The Neurology of Lacrimation – How an Ear Infection Can Cause Dry Eye

By November 14, 2018Articles

by Noelle La Croix, DVM, Dip. ACVO

The Neurology of Lacrimation – How an Ear Infection Can Cause Dry Eye

Neurogenic keratoconjunctivitis sicca (KCS or dry eye) can be a frustrating disease to treat. There are successful drugs to combat dry eye (tacrolimus and cyclosporine) but they sometimes fail in cases with a neurological basis.  In this article I will review the neurology of lacrimation and the pathology of neurogenic KCS.

The trigeminal nerves have both efferent and afferent functions in regulating lacrimation.  These nerves conducts sensory stimuli from the cornea, adnexa, and lacrimal glands to the brain.  Sensory stimulation of the cornea and adnexa causes reflexive lacrimation.  A common example of reflexive lacrimation is crying in reponse to slicing onions.  The slicing releases enzymes which ultimately break down amino acid sulfoxides into a volatile gas (syn-propanethial S-oxide) which then comes into contact with the cornea .  A burning sensation is experienced and lacrimation is stimulated to flush the irritant from the eye.  Similarly, most painful eyes are associated with tear staining via stimulus of the trigeminal nerve.

Tear production can also be stimulated in the absence of noxious stimuli.  Basal levels of tear production result from continuous stimulation of corneal nerve endings.  Diabetic patients have decreased corneal nerve sensitivity and subsequently typically have decreased lacrimation. The most common post-operative complication of Lasik procedures is dry eye secondary to the severing of corneal nerves.  In addition to tear stimulation, corneal nerves also release tropic substances that promote the integrity and overall health of the cornea.  These substances are particularly important in resolving corneal wounds.  Animals with sensory damage to their corneal nerves will often develop dry eye and/or corneal ulcerations (Figure 1).

The trigeminal nerves are also responsible for the efferent arc of lacrimation and they distribute the fibers of the autonomic nervous system to the lacrimal and nictitans glands.  The modulation of lacrimation occurs via parasympathetic (and possibly sympathetic) nerves.  Preganglionic parasympathetic neurons originate from the parasympathetic nuclei of the facial nerves (the rostral salivary nuclei).  The efferent motor neurons of the rostral salivary nuclei lie within the rostral portion of the medulla oblongata, and their fibers exit the brain through the facial canals.

Preganglionic parasympathetic nerves split at the geniculate ganglion of the facial nerves within the dorsal aspect of the petrous temporal bones.  These nerves (which together form the major petrosal nerves) pass through the petrous temporal bones and are associated with the eustachian tubes.  The nerves then join with the deep petrosal nerves forming the nerves of the pterygoid canal.  The parasympathetic aspect of these nerves then synapse with the pterygopalatine ganglia located upon the pterygoideus medial muscles within the floor of each orbit.  Postganglionic parasympathetic neurons follow the zygomatic nerves (the first branch of the maxillary division of the trigeminal nerves) and synapse with the acinar of the lacrimal glands.

Injuries to the parasympathetic nuclei of the facial nerves, pterygopalatine ganglia, and/or pre/postganglionic parasympathetic nerves can lead to neurogenic KCS.  A common cause of neurogenic KCS is otitis media or interna associated with damage of the preganglionic parasympathetic nerves.  In these cases, damage to the facial nerves can also result in a concurrent facial paralysis.  The parasympathetic aspect of the facial nerves also stimulate the lateral nasal glands.  Therefore, facial nerve damage associated with a dry nose (xeromycteria, Figure 2) is also appreciated in some neurogenic KCS patients.

Neurogenic defects can lead to KCS.  Determining and resolving the root cause of these defects can lead to a more effective treatment.  As a simple example, treating an ear infection can sometimes resolve a neurogenic KCS.  If you have further questions about neurogenic KCS please feel free to consult with a veterinary ophthalmologist.

Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006


Figure 1: Corneal ulceration in the right eye and decreased nasal sensitivity secondary to a trigeminal nerve tumor in a 12-year old domestic shorthaired cat.