Neuronal asymmetries in primary visual cortex of dyslexic and nondyslexic brains

Dyslexic brains exhibit histologic changes in the magnocellular (magno) cells of the lateral geniculate nucleus, and consistent with these changes, dyslexics demonstrate abnormal visually evoked potentials and brain activation to magnospecific stimuli. The current study was aimed at determining whether these findings were associated with changes in the primary visual cortex with the prediction that magno components of this cortex would be affected. We measured crosssectional neuronal areas in primary visual cortex (area 17) in dyslexic and nondyslexic autopsy specimens. There was a significant interaction between hemispheres and diagnostic category; ie, nondyslexic brains had larger neurons in the left hemisphere, whereas dyslexic brains had no asymmetry. On the other hand, cell layers associated with magno input from the lateral geniculate nucleus did not show consistent changes in dyslexic brains. Thus, there is a neuronal size asymmetry in favor of the left primary visual cortex in nondyslexics that is absent in dyslexic brains. This is yet another example of anomalous expression of cerebral asymmetry in dyslexia similar to that of the planum temporale, which in our view reflects abnormality in circuits involved in reading. Jenner AR, Rosen GD, Galaburda AM. Neuronal asymmetries in primary visual cortex of dyslexic and nondyslexic brains. Ann Neurol 1999;46:189‐196 Developmental dyslexia may be defined as the relatively selective impairment of reading despite normal intelligence, sensory acuity, motivation, and instruction. In the past 20 years much of the research on this subject has focused on language function. In recent years, however, there has been growing interest in exploring more fundamental sensory processing problems, including auditory and visual perception, which in turn may contribute to the well-documented linguistic deficits. 1‐6 Psychophysical studies have suggested that dyslexics process transient visual stimuli with low-contrast and high-repetition rates (ie, the domain of the magnocellular pathway) more slowly than nondyslexics. The pathway for processing sustained, high-contrast, slow stimuli, the parvocellular pathway, may be spared. 2,7‐13 An anatomical and visual evoked potential (VEP) study provided additional evidence that dyslexics showed a specific defect affecting the magnocellular pathway. Livingstone and colleagues 3 found that, whereas the VEPs of dyslexics and nondyslexics were similar for high-contrast conditions, there was a delay in the early wave (from 0 to N100) in the dyslexic response to lowcontrast stimuli. This delay is thought to implicate abnormal activity early in the magnocellular visual pathway from the retina up to visual area 1 (V1; also area 17 of Brodmann). Consistent with these results, quantitative analysis has shown that the neurons in the magnocellular layers of the lateral geniculate nucleus (LGN) in dyslexics were, on average, 27% smaller than those of the nondyslexics, but there were no measurable differences in the neurons of the parvocellular layers. Additional physiological studies have explored the nature of the visual deficit in dyslexics. Several of these studies 14‐17 have measured VEPs using stimuli that are