| Macula | |
|---|---|
 | |
| Details | |
| Part of | Retina ofhuman eye |
| System | Visual system |
| Identifiers | |
| Latin | macula lutea |
| MeSH | D008266 |
| TA98 | A15.2.04.021 |
| TA2 | 6784 |
| FMA | 58637 |
| Anatomical terminology | |
Themacula (/ˈmakjʊlə/)[1] ormacula lutea is an oval-shaped pigmented area in the center of theretina of thehuman eye and in other animals. The macula in humans has a diameter of around 5.5 mm (0.22 in) and is subdivided into theumbo,foveola,foveal avascular zone,fovea,parafovea, andperifovea areas.[2]
The anatomical macula at a size of 5.5 mm (0.22 in) is much larger than the clinical macula which, at a size of 1.5 mm (0.059 in), corresponds to the anatomical fovea.[3][4][5]
The macula is responsible for the central, high-resolution, color vision that is possible in good light. This kind of vision is impaired if the macula is damaged, as inmacular degeneration. The clinical macula is seen when viewed from the pupil, as in ophthalmoscopy or retinal photography.
The term macula lutea comes fromLatinmacula, "spot", andlutea, "yellow".
The macula is an oval-shaped pigmented area in the center of theretina of thehuman eye and other animaleyes. Its center is shifted slightly away from theoptical axis (laterally, by 5°=1.5 mm).[6]The macula in humans has a diameter of around 5.5 mm (0.22 in) and is subdivided into theumbo,foveola,foveal avascular zone,fovea,parafovea, andperifovea areas.[2]An even smaller central region of highest receptor density (40–80 μm) is sometimes referred to as thefoveal bouquet.[7][8][9][10]The anatomical macula at 5.5 mm (0.22 in) is much larger than the clinical macula which, at 1.5 mm (0.059 in), corresponds to the anatomical fovea.[3][4][5]
The clinical macula is seen when viewed from the pupil, as inophthalmoscopy orretinal photography. The anatomical macula is definedhistologically in terms of having two or more layers ofganglion cells.[11] The umbo is the center of the foveola which in turn is located at the center of the fovea.
The fovea is located near the center of the macula. It is a small pit that contains the largest concentration ofcone cells. The retina's receptor layer contains two types of photosensitive cells, therod cells and the cone cells.
Because the macula is yellow in color, it absorbs excess blue and ultraviolet light that enter the eye and acts as a natural sunblock (analogous to sunglasses) for this area of the retina. The yellow color comes from its content oflutein andzeaxanthin, which are yellowxanthophyllcarotenoids, derived from the diet. Zeaxanthin predominates at the macula, while lutein predominates elsewhere in the retina. There is some evidence that these carotenoids protect the pigmented region from some types ofmacular degeneration. A formulation of 10 mg lutein and 2 mg zeaxanthin has been shown to reduce the risk of age-related macular degeneration progressing to advanced stages, although these carotenoids have not been shown to prevent the disease.[12]
After death orenucleation (removal of the eye), the macula appears yellow, a color that is not visible in the living eye except when viewed with light from which red has been filtered.[13]
Structures in the macula are specialized for high-acuity vision. Within the macula are the fovea and foveola that both contain a high density ofcones, which are nerve cells that arephotoreceptors with high acuity.
In detail, the normal human eye contains three different types of cones, with different ranges of spectral sensitivity. The brain combines the signals from neighboring cones to distinguish different colors. There is only one type of rod, but the rods are more sensitive than the cones, so in dim light, they are the dominant photoreceptors active, and without information provided by the separate spectral sensitivity of the cones it is impossible to discriminate colors. In the foveacentralis, cones predominate and are present at high density. The macula is thus responsible for the central, high-resolution, color vision that is possible in good light; and this kind of vision is impaired if the macula is damaged, for example inmacular degeneration.[14]
The clinical macula is seen when viewed from the pupil, as in ophthalmoscopy or retinal photography.
Whereas loss ofperipheral vision may go unnoticed for some time, damage to the macula will result in loss of central vision, which is usually immediately obvious.The progressive destruction of the macula is adisease known asmacular degeneration and can sometimes lead to the creation of a macular hole. Macular holes are rarely caused by trauma, but if a severe blow is delivered it can burst the blood vessels going to the macula, destroying it.[14]
Visual input from the macula occupies a substantial portion of the brain's visual capacity. As a result, some forms ofvisual field loss that occur without involving the macula are termedmacular sparing. (For example,visual field testing might demonstratehomonymous hemianopsia with macular sparing.)
In the case of occipitoparietal ischemia owing to occlusion of elements of eitherposterior cerebral artery, patients may display corticalblindness (which, rarely, can involve blindness that the patient denies having, as seen inAnton's Syndrome), yet display sparing of the macula. This selective sparing is due to the collateral circulation offered to macular tracts by themiddle cerebral artery.[15] Neurological examination that confirms macular sparing can go far in representing the type of damage mediated by an infarct, in this case, indicating that the caudal visual cortex (which is the principal recipient of macular projections of the optic nerve) has been spared. Further, it indicates that cortical damage rostral to, and including,lateral geniculate nucleus is an unlikely outcome of the infarction, as too much of the lateral geniculate nucleus is, proportionally, devoted to macular-stream processing.[16]
Media related toMacula lutea at Wikimedia Commons| Fibrous tunic (outer) |
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