Dyslexia is a learning disability characterized by an inability to read properly in the absence of any form of mental retardation or lack of intelligence. Common features of the condition include difficulty with manipulation of sounds, spelling, and/or rapid visual/verbal responding. However, these symptoms appear in varying degrees of severity among affected individuals. Of all the forms of dyslexia, the primary form can be hereditary in nature. This type of dyslexia results from a dysfunction in the left cerebral cortex, as opposed to damage to the brain seen in trauma dyslexia. Primary dyslexia is seen more often in boys than girls. Development dyslexia is yet another type of dyslexia resulting from defects in hormonal development in the early stages of fetal development.

Dyslexia is diagnosed based on tests that assess the child's functional reading level and compare it to the reading potential. As in all developmental disorders, early intervention is important for effective management of dyslexia. Special teaching methods and a modified educational environment that meets the specific needs of dyslexic students can make a significant impact. Children who undergo an early remediation program, and who have a supportive home environment have a good prognosis.

The underlying physiologic basis for dyslexia is purported to be abnormal cortical development occurring before the sixth month of fetal brain development. Twin studies have shown a definite genetic basis to at least some forms of dyslexia. Studies have identified several loci and candidate genes that have been implicated in the condition. These include DYX1C1 gene on chromosome 15 (susceptibility to dyslexia1); susceptibility loci on chromosome 6p22, chromosome 2p16-p15, chromosome 3p12-q13, chromosome 18p11.2, chromosome 1p36-p34, and chromosome Xq27.3.