|CRANIAL NERVE VII (FACIAL NERVE) PALSY
SIGNS AND SYMPTOMS
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 ).
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.
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,
Other reports in this section
Eyelids & Eyelashes | Conjunctiva & Sclera | Cornea
Uvea | Vitreous & Retina | Optic Nerve & Brain | Oculosystemic Disease
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