There are different components that make up the precorneal tear film: lipid, aqueous and mucin. The lipid layer is the most superficial and is produced by the meibomian glands located within the eyelid margin. The aqueous component is produced by the orbital lacrimal gland and by the gland of the nictitating membrane. The mucous layer is secreted by the conjunctival goblets cells.
Aqueous production from the lacrimal gland is the result of a complex physiologic process. Both the basal and reflex tears are under the control of the autonomic nervous system. The afferent arm involves the trigeminal nerve (ophthalmic branch), while the efferent component involves the parasympathetic output into the lacrimal gland via the facial nerve.
The preganglionic neurons originate within the parasympathetic nucleus of the facial nerve, located within the rostral portion of the medulla oblongata. These fibres run as part of the facial nerve through the facial canal of the petrous temporal bone (middle ear), branching then into the major (greater) petrosal nerve that synapses with the pterygopalatine ganglion. The post-ganglionic axons innervate the lacrimal gland, the palatine and lateral nasal gland (the latter is very relevant when considering the clinical presentation of neurogenic keratoconjunctivitis sicca – KCS). The lacrimal gland is innervated by the zygomatic and lacrimal nerve (both branches of the trigeminal nerve).
Lesions affecting the efferent pathway will lead to a decrease in tear production and this condition is known as neurogenic KCS.
Patients typically present with an acute history of marked unilateral mucopurulent ocular discharge (Figure 1). Schirmer tear test readings are significantly different between both eyes. The affected eye will normally be lower than 5mm/min and the contralateral eye will be normal. Further examination often identifies a dry nostril (xeromycteria) ipsilateral to the dry eye (Figure 2).
Most patients do not have additional clinical signs. However, other neurological deficits can be detected concurrently depending on the localisation of the lesion, namely: Horner’s syndrome (the sympathetic nerves pass in close proximity to the inner/medial ear) and facial paralysis if the preganglionic nerve (major petrosal nerve) is affected (eg: otitis media and/or interna, petrositis). Erosive lesions to the floor of the medial fossa of the skull can lead to trigeminal nerve deficits such as facial anaesthesia and xeromycteria (dry nasal mucous membranes). Injuries to the pterygopalatine fossa could include periorbital myositis, cellulitis and dental abscessation. Post-ganglionic lesions are commonly identified in cases of orbital trauma.
Other possible causes of dry eye should be ruled out such as: immune-mediated disease (typically bilateral and often of a more gradual onset), congenital (eg: Yorkshire Terrier and English Cocker Spaniel), iatrogenic (eg: excision of nictitating membrane gland), traumatic, infectious (eg: canine distemper virus), radiation therapy, drug-induced (eg: sulphonamides and atropine) and systemic diseases (eg: diabetes mellitus and hypothyroidism). Ideally advanced imaging (eg: CT scan or MRI) should be performed in order to identify possible lesions. However, given that the majority of canine neurogenic KCS cases are idiopathic and in the absence of other neurological deficits these tests do not always need to be performed.
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