Large Animal Neurology. Joe Mayhew
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Название: Large Animal Neurology
Автор: Joe Mayhew
Издательство: John Wiley & Sons Limited
Жанр: Биология
isbn: 9781119477198
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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 СКАЧАТЬ