Visual cortex · Grey Matter
The visual cortex is the part of the occipital lobe, at the back of the brain, that receives the signals from the eyes (relayed through the thalamus) and builds them into what is seen.
Visual cortex. The visual cortex is the part of the occipital lobe, at the back of the brain, that receives the signals from the eyes (relayed through the thalamus) and builds them into what is seen.
The primary visual cortex (V1) lies along the calcarine fissure on the inner face of each occipital lobe, and each hemisphere sees the opposite half of the visual field. Its defining property is retinotopy: neighbouring points in the visual field are handled by neighbouring patches of cortex, so the visual field is laid out across the cortical sheet like a distorted map, with the centre of gaze given far more cortex than the periphery. Beyond V1 a chain of further areas (V2, V3, V3A, motion area MT and others) extracts edges, motion, colour and objects.
Retinotopy is what makes the visual cortex readable from outside. A disturbance that moves across the cortex at a steady speed shows up as a percept that moves across the visual field in the same pattern, which is how the slow march of a migraine aura was traced to the cortex.
It is one of the regions where perturbations of excitability are best studied. Visual auras, occipital seizures and visual stimuli that trigger seizures in photosensitive people all involve this region.
This theme follows a perturbation in visual cortex to three broad fates (a simplification, useful as a map): it fades, it becomes a slow wave of spreading depression, or it becomes a fast synchronous discharge.
A map drawn on a rubber sheet is the picture of retinotopy.
Every street keeps its neighbours, but the city centre has been stretched to cover most of the sheet.
Questions: Why does each hemisphere's visual cortex see the opposite half of the world with both eyes? Each retina is split down the middle: its nasal half sees the outer part of the field on its own side, its temporal half the inner part toward the other side. At the chiasm the nasal fibres cross and the temporal ones stay, so the left optic tract collects everything both eyes see of the right half of the world, and the right tract the left half. That arrangement brings the two eyes' views of the same point to the same hemisphere, which is what the visual cortex needs to compare them and see depth. How can a seizure that starts in the visual cortex spread to both hemispheres? A focal seizure in the occipital lobe first produces what that cortex makes, typically coloured lights or shapes, and it can spread along the cortex to neighbouring areas. It becomes bilateral when the discharge recruits networks that reach both hemispheres, above all the loops between cortex and thalamus: imaging during focal to bilateral tonic-clonic seizures shows the thalamus becoming involved at the moment of spread, and the thalamus relays the rhythm to widespread cortex on both sides. How far a given seizure spreads depends on how well inhibition along the way holds. Why does a stroke in the left occipital lobe blind the right half of both eyes? After the chiasm, the left visual pathway carries the right half of the visual field from both eyes, so destroying the left visual cortex removes that half from each eye's view: a right homonymous hemianopia. Covering one eye does not change the defect, which is how it is told apart from damage to an eye or an optic nerve. With an occipital stroke the central few degrees are often spared, because the occipital pole where central vision is mapped often also receives blood from the middle cerebral artery. Why does imagining or remembering a scene activate the visual cortex? A visual memory is stored largely in the visual areas that processed it, so recalling it means reactivating part of the same cortical pattern. Imaging found that imagined objects activate visual cortex, in some studies even the primary visual cortex, in a pattern that follows the size of the imagined object. The overlap is partial: some patients with damaged visual cortex still imagine well, so imagery relies on higher visual areas and memory more than on V1 itself. What does a seizure in the visual cortex look like from the inside? A seizure in the visual cortex makes that cortex produce what it normally produces, only without input from the eyes, so it is seen as light. The typical form is small, brightly coloured circles or spots, often in the half of the visual field opposite the seizing hemisphere, appearing within seconds and lasting seconds to a few minutes. Some seizures cause a patch of blindness instead, and if the discharge spreads forward, the seizure takes on the signs of the areas it reaches. Why is the primary visual cortex called area 17? In 1909 Korbinian Brodmann stained slices of cortex and found that the thickness and cell makeup of its layers change at sharp borders, and he divided the cortex into 52 numbered areas by that structure alone. The numbers follow the order in which he examined the areas, so neighbours can have distant numbers and the numbers carry no meaning in themselves. They stuck because the borders often coincide with functions: area 17 is the primary visual cortex, 4 the primary motor cortex, 3, 1 and 2 the somatosensory cortex, 41 and 42 the primary auditory cortex, 44 and 45 Broca's area. What can someone who is blind from damage to both visual cortices still do with their eyes? The pupils still react to light, because that reflex runs through the midbrain and never needs the cortex, and the eyes themselves are healthy. Some patients show blindsight: they report seeing nothing, yet point to a light or detect movement in the blind field above chance, through pathways that reach higher visual areas through the superior colliculus and the thalamus without passing V1. Others, in Anton syndrome, deny being blind at all and describe surroundings they cannot see, a failure of awareness added to the loss of vision. Why can light flashing at 15 to 25 times a second trigger seizures in photosensitive people? Each flash drives large numbers of neurons in the visual cortex at the same instant, so a rhythmic flash imposes synchrony from outside, and in a cortex prone to synchronise this can grow into a self-sustaining discharge. Flash rates of about 15 to 25 per second are the most provocative, red and high-contrast patterns are worse, and the risk grows with how much of the visual field the stimulus fills. Why some brains respond this way is only partly known, with a genetic contribution, and photosensitivity is most common in children and adolescents. Why does a migraine aura drift slowly across the visual field? The visual cortex is a map: neighbouring points of the visual field are handled by neighbouring patches of cortex. A wave of spreading depression crossing that map at about 3 mm per minute therefore produces a disturbance that crosses the visual field in the same order, a flickering edge (the wave front) followed by a blind patch (the depressed tissue behind it). Charting his own auras, Lashley estimated in 1941 that the underlying process moved at about 3 mm per minute, and functional MRI in 2001 showed a change in the occipital cortex advancing at about 3.5 mm per minute in step with a subject's aura. Why does a migraine scotoma grow as it moves toward the edge of vision? The visual cortex gives the centre of gaze far more surface than the periphery, so each millimetre of cortex near the map of the centre covers a tiny angle of the visual field and each millimetre near the map of the periphery covers a large one. A wave of spreading depression crossing the cortex at a steady few millimetres per minute therefore appears to speed up and widen as it moves outward through the visual field. The usual pattern, a small flickering spot near the centre that grows into a wide arc drifting to the edge over 5 to 20 minutes, is what a constant-speed wave on that distorted map predicts.