With the ability of light-dark adaptation, human eyes are able to adapt to lighting conditions. These are two opposing processes of the visual system. Disturbances in light-dark adaptation can occur in vitamin A deficiency and after damage to the central nervous visual pathway.
What is light-dark adaptation?
With the ability of light-dark adaptation, human eyes are capable of adapting to lighting conditions. Humans are among the eye-controlled creatures. This means that, from an evolutionary-biological point of view, visual perception has played the most important role in his survival. In order for the human eye to provide a reliable image in permanently changing light conditions and viewing distances, different adaptation processes take place in the eyes. One of these is light-dark adaptation, by which the eye adapts to different light conditions. Light and dark adaptation are two different processes that run in opposite directions. Light adaptation is a special case of daytime vision. It occurs when the visual system as a whole has adapted to luminances above 3.4 cd per square meter. With dark adaptation, the visual system adapts to luminances of less than 0.034 cd per square meter. When a person steps inside a building from full sun, the visual environment appears nearly black for a few seconds. Only a few minutes later is full adaptation achieved and the person recognizes environmental details again. From this point on, the person again finds looking out of the window unpleasant, since the high luminance levels blind the dark-adapted eye. Dark adaptation is based on a resynthesis of the visual pigment in the cones and rods. In light adaptation, on the other hand, the visual pigment decays. For this reason, dark adaptation takes longer than light adaptation.
Function and task
The ability for light-dark adaptation adjusts the human visual perception to the light conditions. The rods of the eye have greater sensitivity to light than the cones. In poor light conditions, the human eye therefore switches from cone vision to rod vision. The greatest cone density is in the fovea centralis. This place is the place of the sharpest vision, so that in the darkness sharp vision is no longer possible and colors are only poorly recognized. The pupil adapts to darkness by contractions of the dilatator pupillae muscle in the form of a dilation to allow more light to enter the eye. In turn, rod sensitivity to light depends on rhodopsin concentration. In brightness, rhodopsin is required for transduction processes. In dark adaptation, the substance is no longer needed for transduction and is accordingly available again in large quantities, giving the eye more sensitivity to light. In addition, during dark adaptation of the eye, lateral inhibition is reduced, allowing the center of receptive fields to extend into the periphery. Each ganglion cell thus receives receptive information from larger retinal areas in the dark. The associated spatial summation also increases the eyes’ sensitivity to light. In the light adaptation of the eyes the opposite changes take place. From rod vision to cone vision, the person sees sharply and in color again. In good light conditions, the pupils are constricted by the parasympathetic sphincter pupillae muscle. The visual pigment concentration decreases and the eyes become less sensitive to light. At the same time, the receptive fields decrease. The processes of light-dark adaptation often cause optical illusions, for example in the form of successive contrast. Black and white patterns on a sheet of paper, for example, are seen by the observer as an inverted pattern after a certain period of observation.
Diseases and ailments
Different conditions can disrupt or pathologically alter light-dark adaptation. One of these conditions is vitamin deficiency. Rods primarily require vitamin A to function without restriction. Dark adaptation switches from cone vision to rod vision. Thus, a person with pronounced vitamin A deficiency can see poorly or not at all in the dark.Since muscles are also involved in the adjustment of pupil width and thus in both types of light-dark adaptation, paralysis may also be responsible for adaptation-related visual disturbances under certain circumstances. Both sympathetically and parasympathetically innervated muscles are required for light-dark adaptation. For this reason, lesions of sympathetic and parasympathetic nerve tissue can cause paralysis that makes light-dark adaptation impossible. Such visual disorders are neurogenic and are usually related to degenerative diseases or other damage to the central nervous system. Disorders related to contrast sensitivity and color perception may also correspond to neurogenic disorders. The most common neurological cause in this context is a lesion of the nerve tissue in the visual pathway. Such a nerve lesion can be due to different triggers. A traumatic trigger can be a craniocerebral trauma. The visual pathway can also be damaged by a stroke. This phenomenon refers to a sudden disturbance of the blood supply to the brain, which causes a regional lack of oxygen and nutrients. The insufficiently supplied tissue dies due to the deficiency symptoms. In the course of the autoimmune disease multiple sclerosis, in turn, different nerve tissue areas of the central nervous system can be damaged. Autoimmunological inflammatory reactions are responsible for the damage, which can cause the tissue to perish. An inflammatory lesion in the area of the visual pathways can also lead to difficulties in light-dark adaptation. Not only autoimmunological inflammation, but also inflammatory reactions to bacterial infections are conceivable causative factors. In addition, tumor diseases or tumor metastases in the brain can cause complaints in light-dark vision if they are located in the area of visual perception or directly at the visual pathway.
