It is an everyday phenomenon that when entering a dark room, initially poor vision improves as the eyes adapt to the light conditions. This is called dark adaptation and is essential for scotopic vision at night.
What is scotopic vision?
Scotopic vision refers to seeing in the dark. Scotopic vision refers to seeing in the dark. In contrast to photopic vision, it is realized by the rod sensory cells of the retina because their increased sensitivity to light makes them particularly well suited for light-dark vision. If the rods are damaged due to inherited or acquired changes, there may be a severe reduction in vision in the dark, known as night blindness.
Function and task
There are two different types of photoreceptors on the retina of the human eye that are needed for vision: Rods and Cones. The cones are responsible for color vision in brightness, also known as photopic vision. The rods take over the visual process in low light or at night, i.e. scotopic vision. The fact that the rod sensory cells of the eye cannot distinguish between different colors is also the reason for our limited color perception in the dark. However, rods and cones are not evenly distributed across the retina. The highest density of sensory cells and thus the sharpest image resolution is achieved at the so-called yellow spot, the fovea centralis. However, only cones are located there, which are of little use in night vision. Therefore, scotopic vision becomes optimal when the eye is aligned in such a way that the image on the retina is not formed on the yellow spot, but next to it (parafoveal). In principle, both types of sensory cells convert light into a signal to the brain by the same mechanism. The energy of the incident light leads to a structural change in a protein, rhodopsin. This triggers a signaling cascade in the cell, as a result of which less glutamate is released. Downstream nerve cells register this and transmit an electrical signal to the brain. During the transition to seeing in the dark, for example when entering a dark room, dark adaptation takes place, consisting of four effects. One quick aspect is the pupillary reflex. In low light conditions, the pupil is dilated so that as much light as possible can fall through the opening of the iris onto the retina. In addition, the light sensitivity of the photoreceptors is increased. Their stimulus threshold is lowered, among other things, by an increased concentration of rhodopsin, which is only possible in darkness. Second, in darkness, there is a switch from cone to rod vision, since the rods per se already have a higher sensitivity to light than the cones. This transition requires a certain amount of time and is also known as the Kohlrausch kink. Finally, as darkness increases, lateral inhibition in the retina decreases and thus the size of the receptive fields increases. The result is a stronger convergence of the signals onto the downstream ganglion cells, which are responsible for transmission to the brain and thus become more excited. However, this increased convergence occurs at the expense of resolving power, or visual acuity.
Diseases and complaints
A defect or weakening of scotopic vision is called night blindness. In this case, dark adaptation can no longer be performed (sufficiently) by the eye, and vision in twilight or darkness is diminished or absent. This disorder can be congenital (congenital) or acquired. However, night blindness can also occur as an accompanying symptom in other disorders. For example, congenital night blindness can be triggered by hereditary mutations in proteins important for the visual process, such as S-arrestin in Oguchi syndrome. Another genetic condition is retinitis pigmentosa, a group of hereditary retinal diseases for which causative mutations in more than 50 different genes are currently known. The onset of this disease, which usually first becomes apparent in childhood, adolescence, or young adulthood, is often indicated by night blindness. In addition to impaired scotopic vision, visual field loss, increased glare sensitivity, and progressive loss of color vision often occur during the course of retinits pigmentosa.Cataract (cataract) also causes symptoms that patients describe as night blindness. However, the cause here is not a malfunction of the rods in the retina, but a clouding of the lens. Similarly, in the course of diabetes mellitus, there may be limitations of scotopic vision, which is called diabetic retinopathy. In addition to night blindness, patients with Leber’s amaurosis often exhibit increased glare sensitivity, nystagmus (involuntary eye tremor), and generally reduced vision. To be distinguished from these forms of night blindness is that caused by vitamin A deficiency. Vitamin A is necessary for the body’s own production of the visual pigment rhodopsin. An improvement of this form of night blindness can therefore be achieved by administration of vitamin A. In western industrialized nations, however, deficiency-induced night blindness is very rare, since the need for vitamin A is easily met by a balanced diet. However, in the case of certain risk factors for vitamin A deficiency, such as various intestinal diseases, inflammation of the pancreas, eating disorders or pregnancy, special attention should be paid to ensuring an adequate supply of vitamin A. In developing countries, vitamin A deficiency due to malnutrition is still a reason for dramatic blindness rates in children.
