| Nyctalopia | |
|---|---|
| Classification and external resources | |
| ICD-10 | H53.6 |
| ICD-9 | 368.6 |
Nyctalopia (from Greek νύκτ-, nykt- "night"; and αλαός, alaos "blindness") is a condition making it difficult or impossible to see in relatively low light. It is a symptom of several eye diseases. Night blindness may exist from birth, or be caused by injury or malnutrition (for example, a lack of vitamin A). It can be described as insufficient adaptation to darkness.
The most common cause of nyctalopia is retinitis pigmentosa, a disorder in which the rod cells in the retina gradually lose their ability to respond to the light. Patients suffering from this genetic condition have progressive nyctalopia and eventually their daytime vision may also be affected. In X-linked congenital stationary night blindness, from birth the rods either do not work at all, or work very little, but the condition doesn't get worse. Another cause of night blindness is a deficiency of retinol, or vitamin A, found in fish oils, liver and dairy products. In the Second World War disinformation was used by the British to cover up the reason for their pilots' successful nighttime missions. Their success was, in the disinformation, attributed to improved night vision and pilots flying night missions were encouraged to eat plenty of carrots, which contain carotenoids and can be converted into retinol. The real reason for their success was their use of advanced radar technologies.
The opposite problem, the inability to see in bright light, is known as hemeralopia and is much rarer.
The outer area of the retina is made up of more rods than cones. The rod cells are the cells that enable us to see in poor illumination. This is the reason why loss of peripheral vision often results in night blindness. Individuals suffering from night blindness not only see poorly at night, but also require some time for their eyes to adjust from brightly lit areas to dim ones. Contrast vision may also be greatly reduced.
Refractive "vision correction" surgery is a widespread cause of nyctalopia due to the impairment of contrast sensitivity function (CSF) which is induced by intraocular light-scatter resulting from surgical intervention in the natural structural integrity of the cornea.[1]
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Aulus Cornelius Celsus, writing ca. 30 AD, described night blindness and recommended an effective dietary supplement: "There is besides a weakness of the eyes, owing to which people see well enough indeed in the daytime but not at all at night; in women whose menstruation is regular this does not happen. But success sufferers should anoint their eyeballs with the stuff dripping from a liver whilst roasting, preferably of a he-goat, or failing that of a she-goat; and as well they should eat some of the liver itself."
Historically, nyctalopia, also known as moonblink, was a temporary night blindness believed to be caused by sleeping in moonlight in the tropics.[2]
An outbreak of nyctalopia affected many of the prisoners at the world's first prisoner-of-war camp at Norman Cross in 1806. They became severely dyspeptic and completely blind from sunset until dawn, to the extent that their fitter companions had to lead them around the camp. Various treatments were tried and failed; finally they were cured with black hellebore, given as snuff, which relieved the dyspepsia and restored their night vision within a few days.[3]
Congenital stationary night blindness is also an opthalmologic disorder in horses with leopard spotting patterns, such as the Appaloosa. It is present at birth (congenital), not sex-linked, non-progressive and affects the animal's vision in conditions of low lighting.[4] CSNB is usually diagnosed based on the owner's observations, but some horses have visibly abnormal eyes: poorly-aligned eyes (dorsomedial strabismus) or involuntary eye movement (nystagmus).[4] In horses, CSNB s has been linked with the leopard complex color pattern since the 1970s.[5] A 2008 study theorizes that both CSNB and leopard complex spotting patterns are linked to the TRPM1 gene.[6] The gene to which Lp has now been localized encodes a protein that channels calcium ions, a key factor in the transmission of nerve impulses. This protein, which is found in the retina and the skin, existed in fractional percentages of the normal levels in homozygous Lp/Lp horses.[4]