eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Reconstructive Surgery

Bell Palsy

Author: Craig H Zalvan, MD, Director of Laryngology, Assistant Professor of Otolaryngology, Head and Neck Surgery, Department of Otorhinolaryngology-Head and Neck Surgery, ENT Faculty Practice
Contributor Information and Disclosures

Updated: Nov 21, 2007

Introduction

Background

Bell palsy, more appropriately known as idiopathic facial paralysis (IFP), is believed to be a virally mediated cranial neuritis affecting the facial nerve due to reactivation of the herpes simplex virus (HSV). IFP accounts for approximately 60-75% of cases of acute facial palsies.

The minimum diagnostic criteria include paralysis or paresis of all muscle groups on one side of the face, sudden onset, and absence of CNS disease. Note that the diagnosis of IFP is made only after other causes of acute peripheral palsy have been excluded.

The treatment of IFP is also controversial, with steroids and antivirals as well as surgical intervention as the mainstay of current therapy. Most patients recover completely with or without treatment. Variable manifestations include otalgia, hyperacusis, decreased tearing, dysgeusia, facial or retroauricular pain, and other cranial neuropathies.

People with acute facial paralysis have a difficult emotional, psychological, and physical challenge. The physicians treating IFP must take into account the aesthetic, functional, and emotional needs of the affected patient. They must be familiar with the natural history of the disease process if they are to counsel the patients effectively about their expectations for recovery and the prevention of complications associated with the paralysis.

Pathophysiology

The exact etiology of IFP remains controversial. Proposed etiologies include viral infection, vascular compromise, autoimmune disease, allergy, and infectious agents. The exact mechanism has not yet been elucidated. The most widely accepted etiology for IFP is a virally mediated cranial neuritis, the agent being herpes simplex virus. This has been demonstrated by numerous serologic, animal, and human studies. Additional support for a viral etiology was seen when intranasal inactivated influenza vaccine was strongly linked to the development of Bell palsy, although whether another component of the vaccine caused the paresis, which was then accompanied by a reactivation of herpes simplex virus, is not clear. Recently, a large population based study found no evidence of increased risk of facial paralysis following pneumococcal vaccine administration.

Frequency

United States

Incidence of IFP is 20-30 patients per 100,000 population. Positive family history of IFP is identified in 8% of patients.

Very few cases are observed during the summer months.

Higher incidence is observed during pregnancy, especially with concurrent preeclampsia.

More people first notice paresis in the morning. Because paresis requires several hours to become evident, it appears that most paresis occurs during sleep.

Mortality/Morbidity

Patients with Bell palsy face a difficult emotional, psychological, and physical challenge. Paralysis, otalgia, decreased tearing, hyperacusis, dysgeusia, facial or retroauricular pain, and other cranial neuropathies may be present.

Bell palsy tends to recur in 7-9% of patients diagnosed with this condition, usually in patients with a family history of IFP or diabetes mellitus.

Sex

The male-to-female ratio is approximately equal, with a slight female predominance in patients younger than 20 years and a slight male predominance in patients older than 40 years.

Age

• The mean age at onset is early to mid forties.
• Slightly higher predominance is observed in patients older than 65 years (59 cases per 100,000 people).
• Lower rate of incidence is observed in children younger than 13 years (13 cases per 100,000 people).

Clinical

History

IFP is a diagnosis of exclusion. All other etiologies of facial paralysis, including traumatic, neoplastic, infectious, congenital, metabolic, immunologic, and autoimmune, should be ruled out.

• Paralysis or paresis of all the muscle groups on one side of the face may occur.
• The onset may be sudden, usually less than 48 hours.
• No evidence of CNS disease is noted. No evidence of ear or cerebellopontine angle disease is noted.
• It may follow recent upper respiratory infection (URI).
• Associated symptoms include the following:
  • Otalgia
  • Hyperacusis (in up to 30% of the patients)
  • Decreased tears
  • Dysgeusia
  • Facial or retroauricular pain
• Some believe that other cranial neuropathies may also be present, however; this is not uniformly accepted. The symptoms in question include the following:
  • Hyperesthesia or dysesthesia of the glossopharyngeal or trigeminal nerves
  • Dysfunction of the vestibular nerve
  • Hyperesthesia of the cervical sensory nerves
  • Vagal or trigeminal motor weakness
• IFP is often abrupt in onset; it usually evolves in less than 2 days.
• Progression of the paresis is possible, but it usually does not progress beyond 7-10 days. A progression beyond this point suggests a different diagnosis.
• If the facial paralysis progresses over weeks to months after the initial diagnosis, then the possibility of a neoplasm should be considered. These include parotid gland neoplasms that can manifest as asymmetric enlargement of the parotid gland or bulging of the parapharyngeal musculature.
• Tumors in the temporal bone such as facial nerve neuromas, meningiomas, hemangiomas, and malignant primary and metastatic lesions should be considered as well.
• Bell palsy rarely recurs. If facial paralysis returns after the initial resolution, another cause should be determined.

Physical

In the grading system developed by House and Brackmann, grades I and II are considered good outcomes, grades III and IV represent moderate dysfunction, and grades V and VI describe poor results. Grade VI is defined as complete facial paralysis; all the other grades are defined as incomplete. An incomplete facial paralysis denotes an anatomically, and to some degree functionally, intact nerve. The degree of facial nerve function should be noted in the chart at the initial visit of the patient.

• Grade I - Normal facial function
• Grade II - Mild dysfunction
  • Slight weakness is noted on close inspection. The patients may have a slight synkinesis.
  • Normal symmetry and tone is noted at rest.
  • Forehead motion is moderate to good, complete eye closure is achieved with minimal effort, and slight mouth asymmetry is noted.
• Grade III - Moderate dysfunction
  • An obvious but not disfiguring difference is noted between both the sides. A noticeable but not severe synkinesis, contracture, or hemifacial spasm is present.
  • Normal symmetry and tone is noted at rest.
  • Forehead movement is slight to moderate, complete eye closure is achieved with effort, and a slightly weak mouth movement is noted with maximum effort.
• Grade IV - Moderately severe dysfunction
  • An obvious weakness and/or disfiguring asymmetry is noted.
  • Symmetry and tone are normal at rest.
  • No forehead motion is observed. Eye closure is incomplete, and an asymmetric mouth is noted with maximal effort.
• Grade V - Severe dysfunction
  • Only a barely perceptible motion is noted.
  • Asymmetry is noted at rest.
  • No forehead motion is observed.
  • Eye closure is incomplete and mouth movement is only slight.
• Grade VI - Total paralysis
  • Gross asymmetry is noted.
  • No movement is noted.
• Other findings: In addition to the facial nerve examination, a full examination of the ear as well as the neck should be performed.
  • Otologic examination includes pneumatic otoscopy and tuning fork examination. An otologic cause should be considered if the history or physical examination demonstrates evidence of acute or chronic otitis media, including a tympanic membrane perforation, otorrhea, cholesteatoma, or granulation tissue, or if a history of previous ear surgery is noted. Vesicles may suggest Ramsay Hunt syndrome (herpes zoster oticus).
  • Parotid/neck examination must be performed to rule out parotid malignancy as a possible cause.
  • Neurologic examination includes complete examination of all the cranial nerves, sensory and motor testing, and cerebellar testing.
• Vesiculation with otalgia and facial pain, facial paralysis, and pruritus or burning may indicate herpes zoster oticus, also known as Ramsay-Hunt syndrome.
• All branches of the facial nerve are involved. If the divisions of the facial nerve are not involved, another cause either locally, such as leprosy, or within the CNS should be considered.
• Paralysis of the facial musculature with sparing of the forehead suggests a central pathology.

Causes

Viral infection, vascular compromise, autoimmune disease, and infectious agents are all proposed etiologies of IFP; the most widely accepted is a virally mediated cranial neuritis caused by the HSV.

Some studies have suggested a possible link to mycoplasma infection and the development of Bell palsy; the mechanism and etiology of this is unknown.^1,2

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