DEVELOPMENTAL
DYSLEXIA
Developmental dyslexia, or developmental reading disorder, is defined as a significant impairment in the development of reading and related skills, such as spelling, writing, and reading comprehension, due to problems with phonologic processing despite adequate intelligence and conventional instruction. This disorder frequently occurs in association with other specific learning disabilities, such as disturbances in auditory comprehension, expressive language, articulation, and visual discrimination. It is the most commonly identified learning disorder, now felt to affect the sexes equally and is often present in siblings and other family members.
Because the primary deficit in
developmental dyslexia is in reading and writing, the abnormality is usually
not identified until the first few years of grade school, the time when
children begin to read. Most parents are not aware of any disorder in their
child before this stage. Because it is common and affects skills recently
acquired by man, developmental dyslexia may have had certain advantages in
preliterate societies, because dyslexic persons often have enhanced
visual-spatial and artistic skills.
Etiologic Theories. Early investigators postulated that developmental
dyslexia was caused by a lesion in the left angular gyrus, an area of the brain
in which a lesion in adults produces word blindness. Later, Orton (1925) felt
that the disorder was caused by equipotential visual association areas in the
two cerebral hemispheres actively competing with each other, with one side
seeing a mirror image of the other. Orton was particularly impressed with
reversals of letters and letter sequences in words, the inconsistency of these
errors, and the ability of some dyslexic students to read better with the aid
of a mirror. Emotional problems and improper instruction were also thought to
cause dyslexia.
Past investigations, including
computed tomography, computed evoked electroencephalographic studies, and
postmortem studies of the brain have all provided evidence of a structural
basis for dyslexia. More recently, MRI has demonstrated a variety of structural
changes in the corpus callosum, left temporal lobes, thalamus, caudate,
inferior frontal gyrus, and cerebellum (Pennington, 1999; Eliez, 2000; Brown,
2011; Leonard, 2001; Rae, 2002; Robichon,
2000; Elnakib, 2012).
Historically, Drake (1968) noted
abnormally formed gyri in the parietal regions and ectopic neurons in
the white matter, arrested during their migration to the cerebral cortex.
Examination of a second brain by Galaburda and Kemper (1979) showed cerebral
cortical abnormalities characterized by focal and verrucose dysplasia in the
sensory speech area (Wernicke’s area) and language dominant left cerebral
hemisphere. The third brain examined showed only verrucose dysplasia almost
exclusively confined to the left cerebral hemisphere (Kemper, 1984). Thus examination
of all three brains has demonstrated minor malformations.
Analysis of human malformations and
animal models indicates that the focal and verrucose dysplasia probably arise
during the later stages of neuronal migration to the cerebral cortex, and
appear to result from the migration of neurons into focal areas of cortical
destruction. In man, neuronal migration to the cerebral cortex occurs from the
8th to approximately the 16th week of gestation. Consistent with this timing is
the presence of ectopic neurons in the white matter in two of the three brains
examined. The nature of this postulated destructive process is unknown.
Geschwind and Behan (1982) have noted a
significant clustering of dyslexia, left-handedness, autoimmune disease, and
migraine in persons related to each other, indicating an association between
these disorders.
Currently, it is felt that developmental
dyslexia is a disorder of network connections as demonstrated by Vandermosten
(2012). By using MRI tractography, adults with dyslexia were noted to have a
reduction in the left arcuate fasciculus, which connects the posterior temporal
and frontal areas. This may represent an area of
decreased myelination.
Treatment. Early identification and evaluation of dyslexia
is essential for proper treatment. The optimal educational approach is
multisensory, including phonemic awareness and enhanced phonologic processing,
where virtually all respond. However, given that dyslexia is a lifelong
disorder, many continue to struggle into adulthood when presented with new or
less familiar words or in reading comprehension settings. Treatment should be
aimed at enabling those to overcome deficits where possible and to learn
strategies to circumvent and compensate for difficulties that cannot be
overcome.
