Anyone who suffers from night blindness or night vision disorders hardly sees in the dark or not at all. Damaged sensory cells in the retina of the eyes, the rod cells, are responsible for this. The defect is either genetic, the result of diseases (such as retinitis pigmentosa) or vitamin A deficiency. Find out everything important about night blindness here.
Night blindness: description
Many know the phenomenon: While you have no difficulty seeing during the day, the problems start at night. Especially in the traffic dazzle oncoming car headlights, you see less sharp and simple light sources form large circles of light, which also make it difficult to see in the dark. Often it is age-related visual impairment, which we colloquially term night blindness. On the other hand, new glasses often help.
However, a true night blindness is the result of another illness or an independent disease. It can be innate or acquired. Affected then see in the twilight or darkness very bad or not at all. The reason for this is damage to the rod cell of the retina in the eye. Depending on the cause, the night blindness remains constant during the course of life or gradually worsens. There is currently no therapy. An exception is the night blindness as a result of vitamin A deficiency. Through the administration of vitamin A improves the vision again.
Color vision and twilight vision
The human eye achieves true excellence: during the day we see the world in bright colors, at night we can orient ourselves well in low light. This is possible thanks to two different cell types in the retina of the eyes, the rod and cone cells. The rod cells allow the light-dark vision and are therefore active mainly at night, the cone cells the color vision, which is why they work mainly during the day.
The transition from day to night vision, however, does not happen suddenly. Instead, in the evening, the cone cells gradually stop functioning (which is why you can not perceive colors at night), and rod cells take on the task of seeing. This process, also called dark adaptation, lasts between 20 and 25 minutes. Only then can we see, for example, outlines in the dark – the rod cells can perceive about 500 different shades.
Main actor: The photopigment rhodopsin
That the different cell types can react to different intensities of light, they owe the so-called rhodopsin. The photosensitive photopigment is composed of a large molecule of opsin and a smaller molecule, the 11-cis-retinal. While the 11-cis-retinal structure is identical in both the cone and rod cells, opsin is present in different composition in the two cell types. This is the reason why rodent cells can only perceive light-dark stimuli and cone cells only color stimuli.
When light hits the pigment, 11-cis retinal changes its structure and activates a number of processes within the cell. At the end of this signal cascade, adjacent nerve cells are activated to transmit the light stimulus to the brain. This analyzes and processes the impulses.
Night blindness: symptoms
Depending on the cause of night blindness, there are additional signs of poor vision in the dark.
Hereditary night blindness: symptoms
Very poor or completely lost vision at night is the typical feature of all forms of night blindness. Symptoms such as increased sensitivity to dazzle, involuntary eye shaking or greatly reduced visual acuity occur depending on the genetic cause:
TheCongenital stationary night blindness remains constant throughout life, but sometimes it improves slightly over time. The visual acuity of the affected person is normal to slightly reduced, the visual field is not restricted. About 60 to 70 percent of those affected also have involuntary eye shaking (nystagmus).
At theOguchi’s disease Apart from night blindness, no additional symptoms are known.
Patients withLiver amaurosis In addition to night blindness, they show drastically reduced eyesight, involuntary eye shaking (nystagmus) and increased sensitivity to glare.
About one third of the patients withFundus albipunctatus develops in addition to night blindness in the course of life an increasing color blindness.
The medical examination in the ophthalmological practice provides further distinguishing features such as numerous bright spots in the retina (Fundus albipunctatus) or a golden yellow coloration of the fundus (= Mizuo-Nakamura in M. Oguchi).
Acquired night blindness: symptoms
If another condition such as retinitis pigmentosa, cataracts, corneal clouding or diabetic retinopathy is the cause of night blindness, there are additional specific symptoms. In inherited retinitis pigmentosa, for example, decreased color vision, low vision, and visual field loss accompany night blindness. These symptoms worsen over the course of life. Those affected also suffer from increased glare sensitivity.
Night blindness: causes and risk factors
Night blindness can have a variety of causes. In all cases, the function of the rod cells is limited or completely damaged. Often the night blindness is the symptom of different, partly hereditary eye diseases. It rarely occurs as an independent and then hereditary disease. Distinguish from these two forms is the night blindness, which is triggered by a vitamin A deficiency.
Congenital night blindness
Various hereditary retinal diseases can trigger night blindness, including:
- Congenital stationary night blindness (group of genetic retinal diseases)
- Oguchi’s disease (Oguchi syndrome)
- Fundus albipunctatus
- Liver amaurosis
Night blind: symptom of diseases
Relatively often, night blindness is the result of hereditary retinitis pigmentosa, a group of inheritable retinal diseases. There are so far more than 51 genes known that can cause night blindness in case of a mutation.
Other eye diseases, such as cataracts or corneal clouding, manifest themselves with increasing symptoms with the symptom night blindness. The night vision disorder is also conceivable as a result of diabetic retinopathy, an eye disease due to diabetes mellitus.
Night blindness due to vitamin A deficiency
In contrast to hereditary or acquired by night blindness, the visual disturbance can also occur as a result of vitamin A deficiency. Because vitamin A is needed, among other things, to build up the rhodopsin. In industrialized countries, night blindness should be extremely rare thanks to a balanced diet. In addition, the liver creates a large vitamin A storage, which is not quickly emptied in a balanced diet. Exceptions may be the time during pregnancy or malnutrition caused by, for example, eating disorders, pancreatitis or intestinal diseases such as Crohn’s disease or celiac disease.
Night blindness: examinations and diagnosis
Whether there is night blindness and, if so, what form, the ophthalmologist determines with the help of various examinations. At first he will talk to you in detail about your complaints and your medical history (anamnesis). Possible questions are:
- Do you not see anything at night or can you perceive low shades?
- Since when do you see bad in the dark?
- Are you night blind on one or both eyes?
To clearly document a night blindness, the ophthalmologist then examines the eyes with an adapter. Thus the physician determines the time, which the eye needs for the dark adaptation – adjustment of the seeing at darkness. The examination also measures what slightest light intensity the eye can still perceive. The physician uses the electroretinogram (ERG) to measure the height at which the rod cells react to incoming light.
In addition, the visual acuity is measured, the color vision checked and the visual field tested. All results together provide the physician with important information about the form of night blindness.
Night blindness: treatment
The congenital forms of night blindness are currently not treatable. However, scientists hope that the hereditary forms of night blindness can be cured in the future using new forms of therapy such as gene therapy or stem cell transplantation.
Retinitis pigmentosa can be treated with electronic retinal implants.
The acquired night blindness as a result of a vitamin A deficiency is treatable: If the cause is in a malnutrition or intestinal or liver diseases, the additional administration of vitamin A can improve the symptoms.
The intake of vitamin A during pregnancy, according to World Health Organization (WHO) seems only in areas where a vitamin A deficiency causes health problems. In developed countries, a balanced and varied diet is often enough to prevent night blindness due to vitamin A deficiency during pregnancy.
Night blindness: disease course and prognosis
The night blindness occurs depending on the cause already in childhood or develops only in the course of life. The innate forms are already noticeable in infancy and do not improve or worsen in the course of life. An exception is congenital stationary night blindness, in which some sufferers notice an improvement over time.
Night blindness as a symptom of retinitis pigmentosa first appears in early childhood, adolescence or middle life. In the course of life, retinitis pigmentosa often leads to progressive loss of visual acuity and even to blindness.
The acquired night blindness as a result of, for example, cataracts, corneal clouding or diabetes mellitus sets in the course of life, depending on the occurrence of the causative disease.
The same applies to the night-blindness as a result of a vitamin A deficiency. Bad vision in the dark begins as soon as the eyes are inadequately supplied with vitamin A.