(Kern and Erb; Power, et al.)
Signs Seen With Cranial Nerve Palsies
Abducens nerve palsy
Trochlear nerve palsy
Oculomotor nerve palsy
Facial nerve paralysis
Potpourri of Neuro-ophthalmic Conditions
Ptosis
Haws
Nystagmus
Hemifacial spasm
Horner's syndrome
Blepharospasm
This chapter is intended to provide highlights of a very complex subject (Bagley, et al.; Neer and Carter; Scagliotti). Some of the conditions are primary whereas others are the result of other ocular or systemic disease.
Produces esotropia (convergent strabismus). Medial rectus over pulls (antagonist is lateral rectus). On tonic reflexes, only lateral movement lacking; dorsal, medial and ventral reflexes normal.
Produces rotational defect of eye and patient compensates with a head tilt; amount of head tilt equals ocular rotation. Rotational defect not seen in horses.
Several muscles involved, but net result usually is downward and slightly lateral deviation of globe. In dorsal and ventral tonic eye reflexes, eyes and head move together; lateral rectus muscle function is normal. Because the iris also is innervated by the oculomotor nerve, pupillary abnormalities also may occur.
Oculomotor nerve palsy and normal pupillary responses: If all extraocular muscles are involved, indicates intracranial lesion. If individual extraocular muscles are affected, indicates peripheral lesion.
Dilated pupil and normal tonic eye reflexes: Indicates peripheral lesion (orbital or intraocular).
Oculomotor nerve palsy and dilated pupil: Lesion could be intraorbital or intracranial.
(Kern and Erb; Power, et al.)
Normal tone of muscles on contralateral side pulls nose toward normal side.
Lip on affected side is flaccid which may lead to self-trauma when chewing food. Drooling is common.
Blinking does not occur on affected side (orbicularis oculi muscle nonfunctional). Exposure keratitis or ulceration may occur, especially in brachycephalic breeds. Reflex retraction of the globe can occur due to intact retractor oculi muscle.
Ear on affected side will droop due if auricular nerve is involved.
Spontaneous cases - no known cause - most common form seen in dogs; rare in cats; may have higher prevalence in boxer dogs. May be temporary or permanent.
Traumatic form - most common form seen in cats. Signs similar to spontaneous form; common in the horse and signs similar to those in small animals; uncommon in dogs.
Cats seem to tolerate this condition better than other species.
Drooping of upper eyelid - innervational deficit of levator or Müller's muscle. Latter most common, and when associated with miosis, enophthalmos (recession of eyeball) and prolapse of the 3rd eyelid, the condition is called Horner's syndrome.
This is a non-veterinary term for protrusion of third eyelids (from 'haw,' non-veterinary term for third eyelid); most common in cats; probably the result of sympathetic 'denervation' to third eyelid.
Cause - unknown.
Treatment - usually best to leave alone - can use topical sympathomimetic drugs if desired - 10% phenylephrine hydrochloride or 1% hydroxyamphetamine (caution: sufficient systemic absorption may occur and cause signs of amphetamine toxicity).
Note well: the third eyelids will protrude whenever there is enophthalmos regardless of cause - must eliminate dehydration, loss of retrobulbar fat, and other problems before diagnosing 'haws.'
This can occur with a variety of neurological conditions involving the central nervous system. The eye may or may not be directly involved. Abnormalities of the eyes, such as congenital cataract or other maldevelopment, may lead to aberrant connections of the retinal ganglion cells to the brain, resulting in nystagmus.
This often is seen as an expected finding in Siamese or Siamese mix cats (Johnson). It also has been seen in cattle (McConnon, et al.).
Treatment is not necessary nor feasible. If the cause can be found and resolved, the nystagmus also should resolve.
Spasm of the muscles supplied by the facial nerve. Usually unilateral.
Cause - often unknown, but may be seen secondary to chronic otitis media with calcification of the ear canal.
Signs - nose is pulled towards affected side, commissure of lip is elevated (grinning effect), spastic partial closure of eyelids on affected side (may result in entropion), and ear on affected side is elevated or pulled towards midline.
Although hemifacial spasm may be confused with facial paralysis, the lesions occur on opposite sides of the face and the nasal deviation is the only common sign (and this is towards the normal side in facial paralysis).
Treatment - none effective. Alcohol block of the auriculopalpebral branch of the facial nerve may control the eyelid spasm; if entropion occurs, corrective surgery may be necessary.
Course - usually permanent; may have Horner's syndrome also because sympathetic nerves damaged while traversing middle ear.
(Kern, et al.; Morgan and Zanotti; Neer; Smith and Mayhew)
Loss of the sympathetic innervation to eye and adnexa. This also may involve other parts of the body depending upon where along the nerve pathway the lesion is located. Refer to a neurology text for more in-depth discussion of non-ocular lesions.
Sometimes no lesion can be found.
Damage to the cranial cervical sympathetic trunk from injury, neoplasms or infections.
Otitis media (especially by ear mites).
Lesions of the first three thoracic spinal cord segments.
Brain lesions.
Damage to sympathetic trunk during jugular vein injections, especially in horses - signs usually transient.
They occur on the side of the lesion.
Miosis due to loss of iris dilator muscle tone; this is not a prominent feature in horses, cattle, goats or sheep.
Enophthalmos due to loss of tone to orbital smooth muscle; this is not a prominent feature in horses, cattle, goats or sheep.
Protrusion of third eyelid due to loss of tone to smooth muscle at base of third eyelid and due to the enophthalmos.
Ptosis due to loss of tone to Müller's muscle.
Horses may have sweating over the face and proximal neck, especially at the base of the ear.
Cattle, cats and dogs may have distention of vasculature and cutaneous heat of the pinna, and sweating over the nostril.
It may be helpful to determine if the lesion is pre- or post-ganglionic (Bistner, et al.) because a pre-ganglionic lesion may be due to a neoplastic lesion in the anterior part of the chest cavity.
This can be done using a direct acting sympathomimetic agent such as phenylephrine and taking advantage of the quicker than normal mydriasis which would be seen if there was a post-ganglionic lesion with denervation supersensitivity. Both eyes need to be treated for comparison.
Alternatively, you can use an indirect acting sympathomimetic agent such as hydroxyamphetamine which will not cause mydriasis if a post-ganglionic lesion is present, but will if a pre-ganglionic one is the case. Both eyes need to be treated for comparison.
Usually none is required for the syndrome per se, but you could use 1-2% epinephrine or 10% phenylephrine drops to replace the loss of sympathetic innervation. However, the most important aspect of this syndrome is finding and treating the cause, if necessary.
Reflex closure of eyelids due to ocular or periocular pain of any cause (or spasm of facial nerve).
Treatment - find the cause and treat it.