Bell Palsy

Bell Palsy: Excerpt from The 5-Minute Pediatric Consult

Stephen J. Falchek, MD

Bell Palsy - BASICS

Bell Palsy - description

• This paralysis may involve all of the modalities affected by the 7th cranial nerve:
  • Mimetic facial movement
  • Taste
  • Cutaneous sensation
  • Hearing acuity
  • Lacrimation
  • Salivation
• The most important feature in diagnosis and management of Bell palsy is the distinction between a peripheral and a central 7th nerve palsy.

Bell Palsy - epidemiology

Bell Palsy - incidence

Annually, incidences range from 3/100,000 in patients <10 years to 25/100,000 in adults. Only 1% of cases have bilateral involvement.

Bell Palsy - pathophysiology

Nearly all cases of true Bell palsy are believed to arise from a viral infection of the facial nerve and, in particular, the geniculate ganglion.

Bell Palsy - etiology

• Idiopathic: Pregnancy related
• Infectious:
  • Herpes simplex virus 1
  • Human herpes virus 6
  • Herpes zoster (without Ramsay-Hunt syndrome)

Bell Palsy - associated conditions

Associated illnesses can cause or predispose to an isolated facial nerve palsy, but are important to distinguish from a classic Bell palsy.

• Rubella
• Lyme disease (Borrelia burgdorferi). In Lyme neuropathy, early reports indicated a preponderance of tic bite histories involving the ipsilateral face, suggesting a retrograde migration of the spirochetes into the nerve and resultant nerve root/arachnoid irritation in at least some cases, as opposed to hematogenous dissemination and CNS penetration.
• Epstein-Barr virus (EBV)
• Cytomegalovirus (CMV)
• Mumps
• HIV
• Mycoplasma pneumoniae

Bell Palsy - DIAGNOSIS

Bell Palsy - signs & symptoms

Bell Palsy - history

• Mastoid or retroauricular pain ipsilateral to the side of developing symptoms (40–50% of patients)
• 50% of patients will have no clear sensory prodrome.
• Bell palsy often follows some identifiable infectious illness, such as viral upper respiratory infection (URI) symptoms, Mycoplasma pneumoniae infection, or infectious mononucleosis. However, an identified antecedent illness is not requisite for the diagnosis.
• The onset is almost always rapid, with progression to a fairly constant state of unilateral paresis or paralysis within hours to 2–3 days.
• As the weakness progresses, the patient (and family members) may note:
  • Difficulty with oral motor tasks (e.g., eating and drinking) due to inability to maintain mouth closure
  • Inability to completely close the eye on the affected side (sometimes leading untrained observers to note an eyelid “droop” on the normal side, due to the contrast with normal eyelid closure and movements)
  • Decreased lacrimation, and eye itching and burning
  • Hyperacusis
  • Ipsilateral facial numbness (less commonly)
  • Distortion of the taste of foods (dysgeusia)
• Bilateral symptoms (<1%) are distinctly rare and suggest an alternative diagnosis, such as Guillain-Barré syndrome or other infectious, inflammatory, or metabolic disease.

Bell Palsy - physical exam

• Weakness of all muscles of mimetic facial movement is noted on the affected side.
• A classic feature of peripheral facial nerve palsies is symmetric weakness or paralysis or both upper (frontalis), mid (orbicularis oculi), and lower (orbicularis oris) muscles on both voluntary and involuntary mimetic movements. Having the patient wrinkle his or her forehead, raise his or her eyebrows, close his or her eyes tightly, and bare his or her teeth or smile, respectively, tests these.
• The examiner will typically note slow or absent spontaneous blinking on the affected side.
• Reflexes, such as the corneal reflex, should be decreased or absent on the affected side, but the consensual response on the unaffected side should be preserved.
• The sensory division of the 7th cranial nerve is tested by examining taste perception on the anterior tongue:
  • This is done by applying, ipsilaterally, swabs soaked in both a sugar solution and a salt solution to the anterolateral aspect of the tongue, without allowing for mouth closure and dispersion of the substances to the other side.
  • Despite complaints of retroauricular pain and unilateral facial “numbness,” abnormalities of cutaneous sensation typically are not verifiable by sensory testing in pure 7th-nerve palsies. The presence of true diminution of sensation should raise the question of other cranial nerve involvement (5th cranial nerve).
• Examination of the external auditory canal on both sides is crucial:
  • Vesicular lesions of the tympanic membrane suggest a zoster-associated palsy (Ramsay-Hunt syndrome).
  • Purulent otitis or evidence of trauma mandate aggressive antibiotic treatment and possibly urgent surgical subspecialty evaluation and imaging of the temporal bone.

Bell Palsy - tests

• Cases of uncomplicated 7th-nerve palsy require no workup.
• Audiologic testing (i.e., brainstem auditory evoked potentials [BAEPs]): These modalities are useful only in distinguishing an isolated 7th-nerve lesion from a combined 7th- and 8th-nerve lesion (such as would be produced by a cerebellopontine angle tumor).
• Nerve conduction studies: In cases of later-than-expected recovery, nerve conduction studies may be of some limited value:
  • Serology for B. burgdorferi: Recommended in all areas where Lyme disease is endemic. Lyme IgM titers are more sensitive for acute infection than are IgG titers.
  • Lumbar puncture and studies for CSF glucose, protein, cell count, culture: Recommended when signs of meningeal inflammation are present (e.g., nuchal rigidity, headache, fever, etc.). A mild pleocytosis may be seen in Lyme disease.

Bell Palsy - imaging

• The decision to defer medical imaging in the evaluation of a typical Bell palsy should be based on a sound clinical history and physical examination. Unusual features should provoke thoughtful review and broader investigation where indicated.
• MRI of the head with gadolinium enhancement: Recommended in cases of unusual presentation or progression, e.g., bilateral involvement, slow progression (over >1 week), or other cranial nerve findings. Several small series have proposed that gadolinium enhancement of the involved seventh nerve predicts a slower or less optimal recovery.

Bell Palsy - differencial diagnosis

• Trauma:
  • Birth (especially forceps pressure to lateral face)
  • Congenital facial palsies should not be regarded as Bell palsy, but rather symptomatic of some other cause.
  • Temporal bone/petrous bone fractures
  • Deep lacerations or trauma to parotid region
• Infection:
  • Purulent otitis media/mastoiditis
  • Basilar meningitis
  • Petrositis (Gradenigo syndrome)
  • Varicella zoster virus (VZV) (Ramsay-Hunt syndrome)
  • Syphilis
  • Trichinosis
  • Tuberculosis
  • Leprosy
• Inflammatory:
  • Sarcoidosis
  • Behcçet disease
  • Giant cell arteritis
  • Polyarteritis nodosa
  • Guillain-Barré syndrome
  • Melkersson-Rosenthal syndrome: Rare neurologic disorder characterized by recurring facial paralysis, swelling of the face and lips (usually the upper lip), and the development of folds and furrows in the tongue
• Tumors:
  • Cerebellopontine angle tumors, osteosarcomas, cholesteatomas, neurofibromas, lymphoma
  • Hyperostosis cranialis interna, osteopetrosis
• Metabolic:
  • Diabetes (nerve ischemia), hyperparathyroidism, hypothyroidism, porphyria
• Congenital/Genetic:
  • Congenital absence or hypoplasia of depressor anguli oris muscle
  • Möbius syndrome
  • Chiari malformation
  • Syringobulbia

Bell Palsy - TREATMENT

Identifying treatable causes of 7th-nerve palsy (e.g., Lyme borreliosis and Ramsay-Hunt syndrome) is crucial for optimizing outcome and preventing comorbidities of these illnesses.

Bell Palsy - general measures

• The decision not to treat true idiopathic 7th-nerve palsy requires the strength of scientific conviction. Patients and families will often require explanation of this approach. In general, the avoidance of unnecessary exposure to antibiotics or corticosteroids should be viewed as a positive feature of this more conservative, evidence-based approach.
• Eye protection and lubrication: A significant risk for corneal injury is best managed by applying artificial tear solutions at least 3–4 times daily and lubricating gels (e.g., Lacri-Lube) at night. Patching and protective eyewear, during active play and sleep, is usually prescribed on the basis of the degree of remaining eyelid closure.
• Corticosteroids: Prednisone, considered only within the 1st 72 hours of symptoms. Recommended dose: 1 mg/kg/d (maximum 30 mg) for 5 days, with or without a taper over the following 5 days.
• Acyclovir: Most clearly indicated for the treatment of Ramsay-Hunt syndrome. It is also used empirically by some practitioners in standard Bell palsy management. Recommended dose: 20 mg/kg/d, divided into 5 times a day, for 10 days; maximum 400 mg 5 times daily. Generally, any evidence of vesicular eruption in the ear canal or face should be treated promptly with acyclovir, as outcomes from VZV-associated palsies are reported to be worse in general.

Bell Palsy - special therapy

Bell Palsy - phys therapy

Although a series of 9 patients treated with a facial muscle exercise program all demonstrated improvement, no controlled studies have been performed to assess the efficacy of facial physiotherapy. It is important to remember that a significant majority of patients with Bell palsy will have complete recovery, thus rendering uncontrolled studies of little use in determining efficacy.

Bell Palsy - medication

• A great deal has been written about the use of corticosteroids, acyclovir or related antivirals, or both, in the treatment of Bell palsy. However, clear evidence supporting the use of either therapy is lacking.
• Antibiotics: In areas where Lyme disease is endemic, many practitioners will begin treatment with oral antibiotics presumptively, while awaiting serologies (recall that the IgM titer is the most useful in the acute setting). (See “Lyme Disease” chapter):

Bell Palsy - first line

Amoxicillin, 50 mg/kg/d divided in 3 doses for 21–28 days

Bell Palsy - second line

For presumed Lyme disease:

• Patients >8 years: Doxycycline, 100 mg b.i.d. for 21–28 days
• Patients of all ages: Cefuroxime, 30 mg/kg/d in 2 divided doses for 21–28 days

Bell Palsy - surgery

Surgical decompression: Previously, surgical decompression of the 7th nerve had been proposed as a possible treatment in cases where recovery was delayed or the clinical course more severe. No clinical evidence to support the benefit of this strategy has emerged. Surgical decompression is best reserved for “other” cases of facial nerve palsy in which there is a definable syndrome of nerve compression due to extrinsic factors, such as exostoses, tumor, etc.

Bell Palsy - FOLLOW UP

Bell Palsy - disposition

Bell Palsy - issues for referral

Subspecialty consultation: Generally, patients are referred if their recovery time is prolonged or if there is a relapsing pattern or other deviations from the expected course. However, the presence of other questionable cranial nerve involvement, recent trauma, meningeal symptoms, or neurologic findings (e.g., eye movement abnormalities, acute hemiparesis, etc.) should be viewed with great concern and evaluated in an urgent-care setting.

Bell Palsy - prognosis

• 60–70% full-recovery rate from isolated 7th-nerve palsy
• Signs of recovering function (generally improving control of mimetic movement) are typically apparent by the 3rd week after onset.
• Of patients with less than total recovery, many will experience at least partial return to normal function; cosmetic results vary in this group.
• Outcome of idiopathic facial palsy as a pregnancy complication seems to be less favorable (~55% full recovery).
• Up to 7% of patients may experience a 2nd occurrence at some point in the future.

Bell Palsy - complications

• Corneal injury, due to decreased lacrimation and poor eye closure
• Several sequelae, generally related to aberrant reinnervation of affected end organs, are observed after an episode of Bell palsy.
• Various synkinesias (abnormal involuntary movements that accompany a normally executed voluntary movement), including the Marin-Amat phenomenon (spontaneous eye closure with mouth opening, or its converse)
• Blepharospasm, hemifacial spasm, facial contractures
• The “crocodile tears” phenomenon (eating provokes ipsilateral tearing) results from crossed reinnervation between lacrimal and salivary parasympathetic fibers.

Bell Palsy - bibliography

1. Alberton DL, Zed PJ. Bell’s palsy: A review of treatment using antiviral agents. Ann Pharmacother. 2006;40(10):1838–1842.
2. Axelsson S, Lindberg S, Stjernquist-Desatnik A. Outcome of treatment with valacyclovir and prednisone in patients with Bell’s palsy. Ann Otol Laryngol. 2003;112:197–201.
3. Grose C, Bonthius D, Afifi AK. Chickenpox and the geniculate ganglion: Facial nerve palsy, Ramsay Hunt syndrome and acyclovir treatment. Pediatr Inf Dis J. 2002;21:615–617.

Bell Palsy - CODES

Bell Palsy - icd9

351.0 Bell palsy

Bell Palsy - FAQ

• Q: How does one differentiate between peripheral facial nerve palsy and a CNS lesion?
• A: A critical step in diagnosis is the differentiation of peripheral from central (upper motor neuron) lesions. With upper motor neuron lesions (above the level of the 7th-nerve nucleus), there is preferential weakness of lower facial musculature and, sometimes, differential paresis of voluntary versus spontaneous emotional mimetic movements. Brainstem lesions, on the other hand, may produce a peripheral-appearing lesion, but almost always have involvement of other pathways and cranial nerve nuclei, e.g., ipsilateral lateral rectus palsy and contralateral somatic hemiplegia (Millard-Gruber syndrome).

Book Source Details

• Book Title: The 5-Minute Pediatric Consult
• Author(s): M. William Schwartz MD; et al.
• Year of Publication: 2008
• Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.

More About Bell's Palsy

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: The 5-Minute Pediatric Consult Authors: M. William Schwartz MD; et al. Publisher: Lippincott Williams & Wilkins Copyright: 2008 ISBN: 0-7817-7577-9

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