Intraocular Pressure Maintains the Shape of the Eye

The shape of the eye is maintained by having it blown up like a soccer ball. The sclera and cornea provide the tough wall, and the inflation pressure is generated by a fluid secretion-reabsorption system much like the CSF system. The ciliary epithelium secretes a CSF-like aqueous humor into the posterior chamber (the space between the iris and the lens). Just as CSF circulates through the ventricles and subarachnoid space and then filters through arachnoid villi, aqueous humor moves through the pupil, into the anterior chamber (between the iris and cornea), gets filtered into a scleral venous sinus (the canal of Schlemm) near the corneoscleral junction, and from there reaches the venous system. The resistance to flow at the filtration site results in a pressure buildup in the aqueous humor. Because the space behind the lens is filled with gelatinous, incompressible vitreous humor, the pressure in the aqueous humor is transmitted throughout the interior of the eye and the shape of the eye is maintained.

The Cornea and Lens Focus Images on the Retina

There’s a big change in refractive index at the interface between air and the front of the cornea, so this is where most of the focusing happens. The lens contributes less because there’s much less change in refractive index going from aqueous humor to lens or from lens to vitreous humor. The major importance of the lens is in adjusting the focus of the eye during accommodation for near vision (see Fig. 17-9 later in this chapter). Contraction of the ciliary muscle relaxes some of the tension on the capsule suspending the lens, allowing the lens to get fatter and the eye to focus on near objects.

The Iris Affects the Brightness and Quality of the Image Focused on the Retina

The pigmented posterior epithelial layers of the iris prevent light from getting into the eye except through the pupil, so regulating the size of the pupil regulates the amount of light reaching the retina (although neural changes in the retina are much more important for regulating the sensitivity of the eye). The pupillary sphincter, innervated by the oculomotor nerve via the ciliary ganglion, makes the pupil smaller (see Figs. 17-7 and 17-8 later in this chapter). The pupillary dilator, innervated by upper thoracic sympathetics via the superior cervical ganglion, makes the pupil larger.

A System of Barriers Partially Separates the Retina from the Rest of the Body

Another indication that the neural retina is really an outgrowth of the CNS is the way its neurons are protected by a similar three-part barrier system. The endothelial cells of retinal capillaries are zipped up by tight junctions, forming a blood-retinal barrier system in the literal sense. The ciliary epithelium, just like the choroid epithelium, prevents diffusion from the ciliary body into aqueous humor. Finally, the retinal pigment epithelium, in a way analogous to the barrier function of the arachnoid, prevents diffusion from the choroid into the retina.

The Retina Is Regionally Specialized

Ganglion cell axons travel along the vitreal surface of the retina, and so they need to pierce the sclera to leave the eye in the optic nerve. They do so by converging on the optic disk, slightly medial to the optic axis, turning 90° posteriorly, and leaving the eye. Here the optic nerve acquires a dural (scleral) sheath continuous with the dural covering of the CNS. (The dural sheath is lined with arachnoid and contains a bit of subarachnoid space; increases in intracranial pressure are therefore transmitted along the optic nerve and cause papilledema, or swelling of the optic disk.) Because there are no photoreceptors at the optic disk, it corresponds to a blind spot in the visual field of each eye. The optics of the eye reverse images on the retina, so the blind spot of each eye lies near the horizontal meridian of the visual field, slightly lateral to the center of the field.

The center of the visual field corresponds to the fovea, a small retinal region in the middle of a pigmented zone called the macula. The fovea is filled with thin, densely packed cones and no rods. All the other neuronal types are pushed toward the periphery, so the center of the fovea is a small pit (THB6 Figure 17-11, p. 425). Outside the fovea, the number of cones diminishes quickly. The packing density of rods, in contrast, first increases rapidly and then declines slowly. We have three different types of cones in terms of the wavelength to which each is most sensitive, so the total cone population can be used for color vision. Rods, on the other hand, come in only one variety but function at lower light levels than do cones. The fovea, with its densely packed cones, is therefore specialized for high spatial acuity and color vision, but only at moderate or high levels of illumination. The region around the fovea, with many rods and few cones, has reasonably good spatial acuity, works at low light levels, but is not very useful for color vision. Finally, the peripheral retina, with few rods and even fewer cones, is mostly good for telling us that something is moving around out there.

Photopigments Are G Protein–Coupled Receptors That Cause Hyperpolarizing Receptor Potentials

Phototransduction is a lot like G protein–coupled synaptic transmission (Fig. 17-3); the equivalent of the postsynaptic receptor protein is opsin, which in the dark binds a particular stereoisomer of a vitamin A derivative (11-cis-retinal). Absorption of a photon by a visual pigment molecule has only one direct effect: It photoisomerizes the 11-cis-retinal, changing the way it fits with opsin. This in turn activates nearby G proteins, each of which activates an enzyme that hydrolyzes cytoplasmic cyclic guanosine monophosphate (cGMP). The surface membranes of photoreceptor outer segments contain cGMP-gated cation channels, so cGMP hydrolysis causes the channels to close and the photoreceptor to hyperpolarize. Hence, light for a photoreceptor is a lot like neurotransmitter release at an unusual G protein–coupled inhibitory synapse—in the light G proteins dissociate, the concentration of a second messenger changes, and cation channels close.

Figure 17-3 Phototransduction in rods. Even though the photopigment-studded membranous disks in cones are open to extracellular space, the transduction process is basically the same (see THB6 Figure 17-16B, p. 431).

Ganglion Cells Have Center-Surround Receptive Fields

Ganglion cells, as mentioned previously, are contrast detectors. The receptive field of each has a center and a surround. The center is a central spot where light causes the cell to fire faster (ON-center) or slower (OFF-center), and the surround is an area where light has just the opposite effect. The result is that if uniform illumination (the level doesn’t matter) covers the whole receptive field, the center and surround more or less cancel each other out. In contrast, if the illumination is nonuniform, either the center or the surround will “win” and the ganglion cell will signal the difference between the two.

The centers of ganglion cell receptive fields result from “straight-through” transmission from receptors to bipolar cells to ganglion cells (Fig. 17-4). The surrounds result from lateral interactions mediated by horizontal and amacrine cells (especially horizontal cells).

Figure 17-4 Formation of center-surround receptive fields in the outer plexiform layer. A, The centers are formed by transmission from photoreceptors to bipolar cells. Photoreceptors release less glutamate when illuminated. ON-center bipolar cells have inhibitory glutamate receptors (−), so the glutamate decrease causes them to depolarize. OFF-center bipolar cells have more typical excitatory glutamate receptors (+), so the glutamate decrease causes them to hyperpolarize. Bipolar to ganglion cell transmission is all excitatory (+). B, Illumination of photoreceptors also sends a signal through horizontal cells, causing neighboring photoreceptors to release more glutamate. This is the basis of the surround effect, producing an effect exactly the opposite of light in the center of the receptive field.

Damage at Different Points in the Visual Pathway Results in Predictable Deficits

Knowledge of the visual pathway enables you to predict the deficits resulting from damage anyplace in the pathway; knowledge of a little terminology allows you to name them (Fig. 17-5) and bewilder the uninitiated. Deficits are generally named for the visual field affected. Heteronymous means the affected fields of the two eyes do not overlap and homonymous means the affected fields overlap to a greater or lesser degree. Therefore, damage in front of the optic chiasm affects only the eye ipsilateral to the damage, damage to the optic chiasm typically causes heteronymous deficits, and damage behind the chiasm causes homonymous deficits. Terms like hemianopia and quadrantanopia mean half or a quarter of a visual field is nonfunctional.

Figure 17-5 Visual field deficits.

Fibers on their way to the upper bank of the calcarine sulcus go through the retrolenticular part of the internal capsule and straight back to the occipital lobe. Fibers on their way to the lower bank go through the sublenticular part and loop out into the temporal lobe (Meyer’s loop) before turning posteriorly toward the occipital lobe (THB6 Figure 17-28, p. 442). Damage in the optic radiation or the occipital lobe sometimes spares part of the large foveal representation, resulting in foveal or macular sparing.

Some Fibers of the Optic Tract Terminate in the Superior Colliculus, Accessory Optic Nuclei, and Hypothalamus

Although most ganglion cell axons terminate in the lateral geniculate nucleus, a smaller number reach other sites: the superior colliculus (orientation to visual stimuli), the nearby pretectal area (pupillary light reflex), other nearby accessory optic nuclei (reflex eye movements), and the suprachiasmatic nucleus of the hypothalamus (entraining circadian rhythms).

Visual Cortex Has a Columnar Organization

A major function of visual cortex is to continue this process of sorting out the different elements of a visual stimulus. Visual cortex is made up of a series of modules, each made up of a number of columns of neurons extending through the cortex. Collectively the columns of a module receive all the visual information from some area of the contralateral visual field—a large area for modules in the peripheral part of the retinotopic map and a small area for modules in the foveal part (THB6 Figure 17-35, p. 449). The neurons in a given column have similar properties: they all respond best to stimuli in a particular part of the visual field, usually are more sensitive to input from one eye or the other, and typically have some other preference in common as well (color, movement in some direction, orientation of a border, etc.).

Visual Information Is Distributed in Dorsal and Ventral Streams

A second major function of visual cortex, once the various elements of visual stimuli have been sorted out, is to export information about these elements to specific areas of visual association cortex that are specialized to deal with them. Thus, there are visual association areas particularly interested in the color of an object, its distance from the eyes, details of its shape, the direction and velocity of movement, and other properties. Although the segregation of functions is far from complete, in general more dorsal areas process information about location and movement and more ventral areas process information about color and form (Fig. 17-6). As a result, rare, selective lesions in visual association areas can cause a selective loss of only some visual capabilities—even something as specific as the ability to recognize faces (THB6 Box 17-2, p. 451).

Figure 17-6 Dorsal and ventral streams in visual association cortex.

Illumination of Either Retina Causes Both Pupils to Constrict

The size of the pupil is determined by the balance between a relatively strong sphincter and a relatively weak dilator (Fig. 17-7). The sphincter receives parasympathetic innervation via the oculomotor nerve and the ciliary ganglion and is normally activated during the pupillary light reflex and the near reflex (next section). The dilator receives sympathetic innervation via the intermediolateral cell column of the spinal cord and the superior cervical ganglion. The preganglionic sympathetic neurons for the dilator can be activated by long descending pathways from the ipsilateral half of the hypothalamus, as well as by other routes.

Figure 17-7 Control of pupil size.

Pupils of significantly unequal size usually signify damage to some aspect of the autonomic innervation of one eye or to the iris itself. A dilated pupil (mydriasis), unresponsive to all stimuli, could be caused by damage to the ipsilateral oculomotor nerve. Such damage, if it affected the entire nerve, would also be accompanied by weakness of the other muscles supplied by the third nerve, most prominently resulting in ptosis (because of a weak levator palpebrae) and lateral strabismus (because of an unopposed lateral rectus). A pupil that was relatively constricted (miosis), but still responsive to light shone through it, could be caused by damage to either its preganglionic or its postganglionic sympathetic innervation, or to fibers on the ipsilateral side of the brainstem as they descend from the hypothalamus to the spinal cord. (In the pons and medulla, the latter fibers are located near the spinothalamic tract.) This would constitute part of Horner’s syndrome and would be accompanied by slight ipsilateral ptosis (weakness of the sympathetically innervated tarsal muscles) but not by any weakness of other extraocular muscles.

A commonly tested cranial nerve reflex is the pupillary light reflex (Fig. 17-8). Light shone through one pupil causes both sphincters to contract equally. The response of the illuminated eye is the direct reflex, and the equal response of the unilluminated eye is the consensual reflex. Afferent impulses for this reflex arc travel along ganglion cell axons in the optic nerve; half of these cross in the optic chiasm. However, they bypass the lateral geniculate nucleus and travel instead through the brachium of the superior colliculus to the pretectal area, just rostral to the superior colliculus at the midbrain-diencephalon junction. Fibers from the pretectal area then distribute bilaterally to the Edinger-Westphal subnucleus of the oculomotor nucleus, where the preganglionic parasympathetic neurons live. Because of the bilateral distribution of fibers both in the optic chiasm and in going from each pretectal area to the oculomotor nuclei, light in one eye causes equal constriction of both pupils. Optic nerve damage produces equal pupils, neither one of which responds to light shone into the eye ipsilateral to the damage, but both of which respond normally to light shone into the contralateral eye. Oculomotor nerve damage, in contrast, causes a dilated ipsilateral pupil that does not respond to light shone into either eye.

Figure 17-8 Circuitry of the pupillary light reflex.

Both Eyes Accommodate for Near Vision

Looking at something nearby causes three things to happen in reflex fashion: (1) Both medial recti contract, converging the eyes; (2) both ciliary muscles contract, allowing the lens to fatten (accommodation) and thus focus the image of the nearby object on the two retinas; and (3) both pupillary sphincters contract, improving the optical performance of the eye. Because this near reflex or accommodation reflex typically involves consciously looking at something, it is not surprising that its pathway involves a loop through visual cortex (Fig. 17-9). The afferent limb is the standard visual pathway through the lateral geniculate nucleus and visual cortex. After one or more synapses in the occipital lobe, the efferent limb involves a projection back through the brachium of the superior colliculus to the pretectal area and/or the superior colliculus and from there to the oculomotor nucleus. (The stop in the superior colliculus is omitted from Fig. 17-9 for simplicity.)

Figure 17-9 Circuitry of the accommodation (near) reflex.