FIGURE 13-16

Coronal section showing orientation of nerve fibers in optic tract. IP, Inferior peripheral; M, macular; SP, superior peripheral.

OPTIC RADIATIONS

The fibers leaving the lateral aspect of the LGN, representing inferior retina, follow an indirect route to the occipital lobe. They pass into the temporal lobe and

STRIATE CORTEX

The superior radiations terminate in the area of the striate cortex above the calcarine fissure, called the cuneus gyrus; the inferior radiations terminate in the region below the calcarine fissure—the lingual gyrus. Thus the cuneus gyrus receives projections from the superior retina and the lingual gyrus from the inferior retina. Only one third of the striate cortex is on the surface of the occipital lobe; the majority is buried within

LGN

Striate cortex

FIGURE 13-17

Retinotopic map representation in lateral geniculate nucleus (or body, LGN). Fibers from ipsilateral (temporal) retina terminate in layers 2, 3, and 5. Fibers from contralateral (nasal) retina terminate in layers 1, 4, and 6. Fibers that originate in neighboring areas of all layers of LGN terminate in same place in striate cortex.

the calcarine fissure, and only a small portion is on the posterolateral aspect of the occipital posterior pole.58 Fibers from the macular area terminate in the most posterior part of the striate cortex, with the superior macular area represented in the cuneus gyrus and the inferior macula represented in the lingual gyrus. The macular projection might extend onto the posterolateral surface of the occipital cortex. The macular area representation occupies a relatively large portion of striate cortex compared with the small macular area in the retina. The macular cells are densely packed, and macular fibers are small caliber. Because macular function involves sharp, detailed vision, the macular representation in the striate cortex is more extensive than the representation of peripheral retinal areas. The most anterior part of the striate cortex, the part adjacent to the parietal lobe, represents the periphery of the nasal retina, corresponding to an area of visual field, the temporal crescent, that is

seen by the contralateral eye only.

FIGURE 13-18

Location of optic radiations in cerebral hemisphere. Meyer loops pass into temporal lobe before passing into parietal lobe.

Retinotopic representation is present in the striate cortex. Those fibers that are adjacent to one another in the layers of the LGN project to the same area in the visual cortex (see Figure 13-17). That is, corresponding points from the two retinas (ipsilateral temporal and contralateral nasal) that represent the same target in the visual field will project to neighboring locations in the primary visual cortex. All the cells in a column correspond to a stimulus presented at the same point in the visual field, and cells in an adjacent column correspond to an adjacent point in the visual field.

Clinical Comment: Visual Field

Testing

THE VISUAL FIELD  is tested monocularly, with the patient looking straight ahead at a fixation point and responding when a target is seen anywhere in the area surrounding that fixation point, usually described to the patient as “seen out of the corner of your eye.” The field can be divided into four quadrants by a vertical line and a horizontal line that intersect at the point of fixation. The point of fixation is seen by the fovea and is eccentric because the temporal field is slightly larger than the nasal field. Inversion and reversal

of the field are caused by the optical system of the eye. The superior field is imaged on the inferior retina and the inferior field on the superior retina; the nasal field is imaged on the temporal retina and the temporal field on the nasal retina (Figure 13-19). This orientation is maintained in the cortex, where the superior field is projected onto the visual cortex inferior to the calcarine fissure, and where the inferior visual field is projected onto the cortex superior to the calcarine fissure.

The reader is cautioned to be aware of the difference between visual fibers and visual fields. Both can be described as nasal, temporal, superior, and inferior.

The visual field seen by the right eye is nearly the same as that seen by the left eye. The nasal part of the field for one eye is the same as the temporal part of the field seen by the other eye, with the exception of the far temporal ­periphery, which is called the temporal crescent. The

temporal­ crescent­ is imaged on the nasal retina of one eye but not on the temporal retina of the other because the depth of the orbit and the prominence of the nose blocks the periphery of the field from the temporal retina. Within each temporal field is an absolute scotoma, the physiologic blind spot, a result of the lack of photoreceptors in the optic disc (Figure 13-20).

Because the fibers that emanate from nasal retina cross in the chiasm, the postchiasmal pathway carries information from the contralateral temporal field and the ipsilateral nasal field. These combined areas can be described as the contralateral hemifield (i.e., the right postchiasmal pathway carries information from the left side of the visual

field for both eyes). Thus, the left side of the field is “seen” by the right striate cortex, paralleling the involvement of the right hemisphere in the motor and sensory activities of the left side of the body. Similarly, objects in the right side of the field are “seen” by the left striate cortex (see Figure 13-1).

Note that reference to the “left side of the visual field” is not the same as the “visual field of the left eye.” Also, some clinicians will refer to the right visual field (meaning the right side of the field) and the left visual field (meaning the left side of the field).

A defect that affects the nasal field of one eye and the temporal­ field of the other eye is described as

homonymous­ . A defect in the field of just one eye must be caused by a disruption anterior to the chiasm. If there is a defect in the fields of both eyes, there are two lesions, one in each prechiasmal pathway, or there is a single lesion in the chiasm or the postchiasmal pathway, where the fibers for the two eyes are brought together. The pattern of the defect, as well as associated signs or symptoms, might aid in determining the location of the damage.

Clinical Comment: Characteristic

Visual Field Defects

Figure 13-21 depicts examples of various visual field defects.

The regular fiber orientation in each structure of the visual pathway can be correlated with a specific pattern of visual field loss. A lesion of the choroid or outer retina will cause a field defect that is similar in shape to the lesion and is in the corresponding location in the field (e.g., if the lesion is in the superior nasal retina, the defect will be in the inferior temporal field).

A lesion in the nerve fiber layer will cause a field defect corresponding­ to the location and configuration of the affected nerve fiber bundle. One of the disease processes­

that affects the nerve fiber layer is glaucoma. If ­temporal retinal fibers are affected, an arcuate defect can be produced­ that curves around the point of fixation­ from the blind spot to termination at the horizontal nasal meridian­

(Figure 13-22). This abrupt edge (at the ­horizontal ­meridian) is called a nasal step and results from the configuration­ of the fibers at the temporal retinal raphe. Less often, a lesion affects a nasal bundle of nerves, producing­ a wedge-shaped defect emanating from the physiologic blind spot into the temporal field.

Injury to the optic nerve is accompanied by a visual field defect, a relative afferent pupillary defect, and atrophy of the affected nerve fibers, which eventually is manifested at the disc. The small-diameter, tightly packed fibers of the macula have the greatest metabolic need and often are affected first in both compressive and ischemic lesions.12

The optic chiasm brings all the visual fibers together; lesions of the chiasm usually will show bitemporal or binasal defects. The most common cause of a bitemporal field defect is

a pituitary gland tumor, and a visual field defect is often the first clinical sign (Figure 13-23, A). A patient may not recognize the field loss because the nasal field of one eye

overlaps the temporal field of the other eye. The crossed fibers seem to be damaged first in compressive lesions such as a tumor.14 This susceptibility to damage might be attributable­

to the purported weak blood supply of the median portion of the chiasm. Consequently, the crossed fibers also are more susceptible to ischemia in a vascular event.41 Involvement of both lateral sides of the chiasm, producing a binasal defect, might be caused by an aneurysm of the internal carotid artery that impinges on the chiasm and displaces it against the other internal carotid artery (Figure 13-23, B).

A single lesion at the optic chiasm and its junction with the optic nerve might be characterized by a central defect in the field of the eye on the same side as the lesion, as well as a superior temporal defect in the field of the opposite eye, because of the inferior nasal fibers that loop into the optic nerve from the contralateral eye. This is known as an anterior junction defect.

A homonymous field defect will be produced by a single lesion in the postchiasmal pathway, as the nasal fibers of the contralateral eye join the temporal fibers of the

ipsilateral eye; visual acuity usually is not affected because one half the fovea is sufficient for 20/20 Snellen acuity­ .14 In this lesion the field loss is present on the side of the field contralateral to the lesion. Other signs or symptoms­ accompanying­ a homonymous defect can help the diagnostician­ determine more exactly the site of the lesion.

A lesion involving the optic tract eventually will produce optic nerve atrophy, which usually becomes evident as optic disc pallor. Because the optic tract is relatively small in cross section, a lesion often damages all of the fibers, causing

a homonymous field defect that affects the entire half of the field; if a partial hemianopia results, the defects will be incongruent.59 The defects in a homonymous field

are congruent if the two defects are similarly shaped and are incongruent if the defect shapes are dissimilar. Because crossed fibers outnumber uncrossed fibers, a lesion of the optic tract may be accompanied by a relative afferent pupillary­ defect of the contralateral eye.14

A lesion in the LGN would affect the contralateral field and eventually also cause optic atrophy; however, there would be no associated pupillary defect. Because of the point-to-point localization in the LGN, lesions here produce ­moderately to completely congruent field defects.42

Damage to the optic radiations or cortex does not normally cause atrophy of the optic nerve because it does not involve the fibers of the retinal ganglion cells. A lesion of the optic radiations causes a contralateral homonymous field defect and, because the fibers are so spread out, the defect often affects only one quadrant. If a lesion of the temporal lobe involves the Meyer loop, a superior quadrant field defect will result; parietal lobe lesions more commonly cause inferior field defects (Figure 13-23, C).14

The characteristic feature of a defect in the occipital lobe is congruency. Congruency depends on how closely fibers from corresponding points of each eye (carrying the same visual field information) are positioned to one another at the site of the lesion. As the fibers reach the occipital lobe and finally the striate cortex, the fibers emanating from corresponding points in the field come together to form a

point-to-point representation of the field. Therefore, a lesion here will cause a congruent defect (Figure 13-24).

When visual association areas within the occipital, ­temporal, and parietal lobes are involved, higher cortical visual processes may be affected. Lesions of the parietal lobe can cause abnormal optokinetic nystagmus and affect visual attention; temporal lobe lesions can cause olfactory ­hallucinations, formed visual hallucinations, or déjà vu phenomenon; injury involving the occipitotemporal cortex can affect object and facial recognition.60 Blind sight occurs when there seems to be some sight in a hemifield but there is no conscious awareness of the sight. That is, a motor reflex response can be elicited with presentation of an unexpected stimulus in the affected field, but the patient has no awareness of the vision. It is likely that subcortical visual responses are mediated at the level of the superior colliculus and that the reflex does not initiate from the visual cortex.