Large Animal Neurology. Joe Mayhew
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of pupillary responses to the swinging light test are useful here as in the evaluation of vision. Consider a bright and alert patient with rather complex responses to visual and light pathway testing. The patient has no menace response but has a normal palpebral response to touch, and is blind with a widely dilated pupil, all in the left eye. There is a normal menace response in the right eye, and light shone in the right eye results in the right pupil constricting and also in a positive dazzle (blink) response. When the light is then swung briskly to enter the left eye, the left pupil is and remains dilated and there is no dazzle response in the left eye. When the light is then quickly retransferred to enter the right eye, the right pupil constricts strongly again. The lesion must involve both the left retina or optic nerve and the left oculomotor parasympathetic fibers. Retrobulbar empyema, cellulitis, or neoplasm can readily explain these findings. With such lesions behind the globe, the sympathetic fibers to the dilator muscles of the pupil can also be involved, confounding this clinical picture further.
CASE STUDY
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