eMedicine Specialties > Neurology > Inflammatory and Demyelinating Diseases

Bell Palsy

Author: Kim Monnell, DO, Consulting Staff, Department of Neurology, Sarasota Memorial Hospital
Coauthor(s): Sally B Zachariah, MD, Associate Professor, Department of Neurology, University of South Florida; Director, Department of Neurology, Division of Strokes, Veteran Affairs Medical Center of Bay Pines; Suzan Khoromi, MD, Fellow, Pain and Neurosensory Mechanisms Branch, National Institute of Dental and Cranial Research, National Institutes of Health
Contributor Information and Disclosures

Updated: Jul 31, 2008

Introduction

Background

Facial paralysis is a disfiguring disorder that has a great impact on the patient. Facial nerve paralysis may be congenital, neoplastic, or result from infection, trauma, toxic exposures, or iatrogenic causes. The most common cause of unilateral facial paralysis is Bell palsy, also known as idiopathic facial paralysis. Bell palsy is thought to account for approximately 60-75% of cases of acute unilateral facial paralysis.

In 1550, Fallopius noted the narrow lumen in the temporal bone through which a part of the seventh cranial nerve passes. In 1828, Charles Bell made the distinction between the fifth and seventh cranial nerves; he noted that the seventh nerve was involved mainly in the motor function of the face and the fifth nerve was concerned mainly with the sensory perception of the face.

Even today, controversy still surrounds the etiology and treatment of Bell palsy. Clinical features of Bell palsy that may help distinguish it from other causes of facial paralysis include sudden onset of unilateral facial paralysis (less than 48 hours), absence of signs and symptoms of CNS disease, and absence of signs and symptoms of ear or posterior fossa disease.

Pathophysiology

The course of the facial nerve is tortuous, both centrally and peripherally (see Media file 1).

The facial nerve nucleus lies within the reticular formation of the pons, adjacent to the fourth ventricle. The facial nerve roots include fibers from the motor, solitary, and salivatory nuclei. The nervus intermedius comprises fibers from salivatory and solitary nuclei (it contains sensory fibers from the tongue, mucosa, and postauricular skin as well as parasympathetic fibers to the salivary and lacrimal glands). The fibers of the facial nerve then course around the sixth cranial nerve nucleus and exit the pons at the cerebellopontine angle. The fibers go through the internal auditory canal along with the vestibular portion of the eighth cranial nerve. The narrowest portion of the internal auditory canal is the labyrinthine segment. This is the location that is thought to be the most common site of compression of the facial nerve in Bell palsy.

The seventh cranial nerve contains parasympathetic fibers to the nose, palate, and lacrimal glands. The preganglionic parasympathetic fibers that originate in the salivatory nucleus join the fibers from nucleus solitarius to form the nervus intermedius. These fibers then synapse with the submandibular ganglion, which has fibers that supply the sublingual and submandibular glands. The fibers from the nervus intermedius also supply the pterygopalatine ganglion, which has parasympathetic fibers that supply the nose, palate, and lacrimal glands.

The facial nerve passes through the stylomastoid foramen in the skull and terminates into the zygomatic, buccal, mandibular, and cervical branches. These nerves serve the muscles of facial expression, which include frontalis, orbicularis oculi, orbicularis oris, buccinator, and platysma. Other muscles innervated by the facial nerve include stapedius, stylohyoid, posterior belly of the digastric, occipitalis, and anterior and posterior auricular muscles. All muscles of the facial nerve are derived from the second brachial arch.

The location of injury of the facial nerve in Bell palsy is peripheral to the seventh nerve nucleus. The injury is thought to occur near or at the geniculate ganglion. If the lesion is proximal to the geniculate ganglion, the motor paralysis is accompanied by gustatory and autonomic abnormalities. Lesions between the geniculate ganglion and the origin of the chorda tympani produce the same effect except that they spare lacrimation. If the lesion is at the stylomastoid foramen, it may result in facial paralysis only.

Bell palsy is thought to be caused by edema and ischemia resulting in compression of the facial nerve in its course through the bony canal. The cause of the edema and ischemia is still being debated. In the past, cold exposure (eg, chilly wind, cold air conditioning, or driving with the car window down) were considered the only triggers to Bell palsy. Several authors believe that the herpes simplex virus (HSV) is a common cause of Bell palsy. However, studying the causal relationship between HSV and Bell palsy is difficult because of the ubiquitous nature of HSV.

In 1972, McCormick first suggested that HSV is responsible for idiopathic facial paralysis.1 This was based on the analogy that HSV was found in cold sores, and he hypothesized that HSV may remain latent in the geniculate ganglion. Since then, autopsy studies have shown HSV in the geniculate ganglion of patients with Bell palsy. Murakami et al performed polymerase chain reaction (PCR) testing for HSV in the endoneural fluid of the seventh nerve of patients who underwent surgery for Bell palsy. Of the 14 patients, 11 were found to have HSV in the endoneural fluid.2 Assuming that HSV is the etiologic agent in Bell palsy is reasonable. If this is true, then the virus is most likely to travel up the axons of the sensory nerves and reside in the ganglion cells. At times of stress, the virus will reactivate, causing local damage to the myelin.

Thus, Bell palsy may be secondary to viral, and/or autoimmune reactions causing the facial nerve to demyelinate, resulting in unilateral facial paralysis.

Frequency

United States

The annual incidence of Bell palsy is approximately 23 cases per 100,000 persons. The right side is affected 63% of the time. Persons with diabetes have a 29% higher risk of being affected by Bell palsy than persons without diabetes. Thus, measuring blood glucose levels at the time of diagnosis of Bell palsy may detect undiagnosed diabetes.

International

The highest incidence was found in a study in Seckori, Japan, in 1986 and the lowest incidence was found in Sweden in 1971. Most population studies generally show an annual incidence of 15-30 cases per 100,000 population.

Mortality/Morbidity

  • Most patients who suffer from Bell palsy have neurapraxia or local nerve conduction block. These patients are likely to have a prompt and complete recovery of the nerve. Patients with axonotmesis, with disruption of the axons, have a fairly good recovery but it is usually not complete. The risk factors thought to be associated with a poor outcome in patients with Bell palsy include (1) age greater than 60 years, (2) complete paralysis, and (3) decreased taste or salivary flow on the side of paralysis (usually 10-25% compared to the patient's normal side). Other factors thought to be associated with poor outcome include pain in the posterior auricular area and decreased lacrimation.
  • Patients generally have a good prognosis; approximately 80-90% of patients recover without noticeable disfigurement within 6 weeks to 3 months. Patients aged 60 years or older have an approximately 40% chance of complete recovery and have a higher rate of sequelae. Patients younger than 30 years have only a 10-15% chance of less than complete recovery and sequelae. If no recovery occurs by 4 months, then the patient is more likely to have sequelae from the disease, which include synkinesis, crocodile tears, and rarely hemifacial spasm.
    • Synkinesis is an abnormal contracture of the facial muscles while smiling or closing the eyes. It may be mild and result in slight movement of the chin when the patient blinks, eye closure with smiling, or contracture around the mouth while blinking. Crocodile tears are observed; patients shed tears while they eat.
    • Facial spasm is a very rare complication of Bell palsy. It occurs as tonic contraction of one side of the face. Spasms are more likely to occur during times of stress or fatigue and may occur during sleep. This condition may occur secondary to compression of the root of the seventh nerve by an aberrant blood vessel, tumor, or demyelination of the nerve root. It occurs most commonly in the fifth and sixth decades of life, and sometimes the etiology is not found. The presence of progressive facial hemispasm with other cranial nerve findings indicates a possibility of a brainstem lesion.
    • Diabetic patients are 30% more likely than nondiabetic patients to have only partial recovery; recurrence of Bell palsy is also more common among diabetic patients.
  • Bell palsy accounts for only 23% of bilateral facial paralysis. The majority of patients with bilateral facial palsy have Guillain-Barré syndrome (GBS), sarcoidosis, Lyme disease, meningitis (neoplastic or infectious), or bilateral neurofibromas (in patients with neurofibromatosis type 2).
  • Bell palsy recurs in 10-15% of patients. It may recur on the ipsilateral or contralateral side of the initial palsy. Recurrence usually is associated with a family history of recurrent Bell palsy. Approximately 30% of patients with recurrent ipsilateral facial palsy were found to have tumors of the seventh nerve or parotid gland. Patients with recurrent ipsilateral facial palsy should undergo MRI or high-resolution CT scan to rule out neoplastic or inflammatory (eg, multiple sclerosis, sarcoidosis) cause of recurrence.

Sex

  • Bell palsy appears to affect the sexes equally. However, young women aged 10-19 years are more likely to be affected than men in the same age group.
  • Pregnant women have a 3.3 times higher risk of being affected by Bell palsy than nonpregnant women; Bell palsy occurs most frequently in the third trimester.

Age

The lowest incidence is found in persons younger than 10 years and the highest incidence in persons aged 60 years or older.

Clinical

History

Bell palsy is a diagnosis of exclusion. The diagnosis must be made on the basis of a thorough history and physical examination and use of diagnostic testing when necessary.

  • Symptoms of Bell palsy
    • Acute onset of unilateral upper and lower facial paralysis (over a 48-h period)
    • Posterior auricular pain
    • Decreased tearing
    • Hyperacusis
    • Taste disturbances
  • The paralysis must include the forehead and lower aspect of the face. The patient may report inability to close the eye or to smile on the affected side. He or she also may report increased saliva on the side of the paralysis. If the paralysis involves only the lower portion of the face, a central cause should be suspected (ie, supranuclear). If the patient complains of contralateral weakness or diplopia in conjunction with the supranuclear facial palsy, a stroke or intracerebral lesion should be strongly suspected.
    • Half of the patients affected with Bell palsy may complain of posterior auricular pain. Ask the patient if he or she has experienced trauma, which may account for the pain and facial paralysis.
    • One third of patients may experience hyperacusis in the ear ipsilateral to the paralysis, which is secondary to weakness of the stapedius muscle.
    • One sixth of patients experience decreased lacrimation.
    • Many patients report numbness on the side of the paralysis. Some authors believe that this is secondary to involvement of the trigeminal nerve, whereas other authors argue that this symptom is probably due to lack of mobility of the facial muscles and not lack of sensation.
  • If a patient has gradual onset of facial paralysis, weakness of the contralateral side, or history of trauma or infection, other causes of facial paralysis must be strongly considered. Patients who have bilateral facial palsy must be evaluated for GBS, Lyme disease, and meningitis.
  • If a patient is from the Northeast, Lyme disease should be considered as a cause of facial paralysis, and serologic testing should be performed. Approximately 5-10% of untreated Lyme patients may have a peripheral seventh nerve palsy. For related information, see Medscape's Lyme Disease Resource Center.
  • Recurrent ipsilateral facial paralysis must raise the suspicion of a tumor of the seventh nerve or parotid gland. If the patient reports sudden onset of hearing loss and severe pain with the onset of facial paralysis, Ramsay Hunt syndrome must be considered.
  • Symptoms associated with seventh nerve neoplasm include slowly progressive paralysis, facial hyperkinesis, severe pain, recurrent palsy, and other cranial nerve involvement. Cerebellopontine tumors may affect the seventh, eighth, and fifth cranial nerves simultaneously. Patients with a progressive paralysis of the facial nerve lasting longer than 3 weeks should be evaluated for neoplasm.

Physical

  • Initial inspection of the patient demonstrates flattening of the forehead and nasolabial fold on the side affected with the palsy.
  • When the patient is asked to raise the eyebrows, the side of the forehead with the palsy will remain flat.
  • When the patient is asked to smile, the face becomes distorted and lateralizes to the side opposite the palsy.
  • The patient is not able to close the eye completely on the affected side. On attempted eye closure, the eye rolls upward and inward on the affected side. This is known as Bell phenomenon and is considered a normal response to eye closure.
  • A careful examination of the head, ears, eyes, nose, and throat (HEENT) must be carried out in all patients with facial paralysis.
    • The external auditory canal must be inspected for vesicles, injection, infection, or trauma.
    • The patient may have decreased sensation to pinprick in the posterior auricular area.
    • The patient who has paralysis of the stapedius muscle will report hyperacusis.
    • Bell phenomenon is observed on attempted eye closure.
    • With weakness/paralysis of the orbicularis oculi muscle (facial nerve innervation) and normal function of the levator muscle (oculomotor nerve innervation) and Mueller muscle (sympathetic innervation), eye closure may be partial or absent. The tear reflex may also be absent in many cases of Bell palsy. For these reasons the patient may have decreased tearing and susceptibility to corneal abrasion and dryness of the eye. The patient may appear to have loss of corneal reflex on the affected side; however, the contralateral eye blinks when testing the corneal reflex on the affected side.
  • A careful oral examination must be performed.
    • Taste and salivation are affected in many patients with Bell palsy.
    • Taste may be assessed by holding the tongue with gauze and testing each side of the tongue independently with salt, sugar, and vinegar. The mouth must be washed after testing with different substances. The affected side has decreased taste as compared to the normal side.
  • Careful neurologic examination is necessary in patients with facial paralysis. A neurologic abnormality warrants neurologic referral and further testing such as MRI of the brain, lumbar puncture, and electromyography (EMG) where appropriate.

Causes

See Pathophysiology.

More on Bell Palsy

Overview: Bell Palsy
Differential Diagnoses & Workup: Bell Palsy
Treatment & Medication: Bell Palsy
Follow-up: Bell Palsy
Multimedia: Bell Palsy
References
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Further Reading

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Keywords

Bell's palsy, idiopathic facial paralysis, facial nerve compression, acute unilateral facial paralysis, bilateral facial palsy, Guillain-Barré syndrome, GBS, sarcoidosis, Lyme disease, meningitis, neoplastic meningitis, infectious meningitis, bilateral neurofibromas, neurofibromatosis type 2, ipsilateral facial palsy

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Contributor Information and Disclosures

Author

Kim Monnell, DO, Consulting Staff, Department of Neurology, Sarasota Memorial Hospital
Kim Monnell, DO is a member of the following medical societies: American Academy of Neurology and American Osteopathic Association
Disclosure: Nothing to disclose.

Coauthor(s)

Sally B Zachariah, MD, Associate Professor, Department of Neurology, University of South Florida; Director, Department of Neurology, Division of Strokes, Veteran Affairs Medical Center of Bay Pines
Sally B Zachariah, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, and American Society of Neuroimaging
Disclosure: Nothing to disclose.

Suzan Khoromi, MD, Fellow, Pain and Neurosensory Mechanisms Branch, National Institute of Dental and Cranial Research, National Institutes of Health
Suzan Khoromi, MD is a member of the following medical societies: American Academy of Neurology, American Pain Society, and International Association for the Study of Pain
Disclosure: Nothing to disclose.

Medical Editor

Milind J Kothari, DO, Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Hershey Medical Center
Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Neurological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Chief Editor

Michael K Racke, MD, Professor, Neurology and Molecular Virology, Immunology, and Medical Genetics; Chairman of Neurology, Chief, Neurology Service, Ohio State University Medical Center
Michael K Racke, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association for the Advancement of Science, American Association of Immunologists, and American Neurological Association
Disclosure: Teva Neuroscience Consulting fee Consulting; Peptimmune Inc. Consulting fee Consulting; Bristol Myers Squibb Consulting fee Consulting; EMD Serono Honoraria Speaking and teaching

 
 
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