This study was designed to determine whether cortical motion processing abnormalities are present in individuals with migraine. Performance was measured using a visual motion coherence task (motion coherence perimetry, MCP) thought to depend on the operation of cortical area V5. Motion coherence thresholds were measured using stimuli composed of moving dots at 17 locations in the central +/- 20 degrees of visual field. Pre-cortical visual function was also measured using frequency doubling perimetry (FDP) at the same 17 locations. Several migraine subjects demonstrated significant pre-cortical visual functional abnormalities, however, most subjects had normal visual fields measured with FDP. Abnormal MCP performance was measured in 15 of 19 migraine-with-aura subjects, and 11 of 17 migraine-without-aura subjects. A decreased ability to detect coherent motion may possibly be explained by an increase in baseline neuronal noise, such as would be consistent with the concept of cortical hyperexcitability in migraine.

When simulated patients made errors, the accuracy and precision of sensitivity estimates were poor when the initial estimate of threshold either overestimated or underestimated the true threshold. This was particularly so for FT and SQ. ZEST demonstrated more consistent error properties than the other two measures.

Previous studies have identified anomalies of cortical visual processing in migraineurs that appear to extend beyond V1. Migraineurs respond differently than controls to transcranial magnetic stimulation of V5, and can demonstrate impairments of global motion processing. This study was designed to assess the integrity of intermediate stages of both motion and form processing in people with migraine. We measured the ability to integrate local orientation information into a global form percept, and to integrate local motion information into a global motion percept. Control subjects performed significantly better than migraineurs on both tasks, suggesting a diffuse visual cortical processing anomaly in migraine.

Several studies have attributed certain visual perceptual alterations in older adults to a likely decrease in GABA (Gamma Aminobutyric Acid) concentration in visual cortex, an assumption based on findings in aged non-human primates. However, to our knowledge, there is no direct evidence for an age-related decrease in GABA concentration in human visual cortex. Here, we estimated visual cortical GABA levels and Glx (combined estimate of glutamate and glutamine) levels using magnetic resonance spectroscopy. We also measured performance for two visual tasks that are hypothesised to be mediated, at least in part, by GABAergic inhibition: spatial suppression of motion and binocular rivalry. Our results show increased visual cortical GABA levels, and reduced Glx levels, in older adults. Perceptual performance differed between younger and older groups for both tasks. When subjects of all ages were combined, visual cortical GABA levels but not Glx levels correlated with perceptual performance. No relationship was found between perception and GABA levels in dorsolateral prefrontal cortex. Perceptual measures and GABA were not correlated when either age group was considered separately. Our results challenge current assumptions regarding neurobiological changes that occur within the aging human visual cortex and their association with certain age-related changes in visual perception.

It is well established that many visual functions deteriorate with age. Perhaps counter-intuitively, a recent study revealed that older people actually require less time to discriminate the direction of motion of large, high contrast moving stimuli than young adults (L. R. Betts, C. P. Taylor, A. B. Sekuler, & P. J. Bennett, 2005). L. R. Betts et al. (2005) proposed their finding as evidence for a reduction of cortical inhibitory function within the aging visual system. There is some neurophysiological support for this suggestion, as broadening of visual cortical neural tuning consistent with reduced inhibitory function has been observed in older animals. Here we explore the perceptual consequences of center-surround suppression within the healthy aging human visual system and report data from a center-surround contrast discrimination task (the Chubb contrast illusion). We predicted that older observers would demonstrate less center-surround suppression than younger subjects (consistent with reduced inhibition). Our data does not support this prediction as perceived contrast was altered more by surround modulation in the older than younger group (t(33) = 2.53, p = 0.02). A possible explanation for our findings is a decrease in perceptual brightness induction in the elderly group. Brightness induction relies on neural synchronization which might be disrupted by aging.

Foveal and midperipheral dysfunction of both M and P pathways was identified in people with glaucoma, in areas of relatively normal visual field performance. These findings are supportive of nonselective neural adaptation abnormalities in early glaucoma.

Normal aging results in a reduction of contrast sensitivity for the low-spatial-frequency-sensitive components of both the M and P pathways. Glaucoma results in a further reduction of sensitivity that is not selective for M or P function. The low-spatial-frequency-sensitive channels of both pathways, which are presumably mediated by cells with larger receptive fields, are approximately equivalently impaired in early glaucoma.

BackgroundThe pathophysiology of migraine is incompletely understood, but evidence points to hyper-responsivity of cortical neurons being a key feature. The basis of hyper-responsiveness is not clear, with an excitability imbalance potentially arising from either reduced inhibition or increased excitation. In this study, we measure centre-surround contrast suppression in people with migraine as a perceptual analogue of the interplay between inhibition and excitation in cortical areas responsible for vision. We predicted that reduced inhibitory function in migraine would reduce perceptual surround suppression. Recent models of neuronal surround suppression incorporate excitatory feedback that drives surround inhibition. Consequently, an increase in excitation predicts an increase in perceptual surround suppression.Methods and FindingsTwenty-six people with migraine and twenty approximately age- and gender-matched non-headache controls participated. The perceived contrast of a central sinusoidal grating patch (4 c/deg stationary grating, or 2 c/deg drifting at 2 deg/sec, 40% contrast) was measured in the presence and absence of a 95% contrast annular grating (same orientation, spatial frequency, and drift rate). For the static grating, similar surround suppression strength was present in control and migraine groups with the presence of the surround resulting in the central patch appearing to be 72% and 65% of its true contrast for control and migraine groups respectively (t(44) = 0.81, p = 0.42). For the drifting stimulus, the migraine group showed significantly increased surround suppression (t(44) = 2.86, p<0.01), with perceived contrast being on average 53% of actual contrast for the migraine group and 68% for non-headache controls.ConclusionsIn between migraines, when asymptomatic, visual surround suppression for drifting stimuli is greater in individuals with migraine than in controls. The data provides evidence for a behaviourally measurable imbalance in inhibitory and excitatory visual processes in migraine and is incompatible with a simple model of reduced cortical inhibitory function within the visual system.