Horner’s syndrome in dogs: aetiology and diagnostic protocol

Introduction

Horner’s syndrome is a neuro-ophthalmological condition that can affect dogs of any age. Breeds including Collies, Shetland, Weimaraner, Doberman, and above all Golden Retrievers, are considered to be predisposed to the condition.^1,2

Horner’s syndrome occurs when one of the sympathetic nerve pathways innervating the eye is damaged and it involves three types of neurons:

• First-order neurons are found in the section connecting the brain to the first thoracic segments of the spinal cord;
• Second-order neurons run from the end of the first-order pathway to the cranial cervical ganglion; and
• Third-order neurons connect the cranial cervical ganglion to the sympathetic nerves of the eye and its adnexa.

As such, Horner’s syndrome can be classified as central, preganglionic or postganglionic depending on the location of the lesion, with postganglionic Horner’s syndrome the most frequent clinical presentation. In any case, the clinical signs in the eye are the same regardless of the lesion’s location.^1,2

Clinical signs

Clinical manifestations of Horner’s syndrome in dogs include:

• Miosis, due to interruption of innervation of the dilator muscle of the iris.
• Enophthalmos, due to a lack of activity of the periorbital muscles that work antagonistically to the retractor bulbi.
• Protrusion of the third eyelid, secondary to enophthalmos.
• Palpebral ptosis, due to a lack of tone of the palpebral muscles and enophthalmos.

In addition, loss of sympathetic innervation may cause ipsilateral peripheral vasodilation and the auricular pavilion may feel warmer on the affected side compared to the contralateral ear. Nasal or conjunctival hyperaemia can also be observed. These latter signs seem to be rare in small animals.^1,2  

Aetiology

Approximately 50% of cases of Horner’s syndrome in dogs are thought to be idiopathic.

Other possible causes include craniocervical trauma (falls, traffic accidents, bites), otitis media/interna, anaesthetic blockades, ear surgeries (bulla osteotomy and ear canal ablation), thoracic surgery or trauma, brachial plexus avulsion, infectious diseases (tick paralysis, neosporosis), fibrocartilaginous embolism, intervertebral disc disease, diabetes and thoracic or intracranial neoplasms.^1-4

Diagnosis of Horner’s syndrome in dogs

In general, the clinical diagnosis of Horner’s syndrome is straightforward and is based on identifying the aforementioned clinical signs. In any case, it is important for vets to confirm that the pupil with miosis is actually the diseased pupil, that is, that there is no disease-related mydriasis, and to rule out other possible causes of miosis (uveitis, endophthalmitis, panophthalmitis or ulcerative keratitis).²

• The application of 1 drop of a cocaine solution (5–10%) is considered the gold standard for the diagnosis of Horner’s syndrome. In healthy dogs, cocaine will dilate the pupil, whereas there is no reaction in patients with bilateral Horner’s syndrome.

In unilateral Horner’s syndrome, there is more marked anisocoria, because the affected pupil does not dilate or only minimally, and the healthy pupil shows full mydriasis. However, this test does not reveal the anatomical location of the lesion. In addition, the legal requirements for obtaining cocaine and the fact it must be applied separately from parasympatholytics mean that it is not used routinely.²

• Apraclonidine (0.5–1%) is used in human medicine to diagnose Horner’s syndrome. In a healthy eye, it has virtually no effect on pupil size, while in affected eyes, it causes pupil dilation, which in patients with unilateral disease manifests as a reduction in anisocoria within 30–45 minutes of administration.²
• Phenylephrine or topical adrenaline is administered to determine the location of the lesion.
• The application of 0.1 mL of 0.001% adrenaline causes the affected pupil to dilate in the first 20 minutes for postganglionic cases, whereas it takes 30–40 minutes in healthy animals or animals with preganglionic Horner’s syndrome.
• If the test is performed with 10% phenylephrine, mydriasis is evident after 5–8 minutes with a postganglionic lesion, but there is no effect on normal eyes or eyes with a preganglionic lesion. In patients with postganglionic Horner’s syndrome, the application of a drop of 1% phenylephrine to the affected eye resolves ocular signs in under 20 minutes, but it does not cause any effect in animals with central or preganglionic disease. It is important to apply phenylephrine in both eyes at the same time. Both pupils will dilate in animals with bilateral disease.^1-3  
• The use of 1% hydroxyamphetamine has been proposed as a means of distinguishing between preganglionic/central (the pupil dilates within 45 minutes) and postganglionic Horner’s syndrome (no effect); however, this test appears to have a higher percentage of false negatives and false positives than phenylephrine.¹

Conclusions

Although the clinical signs of Horner’s syndrome in dogs are easily recognised, it is important to rule out other possible diagnoses first in a patient with anisocoria. The next step is to determine the location of the lesion and establish the causal disease. Either way, owners must be warned that even with an appropriate diagnostic protocol, there is only approximately a 50% chance of identifying the cause.

References

1. Ofri R. (2013). Neuroophthalmology. In: Maggs DJ, Miller PE, Ofri R (Eds). Slatter’s Fundamentals of Veterinary Ophthalmology 5th ed. Elsevier Saunders: 334-371.

2. Zwueste DM, Grahn BH. (2019). A review of Horner’s syndrome in small animals. Can Vet J; 60:81-88.

3. Boydell P. (2000). Idiopathic Horner syndrome in the golden retriever. J Neuroophthalmol; 20: 288-290.

4. Simpson KM, Williams DL, Cherubini GB. (2015). Neuropharmacological lesion localization in idiopathic Horner’s syndrome in Golden Retrievers and dogs of other breeds. Vet Ophthalmol; 18:1-5.