This form of language disorder, unattended by other neurologic signs, is strongly familial, in various series being almost in conformity with an autosomal dominant or sex-linked recessive pattern. Loci on chromosomes 6 and 15 have been implicated but not confirmed. There is also a higher incidence of left-handedness among these persons and members of their families. Shaywitz et al have suggested that the reported predominance of reading disabilities in boys (male-to-female ratios of 2:1 to 5:1) represents a bias in subject selection—many more boys than girls being identified because of associated hyperactivity and other behavioral problems; but to us this does not seem the entire explanation. Our casual clinical experience suggests that there is a genuine and substantial male preponderance. Nonetheless, an estimated 12 to 24 percent of dyslexic children will also have an attention-deficit hyperactivity disorder (ADHD) (see further on).
In the study of dyslexic and dysgraphic children, a number of other apparently congenital developmental abnormalities were documented, such as inadequate perception of space and form (poor performance on form boards and in tasks requiring construction); inadequate perception of size, distance, and temporal sequences and rhythms; and inability to imitate sequences of movements gracefully, as well as slight degrees of clumsiness and reduced proficiency in all motor tasks and games (the clumsy child syndrome as described by Gubbay et al and also by Denckla et al as mentioned earlier in the chapter under “Delays in Motor Development”). These disorders may also occur in brain-injured children; hence there may be considerable difficulty in separating simple delay or arrest in development from a pathologic process in the brain. However, in the majority of dyslexic children these additional features are absent or so subtle as to require special testing for their detection.
A few careful morphometric studies have provided insight into the basis of this disorder. Galaburda and associates studied the brains of 4 males (ages 14 to 32 years) with developmental dyslexia. In each case there were anomalies of the cerebral cortex consisting of minor neuronal ectopias and architectonic dysplasias, located mainly in the perisylvian regions of the left hemisphere. More in conformity with imaging studies noted below, all of the brains were characterized by relative symmetry of the planum temporale, in distinction to the usual pattern of cerebral asymmetry that favors the planum temporale of the left side. Similar changes have been described in 3 women with developmental dyslexia (Humphreys et al). Imaging studies of large numbers of dyslexic patients (as well as some patients with autism and developmental speech delay) have demonstrated an increased prevalence of relative symmetry (reversed or “atypical” asymmetry) of the temporal planes of the two hemispheres (Rosenberger; Hynd et al). It is important to note, however, that not all patients with developmental dyslexia show this anomalous anatomic asymmetry (Rumsey et al). In other studies, a number of variable alterations of cortical organization were found by Casanova and colleagues, most notably, in one case, an enlargement of the minicolumns in the temporal cortex. (A similar developmental change has been found in the brains of individuals with Down syndrome and with autism.)
Leonard and colleagues, using MRI, demonstrated several other gyral anomalies in dyslexic subjects: in the planum temporale and neighboring parietal operculum of both hemispheres, some gyri were missing and others were duplicated. In some dyslexic individuals, the visual evoked to rapid low-contrast stimuli are diminished. This abnormality has been related to a deficit of large neurons in the lateral geniculate bodies (see Livingstone et al).
Specific spelling difficulty probably represents another developmental language disorder, distinct from dyslexia.