Ординатура / Офтальмология / Английские материалы / Small Animal Ophthalmology Secrets_Riis_2002

4.Your patient is an elderly Pekingese dog with bilateral corneal pigmentation and scarring. Touching the cornea with a cotton swab fails to elicit a blink response. Is this likely a problem in the afferent or efferent arm of the reflex?

Brachycephalies have fewer afferent CN- V sensory nerve endings in the cornea than dolichocephalies. This results in reduced frequency of blinking, reduced tear film spread, and chronic keratitis. These complications lessen the compromised corneal sensitivity to compound the problem (i.e., both arms of the reflex are involved).

5.A persistent superficial corneal ulcer in a middle-aged dog will resolve only partially with your treatment for indolent ulceration. Blepharospasm, an indication of corneal pain, is surprisingly absent. Have you checked the response to tactile stimulation?

The dog blinks when under observation but not in response to touching the cornea. Similarly, eyeball retraction is not initiated by touch. Conclude a sensory CN-V lesion. The corneal epithelium

is dependent on normal CN-V innervation. Denervation can result in a nonhealing ulcer. It is important to provide added lubrication to the cornea until the problem resolves or the cause of the deficit is determined. Tarsorrhaphy is also an option. Determine sensory function of the other divisions of CN-V (e.g., the lateral canthus and nares, testing the maxillary branch). Look for evidence of other neuropathies such as facial palsy or cerebellar signs, which point to central verses peripheral disease.

6. Can the lesions responsible for failure of the efferent arm of the blink reflex (i.e., lesions of eN-VII, the facial nerve) be localized?

In these cases, sensation (afferent CN- V) is normal. The animal will retract the eye (CN-VI) and perhaps withdraw its head, but it will fail to blink. The extent of the facial paralysis must be determined. Check for ear and lip droop (Fig. 2). Check for taste sensation with atropine applied to the rostral part of the tongue on the affected side. Taste buds are innervated by special branches of the facial nerve. Check for normal tear production and nostril wetting (see Chapter 10). Concomitant hypalgesia indicating CN- V involvement points to a central (brain) location of lesions.

Figure 2. Lamb withear and lipdroop because of facial palsy.

7. How important is the petrous temporal bone and the inner ear in cases of facial paralysis in the dog?

The facial nerve courses through the petrous temporal bone giving off branches to the lacrimal gland and salivary glands en route to the stylomastoid foramen from where it exits the skull to innervate muscles of facial expression. Inner or middle ear disease such as infections and petrous osteitis can impair CN-VII function. Many cases of otitis media-interna are low-grade, chronic infections that may not carry obvious clinical signs, and facial paralysis is written off as idiopathic. Otitis extern a may not be present. All cases of facial paralysis (and Horner's syndrome) should be given a careful evaluation of the middle ear; this includes radiography of the petrous temporal bone. Increased yawning may be an added sign exhibited. Vestibular signs (e.g.,

nystagmus) may be present as a result either of inner ear involvement or of a lesion in the brain stem (central vestibular signs).

8. Can retinal and optic nerve function be assessed despite the presence of dense cataracts?

This problem confronts the ophthalmologist frequently. The definitive test of retinal function is the electroretinogram (ERG). No matter how dense the cataract, light will pass through the lens, albeit scattered light, to stimulate the retina. The summed electrical potential (in millivolts) generated by a normal retina can be recorded. The ERG may be normal despite optic nerve disease.

9. How should a brisk eyelid closure in response to a very bright light be interpreted?

In this test, called the dazzle response, a very bright light elicits an aversion response seen as a blink of varying speed and intensity in dogs. Humans will avert their gaze, turn away, and even sneeze. This test is not sensitive enough to detect early retinal degenerative disease. The reflex is subcortical. It can be elicited through a cataract. A brisk response is an encouraging sign.

10.Which cranial nerve supplies parasympathetic visceral efferents to the lacrimal gland? Abranch of the facial nerve (CN-VII).

11.What causes neurogenic keratoconjunctivitis sicca (KCS)?

One of the many pathogeneses of KCS is denervation of the gland by a lesion of the facial

nerve. Depending on the location of the lesion, other branches of CN-VII and sometimes CN-V may be involved, with clinical signs consistent with these.

12. How do you interpret the finding of a dry nostril in conjunction with KCS?

Nasal moisture arises primarily from the lateral nasal gland, a serous secreting gland located in the lateral nasal mucosa. Like the lacrimal gland, the nasal gland receives its innervation from a branch of the facial nerve. This branch separates from that to the lacrimal gland at the level of the pterygopalatine ganglion, ventrolateral to the orbital cone and dorsal to the pterygoid muscles. KCS together with a dry nostril (xeromycteria) suggests a preorbital nerve lesion most likely in the petrous temporal bone.

13.Why is it necessary to assess sensation in the lateral canthus area in cases of KCS? The branches of CN-VII that leave the pterygopalatine ganglion as postganglionic efferents

to the lacrimal gland travel to the gland with branches of CN-V, not with CN-VII. These CN-V conduits are sensory to the lateral canthus area. Hypalgesia or anesthesia in the lateral canthal skin, in combination with KCS, enables location of a neuropathy to a peripheral site susceptible to injuries. Remember not all cases of KCS are neurogenic. However, the finding of a CN-VII neuropathy in association with KCS confirms neurogenic KCS.

14.What are the ocular signs of sympathetic denervation (Horner's syndrome)? Assuming that the Homer's syndrome is unilateral, as it is in most cases (Fig. 3), signs in-

clude:

•Miosis in the affected eye. The pupil constriction is relative to the normal eye and is relatively less marked in bright light.

•Enophthalmos. The affected eye recedes into the orbit when the smooth muscle tone of the periorbita is reduced (i.e., "squeeze" on the eyeball is reduced). This sign is the most variable one that is seen.

•Narrowing of the palpebral fissure with loss of tone of upper and lower eyelid smooth muscle. This sign will exaggerate the appearance of enophthalmos

•Third eyelid protrusion. This is mainly passive or secondary to enophthalmos in the dog; it is a direct effect of loss of smooth muscle tone in the cat

Figure 3. Left-sided Horner's syndrome in a cat. Miosis and a narrowed palpebral fissure are the obvious signsin this photograph.

15. What is meant by preversus postganglionic sympathetic denervation?

The term refers to the site of a lesion in relation to the cranial cervical ganglion, an important structure in the understanding of Horner's syndrome.

•The cranial cervical ganglion is the location of the cell bodies from which postganglionic sympathetic axons stream forth to innervate all smooth muscle in the head area.

•The cranial cervical ganglion is located deep to the tympanic bulla.

•Preganglionic fibers arise in the hypothalamus and descend in the cervical spinal cord to levels T I. T2, and T3. After synapsing at this level, the second-order neuron enters the thorax, joins the vagal trunk, and ascends the neck in the jugular groove to synapse in the cranial cervical ganglion.

•Postganglionic fibers travel to the eye and periorbita via the middle ear, go through the cavernous sinus, and then utilize the ramifying fibers of CN-V as a conduit.

16.What are some of the better documented lesions of the firstand second-order neuron (i.e., preganglionic lesions) accounting for Horner's syndrome?

•Hypothalamic neoplasia

•Cervical cord compression

•Brachial plexus avulsion or neoplasia

•Anterior mediastinal space occupying lesions

•Trauma to the jugular groove area including iatrogenic needle stick injuries

17.What are some ofthe documented post-ganglionic lesions accounting for Horner's syndrome?

Middle ear disease including iatrogenic injury with bulla osteotomy.

•Otitis media should not be overlooked.

•Ear examination, despite the common lack of external signs, should be conducted.

•Orbital lesions affecting the ophthalmic division of CN-V traveling through the orbital cone combined with the sympathetics

18.Define strabismus, enophthalmos, and exophthalmos.

Strabismus refers to a deviation of the eyeball from the normal visual axis. It is caused by

abnormal neurologic innervation of extraocular muscles (CN-III, IV, and VI ), primary muscle function disturbances, or space-occupying lesions of the orbit. Remember the vestibular apparatus plays an essential role in the control of eyeball position through its input into the nuclei of CNIII, IV, and VI.

Enophthalmos refers to sinking of the eyeball into the orbit. It should not be confused with active retraction. The most common neurologic cause is Horner's syndrome.

Exophthalmos refers to abnormal protrusion of the eye. This may be passive, as with shallow orbits, or active, as with a space-occupying lesion in the orbit. Apparent exophthalmos oc-

curs in the dog where the animal is blind with widely dilated pupils. A combination of apprehen- sion-increased sympathetic tone in the orbital fascia plus the "staring" attitude of a blind dog contributes to the exophthalmic appearance.

19. How would you expect the eye to deviate with a unilateral lesion of the oculomotor nerve (CN-I1I)?

One should expect lateral strabismus with an inability to fix the gaze medially, dorsally, or ventrally. Bilateral strabismus of this nature is called exotropia. Ptosis (drooping) of the upper eyelid owing to levator palpebrae denervation mayor may not accompany the strabismus of oculomotor nerve dysfunction. Similarly involvement of the pupils would depend on the location and extent of the CN-III lesion.

20. What are the neurologic implications for a dog with a unilateral inability to retract the eyeball?

Eyeball retraction can be induced as a preservation response to noxious stimuli of the eye (afferent CN-V). Usually manual or chemical restriction of simultaneous eyelid closure is necessary. The withdrawal of the eye occurs via the abducens-innervated retractor muscle bundle. The third eyelid will passively protrude. Loss of the retraction response indicates an afferent CN-V or efferent CN-VI lesion. A CN-VI lesion will be associated with medial strabismus.

21. What advice can be given to the worried owner of a cross-eyed cat?

The Siamese breed is relatively prone to this trait although domestic shorthairs are affected as well. The eyes are deviated inward. This is called a convergent strabismus or esotropia. Nystagmus may be seen also. Vision is not normal but adequate. The basis of the syndrome relates to abnormal retinal pathways and projections to visual cortices. The eyes deviate to maximize spatial binocular vision.

22. What is the oculocardiac reflex?

Tension on extraocular muscles or retropulsion of the eye will result in slowing of the heart in the normal animal. Orbital space-occupying lesions or manipulation (e.g., during eye removal) can initiate the reflex.

23.Which cranial nerves comprise the oculocardiac reflex?

Afferent impulses are carried by the ophthalmic branch of CN-V to the sensory nucleus in

the medulla. The efferent arm belongs to the vagus nerve (CN-X). Vagal stimulation induces bradycardia and can induce cardiac arrest.

Review of cranial nerves involved in eye reflexes

24. What is the differential diagnosis for an eye that is blind since birth despite appearing normal with routine examination?

The problem most likely involves the retina or optic nerve and may be unilateral or bilateral. Retinal dysplasia including detachment. This is seen as an inherited trait in some breeds (e.g., rough collie (see Chapter 38). Retinal dysplasia may also be the result of an intrauterine insult to the developing eye (e.g., viral infections, teratogenic drugs). The detached retina looks like a gray

veil behind the lens

Optic nerve hypoplasia. The optic disc is very small, usually indicating an hypoplastic optic nerve (Fig. 4).

Figure 4. Fundus photograph depicting a very small optic disc in a blind puppy.

25.What is the differential diagnosis for sudden blindness in the dog?

Sudden acquired retinal degeneration (SARD). Vision loss is dramatic and bilateral.

Pupillary light reflexes are reduced but seldom absent in the early-presenting case. Retinal examination may be normal or show subtle abnormalities in early stages, progressing to tapetal hyperreflectivity with time. The dog often exhibits polydipsia and polyphagia. Blood cortisol levels are elevated. The dog, however, is not a long-term hyperadrenocorticoid case and does not require therapy for hyperadrenocorticism. Pathogenesis of SARD is not known. Electroretinography (ERG) indicates generalized retinal dysfunction.

Optic neuritis (papilledema). Vision loss is dramatic although not necessarily equal in each eye. Pupils are widely dilated and very poorly or not responsive. The presentation is similar to SARD in that regard. On fundus examination, however, the optic disc is often swollen with retinal vessels climbing up over the protruding disc. The retina may detach and "tent up" around the disc. These features may not always be present and depend on etiology. ERG indicates normal retinal function unless the dog has a concomitant retinitis, in which case the ERG may be suppressed.

26.List the causes of optic neuritis in the dog.

Granulomatous meningoencephalomyelitis (GME) is the most common cause. This multifo-

cal central nervous system disease has a high likelihood of optic nerve involvement (Fig. 5). GME may present initially with signs referable to optic nerve disease only (i.e., sudden blindness with no other neurologic deficit).

•Distemper

•Cryptococcosis and more rarely other mycoses

Figure 5. Fundus photograph of a swollen optic disc consistent with optic neuritis.

•Toxoplasmosis

•Neoplasia in the orbit, chiasm, or base of brain (e.g., pituitary gland)

•Trauma. Consider skull fractures around the basisphenoid, foreign bodies, and iatrogenic trauma following orbital abscess drainage procedures

27.Sudden blindness is encountered with increasing frequency in old cats. Why?

Hypertensive retinopathy with retinal detachments and retinal hemorrhage is seen in the old cat

with blood pressure levels usually exceeding 200 mmHg (Figs. 6 and 7). Funduscopic examination reveals vascular explosions and a billowing retina. The retinopathy is not always bilaterally sym-

Figures 6. Retinal detachment with hemorrhages in a cat with blood pressure recorded at 300 mmHg.

Figure 7. Ultrasound appearance of the retinal detachment with the typical "bird-wing" feature.

metrical. Affected cats may remain relatively more visual in one eye. Therapy directed at blood pressure reduction may preserve vision or even restore vision at times.

28.What are some of the causes of optic neuropathy in cats?

•Cryptococcosis

•Toxoplasmosis

•FIP

•Lymphoma

One should expect signs of retinitis and uveitis with these diseases.

GME does not occur in the cat. Note: Optic disc edema is not a common sign of optic neuropathy in the cat.

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