Page 857 - Clinical Small Animal Internal Medicine

77 Neuroophthalmology 825

Other CNS signs may be evident depending on the spe­
VetBooks.ir cific localization of the lesion.
The presence of concurrent internal and external
ophthalmoplegia should prompt the clinician to evaluate
for intracranial disease to explain involvement of multiple
cranial nerves. Imaging (MRI) is the diagnostic tool of
choice. Treatment is limited unless the underlying cause
is found. Prognosis is poor as most cases progress to
involve adjacent CNS sites.

Trigeminal Nerve Deficit

Two of the three branches of the trigeminal nerve pro­
vide sensory innervation to the eye, adnexa, and perioc­
ular skin. Lateral sensation is primarily via the maxillary
branch and medial sensation via the ophthalmic branch.
Corneal sensation is derived through afferent fibers
within the long ciliary nerves that originate in the
ophthalmic branch. Decreased or absent function is
diagnosed through an absent palpebral reflex (i.e.,
blink response) and an absent corneal reflex. Lack of
sensation must be distinguished from lack of motor
Figure 77.2 Internal ophthalmoplegia in a dog. The right pupil is function (facial nerve deficit) where the patient is unable
normal. The left pupil is mydriatic with an absent direct and to blink. Differentiation is accomplished by attempting
consensual (right to left) PLR. Topical application of 2% to elicit a menace response or dazzle reflex while avoid­
pilocarpine resulted in pupil constriction within five minutes, ing contact with the skin. A patient with trigeminal nerve
confirming an efferent pathway deficit. dysfunction will blink in response whereas animals with
a facial nerve defect will not have a palpebral reflex or
Pharmacologic testing has classically involved the use normal menace response.
of both indirect‐ and direct‐acting parasympathomimetics. The long ciliary nerves derive from the nasociliary
Indirect acting agents, such as topical 0.5% physostig­ nerve, a branch of the ophthalmic branch of the trigemi­
mine, will cause rapid pupillary constriction in cases of nal nerve. Inadequate function of the long ciliary nerves
a preganglionic (proximal to the cilary ganglion) lesion results in corneal anesthesia or hypoesthesia. With loss
due to release of acetylcholine stores at the postgangli­ of these neurons, there is a loss of normal regulatory
onic axon terminals. Direct‐acting agents, specifically neuromediators such as acetylcholine, substance P,
1% to 2% pilocarpine, are more commonly used. One calcitonin gene‐related peptide, and neuropeptide Y
drop of pilocarpine acts directly on the iris sphincter which are instrumental in maintaining normal corneal
muscle by binding to and activating acetylcholine integrity. Neurotrophic keratitis describes pathology
receptors, inducing pupil constriction within 30 min­ resulting from a trigeminal nerve defect. The decrease in
utes. Use of a direct‐acting agent will allow pupil con­ corneal sensation leads to reduced corneal epithelial cell
striction with both pre‐ and postganglionic lesions and proliferation and delayed healing with corneal ulcera­
therefore is useful in differentiating ophthalmoplegia from tion. Neurotrophic keratitis is likely secondary to trigem­
a pupillomotor defect but does not differentiate a pregan­ inal nerve trauma, but as in humans, diabetes mellitus
glionic from a postganglionic site. Lack of pupillary con­ and herpes virus may be predisposing factors.
striction following administration of a topical The mandibular branch of the trigeminal nerve has
parasympathomimetic confirms a pupillomotor defect. both motor and sensory components. It is responsible
In a young dog or one without clinical evidence of iris for motor innervation to the masticatory muscles and
atrophy, pharmacologic mydriasis is commonly the sensation to the mouth, lower face, and ear. Bilateral dis­
cause. A thorough history will aid in diagnosis. ruption of the mandibular branch results in the inability
Internal and external ophthalmoplegia occur as a result to close the mouth. Ninety percent of cases are idiopathic
of oculomotor nerve, ganglion, or nucleus compression. and clinical signs typically resolve over three weeks.
They are a result of neoplasia, trauma, or inflammation Prolonged cases may develop atrophy of the muscles of
at the level of the midbrain, brainstem, or cavernous sinus. mastication. When the pterygoid muscles are affected,