Signs and Symptoms

The seventh cranial nerve (CN VII, facial nerve) is responsible for the voluntary motor innervation to the muscles of facial expression, the stapedius muscle of the inner ear and for sensory innervation to the anterior two-thirds of the tongue.1–7 The orbicularis oculi, responsible for eyelid closure, is under the control of CN VII.1–6 Supranuclear pathway lesions (central or upper motor neuron) affect the contralateral lower face.

Damage either to one of the CN VII nuclei or fascicles, or interruption to its peripheral course (lower motor neuron), will produce characteristic clinical findings that include weakness or paralysis of one side of the face with an inability to voluntarily close the ipsilateral eye. Additional findings on the affected side include flattening of the nasolabial fold, drooping of the corner of the mouth, ectropion, lagophthalmos, decreased tear production, conjunctival injection, corneal compromise, decreased taste sensation and hyperacusis (supersensitivity to sound).1–5

Facial nerve palsy shows no gender preference; men and women are affected equally. Risk factors include trauma, diabetes, pregnancy, herpetic viral infection, ischemic vascular disease and family history.2,6

Facial nerve palsy can either be marked or subtle. In cases of suspected involvement, the clinician must selectively test the involved muscles of the face, looking for asymmetry between the right and left sides. Specifically, patients should be instructed to look up and wrinkle the forehead (moving the frontalis and corrugator muscles), purse the lips and whistle (orbicularis oris muscle), smile and/or puff out the cheeks (buccinator muscle) and squeeze the eyes tightly closed (orbicularis oculi).


Supranuclear motor neurons connecting cortical areas 4 and 6 with the facial nuclei descend as fascicles of the corticobulbar (cortex-to-cranial nerve nuclei) tract through the internal capsule to the level of the lower pons, by way of the cerebral peduncles.2,3 The portion of each facial nucleus that controls the muscles of the upper face (frontalis, orbicularis oculi and corrugator) receives corticobulbar stimulation from the right and left (crossed and uncrossed) precentral motor cortices.

The supranuclear innervations supporting the muscles of facial expression in the lower face is crossed only.2,3,5 The muscles that close the eyes and wrinkle the forehead are bilaterally innervated; therefore, a lesion in the cortex or supranuclear pathway on one side spares eyelid closure and forehead wrinkling but results in contralateral paralysis of the lower face.2,3 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.2–5 Lastly, because supranuclear lesions are upper motor neuron lesions (sometimes referred to as central lesions), they produce spastic rather than flaccid paralysis. This allows the amount of flattening to the nasolabial fold and mouth-corner droop to often be significantly less than its lower motor neuron counterpart.2,3

The facial motor nuclei are located in the lower pontine tegmentum and possess an intimate relationship with the trigeminal nerve (CN V), abducens nuclei (CN VI), cochlear nuclei (CN VIII), medial longitudinal fasciculus (MLF), paramedian pontine reticular formation (PPRF), descending corticospinal fibers and descending sympathetic fibers.

The facial nucleus contains four separate cell groups, each of which innervate specific muscle groups. Motor axons exit the nucleus dorsally, loop around the CN VI nuclei and emerge into the subarachnoid space from the lateral aspect of the pons.2,3,5 Fibers from the superior salivatory and lacrimal nuclei (parasympathetic preganglionic fibers supplying the sublingual, submandibular and lacrimal glands) join the facial nerve as the nervus intermedius at the cerebellopontine angle. CN VIII is present here as well. Lesions at this level include temporal bone fractures and infections, schwannomas, neuromas (cerebellopontine angle tumors) and vascular compressions, producing deficits in hearing, balance, tear production and salivatory flow.2,3,5

The facial and the vestibuloacoustic (CN VIII) nerves enter the internal auditory meatus together.1–3 The facial nerve then departs from the acoustic nerve to enter the fallopian (facial) canal, which courses 30mm through the temporal bone and incorporates the geniculate ganglion.2 Lesions that involve the ganglion include geniculate ganglionitis. Lesions such as acoustic neuroma, which involve cranial nerve VIII, can impair hearing and facial nerve function and produce corneal hypoesthesia. Lesions that begin within the nucleus or along the fascicles are said to involve the final common pathway of neural transmission and are known as lower motor neuron or peripheral lesions.

The first major branch of CN VII, the greater superficial petrosal nerve, traverses the geniculate ganglion, proceeds forward, traverses the dura mater of the middle cranial fossa and synapses in the sphenopalatine ganglion. This structure gives rise to postganglionic fibers, which join the zygomatic and lacrimal nerves of CN V to innervate the lacrimal gland. Lesions here impair reflex tear secretion. It is important to note that when defective tear production accompanies CN V (muscles of mastication) or CN VI palsy, middle cranial fossa disease is indicated.2,3,5

The stapedius branch of CN VII arises from the distal segment of the facial nerve.2,3 Lesions here disable the ability to dampen sound, producing hyperacusis. As the facial nerve continues downward in the facial canal, the chorda tympani branch arises from it. The chorda tympani contains sensory afferent fibers, which transmit taste sensation from the anterior two-thirds of the tongue. It also contains autonomic (parasympathetic preganglionic) nerve fibers, which innervate the submandibular and sublingual salivary glands.2,3 Lesions anywhere along this pathway cause an interruption in salivatory flow and the ability to sense taste from the anterior two-thirds of the tongue.2,3 Lesions of the parotid gland must also be investigated as part of the work-up. Sensory afferents from the external auditory meatus and a small area of skin behind the ear transmit pain, temperature and touch information.2,3

Causes of peripheral CN VII palsy include trauma (21%), cerebellopontine angle tumor (7%), otitis media, herpes zoster oticus (Ramsay-Hunt syndrome), Lyme disease, sarcoidosis, Guillain-Barré syndrome, Epstein-Barr virus, parotid neoplasm, syphilis, diabetes mellitus, herpes simplex infection, pregnancy and HIV.1–11

The term Bell’s palsy is often used to describe idiopathic CN VII dysfunction, and is considered to be the most common diagnosis associated with facial nerve palsy.2,12,13 Bell’s palsy is a diagnosis of exclusion.1–13 It is currently thought to be related to idiopathic inflammation secondary to the reactivation of herpes simplex virus isoform 1 (HSV-1) and/or herpes zoster virus (HZV) from the geniculate ganglia.13

Occasionally, after injury some fibers of CN VII regenerate to erroneously innervate adjacent structures. This phenomenon is known as aberrant regeneration. The result is simultaneous movements of muscles or synkinesis (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 or gustolacrimal tearing).2–5


Care of a patient who presents with CN VII palsy begins with a detailed history and a cursory evaluation of the 12 cranial nerves. Close attention should be given to the affected eyelid’s posture, corneal wetting (tear break-up time), blink posture, secondary epitheliopathy (sodium fluorescein staining) and tear quantity (Schirmer tear testing).

Since Bell’s palsy is a diagnosis of exclusion, medical evaluation should be considered for patients with new-onset facial nerve palsy in an attempt to elicit a cause. The evaluation may include laboratory testing (Lyme titer, rheumatoid factor, erythrocyte sedimentation rate, antinuclear antibody, fluorescent treponemal antibody absorption test, HIV titer), echocardiogram, chest X-ray and contrast-enhanced MRI dependent upon the patient profile, presentation of the palsy, and associated signs and symptoms.1–6

Exposure keratopathy associated with facial nerve palsy can be managed with ocular lubricating drops and ointments. Moisture chamber shields can be attached to spectacle temples to create a moist ocular environment and lessen tear evaporation. Temporary external eyelid weights or bedtime eyelid taping may also be of benefit as a temporary measure in cases that are likely to resolve or as a stopgap measure prior to surgical intervention.7 Partial tarsorraphy can be completed in extreme cases.

Treatment for peripheral facial weakness and facial nerve palsy depends upon the underlying etiology. Should none be found definitively, and the cause is determined to be Bell’s palsy, there are options designed to speed recovery, though typically the condition will resolve in several weeks to months.

There has been controversy regarding the role of oral antivirals in the management of acute Bell’s palsy. Some have shown that there is a limited benefit to oral antiviral medications.14,15 However, the prevailing thought is that oral antivirals alone are not superior to placebo and have no role in management. If they are considered at all it should be done in conjunction with oral steroids.16-18 While oral antiviral medications may have no effect, the prevailing thought is that oral steroids are the mainstay of therapy for Bell’s palsy with strong recommendations to begin treatment within 72 hours of palsy onset.12-14,17,19 The recommended dosing is prednisolone, 60mg/d for five days, with the dosage then tapered for five days.17

Alternate therapies have shown some benefit. These include acupuncture, hyperbaric oxygen therapy and physical therapy.20-22 While there is evidence of benefit, there does not exist enough controlled clinical research to warrant recommending these therapies, though patients who express interest should not be summarily discouraged. In persistent cases of symptomatic facial paralysis, oculoplastic surgery can improve function.23

Clinical Pearls

Patients with idiopathic facial nerve paralysis (Bell’s palsy) typically complain of acute (24–48 hours) unilateral facial weakness with a widening of the palpebral fissure and impaired ability to close the eye.

Chronic, slowly progressive facial nerve palsy suggests a neoplastic etiology.

Bell’s palsy will typically recover within several weeks to months. Per-sistence beyond three months requires re-evaluation.

The number-one concern is corneal protection, using artificial tears, punctal plugs, moisture chambers, internal or external weights or complete or partial tarsorrhaphy.

When a patient presents with acute-onset facial nerve palsy, do not immediately diagnose Bell’s palsy. Instead, perform a thorough history and physical and consider medical and neuroradiologic evaluation to identify a potential cause. Remember, Bell’s palsy is a diagnosis of exclusion.

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2. Gurwood AS, Tasca JM, Kulback E. A review of cranial nerve VII palsy with emphasis on Bell’s palsy. South J Optom 1996;14(3):13–17.

3. May M, Galetta S. The facial nerve and related disorders of the face. In: Glaser JS (ed.), Neurophthalmology (2nd ed.), Philadelphia, J. B. Lippincott Co., 1990:239–77.

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6. Danielides V, Skevas A, van-Cauwenberge P, et al. Facial nerve palsy during pregnancy. Acta Otolaryngol Belg 1996;50(2):131–5.

7. Zwick OM, Seiff SR. Supportive care of facial nerve palsy with temporary external eyelid weights. Optom 2006;77(7):340–2.

8. Sensat ML. Mobius syndrome: A dental hygiene case study and review of the literature. Int J Dent Hyg 2003;1(1):62–7.

9. Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2004;18(4):CD001942.

10. Allen D, Dunn L. Aciclovir or valaciclovir for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2004;1(3):CD001869.

11. Gilbert SC. Bell’s palsy and herpesviruses. Herpes 2002;9(3):70–3.

12. Baugh RF, Basura GJ, Ishii LE, et al. Clinical practice guideline: Bell’s palsy. Otolaryngol Head Neck Surg. 2013;149(3 Suppl):S1-27.

13. Zandian A, Osiro S, Hudson R, et al. The neurologist’s dilemma: A comprehensive clinical review of Bell’s palsy, with emphasis on current management trends. Med Sci Monit. 2014;20:83-90.

14. Albers JR, Tamang S. Common questions about bell palsy. Am Fam Physician. 2014;89(3):209-12.

15. Hato N, Sawai N, Teraoka M, et al. Valacyclovir for the treatment of Bell’s palsy. Expert Opin Pharmacother. 2008;9(14):2531-6.

16. Hato N, Yamada H, Kohno H,et al. Valacyclovir and prednisolone treatment for Bell’s palsy: a multicenter, randomized, placebo-controlled study. Otol Neurotol. 2007;28(3):408-13.

17. Axelsson S, Berg T, Jonsson L, et al. Bell’s palsy – the effect of prednisolone and/or valaciclovir versus placebo in relation to baseline severity in a randomised controlled trial. Clin Otolaryngol. 2012;37(4):283-90.

18. Lockhart P, Daly F, Pitkethly M,et al. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2009;(4):CD001869.

19. Berg T, Bylund N, Marsk E, et al. The effect of prednisolone on sequelae in Bell’s palsy. Arch Otolaryngol Head Neck Surg. 2012;138(5):445-9.

20. Teixeira LJ, Valbuza JS, Prado GF. Physical therapy for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2011;(12):CD006283.

21. Chen N, Zhou M, He L, et al. Acupuncture for Bell’s palsy. Cochrane Database Syst Rev. 2010 Aug 4;(8):CD002914.

22. Holland NJ, Bernstein JM, Hamilton JW. Hyperbaric oxygen therapy for Bell’s palsy. Cochrane Database Syst Rev. 2012 Feb 15;2:CD007288.

23. Sira M, Norris JH, Nduka C, Malhotra R. Transcaruncular Medial Canthal Tendon Plication with Lower Eyelid Suture Sling in Facial Nerve Palsy. Orbit. 2014 Feb 25. [Epub ahead of print].