Physiology of Visual Acuity
20-20 is normal vision. In low light vision, there is low resolution despite the high sensitivity thereof. This is due to spatial summation of rods, so 100 rods could merge into many bipolars, in turn converging on ganglion cells, and the unit for resolution is very large, thus acuity being small. The farther a pattern of white and black lines is presented to a person, the less they can distinguish the lines, culminating to a distance when the pattern is seen as a uniform gray. The angle subtended by the detail at minimum acuity is the resolving power, and its reciprocal is the visual acuity. For example, a visual acuity of 1 subtends 1 minute on the retina, that of 2 is 1/2 minutes (30 seconds) of arc. Visual acuity is much better in bright light than dim light, the former reaching 2 with a bright center and surrounding, the latter perhaps having visual acuity of 0.04 (25 minutes on eye). In this case, the stimulus is 1.7 inches (4.3 cm) and a distance of 20 feet (6.1 m).
Thus, visual acuity, or resolving power, is the property of cones. To resolve detail, the eye's optical system has to project a focused image on the fovea, a region inside the macula having the highest density of cone photoreceptor cells (the only kind of photoreceptors existing on the fovea), thus having the highest resolution and best color vision. Acuity and color vision, despite being mediated by the same cells, are different physiologic functions that do not interrelate except by position. Acuity and color vision can be affected independently.
The grain of a photographic mosaic has just as limited resolving power as the "grain" of the retinal mosaic. In order to see detail, two sets of receptors must be intervened by a middle set. The maximum resolution is that 30 seconds of arc, corresponding to the foveal cone diameter or the angle subtended at the nodal point of the eye. In order to get reception from each cone, as it would be if vision was on a mosaic basis, the "local sign" must be obtained from a single cone via a chain of one bipolar, ganglion, and lateral geniculate cell each. A key factor of obtaining detailed vision, however, is inhibition. This is mediated by neurons such as the amacrine and horizontal cells, which functionally render the spread or convergence of signals inactive. This tendency to one-to-one shuttle of signals is powered by brightening of the center and its surroundings, which triggers the inhibition leading to a one-to-one wiring. This scenario, however, is rare, as cones may connect to both midget and flat (diffuse) bipolars, and amacrine and horizontal cells can merge messages just as easily as inhibit them.
Light travels from the fixation object to the fovea through an imaginary path called the visual axis. The eye's tissues and structures that are in the visual axis (and also the tissues adjacent to it) affect the quality of the image. These structures are: tear film, cornea, anterior chamber, pupil, lens, vitreous, and finally the retina. The posterior part of the retina, called the retinal pigment epithelium (RPE) is responsible for, among many other things, absorbing light that crosses the retina so it cannot bounce to other parts of the retina. Interestingly, in many vertebrates, such as cats, where high visual acuity is not a priority, there is a reflecting tapetum layer that gives the photoreceptors a "second chance" to absorb the light, thus improving the ability to see in the dark. This is what causes an animal's eyes to seemingly glow in the dark when a light is shone on them. The RPE also has a vital function of recycling the chemicals used by the rods and cones in photon detection. If the RPE is damaged and does not clean up this "shed" blindness can result.
As in a photographic lens, visual acuity is affected by the size of the pupil. Optical aberrations of the eye that decrease visual acuity are at a maximum when the pupil is largest (about 8 mm), which occurs in low-light conditions. When the pupil is small (1–2 mm), image sharpness may be limited by diffraction of light by the pupil (see diffraction limit). Between these extremes is the pupil diameter that is generally best for visual acuity in normal, healthy eyes; this tends to be around 3 or 4 mm.
If the optics of the eye were otherwise perfect, theoretically, acuity would be limited by pupil diffraction, which would be a diffraction-limited acuity of 0.4 minutes of arc (minarc) or 20/8 acuity. The smallest cone cells in the fovea have sizes corresponding to 0.4 minarc of the visual field, which also places a lower limit on acuity. The optimal acuity of 0.4 minarc or 20/8 can be demonstrated using a laser interferometer that bypasses any defects in the eye's optics and projects a pattern of dark and light bands directly on the retina. Laser interferometers are now used routinely in patients with optical problems, such as cataracts, to assess the health of the retina before subjecting them to surgery.
The visual cortex is the part of the cerebral cortex in the posterior part of the brain responsible for processing visual stimuli, called the occipital lobe. The central 10° of field (approximately the extension of the macula) is represented by at least 60% of the visual cortex. Many of these neurons are believed to be involved directly in visual acuity processing.
Proper development of normal visual acuity depends on an animal having normal visual input when it is very young. Any visual deprivation, that is, anything interfering with such input over a prolonged period, such as a cataract, severe eye turn or strabismus, or covering or patching the eye during medical treatment, will usually result in a severe and permanent decrease in visual acuity in the affected eye if not treated early in life. The decreased acuity is reflected in various abnormalities in cell properties in the visual cortex. These changes include a marked decrease in the number of cells connected to the affected eye as well as few cells connected to both eyes, resulting in a loss of binocular vision and depth perception, or stereopsis. The period of time over which an animal is highly sensitive to such visual deprivation is referred to as the critical period.
The eye is connected to the visual cortex by the optic nerve coming out of the back of the eye. The two optic nerves come together behind the eyes at the optic chiasm, where about half of the fibers from each eye cross over to the opposite side and join fibers from the other eye representing the corresponding visual field, the combined nerve fibers from both eyes forming the optic tract. This ultimately forms the physiological basis of binocular vision. The tracts project to a relay station in the midbrain called the lateral geniculate nucleus, part of the thalamus, and then to the visual cortex along a collection of nerve fibers called the optic radiations.
Any pathological process in the visual system, even in older humans beyond the critical period, will often cause decreases in visual acuity. Thus measuring visual acuity is a simple test in accessing the health of the eyes, the visual brain, or pathway to the brain. Any relatively sudden decrease in visual acuity is always a cause for concern. Common causes of decreases in visual acuity are cataracts and scarred corneas, which affect the optical path, diseases that affect the retina, such as macular degeneration and diabetes, diseases affecting the optic pathway to the brain such as tumors and multiple sclerosis, and diseases affecting the visual cortex such as tumors and strokes.
Though the resolving power depends on size and packing density of the photoreceptors, the neural system of receptors must interpret this resolving power. As determined from various experiments on the cat, different ganglion cells are tuned to different frequencies of detail, as from a grating, so some ganglion cells have better acuity than others. In humans the results are the same, this time utilizing the same method as well as a device to read electrical changes in the scalp.
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