Bell's palsy: Treatment and prognosis in adults

INTRODUCTION — Idiopathic facial nerve palsy, also referred to as Bell's palsy, is the most common cause of spontaneous peripheral facial paralysis. A viral etiology (ie, activation of the herpes simplex virus) is suspected in most cases of Bell's palsy, although there is no established or widely available method of confirming a viral mechanism in clinical practice.

This review will discuss the treatment and prognosis of Bell's palsy in adults. The pathogenesis, clinical features, and diagnosis of Bell's palsy in adults are discussed separately. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults".)

The clinical features, diagnosis, and management of facial palsy in children are discussed elsewhere. (See "Facial nerve palsy in children".)

INITIAL TREATMENT — The mainstay of pharmacologic therapy for Bell's palsy or facial nerve palsy is early short-term oral glucocorticoid treatment. In severe acute cases, combining antiviral therapy with glucocorticoids may improve outcomes. Eye care is essential for patients with incomplete eye closure (algorithm 1).

Glucocorticoids for all patients — A short-term course of oral glucocorticoids is recommended for all patients with new-onset Bell's palsy [1-4]. Treatment should ideally begin within three days of symptom onset, as this is the setting in which glucocorticoids have been studied and shown to be beneficial. We typically treat patients who are within seven days of symptom onset.

●Dose – Our suggested regimen is prednisone (60 to 80 mg/day) for one week. Studied doses and regimens have varied; in the largest randomized trial, patients were treated with oral prednisolone 60 mg daily for five days followed by a five-day taper by 10 mg per day [5]. A one-week course without taper is simpler and delivers approximately the same total dose.

●Side effects – Glucocorticoids at these doses tend to be well tolerated, with no increase in major or minor adverse effects reported in randomized trials [6]. The most common side effects are temporary sleep disruption, mood swings, high blood pressure, and dyspepsia. Caution is required in patients with diabetes due to the risk of hyperglycemia. (See "Major adverse effects of systemic glucocorticoids".)

Some clinicians routinely coadminister a proton pump inhibitor or H2 receptor antagonist, although the risk of gastric ulceration in this patient population is not well characterized and prevention is primarily supported in patients with additional risk factors (eg, concurrent use of nonsteroidal antiinflammatory drugs). (See "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity".)

●Efficacy – There is high-quality evidence from randomized trials that early glucocorticoids improve outcomes in patients with Bell's palsy [1,6,7]. In a 2016 meta-analysis that included seven trials in 895 patients with Bell's palsy, glucocorticoids reduced the relative risk of incomplete recovery at 6 to 12 months by 37 percent compared with placebo or an inactive control (risk ratio [RR] 0.63, 95% CI 0.50-0.80) [6]. In absolute terms, the risk difference for complete recovery was 11 percent favoring glucocorticoids (83 versus 72 percent; number needed to treat [NNT] to avoid one incomplete recovery, 10, 95% CI 6-20). The majority of trials enrolled patients within 72 hours of the onset of weakness.

Antiviral therapy for severe symptoms — It remains uncertain whether antiviral therapy adds benefit to glucocorticoids in patients with new-onset Bell's palsy, despite many trials and a good rationale. If there is a benefit, it is smaller and more incremental than what is achieved with glucocorticoids.

Absent better data, we suggest coadministration of oral valacyclovir or acyclovir along with glucocorticoids for patients with severe facial palsy (algorithm 1), defined as House-Brackmann (H-B) grade IV or higher (table 1). This practice recognizes the high value of a possible, yet unproven, benefit of antiviral therapy in patients who are at higher risk for unfavorable outcomes, and the relatively low potential for harm of a short course of oral antiviral therapy. In patients with milder presentations, we use glucocorticoids alone, although some clinicians may reasonably choose to treat these patients as well. Antiviral therapy alone (without glucocorticoids) is not recommended [1,3,4].

●Dose – Our suggested regimen for antiviral therapy in patients with severe Bell's palsy is valacyclovir 1000 mg three times daily for one week [5]. Acyclovir 400 mg five times daily for 10 days is an alternative to valacyclovir but is less convenient and has inferior bioavailability.

●Side effects – Valacyclovir and acyclovir tend to be well tolerated. In the largest randomized trial, headache was numerically more common with valacyclovir than placebo [5]. Agitation and hallucinations have been described with both agents, especially in older adults. Dose adjustments are required in patients with kidney impairment.

Efficacy – Meta-analyses of randomized trials have found that antivirals alone are not effective for Bell's palsy [6-10]. Conclusions on whether the combination of glucocorticoid plus antiviral therapy improves outcomes over glucocorticoids alone have been less consistent, and most have found a small benefits or no difference with wide confidence intervals [7-11].

In a meta-analysis of 18 trials in 2786 patients with Bell's palsy, treatment with glucocorticoids alone was associated with a reduced risk of unfavorable recovery compared with a control condition (RR 0.69, 95% CI 0.55-0.87), whereas treatment with antiviral agents alone was not (RR 1.14, 95% CI 0.80-1.62) [7]. In pooled data from eight trials, the same meta-analysis found a trend towards a reduced risk of unfavorable recovery for combined antiviral and glucocorticoid treatment compared with glucocorticoid treatment alone, but the outcome just missed statistical significance (RR 0.75, 95% CI 0.56-1.0). In the two largest individual trials, glucocorticoid treatment alone was effective for Bell's palsy, while antiviral therapy showed no benefit when given alone or in combination with glucocorticoids [5,12]. The absolute risk differences for complete recovery for combined therapy versus glucocorticoids alone were 3.4 percent (favoring combined therapy, 95% CI -4.6 to 11.3) in the largest trial (n = 829) [5] and -3.3 percent (favoring glucocorticoids alone, 95% CI -9.7 to 2.7) in the second-largest trial (n = 551) [12]. In comparison, the risk differences for glucocorticoids versus placebo were larger and statistically significant in both trials (15 percent [95% CI 8-21] and 13 percent [95% CI 7-19], respectively) [1,5,12].

A separate meta-analysis of three trials that compared glucocorticoid plus antiviral therapy with glucocorticoids alone found no benefit for motor recovery but reduced risk of late complications for patents with Bell’s palsy of varying degrees of severity [11]. Based on data from the three retained trials (766 patients), the rates of incomplete recovery with combination therapy were similar to recovery with glucocorticoids alone (RR 0.81, 95% CI 0.38-1.74). However, the benefit of antivirals may have been masked by studies that included patients with mild cases and a favorable prognosis, diluting the benefit of the antivirals in patients with severe symptoms. In addition, in trials that reported on complications of severe palsy (two trials, 469 patients), combination therapy lowered the risk of motor synkinesis (eg, "crocodile tears") compared with glucocorticoids alone (RR 0.56, 95% CI 0.36-0.87).

Eye care to prevent corneal injury — All patients with Bell's palsy should be assessed for the completeness of eyelid closure. For those with incomplete closure (ie, sclera remains visible when the patient is asked to close the eye), meticulous eye care is required to prevent corneal injury [2]. In addition to physical exposure due to eyelid weakness, the cornea is at increased risk for dryness and abrasion due to reduced tear production from the lacrimal gland, which is also innervated by the facial nerve.

Eye care includes the following:

●Waking hours – Patients should use artificial tear drops (liquid or gel) four times daily and up to hourly if needed. Gel formulations may cause transient blurry vision when applied. Artificial tears are available over the counter. Formulations with preservatives are safe for use four times a day, but preservative-free formulations are probably safer for more frequent application. (See "Dry eye disease", section on 'Artificial tears'.)

Protective glasses or goggles can be worn to physically protect the eye from external trauma. Some patients may prefer to tape the eyelid closed during the day to prevent exposure, using the same procedure as described for sleep. Patches are generally not recommended because there is a tendency for the eye to open under the patch and expose the cornea.

Patients with refractory eye dryness and exposure symptoms should be referred to ophthalmology for discussion of additional options such as a scleral lens, adhesive moisture chambers, temporary-suture tarsorrhaphy, and gold or platinum eyelid weighting [13]. (See 'Eyelid weights and tarsorrhaphy' below.)

●During sleep – Overnight and during naps, an ointment formulation of artificial tears should be applied to further protect the eye when it is most vulnerable. In addition, the eye can be carefully taped shut using a medical-grade waterproof transparent dressing or tape [13]. The eye should be examined to make sure the eyelid remains completely closed under the dressing. Patching without taping is not generally recommended because the cornea remains exposed under the patch.

Other therapies

●Physical therapy – We do not routinely prescribe physical therapy for newly diagnosed Bell's palsy, since most patients will recover function spontaneously. Nevertheless, physical therapy is often incorporated into multimodal interventions for patients with incomplete recovery. Limited data support the utility of facial exercise therapy for some patients with severe symptoms [14]. (See 'Role of physical and stimulation therapies' below.)

●Surgical decompression (not recommended) – Some have advocated surgical decompression of the facial nerve via open middle cranial fossa craniectomy in severely affected patients with early motor nerve conduction studies (NCS) that show at least 90 percent degeneration of the facial nerve in the first 3 to 14 days after symptom onset, based on results of observational studies [15]. However, this approach for patient selection has not been confirmed prospectively nor widely accepted [2].

Potential serious harms of middle cranial fossa surgery to decompress the labyrinthine segment of the bony facial canal include permanent unilateral hearing loss [16,17]. Other risks include seizures, cerebrospinal fluid leak, and facial nerve injury [18].

A systematic review updated in 2021 found only two small randomized trials comparing surgery and nonsurgical control groups [19]. The methodologic quality of both trials was very low, and there was no difference in outcome between the treatment groups in either trial. The authors concluded that there is insufficient evidence to decide whether surgery for Bell's palsy is beneficial. Similar conclusions were reached in an earlier systematic review from the American Academy of Neurology that identified four nonrandomized, prospective studies comparing patients treated with surgery versus no surgery [16].

FOLLOW-UP CARE — Patients with acute Bell's palsy require follow-up to confirm improvement of facial weakness, monitor for ocular complications, and identify patients with incomplete recovery who may benefit from referral to a multidisciplinary facial nerve clinic [2].

New or worsening symptoms — The weakness in patients with Bell's palsy typically evolves quickly to reach a nadir within one to two days of the onset of symptoms. The timing and pace of early recovery is variable and may wax and wane slightly, but the general course should be one of stability by three weeks and gradual improvement by two to three months.

Worsening facial weakness beyond three weeks of presentation and/or development of any new neurologic symptoms (eg, diplopia, facial numbness, ataxia) should prompt reevaluation for alternative etiologies. Brain magnetic resonance imaging (MRI) with contrast is generally indicated, along with additional studies depending on the clinical presentation (eg, screening laboratories for underlying systemic disease or infection, lumbar puncture). (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on 'Differential diagnosis'.)

Incomplete recovery by three to four months — Patients with incomplete recovery of facial function following Bell's palsy can have varying degrees of facial weakness, hypertonia, and synkinesis, with functional problems related to incomplete eye closure, brow ptosis, and nasal valve collapse [20]. Follow-up is essential (algorithm 1) for eye care, psychologic support, and management of long-term sequelae. (See 'Prognosis' below and 'Management of incomplete or aberrant recovery' below.)

A diagnosis of Bell's palsy is doubtful if some facial function, however small, has not returned within three to four months. If not previously performed, brain MRI and computed tomography (CT) with appropriate technique and slice thickness to image the full course of the facial nerve in the skull base and parotid gland should be obtained in patients with no recovery at this stage. Motor nerve conduction studies (NCS) and electromyography (EMG) can also be used to quantify the degree of axonal damage and assess for evidence of subclinical reinnervation. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on 'Imaging studies' and "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on 'Electrodiagnostic studies'.)

PROGNOSIS

Recovery of facial nerve function — The prognosis of Bell's palsy is very good. Approximately 70 percent of patients are expected to recover spontaneously by three to six months [21], and rates of complete recovery increase to approximately 80 to 85 percent with glucocorticoid treatment [22]. (See 'Glucocorticoids for all patients' above.)

The main risk factor for incomplete recovery is the severity of weakness at presentation using the House-Brackmann (H-B) grading scale (table 1) [21-23]. Other grading systems (eg, the Sunnybrook Facial Grading System [24]) are similar and sometimes favored [25-28].

In a contemporary study of over 1300 adults with Bell's palsy, 70 percent of patients presented with moderate weakness (H-B grade III or IV) and 30 percent had severe weakness (H-B grade ≥V) [22]. On multivariable analysis, severe baseline weakness was associated with approximately 2.5 times the risk of unfavorable outcome, defined as H-B grade ≥III at six-month follow-up (odds ratio [OR] 2.62, 95% CI 1.93-3.57). In absolute terms, 84 percent of patients with moderate weakness improved to H-B grade II or better by six months, compared with 69 percent of those with severe weakness at presentation. Additional baseline clinical factors associated with worse outcome included age ≥40 years, diabetes, and uncontrolled hypertension.

Recovery of facial paresis appears slightly worse in patients who develop the disease during pregnancy. A retrospective study of 77 patients with pregnancy-related Bell's palsy compared recovery outcome in pregnant patients with that of nonpregnant patients [29]. All patients in all groups with incomplete paralysis ultimately recovered satisfactory function. However, more pregnant patients developed complete paralysis (65 versus 50 percent for nonpregnant patients). Pregnant patients (as well as nonpregnant patients) with complete paralysis are less likely to recover satisfactory function than the other groups (52 versus 77 to 88 percent). The fact that pregnant patients are less likely to receive treatment may also contribute to an apparent poorer prognosis [30,31].

Nerve conduction studies (NCS) and electromyography (EMG) of the facial nerve can be used to help predict recovery in patients with severe weakness. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on 'Electrodiagnostic studies'.)

Complications of regeneration — Synkinesia and contractures of the face develop in approximately 15 percent of patients as a late complication of Bell's palsy due to disorganized and misdirected nerve regrowth [21].

Synkinesia refers to involuntary contraction or twitching of part of the facial musculature upon voluntary facial movement. For example, twitching of the angle of the mouth may occur when the patient blinks forcefully, or contracture of the orbicular oculi and narrowing of the palpebral fissure may occur with smiling. Nonmotor synkinesias can also develop due to misdirected autonomic fibers. In the syndrome of gustatory tearing or "crocodile tears," a salivary stimulus results in excess lacrimation. Less commonly, salivation causes facial sweating.

Most synkinesia after Bell's palsy is mild and may not be noticed by the affected individual. More severe or bothersome synkinesia can be treated with botulinum toxin injections. (See 'Botulinum toxin for synkinesias' below.)

Psychological impact — Chronic facial weakness has both physical and psychological implications, with negative effects on socialization and emotional well-being. Facial disfigurement can cause psychosocial distress resulting in decreased quality of life and increased risk for depression and anxiety [32-34]. Patients may suffer from poor self-confidence, phobic avoidance, and social isolation [35]. Of 22,594 patients surveyed at the Edinburgh facial palsy clinic, one-half exhibited a considerable degree of psychological distress and restriction in social activities as a consequence of their facial palsy [36].

Psychosocial distress may also occur in some patients without severe facial weakness. In a meta-analysis of 23 studies reporting quality-of-life outcomes among 3746 patients with peripheral facial weakness, the psychological burden was only weakly correlated with the severity of facial weakness (0.36, 95% CI 0.24-0.46) [37]. Other factors may include older age, female sex, and higher depression or anxiety scores on testing [38-40].

Risk of recurrent Bell's palsy — Recurrent attacks of Bell's palsy on either the ipsilateral or contralateral side have been observed in 7 to 15 percent of patients [41-44]. In one of the larger natural history studies with prolonged follow-up, the mean time to recurrence was approximately 10 years [44]. Due to the rarity, alternative etiologies should also be considered at the time of recurrence. In one referral center series, one-quarter of 53 patients with recurrent Bell's palsy were found to have an alternative etiology, most commonly Melkersson-Rosenthal syndrome, neurosarcoidosis, or facial nerve schwannoma [45]. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on 'Melkersson-Rosenthal syndrome'.)

Pregnancy may be a risk factor for recurrence of Bell's palsy [46]. Additional risk factors are not well defined. Some patients with recurrent attacks have a family history of multiple attacks, suggesting a genetic predisposition to Bell's palsy. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on 'Epidemiology'.)

MANAGEMENT OF INCOMPLETE OR ABERRANT RECOVERY — Patients with incomplete or aberrant recovery may benefit from a multimodality approach and referral to facial plastic and reconstructive surgery. Patients with persistent severe deficits may be candidates for chemodenervation with botulinum toxin injections and selective surgical procedures to improve function and appearance [13,20,47].

Botulinum toxin for synkinesias — Botulinum toxin injections may benefit patients with synkinesis, facial spasm, or hyperlacrimation ("crocodile tears") [20,48,49].

In facial synkinesis, botulinum toxin is used to selectively inhibit muscle contractility. Common facial muscle targets include the orbicularis oculi, depressor anguli oris, depressor labii inferioris, mentalis, and platysma [50]. Some patients develop compensatory hyperfunction and hypertrophy in the contralateral side of the face that may also be targeted with botulinum toxin to improve symmetry.

Eyelid weights and tarsorrhaphy — Insertion of a gold or platinum weight into the upper eyelid is the most common dynamic technique used to treat persistent severe lagophthalmos after Bell's palsy. Platinum weights are smaller than gold implants and may be less allergenic and prone to extrusion [13]. Lower eyelid lag may also need to be addressed in patients with severe paralysis by suspension or augmentation techniques. Palpebral springs may be an option in patients who fail eyelid weights.

Cosmetic procedures — Brow ptosis due to prior Bell's palsy can exacerbate lagophthalmos and contribute to poor cosmetic recovery. Correction via brow lift procedures may enhance facial symmetry and cosmetic appearance [20]. Cosmetic and functional improvement may be possible with facial reanimation surgery, although it is rarely done [20,51-53].

Role of physical and stimulation therapies — Physical therapy encompasses a range of interventions for Bell's palsy, including but not limited to facial exercises, mime therapy, massage, electrical stimulation, acupuncture, heat therapy, and biofeedback. Although not supported by high-quality data, physical therapy is an integral component of most multidisciplinary care plans in patients with severe weakness and incomplete recovery [50].

A systematic review of physical therapy for Bell's palsy identified 12 controlled trials with 872 participants, including four trials of electrical stimulation, three of exercises, and five of acupuncture compared or combined with another form of physical therapy [54]. Facial exercises did not reduce the proportion of patients with incomplete recovery at six months. One low-quality trial reported that facial exercises reduced the rate of synkinesis at three months. Another low-quality trial of 34 subjects with persistent facial palsy that lasted more than nine months found that exercises (mime therapy) led to some improvement in facial function at one year. Similarly, studies of electrical stimulation or acupuncture have failed to find significant benefit or harm. However, a subsequent trial has reported benefit of electrical simulation on facial nerve disability scores and electrophysiologic outcomes for some patients with Bell’s palsy [55].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bell's palsy".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Bell's palsy (The Basics)")

●Beyond the Basics topic (see "Patient education: Bell's palsy (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Definition and pathogenesis – Bell's palsy, also referred to as idiopathic facial nerve palsy or facial nerve palsy of suspected viral etiology, is the most common cause of acute spontaneous peripheral facial paralysis. Inflammation, nerve edema, and herpes simplex virus (HSV) reactivation are thought to play a role in pathogenesis in most patients. (See 'Introduction' above.)

●Initial treatment

•Glucocorticoids for all patients – For all patients with new-onset Bell's palsy, we recommend oral glucocorticoids (Grade 1B). Early treatment (eg, within three days of symptom onset) increases the rate of complete recovery. We typically treat patients who are within seven days of symptom onset. Our suggested regimen is prednisone (60 to 80 mg/day) for one week without a taper. (See 'Glucocorticoids for all patients' above.)

•Antiviral therapy for patients with severe palsy – For patients with severe facial palsy at presentation, defined as House-Brackmann grade IV or higher (table 1), we suggest adjunctive oral antiviral therapy rather than glucocorticoids alone (Grade 2C). The benefit of antiviral therapy for recovery is uncertain, but treatment appears to be safe in most people. The usual regimen is valacyclovir 1000 mg three times daily for one week. Acyclovir (400 mg five times daily for 10 days) is an alternative to valacyclovir but is less convenient and has inferior bioavailability. (See 'Antiviral therapy for severe symptoms' above.)

•Prevent corneal injury – We assess all patients for the completeness of eye closure. For those with incomplete closure, we advise meticulous eye care to prevent corneal injury (see 'Eye care to prevent corneal injury' above):

-Waking hours – Apply artificial tears (liquid or gel) four times daily and up to hourly if needed and eye protection (eg, glasses or goggles) to protect from trauma.

-During sleep – Apply artificial tears ointment and tape the eyelid shut. We advise not using an eye patch without taping as this leaves the cornea exposed.

We instruct patients to monitor for and report any ocular complications (eg, corneal abrasion, foreign body injury).

●Follow-up management – For patients whose symptoms worsen >3 weeks from symptom onset and for those with incomplete recovery at three to four months, we advise further evaluation to exclude other causes of facial palsy and to identify opportunities for additional treatment. (See 'Follow-up care' above.)

Patients with incomplete or aberrant recovery may be candidates for botulinum toxin injections or selective surgical procedures to improve function and appearance. (See 'Management of incomplete or aberrant recovery' above.)

●Prognosis – The prognosis of Bell's palsy is very good. Approximately 80 to 85 percent experience a full recovery of facial nerve function by six months. The main risk factor for incomplete recovery is severity of weakness at the time of presentation (table 1). Synkinesias due to aberrant or disorganized nerve regrowth affect approximately 15 percent of patients. (See 'Prognosis' above.)