the left optic nerve, the unambiguous description would be as follows. The patient is blind in the left eye only and has no menace response in the left eye with normal facial nerve function and normal palpebral reflexes. The left pupil is widely dilated, and light directed into the left eye causes no response in either pupil. Light directed into the right eye causes the right pupil to constrict but the left pupil remains dilated.
Sympathetic innervation to the eyes and head
Although not classical cranial nerves, these neuronal fibers are involved in pupillary function and can be conveniently considered here. Nuclei within the brain that control sympathetic motor function are in the hypothalamus, midbrain, pons, and medulla oblongata. First‐order neuronal fibers descend through the midbrain, medulla, and cervical spinal cord to synapse on cell bodies in the lateral intermediate gray columns in the thoracolumbar spinal cord. The preganglionic, second‐order, sympathetic cell bodies supplying the head and neck are situated in this position in the cranial thoracic segments, T1–T3. Axons leave these segments of the spinal cord, traverse the cranial thorax,19 ascend the neck in the cervical sympathetic trunk adjacent to the vagus nerve, and pass to the cranial cervical ganglion that lies under the cranial part of the atlas. In the horse, this ganglion is on the caudodorsal wall of the medial compartment of the guttural pouch. Postganglionic, third‐order, sympathetic fibers leave the cranial cervical ganglion to innervate the glands, smooth muscles and blood vessels of the eyeball, and the head and cranial cervical area at the level of C1 and C2 (Figure 2.10). Sympathetic fibers supplying the skin of the neck from C2–C8 leave the parent bundles in the thorax and pass cranially as the vertebral nerve with the vertebral vessels all running within the lateral vertebral foramina to join the segmental vertebral nerves supplying each cervical dermatome.
Damage to the sympathetic supply to the eye and its associated structures results in slight ptosis of the upper lid, a miosis or constriction of the pupil, slight enophthalmos, and a slight protrusion of the nictitating membrane. Vision and the pupillary light responses are unaffected. In most species, this is referred to as the Horner syndrome. Prominent in horses is a resulting change in eyelash angle that occurs due to loss of innervation of eyelid muscles under sympathetic control, especially the m. arectores cilliorum, all of which help maintain a relatively horizontal eyelash angle.
In the horse at least, lesions involving the sympathetic supply to the head result in these ophthalmic signs, as well as additional signs consisting of dilation of facial blood vessels, hyperemia of nasal and conjunctival mucous membranes, and increased temperature and sweating of the face. Sweating is most prominent at the base of the ear—due to a high sweat gland population there—and can extend a variable distance down the neck dependent upon the exact lesion site. Ptosis is the eye sign most consistently observed in large animals, and this may be the only sign with retrobulbar sympathetic involvement but usually accompanied by periorbital sweating in horses. However, with more proximal lesions of the sympathetic supply to the head in horses, there is usually prominent sweating and vasodilation of the sympathetically denervated skin.20, 21 Lesions in the region of the guttural pouch and cranial cervical ganglion will result in sweating of the face and the cranial neck down to the level of C2.22 Most likely the postganglionic fibers follow branches of the trigeminal nerve, thus some lesions of these branches have resulted in localized sweating of the rostral face only with infraorbital involvement of the maxillary branches in the absence of signs of eye involvement. Lesions further down the neck involving the sympathetic trunk may result in sweating of the face and the neck extending down to the level of C3. Lesions in the thoracic inlet can result in this sweating extending down to the level of the shoulder with involvement of other thoracic sympathetic nerves in addition to the cranial cervical sympathetic trunk. Selective lesions in the neck involving segmental branches from the paravertebral nerve that passes up the vertebral lateral foramina can result in linear saddles of sweating over the neck between C3 and C8 dermatomal segments. Although extremely rare, lesions of the spinal cord involving the descending sympathetic pathway can result in eye involvement and sweating of the whole side of the body ipsilateral to the lesion. This is because all the sympathetic fibers leaving the spinal cord have lost their central motor neuron connections and are thus decentralized and nonfunctional.
Figure 2.10 Sympathetic pathways showing outflow from CNS to face, neck, and trunk.
The reason for sweating with cutaneous sympathetic denervation in horses is not entirely clear as equine skin probably has predominantly cholinergic, not adrenergic neural supply, and although nerve endings are close to sweat glands and their accompanying prominent small blood vessels, they may not actually innervate the glandular secretory cells.20 An explanation is that loss of sympathetic supply results in cutaneous vasodilation that brings more circulating adrenalin to the sweat glands, and this hormone has a powerful sudomotor effect in that species.
Cattle that have lost the sympathetic supply to the head show the same signs involving the eye and periorbit, dilated blood vessels over the pinna, and a lack of sweat production on the muzzle. Only eye signs have been detected with sympathetic denervation of the head and neck in sheep and goats, although this could be studied with greater diligence.
Sympathetic innervation to the trunk
Other first‐order neuronal fibers descend through the midbrain, medulla, and cervical spinal cord to synapse on second‐order cell bodies in the lateral intermediate gray columns in the thoracolumbar spinal cord to leave the T‐L spinal cord segmentally, supplying the sympathetic trunk that supplies third‐order neurons to glands (including the adrenal) and blood vessels over the trunk and remainder of the body. Damage anywhere along this pathway can result in diffuse (proximal lesions) or selective (more distal lesions) sweating over the caudal body.
Is it not interesting to ponder the systemic effects of decentralizing the adrenal medulla on one or both sides?
Oculomotor nerve—CN III; trochlear nerve—CN IV; abducens nerve—CN VI
In addition to parasympathetic innervation of the pupillary constrictor smooth muscles, the oculomotor nerve also innervates the somatic extraocular muscles, along with the trochlear and abducens nerves. The function of these muscles and nerves is tested by observing the normal position of the eyes within the bony orbits and by observing eye movement. An abnormal eye position or strabismus results when these nerves or muscles are damaged. Physical deformity of the bony orbit and prominent, particularly congenital, blindness all can result in degrees of abnormal eye position.
When evaluating eye position and movement, consideration must be given to the normal response of the eyes to head posture and movement. When the nose of a large animal is elevated to extend the head, the eyes tend to maintain a horizontal axis and thus move ventrally in the bony orbits. As the head is moved to one side, the eyes move in a rhythmical manner until head movement stops. There is slow phase movement in the direction opposite to the direction of head movement, followed by a fast (catch‐up) phase in the direction of head movement. These eye movements are regarded as physiologic vestibular nystagmus and result from the connection from the vestibular apparatus in the inner ear and the medullary vestibular nuclei to the nuclei of the cranial nerves controlling eye movement, CNs III, IV and VI. Normal inducible vestibular nystagmus thus requires an intact vestibular system, intact cranial nerves III, IV, and VI, and the connections between all of these in the medial longitudinal fasciculus.
The forms of strabismus described for paralysis of each of these cranial nerves should be present in all positions of the head. Such examples of true strabismus are not often encountered in large animals. Mydriasis is seen with oculomotor nerve disease, and a tendency for lateral eyeball deviation