IN-DEPTH INTERACTIVE: NEUROLOGY


mal vision. Before terminating on the facial nu- cleus in the ipsilateral medulla oblongata, the menace pathway passes through the ipsilateral cer- ebellum (Fig. 2A). For example, in normal neo- nates up to 2 weeks of age and in Arabian foals with cerebellar abiotrophy, there is no menace response, but the horse can see. In these settings, vigorous threatening gestures toward the eye may cause re- traction of the eyeball and evasive movements of the head but not blinking. Head-bobbing, limb hy- permetria, and ataxia are expected in horses with abnormal menace responses that result from cer- ebellar dysfunction.


Clinical examples: (1) melanoma in caudal fossa of skull that puts pressure on the cerebellum and (2) Halicephalobus gingivalis aberrant par- asite migration.


Lesion 3—contralateral optic tract: Because “vi- sion” fibers functionally cross en masse at the chi- asm, transection of the right optic tract causes blindness and menace deficit in the left eye. How- ever, enough “light” fibers project ipsilaterally to the midbrain to sustain a normal PLR, and because many of these fibers cross to the other side in the midbrain, both direct and indirect reflexes remain intact.


Clinical examples: Pressure from (1) expanding local tumor (pituitary adenoma, meningioma) and (2) S. equi (strangles) cerebral abscess.


Lesion 4—ipsilateral optic nerve: With injury to the left optic nerve, sensory input to all reflexes from that eye are lost, so the horse has defects in direct PLRs, menace and vision in the left eye, and indirect PLRs to the right eye. In contrast, motor innerva- tion of the pupil is intact, so pupil size (responding to ambient light in the right eye) and indirect PLRs to the left eye are present.


Clinical examples: (1) a yearling colt that has flipped over backward while being handled, striking the poll, causing the cerebrum to “bounce” and tearing its connection to the left optic nerve; (2) a small ethmoid hematoma that grows backward in a Mammoth Mule molly and compresses the optic nerve against the sphenoi- dal bone.


Lesion 5—ipsilateral oculomotor nerve: Motor function to the sphincter of the right pupil is lost, so left PLRs (direct and indirect from the right eye) are absent, and the pupil is dilated and fixed; all other functions are normal.


Clinical examples: (1) peripheral: horse is kicked in the skull and fractures skull through the sphenoidal bone; the pupil is dilated and fixed, the eye is rotated laterally and down, and


194 2015  Vol. 61  AAEP PROCEEDINGS


the upper eyelid is drooped; (2) central: after trauma to the left side of the skull, a portion of the left cerebrum herniates caudally (tran- stentorially) and compresses the oculomotor nerve.


Lesion 6—ipsilateral facial nerve: Inability to blink affects only the menace on the same side and is detected independently by performing the left pal- pebral reflex.


Clinical examples: (1) distal: horse cast in a stall overnight while wearing a halter and after thrashing in lateral recumbency injures the fa- cial nerve behind the vertical ramus of the man- dible; (2) proximal: great petrosal branch of the facial nerve damaged within the petrous temporal bone when that bone is fractured when temporohyoid osteoarthropathy is precip- itated by placing a stomach tube in a horse with a fused temporohyoid joint.


4. Syndrome 3: Exposure Keratitis Versus Dry Eye— Different Levels of Facial Nerve Paralysis With Very Different Consequences for the Cornea


Maintenance of a tear film over the corneal surface is essential for normal corneal function and viability and requires both production of tear components (i.e., water, lipids, mucus) and their distribution across the corneal surface. Functions controlled by motor components of the facial nerve (VII) are in- volved in both phases: (1) a parasympathetic branch (great petrosal nerve) of VII exits the facial canal within the petrous temporal bone and inner- vates the water-producing lacrimal and nictitans glands, and (2) after the facial nerve emerges from the stylomastoid foramen of the petrous temporal bone, it gives rise to the auriculopalpebral nerve caudal to the vertical ramus of the mandible; palpe- bral branches of this nerve innervate the striated muscle that provides the blinking action—the orbic- ularis oculi. Blinking in turn serves to distribute the tear film and to squeeze out lipids from meibo- mian glands along the rim of the eyelids. Thus, injury of the facial nerve distal to the great petrosal nerve branch and proximal to the auriculopalpebral nerve causes eyelid paralysis and exposure keratitis while more proximal injury additionally causes dry eye (also known as keratoconjunctivitis sicca) be- cause of the loss of lacrimal gland secretions.


Exposure keratitis (somatic motor VII denervation): In bright and otherwise healthy horses, eyelid pa- ralysis frequently has no clinical effect. Presum- ably, in response to the irritation of incipient desiccation of the cornea in affected horses, there is frequent reflex retraction of the eyeball (Figs. 3 and 4). This is part of the corneal reflex that may be elicited during the neurologic examination and re- quires the trigeminal nerve (V) for its afferent com- ponent and abducent nerve (VI) for the efferent or


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