Night blindness

Night blindness or Nyctalopia is inability or difficulty in seeing in the night or poor light. While it is congenital in some, in others it is caused due to injury, certain drugs or other causes. This causes problems especially during driving at night. Persons suffering from night blindness tend to notice reduced contrast vision; as their eyes take more time to adjust from brightly lit areas to dim ones. Some causes for night blindness are cataract and nearsightedness. An ophthalmologist might conduct tests such as retinal exam, color vision testing and pupil light reflex.

Hemeralopia is the opposite of night blindness where a person is unable to see in bright light or suffer acute discomfort in the eyes. Hemeralopia can occur owing to many conditions - Cone dystrophy (genetic condition in which cones are lost in the retina), Cohen Syndrome and even Cataracts. Some drugs can cause temporary Hemeralopia in some cases. ( eg.Trimethadione) Wearing dark glasses or neutral density filters in the correcting lens could mitigate the pain.

Electroretinography

Electroretinography or ERG is an eye test used to detect the abnormal function of the retina. The rods, cones and the ganglion cells of the eyes are examined during this test. An electrode is placed on the cornea to measure the electrical response to the light in the retina and the back of the eye. This test helps identify any defects in the retina and can help in identifying if retinal surgery is required.

ERG Procedure

Patient's eyes are dilated and anesthetic drops are placed on the eyes. Eyes are kept open using a speculum and an electrode is placed in the eye. Another electrode is placed on the skin. The patient is made to watch a standardized light stimulus or flash ERG. The signal received is measured according to its amplitude. The readings are taken when the room is normally lit and when the room is dark. If the tests are normal, it will display a normal A and B pattern for each flash.

Abnormal results can indicate:

• Congenital night blindness
  
• Cone Rod Dystrophy (CRD)
  
• Retinal detachment
  
• Vitamin A deficiency
  
• Trauma
  

Vitamin A

Vitamin A is a fat soluble vitamin which is derived from beta carotene which plays a significant role in the process of vision and other important metabolic pathways pertaining to cell division and genetic expression. The significant forms of vitamin A include retinol, retinal, retinoic acid and retinyl esters. There are approximately six hundred derivatives of beta carotenes and the most important form is retinol.

Functions of Vitamin A

Vitamin A is essential for many metabolic pathways in the body. It is the chief requirement for the function of the rhodopsin protein located in the retina to absorb light and to differentiate functions of the cornea and the conjunctival membranes. Vitamin A is essential for normal functioning of the retina. Apart from this, vitamin A plays a significant role in immune system functions, cell signaling and cellular communication and reproduction. The functions and pathways associated with vitamin A are directly related to the functionality of vital organs such as heart, brain, lungs, liver and kidneys. Hence vitamin A is also known as an important antioxidant. Besides it is required for the growth and differentiation of epithelial tissue, normal growth of bone and embryonic development. Most of our body's Vitamin A is stored in the liver in the form of retinyl esters.

Vitamin A Deficiency: Poor adaptation of vision to darkness or what is known as night blindness is an early symptom that may be followed by degenerative changes in the retina. Degenerative changes in eyes and skin are commonly observed in vitamin A deficiency. The predominant form of vitamin A deficiency is Nyctalopia or night blindness. This occurs as result of retinol imbalance which is the chief derivative of vitamin A. In third-world, vitamin A deficiency is the primary cause of blindness. Pregnant and lactating women, premature children, children living in rural areas of developing countries and patients who have a history of liver diseases such cirrhosis and cystic fibrosis are most susceptible to Vitamin A deficiency. Severe or prolonged deficiency may lead to dry eye or Xerophthalmia (dryness in conjunctiva and cornea of the eye) that can result in corneal ulcers, inflammation, ridge formation, scarring and eventually blindness. Xerophthalmia is due to lacrimal gland dysfunction. Other associated conditions include keratomalacia and follicular hyperkeratosis. Another important consequence of Vitamin A deficiency is acquired immunodeficiency disease, with an increased incidence of death related to infectious diseases. Vitamin A deficiency is associated with increased disease progression and mortality in HIV patients.

World Health Organization (WHO) Recommendations for Vitamin A:
Supplementation may be required in cases where the blood Vitamin A level falls below 20 µg/dL.
Severe deficiency is < 10 µg/dL

Food sources and recommended dietary allowance

Vitamin A is naturally available in dairy products such as milk, cheese, curd, cream. Meat products like liver and fish oil and leafy vegetables are excellent sources of vitamin A. Other sources include pumpkin, potatoes, broccoli, cereals, beans and cow peas. Studies indicate that the intensity of the fruit or vegetable color is directly proportional to the amount of vitamin A present in it. The recommended intake of vitamin A per day for children 500 micrograms, males 1000 micrograms and females 800 micrograms respectively.

RDAs (recommended dietary allowance) for vitamin A are given as mcg of retinol activity equivalents (RAE) to account for the different bioactivities of retinol and provitamin A carotenoids. FDA may introduce new labeling regulations in the near future which may result in listing Vitamin A with RAE values rather than in IU.
The following table shows conversion rates of mcg of RAE (retinol activity equivalents):

• 1 IU retinol = 0.3 mcg RAE
  
• 1 IU beta carotene from dietary supplements = 0.15 mcg RAE
  
• 1 IU beta carotene from food = 0.05 mcg RAE
  
• 1 IU alpha carotene or beta-cryptoxanthin = 0.025 mcg RAE
  

Essentially all dietary sources of vitamin A are converted into retinol by the body: 1 mcg of physiologically available retinol is equivalent to the following amounts from dietary sources:

• 1 mcg of retinol
  
• 12 mcg of beta carotene
  
• 24 mcg of alpha carotene or beta cryptoxanthin
  

Hypervitaminosis A: Vitamin A in excess can be toxic. According to WHO, values in excess of 120 µg/dL is Hypervitaminosis A. Chronic vitamin A over dosage may be a serious issue in normal adults who take more than 15 mg per day and in children who take more than 6 mg per day of vitamin A over a period of several months. Symptoms can include :

• Dry skin
  
• Cheilosis
  
• Glossitis
  
• Hypercalcemia
  
• Hyperlipidemia
  
• Amenorrhea
  
• Liver fibrosis with portal hypertension
  
• pseudotumor cerebri
  
• increased intracranial pressure and Papilledema
  
• lymph node enlargement
  

Other than that some symptoms such as pain, vomiting, alopecia and bone demineralization may result due to excessive intake of Vitamin A. In pregnant women, an over dose of Vitamin A over a period of time may result in spontaneous abortions or Congenital malformations, craniofacial abnormalities and valvular heart disease in the baby.

However, unlike preformed Vitamin A, beta-carotene is not known to be teratogenic (reproductive toxicity). Even a relatively large supplemental doses of beta carotene or eating carotenoid rich food for long duration need not result in toxicity always. Rarely a reversible condition known as carotenodermia - where the skin turns yellow/orange might be the result of long term over dosage of beta carotene.