Handbook of Ocular Disease Management - Cranial Nerve VII (facial nerve) Palsy

CRANIAL NERVE VII (FACIAL NERVE) PALSY

SIGNS AND SYMPTOMS
The prevalence of idiopathic cranial nerve VII (CN VII) palsy ranges from 10/100,000 to 40/100,000 with an average of 21/100,000. Occurrences are highest in adults over 70. Recurrence of idiopathic CN VII palsy ranges between 6 to 11 percent.

Cranial nerve VII innervates the muscles of facial expression and the stapedius muscle of the inner ear. The orbicularis oculi, responsible for eyelid closure, is controlled by CN VII. Damage to the nerve or its peripheral course produces weakness or paralysis of one side of the face with an inability to close the ipsilateral eye. Additional findings on the affected side include flattening of the nasal labial fold, droop of the corner of the mouth, ectropion, lagophthalmos, decreased tear production, dry eye, conjunctival injection, corneal compromise, decreased sense of taste and hyperacusis (supersensitivity to sound).

Occasionally, following injury, some fibers of CN VII regenerate to erroneously innervate adjacent structures. The result is simultaneous movements of muscles (e.g. the corner of the mouth contracts on attempted eyelid closure) or the stimulation of glands supplied by the redistributed branches of CN VII when the nerve is activated (e.g. excessive lacrimation upon eating, known as crocodile tearing ).

PATHOPHYSIOLOGY
The muscles that close the eyes and wrinkle the forehead are bilaterally innervated. A unilateral lesion in the cortex or supranuclear pathway spares eyelid closure and forehead wrinkling but results in contralateral paralysis of the lower face. Since the area of the cortex associated with facial muscle function lies near the motor representation of the hand and tongue, weakness of the thumb, fingers and tongue ipsilateral to the facial palsy is not uncommon.

The facial nucleus contains four separate cell groups that innervate specific muscle groups. Lesions of the fibers of the superior salivatory and lacrimal nuclei (parasympathetic preganglionic fibers supplying the sublingual, submandibular and lacrimal glands) include temporal bone fractures and infections, schwannomas, neuromas (cerebellopontine angle tumors) and vascular compression, producing deficits in hearing, balance, tear production and salivatory flow.

Lesions that involve the ganglion include geniculate ganglionitis (Ramsey-Hunt syndrome: zoster oticus). Lesions such as acoustic neuroma that also involve cranial nerve VIII can impair hearing, facial nerve function and produce corneal hypoesthesia (CN V).

Lesions of the zygomatic and lacrimal nerves impair reflex tear secretion. Middle cranial fossa disease is indicated when defective tear production accompanies CN V (muscles of mastication) or CN VI palsy.

Lesions of the facial nerve disable the ability to dampen sound, producing hyperacusis. Lesions to sensory afferent fibers that transmit taste (fibers that also innervate the salivary glands) cause an interruption in salivatory flow and an inability to sense taste from the anterior two-thirds of the tongue.

The portion of the facial nerve that contains the motor fibers that innervate the muscles of facial expression exits the stylomastoid foramen and enters the substance of the parotid gland before distribution. Therefore, investigate lesions of the parotid gland also as part of the work up.

Lesions that occur within the cortical, extrapyramidal or brainstem levels are known as central lesions. Lesions outside the brain are referred to as peripheral. The common causes of peripheral CN VII palsy include cerebellopontine angle tumor (7 percent), trauma (21 percent), otitis media, herpes zoster oticus (Ramsey-Hunt syndrome), Lyme disease, sarcoidosis, parotid neoplasm, syphilis, diabetes mellitus, pregnancy and HIV.

MANAGEMENT
First obtain a complete history. Perform a cursory evaluation of the 12 cranial nerves as well as a comprehensive ocular examination with dilated fundus and optic nerve evaluation. Pay close attention to the affected eyelid's posture, corneal wetting (tear break up time), blink posture, tear quality (sodium fluorescein staining) and tear quantity (Schirmer tear testing). In cases where diagnosis is questionable, ask the patient to close both eyes while you try to open the lid. If one lid is significantly easier to open than the other, suspect CN VII palsy.

You can manage exposure keratopathy with ocular lubricating drops and ointments. Moisture chamber patches (e.g. Guibora eye patch) or eyelid taping are also possible solutions. Moisture chamber shields can be attached to spectacle temples to create a moist ocular environment and lessen tear evaporation. Since idiopathic facial nerve palsy is a diagnosis of exclusion, order laboratory testing (Lyme titer, rheumatoid factor, erythrocyte sedimentation rate, antinuclear antibody, echocardiogram, fluorescent treponemal antibody absorption test, HIV titer, chest X-ray), lumbar puncture (in patients with suspected neoplasm), CT and MRI and/or appropriate referrals (otolaryngology, neurology, neurosurgery).

CLINICAL PEARLS

Most cases (53 percent) of unilateral facial weakness are idiopathic. These lesions are thought to occur secondary to idiopathic inflammation, viral infection or vascular compression of CN VII. Given the extensive neurology of CN VII, idiopathic "Bell's Palsy" is a diagnosis of exclusion.
Patients with idiopathic facial nerve paralysis (Bell's Palsy) typically complain of acute (24 to 48 hours) unilateral facial weakness with a widening of the palpebral fissure and impaired ability to close the eye.
Risk factors include diabetes, pregnancy and family history.
Chronic, slowly progressive facial nerve palsy suggests neoplasm. The presence of a parotid mass suggests tumor of the gland.
Paralysis of the lower face that spares eyelid closure and forehead wrinkling indicates a lesion in the contralateral cerebral cortex.

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