Bell Palsy : by Craig H Zalvan

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http://www.emedicine.com/ent/topic719.htm

Bell Palsy

Article Last Updated: Nov 21, 2007

AUTHOR AND EDITOR INFORMATION

Section 1 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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

Craig H Zalvan is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Laryngological Rhinological and Otological Society, American Medical Association, Medical Society of the State of New York, New York County Medical Society, Triological Society, and Voice Foundation

Editors: B Viswanatha, MBBS, MS, DLO, Professor of ENT, Sri Venkateshwara ENT Institute, Victoria Hospital, Bangalore Medical College and Research Institute, India; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Dominique Dorion, MD, MSc, FRCSC, Program Director and Division Chair, Professor of Surgery, Division of Otolaryngology, University of Sherbrooke, Canada; Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders; Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Author and Editor Disclosure

Synonyms and related keywords: Bell palsy, Bell's palsy, BP, acute facial paralysis, idiopathic facial paralysis, IFP, facial palsy, lower motor neuron facial paresis, lower motor neuron facial paralysis, cranial nerve VII, CN VII

INTRODUCTION

Section 2 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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

Section 3 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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}

DIFFERENTIALS

Section 4 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Traumatic

Birth trauma
Temporal bone fracture
Barotrauma
Facial trauma

Neurologic

Cranial nerve syndromes

Systemic

Diabetes mellitus
Alcoholic neuropathy
Hyperthyroidism
Pregnancy

Infectious

Acute otitis media
Chronic otitis media
Herpes zoster oticus
Necrotizing otitis media
Cholesteatoma
Mumps
Mononucleosis
Lyme disease
Viral syndromes
Tuberculosis

Vascular

Benign intracranial hypertension
Intratemporal aneurysm

Toxic

Thalidomide
Tetanus
Carbon monoxide

Neoplastic

Acoustic neuroma
Glomus tumors
Facial nerve neuroma
Metastatic disease
Fibrous dysplasia

Iatrogenic

Surgical
Embolization
Anesthesia nerve blocks

Idiopathic

Melkersson-Rosenthal syndrome
Autoimmune syndrome
Multiple sclerosis
Myasthenia gravis
Sarcoidosis
Amyloidosis
Wegener granulomatosis
Kawasaki disease

WORKUP

Section 5 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• For endemic areas, Lyme titers may be appropriate in patients presenting for the first time.
• For recurrent episodes of IFP, further workup should include diagnostic eval‎uation based on the differential diagnosis.
• Antineutrophil cytoplasmic antibody (cANCA) levels are indicated if applicable to exclude Wegener granulomatosis.

Imaging Studies

• MRI with gadolinium enhancement is indicated at initial examination when the history and physical examination findings are consistent with the diagnosis of acute IFP.

·          

• MRI with gadolinium may demonstrate enhancement of the nerve within the facial canal at the labyrinthine and geniculate segments or the internal auditory canal.
• Little correlation between the enhancement of the facial nerve and the clinical outcome has been noted. However, a recent analysis of early MRIs with gadolinium of the intratemporal facial nerve demonstrated the ability to predict the long-term outcome of the facial paralysis; these findings (increased signal intensity in the internal auditory canal after administration of gadolinium) correlated favorably with those of electrodiagnostic testing.
• Thus, MRI is useful as a means of excluding other pathologies as the cause of paralysis.
• Radiological eval‎uation by CT scanning and other methods is indicated if other associated physical findings indicate or if the paresis is progressive and unremitting. CT scanning demonstrates the architecture of the temporal bone and may be used if some other pathology is suspected.

Other Tests

• Audiometry

·          

• All patients should undergo audiography and early latency auditory evoked potentials (AEP).
• Typically, the hearing threshold is not affected by IFP.
• Impedance testing may reveal an absent or diminished stapedial reflex because of paresis of the stapedial branch of the facial nerve.
• Electrodiagnostic testing

·          

• This may be an important adjunct in determining the prognosis of IFP.
• It is reserved for patients with complete paralysis or for those demonstrating progression from partial to complete paralysis.
• Electroneuronography

·          

• This is a physiological test that uses electromyography to objectively measure the difference between potentials generated by the facial musculature on both sides of the face in response to a supramaximal electrical stimulation of the facial nerve.
• Because all electrodiagnostic testing is performed on the nerve distal to the proposed site of injury, sufficient time is needed for Wallerian degeneration to occur, usually 48-72 hours. Testing should begin 3 days from the onset of complete paralysis.
• Electrodiagnostic testing measures the facial nerve degeneration indirectly. If a patient does not reach 90% degeneration within the first 3 weeks of onset of paralysis, some studies suggest the prognosis is excellent, with over 80-100% of the patients recovering with excellent function. The patients who reach over 90% degeneration within the first 3 weeks of onset of paralysis have a much more guarded prognosis, with only 50% having good recovery of facial motion.
• The rate of degeneration also predicts the prognosis. Those who have 90% degeneration by 5 days have a worse prognosis than those with 90% degeneration at 14 days.
• Electromyography

·          

• This is an electrodiagnostic test that measures electrical activity of the striated muscle via electrode placement within the muscle, and findings reflect the health of the facial nerve.
• Early voluntary contraction within 2 weeks of paralysis indicates a good prognosis. Short waves signify denervation.
• Blepharokymographic analysis

·          

• Blepharokymographic analysis, a high-speed eyelid motion-analysis system, has been recently used to eval‎uate movement of the eyelids. Computerized based analysis may prove helpful in diagnosing Bell palsy, predicting prognosis, and eval‎uating response to therapeutic measures such as a gold weight placement.

TREATMENT

Section 6 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

Although true IFP has a good recovery in 71% of cases, with or without treatment, the standard is to treat all patients who have this condition.

Current diagnostic technology cannot predict which patients will experience sequelae, which ones will progress to complete paralysis, and which ones will recover completely.

• Glucocorticoid therapy

·          

• The current treatment of IFP is 20 mg of prednisone orally qid. Its effectiveness has been demonstrated by double-blind placebo-controlled studies.
• The patients treated with corticosteroids had an improved clinical course and had fewer incidents of synkinesis and other sequelae than those treated with placebo, but a reliably good result does not always occur. However, conflicting studies that do not demonstrate as strong a significance exist. Larger trials are now underway.
• Another study demonstrated that prednisone significantly decreased the pain associated with IFP.
• Unless contraindications exist, patients are treated with 1 mg/kg of prednisone up to 80 mg/d for 7-10 days.
• The earlier the treatment is instituted, the better the prognosis.
• If the paralysis is incomplete or improving, then the dosage can be tapered rapidly. However, if progression of the paralysis is noted or if paralysis is complete, then the full dose of corticosteroid therapy should be continued for 7-10 days and then tapered off.
• Antiviral therapy

·          

• Because of the recent evidence implicating HSV as the likely cause of IFP, antiviral therapy in the form of acyclovir has been added to the treatment regimen.
• Early studies demonstrated an improved prognosis in patients treated with a combination of prednisone and acyclovir (400 mg 5 times daily), famciclovir (500 mg tid), or valacyclovir (500 mg tid). Patients also experienced improved return of volitional muscle motion with less likelihood of partial nerve degeneration.
• However, analysis of 5 additional studies in a systematic review of the literature failed to demonstrate significant evidence of the efficacy of antiviral treatment. In patients with a known history of vesiculation, those with recent exposure to a viral infection, and in patients who are immunocompromised addition of antiviral medication may be of some benefit, especially given the low incidence of adverse reactions to these medications.
• A recent prospective, multicenter, randomized placebo-controlled study of 221 patients found a statistically significant rate of improvement with treatment including valacyclovir (1000mg/d for 5d) and prednisolone. Another recent randomized, multicenter, controlled study failed to detect a statistically significant difference with the addition of valacyclovir; however, this study did find a 34% reactivation rate of herpes simplex virus type 1 (HSV1) or varicella-zoster virus in patients with acute onset facial paralysis. In addition, some authors have suggested that those patients with HSV1 reactivation did benefit from the addition of valacyclovir.

Surgical Care

Surgical decompression of the facial nerve is, at times, an option in the treatment of IFP. Because prognosis for complete recovery is very good in patients with incomplete facial paralysis, aggressive surgical therapy is not indicated. However, numerous studies have suggested a role for surgical decompression in patients with complete paralysis and electrophysiologic degeneration as demonstrated by decrease in the electroneurography amplitude of greater than 90-95%.

Controversy remains in the literature as to which surgical approach should be used. Because the primary area of pathology of the facial nerve is the labyrinthine segment and this region can be most safely and effectively decompressed by a middle fossa subtemporal craniotomy, support for the middle fossa subtemporal craniotomy approach has been considerable. The transmastoid approach, while accessing the mastoid and tympanic segments of the facial nerve, is less favored because of its limited access to the labyrinthine segment of the facial nerve. Studies have shown greater efficacy of surgical decompression with earlier intervention.

• A recent study compared a cohort of patients with degeneration greater than 90% who underwent middle fossa decompression with a cohort of similar patients who chose not to pursue surgical decompression. The surgical group exhibited a House-Brackmann grade I or II in 91% of the cases. The nonsurgical group had a poor result in 58% of the patients, with a House-Brackmann grade III or IV at 7 months. This study also demonstrated that best results were obtained if the decompression was attempted within 14 days after the onset of paralysis.
• Another recent study compared two groups of patients with greater than 95% degeneration after steroid treatment. In one group, decompression was performed from the labyrinthine segment to the stylomastoid foramen using a transmastoid approach. The other group was observed. The results demonstrated a significant improvement in the recovery of facial function in the surgical group. This study also demonstrated a trend toward better recovery with earlier intervention.
• Thus, the literature supports a role for surgical decompression either by a transmastoid or middle fossa subtemporal craniotomy approach dependent upon the clinical and surgical experience of the surgeon. The patient should be informed about the possible risks, although rare, that exist with both approaches.

MEDICATION

Section 7 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Glucocorticoids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Drug Name	Prednisone (Deltasone, Meticorten, Orasone, Sterapred)
Description	Glucocorticoid absorbed readily from GI tract. It has anti-inflammatory and immune-modulating effects and profound and varied metabolic effects. Used in the treatment of idiopathic facial paralysis.
Adult Dose	20 mg PO qid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI bleeding or ulceration
Interactions	Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

FOLLOW-UP

Section 8 of 9 ?/div>

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Outpatient Care

• Eye care

·          

• Treatment options are limited when recovery is incomplete. However, in general, any facial nerve weakness that limits the ability of the patient to blink requires vigilant eye care, including hourly saline eye drops and nightly ophthalmic ointment and eye protection.
• Further long-term management of ocular complications includes gold weight placement and lid-shortening procedures.
• Management strategy: The management strategy described by Gantz in 1999 is as follows:

·          

• Acute paresis, day 0-14: The patient is started on prednisone and followed up in 5 days. If the paresis remains or is improved, then the patient is followed up in 1 month. If the paresis progresses, then electroneuronography is performed and the paralysis protocol provided below is followed. If the acute paresis persists for longer than 14 days, then the patient is observed and followed up in 6 months.
• Acute paralysis
• Day 0-3: The patient is started on prednisone and followed up in 3 days.
• Day 3-14: Electroneuronography is performed. If less than 90% degeneration is noted, then the patient is started on prednisone and followed up in 14 days depending on the findings of electroneuronography. If greater than 90% degeneration is noted, then middle cranial fossa decompression should be considered.
• Day 14 and after: The patient is followed up in 6 months.

Prognosis

• Most patients have an excellent prognosis, both functionally and aesthetically. Even if a patient presents with a complete paralysis, over 70% have a full recovery.
• The most important prognostic factor is whether the paralysis is complete or incomplete on presentation.
• An abrupt onset, early return of function, partial paralysis, and no signs of other diseases indicate a good prognosis.
• Signs of spontaneous remission are observed in 85% of patients within 3 weeks of the initial paresis.
• Patients who do not progress to complete facial paralysis have an excellent prognosis for the recovery of facial motor function, with over 94% recovering completely.
• In about 15% of the patients, recovery does not begin until 3-6 months after the onset of paralysis.
• The sooner the recovery, the less likely are the chances that sequelae will develop. If some restoration of function is noted within 3 weeks, then the recovery is most likely to be complete. If the recovery begins between 3 weeks and 2 months, then the ultimate outcome is usually satisfactory. If the recovery does not begin until 2-4 months from the onset, likelihood of permanent sequelae, including residual paresis and synkinesis, is higher.
• The sequelae include dysgeusia, ageusia, dysesthesias, synkinesis, residual weakness, facial spasms, and tics.
• Multiple coincident factors associated with a bad prognosis are as follows: (1) hyperacusis, (2) diabetes mellitus, (3) hypertension, (4) decreased tears, (5) age more than 60 years, and (6) severe aural, anterior facial, or radicular pain.

Patient Education

• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education article Bell Palsy.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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