The relationship between brain activity and reading performance was examined to test the hypothesis that dyslexia involves a deficit in a specific visual pathway known as the magnocellular (M) pathway. Functional magnetic resonance imaging was used to measure brain activity in dyslexic and control subjects in conditions designed to preferentially stimulate the M pathway. Dyslexics showed reduced activity compared with controls both in the primary visual cortex and in a secondary cortical visual area (MT؉) that is believed to receive a strong M pathway input. Most importantly, significant correlations were found between individual differences in reading rate and brain activity. These results support the hypothesis for an M pathway abnormality in dyslexia and imply a strong relationship between the integrity of the M pathway and reading ability.Developmental dyslexia can be defined as an unexpectedly low reading ability given an individual's intelligence quotient that cannot be explained by other factors such as motivation, learning opportunity, sensory acuity, or brain injury. Estimates of dyslexia's prevalence range from 3 to 9% (1, 2). The etiology of dyslexia as well as specific sensory deficits in dyslexia remain controversial.A particularly controversial issue is whether dyslexia involves a visual deficit. One subdivision of the visual system, known as the magnocellular (M) pathway, begins at the level of the ganglion cells in the retina, projects through the M layers of the lateral geniculate nucleus, and terminates in the primary visual cortex (V1) (3, 4). There are several lines of evidence for an M pathway deficit in dyslexia, including abnormally small cells in the M layers of the LGN (5), impaired perceptual performance (6-11), and reduced electrophysiological responses (5, 12-14) to stimuli processed mainly by the M pathway. Furthermore, a recent functional MRI (fMRI) study (15) reported that dyslexics showed essentially no significant activity in a cortical visual area (MTϩ that consists of area MT along with adjacent motion sensitive areas) that is believed to receive a strong M pathway input. Several perceptual and electrophysiological studies have, however, failed to find evidence for an M pathway deficit (16)(17)(18)(19)(20).Our study was designed to test two predictions of the M deficit hypothesis. First, the degree of the M pathway deficit should be strongly correlated with the severity of reading difficulty. Second, it should be possible to demonstrate physiological differences at least as early as V1.
MATERIALS AND METHODSBlood oxygenation level-dependent fMRI (21-23; for review, see ref. 24) was used to measure brain activity in five dyslexic and five control subjects. Each subject participated in several scanning sessions: one to obtain a standard, high resolution, anatomical scan, one to define the early visual areas including V1, and at least three more sessions to measure fMRI response amplitude as a function of stimulus contrast (contrast is defined as the maximum minus the mini...