Ординатура / Офтальмология / Английские материалы / Slatter's Fundemental of Vetrinary Ophthalmology 4th edition_Maggs, Miller, Ofri_2008

Lewis DG, et al. (1986): Congenital microphthalmia and other developmental ocular anomalies in the Doberman. J Small Anim Pract 27:559.

Lightfoot RM, et al. (1996): Retinal pigment epithelial dystrophy in Briard dogs. Res Vet Sci 60:17.

MacMillan AD, Lipton DE (1978): Heritability of multifocal retinal dysplasia in American cocker spaniels. J Am Vet Med Assoc 172:568.

Matz-Rensing K, et al. (1996): Retinal detachment in horses. Equine Vet J 28:111.

McLeod DS, et al. (1998): Clinical and histopathologic features of canine oxygen-induced proliferative retinopathy. Invest Ophthalmol Vis Sci 39:1918.

McLeod DS, et al. (1996): Vaso-obliteration in the canine model of oxygeninduced retinopathy. Invest Ophthalmol Vis Sci 37:300.

McLeod DS, et al. (1996): Vasoproliferation in the neonatal dog model of oxygen-induced retinopathy. Invest Ophthalmol Vis Sci 37:1322.

Meyers VN, et al. (1983): Short-linked dwarfism and ocular defects in the Samoyed dog. J Am Vet Med Assoc 183:975.

Miller PE, et al. (1998): Photoreceptor cell death by apoptosis in dogs with sudden acquired retinal degeneration syndrome. Am J Vet Res 59:149.

Millichamp NJ (1988): Progressive retinal atrophy in Tibetan terriers. J Am Vet Med Assoc 192:769.

Munroe G (2000): Survey of retinal haemorrhages in neonatal thoroughbred foals. Mol Ther 12:1072.

Narfström K, Ekesten B (1999): Diseases of the canine ocular fundus, in Gelatt KN (editor): Veterinary Ophthalmology, 3rd ed. Lippincott Williams & Wilkins, Philadelphia.

Narfström K, Ekesten B (1998): Electroretinographic evaluation of papillons with and without hereditary retinal degeneration. Am J Vet Res 59:221.

Narfström K, et al. (2003): Functional and structural recovery of the retina after gene therapy in the RPE65 null mutation dog. Invest Ophthalmol Vis Sci 44:1663.

Narfström K, et al. (2002): Guidelines for clinical electroretinography in the dog. Doc Ophthalmol 105:83.

Narfström K, et al. (1995): Clinical electroretinography in the dog with Ganzfeld stimulation: a practical method of examining rod and cone function. Doc Ophthalmol 90:279.

Narfström K, et al. (1994): Hereditary retinal dystrophy in the Briard dog: clinical and hereditary characteristics. Vet Comp Ophthalmol 4:85.

Narfström K, et al. (1989): The Briard dog: a new animal model of congenital stationery night blindness. Br J Ophthalmol 73:750.

Narfström K, et al. (1988): Hereditary retinal degeneration in the Abyssinian cat: developmental studies using clinical electroretinography. Doc Ophthalmol 69:111.

Narfström K, et al. (1985): Progressive retinal atrophy in the Abyssinian cat: studies of the DC-recorded electroretinogram and the standing potential of the eye. Br J Ophthalmol 69:618.

Narfström K, Nilsson SE (1985): Hereditary retinal degeneration in the Abyssinian cat: correlation of ophthalmoscopic and electroretinographic findings. Doc Ophthalmol 60:183.

Nelson DL, Macmillan AD (1983): Multifocal retinal dysplasia in field trial Labrador retrievers. J Am Anim Hosp Assoc 19:388.

Nilsson SEG, et al. (1992): Changes in the DC electroretinogram in Briard dogs with hereditary congenital stationery night blindness and partial day blindness. Exp Eye Res 54:291.

Nunnery C, et al. (2005): Congenital stationary night blindness in a thoroughbred and a paso fino. Vet Ophthalmol 8:415.

Ofri R, Narfstrom K (2007): Light at the end of the tunnel? Advances in the understanding and treatment of glaucoma and inherited retinal degeneration. Vet J (E-pub ahead of print).

Ofri R, et al. (1996): Feline central retinal degeneration in captive cheetahs (Acinonyx jubatus). J Zoo Wildl Med 27:101.

O’Toole DO, et al. (1983): Retinal dysplasia of English springer spaniel dogs: light microscopy of the postnatal lesions. Vet Pathol 20:298.

Parshall C, et al. (1991): Photoreceptor dysplasia: an inherited progressive retinal atrophy of miniature schnauzer dogs. Prog Vet Comp Ophthalmol 1:187.

Paulsen ME, et al. (1989): Blindness and sexual dimorphism associated with vitamin A deficiency in cattle. J Am Vet Med Assoc 194:933.

Peiffer RL, Fischer CA (1983): Microphthalmia, retinal dysplasia and anterior segment dysgenesis in a litter of Doberman pinschers. J Am Vet Med Assoc 183:875.

Petersen-Jones S (2005): Advances in the molecular understanding of canine retinal diseases. J Small Anim Pract 46:371.

Petersen-Jones SM, Zhu FX (2000): Development and use of a polymerase chain reaction-based diagnostic test for the causal mutation of progressive retinal atrophy in Cardigan Welsh corgis. Am J Vet Res 61:844.

Pion PD, et al. (1987): Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy. Science 237:764.

RETINA 317

Pizzirani S (2003): Transpupillary diode laser retinopexy in dogs: ophthalmoscopic, fluorescein angiographic and histopathologic study. Vet Ophthalmol 6:227.

Rabin AR, et al. (1973): Cone and rod responses in nutritionally induced retinal degeneration in the cat. Invest Ophthalmol Vis Sci 12:694.

Rampazzo A, et al. (2005): Collie eye anomaly in a mixed-breed dog. Vet Ophthalmol 8:357.

Reppas GP, et al. (1995): Trauma-induced blindness in two horses. Aust Vet J 72:270.

Riis R, et al. (1999): Ocular manifestations of equine motor neuron disease. Equine Vet J 31:99.

Rubin LF (1971): Hemeralopia in Alaskan malamute pups. J Am Vet Med Assoc 158:1699.

Rubin LF (1968): Heredity of retinal dysplasia in Bedlington terriers. J Am Vet Med Assoc 152:260.

Rubin LF (1963): Atrophy of rods and cones in the cat retina. J Am Vet Med Assoc 142:1415.

Sandberg MA, et al. (1986): Full field electroretinograms in miniature poodles with progressive rod-cone degeneration. Invest Ophthalmol 27:1179.

Santo-Anderson R, et al. (1980): An inherited retinopathy in collies: a light microscopic study. Invest Ophthalmol Vis Sci 19:1281.

Schaffer EH, Wallow IHL (1975): Rhegmatogenous bilateral retinal detachment in a poodle dog. J Comp Pathol 85:195.

Schmidt GM, et al. (1979): Inheritance of retinal dysplasia in the English springer spaniel. J Am Vet Med Assoc 174:1989.

Shelah M, et al. (2007): Acute blindness in a dog caused by an explosive blast. Vet Ophthalmol 10:196.

Slatter D, et al. (1980): Progressive retinal degeneration in the greyhound. Aust Vet J 56:106.

Slatter D, et al. (1980): Stypandra spp. (“blindgrass”) poisoning in ruminants— ocular and neurological findings in spontaneous cases. Aust Vet J 57:132.

Slater JD, et al. (1992): Chorioretinopathy associated with neuropathology following infection with equine herpesvirus-1. Vet Rec 131:237.

Storey ES, et al. (2005): Multifocal chorioretinal lesions in borzoi dogs. Vet Ophthalmol 8:337.

Tao W, et al. (2002): Encapsulated cell-based delivery of CNTF reduces photoreceptor degeneration in animal models of retinitis pigmentosa. Invest Ophthalmol Vis Sci 43:3292.

Taylor RM, Farrow BR (1992): Ceroid lipofuscinosis in the border collie dog: retinal lesions in an animal model of juvenile batten disease. Am J Med Genet 42:622.

Url A, et al. (2001): Equine neuronal ceroid lipofuscinosis. Acta Neuropathol (Berl) 101:410.

Vainisi SJ, Packo KH (1995): Management of giant retinal tears in dogs. J Am Vet Med Assoc 206:491.

Watson P, Bedford PGC (1992): The pigments of retinal pigment epithelial dystrophy in dogs. Vet Pathol 29:5.

Watson WA, et al. (1972): Progressive retinal degeneration (bright blindness) in sheep: a review. Vet Rec 91:665.

Witzel DA, et al. (1977): Night blindness in the appaloosa: sibling occurrence. J Equine Med Surg 1:383.

Witzel ED, et al. (1977): Electroretinography of congenital night blindness in an appaloosa filly. J Equine Med Surg 1:266.

Wolf ED, et al. (1978): Rod-cone dysplasia in the collie. J Am Vet Med Assoc 173:1331.

Woodford BJ, et al. (1982): Cyclic nucleotide metabolism in inherited retinopathy in collies. Exp Eye Res 34:703.

Wrigstad A, et al. (1995): Neuronal ceroid lipofuscinosis in the Polish owczarek nizinny (PON) dog: a retinal study. Doc Ophthalmol 91:33.

Wrigstad A, et al. (1994): Slowly progressive changes of the retina and the retinal pigment epithelium in Briard dogs with hereditary retinal dystrophy. Doc Ophthalmol 87:337.

Wyman M, et al. (2005): Ophthalmomyiasis (interna posterior) of the posterior segment and central nervous system myiasis: Cuterebra spp. in a cat. Vet Ophthalmol 8:77.

Yanoff M, et al. (1970): Oxygen poisoning of the eyes: comparison in cyanotic and acyanotic dogs. Arch Ophthalmol 84:627.

Zeiss CJ, et al. (2006): CNTF induces dose-dependent alterations in retinal morphology in normal and rcd-1 canine retina. Exp Eye Res 82:395

Zeiss CJ, et al. (2000): Mapping of X-linked progressive retinal atrophy (XLPRA), the canine homolog of retinitis pigmentosa 3 (RP3). Hum Mol Genet 9:531.

Zhang Q, et al. (1999): Photoreceptor dysplasia (pd) in miniature schnauzer dogs: evaluation of candidate genes by molecular genetic analysis.

J Hered 90:57.

Neuroophthalmology should not be a daunting study. If anatomy, physiology, and pathology of the ocular and visual innervation are understood, a diagnosis can be reached through deduction and elimination rather than from memory.

The following cranial nerves are significant in relation to ocular functions:

•Optic nerve: Cranial nerve (CN) II—relays the visual signal from the retina to the central nervous system (CNS)

•Oculomotor nerve: CN III—innervates four extraocular muscles (dorsal, medial, and ventral recti and the ventral oblique) and the levator palpebral muscle (elevating the upper eyelid); also provides parasympathetic innervation to the iris sphincter

•Trochlear nerve: CN IV—innervates the dorsal oblique muscle

•Trigeminal nerve: CN V—its ophthalmic and maxillary branches provide sensory innervation to the eye and its accessory organs, including the cornea, conjunctiva, lacrimal gland, and periocular skin

•Abducens nerve: CN VI—innervates the lateral rectus and retractor bulbi muscles

•Facial nerve: CN VII—innervates the various muscles controlling the blink response

In addition, significant parts of the CNS are devoted to vision processing and ocular control. Therefore the workup of the neuroophthalmologic patient requires comprehensive neurologic and systemic examinations, in addition to a thorough neuroophthalmologic examination (Table 16-1). This chapter reviews the examination, clinical signs, and diseases of the neuroophthalmologic patient.

ASSESSING VISION AND PUPILLARY LIGHT REFLEXES

Vision and the Menace Response

Vision is initially evaluated as the patient walks into the clinic or examination room. The ability to navigate in these unfamiliar surroundings may reveal visual deficits. A more direct assessment is made by testing the animal’s response to a menacing gesture. The menace response is evoked by making a threatening gesture with the hand at each eye while the other hand covers the opposite eye. If the other eye is not covered, an alert animal that is unilaterally blind in the eye being tested may observe the

threat with its normal eye and respond by blinking bilaterally, thus creating a false positive response (i.e., a blink “response” in a blind eye). It is crucial to the validity of this test that the threatening hand does not touch the patient or create enough air currents to be felt by the patient, which may also generate a false positive response (Figure 16-1).

The normal response to this threat is a rapid blink and closure of the palpebral fissure. The anatomic pathways of the afferent and efferent components are depicted in Figure 16-2. The afferent component of the response is relayed by the optic nerve, through the optic chiasm, optic tract, lateral geniculate nucleus (LGN), and optic radiation to the visual cortex located in the occipital lobe. It is assumed that the visual cortex projects to the motor cortex, which in turn projects via the internal capsule and crus cerebri to the facial nuclei in the medulla, and from there the facial nerve (CN VII) relays the efferent signal to the eyelid muscles. The complexity of this pathway implies that the resulting blinking is not a reflex but a learned response. Therefore this response may not become fully developed until 10 to 12 weeks of age in some small animals. It is usually present by 5 to 7 days in foals and calves. As a result, menace testing in young patients may result in a false negative result, as the animal does not blink even though it can see.

Crossover of optic nerve fibers occurs at the optic chiasm (Figure 16-3). Consequently, the left occipital cortex receives the axons of the lateral retina of the left eye (inputting from the right visual field) as well as the axons of the medial retina of the right eye (inputting, again, from the right visual field) (see orange pathways in Figure 16-3). The right occipital cortex inputs from the left visual fields of both eyes (see green pathways in Figure 16-3). In humans, where 50% of the axons cross over in the chiasm, the left occipital cortex inputs the right visual hemifield of both eyes, and the right occipital cortex inputs the left visual hemifield (orange and green pathways, respectively, in Figure 16-3). In animals, where a greater percentage of fibers cross over, the left occipital cortex will input a greater proportion of the right visual field of the right eye and a smaller proportion of the right visual field of the left eye. Therefore, in humans, a lesion in the left optic radiation or occipital cortex, for example, will cause a loss of the right visual hemifield, with symmetric deficits in both eyes (homonymous hemianopia). In animals, however, such a lesion will cause greater deficits in the visual field of the right eye than those of the left eye. In the dog, where 25% of the fibers

Table 16-1 Summary of the Neuroophthalmologic

Examination

FIGURE 16-1. The menace response of the right eye is tested while the left eye is being covered. This eliminates the possibility of a blinking response generated by the visual, untested eye. To eliminate stimulation due to air movement or touching of hair, the menacing gesture may be made behind a transparent glass or plastic sheet.

1

2

3

4

Diencephalon

8

5

15

Myel.

FIGURE 16-2. Anatomic pathway of the menace response: The afferent component of the response is relayed from the retina (1) by the optic nerve (2), through the optic chiasm (3), optic tract (4), lateral geniculate nucleus (5) and optic radiation (6) to the visual cortex (7) located in the occipital lobe. Note that the afferent pathways common to the pupillary light reflex and menace response (up to the level of the proximal optic tract) are colored in lighter shades. Afferent pathways that serve only the menace pathways (from the distal optic tract onward) are depicted in darker shades. It is assumed that the visual cortex projects to the motor cortex, which in turn projects via the internal capsule (8) and crus cerebri

(9) to the facial nuclei (15) in the medulla, and from there the facial nerve (cranial nerve VII) relays the efferent signal to the eyelid muscles (16). The cerebellum participates in modulating the menace response and integrating function of the motor cortex, using pathways that include: 10, longitudinal fibers of pons; 11, pontine nucleus; 12, transverse fibers of pons and middle cerebellar peduncle; 13, cerebellar cortex; 14, efferent cerebellar pathway; 15, facial nuclei; 16, facial muscles—orbicularis oculi. The wiggling line (~) indicates axons crossing the midline of the brain. (Modified from de Lahunta A [1983]: Veterinary Neuroanatomy and Clinical Neurology, 2nd ed. Saunders, Philadelphia.)

remain on the ipsilateral side and 75% of the fibers cross over in the chiasm, a unilateral lesion will cause deficits of 25% and 75% in the visual fields of the ipsilateral and contralateral eye, respectively. In the cat, the respective figures are 33% and 67%. In dogs and cats such visual deficits are difficult to detect as an animal moves in its surroundings. Occasionally, the animal may bump into an object on the side opposite the lesion, but often there is no evidence of visual deficit because 25% to 33% of the visual field is relayed to the unaffected lobe. In horses, sheep, and cattle with 80% to 90% decussation of optic nerve axons there is a greater tendency to walk into objects on the side of the visual deficit, contralateral to the lesion. Theoretically, these deficits could be tested separately by threats from the lateral and medial visual fields. However, this approach is unreliable, and in all domestic animals menace reflex is poor or absent on the side contralateral to the lesion.

If the menace response does not occur, the examiner should rule out another potential cause of false negative responses by checking the facial nerve innervation of the orbicularis oculi. It

is possible that the patient is visual but cannot blink due to facial nerve paralysis. This is checked by touching the lateral and medial canthi of the eyelids to test the palpebral reflex, which is expressed as a blink in response to the tactile stimulation. Another way to rule out a false negative response caused by facial nerve paralysis is to carefully watch the eye while performing the menace test. If a facial nerve paralysis exists, forehead or eye retraction is observed when that eye is threatened, but no blinking is observed. With slight retraction of the eye, the third eyelid passively protrudes. A patient with a facial nerve paralysis may therefore have “flashing third eyelid,” which is an indication that vision is intact. If there is no facial nerve paralysis and no menace response occurs, the animal should be lightly struck two or three times with the threatening hand, and then the threat should be repeated without touching the patient. This procedure often arouses and directs the attention of the patient and is then followed by a normal response. Significant cerebellar disease may also cause

Occipital cortex

FIGURE 16-3. Central visual pathway for conscious perception includes the retina, optic nerve, optic chiasm, optic tract, lateral geniculate nucleus, optic radiation, and occipital cortex. Note that the afferent pathways common to the pupillary light reflex and menace response (up to the level of the proximal optic tract) are colored in lighter shades. Afferent pathways that serve only the menace pathways (from the distal optic tract onward) are depicted in darker shades. Because of the crossover in the chiasm, the left occipital cortex receives the axons of the lateral retina of the left eye (inputting from the right visual field) as well as the axons of the medial retina of the right eye (inputting, again, from the right visual field). In humans, where 50% of the axons cross over in the chiasm, the left occipital cortex therefore inputs the right visual hemifield of both eyes. In animals, where a greater percentage of fibers cross over, the left occipital cortex will input a greater proportion of the right visual field of the right eye and a smaller proportion of the right visual field of the left eye. Therefore, in humans, a lesion in the left optic radiation or occipital cortex will cause a loss of the right visual hemifield, with symmetric deficits in both eyes. In animals, the resulting deficits from the right eye will be greater than those from the left eye. (Modified from de Lahunta A [1973]: Small animal neuroophthalmology. Vet Clin North Am 3:491.)

lack of menace response in a visual animal, as pathways from the visual cortex to the facial nucleus likely run through the cerebellum (see Figure 16-2).

In patients in which results of the menace testing are equivocal, vision can be assessed using any of the three following tests:

Tracking Moving Objects

Vision can be assessed in young small animals that may not yet have learned the menace response, and occasionally in stoic older animals, by throwing cotton balls in the air in front of the animal. A normal, alert animal that may not readily respond to a menace gesture will follow the cotton ball. Avoid throwing heavier objects that cause significant air movement or noise, because the animal may respond to these stimuli. Some animals, especially cats, will follow the red light emitted by a laser pointer. Young, hungry calves and foals often follow a moving hand or a nursing bottle.

Maze Test

This test assesses the patient’s ability to navigate through an obstacle course. The test may be conducted with one eye covered to assess unilateral vision. It can also be conducted both in light and dim environments (to test for early signs of inherited retinopathies). The patient’s performance in the course should always be compared with that of normal animals.

Visual Placing Postural Reaction

In the visual placing postural reaction test, the animal is held off the ground and brought to a table edge. If it sees the table, it elevates its limbs to place them on the table’s surface before the limbs touch the table. A blind animal does not elevate the limbs until they touch the table’s edge (Figure 16-4).

Pupillary Light Reflex

The Anatomic Basis of the Pupillary Light Reflex

The afferent and efferent pathways controlling pupil size and reaction are depicted in Figure 16-5. The size of the pupil at rest represents a balance between two anatagonistic forces: (1) the amount of incident light stimulating the retina and influencing the oculomotor neurons to constrict the pupil (parasympathetic innervation through CN III), and (2) the emotional status of the patient (e.g., fear, anger, or excitement), which influences the sympathetic system and causes pupillary dilation. In the resting pupil, both pupillary dilator (sympathetic) and the antagonistic pupillary sphincter (parasympathetic) muscles are active. The relative resting parasympathetic and sympathetic innervation and resulting muscle tone determine the size of the pupil (see Figure 16-5, efferent pathways A and B, respectively). The pupillary sphincter (or constrictor) is the more powerful of the two muscles.

As noted, pupillary constriction and pupillary light reflex (PLR) are controlled by the parasympathetic system. The afferent pathway to the parasympathetic oculomotor nucleus is via the optic nerve to the optic chiasm (where some crossing occurs), through both optic tracts, over the LGNs without forming a synapse, and ventrally into the region between the thalamus and the rostral colliculus, called the pretectal area.

16-4. The placement reflex is evaluated in cases in which the menace response is inconclusive. The animal is suspended in the air and led toward a table. A visual animal will extend its forelimbs toward the approaching surface. This reflex is composed of an afferent visual response and an efferent motor response.

Synapse takes place in the pretectal nuclei in the mesencephalon (see Figure 16-5). Crossing between sides occurs between the pretectal nuclei via the caudal commissure. Axons of the pretectal cell bodies pass to the Edinger-Westphal (parasympathetic oculomotor) nucleus of both sides. The parasympathetic axons leave the mesencephalon with the motor axons of CN III (that control four of the extraocular muscles and the levator palpebral muscle), and enter the orbit through the orbital fissure. The ciliary ganglion is located at the rostral end of the oculomotor nerve, ventral to the optic nerve (see Figures 16-5 and 16-6). Preganglionic parasympathetic axons of the oculomotor nerve synapse here with the cell bodies of the postganglionic axons. The postganglionic axons pass via short ciliary nerves, enter the globe adjacent to the optic nerve, and innervate the ciliary body and pupillary constrictor muscles. The feline eye has

16-5. Neuroanatomic tracts controlling the pupil size and response include parasympathetic (A) and sympathetic (B) pathways. The afferent pathway to the parasympathetic oculomotor nucleus is via the optic nerve to the optic chiasm (where some crossing occurs), through both optic tracts, over the lateral geniculate nucleus (without forming a synapse) to synapse in the pretectal nuclei in the mesencephalon. Note that fibers inputting to the lateral geniculate nucleus and visual cortex diverge in the middle of the optic tract; these are depicted in darker shades of green and orange. Crossing of the afferent PLR fibers between sides occurs between the pretectal nuclei via the caudal commissure. Axons of the pretectal cell bodies pass to the Edinger-Westphal (parasympathetic oculomotor) nucleus of both sides. The parasympathetic axons leave the mesencephalon with the motor axons of cranial nerve III, enter the orbit through the orbital fissure, and synapse in the ciliary ganglion. The postganglionic axons pass via short ciliary nerves, enter the globe adjacent to the optic nerve, and innervate the pupillary constrictor muscles. Preganglionic sympathetic cell bodies are located in the first three segments of the thoracic spinal cord (T1-T3). These preganglionic axons join the thoracic sympathetic trunk inside the thorax and terminate in the cranial cervical ganglion. The postganglionic fibers pass between the tympanic bulla and the petrosal bone into the middle ear cavity and continue to the eye, where they innervate the iris dilator muscle. (Modified from de Lahunta A [1983]: Veterinary Neuroanatomy and Clinical Neurology, 2nd ed. Saunders, Philadelphia.)

only two short ciliary nerves, each serving half of the iris. A partial parasympathetic lesion may therefore cause a hemidilated pupil (partial internal ophthalmoplegia) in the cat.

The anatomy of the sympathetic pathway, responsible for pupil dilatation, is discussed later in this chapter (see Sympathetic Lower Motor Neuron Innervation).

Testing the Pupillary Light Reflex

The size and response of pupils to light are assessed after the menace test. If there is a visual deficit, localization of the lesion depends on a careful examination of the eyes and the pupils.

First, the size of the pupils at rest (without stimulation) should be evaluated both in normal room light and in dim light. If the pupils cannot be seen without extra light, a dim penlight is held in front of the nose of the patient and at a distance that will just allow the pupillary margins to be seen, without stimulating them. The size of the pupils is assessed and compared with each other to determine if there is anisocoria (unequal pupils).

Next, the reaction to strong light is tested. Because of the crossover in the optic chiasm and mesencephalon (see Figure 16-5), stimulation of the retina of one eye with a bright source of light causes constriction of both pupils. First the examiner evaluates the direct PLR by shining a bright light into one eye while observing the reaction of its pupil. To evaluate the indirect PLR, the examiner shines a bright light into one eye while observing the reaction of the contralateral pupil. The patient should be relaxed for this part of the examination, because circulating epinephrines and sympathetic stimulation may interfere with the PLR.

It is important to remember that PLR, as well as the following four tests described next, evaluate subcortical reflexes. Therefore they are not indicators of vision and may be normal in a blind animal (e.g., in cases of cortical disease). Furthermore, the PLR is remarkably resistant to serious ocular diseases that substantially reduce its afferent input. Animals with extensive retinal disease (e.g., progressive rod-cone degeneration) or mature cataracts can be functionally blind and yet their pupils may still respond to bright light. However, these animals have pupils that are dilated more than normal in the room light because they do not react to incident light in the room. This helps distinguish them from cases of central blindness, where pupils constrict in response to incident light. If the clinician is not aware of this possibility, he or she may erroneously diagnose a lesion in the central visual pathways in that patient (based on the presence of PLR in a blind animal).

Swinging Flashlight Test

A swinging flashlight test is used by some clinicians. In a normal animal, a quick redirection of a flashlight from one eye to the other (by swinging it from side to side) should reveal semiconstriction of the second pupil. The second pupil initially underwent limited constriction owing to the consensual stimulus from the first eye; swinging the flashlight causes further constriction, because now the second eye is stimulated directly. On the other hand, if a retinal or optic nerve disease is present in the second eye, swinging the flashlight to this eye will result in a dilatation of its pupil. This is because the second pupil initially underwent limited constriction owing to the consensual stimulation from the first eye; however, when the light

is moved to the diseased eye, it dilates as it receives no direct stimulation. This quick dilation of the second pupil, called a positive swinging flashlight test result or presence of the

Marcus Gunn sign, is considered pathognomonic for a prechiasmal lesion.

Pupillary Escape

Another phenomenon often seen with pupil assessment is pupillary escape. When a light is applied to the eye the pupil constricts and then immediately dilates slightly. This is due to light adaptation of the photoreceptors and is more common with weak light sources.

Dazzle Reflex

If the PLR cannot be evaluated (e.g., due to severe corneal edema or hyphema), the dazzle reflex is also often helpful in lesion localization. Shining a bright light into the eye elicits a subcortically mediated, reflex rapid eye blink (Figure 16-7). Because this is a subcortical reflex, it may be present in a blind animal. This response involves CN II, the rostral colliculus, and CN VII. Therefore it will be present in an animal blinded by a cerebrocortical lesion but absent in a patient blinded by subcortical diseases.

Electrophysiology

Retinal function can also be evaluated electrophysiologically, using electroretinography to record the responses of the retina

to light stimulation. The test is described in detail in Chapter 15. It may be used to determine whether blindness is caused by retinal or postretinal disease. Placing the active electrode over the visual cortex, rather than on the cornea, allows for the recording of visual evoked potentials, which are useful in determining cortical function and vision.

FIGURE 16-7. The dazzle reflex is evoked with use of a strong light source. The efferent arm of the reflex causes the patient to squint. This is a subcortical reflex, and the squinting does not necessarily mean that the animal is visual.

LESIONS IN PATIENTS WITH VISUAL AND PUPILLARY LIGHT REFLEX DEFICITS

Based on the results of the visual performance and PLR tests, patients with deficits may be divided into one of three categories:

•Blind patients with normal PLRs

•Blind patients with abnormal PLRs

•Visual patients with abnormal PLRs

This simple categorization is the first step in localizing the pathologic lesion (Table 16-2 and Figures 16-8 to 16-12). It assumes that ophthalmic examination did not reveal any pathology that would prevent light from reaching the retina (e.g., hyphema, cataract).

Lesions in Blind Patients with Normal Pupillary Light Reflexes

Based on the anatomy of the PLR pathway, the size of the pupils and their response to light are normal in blind animals with disease limited to the distal optic tract (after the afferent PLR fibers have diverged), LGN, optic radiations, and/or visual cortex (see dark green and dark orange pathways, Figures 16-2 and 16-3).

Bilateral cerebral lesions that cause blindness include prosencephalic hypoplasia with no cerebral hemispheres (calves), hydranencephaly (calves, lambs), cerebral contusion, cerebral edema (following trauma, postictal, or due to spaceoccupying lesions), viral encephalitis, thrombotic meningoencephalitis (Haemophilus somnus in cattle), inflammatory diseases such as granulomatous meningoencephalitis (GME) in dogs and horses, metabolic disorders (hypoglycemia, hepatic encephalopathy), poisonings, and nutritional and storage diseases. These diseases are discussed at the end of the chapter (see Diseases of the Central Visual Pathways).

The most common causes of a unilateral cerebral lesion with contralateral visual deficit are neoplasms in small animals and abscesses in large animals. Others are cerebral infarction (most common in cats), protozoan encephalitis in horses, chronic canine distemper encephalitis, Toxoplasma granulomas,

GME in dogs, thrombotic meningoencephalitis in cattle, and parasitic cysts (coenurosis in sheep) or migrations. These diseases are discussed at the end of this chapter (see Diseases of the Central Visual Pathways).

Lesions in Blind Patients with Abnormal Pupillary Light Reflexes

As can be seen in Figures 16-2, 16-3, and 16-5, the afferent fibers of the PLR and visual signal run together from the retina through the optic nerve, optic chiasm, and proximal optic tract, diverging just before the LGN (see light green and light orange pathways in these figures). Minor lesions in this common pathway (e.g., early retinal degeneration) may cause visual deficits without affecting the PLR. This is because, as noted earlier, the PLR is resistant to deficits in afferent input. Therefore if a lesion in this common pathway is significant enough to cause a pupillary abnormality, it usually also causes blindness. Converesely, if the eye is blind due to an afferent lesion, the PLR is almost always abnormal (though not necessarily absent). As a rule, afferent lesions that interrupt this pathway occur in the retina, optic nerve, or optic chiasm (see Figures 16-8 and 16-9). Rarely both proximal optic tracts are affected sufficiently to cause pupillary abnormalities, because the tracts are spread out over a relatively large area. A single optic tract lesion is rare and may cause no PLR abnormality (due to the crossover in the pretectal and oculomotor nuclei) (see Figure 16-10).

A patient with a unilateral lesion in the retina or optic nerve has no menace response in that eye. The pupil in that eye may be slightly larger (because it receives no direct parasympathetic stimulation from incident light), although it is not fully dilated (due to the indirect stimulation from the unaffected eye) (Figure 16-13). Light directed into the affected eye causes no response in either eye. Light directed into the unaffected eye elicits a bilateral response (see Figure 16-8). To assess direct and indirect responses, the examiner moves the light back and forth between the eyes. In an animal with a unilateral lesion, as the light is directed from the unaffected eye to the affected eye, the pupil in the affected eye dilates back to the resting

state created by the room light (indirectly, through the unaffected eye). This is because the strong light source was taken away from the unaffected eye (thereby removing the indirect stimulation) and the lesion in the affected eye has interrupted the direct afferent pathway for this reflex. This phenomenon is readily apparent as the light is repeatedly moved between the eyes. Further confirmation of a unilateral lesion is made by covering the normal eye and observing further dilation of the pupil in the affected eye which is no

longer stimulated indirectly by room light through the normal, covered eye.

Common causes of unilateral lesions resulting in PLR and visual deficits include retinal detachment, glaucoma, and retrobulbar abscess or neoplasia. Trauma to the optic nerve is another common cause of unilateral lesions. The trauma may cause direct avulsion of the axons at the level of the optic canals or interference with the vascular supply of the intracanalicular part of the optic nerve. This problem may be

more common in horses and in brachycephalic dogs. Ophthalmoscopic examination often shows optic disc atrophy, with secondary retinal degeneration.

Severe bilateral retinal, optic nerve, or optic chiasm lesions cause blindness with dilated pupils that are unresponsive to light (see Figure 16-9). Bilateral retinal diseases include retinal detachment, end-stage retinal degeneration, SARD, and glaucoma. The most common optic nerve disease to affect vision and PLR is optic neuritis. The disease may be infective (e.g., distemper, cryptococcosis, toxoplasmosis) or inflammatory (GME) though it is frequently idiopathic in nature. It can affect both optic nerves and the optic chiasm, and the patient presents with blindness and fixed, dilated pupils (optic neuritis is discussed under Diseases of the Optic Nerve). In young cattle, vitamin A deficiency may cause optic nerve

compression from stenosis of the optic canals. Rarely in cats does ischemic encephalopathy syndrome result in infarction of the optic chiasm.

The optic chiasm may be compressed by extramedullary space-occupying lesions near the hypophyseal fossa. Pituitary neoplasms are the most common tumor in this site, although meningiomas and germ cell neoplasms (teratomas) have also been reported. The latter are more common in dogs younger than 5 years. Diseases of the optic nerve and chiasm are discussed further at the end of the chapter (see Diseases of the Central Visual Pathways).

A retrobulbar or intracranial lesion that affects both the optic nerve and the parasympathetic part of the oculomotor nerve causes a widely dilated pupil in the ipsilateral eye at rest (see Figures 16-8 and 16-11). Because of CN II involvement there

is no menace response from this affected eye, and light directed into the affected eye elicits no response in either eye. Light directed into the unaffected eye causes pupillary constriction only in that eye (due to CN III lesion in the affected eye). In addition to loss of PLR, a complete oculomotor nerve deficit will also cause ventrolateral strabismus and ptosis due to denervation of four extraocular muscles and the levator palpebral muscle. However, lesions that involve only the oculomotor nerve, and do not affect vision, may also occur. These are discussed later (see Lesions Causing Pupillary Light Reflex Abnormalities in Visual Patients).

Pupils in Patients with Intracranial Injury

Pupillary abnormalities are common after intracranial trauma. They may also accompany severe acute brain lesions such as those found in polioencephalomalacia and lead poisoning in ruminants. Evaluation of the size of the pupils is important to the assessment both of the location and extent of brain

damage from intracranial injury and to evaluate the response to therapy. Pupil size and prognosis in intracranial injury are shown in Table 16-3.

Brainstem contusion with hemorrhage and laceration of the midbrain and pons is a common sequel of trauma. The parenchymal components of the oculomotor neurons are interrupted, causing both pupils to be widely dilated and unresponsive, a grave sign. Affected animals are also recumbent and semicomatose or comatose. Severe caudal brainstem lesions that are life threatening also result in partly dilated, fixed, unresponsive pupils.

Injuries that predominately involve the prosencephalon often result in very miotic pupils. Severe bilateral miosis is a sign of acute, extensive brain disturbance that by itself is not necessarily of any localizing value. The return of the pupils to normal size and response to light is a favorable prognostic sign and indicates recovery from the brain disturbance, especially following trauma. However, progression from bilateral miosis to bilateral mydriasis with fixed pupils that are unresponsive to