Background: Magnocellular deficit theory is among the different hypotheses that have been proposed to explain the pathophysiology of developmental dyslexia (DD). Dysfunction of the magnocellular system in DD has been ...Background: Magnocellular deficit theory is among the different hypotheses that have been proposed to explain the pathophysiology of developmental dyslexia (DD). Dysfunction of the magnocellular system in DD has been investigated using mainly visual evoked potentials (VEPs), particularly transient VEPs, although recently abnormal steady-state VEPs have also been reported. The brain regions responsible for the abnormal VEPs in DD have yet to be elucidated, however. In this study, we performed functional magnetic resonance imaging and electroencephalography (fMRI-EEG) simultaneously to elucidate the brain areas that were found in a previous study to be activated through stimulation of the magnocellular system, and then investigated the mechanism involved in the dysfunction seen in DD.Methods: Subjects were 20 healthy individuals (TYP group;13 men, 7 women;mean ± standard deviation age, 26.3 ± 5.53 years) and 2 men with DD (aged 42 and 30 years). Images of brain activity were acquired with 3-Tesla MRI while the viewing the reversal of low-spatial frequency and low-contrast black-and-white sinusoidal gratings. EEG was recorded concurrently to obtain steady-state VEPs.Results: Stimulus frequency-dependent VEPs were observed in the posterior region of the brain in the TYP group;however, VEP amplitudes in both DD patients were clearly smaller than those in TYP. fMRI images revealed that both the primary and secondary visual cortices were activated by black-and- white sinusoidal gratings in the TYP group, whereas activity in the visual cortex overall was reduced in both DD patients.Conclusions: Present low spatial and high reversal frequency visual stimuli activated the primary visual cortex presumably through predominant activation of the magnocellular pathway. This finding indicates that some cases of adult patients of DD involve impairment of the visual magnocellular system.展开更多
文摘Background: Magnocellular deficit theory is among the different hypotheses that have been proposed to explain the pathophysiology of developmental dyslexia (DD). Dysfunction of the magnocellular system in DD has been investigated using mainly visual evoked potentials (VEPs), particularly transient VEPs, although recently abnormal steady-state VEPs have also been reported. The brain regions responsible for the abnormal VEPs in DD have yet to be elucidated, however. In this study, we performed functional magnetic resonance imaging and electroencephalography (fMRI-EEG) simultaneously to elucidate the brain areas that were found in a previous study to be activated through stimulation of the magnocellular system, and then investigated the mechanism involved in the dysfunction seen in DD.Methods: Subjects were 20 healthy individuals (TYP group;13 men, 7 women;mean ± standard deviation age, 26.3 ± 5.53 years) and 2 men with DD (aged 42 and 30 years). Images of brain activity were acquired with 3-Tesla MRI while the viewing the reversal of low-spatial frequency and low-contrast black-and-white sinusoidal gratings. EEG was recorded concurrently to obtain steady-state VEPs.Results: Stimulus frequency-dependent VEPs were observed in the posterior region of the brain in the TYP group;however, VEP amplitudes in both DD patients were clearly smaller than those in TYP. fMRI images revealed that both the primary and secondary visual cortices were activated by black-and- white sinusoidal gratings in the TYP group, whereas activity in the visual cortex overall was reduced in both DD patients.Conclusions: Present low spatial and high reversal frequency visual stimuli activated the primary visual cortex presumably through predominant activation of the magnocellular pathway. This finding indicates that some cases of adult patients of DD involve impairment of the visual magnocellular system.
