illnesses like stress disorders. While prolonged overexposure to stress-induced Cortisol or Glucocorticoids is associated with damage to “muscle tissue, steroid diabetes, infertility, inhibition of growth, inhibition of the inflammatory responses, and suppression of the immune system” (Carlson, 2009, p. 603). 

Prolonged exposure to stress can cause brain abnormalities, specifically in the hippocampus and amygdala formations, as seen in studies of patients with PTSD and Stress disorders (Carlson, 2009, p. 607). PTSD is a psychological disorder that results from exposure to a situation of extreme danger and stress and includes distressing symptoms like recurrent dreams or intrusive recollections of trauma that interfere with social activities and cause a feeling of hopelessness (Carlson, 2009, p. 606). The hippocampus plays a vital part in contextual learning including participating in the recognition of the context in which traumatic experiences occur and later helping one distinguish safe from dangerous context (Carlson, 2009, p. 607). One hypothesis suggests that after a person is attacked by something a traumatic trigger is created and stored with traumatic stimuli, however, because of the damage to the hippocampus the ability to distinguish actual traumatic stimuli from similar stimuli is impaired resulting in the activation of the amygdala and the trigger of an emotional response in the face of similar stimuli (Carlson, 2009, p. 607). The prefrontal cortex can exert an inhibitory effect on the amygdala and suppress emotional reactions including the loss of conditioned emotional responses like fear (Carlson, 2009, p. 607). Evidence suggests that actions from prefrontal cortex inhibiting the activity of the amygdala may be liable for emotional reactions and psychological symptoms such as difficulty falling or staying asleep, irritability, outbursts of anger, difficulty in concentrating, and heightened reactions to sudden noises or movements found in persons with PTSD (Carlson, 2009, p. 607-608).

             The above changes in physiological fight or flight response to stress and its effects on cognitive or emotional changes would be similar in most persons who were living under these same stressors, what would likely differ is the length of duration before the onset of symptoms that impair function. If the same stressor was being experienced by a person of the opposite sex or someone much older or younger there might be some differences in how they react emotionally. For example, men may be less tearful and frightened and react with more anger and hostility, while an older or wiser person may feel unabashed and a younger person may be completely depressed and express with hyperactivity and impulsivity, instead of displaying fear and tears. How someone reacts to a stressor is largely based on their ability and resources to deal with the problems, how much social support they have, their previous trauma experiences, personality, temperament, coping skill and lastly, how long the stressor persists.

The four most important behavioral strategies I would suggest one implement immediately to reduce the effects of stress on my body is cared for themselves by making sure they get adequate sleep, sun, nutrition, and exercise.

Getting proper nutrition is important because nutrients play a vital role in neurotransmitter metabolism. Vitamin deficiencies are often found in subjects with depression and being properly nourished supplies the body with minerals such as calcium, iron, magnesium, selenium, and zinc that aid in preventing depression, irritability, and mood swings (Masley, 2013). One of the most important things one can do to combat stress is to work on making sure they have a stock of healthy ready to eat items handy.

Exercise has been shown to increase serotonin function, so exercising can help induce a positive mood (Young, 2007). Several studies have confirmed a relationship between serotonin and mood, indicating that less serotonin correlates with more negative moods (Young, 2007). Studies that have researched exercise and the relationship with mood concluded that exercise has antidepressant and anxiolytic effects, plus increases brain serotonin function (Young, 2007).

Get more sunlight, which can help increase serotonin levels and improve mood.  A studied has demonstrated a “positive correlation between serotonin synthesis and the hours of sunlight received” that day; therefore, increasing my sunlight can also help me fight feelings of depression (Young, 2007).

Why exactly the brain needs to sleep is perhaps poorly understood, but it is clear that decreases in sleep later results in poor cognitive function and psychological symptoms because sleep deprivation impairs cerebral functioning (Carlson, 2009, p. 310). As the brain activity utilities glycogen as fuel for the neural activity it levels drop producing extracellular adenosine chemicals, which then accumulate prohibiting normal neural activity (Carlson, 2009). This chemical toxicity produces both the cognitive and emotional effects that are seen during sleep deprivation and the process that occurs during sleep helps restock glycogen for tomorrow.

Poor sleep results in poor cognitive performance because it is during sleep, particularly during slow-wave and REM state, that our brains restore cognitive function and process information (Carlson, 2009). Increases in mental activity, including dealing with stressors, would cause an increased need for slow-wave sleep to facilitate the consolidation of explicit memories (Carlson, 2009, p. 307). REM sleep is equally important and is believed to play a major role in the development and learning, particularly the consolidation of long-term memories and implicit memories (Carlson, 2009, p. 309). Decreased sleep also causes increases in highly reactive oxidizing agents called free radicals within the brain (Carlson, 2009, p. 307). During a process called oxidative stress, free radicals can bind with electrons from other molecules and damage the cells that they inhabit (Carlson, 2009, p. 307). The decreased metabolic rate during slow-wave sleep allows for the restorative mechanisms to eliminate free radicals before damage occurs (Carlson, 2009, p. 307). Clearly, getting enough regular sleep will improve my cognitive function and emotional well-being.

The most important skill one must demonstrate to implement these is time management.

References

Carlson, N. R. (2009). Physiology of Behavior, 10th Edition. Pearson Learning Solutions. VitalBook file.

Mills, H.  Reiss, N.  Dombeck, M. (2008). Cognitive Therapy Techniques for Stress Reduction.  MentalHelp.  Retrieved from http://www.mentalhelp.net/poc/view_doc.php?type=doc&id=15667&cn=117

Masley, J. (February, March 2005). The role of exercise, nutrition, and sleep in the battle against depression. Mental Health Matters. 2(5,6). Gratiot Medical Center: An Affiliate of MidMichigan Health. http://fhpcc.com/PDFs/RolesAgainstDepression.pdf

Young, S. M. (2007). How To Increase Serotonin in the Human Brain Without Drugs. Journal of Psychiatry Neurosci. 2007 November; 32(6): 394–399. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077351/