Martin Furr
Horner’s Syndrome
Horner’s syndrome (HS), a constellation of clinical signs reflecting sympathetic denervation of structures of the head, has been reported in humans and a number of veterinary species. The syndrome is named after the Swiss physician Johann Horner (1869), but the first report has also been attributed to Francois Pourfour du Petit in 1727. Although several descriptions of HS have been published, there are no specific reports of prevalence. The condition is relatively uncommon.
Anatomy, Pathophysiology, and Clinical Signs
Sympathetic neurons innervating the head arise from the brainstem in the region of the midbrain, pons, and ventrolateral aspect of the medulla oblongata, and descend in the lateral funiculus of the spinal cord to synapse, at the level of the cranial thoracic segments, on the nerve cell bodies that give rise to the sympathetic trunk. Axons exit the central nervous system (CNS) at T1-T2, course through the anterior mediastinum, and ascend as the cervicosympathetic trunk intimately associated with the carotid artery, terminating in the cranial cervical ganglion (CCG), which lies on the caudodorsal surface of the medial compartment of the guttural pouch. Postganglionic neurons arising from the CCG innervate the pupillary dilator and retrobulbar muscles of the eye, smooth muscles of the eyelids, and sweat glands of the skin.
The clinical signs of HS can arise secondary to damage to any of the nerves comprising the described sympathetic pathway (Box 86-1). Damage to the cervical sympathetic trunk associated with intravenous injections, perivascular inflammation or abscesses, myositis of the cervical muscles, lacerations, or blunt force trauma appear to be the most common. Central nervous system lesions arising from many causes can also lead to HS, and thoracic or pleural disease arising from mediastinal abscesses or masses may also cause HS. Damage to the CCG or postganglionic neurons can arise from blunt force trauma to the head, periorbital masses, guttural pouch empyema or mycosis, and mandibular fracture with associated soft tissue damage. In most cases, the signs are unilateral, as is evident from the nature of the inciting causes, but bilateral HS has been reported in horses with cranial mediastinal masses.
Clinical signs of HS are classically described as consisting of ptosis, miosis, and enophthalmos. In the horse, increased sweating is a prominent component of the illness, unlike in humans, and hyperemia of the nasal mucosa on the affected side is occasionally seen. However, the clinical signs and presentation are often not straightforward; signs may vary in magnitude, and not all signs may be present in each individual. The clinical signs of HS are reported to vary with the site and chronicity of the lesion. In experimentally induced HS in which the cervical sympathetic trunk was surgically transected, clinical signs consistently included ptosis, miosis, enophthalmos, prolapsed nictitating membrane, and unilateral sweating. Hyperemia of the nasal mucosa was variably seen (in two of six experimental animals), as was increased skin temperature as assessed by thermography. These findings were reported to be of variable severity, however, so there also appears to be substantial interanimal variability in the expression of clinical signs.
Loss of sympathetic innervation to the skin leads to sweating in the horse; with a unilateral lesion, sweating will begin at the base of the ear, follow a well-demarcated boundary down the center of the head, and extend as far caudal as the first cervical vertebrae. In experimentally induced HS, this persists for only the first 48 hours or so, after which sweating becomes patchy and inconsistent. In many reported clinical cases, however, prominent sweating persists for many days to weeks, and most likely reflects variation in the magnitude of nerve dysfunction.
Ptosis has been reported by many authors to be one of the most consistent and distinct features of HS in horses. Ptosis is caused by decreased tone of the smooth muscle of the eyelid and is more easily discerned in subtle cases by viewing the eyelash angle from a frontal view; with ptosis, the eyelashes will be pointing down, rather than laterally. Enophthalmos arises from reduced tone of the retractor bulbi muscle but is usually mild, and prolapse of the third eyelid may or may not be seen, depending on the degree of enophthalmos. The miosis observed with HS in horses is also usually mild, with a maximal difference in pupil size of no more than 2 to 3 mm, compared with the unaffected side.
Although it has been seen, laryngeal hemiplegia is not reported to be a common clinical finding in horses with HS. This may be because many horses with HS do not routinely undergo endoscopic evaluation, and a higher incidence of laryngeal hemiplegia might be seen in horses with HS if endoscopy was performed. Laryngeal hemiplegia was observed as a complication in 2 of 10 horses with HS in one case series, and has been reported sporadically in other reports.
