Neuro‐ophthalmic Syndromes

Neuro‐ophthalmic Syndromes

Neuro‐ophthalmic syndromes occur as the result of an insult to the segments of the nervous system that innervate or influence the functions of the eye and adnexa. Neuro‐ophthalmology is a complex field, and although there are several syndromes recognized in veterinary medicine, their diagnosis and understanding can be difficult and incomplete. Patients with these syndromes present to either the ophthalmologist or the neurologist; often in large and referral veterinary practices these two disciplines will examine the patient, and combine their talents and experiences for the benefit of the patient. Optic neuritis that can be grouped with these syndromes is discussed in Chapter 13. Prognosis and treatment of neuro‐ophthalmic conditions depends upon the location and etiology of the lesion.

Horner’s Syndrome

Horner’s syndrome is best understood and most frequently diagnosed in the dog. However, Horner’s syndrome occurs in all of the most common domestic species and can indicate significant neurological disease.

Horner’s Syndrome in the Dog

Horner’s syndrome in the dog results from an interference of the sympathetic innervation to the eye and periocular structures. It results in miosis, ptosis (drooping of the upper eyelid), enophthalmos (eye appears recessed), and protrusion of the nictitating membrane (Figure 19.1). With these clinical signs, anisocoria (difference in pupil size between the two eyes) and a narrowed palpebral fissure also occur.

Photo of a dog with Horner’s syndrome characterized by miosis, protrusion of the nictitating membrane, ptosis or drooping of the upper eyelid, and relative enophthalmia.
Photo of a Golden Retriever dog with idiopathic Horner’s syndrome.
Photo of a cat with Horner’s syndrome.

Figure 19.1 (A) Horner’s syndrome in the dog is characterized by miosis, protrusion of the nictitating membrane, ptosis or drooping of the upper eyelid, and relative enophthalmia. (B) Idiopathic Horner’s syndrome in a Golden Retriever. (C) Horner’s syndrome in a cat.

The clinical signs seen in Horner’s syndrome occur when damage has been incurred anywhere along the three neuron pathways that dictate sympathetic control of the eye. Provocative pharmacologic testing (topical cocaine, 10% phenylephrine, and 1% hydroxyamphetamine) can be used to localize the lesion and differentiate between first and third order lesions.

The most frequent causes for Horner’s syndrome in the dog are trauma, brachial plexus root avulsion, otitis media/interna, thoracic and intracranial tumors. Prognosis is determined by the etiology. Idiopathic Horner’s syndrome occurs fairly commonly in the Golden Retriever. Signs and causes of Horner’s syndrome are similar in the cat.

Horner’s Syndrome in Large Animals

The clinical signs of Horner’s syndrome in horses include miosis, ptosis, enophthalmia, and protrusion of the nictitating membrane (Figure 19.2). In addition, cutaneous facial and cervical hyperthermia and sweating occurs on the affected side. The causes of Horner’s syndrome in horses include mycotic guttural pouch infections, trauma of the basisphenoid area, polyneuritis equi syndrome (cauda equina neuritis), equine protozoa myeloencephalitis, esophageal rupture, and after intravenous injections of xylazine, vitamin C/selenium, and phenylbutazone. Prognosis is determined by the contributing cause and response to therapy. Horner’s syndrome in bovids manifests with ipsilateral anhydrosis (absence of sweating) of the nasal planum, rather than upregulated facial sweating as in the horse.

Photo of a horse with wound at its neck.

Figure 19.2 Horner’s syndrome in the foal is exhibited as miosis, protrusion of the nictitating membrane, ptosis or partial drooping of the upper eyelid, relative enophthalmia, and regional sweating of the area behind the orbit (note the wet hair). Guttural pouch infections and trauma are common causes of Horner’s syndrome in the horse.

Facial Nerve Paralysis and Neuroparalytic Keratitis

Facial nerve paralysis is one of the more frequent neuro‐ophthalmic disorders in the dog. Presentation is often based on nonophthalmic facial changes. The clinical signs of facial nerve paresis and/or paralysis include ear movement, drooping of upper and lower lips and commissures of the mouth, drooling, food collecting in the buccal area, and lack of nostril movements (Figure 19.3). The eyelids (especially the upper lid) fail to blink and protect the eye and often result in neuroparalytic keratitis (see also Figure 8.10). Touching the eyelids fails to induce the blink reflex. Because the lids do not function to protect the globe and distribute tear fluid, the globe is at risk for exposure keratitis and ulceration. Keratoconjunctivitis sicca (KCS) can also be present, so tear production should be measured with Schirmer’s tear test when the diagnosis of facial paralysis is made.

Photo of a dog with drooping upper lip and drooping lower eyelid due to facial nerve paralysis.
Photo of a dog’s eye affected with neuroparalytic keratitis and conjunctivitis.

Figure 19.3 (A) Facial nerve paralysis in the dog is evidenced as an impaired or absent blink reflex, variable ptosis, and a drooping lower eyelid. Additional facial nerve abnormalities, such as drooping of the upper lip, may also be present. Manipulation of this dog’s upper eyelid resulted in no attempt to close the palpebral fissure. (B) Neuroparalytic keratitis results from dysfunction of the facial nerve, impairment of the blink reflex, and reduced protection of the eyelid to the cornea and conjunctiva. The result in this dog is drooping of the lower eyelid and conjunctivitis, with the possibility of future keratitis or corneal ulceration.

Facial nerve lesions are central (tumor, inflammation) or peripheral (trauma, otitis media or interna), with the latter having a better prognosis. Causes of facial nerve dysfunction in dogs and cats are surgical and nonsurgical trauma, neoplasia, and otitis media or interna. The condition can be idiopathic in some cases. In cattle, facial nerve paralysis has been associated with dehorning and Listeria sp. infections.

Short‐term medical therapy includes topical lubricants and oral or topical pilocarpine to stimulate tear production when indicated. Long‐term strategies to protect the cornea usually include temporary or permanent partial tarsorrhaphy. If facial nerve function does not improve and the globe is compromised, enucleation may be indicated.

Hemifacial Spasms in the Dog

Hemifacial spasms result in a narrowed palpebral fissure and an asymmetrical face secondary to the facial muscles’ contractions (Figure 19.4). Horner’s syndrome may also be present, and when combined with hemifacial spasms usually occurs secondary to otitis media. Treatment is directed at the underlying condition.

Photo of a dog with narrowed palpebral fissure and distorted face due to hemifacial spasms.

Figure 19.4

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Jul 24, 2020 | Posted by in INTERNAL MEDICINE | Comments Off on Neuro‐ophthalmic Syndromes

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