Night Blindness

Night Blindness: Blindness or dimness in dim light is a condition called blindness. The term blindness is derived from the fact that it looks better during the day but less visible at night. The pigment in the conjunctiva of the retina of the eye is decomposed due to the fall of light on the pigment. To these chemical changes, the cone-rods are the sensors of the nerve fibers (nerves) that are photosensitive [⟶ eye]. This pigment is called ‘rhodopsin’ and requires vitamin A for its sale and its deficiency is the main cause of blindness.

Night blindness is a symptom of some diseases. Night blindness is a major symptom of retinal pigment degeneration due to degeneration of cone-rods. Due to the defect in the regeneration of retinal detachment in the retinal detachment, the sensory perception is reduced. Sometimes this disorder is congenital. Night blindness may be due to nutritional defects of the eyeball (e.g., vitiligo). In the congenital form ‘Oguchi disease’ c. In a disorder known as Oguchi, a Japanese ophthalmologist, after keeping the patient in complete darkness for two to three hours, the ophthalmologist examines the retina (yellow at the base of the retina) for a yellow or gray color. Over time, its natural orange-red color reappears. Congenital short-sightedness (parallel rays from a distant object not falling on the retina and concentrating on it) is accompanied by blurred vision, blurred vision (with both eyes moving as usual when they look at an object, or subtle movements or movements).

Vitamin A deficiency is a major cause of this blindness. The human retina is sensitive to both colorless and pigmented stimuli. It consists of the main part of the cones. Each retina contains 12.5 million rods and 70 million cones, and their sensations travel through the optics to the outermost part of the brain (the outermost part of the brain).

Appearance of light in rods is essential for exposure to dim light. This pigment is made up of a pigment called protein and retinin and is stable in dim light. It decomposes in intense light to separate proteins and retinins, and this compound is called viscous. At this stage, the tamunukulan (regeneration of the viscera in dim light and dilation of the doll) disappears. As the intensity of light increases, regeneration occurs and adaptation is established. If intense light is kept on, proteins and vitamins A are formed by decomposition and this compound is called optical whitening. It is insensitive to light. Vitamin A is absorbed by the blood. As the intensity of light decreases, sebaceous glands are formed and the supply of essential nutrients is provided by the bloodstream. Therefore, deficiency of this vitamin causes slowing of thyroid adaptation. Chemical changes caused by light and darkness in the viscera. Shown in Fig. 2. This is called 'Drugnilarun Chakra'.

Apart from the above physical causes, there may be anatomical or functional night blindness. Psychological night blindness is more prevalent in developed countries like England. It is also called manic night blindness. In this deformity where there is no defect in the eye examination, the patient often describes his complaint in a dramatic manner. This disorder is found in coal miners and in front-line soldiers who have to work constantly in dim light, which is a constant threat to their lives. Aviators can also have night blindness. A driver with night blindness is only 2-3 m in the bright light of the next lights. The road to the top is visible. On the other hand, a driver who is not visually impaired can see the road up to several meters clean.

The exact opposite of night blindness is called blindness, which means looking better in dim light than in bright light. This lesion is found in tobacco-induced retinal detachment. Opacity in the center of the sphincter (the transparent part of the front of the iris) and opacity in the center of the eyeball look good in low light, as more light can penetrate due to the dilated pupil.

Vitamin A deficiency night blindness is cured by proper amounts of that vitamin. Most patients do not recover if there is conical degeneration.

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