Bell Palsy Treatment & Management: Approach Considerations, Pharmacologic Therapy, Local Treatment, bell’s palsy treatment prednisone.

Bell Palsy Treatment & Management

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Because persons with true Bell palsy generally have an excellent prognosis, and because spontaneous recovery is fairly common, treatment of Bell palsy is still controversial. The goals of treatment are to improve facial nerve (seventh cranial nerve) function and reduce neuronal damage.

Many issues must be addressed in treating patients with Bell palsy. The most important is the onset of symptoms. Treatment may be considered for patients who present within 1-4 days of the onset of paralysis.

Patients with Bell palsy frequently present to the emergency department (ED). The role of the ED clinician consists of the following:

The American Academy of Neurology (AAN) published a practice parameter in 2001 stating that steroids are probably effective and acyclovir (with prednisone) is possibly effective for the treatment of Bell palsy. There was insufficient evidence for recommendations on facial decompression surgery. [45]

In 2012, the AAN released guidelines stating that steroids are highly likely to be effective and increase the likelihood of recovery of facial nerve function in new-onset Bell palsy [6, 8] Guidelines from the American Academy of Otolaryngology—Head and Neck Surgery Foundation also recommend the use of corticosteroids. [1]

A variety of nonpharmacologic measures have been used to treat Bell palsy, including physical therapy (eg, facial exercises, [46] neuromuscular retraining [47] ) and acupuncture. [48] No adverse effects of these treatments have been reported. Reviews suggest that physical therapy may result in faster recovery and reduced sequelae, but further randomized, controlled trials are needed to confirm any benefit.

Surgical options

Surgical options for Bell palsy include the following:

Anecdotal evidence suggests that surgical repair by using a combination of procedures tailored to the patients’ clinical findings works well for improving symptoms and exposure. Most patients who have had severe corneal exposure from lagophthalmos with or without paralytic ectropion have received a combination of lateral tarsal strip placement, SOOF lift, and gold-weight implantation. Patients without severe exposure have received a single procedure or combinations of procedures.

Pharmacologic Therapy

The most widely accepted treatment for Bell palsy is corticosteroid therapy. However, the use of steroids is still controversial because most patients recover without treatment. Antiviral agents have also been studied in this setting, as have combinations of the 2 types of drugs.

Corticosteroids

As previously mentioned, 2012 guidelines from the AAN state that steroids are highly likely to be effective and increase the likelihood of recovery of facial nerve function in new-onset Bell palsy [6, 8]

Guidelines from the American Academy of Otolaryngology–Head and Neck Surgery Foundation (AAO-HNSF) were issued in November 2013 that also support the AAN guidelines. The guidelines recommend use of corticosteroids within 72 hours from the onset of symptoms. Antiviral agents (eg, acyclovir, valacyclovir) may be considered if a viral etiology is suspected, but only in combination with corticosteroids. [49]

Many trials have been carried out to study the efficacy of prednisone in Bell palsy. In 1972, for example, Adour et al conducted a large, controlled clinical trial that found that 89% of patients treated with prednisone had full recovery, compared with 64% of patients treated with placebo. [50]

This trial and other early studies, however, showed conflicting results for steroid use in treating Bell palsy, [51] and they were limited in their size.

However, 3 subsequent randomized, controlled trials showed significant improvement in outcomes when prednisolone was started within 72 hours of symptom onset. [12, 13, 52] Based on these 3 studies, steroids should be strongly considered to optimize outcomes. Once the decision to use steroids is made, the consensus is that this treatment should be started immediately.

One of the 3 studies—a double-blind, randomized trial from Scotland involving 551 patients with Bell palsy who were recruited within 72 hours of symptom onset—demonstrated that early treatment with prednisolone can significantly improve the chances of complete recovery at 3 and 9 months. [12] In contrast, acyclovir given alone did not show any significant difference in the rate of facial recovery compared with placebo, and there was no additional benefit from combining acyclovir and prednisolone compared with prednisolone alone.

A larger double-blind, controlled trial showed that prednisolone significantly shortened the time to complete recovery, while valacyclovir did not affect facial recovery compared with placebo. [13] Further analysis showed that patients treated with prednisolone within 48 hours had significantly higher rates of complete recovery than did those who were not treated, whereas no significant difference in recovery rate was seen between patients treated at 49-72 hours and untreated patients. [53]

The recommended dose of prednisone for the treatment of Bell palsy is 1 mg/kg or 60 mg/day for 6 days, followed by a taper, for a total of 10 days. Caution should be used in patients with any of the following:

High-dose steroids (>120 mg/day of prednisone) have been safely used to treat Bell palsy in patients with diabetes [54, 55] ; however, optimal dosing has not been established. Caution should be used in these cases because of the risk of hyperglycemia.

Antiviral agents

Evaluation of the use of antiviral medicines in Bell palsy has shown limited benefit from these drugs, [38, 56] with 3 randomized, controlled trials having demonstrated no benefit from them. [12, 13, 52] However, given the evidence suggesting that a large percentage of Bell palsy cases may result from a viral infection, [24, 57] the use of antiviral agents may be reasonable in certain situations.

The 2001 AAN practice perameter suggested that the use of acyclovir for the treatment of Bell palsy is only possibly effective and that therapy with this agent alone is not effective in facial recovery. [45] According to the academy’s 2012 guidelines, benefit from antivirals has not been established and, at best, is likely to be modest. [6, 8]

The Scottish study cited earlier suggested that prednisolone, and not acyclovir, is useful for facial recovery in Bell palsy. [12]

A Cochrane review found no significant benefit to the use of antivirals over placebo in reducing the rate of incomplete recovery from Bell palsy. [58] This meta-analysis looked at 7 studies involving a total of 1987 patients treated between 1966 and 2008.

Acyclovir (Zovirax) is administered at a dosage of 400 mg orally 5 times daily for 10 days. Evidence supports HSV as a major cause of Bell palsy; if varicella zoster virus (VZV) is suspected, higher doses may be needed (800 mg orally 5 times daily).

Valacyclovir (Valtrex), taken orally in doses of 500 mg twice daily for 5 days, may be used instead of acyclovir. Although it is more expensive, it may be associated with better compliance. If VZV is the cause of Bell palsy, higher doses may be needed (1000 mg orally 3 times daily). Because of the increased cost and greater risk of side effects with higher doses, however, valacyclovir cannot be routinely recommended for the treatment of Bell palsy at this time.

Corticosteroid-antiviral combinations

A prospective randomized trial with 101 patients comparing prednisone with acyclovir demonstrated that the prednisone group had better clinical recovery. [59] In another prospective, randomized trial, with 99 patients, the combination of prednisone and acyclovir was more effective than prednisone monotherapy in preventing nerve degeneration, as measured by electrodiagnostic tests. [60]

A Japanese randomized, prospective study of 221 patients with Bell palsy showed significant improvement in facial function using a combination of prednisone and valacyclovir therapy versus using prednisone alone. This improvement was noted in patients who had severe to complete facial palsy. [57]

Quant et al conducted a meta-analysis of published studies from 1984 to January 2009 that showed no improved benefit (with respect to degree of facial muscle recovery in patients with Bell palsy) from the use of corticosteroids plus antiviral agents as compared with corticosteroid therapy alone. [61] Six trials (representing pooled data from 1145 patients) were examined and included 574 patients who received corticosteroids alone and 571 patients who received corticosteroids and antiviral agents.

Quant et al suggest that the routine use of antiviral agents is not warranted; however, future studies should improve diagnostic efforts to identify herpes virus as a potential etiology. Additionally, newer antiviral agents may prove more beneficial than older antiviral agents used in the studies analyzed to date. [61]

Contrary to the meta-analyses by Quant et al and Cochrane, de Almeida and colleagues found that antiviral agents, when combined with corticosteroids, were associated with greater risk reduction of borderline significance than were corticosteroids alone. [62] Their meta-analysis examined 18 trials involving a total of 2786 patients.

If antiviral agents are used, they should be initiated in conjunction with corticosteroids. Future studies will be needed to determine which population will most benefit from antiviral therapy.

Local Treatment

It is universally accepted that eye care is imperative in Bell palsy. The patient’s eye is at risk for drying, corneal abrasion, and corneal ulcers.

In most cases, topical ocular lubrication (with artificial tears during the day and lubricating ophthalmic ointment at night, or occasionally ointment day and night) is sufficient to prevent the complications of corneal exposure. [9] Punctal plugs may be helpful if dryness of the cornea is a persistent problem.

Occluding the eyelids by using tape or by applying a patch for 1 or 2 days may help to heal corneal erosions. Care must be taken to prevent worsening the abrasion with the tape or patch by ensuring that the eyelid is securely closed. Clear plastic wrap, cut to 8 X 10 cm and applied with generous amounts of ointment as a nighttime occlusive bandage, may be required.

External eyelid weights are available to improve mechanical blink. The weights are attached to the upper lid with an adhesive and are available in different skin tones.

Lower-lid ectropion or droop can temporarily be helped by applying tape below the lid margin in the center of the lower lid; the lid is pulled laterally and upward to anchor on the orbital rim.

Botulinum toxin can be injected transcutaneously or subconjunctivally at the upper border of the tarsus and aimed at the levator muscle to produce complete ptosis and to protect the cornea. [4] Botulinum toxin may help in relaxing the facial muscles after they have developed mass contraction, though the results are not as satisfying in patients with Bell palsy as in patients with idiopathic hemifacial spasm.

Facial Nerve Decompression

Surgery to decompress the facial nerve is controversial. Patients with a poor prognosis, identified by facial nerve testing or persistent paralysis, appear to benefit the most from surgical intervention. However, studies have been mixed as far as benefit from surgery. [45]

Surgery may be considered in patients with complete Bell palsy that has not responded to medical therapy and with greater than 90% axonal degeneration, as shown on facial nerve EMG within 3 weeks of the onset of paralysis. [63, 31] The problem must be localized with MRI. The surgeon can then decide if the maxillary segment should be decompressed externally or if the labyrinthine segment and geniculate ganglion should be decompressed with a middle fossa craniotomy.

A study in patients with greater than 90% degeneration demonstrated superior results in the cohort that underwent middle fossa decompression, compared with the cohort that chose not to pursue surgical decompression. In the surgical group, 91% of cases exhibited a postoperative House-Brackmann grade of I or II. In the nonsurgical group, 58% of the patients had a poor result, with a House-Brackmann grade of III or IV at 7 months. The best surgical results were obtained when the procedure was done within 14 days after the onset of paralysis. [64]

Subocularis Oculi Fat Lift

The SOOF is deep to the orbicularis oculi muscle and superficial to the periosteum below the inferior orbital rim. An SOOF lift is designed to lift and suspend the midfacial musculature. The procedure may also elevate the upper lip and the angle of the mouth to improve facial symmetry.

Lateral tarsal strip procedure

An SOOF lift is commonly performed in conjunction with a lateral tarsal strip procedure to correct horizontal lower-lid laxity and to improve apposition of the lid to the globe. [65] First, lateral canthotomy and cantholysis is performed. Then, the anterior lamella is removed, and the lateral tarsal strip is shortened and attached to the periosteum at the lateral orbital rim.

Implants in Eyelid

Implantable devices have been used to restore dynamic lid closure in cases of severe, symptomatic lagophthalmos. These procedures are best for patients with poor Bell phenomenon and decreased corneal sensation. Gold or platinum weights, a weight-adjustable magnet, or palpebral springs can be inserted into the eyelids. Pretarsal gold-weight implantation is most commonly performed.

The implants are inert and composed of 99.99% pure gold or platinum. Sizes range from 0.6-1.8 g. The weight allows the upper eyelid to close with gravity when the levator palpebrae are relaxed. Therefore, patients must sleep with their head slightly elevated.

The implants are easily removed if nerve function returns. Complications include migration of the implant, inflammation, allergic reaction, and extrusion.

Tarsorrhaphy

Tarsorrhaphy decreases horizontal lid opening by fusing the eyelid margins together, increasing support of the precorneal lake of tears and improving coverage of the eye during sleep. The procedure can be done in the office and is particularly suitable for patients who are unable or unwilling to undergo other surgery. It can be completed as either a temporary or a permanent measure. Permanent tarsorrhaphy is performed if nerve recovery is not expected.

Tarsorrhaphy can be performed laterally, centrally, or medially. The lateral procedure is the most common; however, it can restrict the monocular temporal visual field. Central tarsorrhaphy offers good corneal protection, but it occludes vision and can be cosmetically unacceptable. Medial or paracentral tarsorrhaphy is performed lateral to the lacrimal puncta and can offer good lid closure without substantially affecting the visual field.

Muscle Transposition, Nerve Grafting, and Brow Lift

Transposition of temporalis

Transposition of the temporalis muscle can be used to reanimate the face and to provide lid closure by using the fifth cranial nerve. Strips from the muscle and fascia are placed in the upper and lower lids as an encircling sling. Patients initiate movement by chewing or clenching their teeth.

Facial nerve grafting or hypoglossal-facial nerve anastomosis

Reinnervation of the facial nerve by means of facial nerve grafting or hypoglossal-facial nerve anastomosis can be used in cases of clinically significant permanent paralysis to help restore relatively normal function to the orbicularis oculi muscle or eyelids.

Direct brow lift

Brow ptosis is repaired with a direct brow lift. Care should be taken in the presence of corneal decompensation because lifting the brow can cause worsening of lagophthalmos, especially if lid closure is poor. A gold-weight implant can be placed or lower-lid resuspension can be performed simultaneously to prevent this complication.

Consultations and Monitoring

Consultations

If the patient’s paralysis is not resolving or is progressing to complete paralysis, a thorough neurologic assessment and an examination of the head, eyes, ears, nose, and throat should be performed to rule out neoplastic causes of facial nerve palsy.

If the initial diagnostic impression based on the history and physical examination of the patient is not Bell palsy, then consultation with a neurologist or otolaryngologist is needed. For example, consultation with an otolaryngologist should be made for the patient who has facial palsy and pain and in whom the ear, nose, and throat examination does not show auricular vesicles (as in Ramsay Hunt syndrome). These patients should be evaluated for malignancy or other structural lesions of the facial nerve.

Consultation with a neurologist or otolaryngologist should also be sought if the paralysis persists for several months.

An evaluation by an otolaryngologist may be indicated for patients with a prolonged course, for the consideration of surgical decompression of the facial nerve. Patients who report persistent dry eye or painful eye should be referred to an ophthalmologist. An evaluation by a specialist in infectious disease may be indicated if results of laboratory studies are positive for Lyme disease, syphilis, or HIV infection.

Monitoring

The patient should be monitored if the initial EMG shows that the function of the involved facial muscles is less than 25% of the normal side’s facial muscle function. If the residual paralysis is severe, the patient should be referred for counseling.

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Contributor Information and Disclosures

Danette C Taylor, DO, MS, FACN Senior Staff Neurologist, Henry Ford Health Systems; Clinical Assistant Professor, Department of Neurology and Ophthalmology, Michigan State University College of Osteopathic Medicine

Sally B Zachariah, MD Associate Professor, Department of Neurology, University of South Florida College of Medicine; Director, Department of Neurology, Division of Strokes, Veteran Affairs Medical Center of Bay Pines

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

Edward Bessman, MD Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Disclosure: Nothing to disclose.

Dominique Dorion, MD, MSc, FRCSC, FACS Vice Dean and Associate Dean of Resources, Professor of Surgery, Division of Otolaryngology-Head and Neck Surgery, University of Sherbrooke Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Thomas R Hedges III, MD Director of Neuro-Ophthalmology, New England Eye Center; Professor, Departments of Neurology and Ophthalmology, Tufts University School of Medicine

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center

Disclosure: Nothing to disclose.

Suzan Khoromi, MD Fellow, Pain and Neurosensory Mechanisms Branch, National Institute of Dental and Cranial Research, National Institutes of Health

Disclosure: Nothing to disclose.

Milind J Kothari, DO Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Penn State Milton S Hershey Medical Center

Disclosure: Nothing to disclose.

Andrew W Lawton, MD Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center

Disclosure: Nothing to disclose.

Bruce Lo, MD Medical Director, Sentara Norfolk General Hospital; Assistant Professor, Assistant Program Director, Core Academic Faculty, Department of Emergency Medicine, Eastern Virginia Medical School

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation Unrestricted gift Unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy Ownership interest Management position; Cerescan Imaging Honoraria Consulting; GYRUS ACMI Honoraria Consulting

Kim Monnell, DO Neurology Consulting Staff, Department of Medicine, Bay Pines VA Medical Center

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University School of Medicine

Disclosure: Nothing to disclose.

B Viswanatha, MBBS, MS, DLO Professor of Otolaryngology (ENT), Chief of ENT III Unit, Sri Venkateshwara ENT Institute, Victoria Hospital, Bangalore Medical College and Research Institute; PG and UG Examiner, Manipal University, India and Annamalai University, India

B Viswanatha, MBBS, MS, DLO is a member of the following medical societies: Association of Otolaryngologists of India, Indian Medical Association, and Indian Society of Otology

Disclosure: Nothing to disclose.

Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Disclosure: Nothing to disclose.

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

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