Large Animal Neurology. Joe Mayhew

side of the trunk, neck, and head as well as the eye signs of Horner syndrome.¹⁸ Of some diagnostic interest is that at least for horses with acute sympathetic lesions and distributions of sweating, the administration of α‐2 agonist sedative drugs will result in expected sweating over normal skin of the body but often reverses the vasodilation and sweating over the sympathetically denervated skin such that it becomes dry.

Figure 10.3 Left Horner syndrome present in this horse (A) is evident as moderate ptosis, lowering of the upper eyelashes and miosis (C) compared with the unaffected side (B). Note that there is still an angle present at the medial margin of the upper lid that is usually much less apparent with the ptosis seen with facial CN VII paralysis.

Figure 10.4 In this case of acute, temporary, experimental Horner syndrome induced by local anesthetic blockade of the cervical sympathetic trunk, a slightly constricted pupil is evident (A) compared with the normal eye (B). In horses, loss of sympathetic tone to superficial blood vessels induces vasodilation and this can be seen on any affected mucous membrane such as the pharynx and larynx, and the bulbar conjunctiva in this case (A). Ptosis is not evident as the eyelids are being held open.

Figure 10.5 This horse is suffering from guttural pouch (GP) mycosis with evidence of pharyngeal dysphagia (A) along with left‐sided Horner syndrome shown as mild ptosis of the upper lid (arrowhead in (B)) and accompanied by facial sweating (A) down to the level of C2 on the neck and even evident under the eye on the left (D) compared with the right (C) side. This is to be distinguished from facial nerve paralysis in that there is no weakness to closing the eyelids when there is loss of sympathetic tone to the eyelids. The classical signs of Horner syndrome are seen in the horse’s left eye (D) when compared to the normal right eye (C). Mild miosis and enophthalmos with slight protrusion of the nictitating membrane are evident along with the ptosis. A prominent component of the ptosis in this syndrome compared with facial paralysis is the lower angle of the upper eyelashes (D) rather than marked lowering of the upper lid, especially the medial aspect, that more typifies facial paralysis. A useful test to help confirm the presence of Horner syndrome is to instill 0.5 mL of 0.5% phenylephrine into the conjunctival sac and observe for correction of the lowered eyelashes. This is shown in (E) where a case of bilateral Horner syndrome has been treated on the right side to correct the ptosis (yellow arrows).

Figure 10.6 This horse was injected with local anesthetic solution in the caudal cervical region. It demonstrated Horner syndrome and sweating over the face and cranial cervical region, especially at the base of the ear. Additionally, there was prominent sweating on the neck over the C₃ to C₆ dermatomes. The local anesthetic solution almost certainly spread caudally along the cervical vagosympathetic trunk to the region of the cervicothoracic ganglion. This would then produce blockade of the sympathetic supply to the skin of the neck at the levels of C3 to C6 in addition to blocking the cervical sympathetic trunk that causes sweating over C1 and C2 only (See also Figure 2.10).

Sympathetic denervation of the head in cattle includes the eye signs of ptosis of the upper eyelid, miosis, and subtle enophthalmos as described in other species, with dilated vessels on the pinnae, warm face and ears, and an absence of droplets of sweat forming on the muzzle (Figure 10.7). ^{Eye signs in Horner syndrome are even less prominent in large animal species other than horses and cattle.14,15,19 Interestingly, it may be reasonable to expect ectoparasites such as ticks to be attracted to skin with altered temperature.27 Facial analgesia was present in a cow that had an ocular squamous cell carcinoma invading the trigeminal nerve. Part of the syndrome included a specific and dense infestation of ticks only on the denervated skin of the face.27 This most probably resulted from cutaneous vasodilation caused by interruption of postganglionic sympathetic fibers distal to those innervating the eyeball that had joined the trigeminal nerve to innervate the skin and blood vessels of the remainder of the face.}

Figure 10.7 Loss of sympathetic control to the blood vessels and glands of the muzzle in cattle results in a loss of fluid production by the nasal glands. This cow had a lesion in the left cranial neck causing Horner syndrome and a dry muzzle on the left side (arrows). Because of the chronicity of the dry muzzle, desiccation and excoriation had begun to occur (arrowhead).

Accompanying generalized signs of autonomic failure, horses affected by equine dysautonomia, commonly known as grass sickness, often show bilateral ptosis.^{28, 29} Muscles (and their innervation) of the upper eyelid that when paralyzed may result in ptosis of the upper eyelids are the levator palpebrae superioris (CN III), the levator anguli oculi medialis (CN VII), and Müller tarsal smooth muscle (sympathetic).³⁰ In grass sickness cases, there is no evidence for the ptosis being due to somatic facial or oculomotor dysfunction, and the evidence points to this being due to sympathetic dysfunction. Indeed, the ptosis can be readily reversed (Figure 10.8) using a low dose of topical α‐1 adrenergic agonist (0.5 mL of 0.5% phenylephrine eye drops). Not only does the upper eyelid ptosis resolve within 10–30 min, but the lowered angle of the upper eyelashes (i.e., pointing toward the ground), so characteristic of grass sickness, also resolves and often quite impressively so compared to the untreated side. This lower eyelash angle present in grass sickness cases is likely due to paralysis of the smooth muscle innervating the eyelashes themselves, the arrectores ciliorium, present in horses and cattle but not in humans and dogs. This phenylephrine eye drop test is thus useful to assist in the diagnosis of grass sickness and other causes of Horner syndrome at least in horses.³¹

Figure 10.8 This horse has left‐sided Horner syndrome (A). About 20 min following instillation of 0.5 mL of 0.5% phenylephrine into the left conjunctival sac, the ptosis is resolved (B) helping to confirm hypersensitivity to adrenergic compounds in the sympathetically denervated structures. An apparently excessive sweat response to phenylephrine also is seen around the orbit (B).

      Third‐order sympathetic neuronal fibers do not pass through