Dyslexia is an unexpected impairment in reading and spelling despite a normal intellect.
Description
Dyslexia was first described by Hinshelwood in 1896. Orton originally hypothesized that dyslexia results from a dysfunction in visual memory and visual perception due to a delayment in maturation. Most dyslexics also display poor writing ability. Dyslexia is a classical primary reading disorder and should be differentiated from secondary disorders such as mental retardation, educational or environmental deprivation, or physical/organic diseases. The disorder results as a combination of genetic and environmental causes, which can induce variations in the behavioral, cognitive, and physiological measures related to reading disability. Dyslexia was previously called congenital word blindness. Dyslexia is a reading disorder, not caused by lowered motivation, inadequate learning opportunity or any overt neurological disability. Reading is a complex process which involves multiple systems to process the information cognitively and physiologically. In simple terms reading typically begins with a visual sensation stimuli and processing the text via the visual pathway in the brain (from the retina in the eye, the impulse goes in the brain to the lateral geniculate nuclei and primary visual cortex, the occipital lobe, located in the back of the head, which functions to process and integrate incoming visual information). Input information from vision is probably integrated with other neuronal systems that include language-specific rules, learned information and symbolic images into components of language thinking related to reading. Reading-related thinking is correlated with high activity in the left-hemisphere cortical regions, and language processing centers in the brain. Additionally, learning to read is also related to the learning process, which is mediated by the cerebellum and on relay feedback mechanisms between related areas of the brain.
Deficits in reading may stem from disruptions of simple sensory impairments to more complex problems involving thinking related to language. There are several subtypes of dyslexias and they can be categorized as either central or peripheral dyslexias (of which there are two, attentional dyslexia and neglect dyslexia), which result from impairment to brain processes that are capable of converting letters on the page into visual word forms. There are two types of peripheral dyslexias called attentional dyslexia, and neglect dyslexia. The attentional dyslexia subtype is a rare disorder of attention control, typically correlated with damage to the left parietal lobe (located on the sides of the head). The attentional dyslexia causes an impairment of reading words in sentences, since the defect causes many words to be visible at the same time. Neglect dyslexia is usually due to brain damage, and causes an impairment of reading because the affected person misidentifies letters in certain spatial regions of either a word or a group of words. The defect for neglect dyslexia subtype is associated with the right parietal lobe. Neglect dyslexia can be further divided into left neglect dyslexia and right neglect dyslexia. In the left neglect dyslexia subtype, the affected person experiences difficulty reading initial letters of the word, which may cause a letter(s) to be substituted, omitted or added. The right neglect dyslexia subtype causes a patient to have letter errors at the end of the word.
Letter-by-letter reading (LBL, pure alexia, or pure word blindness) is another form of peripheral dyslexia causing patients to have very slow reading performance with large effects on word length and response time. There is damage to the prestriate cortex of the occipital cortex and most patients also have a dense right visual field deficit. The damage impairs the word-form system in an abnormal way so that written words seem as random letter strings.
Central dyslexias are typically caused by disruption to neuronal processes correlated with sound analysis and meaning of written words. There are two major subtypes of central dyslexias which either impair semantic reading or nonsemantic reading. Semantic reading dyslexia is also referred to as deep and phonologic dyslexia. Semantic reading is due to extensive damage to the left hemisphere which results in a deficit whereby patients can only assemble the pronunciation of a word by first assessing its meaning. Affected individuals also make visual errors when reading. Nonsemantic reading, due to damage of the left temporal lobe causes patients to have difficulty reading exception words (i.e. shove), but can read correctly words that are common and similar (i.e. love).
Demographics
It is thought that dyslexia is the most common neurobehavioral disorder affecting children. The prevalence (existing cases) ranges from 5-10% of school-aged children (school and clinic identified) in the United States. However, these rates may be significantly more (up to 17.5%) in unselected populations. Research indicates that dyslexia is a chronic and persistent disorder. Evidence concerning gender predilection remains controversial. Dyslexia may also co-occur with another disorder called attention deficit/hyperactivity disorder (ADHD, 40% comorbidity). Dyslexia affects approximately 80% of children identified as manifesting a learning disorder.
Causes and symptoms
Persons affected with dyslexia have dysfunction developing an awareness of spoken and written words and segmenting smaller units of sound that are essential in an alphabetic language like English. Patients lose the ability to link and map printed symbols (letters) to sound.
Dyslexia runs in families. Studies demonstrate concordance rates of 68% for monozygotic twins and 37% for dizygote twins (Colorado Twin Study of Reading Disability). However, the genetic transmission is not simple and does not follow classical knowledge of trait heritability. Findings suggest that several genetic factors determine reading ability and the interactions of some or all factors determine the ultimate ability to read.
Evidence from neurobiological research utilizing high resolution imaging techniques, and brain measurement studies indicate differences in left temporo-parieto-occipital brain regions in dyslexic patients when compared to nonimpaired readers. Furthermore, evidence using functional brain imaging techniques in adult and children with dyslexia demonstrates a failure of normal left hemisphere posterior brain systems during reading with increased brain activation in frontal regions. This data indicates that impairment of posterior reading systems results in a disruption of the smoothly functioning and integrated reading system seen in nonimpaired persons. The impairment of posterior reading systems causes dyslexic persons to shift to ancillary neuronal systems to compensate for the deficit. It is the impairment in the posterior reading systems that prevents the development of skilled reading. Postmortem studies (confirmed in live subjects using MRI imaging) indicate a lack of symmetry in language-associated regions in the brain. The abnormal symmetry is associated with the common linguistic deficits that are characteristic of dyslexia.
The specific signs of dyslexia in both adults and school-aged children are similar. Patients exhibit inaccurate and labored decoding, word recognition, and text reading. They also exhibit difficulties in spelling and remain slow readers. Typical early symptoms can include difficulty playing rhyming games and problems with learning numbers and letters. Children often avoid reading independently and are unusually happy at the opportunity for parents to read to them.
Diagnosis
All cases and ages are diagnosed clinically by a combination of careful medical history, observation and psychological testing. There is no one test that is sufficient to render a definitive diagnosis. Rather, the diagnosis is made based on the results of all the clinical data attained. Dyslexia can be distinguished from other learning disorders by identifying the phonologic deficit. Family history and collateral data obtained from school and test results are essential. Tests to determine attention, memory, intelligence and math and language skills may be administered to establish the diagnosis.
Treatment team
The treatment team can consist of a neurologist, a pediatrician, and special education instructors. A clinical psychologist can perform psychological assessments (psychometric testing) to help establish the diagnosis. School and/or college counselors also comprise part of an effective and integrated treatment team.
Treatment
The management for dyslexic patients is lifelong. Early identification and intervention (remediation) of reading deficits involves specialist education. Intervention programs must systematically and explicitly teach phonics ensuring a clear understanding of how letters are linked to sounds (phonemes) and spelling. Typically individualized teaching is recommended to provide a balanced remedial program providing systematic instruction on phonemic awareness, phonics, vocabulary fluency and comprehension strategies. A well-integrated treatment program also includes opportunities for writing, reading, and discussing literature. A well-executed treatment program considers each component of the reading process to improve phonemic awareness and the ability to manipulate speech sounds.
Treatment for older persons (high school, college, and graduate school) is accommodation rather than remediation. College students require extra time with examination and reading/writing assignments. Other accommodations include recorded books, tape recorders in the classroom, tutorial services, alternatives to multiple choice questions and computer availability with spelling checkers.
Recovery and rehabilitation
Rehabilitation for dyslexics is a lifelong process. Early intervention in younger patients consists of a highly structured, integrated, systematic and explicit treatment program. A balanced treatment program should include the meaning and phonetic approaches to reading to ultimately improve language development (since dyslexia is a language-based disorder.) The program should allow for personalized instruction. Older persons require accommodation in college and at work versus remediation.
Clinical trials
There are two current clinical research trials entitled: Comprehensive Program to Improve Reading and Writing Skills in At-Risk and Dyslexic Children; and Using MRI to Evaluate Instructional Programs for Children with Developmental Dyslexia. Information can be obtained from http://www.ClinicalTrails.com.
Prognosis
Dyslexia is a lifelong disorder, but improvement is possible. Multiple learning disabilities can be expected, since the brain connections for reading, spelling, listening, speaking, and writing are part of the linguistic system. The prognosis can ultimately depend on associated comorbidities (other disorders associated with the primary disorder), early detection and intervention, and an intensive and comprehensive treatment plan.
Special concerns
Early recognition, intervention, and family members are important. Remediation programs must be delivered by highly-trained specialists, and treatment should be individualized.
BOOKS
Behrman, Richard, E., et al., eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia: Saunders, 2004.
PERIODICALS
Brow, W. E., A. L. Reiss, and S. Eliez. "Preliminary evidence of widespread morphological variations of the brain in dyslexia." Neurology 56, no. 6 (March 2001).
Bub, Danial. "Alexia and related reading disorders." Neurological clinics 21, no. 2 (May 2003).
Francks, C., and L. Macphie. "The genetic basis of dyslexia." The Lancet Neurology 1, no. 8 (December 2002).
Olitsky, Scott E. "Reading disorders in children." Pediatric Clinics of North America 50, no. 1 (February 2003).
Wood, F., and E. L. Grigorenko. "Emerging Issues in the Genetics of Dyslexia: A Methodological Preview." Journal of Learning Disabilities 34, no. 6 (November-December 2001).
The National Center for Learning Disabilities. 381 Park Avenue South, Suite 1401, New York, NY 10016. (212) 545-7510 or 888-575-7373; Fax: (212) 545-9665. <http://www.ncld.org>.
The International Dyslexia Association. 8600 LaSalle Road, Baltimore, MD 21286-2044. 410-296-0232 or 800-ABCD123; Fax: 410-321-5069. <http://www.interdys.org>.
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