Introduction
Dark adaptation means recovery of visual senses in the dark after exposure to bright light. Light plays a crucial role in vision. The light particles or photons initiate neural and molecular events that aid in the visualization of the objects. As the eye can detect light within a broad spectral domain, it is necessary to determine the range of the light for visualization. In 1965 Aubert did the first test to determine the absolute intensity threshold and the minimum luminance of light to visualization. Rod and cone photoreceptor cells play a crucial role in the adaptation process to light intensity. Any pathological condition that disrupts photoreceptor cells' form and function may cause impaired light adaptation mechanisms.
What Is the Mechanism of Dark Adaptation?
Duplicity theory can explain the dark adaptation mechanism. According to this theory, the cone cells are responsible for vision above the luminance level of 0.03 candela per square meter. This type of vision is known as photopic vision. This allows higher visual acuity and color perception. At this point, a sudden drop in luminance causes blackness in the eye. This is because cone cells cease to perform in the absence of light. And also, all the rod pigments were bleached out due to the presence of light. Gradually, the rhodopsin regenerates, and the retina's sensitivity increases over time. The size of the pupil also changes during this process.
What Are the Controlling Factors?
The controlling factors of dark adaptation are:
- Intensity and Duration of the Pre-Adapting Light - The intensity of the pre-adapting light determines the time and duration of the dark adaptation. Higher luminance of the pre-adapting light causes higher involvement of cone photoreceptors. As a result, more bleaching of the rod pigments occurs. This causes a delay in the dark adaptation. On the other hand, low luminous intensity is responsible for more abrupt dark adaptation.
- The Wavelength of the Threshold Light - The difference between rod and cone break is affected by the wavelength of the light. The rod and cone difference is minimal, with a long wavelength of light. This is because rods and cones have had similar sensitivity toward longer wavelengths of light. On the other hand, the increased differences between rods and cones can be seen in the presence of shorter wavelengths of light.
- Rhodopsin Regeneration - In the presence of light, the rhodopsin bleaches. The more light intensity, the more rhodopsin takes place. Any problem in the rhodopsin regeneration process causes a delay in the dark adaptation. A one percent rise in the bleaching of rhodopsin decreases the dark adaptation threshold by 10 times. On the contrary, bleaching of cone photopigment does not affect dark adaptation.
What Are the Diseases Cause Slow Dark Adaptation?
Diseases related to photoreceptor cells are responsible for delayed dark adaptation. These diseases are:
1. Fundus Albipunctatus - This is a rare congenital disorder characterized by night blindness. The mutation of the RDH5 gene causes this hereditary disorder. This gene encodes the enzyme 11-cis retinol dehydrogenase, which catalyzes and recycles the cone and rod photopigments. This is characterized by worsening visual acuity in the presence of dim light. White-yellowish retinal lesions of various sizes and shapes can be detected on fundus examination. Scotopic electroretinography (a test to measure the retina's electrical activity) shows decreased rod cell response. Multifocal electroretinogram (rapid assessment of retinal function) shows reduced cone density.
2. Systemic Vitamin A Deficiency - Vitamin A deficiency is one of the most common causes of delayed dark adaptation or night blindness. This is a fat-soluble vitamin whose deficiency is mainly seen in poor countries. Improper breastfeeding and mother malnutrition cause poor infant intake and are responsible for vitamin A deficiency. Other than this, chronic diarrhea, celiac disease (an immune response against eating gluten), cystic fibrosis (an inherited disorder that causes the thickening of sweat, mucus, and digestive juice), bile duct blockage, and liver function disorders. Its deficiency causes the impaired formation of rhodopsin. The clinical manifestations are:
- Night Blindness: Difficulty in seeing in less.
- Conjunctival Xerosis: Dryness of conjunctiva.
- Bitot’s Spots: Elevated white foamy lesion on the bulbar conjunctiva near the limbus.
- Corneal Ulcer: Ulceration in the cornea with a punched-out appearance.
3. Age-Related Maculopathy - This is an acquired disorder characterized by degeneration of the retina. Due to age-related changes or the presence of risk factors (smoking, genetic factors, hypertension), modification and thinning of retinal pigment epithelium and photoreceptor cells occurs. Patients often complain of distorted near vision and blurred vision. The clinical manifestations are:
- Geographic atrophy of the retina.
- Accumulation of blood at the sub-retinal level.
- Fibrosis at the sub-retinal region.
- Thickening of Bruch’s membrane and the deposition of neutral lipids.
- Presence of blind spot in the visual field.
- Formation of new blood vessels in the choroid region.
4. Stargardt Macular Dystrophy - This is a genetic disorder characterized by fatty deposition on the ocular surface. This is caused by the mutation of the ABCA4 gene located on chromosome 1. This gene mutation causes lipofuscin-like molecules to be deposited on the retinal surface. These molecules are toxic to the retinal pigmented epithelium and photoreceptors. As a result of which destruction of photoreceptor cells. The clinical features of this disease are:
- Blurred vision.
- Presence of blind spot in the visual field.
- Color blindness.
- “Fish-tail” or pisciform lesions present within the macula.
5. Bothnia Dystrophy - It is a rare retinal dystrophy caused by the cellular retinaldehyde-binding protein. This disease is mainly seen in Northern Sweden region. The retinaldehyde-binding protein mutation causes retinol's impaired metabolism and disrupts visual pigment regeneration. As a result, patients develop night blindness from early childhood. Clinical features are:
- Retinal hypopigmentation.
- Central Maculopathy - Loss of central vision, color blindness.
- Decreased visual acuity.
6. Sorsby Fundus Dystrophy - This is an autosomal dominant disorder degenerative disorder. This is characterized by mutations in the Tissue Inhibitor of the metalloproteinase-3 (TIMP3) gene. The main characteristic feature of this disorder is the deposition of TIMP3 protein. These protein molecules appear as 20–30 millimeter thick, amorphous deposits on the basement membrane of retinal pigmented epithelium. Other clinical features are
- Drusen (yellow spot) and “pisciform” lesions in the fourth decade of life.
- Thinning of retina and choroid.
Conclusion:
Light is essential for visualization. Adaptation to the intensity of the light is an integral part of the visual princess. Rods and cones play an important role in this adaptive process. The functionality of rods is essential for dark adaptation. Pathological conditions affecting rods' form and function affect the dark adaptation process.
