Macula of retina

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This article is about the macula of the human eye. For other uses of the term macula, see Macula (disambiguation).
Macula of retina
Blausen 0389 EyeAnatomy 02.png
Human eye cross-sectional view, with macula near center.
Latin macula lutea
Gray's p.1015
MeSH Macula+Lutea
Anatomical terminology
Fundus photographs of the right eye (left image) and left eye (right image), seen from front so that left in each image is to the person's right. The gaze is into the camera, so in each picture the macula is in the center of the image, and the optic disk is located towards the nose.

The macula or macula lutea (from Latin macula, "spot" + lutea, "yellow") is an oval-shaped highly pigmented yellow spot near the center of the retina of the human eye. It has a diameter of around 6 mm[1] and is often histologically defined as having two or more layers of ganglion cells. Near its center is the fovea, a small pit that contains the largest concentration of cone cells in the eye and is responsible for central, high resolution vision. The macula also contains the parafovea and perifovea.

Structure[edit]

Color[edit]

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 colour comes from its content of lutein and zeaxanthin, which are yellow xanthophyll carotenoids, 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 of macular degeneration.

Function[edit]

Structures in the macula are specialized for high acuity vision. Within the macula are the fovea and foveola which contain a high density of cones (photoreceptors with high acuity).

Clinical significance[edit]

Whereas loss of peripheral 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 a disease known as macular 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.

Visual input from the macula occupies a substantial portion of the brain's visual capacity. As a result, some forms of visual field loss can occur without involving the macula; this is termed macular sparing. (For example, visual field testing might demonstrate homonymous hemianopsia with macular sparing.)

In the case of Occipitoparietal ischemia owing to occlusion of elements of either posterior cerebral artery, patients may display cortical blindness (which, rarely, can involve blindness that the patient denies having, as seen in Anton's Syndrome), yet display sparing of the macula. This selective sparing is due to the collateral circulation offered to macular tracts by the middle cerebral artery.[2] 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.[3]

See also[edit]

This article uses anatomical terminology; for an overview, see anatomical terminology.

References[edit]

  1. ^ Anita Hendrickson, 2005. Organization of the Adult Primate Fovea. In: P. Penfold, J. Provis, 2005. Macular Degeneration. Berlin: Springer. Ch.1.
  2. ^ Helseth,, Erek. "Posterior Cerebral Artery Stroke". Medscape Reference. Medscape. Retrieved 23 October 2011. 
  3. ^ Siegel, Allan; Sapru, Hreday N. (2006). Betty Sun, ed. Essential Neuroscience (First Revised ed.). Baltimore, Maryland: Lippincott Williams & Wilkins. ISBN 978-0-7817-9121-2. 

Additional images[edit]

External links[edit]