Читать книгу Large Animal Neurology - Joe Mayhew - Страница 114

Picture a patient being examined for visual and light acuity, but outside in daylight with both pupils somewhat constricted. The right menace response appears to be less than that for the left eye with no convincing anisocoria detectable in shaded but bright daylight. The left pupil responds directly to light shone in the left eye. The right pupil does respond to light shone in the right eye, although being in daylight it is not possible to be convinced of any asymmetry in the rate or degree of pupillary responsiveness. Where is the lesion? With such information available, a partial lesion should be in the left central visual pathways, i.e., postchiasmal. However, now note the responses to the swinging light test using a very bright light source. Light shone in the left eye results in pupillary constriction in that eye. The light is quickly swung to be redirected into the right eye, avoiding a dazzle response. Although the right pupil is initially constricted it dilates back to its resting size as light reaches that eye! When the light is swung quickly to be redirected into the left eye again the left pupil, that may or may not initially appear somewhat dilated, responds by constricting very well. This can be repeated as the light is quickly redirected into each eye in turn, pausing long enough to observe each pupillary size and response. Also, being outside, when the left eye is covered for 10 s with a hand the right pupil dilates to a resting state. When the right eye is covered the left pupil remains constricted as appropriate for the degree of bright ambient light. Indeed, such maneuvers may allow convincing anisocoria to become more apparent with the right pupil becoming less constricted than the left pupil. At least one lesion is in the right eye or right optic nerve. When a darkened examination space becomes available, anisocoria with right relative mydriasis should then be noted. Two points are of note in this case. First, we are often not discerning enough to visually detect minor degrees of anisocoria; and second, outside, even in shaded daylight, there is enough ambient light entering the normal eye to maintain considerable pupillary constrictor tone in the blind eye.

With anisocoria, particularly when due to partial lesions, it can sometimes be difficult to determine which pupil is abnormal. As a rule, an abnormally small pupil (i.e., sympathetic denervation) in one eye will not dilate fully in darkness, but it will respond to light directed into that eye and into the other, normal eye. In comparison, a unilateral abnormally dilated pupil (i.e., parasympathetic denervation) will be most evident in bright light and will not constrict fully in response to light shone into either eye. With reference to bright light, it should be remembered that daylight, and especially direct sunlight, is so much more powerful than any portable light source. It is thus best to perform light pathway tests both in ambient and in quite dim lighting.

A mydriatic pupil with normal vision is seen with parasympathetic oculomotor nerve involvement in large animals, although this is not commonly seen in isolation. The accompanying classical lateral and ventral (down and out) strabismus with ptosis due to somatic motor CN III lesions is also not often seen in large animals but occurs with basilar and sphenoidal sinus diseases. When mydriasis with an inability of the iris to constrict is found with no other neurologic abnormalities, previous atropine therapy must be considered (Figure 10.2). Many asymmetric inflammatory, traumatic, and vascular brain diseases can result in midbrain oculomotor involvement and anisocoria. Space‐occupying and other forebrain lesions associated with brain swelling can result in subsequent ventral pressure on the midbrain and hence onto the oculomotor nerves (Figure 4.8). When such lesions are asymmetric, they then cause anisocoria with poorly responsive pupils that can be accompanied by degrees of blindness, depending on whether the optic nerves and light pathways are also affected.

Figure 10.2 With this degree of bilateral pupillary dilation found in normal ambient room light (yellow bar), the possibility that it is due to a frightened or painful patient must be considered. Especially if this is asymmetric, the effects of previous application of a mydriatic have also to be considered. This patient had received one application of atropine in this left eye 36 h previously and even in sunlight left mydriasis was maintained (see also Figure 13.2).

In accordance with the global trend for the use of nonpossessive eponyms,¹² we shall use the descriptor Horner syndrome—as opposed to Horner’s syndrome—to describe the signs associated with sympathetic denervation (decentralization) of the head of animals. The degree of miosis seen in sympathetic denervation of the eye (Horner syndrome) is very variable and not dramatic in large animals, and neither is enophthalmos and protruding nictitating membrane (Figures 10.3 and 10.4).^313–19 Horner syndrome in horses consists of miosis and ptosis of the upper eyelid as in other species, and these signs alone can be seen with retrobulbar lesions involving postganglionic sympathetic fibers. Ptosis is due to paralysis of the sympathetically innervated Műller superior tarsal smooth muscle. In addition, hyperemic mucous membranes of the head (Figure 10.3), hyperthermia of the face,^20,21 and in horses sweating of the face and cranial neck are evident with more proximal sympathetic lesions (Figures 2.10, 10.5, and 10.6). These latter findings are caused by the interruption of sympathetic fibers to the skin (blood vessels and sweat glands) of the head and neck.¹⁹ Although sweat glands in horses, as in other mammals, may not be directly innervated,²² sympathetic denervation of the head causes cutaneous vasodilation so that more circulating adrenalin is brought to the sweat glands, and this neurohormone has powerful sudomotor effects in horses.^22,23 If the sympathetic fibers are affected at the level of, or distal to, the cranial cervical ganglion in the wall of the guttural pouch, sweating over the head projects caudal only to the level of the atlas. Preganglionic lesions proximal to this level, as in the neck, result in sweating further down the neck to the level of the axis to C3.^{18, 21} Cranial thoracic lesions can affect the sympathetic fibers not only in the cervical sympathetic trunk, but also those innervating the skin of the remainder of the neck traveling with the vertebral nerve and segmental dorsal spinal nerve roots (Figure 2.10). Then, there is sweating over the whole neck and head (Figures 2.10 and 10.6). A first‐order sympathetic neuronal lesion in the descending, tectotegmento‐spinal tract in the brainstem or cervical spinal cord results in sweating on the whole 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 the petrosal bone as in small animal species; therefore, Horner syndrome is usually not recognized with otitis media in large animals or with petrosal bone fractures. Inadvertent perijugular injection of drugs is a relatively frequent cause of Horner syndrome when the compound spreads to the adjacent cervical vagosympathetic trunk. The effect with local anesthetic compounds including α‐2 drugs is usually temporary. But depending on the degree of tissue inflammation caused by other, more irritant compounds, any resulting Horner syndrome can last for hours to months and may be permanent. In horses, the sympathetic fibers innervating the eye are more often damaged in and around the guttural pouch in the region of the cranial cervical ganglion. Finally, many systemic toxins, such as those mediated by atropine‐like alkaloids and the common antimuscarinic colic drug butylscopolamine, cause degrees of mydriasis (Figure 10.1), and those acting with anticholinesterase activity can result in miosis.