U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001.

  • By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.
Cover of Neuroscience

Neuroscience. 2nd edition.

Show details

Visual Field Deficits

A variety of retinal or more central pathologies can cause visual field deficits that are limited to particular regions of visual space. Because the spatial relationships in the retinas are maintained in central visual structures, a careful analysis of the visual fields can often indicate the site of neurological damage. Relatively large visual field deficits are called anopsias and smaller ones are called scotomas (see Box A). The former term is combined with various prefixes to indicate the specific region of the visual field from which sight has been lost (Figures 12.7 and 12.8).

Figure 12.7. Course of the optic radiation to the striate cortex.

Figure 12.7

Course of the optic radiation to the striate cortex. Axons carrying information about the superior portion of the visual field sweep around the lateral horn of the ventricle in the temporal lobe (Meyer's loop) before reaching the occipital lobe. Those (more...)

Figure 12.8. Visual field deficits resulting from damage at different points along the primary visual pathway.

Figure 12.8

Visual field deficits resulting from damage at different points along the primary visual pathway. The diagram on the left illustrates the basic organization of the primary visual pathway and indicates the location of various lesions. The right panels (more...)

Damage to the retina or one of the optic nerves before it reaches the chiasm results in a loss of vision that is limited to the eye of origin. In contrast, damage in the region of the optic chiasm—or more centrally—results in specific types of deficits that involve the visual fields of both eyes (Figure 12.8). Damage to structures that are central to the optic chiasm, including the optic tract, lateral geniculate nucleus, optic radiation, and visual cortex, results in deficits that are limited to the contralateral visual hemifield. For example, interruption of the optic tract on the right results in a loss of sight in the left visual field (that is, blindness in the temporal visual field of the left eye and the nasal visual field of the right eye). Because such damage affects corresponding parts of the visual field in each eye, there is a complete loss of vision in the affected region of the binocular visual field, and the deficit is referred to as a homonymous hemianopsia (in this case, a left homonymous hemianopsia).

In contrast, damage to the optic chiasm results in visual field deficits that involve noncorresponding parts of the visual field of each eye. For example, damage to the middle portion of the optic chiasm (which is often the result of pituitary tumors) can affect the fibers that are crossing from the nasal retina of each eye, leaving the uncrossed fibers from the temporal retinas intact. The resulting loss of vision is confined to the temporal visual field of each eye and is known as bitemporal hemianopsia. It is also called heteronomous hemianopsia to emphasize that the parts of the visual field that are lost in each eye do not overlap. Individuals with this condition are able to see in both left and right visual fields, provided both eyes are open. However, all information from the most peripheral parts of visual fields (which are seen only by the nasal retinas) is lost.

Damage to central visual structures is rarely complete. As a result, the deficits associated with damage to the chiasm, optic tract, optic radiation, or visual cortex are typically more limited than those shown in Figure 12.8. This is especially true for damage along the optic radiation, which fans out under the temporal and parietal lobes in its course from the lateral geniculate nucleus to the striate cortex. Some of the optic radiation axons run out into the temporal lobe on their route to the striate cortex, an anomaly called Meyer's loop (see Figure 12.7). Meyer's loop carries information from the superior portion of the contralateral visual field. More medial parts of the optic radiation, which pass under the cortex of the parietal lobe, carry information from the inferior portion of the contralateral visual field. Damage to parts of the temporal lobe with involvement of Meyer's loop can thus result in a superior homonymous quadrantanopsia; damage to the optic radiation underlying the parietal cortex results in an inferior homonymous quadrantanopsia.

Injury to central visual structures can also lead to a phenomenon called macular sparing, i.e., the loss of vision throughout wide areas of the visual field, with the exception of foveal vision. Macular sparing is commonly found with damage to the cortex, but can be a feature of damage anywhere along the length of the visual pathway. Although several explanations for macular sparing have been offered, including overlap in the pattern of crossed and uncrossed ganglion cells supplying central vision, the basis for this selective preservation is not clear.

By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.

Copyright © 2001, Sinauer Associates, Inc.
Bookshelf ID: NBK10912

Views

  • Cite this Page

Related Items in Bookshelf

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...