A 77-year-old Caucasian female was referred to the clinic for a corneal evaluation secondary to worsening lagophthalmos produced by cranial nerve (CN) VII damage in her left eye. The issue occurred as a result of the removal of an acoustic neuroma. Her systemic history was remarkable for acoustic neuroma which was removed surgically approximately two weeks prior.
Her previous ocular history was contributory as the lagophthalmos was aggravated by an old cosmetic ptosis repair to her left eye three years earlier.
In response to the inability of the lid to cover the cornea, she was referred to an ear, nose and throat specialist who placed gold weights into the superior lid of her left eye. When the desired effect was inadequate, the ophthalmology department was consulted. She denied allergies of any kind.
Her best corrected entering visual acuities were 20/20, OU at distance and near. An external examination uncovered poor facial nerve function of her left eye with an inability to voluntarily close it or adequately cover the cornea using the Bell’s phenomenon. No evidence of afferent pupillary defect was noted. The pertinent findings are demonstrated in the photographs. Goldmann applanation tonometry measured 15mm Hg OU.
The dilated fundus findings were normal peripherally and centrally with normal nerves and maculae.
Additional studies included examination of the eyelids (for their ability to close), examination of the Bell’s reflex (and its ability to cover the cornea when employed), sodium fluorescein instillation (to assess the amount of corneal and conjunctival compromise) and corneal sensitivity testing (to assess the integrity of tissue’s physiologic response).
Use of a combination of thick artificial tear drops and ointments in concert with the placement of moisture chamber was evaluated over the course of one week. The placement of scleral contact lenses was not considered.
The diagnosis in this issue is left paralytic (lower motor neuron) CN VII palsy secondary to the iatrogenic complications of acoustic neuroma (cerebellopontine angle tumor) removal aggravated by the effects of internal scarring produced by a previous left ptosis repair.
The muscles which control the voluntary responses of smiling, frowning, grimacing and eyelid closure (the muscles of facial expression) depend on signals which originate in the facial motor area of the precentral gyrus (Brodman’s areas 4 and 6, adjacent to the lateral Sylvian fissure) of the frontal cerebral cortex.1-9 Supranuclear motor neurons (above the nucleus) connecting cortical areas 4 and 6 with the facial nerve nuclei in the pons descend as fascicles of the corticobulbar tract (cortex to cranial nerve nuclei) through the internal capsule by way of the cerebral peduncles.1,2
The portion of each facial nucleus which controls the muscles of the upper face (frontalis, orbicularis oculi, and corrugator supercilli) receives corticobulbar stimulation from both the right and left (via crossed and uncrossed pathways) precentral motor corticies.1-9 The supranuclear innervation supporting the muscles of the lower face is crossed only.2,4 The muscles that close the eyes and wrinkle the forehead are bilaterally innervated; therefore a unilateral lesion in the cortex or supranuclear pathway spares eyelid closure and forehead wrinkling but results in contralateral paralysis of the lower face.2,4 This is known as a “central” or upper motor neuron lesion. Since the area of the cortex associated with facial muscle function lies near the cerebral motor representation of the hand and tongue, weakness of the thumb, fingers and tongue, ipsilateral to the facial palsy (on the same side) is not uncommon. Finally, because supranuclear lesions are upper motor neuron lesions, they produce a relative, spastic paralysis with the amount of flattening to the nasolabial fold and mouth-corner-droop being significantly less than its lower motor neuron counterpart.1-4
An injury to the final common pathway of a nerve from its nucleus to its end organ (a muscle or a gland) is also known as a “peripheral” or lower motor neuron palsy. The facial nerve innervates the muscles of facial expression, the lacrimal gland, the submaxillary and sublingual salivary glands and the taste receptors on the anterior two thirds of the tongue. Complete facial nerve palsy produces the characteristic clinical findings which include weakness or paralysis of one side of the face with an inability to close the ipsilateral eye (lagophthalmos).1-9 Additional findings include ipsilateral flattening of the nasal labial fold, droop of the corner of the mouth, paralytic ectropion, decreased tear production, dry mouth, decreased taste and hypersensitivity to loud sounds (hyperacousis) secondary to the lack of ability to dampen sounds.10,11
The common causes of peripheral (lower motor neuron) CN VII palsy include cerebellopontine angle tumor (i.e., acoustic neuroma-7% ), trauma (21%), otitis media, herpes zoster oticus (Ramsey-Hunt syndrome), Lyme disease, sarcoidosis, parotid neoplasm, syphilis, diabetes mellitus, pregnancy, HIV, Guillain– Barre syndrome and surgical trauma.1-13 The incidence varies between 17 and 35 cases per 100,000.13
Many factors are involved in determining the appropriate treatment of these patients: the underlying cause, expected duration of nerve dysfunction, anatomical manifestations, severity of symptoms and objective clinical findings.13 In the acute phase, the main priority should be to ensure adequate corneal protection.10-13 Treatment depends on the degree of corneal damage as well as the risk for the corneal damage based on the amount of lagophthalmos, the quality of Bell’s phenomenon, the presence or absence of corneal sensitivity and the degree of lid retraction.9-15 The main therapy is intensive lubrication via artificial tear drops and ointments. Other treatments include eye lid taping overnight, moisture chamber placement during the day, botulinum toxin injection to relax the eye lid muscles which keep the eye open, encircling palpebral springs, eyelid gold weight implants (lid loading), scleral contact lenses and tarsorrhaphy.9-16
The procedure itself is not complicated. Temporary suture tarsorrhaphy (TST), consists of a suture through the upper and lower eyelid’s posterior lamella ending superiorly or inferiorly with unconnected and untied running ends of the suture. These ends are available for either a simple half overhand knot tie or taping.17 This allows the lid closure created by the TST to be adjustable and openable so medicines can be periodically placed into the eye.17 The most common complication of the procedure is the erosion of the suture through the tissues.17 This can be remedied by including a bolster (additional material through which the suture is passed reducing the risk of suture tissue erosion).17 The TST is faster and simpler, requires fewer materials and reduced the risks of complications including eyelid margin necrosis and lash loss from vascular compromise.17
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12. Toulgoat F, Sarrazin JL, Benoudiba F, et al. Facial nerve: from anatomy to pathology. Diagn Interv Imaging. 2013t;94(10):1033-42.
13. Portelinha J, Passarinho MP, Costa JM. Neuro-ophthalmological approach to facial nerve palsy. Saudi J Ophthalmol. 2015;29(1):39-47.
14. Trivedi D, McCalla M, Squires Z, Parulekar M. Use of cyanoacrylate glue for temporary tarsorrhaphy in children. Ophthal Plast Reconstr Surg. 2014;30(1):60-3.
16. Manodh P, Devadoss P, Kumar N. Gold weight implantation as a treatment measure for correction of paralytic lagophthalmos. Indian J Dent Res. 2011;22(1):181.
17. McInnes AW, Burroughs JR, Anderson RL, McCann JD. Temporary suture tarsorrhaphy. Am J Ophthalmol. 2006;142(2):344-6.