Dyslexia is a learning disability that makes itself manifest primarily as a difficulty with written language, particularly with reading. It is separate and distinct from reading difficulties resulting from other causes, such as a non-neurological deficiency with vision or hearing, or from poor or inadequate reading instruction. suggests that dyslexia results from differences in how the brain processes written and spoken language. Although dyslexia is thought to be the result of a neurological difference, it is not an intellectual disability. Dyslexia is diagnosed in people of all levels of intelligence. Dyslexia is a learning difficulty which holds no simple definition; psychologists continue to have difficulties providing clear cut answers as to what it is or how it is actually caused.

History

Identified by Oswald Berkhan in 1881, the term 'dyslexia' was later coined in 1887 by Rudolf Berlin, an ophthalmologist practicing in Stuttgart, Germany. He used the term to refer to a case of a young boy who had a severe impairment in learning to read and write in spite of showing typical intellectual and physical abilities in all other respects.

In 1896, W. Pringle Morgan, a British physician, from Seaford, East Sussex, England published a description of a reading-specific learning disorder in a report to the British Medical Journal titled "Congenital Word Blindness". This described the case of a 14-year-old boy who had not yet learned to read, yet showed normal intelligence and was generally adept at other activities typical of children of that age.

During the 1890s and early 1900s, James Hinshelwood, a British ophthalmologist, published a series of articles in medical journals describing similar cases of congenital word blindness, which he defined as "a congenital defect occurring in children with otherwise normal and undamaged brains characterised by a difficulty in learning to read." In his 1917 book Congenital Word Blindness, Hinshelwood asserted that the primary disability was in visual memory for words and letters, and described symptoms including letter reversals, and difficulties with spelling and reading comprehension.

An early researcher in dyslexia was Samuel T. Orton, a neurologist who worked primarily with stroke victims. In 1925 Orton met a boy who could not read and who exhibited symptoms similar to stroke victims who had lost the ability to read. Orton began studying reading difficulties and determined that there was a syndrome unrelated to brain damage that made learning to read difficult. Orton called the condition strephosymbolia (meaning 'twisted signs') to describe his theory that individuals with dyslexia had difficulty associating the visual forms of words with their spoken forms. Orton observed that reading deficits in dyslexia did not seem to stem from strictly visual deficits. He believed the condition was caused by the failure to establish hemispheric dominance in the brain. He also observed that the children he worked with were disproportionately left- or mixed-handed, although this finding has been difficult to replicate. Orton's hypothesis concerning hemispheric specialization was borne out by post-mortem studies in the 1980s and 1990s establishing that the left planum temporale, a brain area associated with language processing, is physically larger than the corresponding right area in the brains of non-dyslexic subjects, but that these brain areas are symmetrical or slightly larger on the right for dyslexic subjects. FMRI imaging studies of children and young adults reported in 2003 provide further support, demonstrating that increases in age and reading level are associated with a suppression of right hemispheric activity.