Pigment Epithelium of the Retina

This epithelium is composed of a single layer of cuboidal cells with their base on a basement membrane apposed to the choroid and their apex facing the photosensitive layer across the potential space of the neural tube (lumen of the optic cup).^159,217 This epithelium is entirely derived from the outer wall of the optic cup. Numerous processes of the apical cell membrane and cytoplasm interdigitate with the processes of the external segments of the photoreceptor rods and cones. In cats, this structure is quite elaborate, with specialized sheetlike projections from the apical surface of the pigment epithelium ensheathing the external segments of the cones and, to a lesser degree, the rods. This close arrangement may facilitate the role of the pigment epithelium in the regeneration of rhodopsin, the visual pigment in the rods, and the removal of degenerate rod membranous lamellae by pigment-cell phagocytosis. Many melanin granules fill the apical cytoplasm of the pigment cells throughout the retina, except over the area occupied by the tapetum lucidum in the adjacent choroid. The presence of these pigment granules partly accounts for the dark color of the non-tapetal portion of the fundus observed with the ophthalmoscope. The tapetum lucidum in the choroid is rendered more visible by the absence of melanin pigment in this pigment epithelium. These pigment cells and the photoreceptor neurons are nourished by the vessels of the choriocapillaris layer of the choroid. This layer is adjacent to the scleral side of the pigment epithelial cells. Exchange of substances between these choroidal vessels and the photoreceptor neurons must pass through the pigment epithelial cells.

Photosensitive Layer

The photosensitive layer,² divided into two segments, represents the dendritic zone and cell body of the special somatic afferent neuron, the photoreceptor cell.^210,217 The external and internal segments of the layer are composed of modifications of the cell processes and the bodies of the rod and cone cells. Their nuclei are in the external nuclear layer. The external segment of the photosensitive layer represents the dendritic zones of these neurons. For each neuron (rod and cone), the component in the external segment consists of parallel lamellae within an elongate cell process. These lamellae are orderly stacks of flattened, double-membrane sacs in the form of disks. These membranes are oriented transversely to the axis of the cell process. They are formed at the base of the external segment from the modified cilium located there. These membranes are continually being produced. They migrate distally (away from the vitreous) and are cast off at the outer portion, where they are phagocytized by the pigment epithelial cells.^73,131,220 In the rods, these membranes contain the visual pigment rhodopsin, the photoreceptor substance responsible for light absorption and the initiation of the visual stimulus. A similar substance, iodopsin, is in the cone membranous lamellae. The rod cells are sensitive to low levels of illumination (night vision) and are more abundant in nocturnal animals. Cone cells respond to high levels of illumination (day vision) and are responsible for initiating color vision.

The external segment is connected to the internal segment by a slender stalk containing the modified cilium. The internal segment, called the ellipsoid, is elongated in rods and oval in cones and is composed mostly of endoplasmic reticulum and numerous mitochondria. The ellipsoid is a modification of the cell body of these photoreceptor special somatic afferent neurons.

External Limiting Membrane

The external limiting membrane consists of the junctional complexes between the photoreceptor neurons and the supporting radial astrocytes (the cells of Muller). These latter cells surround and support all the neural elements of the retina between the internal limiting membrane adjacent to the vitreous and the external limiting membrane, which is on the scleral side of the external nuclear layer between the internal segments and the nuclei of the photoreceptor neurons.

External Nuclear Layer

The external nuclear layer is composed of the nuclei of the cell bodies of the photoreceptors, which are special somatic afferent neurons. The cone nuclei are located adjacent to the external limiting membrane. The rod nuclei are smaller than cone nuclei and constitute most of this layer. They extend in several layers toward the vitreal surface of the retina. In the dog retina, the ratio of rod cells to cone cells is estimated to be approximately 18 to 1. The number of cone cells increases toward the central area of the retina. Rod cells predominate in the retinas of all the domestic animals that have been studied and are more common in animals that are active during the night when illumination is limited. Axons of the rod and cone cells course vitreally into the next layer.

External Plexiform Layer

The external plexiform layer¹²² is composed of the axons and telodendria of the photoreceptor neurons and the axons and dendritic zones of the bipolar neurons and their synaptic arrangements. Intermingled with these neuronal processes are the processes of horizontal cells. The horizontal cell is an interneuron transmitting between different groups of photoreceptor neurons.

Internal Nuclear Layer

The internal nuclear layer consists primarily of the nuclei in the small cell bodies of bipolar neurons, which are the second neurons in the visual pathway and, similar to the photoreceptor neurons, are restricted to the retina. Bipolar neurons connect photoreceptor neurons with the ganglion neurons in the visual pathway. The dendritic zone of the bipolar neuron is in the external plexiform layer. The axon courses from the external plexiform layer, through the internal nuclear layer, and into the internal plexiform layer, where the telodendron is located. The cell body with its nucleus is situated along the axon in the internal nuclear layer, accounting for its bipolar characteristics. On the scleral surface of this internal nuclear layer are the cell bodies of the horizontal interneurons. On the vitreal surface are the cell bodies of another interneuron, the amacrine cell. This interneuron is in synaptic relationship with the bipolar neurons, ganglion neurons, and other amacrine interneurons. In addition, the nuclei of the radial astrocytes are located in this layer. Whereas many rod cells are in synaptic contact with one bipolar neuron, only one cone cell may be synapsing on a bipolar neuron. Thus convergence of rod cell activity on the bipolar neurons takes place.

Internal Plexiform Layer

The internal plexiform layer^123,124 is composed primarily of the axons and telodendria of the bipolar neurons and the axons and dendritic zones of the ganglion neurons and their synaptic arrangements. In addition, the processes of the amacrine interneurons extend throughout this layer.

Ganglion Layer

This neuronal ganglion layer contains the cell bodies and nuclei of the third neuron in the visual pathway.* These cell bodies and nuclei are large multipolar neurons with a large cell body and nucleus that comprise an incomplete layer one to two cells thick between the internal plexiform layer and the nerve fiber layer. This neuron transmits the visually induced impulse to the brain by way of its axon in the optic nerve. Endoplasmic reticulum, Nissl substance, is evident in the cytoplasm of these neuronal cell bodies. These cell bodies vary in size from 6 to 35 microns in diameter. The smallest cell bodies have axons that project to the rostral colliculus. The larger cell bodies have axons that project mostly to the lateral geniculate nucleus. Functional differences may be found between the medial (nasal) and lateral (temporal) portions of the retina. Mean ganglion neuron size is greater in the lateral retina than in the medial retina, suggesting a greater projection from the lateral retina (medial visual field in space) to the lateral geniculate nucleus of the thalamus for cerebral projection. An increased number of ganglion neurons can be found in the area centralis, where the smaller cell bodies predominate. Remember that the term for this layer, ganglion, is a misnomer because it implies that these neurons are outside the CNS, which is incorrect.

Nerve Fiber Layer

The nerve fiber layer consists of the axons of the ganglion neurons coursing on the vitreal surface of the retina to the optic disk. These axons are unmyelinated until they penetrate the sclera at the optic disk. Their myelination by oligodendrocytes at this point accounts for the white color of the optic disk. The nerve fiber layer is most thick in the vicinity of the optic disk. The separation of scleral collagen fibers at the point where the axons of ganglion neurons penetrate the sclera to form the optic nerve is called the area cribrosa. Stellate astrocytes are located in this nerve fiber layer.

Internal Limiting Membrane

The internal limiting membrane is formed by the basal cell membrane of the radial astrocyte and a basement membrane adjacent to the vitreous.

Figs. 14-5 and 14-6 show examples of these layers in a dog and horse eye.

Figure 14-5 Microscopic section of the pars optica retina of a dog’s eye. The pigment at the top is in the inner (vitreal) portion of the choroid. Beneath this portion, in order, is the tapetum lucidum of the choroid (1), the pigment epithelium of the retina (without pigment), the external segments of the photosensitive layer, (densely stained), the internal segments of the photosensitive layer (2), the external nuclear layer (nuclei of rods and cones) (3), outer plexiform layer (4), inner nuclear layer (primarily nuclei of bipolar cells) (5), inner plexiform layer (6), ganglion cell layer (single layer of large neurons) (7), and nerve fiber layer (8). The vitreous (9) is at the bottom.

Figure 14-6 Microscopic section of the pars optica retina of a horse eye. At the top is a small inner (vitreal) portion of the choroid where no tapetum lucidum is found. The single layer of pigmented cells adjacent to the choroid is the pigment epithelium of the retina. The remaining layers can be identified below as in the previous figure of the dog retina.

Area Centralis

Humans have a round area for most distinct vision located dorsolateral to the optic disk known as the macula (spot), fovea, or central area. This portion of the retina has the highest resolving power necessary for acute vision. In this area, the retina is composed of only cone cells in the photoreceptor layer, and other modifications occur to facilitate its function for visual acuity. For most precise close-up vision such as reading extraocular neuromuscular mechanisms are responsible for the visual field being focused on this central area in each eyeball. Domestic animals have various modifications of this area. In no species of domestic animal is this area readily seen with the ophthalmoscope, except possibly in some cats. In the cat, this area may be identified as a pale streak or oval in the area of the tapetum lucidum dorsolateral to the optic disk in which the blood vessels (arterioles) converge (Fig. 14-7).²⁰⁹ The area itself is devoid of any large blood vessels. In this area centralis in the cat, an increase in the number of cone cells relative to rod cells can be found in the photosensitive layer, with an overall increase in thickness of the external nuclear layer. The length of the external segments of the photoreceptor cells is increased. The bipolar and ganglion neurons in this area are increased in number as well. The axons in the nerve fiber layer form an arc as they leave the area centralis and course to the optic disk. If the area centralis is defined as a region of the pars optica retina in which ganglion neuron density increases to a peak, then, in all ungulates, this is evident as a streak of high cell density extending horizontally dorsal to the optic disk. This increase in ganglion neurons is maximal near the lateral end of the visual streak, which corresponds approximately to the location of area centralis in cats.

Figure 14-7 Relationship of optic disk and the area centralis (AC) in the retina of a cat.

Optic Disk

The optic disk at the origin of the optic nerve varies in shape in the domestic animals, as well as between breeds of dogs, from round to oval to triangular.^15,141,218 It is usually slightly ventrolateral to the posterior pole of the eyeball and varies in its relationship to the level of the tapetum lucidum. In toy breeds, the optic disk may be in the retina entirely inferior to the inferior border of the tapetum lucidum. In medium-size breeds, it is usually halfway over the inferior border of the tapetum lucidum. In large breeds, it may be entirely over the area of the tapetum lucidum. In cats, the optic disk is small, round, and always over the area of the tapetum lucidum. In horses and ruminants, it is just inferior to the inferior border of the tapetum lucidum. The degree of myelination of the optic disk varies between species of domestic animal, with it being the most developed in the dog and least in cattle. The size and arrangement of the blood vessels at the optic disk also vary between species and are the least prominent in the horse and limited to the periphery of the optic disk. Some examples of photographs of the fundus of a normal dog, cat, cow, and horse can be found in Figs. 14-8 through 14-11.

Figure 14-8 Fundus of the eye of a medium-sized dog breed. Note the abundant myelination of the optic disk, which is at the inferior border of the choroidal tapetum lucidum. Note the veins located in the center of the optic disk.

Figure 14-9 Fundus of a cat eye with the optic disk positioned over the area of the choroidal tapetum lucidum. Note that the optic disk is small, and all of the blood vessels are at the margin of the optic disk.

Figure 14-10 Fundus of a cow eye. Note the optic disk at the inferior border of the choroidal tapetum lucidum with the large tortuous blood vessels and the minimal myelination.

Figure 14-11 Fundus of a horse eye. Note the prominent optic disk just below the inferior border of the choroidal tapetum lucidum (non–tapetal nigrum area). Note the very small blood vessels only located at the margin of the optic disk.

Optic Nerve

The growth of the ganglion neuronal axons through the embryonic optic stalk produces the optic nerve.* In reality, the term optic nerve is a misnomer, given that a nerve is defined as a bundle of neuronal axons outside the CNS and myelinated by Schwann cells. The optic nerve is, in fact, a tract of the CNS based on its origin within the optic cup, which is an extension of the rostral portion of the neural tube that forms the prosencephalon. The axons in the optic nerve are myelinated by oligodendroglia, and this nerve contains astrocytes. The optic nerve is surrounded by meninges and a subarachnoid space. Extensions of the pia course through the nerve as septa. This structure has clinical importance because the optic nerve is subject to diseases of the CNS and not the peripheral nervous system. When contrast is injected into the cerebellomedullary cistern to produce a myelogram and the head is lowered to direct the contrast into the cranial cavity, an encephalogram is produced. The contrast in the subarachnoid space around the brain surrounds the optic nerve from the middle cranial fossa rostrally to the posterior surface of the eyeball, forming an optic thecogram.

The optic nerves course caudally in the orbit surrounded by their meninges, extraocular muscles, and periorbita. They enter the skull through the optic canals of the presphenoid bone, which have considerable length in the horse. The optic nerves join at the optic chiasm ventral to the rostral aspect of the hypothalamus and rostral to the hypophysis.

Optic Chiasm and Tract

At the optic chiasm in domestic animals, a majority of the axons in each optic nerve cross to enter the opposite optic tract. These axons are destined to influence the contralateral occipital lobes of the cerebral hemispheres (Fig. 14-12).^31,37,89,188 This arrangement corresponds to the pattern that most sensory modalities that can be localized in space (general proprioception, general somatic afferent) are represented contralaterally in the brain. The factor that determines whether ganglion neuronal axons cross or not in the chiasm is the subject of extensive ongoing investigations. Research has shown that the signal molecule, sonic hedgehog, that is produced in retinal ganglion neurons plays a role in this development.

Figure 14-12 Central visual pathway for conscious perception.

In fish and birds, all of the optic nerve axons cross in the optic chiasm. In mammals, partial decussation develops in relationship to the development of a binocular field of vision, with frontal positioning of the eyes and the ability to perform coordinated conjugate movements of the eyeballs, including convergence. In primates, in whom this feature is most developed, the degree of decussation is slightly over 50%. Estimates suggest that the degree of decussation in the cat is 65%; in dogs, 75%; and in the horse and farm animals, 80% to 90%. Based on this information, the cat most closely resembles the primate in degree of decussation, frontal positioning of the eyes, and presumably conjugate movements of the eyeballs. As the visual system becomes more complex along with the capability for binocular vision, decussation in the optic chiasm decreases. In avian species, decussation is 100%. The Siamese cat and white Persian tiger have been found to have an increased number of axons that cross in the optic chasm, which is reflected in an altered lamination of the lateral geniculate nucleus. Congenital pendular nystagmus and a convergent strabismus have been considered to be related to this altered visual system architecture in these species.* This feature was described in Chapter 12.

The axons that cross in the optic chiasm come from ganglion neurons in the medial (nasal) aspect of the retina (see Fig. 14-12).^197,200 Axons from ganglion neurons in the lateral (temporal) aspect of the retina remain ipsilateral in their course through the central visual pathway. Neuroanatomic studies in the cat have determined that this division between medial and lateral portions of the retina, based on the axons that cross in the chiasm, is a vertical line approximately through the area centralis. This arrangement was initially determined by cutting one optic tract and studying the retrograde degeneration that occurred in the ganglion neurons of the retina, the axons of which were severed (Fig. 14-13). Studies using horseradish peroxidase injected into the lateral geniculate nucleus of the thalamus have further confirmed this nasotemporal division of the retina.

Figure 14-13 Origin in retinal ganglion layer of axons in the optic tract of the cat.

The optic tracts course caudodorsolateral over the side of the diencephalon, progressing from ventral to lateral to caudal in relationship to the internal capsule to reach the lateral geniculate nucleus.¹⁹ This nucleus forms a caudodorsolateral protrusion of the thalamus (see Fig. 2-2 through 2-6). Each optic tract contains axons mostly from the medial retina of the contralateral eyeball and the lateral retina of the ipsilateral eyeball. The visual field is defined as the area in space observed by each eyeball when fixed at any one moment. Therefore light from the lateral half of the visual field of each eyeball will stimulate the medial retina, and light from the medial half of the visual field will stimulate the lateral retina. Thus each optic tract contains the axons of neurons in which light generates an impulse from the same half of the visual field of each eyeball. That is, the left optic tract contains the axons of neurons stimulated by light from the right half of the visual field of the left and right eyeballs. Objects in the right visual field of each eyeball are therefore represented in the left central visual pathways.

When the optic tract reaches the level of the lateral geniculate nucleus, two basic courses can be followed: (1) a pathway for conscious perception and (2) a reflex pathway.

Pathway for Conscious Perception— Visual Cortex

Approximately 80% of the optic tract axons in the cat terminate in the lateral geniculate nucleus (see Figs. 2-4 through 2-6). This nucleus contains neuronal cell bodies organized in specific laminae.* A retinotopic anatomic relationship is maintained throughout the central visual pathway. This relationship is reflected in the laminar pattern of the lateral geniculate nucleus. The axons of the neuronal cell bodies in the lateral geniculate nucleus project into the internal capsule and course caudally as the optic radiation in the caudal limb of the internal capsule, which forms the lateral wall of the lateral ventricle (see Figs. 2-5, 2-6). These axons terminate in the cerebral (visual) cortex on the lateral, caudal, and medial aspects of the occipital lobe.^72,150 The gyri that comprise this area include the caudal part of the marginal, ectomarginal (laterally), occipital (caudally), and the splenial (medially) gyri. This pathway from the optic tract to the lateral geniculate nucleus to the optic radiation of the internal capsule to the visual cortex must be intact for normal conscious visual perception to occur.

Various portions of the visual cortex have connections to the visual cortex of the opposite cerebrum via the corpus callosum, to the motor cortex of both cerebral hemispheres, to the cerebellum by way of the pons, to the rostral colliculus, and to the mesencephalic tegmentum and nuclei of cranial nerves III, IV, and VI directly or indirectly through the rostral colliculus.

Similar to the arrangement in the optic tract, the lateral geniculate nucleus, optic radiation, and visual cortex on one side of the brain contain neurons stimulated by light from objects in the contralateral half of the visual fields of each eyeball. This route is a retinotopic pathway in that specific anatomic portions of the retina are represented in specific anatomic portions of the optic tract, lateral geniculate nucleus, optic radiation, and visual cortex. These retinal areas have a specific representation in the visual field of each eyeball.

In primates, the visual cerebral cortex is divided into functional areas. Area 17 is for vision of stationary objects. Areas 18 and 19 function in panoramic vision for movement, spatial relationship, and depth perception. For normal object vision, interaction is required between the visual cortex and the rostral colliculus. For normal panoramic vision, interaction is required between the visual cortex and the mesencephalic tegmentum. Removal of the rostral colliculus on one side causes hemianopsia in the contralateral visual field for object vision. Bilateral rostral collicular lesions cause blindness for stationary objects. Visual perception of movement and spatial orientation are lost with lesions of the mesencephalic tegmentum. Unilateral lesions of the tegmentum cause a contralateral deficit in addition to causing a severe torsion of the head such that it tilts more than 90 degrees to the side opposite the lesion. Blindfolding corrects this postural dystonia, indicating its visual basis.

In cats, functional differences between the medial (nasal) and lateral (temporal) portions of the retinal ganglion neurons have been found. These neurons in the lateral retina have a greater projection to the thalamus and visual cortex, whereas more of the medial retinal ganglion neurons project to the rostral colliculus. After bilateral removal of the visual cortex of the occipital lobes, some visual orienting responses persist. These cats can detect objects introduced into the lateral visual field of each eye presumably by using their rostral collicular projection, which is more abundant from the medial retina. Total bilateral rostral colliculectomy causes immediate inattention to all visual stimuli and loss of both visual placing and the menace responses. These functions return in a few days to a week. Obviously the cerebral cortex and rostral midbrain have extensive interaction in mediating visually guided behavior. From a clinical perspective, we do not feel confident that we can make an anatomic diagnosis of a rostral collicular lesion.

Reflex Pathway

Two reflex pathways exist for the optic tract axons. One pathway subserves the pupillary light reflex function, and the other pathway involves reflexes concerned with somatic motor responses to retinal activity.

For the pupillary light reflex, approximately 20% of the optic tract axons in the cat pass over the lateral geniculate nucleus to terminate in the mesencephalic pretectal nucleus or the rostral colliculus (see Fig. 2-5 through 2-7). The pretectal nucleus functions in the pupillary light reflex pathway. Optic tract axons terminate in this nucleus. Most of the axons of the neuronal cell bodies in the pretectal nuclei cross in the caudal commissure to synapse in the contralateral general visceral efferent (GVE) parasympathetic oculomotor nucleus. Thus light entering one eye will have its greatest effect on the pupil of that eye because of the crossing of the majority of the axons in the optic chiasm and again at the caudal commissure.

For somatic motor responses to retinal activity, the axons that course into the rostral colliculus form the brachium of the rostral colliculus, which lies between the lateral geniculate nucleus and the rostral colliculus. The rostral colliculus is also a laminated structure, and, in addition to the optic tract axons, it receives axons from the cerebral cortex (especially the visual cortex) and the spinal cord via the spinomesencephalic (spinotectal) tract in the ventral funiculus. Recall from Chapter 3 that the tectum of the mesencephalon is the roof composed of the four colliculi. Tectonuclear axons of cell bodies in the rostral colliculus project to the tegmentum of the midbrain and medulla to influence the nuclei of cranial nerves III, IV, and VI. A tectospinal tract courses caudally from the rostral colliculus, decussates in the midbrain, and continues through the medulla into the ventral funiculus of the cervical spinal cord to contribute to the upper motor neuron that influences the lower motor neurons in the gray matter of the cervical spinal cord.¹⁵³ These rostral collicular efferent tracts are important in the activation of muscles concerned with the orientation of the eyes, head, and neck in response to visual input. Think of the muscles that are activated for you to follow the action in a sports event or in your response to a flashbulb. Tectothalamic axons project to the thalamus for feedback to the cerebral cortex, and tectocerebellar axons project to the cerebellum via the rostral cerebellar peduncle. All of these pathways function in the coordination of head, neck, and eyeball movements in response to visual stimuli.

Clinical Tests

Vision can be tested by watching the patient walk in a strange environment or through a maze of obstacles. Owners may be unaware of a loss of vision in their pet if its activity is confined to their home or yard and especially if no stairs are available to negotiate. Owners rarely detect unilateral visual loss. In the neurologic examination, vision is evaluated by the menace response and pupillary light reflexes. ^44,46

Menace Response Test

The menace response test consists of making a menacing gesture with the hand directed at one eye while the other eye is covered and observing closure of the eyelids. You can perform this test as you face your patient or while standing over your patient facing in the same direction. Care must be taken not to touch any of the facial hairs or to create too much air turbulence because a palpebral reflex will be elicited. Cover one eye with your hand that is holding the head and lightly tap the eyelids or the side of the face of the eye being tested so that the patient is aware of the test and to be sure the facial nerve functions normally. The menace response is a learned response that requires the entire peripheral and central components of the visual system pathway and connections from the cerebrum to the brainstem with activation of the facial neurons in the medulla. Being a learned response, it is often absent in young animals. It is, however, usually present in foals and calves by 1 to 2 weeks of age and by 10 to 12 weeks of age in puppies and kittens. In patients with facial nerve paralysis, look for retraction of the eyeball away from the menacing gesture, which will be indicated by a brief protrusion of the third eyelid. Occasionally, this patient will retract its entire head away from the gesture. Based on the observation of numerous kinds of lesions located in the cerebral components of this visual pathway, it has been established that these areas are all necessary for the perception of vision required for this menace response. Experimental studies have defined a role for the rostral colliculus in the normal menace response, but the rarity of lesions localized to one or both rostral colliculi does not permit any similar clinical conclusion.

In all domestic animals, diffuse cerebellar disorders, especially those that involve the interposital and lateral cerebellar nuclei, have often been observed to cause a failure of the menace response to elicit eyelid closure bilaterally. The palpebral reflex is normal, as is their vision, based on eyeball or head retraction. The assumption is either that the pathway that mediates this response passes through the cerebellum to reach the facial neurons (Fig. 14-14) or that the cerebellar lesion causes inhibition of the cerebrocortical neurons involved in this response. An anatomic pathway was described in Chapter 13 on the cerebellum that involves a synapse in the pontine nuclei, a cerebropontocerebellar pathway. Alternatively a pathway may involve the rostral colliculus with or without a pontine relay, a cerebrotectopontocerebellar pathway¹¹⁵ or cerebrotectocerebellar pathway. See Video 13-22 and Video 13-23 in Chapter 13 for a good example of this feature in Arabian foals with a diffuse cerebellar cortical abiotrophy. In the horse and dog, we have observed a unilateral loss of the menace response in patients with a large unilateral cerebellar lesion on the same side as the menace deficit. This loss may be explained by the crossing that occurs from the cerebrum to the cerebellum at the pontine nucleus (see Fig. 14-14).

Figure 14-14 An anatomic pathway for the menace response. Mes., Mesencephalon; Met.,metencephalon; Myel., myelencephalon. indicates axons crossing the midline of the brain. A lesion in the left cerebellar hemisphere would prevent a response to a menace directed at the left eye from its left visual field (A) because 65% to 90% of the optic nerve axons cross in the optic chiasm.

1 Retina

2 Optic nerve

3 Optic chiasm

4 Optic tract

5 Lateral geniculate nucleus

6 Optic radiation

7 Visual cortex

8 Internal capsule association fiber

9 Motor cortex

10 Internal capsule projection fiber

11 Crus cerebri

12 Longitudinal fibers of the pons

13 Pontine nucleus

14 Transverse fibers of the pons and middle cerebellar peduncle

15 Cerebellar cortex

16 Efferent cerebellar pathway

17 Facial nuclei

18 Facial muscles-orbicularis oculi

Clinical Signs

See Table 14-1. Refer to Fig. 7-1 to help you determine what to expect with the following location of lesions. The degree of visual deficit depends on the location and extent of the lesion in the visual pathway.

Table 14-1 Clinical Signs of Visual System Lesions

Lesions that destroy the retina or optic nerve in one eye cause blindness and a normal to slightly dilated pupil in that eyeball. Pupil size may be normal in the affected eye if enough light enters the normal eyeball to stimulate both oculomotor nuclei. This lesion does not usually cause any disorientation observable in the gait or posture in domestic animals. No head tilt or any neck curvature is observed; in birds, the lesion may cause a head tilt toward the blind eye. No palpebral closure to the menace gesture made toward the affected eye is observed, but the palpebral reflex is normal. Light directed into the affected blind eyeball produces no response in either eyeball. Light directed into the normal eyeball causes both pupils to constrict. In the pupillary light reflex pathway, many of the afferents cross both in the optic chiasm, as well as in the pretectum, to influence both oculomotor nuclei. Observing both eyes simultaneously is often difficult. The best way to observe the pupillary response in both eyes is to swing the light source, which is held close to the eye, continually from one eye to the other and back again. This action is called the swinging light maneuver. The speed is determined by how fast you can observe the response in the eye when you swing the light to that eye. As you swing the light from one eye to the other, both pupils constrict when the light is directed into the normal eyeball, However, as the light swings back to the affected eye, that pupil will be dilating back to its original size in room light. If the pupil had not constricted when the light was directed into the normal eye, no change would be seen when the light was moved into the affected eye. If you cover the normal eye with your hand, the pupil in the affected eye will dilate because you have eliminated the only source of light to the oculomotor nuclei.

Bilateral retinal or optic nerve disease that is total causes blindness with both pupils widely dilated and unresponsive to light directed into either eyeball. Sudden acquired retinal degeneration syndrome (SARDS) and optic neuritis are each a common causes of this. Ordinarily, very severe retinal or optic nerve lesions are needed to prevent the pupils from constricting to a bright source of light. In most instances, vision will disappear before the loss of the pupillary light reflex. Therefore an animal may be blind from retinal or optic nerve disease but still have pupils that respond to a bright source of light. However, the pupils may be slightly dilated in the relatively subdued room light. Remember that the light source used for the pupillary light reflex is very bright, and if any retinal or optic nerve axons are intact, a pupillary light reflex will be observed. Another way to consider this factor is that, as a disease process progressively interferes with retinal or optic nerve function, vision will be lost before the pupillary light reflex. If blindness occurs slowly and the patient is confined to a small environment, the visual deficit may not be noticed. Blind animals may adjust well to their normal surroundings. Owners often describe an acute onset of blindness in their dogs that have either SARDS or optic neuritis, both of which are progressive diseases. These patients have undoubtedly been losing their vision for some time and only when most of these structures have lost their function does the patient appear to be suddenly blind.

Unilateral lesions in the optic tract, lateral geniculate nucleus, optic radiation, and visual cortex result in a visual deficit in the contralateral visual field of each eyeball. Because of the degree of decussation in the optic chiasm, the visual deficit can be appreciated only in the contralateral eyeball. This abnormality is called hemianopsia because a visual field deficit occurs in 50% of the total visual field. In the dog, this level represents approximately a 25% retinal dysfunction in the ipsilateral eyeball and a 75% retinal dysfunction in the contralateral eyeball. In the dog and cat, the visual deficit is most evident in the failure of the menace response in the contralateral eye. This aspect is very reliable despite the still-intact function of the lateral retinal neurons that do not decussate in the optic chiasm. The visual deficit may be difficult to detect as the patient moves around in its surroundings. Occasionally, an object may be bumped on the side opposite to that of the lesion. However, in many instances, no evidence of a visual deficit is observed. Unilateral blindfolding and maze testing of the patient may be helpful. In the large animals with 80% to 90% of the optic nerve axons crossing in the optic chiasm, a greater tendency exists for the patient to walk into objects on the side of the visual deficit, contralateral to the lesion.

All domestic animals with these unilateral lesions in the central visual pathway exhibit a poor to absent palpebral closure response to menacing gestures to the eyeball that is contralateral to the lesion. If the examiner is careful, this test can be reliably performed without using a transparent barrier between the hand and the eyeball to prevent air currents and direct contact with facial hairs. The dropping of cotton balls, which some recommend instead of the menace test, is unreliable and awkward to perform. In small animals, the eye not being tested must be covered. By menacing the eye from both the medial and lateral visual fields when a lesion exists in the contralateral central visual pathway, you may determine that the deficit is more pronounced when the lateral visual field is tested.

In unilateral lesions of the central visual pathway caudal to the optic chiasm, the pupillary light reflex responses are usually normal. The logical assumption is that a unilateral lesion in the optic tract will cause a decreased pupillary light reflex in the contralateral eyeball because most of the optic nerve axons cross in the optic chiasm and most of the axons of pretectal neurons cross back to the oculomotor nucleus on the side of the eyeball that is stimulated (see Fig. 7-1). In our experience, this difference in the pupillary light reflex response between the two eyeballs with a unilateral optic tract lesion has been difficult to appreciate.

Bilateral lesions in the optic tracts and the lateral geniculate nuclei that involve the pathway to the pretectal nuclei, if complete, will cause blindness with dilated pupils that are unresponsive to light. More often the lesions here are partial, and clinical signs are difficult to determine. Canine distemper virus often produces extensive demyelinating lesions in the optic tracts without obvious clinical deficits of vision or pupillary function.

The central visual pathway from the lateral geniculate nucleus to the visual cortex contains no neurons in the pupillary light reflex pathway, and therefore lesions here cannot interfere with this reflex. Bilateral lesions here can cause complete blindness with normal pupillary light reflexes.

Abnormal Pupils

The following four case examples provide cases of clinical disorders that involve the pupillary light reflex. See Table 7-1 and the description of similar clinical disorders in Chapter 7.