Several behavioral studies have shown that developmental dyslexics do poorly in tests requiring rapid visual processing. In primates fast, low-contrast visual information is carried by the magnocellular subdivision of the visual pathway, and slow, high-contrast information is carried by the parvocellular division. In this study, we found that dyslexic subjects showed diminished visually evoked potentials to rapid, low-contrast stimuli but normal responses to slow or highcontrast stimuli. The abnormalities in the dyslexic subjects' evoked potentials were consistent with a defect in the magnocellular pathway at the level of visual area 1 or earlier. We then compared the lateral geniculate nuclei from five dyslexic brains to five control brains and found abnormalities in the magnocelular, but not the parvocellular, layers. Studies using auditory and somatosensory tests have shown that dyslexics do poorly in these modalities only when the tests require rapid discriminations. We therefore hypothesize that many cortical systems are similarly divided into a fast and a slow subdivision and that dyslexia specifically affects the fast subdivisions.Developmental dyslexia is the selective impairment of reading skills despite normal intelligence, sensory acuity, motivation, and instruction. Several perceptual studies have suggested that dyslexic subjects process visual information more slowly than normal subjects. The flicker fusion rate, which is the fastest rate at which a contrast reversal of a stimulus can be seen, is abnormally slow in dyslexic children at low spatial frequencies and low contrasts (1). Moreover, such visual abnormalities were reported to be found in >75% of the reading-disabled children tested (2). When two visual stimuli are presented in rapid succession, the two images fuse and appear as a single presentation; the temporal separation necessary to distinguish two presentations measures visual persistence, and this is up to 100 msec longer for dyslexic than for normal children, particularly for low spatial frequency stimuli (3-6). Dyslexic subjects also have trouble distinguishing the order of two rapidly flashed visual stimuli (7). In contrast, dyslexics perform normally on tests having prolonged stimulus presentations (2).These perceptual studies suggest an abnormality in dyslexia affecting some part of the visual system that is fast and transient and has high contrast sensitivity and low spatial selectivity. Exactly these properties characterize the magnocellular subdivision of the visual pathway (8, 9). The primate visual system is composed mainly of two major processing pathways that remain largely segregated and independent throughout the visual system. This subdivision begins in the retina but is most apparent in, and was first discovered in, the lateral geniculate nucleus (LGN), where cells in the ventral, or magnocellular, layers are larger than cells in the dorsal, or parvocellular, layers. In the retina and the LGN, the magno and parvo subdivisions differ physiologically in four major...

We report the neuroanatomical findings in 4 consecutively studied brains of men with developmental dyslexia. The patients, who ranged in age between 14 and 32 years, were diagnosed as dyslexic during life. Nonrighthandedness and several autoimmune and atopic illnesses were present in the personal and family histories. All brains showed developmental anomalies of the cerebral cortex. These consisted of neuronal ectopias and architectonic dysplasias located mainly in perisylvian regions and affecting predominantly the left hemisphere. Furthermore, all brains showed a deviation from the standard pattern of cerebral asymmetry characterized by symmetry of the planum temporale. The neuroanatomical findings in these 4 patients are discussed with reference to developmental cortical anomalies, cerebral asymmetries, reorganization of the brain after early lesions, and the association between learning disorders, left handedness, and diseases of the immune system.

When the landmark patient Phineas Gage died in 1861, no autopsy was performed, but his skull was later recovered. The brain lesion that caused the profound personality changes for which his case became famous has been presumed to have involved the left frontal region, but questions have been raised about the involvement of other regions and about the exact placement of the lesion within the vast frontal territory. Measurements from Gage's skull and modern neuroimaging techniques were used to reconstitute the accident and determine the probable location of the lesion. The damage involved both left and right prefrontal cortices in a pattern that, as confirmed by Gage's modern counterparts, causes a defect in rational decision making and the processing of emotion.

A new cytoarchitectonic study of the human auditory cortex was undertaken in the light of recent knowledge concerning the architecture, fiber connectivity, and physiology of this region in the monkey. The survey of three normative human brains (six hemispheres) processed in whole-brain serial sections disclosed a cytoarchitectonic organization of the cortical auditory region similar to that in the macaque. Unlike the monkey, auditory-related cortex was found in parietal operculum and inferior parietal lobule. Similarities in cortical architectonics between human and monkey brains may provide a rationale for the application of knowledge concerning animal physiology and connectivity to man.