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

during fundus examination. Lesions are unilateral, are nonprogresive, do not affect vision or PLR, and are not preceded or accompanied by hemorrhages around the disc. Proliferative optic neuropathy was formerly reported as astrocytoma, but histologic studies indicate that it is a lipid storage disorder.

Optic neuropathy in horses may also be ischemic, due to trauma or following ligation of the internal and external carotid arteries (to treat epistaxis caused by guttural pouch mycosis) (see Figure 15-55 in Chapter 15). Although initially the affected optic nerve appears normal, edema, hyperemia, and hemorrhages may be observed after 24 hours, and irreversible blindness is a common sequel.

NEOPLASMS. Primary neoplasms affecting the optic nerve include meningioma, glioma, and astrocytoma. They are uncommon in all species. Secondary metastatic neoplasms may also occur.

Clinical Signs. The clinical signs of neoplasms of the optic nerve are as follows:

•Mydriasis and abolition of the direct PLR in the affected eye, and the consensual PLR to the unaffected eye. With a large infiltrating orbital mass, the consensual reflex from the contralateral eye to the affected eye may be abnormal because of destruction of efferent nerves of CN III. In such cases, strabismus and ptosis will also be noted.

•Orbital neoplasms may cause papilledema and/or optic neuritis that will eventually progress to optic neuropathy (see following section).

FIGURE 16-35. Proliferative optic neuropathy in a horse. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

•The optic nerve head or posterior section of the globe may be indented by the retrobulbar mass. Retinal edema and folds resulting from pressure exerted by orbital masses on the posterior of the globe may also be observed ophthalmoscopically.

•Progressive exophthalmous that may even lead to ptosis of the globe. Position of the globe and direction of the visual axis may assist in determining the position

of the mass. Exophthalmous caused by retrobulbar neoplasia can be differentiated from that caused by a retrobulbar abscess as the latter is painful and of acute onset, whereas the former is nonpainful and slowly progressive.

Treatment. Imaging techniques, including radiography, computed tomography and magnetic resonance imaging, may be used to delineate the extent of the tumor. In cases of retrobulbar tumors, cytology samples may be obtained using ultraound-guided fine needle aspiration. Treatment of optic neoplasms consists of anterior or lateral orbitotomy if the globe is to be saved, or orbital exenteration if the neoplasm is too extensive or infiltrates the globe or secondary lesions are present in the globe.

OPTIC NEUROPATHY

Etiology. Optic neuropathy is atrophy of the optic nerve. The condition has numerous causes and is the end stage of

numerous pathologic processes. Some of the more common processes are as follows:

•Advanced retinal degeneration of any type, as the degeneration eventually spreads to the RGCs and their axons

•Glaucoma, as the RGCs and their axons are damaged by the elevation in intraocular pressure

•Orbital disorders (e.g., retrobulbar abscess, orbital cellulitis, canine extraocular myositis)

•Intraorbital nerve damage secondary to traumatic proptosis in dogs and cats

•Sequel to optic neuritis

•Prolonged papilledema

•Intraorbital and intracranial neoplasia

Clinical Signs. The clinical signs of optic atrophy are as follows:

•Pale, grayish white, shrunken disc with extensive papillary and peripapillary pigmentation (similar in appearance to Figure 16-28, A)

•Slight depression of the disc surface

•Exposure and increased visibility of the lamina cribrosa

•Attenuation of retinal vessels

Treatment. Except to prevent further damage to the nerve by the original cause, treatment of optic neuropathy has no effect.

Diseases of the Optic Chiasm

The most common disease of the optic chiasm is pituitary neoplasia. In domestic animals, unlike in humans, the pituitary gland is located caudal to the optic chiasm. Therefore most pituitary neoplasms expand into the hypothalamus, and the chiasm is affected only in advanced stages of growth. The result is bilateral visual and PLR deficits. Occasionally, the cerebral infarction syndrome in cats causes ischemic encephalopathy and necrosis of the optic chiasm, with blindness and dilated, unresponsive pupils (see Diseases of the Optic Radiation and Visual Cortex).

In severe proptosis or traction during enucleation, the optic chiasm may be traumatized, thus causing optic neuropathy and blindness in the contralateral eye that was not affected initially. This condition is most commonly seen in cats, as the retrobulbar optic nerve is particularly short in this species.

Diseases of the Optic Tracts

BILATERAL DISEASE. Incomplete bilateral optic tract lesions may produce partial bilateral visual deficit with variable pupillary responses. The most common histopathologic finding

in optic tract disease is demyelination. It may be caused by canine distemper, which has a predilection for the optic tracts. As noted previously, the virus may also cause optic neuritis, and the dog will present with signs of optic nerve inflammation. However, often no clinical visual deficit is observed, and optic tract demyelination may be the only pathology. The diagnosis is confirmed by PCR testing of various tissues, notably conjunctival swabs and blood samples. The disease is discussed in detail in Chapter 18. Demyelination of the optic tracts may also be seen in some storage diseases (see later). Occasionally, canine pituitary neoplasms affect the optic tracts when the hypothalamus is invaded or compressed by the neoplasm.

UNILATERAL DISEASE. Neoplasms in the hypothalamus and thalamus may encroach on one optic tract, causing a visual deficit in the contralateral eye, but PLRs are unaffected.

Because of close approximation of the internal capsule and rostral crus cerebri to the optic tract, space-occupying lesions in the lateral hypothalamus or thalamus (or both) that affect the optic tract usually also affect the internal capsule and rostral crus cerebri. The result is mild contralateral hemiparesis, which often is not evident in the gait but is demonstrable as asymmetry with postural testing.

Traumatic or ischemic lesions that cause necrosis of these tissues on one side can result in the same residual neurologic signs, that is, contralateral visual deficit and postural reaction deficit (“hemiparesis”).

Diseases of the Lateral Geniculate Nucleus

Destruction of the LGN produces signs similar to those observed with distal optic tract lesions. It may be caused by any multifocal or diffuse brain disease that involves the thalamus and LGN, or by inflammatory, neoplastic, or storage diseases. An abnormality in the retinogeniculate projections and neuronal organization in this nucleus occurs in albinotic cats of all sizes, from Siamese cats to tigers, and in minks. In some animals it is associated with congenital esotropia and nystagmus.

Diseases of the Optic Radiation and Visual Cortex

UNILATERAL DISEASE. Unilateral lesions of the optic radiation and visual cortex produce hemianopia in the contralateral visual field. Pupillary size and response to light are normal. Common lesions of these structures and their clinical signs are as follows:

Neoplastic Lesions. Neoplasms produce progressive signs of neurologic deficit. Convulsions or changes in behavior may accompany the visual deficit.

Traumatic Lesions. Traumatic lesions causing necrosis may leave a residual neurologic defect limited to a contralateral visual deficit. If the entire hemisphere is involved, a contralateral postural reaction deficiency may be seen on neurologic examination. Immediately after an injury the neurologic signs may be more extensive, suggesting diffuse cerebral disturbance. As hemorrhage and edema subside, the residual neurologic deficits relate to areas of necrotic tissue.

Feline Ischemic Encephalopathy. This is a syndrome consisting of peracute signs of unilateral cerebral disturbance in adult cats of all ages and both sexes, believed to be caused by aberrant migration of Cuterebra. CNS signs are variable, with some animals showing only severe depression with mild ataxia, circling, or both, whereas others circle continuously. Other cases begin with seizures and consist of tonic or clonic activity of the muscles on one side of the head, trunk, and limbs. Changes in attitude and behavior are common and may involve severe aggression. Pupils are often dilated, and blindness may be apparent. For the first 1 to 2 days, observable hemiparesis may be present. Acute signs usually resolve in a few days, leaving signs of a nonprogressive unilateral cerebral lesion. The loss of neurons in the visual cerebral cortex or optic radiation causes contralateral loss of the menace reflex, with normal pupillary reflexes.

Unilateral cerebral lesions are usually in the frontal lobe. Examination may demonstrate a unilateral facial hypalgesia contralateral to the cerebral lesion. No other cranial nerve deficits have been observed. Ischemic necrosis of the cerebral hemisphere is variable and is usually unilateral but occasionally bilateral. The necrosis may be multifocal or the infarction may involve up to two thirds of one entire cerebrum. Vascular occlusion occurs most commonly in the middle cerebral artery. Most cats with cerebral vascular disease survive, but behavioral changes and uncontrollable seizures may persist.

Unilateral Cerebral Abscess. In horses, abscesses caused by

Streptococcus equi or by Sarcocystis neurona may affect the optic radiation and cause a contralateral visual deficit with normal pupillary reflexes. Expansion of the lesion with accompanying cerebral edema raises intracranial pressure and causes the occipital lobes to herniate ventral to the tentorium cerebelli. The herniation further compromises function of the visual cortex bilaterally, and total blindness results if both sides are affected. Similar signs occur in ruminants with

Corynebacterium pyogenes abscess.

Encephalitis. In encephalitis caused by Toxoplasma gondii, a space-occupying granuloma may be produced in the optic radiation and cause a contralateral visual deficit. CSF contains inflammatory cells, often with neutrophils and increased amounts of protein.

BILATERAL DISEASE. Total blindness with normal PLRs is characteristic of bilateral visual cortex lesions. Common lesions and their findings are as follows:

Canine Distemper. Chronic encephalitis due to canine distemper may result in demyelination and astrocytosis of the optic radiation. This is a sclerosing encephalitis that may produce a unilateral or bilateral visual deficit with normal pupillary function. Chorioretinitis may be visible ophthalmoscopically. The disease is discussed in detail in Chapter 18.

Thromboembolic Meningoencephalitis. Infarction of the cerebral white matter by septic emboli occurs in cattle afflicted with thromboembolic meningoencephalitis caused by H. somnus. Visual deficits may result. Severe ophthalmoscopically visible retinal lesions are the probable cause of visual deficits and are

NEUROOPHTHALMOLOGY 349

of considerable use in diagnosis (see Figure 15-49, C in Chapter 15).

Metabolic Diseases. Cortical blidness may also be caused by a number of metabolic diseases, notably hepatic and uremic encephalopathy, and hypoglycemia. The diseases may also affect the brainstem, resulting in subsequent PLR and eye movement abnormalities.

Inflammations. Cortical blindness may be caused by GME, an idiopathic inflammation characterized by formation of granulomas in the visual pathways, including the visual cortex. Immunosuppresive treatment is recommended, though prognosis is grave. The treatment and prognosis are similar in necrotizing meningoencephalitis, a disease of the cerebral hemispheres in small breed dogs.

Ischemic Necrosis of Cerebrum. Anesthetic overdose leading to prolonged apnea and cardiac arrest may cause diffuse ischemic necrosis of the cerebrum. Animals may recover, the only residual deficit being blindness with intact pupillary reflexes.

Poisonings in Cattle and Sheep. Severe cerebral disturbance, including frequent blindness, is seen in cattle and sheep with polioencephalomalacia, or thiamine (vitamin B1) deficiency. The visual deficit is due to necrosis of the visual cortex caused by elevation in thiaminase levels following ingestion of bracken fern or excess thiaminase production in the rumen. Lead poisoning causes similar acute necrosis of the cerebral cortex and associated blindness. Similarly, severe water intoxication with cerebral disturbance may cause blindness.

Intoxication by wheat seed fungicide containing mercury has been reported in cattle and pigs. The metal causes chronic degeneration of neurons in the cerebral cortex and replacement of astrocytes. Convulsions and blindness may appear in the chronic stages. Mercury toxicity also occurs in dogs and cats.

Tentorial Herniation. As noted in the previous section, space-occupying granulomas caused by a number of infective agents may cause cerebral edema, leading to elevation in intracranial pressure, bilateral ventral occipital lobe herniation, and blindness. The same explanation for bilateral signs of visual deficit from tentorial herniation can be offered for any spaceoccupying cerebral lesion or cerebral swelling after injury. Head injury that causes progressive cerebral edema causes blindness. The pupillary activity varies with the extent of brainstem involvement (see Pupils in Patients with Intracranial Injury).

Hypoplasia of the Prosencephalon in Calves. In calves with hypoplasia of the prosencephalon, the rostral portion of the malformed diencephalon protrudes through a defect in the calvaria and is attached to the adjacent skin. The skull is flatter than normal to conform to the malformed brain, which consists of a brainstem with a small cerebellum and no cerebral hemispheres. The lack of cerebral tissue causes visual deficit despite a functional brainstem. Affected animals may be able to stand and usually live for a few days.

Hydranencephaly. In hydranencephaly the cerebral hemispheres are reduced to a membranous sac filled with CSF, which may cause a “dummy” syndrome in calves and lambs with ataxia and visual deficit. This disorder may be caused by Akabane virus in cattle and bluetongue virus in sheep.

Obstructive Hydrocephalus. Obstructive hydrocephalus is caused by obstructions in CSF flow and drainage, leading to accumulation of fluid in the lateral ventricles or subaracnoid space. The elevation in pressure compromises the optic radiation in the internal capsule, in which it forms the lateral

wall of the dilated lateral ventricle. Bilateral visual deficits and ataxia are common signs, reflecting attenuation of the cerebral white matter, optic radiation, and visual cortex.

Additional Neuroophthalmic Diseases

Vitamin A Deficiency

Vitamin A deficiency is of clinical, ophthalmic, and economic significance in cattle, pigs, and sheep. The disease affects the visual system through two mechanisms. In young animals, it causes abnormal thickening of growing bones, including the bones around the optic canal. This thickening leads to constriction and compressions of the optic nerve. Clinical signs are as follows (see Figures 15-52 and 15-53 in Chapter 15):

•Papilledema. As the deficiency progresses, papilledema worsens, the optic disc enlarges and becomes pink and pale, and details of the central optic disc are obscured. In the later stages or if treatment is not given, irreversible optic nerve atrophy occurs and the optic disc becomes gray, flat, and shrunken.

•Tortuous retinal blood vessels, which later become attenuated

•Retinal detachment and hemorrhage

•Retrograde degeneration of the retina, especially in the peripapillary region

•Anterograde degeneration of the optic chiasm and tracts

•Mottling of the tapetum and pallor of the nontapetum

•Reduced CSF absorption, leading to increased CSF pressure, ataxia, tetraparesis, and seizures

As vitamin A is used in the synthesis of visual photopigments in the rods (see Chapter 15), hypovitaminosis A will also impair rod function, leading to night blindness. In chronic deficiencies, progressive loss of vision and complete retinal degeneration will occur.

Clinical signs become apparent when vitamin A levels have dropped to about 20 Mg/dL of blood or 2 Mg/g of liver. For diagnosis of vitamin A deficiency, liver levels are more reliable than blood levels. Affected animals should be treated as follows:

1.Vitamin A (water-soluble preparation) at 440 IU/kg intramuscularly

2.Provision of rations containing vitamin A, 65 IU/kg body weight per day

Storage Diseases

Inherited storage diseases of the nervous system occur in most domestic species and are models of comparable diseases in

Table 16-11 Clinical Signs of Meningitis

humans. All are progressive, degenerative disorders of the nervous system, usually of a recessive nature. The onset is usually some time after weaning. Signs represent diffuse involvement of the nervous system but often begin with pelvic limb ataxia and paresis. In the advanced stages of many of these diseases blindness is common because the retina or visual pathways are affected.

Storage diseases are usually caused by an absence or severe deficiency of a specific degradative enzyme, which leads to abnormal accumulation of the sub-strate normally metabolized by that enzyme. These metabolic disorders may be expressed in neurons by the accumulation of complex lipids in neuronal cytoplasm (lipodystrophy) or in the myelin by demyelination and accumulation of complex lipids in macrophages (leukodystrophy). Leukodystrophy involves an abnormal metabolism of myelin and its subsequent degeneration, whereas lipodystrophy consists of abnormal neuronal metabolism associated with accumulations of complex lipids in neurons and their subsequent degeneration.

Meningitis

Canine meningitis may cause various neurologic and neuroophthalmologic deficits, depending on the cause (Table 16-11).

Cerebellar Disease

It is assumed that the pathway between the visual cortex and the facial nucleus passes through the cerebellum (see Figure 16-2). Therefore significant cerebellar disease will interrupt the efferent pathway of the menace response. Patients will have no menace response, even though they are visual. Animals with this condition also have significant signs of cerebellar ataxia. A unilateral cerebellar lesion causes an ipsilateral menace deficit with normal vision. This occurs because of the crossing of the visual pathway in the optic chiasm and the reciprocal interaction between the cerebrum on one side and the opposite cerebellar hemisphere.

Involvement of the cerebellum may also cause vestibular disturbance, with loss of equilibrium, nystagmus, bizarre postures, and a broad-based staggering gait with jerky movements as well as a tendency to fall to the side or back, especially if the thoracic limbs are elevated. Abnormal nystagmus is observed only occasionally.

Occasionally in animals with significant cerebellar disease that involves the cerebellar nuclei, one palpebral fissure is slightly wider or one third eyelid is mildly elevated. The pathogenesis of these signs in poorly understood, even though they have also been reproduced experimentally.

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ANATOMY

The orbit is the cavity that encloses the eye. The two orbital patterns in domestic animals are as follows:

•Incomplete bony orbit, found in dogs and cats (Figures 17-1 to 17-3)

•Complete bony orbit, found in horses, oxen, sheep, and pigs (Figures 17-4 and 17-5)

The orbit separates the eye from the cranial cavity, and the foramina and fissures in its walls determine the path of blood vessels and nerves from the brain to the eye. The walls of the equine orbit are formed by the frontal, lacrimal, zygomatic, temporal, presphenoid, palatine, and maxillary bones, which are similar in other species. In the dog and cat the dorsolateral portion of the orbit is spanned by the dense collagenous orbital ligament, which passes from the zygomatic process of the frontal bone to the frontal process of the zygomatic bone. The basic foramina and fissures of the orbit are the orbital, rostral and caudal alar, oval, supraorbital, ethmoidal, lacrimal, maxillary, sphenopalatine, round, and palatine. In cattle, the orbital foramen and the foramen rotundum fuse to form the foramen orbitorotundum. The vessels and nerves that pass through these foramina and fissures in the dog are shown in Figures 1-16, 1-17, and 1-19 to 1-22 in Chapter 1 and Figure 17-6.

The position of the orbit within the skull varies with species. In cattle, sheep, and horses the eyes are situated laterally, giving panoramic vision, whereas in dogs and cats the eyes are located more anteriorly, which emphasizes binocular overlap between the two eyes. The visual, orbital, and optic axes, defined as follows, do not coincide (Figure 17-7):

•Visual axis: Line from the center of the most sensitive area of the retina to the object viewed

•Orbital axis: Line from the apex of the orbit to the center of the external opening

•Optic axis: Line from the center of the posterior pole of the eye through the center of the cornea

The angle formed by the optic axes, a measure of binocular overlap, is shown in different species in Figures 17-8 to 17-10.

The relationships of the orbit to the paranasal sinuses, teeth, zygomatic gland, and ramus of the mandible are important, because they affect incidence, diagnosis, and pathogenesis of clinical diseases of the eye and orbit, as follows:

•Infections of the sinuses or nasal cavity may enter the orbit in all domestic species (Figure 17-11). The junction of the frontal, lacrimal, and palatine bones in the medial wall of the canine orbit (see Figures 17-2 and 17-11) is often thin and may be eroded by disease processes in the nasal cavity, which then enter the orbit. The bone is thicker in horses (Figure 17-12).

•Fractures of walls of the sinuses can cause emphysema, with gas visible beneath the conjunctiva or palpable under the skin.

•Infections of the roots of the molar teeth can affect the orbit, uvea, and periocular area in dogs and cats.

•Enlargement of the canine and feline zygomatic salivary gland may cause increased pressure within the orbit or protrusion of the gland into the ventral conjunctival fornix (Figure 17-13). When the mouth is opened, especially in dogs and cats with greater mobility of the mandible, the vertical ramus of the mandible moves forward, exerting pressure on the orbital contents. This is painful if orbital contents are inflamed.

The orbital contents are completely enclosed in a sheet of connective tissue—the periorbita—that lies next to the bone in the bony parts of the orbital wall and that is thicker laterally where the wall is incomplete (in carnivores). The periorbita is reflected over the extraocular muscles and forward over the globe to become Tenon’s capsule, lying beneath the conjunctiva (Figure 17-14). The periorbita is continuous with the periosteum of the facial bones at the orbital rim, with the orbital septum anteriorly, and with the dura mater of the optic nerve. The orbital fat pad lies between the periorbita and the extraocular muscles. Intraorbital fat lies between the muscles and fascial layers (Figure 17-15). In animals with an incomplete bony orbit, the masticatory muscles play a critical role in providing posterior support for the orbital contents. Orbital disease processes may thus be located in one of the following three planes:

•Within the muscle cone

•Outside the muscle cone but within the periorbita

•Within the orbit but outside the periorbita (e.g., posterior to the periorbita laterally where there is no bony wall, as occurs in myositis of the temporal muscle)

The lacrimal gland lies beneath the orbital ligament on the dorsolateral surface of the globe (see Figure 17-14). The base of the third eyelid and gland is held down by the orbital retinaculum, which are poorly defined sheets of collagenous

Zygomatic Wing of sphenoid

FIGURE 17-1. Bones of the skull, hyoid apparatus, and laryngeal cartilages, lateral aspect. (Modified from Evans HE [1993]: Miller’s Anatomy of the Dog, 3rd ed. Saunders, Philadelphia.)

Frontal

(cut)

FIGURE 17-2. Skull, lateral aspect (zygomatic arch removed). (Modified from Evans HE [1993]: Miller’s Anatomy of the Dog, 3rd ed. Saunders, Philadelphia.)

Incisor teeth

FIGURE 17-3. Dorsal view of the canine skull. (Modified from Getty R [1975]: Sisson and Grossman’s the Anatomy of the Domestic Animals, 5th ed. Saunders, Philadelphia.)

ORBIT 353

FIGURE 17-4. Left lateral view of the equine skull. Note the enclosed dorsolateral surface of the orbit. (Modified from Dyce KM, et al. [2002]: Textbook of Veterinary Anatomy, 3rd ed. Saunders, Philadelphia.)

Orbit

Zygomatic

Lacrimal

Facial crest

Maxilla

Infraorbital foramen

Nasal

Nasal process of incisive

Body of incisive

Interincisive canal

FIGURE 17-5. Dorsal view of the equine skull. (Modified from Getty R [1975]: Sisson and Grossman’s the Anatomy of the Domestic Animals, 5th ed. Saunders, Philadelphia.)

tissue continuous with the periorbita but that contain smooth muscle with sympathetic innervation.

Extraocular Muscles

Seven extraocular muscles control movements of the globe (Figure 17-16; Table 17-1). The extraocular muscles arise from the annulus of Zinn, which circles the optic foramen and orbital fissure, and insert onto the globe. Neurologic abnormalities in their function are discussed in Chapter 16.

PATHOLOGIC MECHANISMS

Because the orbit forms a semiclosed space, increases and decreases in the volume of its contents affect the position of the

ORBIT 355

FIGURE 17-10. Visual field of the horse, showing a smaller binocular field, large panoramic uniocular areas, and a minute blind area.

eye in relation to the orbital rim and to the other eye. Spaceoccupying lesions (Figure 17-17) push the eye forward, causing exophthalmos, and often the third eyelid also protrudes as it is passively forced out of the orbit. In dogs and cats orbital masses usually result in swelling of the tissues caudal to the last upper molar tooth, because the orbital floor is only soft tissue in this area. With decreased volume of the orbital contents (e.g., dehydration or atrophy of fat or muscle), the eye sinks further into the orbit—enophthalmos—and the third eyelid protrudes. Osteomyelitis of the bones forming the orbit due to organisms such as Cryptococcus and Actinomyces spp. may also cause exophthalmos.

The position of space-occupying lesions alters the direction of displacement of the globe and is used to determine the site of the offending mass (Figure 17-18) and the optimal route of surgical exploration.

Because the subconjunctival tissues and the orbit are connected, orbital diseases frequently cause chemosis. If the orbital lesion compresses the orbital veins, posterior venous drainage diminishes and chemosis is further increased. In horses, orbital swelling or inflammation commonly causes filling of the depression superior to the upper eyelid.

Muscle fascial sheaths

FIGURE 17-12. Transverse section through head of horse at level of orbital cavities; rostral surface of section. A, Ethmoidal labyrinth; B, dorsal nasal conchal sinus; C, frontal sinus; D, sphenopalatine sinus; E, vomer bone; F, zygomatic process of frontal bone; G, palatine bone; H, mandible; 1, perpendicular plate (lamina); 2, tectorial plate; 3, orbital plate; 4, basal plate; 2-4, papyraceous plate; 5, dorsal nasal concha (endoturbinate I); 6, middle nasal concha (endoturbinate II); 7-10, endoturbinates II-VI, respectively. (Modified from Getty R [1975]: Sisson and Grossman’s the Anatomy of the Domestic Animals, 5th ed. Saunders, Philadelphia.)

Check ligament

FIGURE 17-14. Divisions of the periorbita.

FIGURE 17-15. Loss of orbital fat and masticatory muscle mass, as in this aged golden retriever, can result in profound enophthalmia. (Courtesy University of Wisconsin–Madison Veterinary Ophthalmology Service Collection.)