Evidence of a neurological basis for developmental dyslexia is reviewed by a researcher from the Cognitive Neurology Laboratory, Department of Neurology, Marseille, France. Beginning with the neuroanatomical findings (cortical malformations - ectopias and dysplasias, and absence of normal asymmetry of the planum temporale) of the Boston school (Galaburda et al, 1985, 1989; Cohen et al, 1989), and interhemispheric corpus callosal deficits (Hynd et al, 1995); subsequent areas of investigation covered include the central role of phonological disorders (grapheme-to-phoneme conversion deficit) in dyslexia, an insensitivity to auditory frequency awareness and modulation (Manis et al, 1997); the demonstration of a visual processing deficit (the ‘magnosystem’ theory (Livingston et al, 1991), and ‘dyseidetic’ (Boder, 1973) subgroup); the ‘temporal (rate)-processing’ theory (Tallal and Piercy, 1973), the dyslexics’ inability to process rapidly successive auditory or visual stimuli (a ‘dyschronia’ (Llinas, 1993)); the contribution of electrophysiological studies (event-related potentials, mismatch negativity, P300, and N400 (Taylor, 1995)), brain functional imaging (magnetoencephalography (Salmelin et al, 1996), functional MRI, PET during phonological tasks), and a working hypothesis and method of remediation based on the temporal processing deficit theory. Evidence points to a multi-system deficit related to temporal processing. The brain of dyslexics is unable to process stimuli presented in rapid succession, which accounts in part for the perceptual, motor, and cognitive impairments frequently associated with learning disorders. Recently proposed training methods include acoustically modified speech to correct the temporal processing deficit described in dyslexics (Merzenich et al, 1996; Tallal et al, 1996). 
COMMENT. Developmental dyslexia is defined as a neurologically-based, often familial, disorder which interferes with the acquisition and processing of language. Dyslexia is one of several distinct learning disabilities. It is a specific language-based disorder of constitutional origin, characterized by difficulties in single word decoding that reflect insufficient phonological processing. (See Millichap JG. Attention Deficit Hyperactivity and Learning Disorders. PNB Publ, Revised 2001, for definitions and references to dyslexia, LD, and ADHD). Several methods of reading remediation have been reviewed by educators, including multisensory, modified alphabets, language-experience, individualized reading, synthetic phonics, linguistic decoding, and phonics systems (Millichap N, 1986). The multisensory approach to treatment of dyslexia is the most usual remediation employed by educators (Pavoni B, 2000).
The theory that dyslexia is due to an immaturity of cerebral function is supported by the pathological and neuroimaging evidence of developmental cerebral anomalies and electrophysiological studies. The anatomical location of the anomalies strongly supports the “phonological-linguistic,” or deficient speech sound and decoding theory of dyslexia (Denckla MB, In Progress in Pediatric Neurology II. PNB Publ, 1994;p174). The left temporal-parietal area appears to be most critical in location of normal reading ability, but additional areas of the left hemisphere may be involved also. Some reports of acquired dyslexia following surgery on the brain have involved the left frontal lobe. A “disconnection theory” for dyslexia, involving impaired relays between the anterior and posterior areas of the left brain, has been proposed based on PET studies (Paulesu et al, 1996).
Dyslexia occurs in 5 to 10% of school children, at all levels of intelligence, from superior to low normal. Dyslexia may be an isolated abnormality or may be associated with other learning disabilities. Reading and spelling disability overlaps with ADHD and shows similar genetic characteristics but different brain localizations. Anatomically, left hemisphere deficits underly reading and other learning disabilities, whereas the right frontal lobe is involved in ADHD.