Motion-onset visual evoked potentials improve the diagnosis of glaucoma

Abstract

Chronic glaucoma has been shown preferentially to damage larger retinal cells and optic nerve fibres that provide the input to the magnocellular visual pathway. We compared the motion-onset visual evoked potentials (primarily the magnocellular system) with those to standard pattern reversal in 20 patients with bilateral chronic glaucoma. For motion-onset visual evoked potentials, the pattern (isolated 40' checks of 10% contrast) moved in four cardinal directions (varied randomly from trial to trial) at a velocity of 10 deg/s for 20 ms, with an interstimulus interval of 1 s. In pattern-reversal stimulation, the checkerboard reversed at a rate of 2 reversals per second. In 60% of the eyes investigated, the results of both types of visual evoked potentials correlated, showing either normal (27.5%) or increased (32.5%) latencies. In the remaining 40% of the eyes, the normal pattern-reversal visual evoked potential latencies were accompanied by prolonged motion-onset visual evoked potentials. The high occurrence of delayed motion-onset visual evoked potentials in our patients confirms the primary magnocellular loss in chronic glaucoma and suggests that the motion-onset VEPs are suitable for detection of glaucomatous changes.

A primer on motion visual evoked potentials

“…Nevertheless, the idea that glaucoma might be detected using motion VEPs attracted interest. Results by Kubová et al [110] suggest that the amplitude of the N2 is hardly affected by chronic glaucoma, while the latency appears to be a more sensitive indicator of glaucoma than the pattern-reversal P100 latency. In a study by Korth et al [123] both amplitude and latency were affected in patients with open-angle glaucoma.…”

“…Therefore, in some studies a 'virtual electrode' was introduced corresponding to the occipito-temporal electrode with the largest response as determined individually for each subject [e.g., 42, 107,110].…”

Brain activity in visual cortex predicts individual differences in reading performance

“…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)(7)(8)(9)(10)(11), and reduced electrophysiological responses (5,(12)(13)(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.…”

Chromatic-achromatic perimetry in four clinic cases: Glaucoma and diabetes

“…4 ], in agreement with the literature that shows that this mechanism is usually selectively affected by this pathology. [ 20 21 22 23 24 25 26 27 28 29 ] With the G2 patient, all perimetric tests exhibit significant losses in MD and the shape of the visual field is also abnormal [ Fig. 5 ].…”