Page 858 - Clinical Small Animal Internal Medicine

826 Section 8 Neurologic Disease

nerve paralysis still have normal sensation and may
VetBooks.ir retract their eye and elevate the third eyelid in response
to a menacing gesture or painful stimulus applied to the
adnexa. Animals with a trigeminal nerve defect have a
normal menace response.
Without the ability to close the eyelids completely,
neuroparalytic keratitis may arise due to chronic cor­
neal exposure and tear film evaporation. With progres­
sion, corneal vascularization, scarring, and ulceration
ensue (see Figure 77.3). Corneal protection is the treat­
ment of choice and involves the use of topical lubri­
cants, topical antibiotics, and possibly placement of a
temporary tarsorrhaphy. If the parasympathetic fibers
that run with the facial nerve to the lacrimal gland are
Figure 77.3 Neurotrophic and neuroparalytic keratitis in a dog. affected, neurogenic dry eye will occur. Approximately
Note the left eye is enophthalmic, the third eyelid is elevated, the 20% of dogs with facial nerve paralysis develop neuro­
ocular surface is dry, and a deep, infected stromal corneal ulcer is
present. Also note the severe masseter and temporalis muscle genic dry eye that can be diagnosed by a routine
atrophy. Neuroophthalmic localization of the lesion is at the Schirmer tear test. Concurrent neurogenic dry eye
petrosal temporal bone. hastens corneal deterioration. Treatment with oral or
topical parasympathomimetics will aid in return of
tear production due to denervation hypersensitivity
secondary enophthalmos and passive third eyelid eleva­ and upregulation of acetylcholine receptors at the lac­
tion may occur (Figure 77.3). rimal gland.
Treatment for trigeminal nerve defects is supportive. Facial nerve paralysis is reported to be idiopathic in
Topical lubricating agents are recommended to support 75% of dogs and 25% of cats. Other causes include
surface ocular health and symptomatic treatment for surgery, trauma, neoplasia, hypothyroidism, and otitis
secondary corneal ulceration is indicated when necessary. media. Total ear canal ablation and bulla osteotomy
As most cases are secondary to trauma or are idiopathic, surgery results in facial nerve paralysis or paresis in
prognosis for return of function is fair. Other reported 49% of dogs and cats. Median time to restoration of
causes of trigeminal dysfunction include neoplasia and function is 2–4 weeks. Neoplasia is an uncommon
polyneuritis of unknown origin. cause in dogs, but the most common in cats. Inflam­
mation of the middle or inner ear is often present with
facial nerve paralysis. With primary or secondary pet­
Facial Nerve Paralysis rosal bone inflammation, other neuropathies may
become apparent. The trigeminal, vestibulocochlear,
The efferent arm of the palpebral, menace, corneal, and glossopharyngeal, and oculosympathetic and parasym­
dazzle reflex are all mediated by the facial nerve. The pathetic nerves course through the petrosal bone.
facial nerve arises at the facial nucleus in the brainstem Therefore, additional clinical signs may include ocular
and courses with the vestibulocochlear nerve through and facial anesthesia or hypoesthesia, neurotrophic
the petrosal bone before branching. Ultimately, the keratitis, masticatory muscle atrophy, vestibular dis­
zygomatic branch innervates the orbicularis oculi and ease, loss of taste sensation, and Horner’s syndrome.
retractor anguli oculi muscles and controls the blink­ Fifty to sixty percent of dogs and cats with facial nerve
ing response. Clinical signs associated with facial nerve paralysis will have additional signs, with vestibular dis­
paralysis may be restricted to the eye or may also involve ease most common in cats and hypothyroidism or ves­
other structures, depending on the site affected. tibular disease most common in dogs.
Nonocular clinical signs associated with facial nerve Treatment of facial nerve paralysis involves addressing
paralysis may include deviation of the nasal septum the underlying cause when present. All patients with
toward the unaffected side, drooping of the ipsilateral lip facial nerve paralysis should have a thorough otic exam
or pinna, and lack of sensation to the inner pinna. Ocular and a thyroid level completed. If an underlying cause is
signs of facial nerve paralysis include an absent palpebral not found, and true idiopathic facial nerve paralysis
reflex, neuroparalytic keratitis, and, potentially, neuro­ exists, supportive care to involve ocular lubrication and
genic dry eye. protection is indicated. Prognosis for return to function
Differentiation of facial nerve paralysis from trigeminal is guarded, with some cases improving in several weeks
nerve dysfunction can be difficult. Animals with facial and others never.