Guyton and Hall Textbook of Medical Physiology, 12th Ed


The Eye

III. Central Neurophysiology of Vision

Visual Pathways

image Figure 51-1 shows the principal visual pathways from the two retinas to the visual cortex. The visual nerve signals leave the retinas through the optic nerves. At the optic chiasm, the optic nerve fibers from the nasal halves of the retinas cross to the opposite sides, where they join the fibers from the opposite temporal retinas to form the optic tracts. The fibers of each optic tract then synapse in the dorsal lateral geniculate nucleus of the thalamus, and from there, geniculocalcarine fibers pass by way of the optic radiation (also called the geniculocalcarine tract) to the primary visual cortex in the calcarine fissure area of the medial occipital lobe.


Figure 51-1 Principal visual pathways from the eyes to the visual cortex.

(Modified from Polyak SL: The Retina. Chicago: University of Chicago, 1941.)

Visual fibers also pass to several older areas of the brain: (1) from the optic tracts to the suprachiasmatic nucleus of the hypothalamus, presumably to control circadian rhythms that synchronize various physiologic changes of the body with night and day; (2) into the pretectal nuclei in the midbrain, to elicit reflex movements of the eyes to focus on objects of importance and to activate the pupillary light reflex; (3) into the superior colliculus, to control rapid directional movements of the two eyes; and (4) into the ventral lateral geniculate nucleus of the thalamus and surrounding basal regions of the brain, presumably to help control some of the body’s behavioral functions.

Thus, the visual pathways can be divided roughly into an old system to the midbrain and base of the forebrain and a new system for direct transmission of visual signals into the visual cortex located in the occipital lobes. In humans, the new system is responsible for perception of virtually all aspects of visual form, colors, and other conscious vision. Conversely, in many primitive animals, even visual form is detected by the older system, using the superior colliculus in the same manner that the visual cortex is used in mammals.

Function of the Dorsal Lateral Geniculate Nucleus of the Thalamus

The optic nerve fibers of the new visual system terminate in the dorsal lateral geniculate nucleus, located at the dorsal end of the thalamus and also called the lateral geniculate body, as shown in Figure 51-1. The dorsal lateral geniculate nucleus serves two principal functions: First, it relays visual information from the optic tract to the visual cortex by way of the optic radiation (also called the geniculocalcarine tract). This relay function is so accurate that there is exact point-to-point transmission with a high degree of spatial fidelity all the way from the retina to the visual cortex.

Half the fibers in each optic tract after passing the optic chiasm are derived from one eye and half from the other eye, representing corresponding points on the two retinas. However, the signals from the two eyes are kept apart in the dorsal lateral geniculate nucleus. This nucleus is composed of six nuclear layers. Layers II, III, and V (from ventral to dorsal) receive signals from the lateral half of the ipsilateral retina, whereas layers I, IV, and VI receive signals from the medial half of the retina of the opposite eye. The respective retinal areas of the two eyes connect with neurons that are superimposed over one another in the paired layers, and similar parallel transmission is preserved all the way to the visual cortex.

The second major function of the dorsal lateral geniculate nucleus is to “gate” the transmission of signals to the visual cortex—that is, to control how much of the signal is allowed to pass to the cortex. The nucleus receives gating control signals from two major sources: (1) corticofugal fibers returning in a backward direction from the primary visual cortex to the lateral geniculate nucleus, and (2) reticular areas of the mesencephalon. Both of these are inhibitory and, when stimulated, can turn off transmission through selected portions of the dorsal lateral geniculate nucleus. Both of these gating circuits help highlight the visual information that is allowed to pass.

Finally, the dorsal lateral geniculate nucleus is divided in another way: (1) Layers I and II are called magnocellular layers because they contain large neurons. These receive their input almost entirely from the large type Y retinal ganglion cells. This magnocellular system provides a rapidly conducting pathway to the visual cortex. However, this system is color blind, transmitting only black-and-white information. Also, its point-to-point transmission is poor because there are not many Y ganglion cells, and their dendrites spread widely in the retina. (2) Layers III through VI are called parvocellular layers because they contain large numbers of small to medium-sized neurons. These neurons receive their input almost entirely from the type X retinal ganglion cells that transmit color and convey accurate point-to-point spatial information, but at only a moderate velocity of conduction rather than at high velocity.

Organization and Function of the Visual Cortex

Figures 51-2 and 51-3 show the visual cortex located primarily on the medial aspect of the occipital lobes. Like the cortical representations of the other sensory systems, the visual cortex is divided into a primary visual cortex and secondary visual areas.


Figure 51-2 Visual cortex in the calcarine fissure area of the medial occipital cortex.


Figure 51-3 Transmission of visual signals from the primary visual cortex into secondary visual areas on the lateral surfaces of the occipital and parietal cortices. Note that the signals representing form, third-dimensional position, and motion are transmitted mainly into the superior portions of the occipital lobe and posterior portions of the parietal lobe. By contrast, the signals for visual detail and color are transmitted mainly into the anteroventral portion of the occipital lobe and the ventral portion of the posterior temporal lobe.

Primary Visual Cortex

The primary visual cortex (see Figure 51-2) lies in the calcarine fissure area, extending forward from the occipital pole on the medial aspect of each occipital cortex. This area is the terminus of direct visual signals from the eyes. Signals from the macular area of the retina terminate near the occipital pole, as shown in Figure 51-2, whereas signals from the more peripheral retina terminate at or in concentric half circles anterior to the pole but still along the calcarine fissure on the medial occipital lobe. The upper portion of the retina is represented superiorly and the lower portion inferiorly.

Note in the figure the large area that represents the macula. It is to this region that the retinal fovea transmits its signals. The fovea is responsible for the highest degree of visual acuity. Based on retinal area, the fovea has several hundred times as much representation in the primary visual cortex as do the most peripheral portions of the retina.

The primary visual cortex is also called visual area I. Still another name is the striate cortex because this area has a grossly striated appearance.

Secondary Visual Areas of the Cortex

The secondary visual areas, also called visual association areas, lie lateral, anterior, superior, and inferior to the primary visual cortex. Most of these areas also fold outward over the lateral surfaces of the occipital and parietal cortex, as shown in Figure 51-3. Secondary signals are transmitted to these areas for analysis of visual meanings. For instance, on all sides of the primary visual cortex is Brodmann’s area 18 (see Figure 51-3), which is where virtually all signals from the primary visual cortex pass next. Therefore, Brodmann’s area 18 is called visual area II, or simply V-2. The other, more distant secondary visual areas have specific designations—V-3, V-4, and so forth—up to more than a dozen areas. The importance of all these areas is that various aspects of the visual image are progressively dissected and analyzed.

The Primary Visual Cortex Has Six Major Layers

Like almost all other portions of the cerebral cortex, the primary visual cortex has six distinct layers, as shown in Figure 51-4. Also, as is true for the other sensory systems, the geniculocalcarine fibers terminate mainly in layer IV. But this layer, too, is organized into subdivisions. The rapidly conducted signals from the Y retinal ganglion cells terminate in layer IVcα, and from there they are relayed vertically both outward toward the cortical surface and inward toward deeper levels.


Figure 51-4 Six layers of the primary visual cortex. The connections shown on the left side of the figure originate in the magnocellular layers of the lateral geniculate nucleus (LGN) and transmit rapidly changing black-and-white visual signals. The pathways to the right originate in the parvocellular layers (layers III through VI) of the LGN; they transmit signals that depict accurate spatial detail, as well as color. Note especially the areas of the visual cortex called “color blobs,” which are necessary for detection of color.

The visual signals from the medium-sized optic nerve fibers, derived from the X ganglion cells in the retina, also terminate in layer IV, but at points different from the Y signals. They terminate in layers IVa and IVcβ, the shallowest and deepest portions of layer IV, shown to the right in Figure 51-4. From there, these signals are transmitted vertically both toward the surface of the cortex and to deeper layers. It is these X ganglion pathways that transmit the accurate point-to-point type of vision, as well as color vision.

Vertical Neuronal Columns in the Visual Cortex

The visual cortex is organized structurally into several million vertical columns of neuronal cells, each column having a diameter of 30 to 50 micrometers. The same vertical columnar organization is found throughout the cerebral cortex for the other senses as well (and also in the motor and analytical cortical regions). Each column represents a functional unit. One can roughly calculate that each of the visual vertical columns has perhaps 1000 or more neurons.

After the optic signals terminate in layer IV, they are further processed as they spread both outward and inward along each vertical column unit. This processing is believed to decipher separate bits of visual information at successive stations along the pathway. The signals that pass outward to layers I, II, and III eventually transmit signals for short distances laterally in the cortex. Conversely, the signals that pass inward to layers V and VI excite neurons that transmit signals much greater distances.

“Color Blobs” in the Visual Cortex

Interspersed among the primary visual columns, as well as among the columns of some of the secondary visual areas, are special column-like areas called color blobs. They receive lateral signals from adjacent visual columns and are activated specifically by color signals. Therefore, these blobs are presumably the primary areas for deciphering color.

Interaction of Visual Signals from the Two Separate Eyes

Recall that visual signals from the two separate eyes are relayed through separate neuronal layers in the lateral geniculate nucleus. These signals still remain separated from each other when they arrive in layer IV of the primary visual cortex. In fact, layer IV is interlaced with stripes of neuronal columns, each stripe about 0.5 millimeter wide; the signals from one eye enter the columns of every other stripe, alternating with signals from the second eye. This cortical area deciphers whether the respective areas of the two visual images from the two separate eyes are “in register” with each other—that is, whether corresponding points from the two retinas fit with each other. In turn, the deciphered information is used to adjust the directional gaze of the separate eyes so that they will fuse with each other (be brought into “register”). The information observed about degree of register of images from the two eyes also allows a person to distinguish the distance of objects by the mechanism of stereopsis.

Two Major Pathways for Analysis of Visual Information—(1) The Fast “Position” and “Motion” Pathway; (2) The Accurate Color Pathway

Figure 51-3 shows that after leaving the primary visual cortex, the visual information is analyzed in two major pathways in the secondary visual areas.

1. Analysis of Third-Dimensional Position, Gross Form, and Motion of Objects. One of the analytical pathways, demonstrated in Figure 51-3 by the black arrows, analyzes the third-dimensional positions of visual objects in the space around the body. This pathway also analyzes the gross physical form of the visual scene, as well as motion in the scene. In other words, this pathway tells where every object is during each instant and whether it is moving. After leaving the primary visual cortex, the signals flow generally into the posterior midtemporal area and upward into the broad occipitoparietal cortex. At the anterior border of the parietal cortex, the signals overlap with signals from the posterior somatic association areas that analyze three-dimensional aspects of somatosensory signals. The signals transmitted in this position-form-motion pathway are mainly from the large Y optic nerve fibers of the retinal Y ganglion cells, transmitting rapid signals but depicting only black and white with no color.

2. Analysis of Visual Detail and Color. The red arrows in Figure 51-3, passing from the primary visual cortex into secondary visual areas of the inferior, ventral, and medial regions of the occipital and temporal cortex, show the principal pathway for analysis of visual detail. Separate portions of this pathway specifically dissect out color as well. Therefore, this pathway is concerned with such visual feats as recognizing letters, reading, determining the texture of surfaces, determining detailed colors of objects, and deciphering from all this information what the object is and what it means.

Neuronal Patterns of Stimulation During Analysis of the Visual Image

Analysis of Contrasts in the Visual Image

If a person looks at a blank wall, only a few neurons in the primary visual cortex will be stimulated, regardless of whether the illumination of the wall is bright or weak. Therefore, what does the primary visual cortex detect? To answer this, let us now place on the wall a large solid cross, as shown to the left in Figure 51-5. To the right is shown the spatial pattern of the most excited neurons in the visual cortex. Note that the areas of maximum excitation occur along the sharp borders of the visual pattern. Thus, the visual signal in the primary visual cortex is concerned mainly with contrasts in the visual scene, rather than with noncontrasting areas. We noted in Chapter 50 that this is also true of most of the retinal ganglion because equally stimulated adjacent retinal receptors mutually inhibit one another. But at any border in the visual scene where there is a change from dark to light or light to dark, mutual inhibition does not occur, and the intensity of stimulation of most neurons is proportional to the gradient of contrast—that is, the greater the sharpness of contrast and the greater the intensity difference between light and dark areas, the greater the degree of stimulation.


Figure 51-5 Pattern of excitation that occurs in the visual cortex in response to a retinal image of a dark cross.

Visual Cortex Also Detects Orientation of Lines and Borders—“Simple” Cells

The visual cortex detects not only the existence of lines and borders in the different areas of the retinal image but also the direction of orientation of each line or border—that is, whether it is vertical or horizontal or lies at some degree of inclination. This is believed to result from linear organizations of mutually inhibiting cells that excite second-order neurons when inhibition occurs all along a line of cells where there is a contrast edge. Thus, for each such orientation of a line, specific neuronal cells are stimulated. A line oriented in a different direction excites a different set of cells. These neuronal cells are called simple cells. They are found mainly in layer IV of the primary visual cortex.

Detection of Line Orientation When a Line Is Displaced Laterally or Vertically in the Visual Field—“Complex” Cells

As the visual signal progresses farther away from layer IV, some neurons respond to lines that are oriented in the same direction but are not position specific. That is, even if a line is displaced moderate distances laterally or vertically in the field, the same few neurons will still be stimulated if the line has the same direction. These cells are called complex cells.

Detection of Lines of Specific Lengths, Angles, or Other Shapes

Some neurons in the outer layers of the primary visual columns, as well as neurons in some secondary visual areas, are stimulated only by lines or borders of specific lengths, by specific angulated shapes, or by images that have other characteristics. That is, these neurons detect still higher orders of information from the visual scene. Thus, as one goes farther into the analytical pathway of the visual cortex, progressively more characteristics of each visual scene are deciphered.

Detection of Color

Color is detected in much the same way that lines are detected: by means of color contrast. For instance, a red area is often contrasted against a green area, a blue area against a red area, or a green area against a yellow area. All these colors can also be contrasted against a white area within the visual scene. In fact, this contrasting against white is believed to be mainly responsible for the phenomenon called “color constancy”; that is, when the color of an illuminating light changes, the color of the “white” changes with the light, and appropriate computation in the brain allows red to be interpreted as red even though the illuminating light has changed the color entering the eyes.

The mechanism of color contrast analysis depends on the fact that contrasting colors, called “opponent colors,” excite specific neuronal cells. It is presumed that the initial details of color contrast are detected by simple cells, whereas more complex contrasts are detected by complex and hypercomplex cells.

Effect of Removing the Primary Visual Cortex

Removal of the primary visual cortex in the human being causes loss of conscious vision, that is, blindness. However, psychological studies demonstrate that such “blind” people can still, at times, react subconsciously to changes in light intensity, to movement in the visual scene, or, rarely, even to some gross patterns of vision. These reactions include turning the eyes, turning the head, and avoidance. This vision is believed to be subserved by neuronal pathways that pass from the optic tracts mainly into the superior colliculi and other portions of the older visual system.

Fields of Vision; Perimetry

The field of vision is the visual area seen by an eye at a given instant. The area seen to the nasal side is called the nasal field of vision, and the area seen to the lateral side is called the temporal field of vision.

To diagnose blindness in specific portions of the retina, one charts the field of vision for each eye by a process called perimetry. This is done by having the subject look with one eye closed and the other eye looking toward a central spot directly in front of the eye. Then a small dot of light or a small object is moved back and forth in all areas of the field of vision, and the subject indicates when the spot of light or object can be seen and when it cannot. Thus, the field of vision for the left eye is plotted as shown in Figure 51-6. In all perimetry charts, a blind spot caused by lack of rods and cones in the retina over the optic disc is found about 15 degrees lateral to the central point of vision, as shown in the figure.


Figure 51-6 Perimetry chart, showing the field of vision for the left eye.

Abnormalities in the Fields of Vision

Occasionally, blind spots are found in portions of the field of vision other than the optic disc area. Such blind spots are called scotomata; they frequently are caused by damage to the optic nerve resulting from glaucoma (too much fluid pressure in the eyeball), from allergic reactions in the retina, or from toxic conditions such as lead poisoning or excessive use of tobacco.

Another condition that can be diagnosed by perimetry is retinitis pigmentosa. In this disease, portions of the retina degenerate, and excessive melanin pigment deposits in the degenerated areas. Retinitis pigmentosa usually causes blindness in the peripheral field of vision first and then gradually encroaches on the central areas.

Effect of Lesions in the Optic Pathway on the Fields of Vision

Destruction of an entire optic nerve causes blindness of the affected eye.

Destruction of the optic chiasm prevents the crossing of impulses from the nasal half of each retina to the opposite optic tract. Therefore, the nasal half of each retina is blinded, which means that the person is blind in the temporal field of vision for each eye because the image of the field of vision is inverted on the retina by the optical system of the eye; this condition is called bitemporal hemianopsia. Such lesions frequently result from tumors of the pituitary gland pressing upward from the sella turcica on the bottom of the optic chiasm.

Interruption of an optic tract denervates the corresponding half of each retina on the same side as the lesion; as a result, neither eye can see objects to the opposite side of the head. This condition is known as homonymous hemianopsia.

Eye Movements and Their Control

To make full use of the visual abilities of the eyes, almost equally as important as interpretation of the visual signals from the eyes is the cerebral control system for directing the eyes toward the object to be viewed.

Muscular Control of Eye Movements

The eye movements are controlled by three pairs of muscles, shown in Figure 51-7: (1) the medial and lateral recti, (2) the superior and inferior recti, and (3) the superior and inferior obliques. The medial and lateral recti contract to move the eyes from side to side. The superior and inferior recti contract to move the eyes upward or downward. The oblique muscles function mainly to rotate the eyeballs to keep the visual fields in the upright position.


Figure 51-7 Extraocular muscles of the eye and their innervation.

Neural Pathways for Control of Eye Movements

Figure 51-7 also shows brain stem nuclei for the third, fourth, and sixth cranial nerves and their connections with the peripheral nerves to the ocular muscles. Shown, too, are interconnections among the brain stem nuclei by way of the nerve tract called the medial longitudinal fasciculus. Each of the three sets of muscles to each eye is reciprocally innervated so that one muscle of the pair relaxes while the other contracts.

Figure 51-8 demonstrates cortical control of the oculomotor apparatus, showing spread of signals from visual areas in the occipital cortex through occipitotectal and occipitocollicular tracts to the pretectal and superior colliculus areas of the brain stem. From both the pretectal and the superior colliculus areas, the oculomotor control signals pass to the brain stem nuclei of the oculomotor nerves. Strong signals are also transmitted from the body’s equilibrium control centers in the brain stem into the oculomotor system (from the vestibular nuclei by way of the medial longitudinal fasciculus).


Figure 51-8 Neural pathways for control of conjugate movement of the eyes.

Fixation Movements of the Eyes

Perhaps the most important movements of the eyes are those that cause the eyes to “fix” on a discrete portion of the field of vision. Fixation movements are controlled by two neuronal mechanisms. The first of these allows a person to move the eyes voluntarily to find the object on which he or she wants to fix the vision; this is called the voluntary fixation mechanism. The second is an involuntary mechanism that holds the eyes firmly on the object once it has been found; this is called the involuntary fixation mechanism.

The voluntary fixation movements are controlled by a cortical field located bilaterally in the premotor cortical regions of the frontal lobes, as shown in Figure 51-8. Bilateral dysfunction or destruction of these areas makes it difficult for a person to “unlock” the eyes from one point of fixation and move them to another point. It is usually necessary to blink the eyes or put a hand over the eyes for a short time, which then allows the eyes to be moved.

Conversely, the fixation mechanism that causes the eyes to “lock” on the object of attention once it is found is controlled by secondary visual areas in the occipital cortex, located mainly anterior to the primary visual cortex. When this fixation area is destroyed bilaterally in an animal, the animal has difficulty keeping its eyes directed toward a given fixation point or may become totally unable to do so.

To summarize, posterior “involuntary” occipital cortical eye fields automatically “lock” the eyes on a given spot of the visual field and thereby prevent movement of the image across the retinas. To unlock this visual fixation, voluntary signals must be transmitted from cortical “voluntary” eye fields located in the frontal cortices.

Mechanism of Involuntary Locking Fixation—Role of the Superior Colliculi

The involuntary locking type of fixation discussed in the previous section results from a negative feedback mechanism that prevents the object of attention from leaving the foveal portion of the retina. The eyes normally have three types of continuous but almost imperceptible movements: (1) a continuous tremor at a rate of 30 to 80 cycles per second caused by successive contractions of the motor units in the ocular muscles, (2) a slow drift of the eyeballs in one direction or another, and (3) sudden flicking movements that are controlled by the involuntary fixation mechanism.

When a spot of light has become fixed on the foveal region of the retina, the tremulous movements cause the spot to move back and forth at a rapid rate across the cones, and the drifting movements cause the spot to drift slowly across the cones. Each time the spot drifts as far as the edge of the fovea, a sudden reflex reaction occurs, producing a flicking movement that moves the spot away from this edge back toward the center of the fovea. Thus, an automatic response moves the image back toward the central point of vision.

These drifting and flicking motions are demonstrated in Figure 51-9, which shows by the dashed lines the slow drifting across the fovea and by the solid lines the flicks that keep the image from leaving the foveal region. This involuntary fixation capability is mostly lost when the superior colliculi are destroyed.


Figure 51-9 Movements of a spot of light on the fovea, showing sudden “flicking” eye movements that move the spot back toward the center of the fovea whenever it drifts to the foveal edge. (The dashed lines represent slow drifting movements, and the solid lines represent sudden flicking movements.)

(Modified from Whitteridge D: Central control of the eye movements. In Field J, Magoun HW, Hall VE (eds): Handbook of Physiology. vol. 2, sec. 1. Washington, DC: American Physiological Society, 1960.)

Saccadic Movement of the Eyes—A Mechanism of Successive Fixation Points

When a visual scene is moving continually before the eyes, such as when a person is riding in a car, the eyes fix on one highlight after another in the visual field, jumping from one to the next at a rate of two to three jumps per second. The jumps are called saccades, and the movements are called opticokinetic movements. The saccades occur so rapidly that no more than 10 percent of the total time is spent in moving the eyes, with 90 percent of the time being allocated to the fixation sites. Also, the brain suppresses the visual image during saccades, so the person is not conscious of the movements from point to point.

Saccadic Movements During Reading

During the process of reading, a person usually makes several saccadic movements of the eyes for each line. In this case, the visual scene is not moving past the eyes, but the eyes are trained to move by means of several successive saccades across the visual scene to extract the important information. Similar saccades occur when a person observes a painting, except that the saccades occur in upward, sideways, downward, and angulated directions one after another from one highlight of the painting to another, and so forth.

Fixation on Moving Objects—“Pursuit Movement.”

The eyes can also remain fixed on a moving object, which is called pursuit movement. A highly developed cortical mechanism automatically detects the course of movement of an object and then rapidly develops a similar course of movement for the eyes. For instance, if an object is moving up and down in a wavelike form at a rate of several times per second, the eyes at first may be unable to fixate on it. However, after a second or so, the eyes begin to jump by means of saccades in approximately the same wavelike pattern of movement as that of the object. Then, after another few seconds, the eyes develop progressively smoother movements and finally follow the wave movement almost exactly. This represents a high degree of automatic subconscious computational ability by the pursuit system for controlling eye movements.

Superior Colliculi Are Mainly Responsible for Turning the Eyes and Head Toward a Visual Disturbance

Even after the visual cortex has been destroyed, a sudden visual disturbance in a lateral area of the visual field often causes immediate turning of the eyes in that direction. This does not occur if the superior colliculi have also been destroyed. To support this function, the various points of the retina are represented topographically in the superior colliculi in the same way as in the primary visual cortex, although with less accuracy. Even so, the principal direction of a flash of light in a peripheral retinal field is mapped by the colliculi, and secondary signals are transmitted to the oculomotor nuclei to turn the eyes. To help in this directional movement of the eyes, the superior colliculi also have topological maps of somatic sensations from the body and acoustic signals from the ears.

The optic nerve fibers from the eyes to the colliculi, which are responsible for these rapid turning movements, are branches from the rapidly conducting Y fibers, with one branch going to the visual cortex and the other going to the superior colliculi. (The superior colliculi and other regions of the brain stem are also strongly supplied with visual signals transmitted in type W optic nerve fibers. These represent the oldest visual pathway, but their function is unclear.)

In addition to causing the eyes to turn toward a visual disturbance, signals are relayed from the superior colliculi through the medial longitudinal fasciculus to other levels of the brain stem to cause turning of the whole head and even of the whole body toward the direction of the disturbance. Other types of nonvisual disturbances, such as strong sounds or even stroking of the side of the body, cause similar turning of the eyes, head, and body, but only if the superior colliculi are intact. Therefore, the superior colliculi play a global role in orienting the eyes, head, and body with respect to external disturbances, whether they are visual, auditory, or somatic.

“Fusion” of the Visual Images from the Two Eyes

To make the visual perceptions more meaningful, the visual images in the two eyes normally fuse with each other on “corresponding points” of the two retinas. The visual cortex plays an important role in fusion. It was pointed out earlier in the chapter that corresponding points of the two retinas transmit visual signals to different neuronal layers of the lateral geniculate body, and these signals in turn are relayed to parallel neurons in the visual cortex. Interactions occur between these cortical neurons to cause interference excitation in specific neurons when the two visual images are not “in register”—that is, are not precisely “fused.” This excitation presumably provides the signal that is transmitted to the oculomotor apparatus to cause convergence or divergence or rotation of the eyes so that fusion can be re-established. Once the corresponding points of the two retinas are in register, excitation of the specific “interference” neurons in the visual cortex disappears.

Neural Mechanism of Stereopsis for Judging Distances of Visual Objects

In Chapter 49, it is pointed out that because the two eyes are more than 2 inches apart, the images on the two retinas are not exactly the same. That is, the right eye sees a little more of the right-hand side of the object, and the left eye a little more of the left-hand side, and the closer the object, the greater the disparity. Therefore, even when the two eyes are fused with each other, it is still impossible for all corresponding points in the two visual images to be exactly in register at the same time. Furthermore, the nearer the object is to the eyes, the less the degree of register. This degree of nonregister provides the neural mechanism for stereopsis, an important mechanism for judging the distances of visual objects up to about 200 feet (60 meters).

The neuronal cellular mechanism for stereopsis is based on the fact that some of the fiber pathways from the retinas to the visual cortex stray 1 to 2 degrees on each side of the central pathway. Therefore, some optic pathways from the two eyes are exactly in register for objects 2 meters away; still another set of pathways is in register for objects 25 meters away. Thus, the distance is determined by which set or sets of pathways are excited by nonregister or register. This phenomenon is called depth perception, which is another name for stereopsis.

Strabismus—Lack of Fusion of the Eyes

Strabismus, also called squint or cross-eye, means lack of fusion of the eyes in one or more of the visual coordinates: horizontal, vertical, or rotational. The basic types of strabismus are shown in Figure 51-10: (1) horizontal strabismus, (2) torsional strabismus, and (3) vertical strabismus. Combinations of two or even all three of the different types of strabismus often occur.


Figure 51-10 Basic types of strabismus.

Strabismus is often caused by abnormal “set” of the fusion mechanism of the visual system. That is, in a young child’s early efforts to fixate the two eyes on the same object, one of the eyes fixates satisfactorily while the other fails do so, or they both fixate satisfactorily but never simultaneously. Soon the patterns of conjugate movements of the eyes become abnormally “set” in the neuronal control pathways themselves, so the eyes never fuse.

Suppression of the Visual Image from a Repressed Eye

In a few patients with strabismus, the eyes alternate in fixing on the object of attention. In other patients, one eye alone is used all the time, and the other eye becomes repressed and is never used for precise vision. The visual acuity of the repressed eye develops only slightly, sometimes remaining 20/400 or less. If the dominant eye then becomes blinded, vision in the repressed eye can develop only to a slight extent in adults but far more in young children. This demonstrates that visual acuity is highly dependent on proper development of central nervous system synaptic connections from the eyes. In fact, even anatomically, the numbers of neuronal connections diminish in the visual cortex areas that would normally receive signals from the repressed eye.

Autonomic Control of Accommodation and Pupillary Aperture

Autonomic Nerves to the Eyes

The eye is innervated by both parasympathetic and sympathetic nerve fibers, as shown in Figure 51-11. The parasympathetic preganglionic fibers arise in the Edinger-Westphal nucleus (the visceral nucleus portion of the third cranial nerve) and then pass in the third nerve to the ciliary ganglion, which lies immediately behind the eye. There, the preganglionic fibers synapse with postganglionic parasympathetic neurons, which in turn send fibers through ciliary nerves into the eyeball. These nerves excite (1) the ciliary muscle that controls focusing of the eye lens and (2) the sphincter of the iris that constricts the pupil.


Figure 51-11 Autonomic innervation of the eye, showing also the reflex arc of the light reflex.

(Modified from Ranson SW, Clark SL: Anatomy of the Nervous System: Its Development and Function, 10th ed. Philadelphia: WB Saunders, 1959.)

The sympathetic innervation of the eye originates in the intermediolateral horn cells of the first thoracic segment of the spinal cord. From there, sympathetic fibers enter the sympathetic chain and pass upward to the superior cervical ganglion, where they synapse with postganglionic neurons. Postganglionic sympathetic fibers from these then spread along the surfaces of the carotid artery and successively smaller arteries until they reach the eye. There, the sympathetic fibers innervate the radial fibers of the iris (which open the pupil), as well as several extraocular muscles of the eye, which are discussed subsequently in relation to Horner’s syndrome.

Control of Accommodation (Focusing the Eyes)

The accommodation mechanism—that is, the mechanism that focuses the lens system of the eye—is essential for a high degree of visual acuity. Accommodation results from contraction or relaxation of the eye ciliary muscle. Contraction causes increased refractive power of the lens, as explained in Chapter 49, and relaxation causes decreased power. How does a person adjust accommodation to keep the eyes in focus all the time?

Accommodation of the lens is regulated by a negative feedback mechanism that automatically adjusts the refractive power of the lens to achieve the highest degree of visual acuity. When the eyes have been focused on some far object and must then suddenly focus on a near object, the lens usually accommodates for best acuity of vision within less than 1 second. Although the precise control mechanism that causes this rapid and accurate focusing of the eye is unclear, some of the known features are the following.

First, when the eyes suddenly change distance of the fixation point, the lens changes its strength in the proper direction to achieve a new state of focus within a fraction of a second. Second, different types of clues help to change the lens strength in the proper direction:

1. Chromatic aberration appears to be important. That is, red light rays focus slightly posteriorly to blue light rays because the lens bends blue rays more than red rays. The eyes appear to be able to detect which of these two types of rays is in better focus, and this clue relays information to the accommodation mechanism whether to make the lens stronger or weaker.

2. When the eyes fixate on a near object, the eyes must converge. The neural mechanisms for convergence cause a simultaneous signal to strengthen the lens of the eye.

3. Because the fovea lies in a hollowed-out depression that is slightly deeper than the remainder of the retina, the clarity of focus in the depth of the fovea is different from the clarity of focus on the edges. This may also give clues about which way the strength of the lens needs to be changed.

4. The degree of accommodation of the lens oscillates slightly all the time at a frequency up to twice per second. The visual image becomes clearer when the oscillation of the lens strength is changing in the appropriate direction and becomes poorer when the lens strength is changing in the wrong direction. This could give a rapid clue as to which way the strength of the lens needs to change to provide appropriate focus.

The brain cortical areas that control accommodation closely parallel those that control fixation movements of the eyes, with analysis of the visual signals in Brodmann’s cortical areas 18 and 19 and transmission of motor signals to the ciliary muscle through the pretectal area in the brain stem, then through the Edinger-Westphal nucleus, and finally by way of parasympathetic nerve fibers to the eyes.

Control of Pupillary Diameter

Stimulation of the parasympathetic nerves also excites the pupillary sphincter muscle, thereby decreasing the pupillary aperture; this is called miosis. Conversely, stimulation of the sympathetic nerves excites the radial fibers of the iris and causes pupillary dilation, called mydriasis.

Pupillary Light Reflex

When light is shone into the eyes, the pupils constrict, a reaction called the pupillary light reflex. The neuronal pathway for this reflex is demonstrated by the upper two black arrows in Figure 51-11. When light impinges on the retina, a few of the resulting impulses pass from the optic nerves to the pretectal nuclei. From here, secondary impulses pass to the Edinger-Westphal nucleus and, finally, back through parasympathetic nerves to constrict the sphincter of the iris. Conversely, in darkness, the reflex becomes inhibited, which results in dilation of the pupil.

The function of the light reflex is to help the eye adapt extremely rapidly to changing light conditions, as explained in Chapter 50. The limits of pupillary diameter are about 1.5 millimeters on the small side and 8 millimeters on the large side. Therefore, because light brightness on the retina increases with the square of pupillary diameter, the range of light and dark adaptation that can be brought about by the pupillary reflex is about 30 to 1—that is, up to as much as 30 times change in the amount of light entering the eye.

Pupillary Reflexes or Reactions in Central Nervous System Disease

A few central nervous system diseases damage nerve transmission of visual signals from the retinas to the Edinger-Westphal nucleus, thus sometimes blocking the pupillary reflexes. Such blocks may occur as a result of central nervous system syphilis, alcoholism, encephalitis, and so forth. The block usually occurs in the pretectal region of the brain stem, although it can result from destruction of some small fibers in the optic nerves.

The final nerve fibers in the pathway through the pretectal area to the Edinger-Westphal nucleus are mostly of the inhibitory type. When their inhibitory effect is lost, the nucleus becomes chronically active, causing the pupils to remain mostly constricted, in addition to their failure to respond to light.

Yet the pupils can constrict a little more if the Edinger-Westphal nucleus is stimulated through some other pathway. For instance, when the eyes fixate on a near object, the signals that cause accommodation of the lens and those that cause convergence of the two eyes cause a mild degree of pupillary constriction at the same time. This is called the pupillary reaction to accommodation. A pupil that fails to respond to light but does respond to accommodation and is also very small (an Argyll Robertson pupil) is an important diagnostic sign of central nervous system disease such as syphilis.

Horner’s Syndrome

The sympathetic nerves to the eye are occasionally interrupted. Interruption frequently occurs in the cervical sympathetic chain. This causes the clinical condition called Horner’s syndrome, which consists of the following effects: First, because of interruption of sympathetic nerve fibers to the pupillary dilator muscle, the pupil remains persistently constricted to a smaller diameter than the pupil of the opposite eye. Second, the superior eyelid droops because it is normally maintained in an open position during waking hours partly by contraction of smooth muscle fibers embedded in the superior eyelid and innervated by the sympathetics. Therefore, destruction of the sympathetic nerves makes it impossible to open the superior eyelid as widely as normally. Third, the blood vessels on the corresponding side of the face and head become persistently dilated. Fourth, sweating (which requires sympathetic nerve signals) cannot occur on the side of the face and head affected by Horner’s syndrome.


Bridge H., Cumming B.G. Representation of binocular surfaces by cortical neurons. Curr Opin Neurobiol. 2008;18:425.

Buttner-Ennever J.A., Eberhorn A., Horn A.K. Motor and sensory innervation of extraocular eye muscles. Ann N Y Acad Sci. 2003;1004:40.

Collewijn H., Kowler E. The significance of microsaccades for vision and oculomotor control. J Vis. 2008;8(20):1-21.

Crawford J.D., Martinez-Trujillo J.C., Klier E.M. Neural control of three-dimensional eye and head movements. Curr Opin Neurobiol. 2003;13:655.

Derrington A.M., Webb B.S. Visual system: how is the retina wired up to the cortex? Curr Biol. 2004;14:R14.

Guyton D.L. Ocular torsion reveals the mechanisms of cyclovertical strabismus: the Weisenfeld lecture. Invest Ophthalmol Vis Sci. 2008;49:847.

Hikosaka O., Takikawa Y., Kawagoe R. Role of the basal ganglia in the control of purposive saccadic eye movements. Physiol Rev. 2000;80:953.

Kandel E.R., Schwartz J.H., Jessell T.M. Principles of Neural Science, ed 4. New York: McGraw-Hill, 2000.

Kingdom F.A. Perceiving light versus material. Vision Res. 2008;48:2090.

Klier E.M., Angelaki D.E. Spatial updating and the maintenance of visual constancy. Neuroscience. 2008;156:801.

Krauzlis R.J. Recasting the smooth pursuit eye movement system. J Neurophysiol. 2004;91:591.

Luna B., Velanova K., Geier C.F. Development of eye-movement control. Brain Cogn. 2008;68:293.

Martinez-Conde S., Macknik S.L., Hubel D.H. The role of fixational eye movements in visual perception. Nat Rev Neurosci. 2004;5:229.

Munoz D.P., Everling S. Look away: the anti-saccade task and the voluntary control of eye movement. Nat Rev Neurosci. 2004;5:218.

Nassi J.J., Callaway E.M. Parallel processing strategies of the primate visual system. Nat Rev Neurosci. 2009;10:360.

Parker A.J. Binocular depth perception and the cerebral cortex. Nat Rev Neurosci. 2007;8:379.

Peelen M.V., Downing P.E. The neural basis of visual body perception. Nat Rev Neurosci. 2007;8:636.

Pelli D.G. Crowding: a cortical constraint on object recognition. Curr Opin Neurobiol. 2008;18:445.

Pierrot-Deseilligny C., Milea D., Muri R.M. Eye movement control by the cerebral cortex. Curr Opin Neurol. 2004;17:17.

Roe A.W., Parker A.J., Born R.T., et al. Disparity channels in early vision. J Neurosci. 2007;27:11820.

Sharpe J.A. Neurophysiology and neuroanatomy of smooth pursuit: lesion studies. Brain Cogn. 2008;68:241.


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