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19/5/2020 Bell's palsy: Treatment and prognosis in adults - UpToDate

Official reprint from UpToDate®


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Bell's palsy: Treatment and prognosis in adults


Author: Michael Ronthal, MD
Section Editor: Jeremy M Shefner, MD, PhD
Deputy Editor: April F Eichler, MD, MPH

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Apr 2020. | This topic last updated: Nov 05, 2019.

INTRODUCTION

Bell's palsy is the appellation commonly used to describe an acute peripheral facial palsy of unknown
cause. However, the terms "Bell's palsy" and "idiopathic facial paralysis" may no longer be considered
synonymous, as herpes simplex virus activation is the likely cause of Bell's palsy in most cases. A
peripheral facial palsy is a clinical syndrome of many causes, and evaluation requires more than a
superficial examination.

This review will discuss the treatment and prognosis of Bell's palsy (ie, idiopathic facial nerve palsy or
facial nerve palsy of suspected viral etiology). Other clinical aspects of this disorder are reviewed
separately. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults".)

The treatment of facial nerve palsy related to Lyme disease is discussed elsewhere.

ACUTE TREATMENT

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

Glucocorticoid and antiviral therapy — We recommend early treatment with oral glucocorticoids for
all patients with idiopathic facial nerve palsy (Bell's palsy) or facial nerve palsy of suspected viral
etiology, consistent with current guidelines [1-4]. Treatment should preferably begin within three days of
symptom onset. Our suggested regimen is prednisone (60 to 80 mg/day) for one week.

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The suspicion that Bell's palsy is caused by herpes simplex virus in most patients led to trials of antiviral
therapy. Compared with placebo, these trials found no benefit for antiviral therapy alone. However, it is
possible, but not proven, that the addition of antivirals to glucocorticoids is beneficial, particularly for the
subgroup of patients with severe facial palsy, defined as House-Brackmann grade IV or higher (table 1).
Until certainty is reached, we suggest early combined therapy with prednisone (60 to 80 mg per day)
plus valacyclovir (1000 mg three times daily) for one week for patients with severe facial palsy at
presentation, defined as House-Brackmann grade IV or higher (table 1). Acyclovir (400 mg five times
daily for 10 days) is an alternative to valacyclovir but is less convenient and has inferior bioavailability.

The evidence for glucocorticoid and antiviral therapy is presented in the next sections.

Meta-analyses — A number of meta-analyses have evaluated trials testing glucocorticoids and


antiviral therapy for Bell's palsy [5-9]. Across studies, there is consistency in the conclusion that
glucocorticoids reduce the risk of incomplete recovery of facial nerve function by approximately 30 to 40
percent compared with no glucocorticoids or antivirals alone. In a meta-analysis that included seven
trials in 895 patients, the absolute rate of incomplete recovery was 17 percent with glucocorticoids and
28 percent with no glucocorticoids (number needed to treat to avoid one incomplete recovery, 10, 95%
CI 6-20) [9].

Conclusions on whether the combination of glucocorticoids plus antivirals improves outcomes over
glucocorticoids alone have been less consistent, and most have found no clear difference and wide
confidence intervals. The following examples illustrate the range of the findings:

● In a meta-analysis involving 18 trials and 2786 patients, treatment with glucocorticoids alone was
associated with a reduced risk of unfavorable recovery compared with a control condition (relative
risk [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) [5]. 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).

● A separate meta-analysis identified three trials at low risk of bias comparing glucocorticoid plus
antiviral therapy with glucocorticoids alone in patients with Bell's palsy of varying degrees of
severity; 10 other trials were excluded due to multiple sources of bias [10]. Based on data from the
three retained trials (766 patients), there was no clear difference in rates of incomplete recovery
with combination therapy compared with glucocorticoids alone (RR 0.81, 95% CI 0.38-1.74). In
trials that reported on complications of severe palsy (two trials, 469 patients), combination therapy
lowered the risk of motor synkinesis or crocodile tears compared with glucocorticoids alone (RR
0.56, 95% CI 0.36-0.87). For the subgroup of patients with severe palsy (two trials, 98 patients),

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combination therapy had no clear effect on incomplete recovery at month 6 compared with
glucocorticoids alone, although the result was again imprecise (RR 0.82, 95% CI 0.57-1.17).

Methodologic differences probably account for differences in precision in these two meta-analyses.
Neither excludes the possibility of marginal benefit when antiviral therapy is combined with
glucocorticoids. However, the trend towards benefit was driven largely by the smaller, lower-quality
trials.

Randomized trials — Randomized trials have established the effectiveness of early short-term oral
glucocorticoid treatment for idiopathic facial nerve palsy (Bell's palsy) or facial nerve palsy of suspected
viral etiology [11-17]. In the two highest-quality trials, glucocorticoid treatment alone was effective for
Bell's palsy, while antiviral treatment showed no benefit when given alone or when combined with
glucocorticoids [15,17].

● The largest trial studied 829 adults with Bell's palsy who were randomly assigned within 72 hours of
onset to one of four treatment groups [17]:

• Placebo plus placebo.

• Prednisolone (60 mg daily for five days, then tapered by 10 mg daily, for a total treatment
length of 10 days) plus placebo.

• Valacyclovir (1000 mg three times daily for seven days) plus placebo.

• Prednisolone (10 days) plus valacyclovir (seven days).

• At one-year follow-up, the time to complete recovery of facial function was significantly shorter
for patients treated with prednisolone compared with those not treated with prednisolone
(hazard ratio [HR] 1.4, 95% CI 1.18-1.64) [17]. By contrast, time to recovery was no different
for patients treated or not treated with valacyclovir (HR 1.01, 95% CI 0.85-1.19). Furthermore,
time to recovery with the addition of valacyclovir to prednisolone was no better than with
prednisolone alone. In a separate analysis, treatment with prednisolone significantly reduced
the proportion of patients at one year with mild and moderate sequelae (ie, facial asymmetry,
facial weakness, and synkinesis) [18].

● An earlier trial evaluated 551 adults (age 16 or older) who were recruited within 72 hours after
symptom onset and assigned to 10 days of treatment with either oral prednisolone (25 mg twice
daily), acyclovir (400 mg five times daily), both prednisolone and acyclovir, or placebo [15].
Outcome data were available for 496 patients. The following observations were noted:

• The primary outcome measure, complete recovery of facial function, was significantly more
likely for patients assigned to treatment with prednisolone than for those not assigned to
prednisolone at both three months (83 versus 64 percent, adjusted OR 2.44, 95% CI 1.55-
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3.84) and nine months (94 versus 82 percent, adjusted OR 3.32, 95% CI 1.72-6.44) [15]. The
corresponding number needed to treat to achieve one additional complete recovery was six
and eight at the two time periods.

• There was no significant difference in the rate of complete facial recovery for patients assigned
to acyclovir (400 mg five times daily) compared with those not assigned to acyclovir at either
three months (71 versus 76 percent, adjusted OR 0.86, 95% CI 0.55-1.32) or nine months (85
versus 91 percent, adjusted OR 0.61, 95% CI 0.33-1.11) [15]. Similarly, there was no additional
benefit of combined acyclovir and prednisolone treatment compared with prednisolone alone.

The results of other lower-quality trials have suggested benefit or a trend towards benefit for antiviral
therapy combined with glucocorticoids [11,14,16,19]. The largest such trial randomly assigned 221
patients within seven days of Bell's palsy onset to treatment with either valacyclovir (500 mg twice daily
for five days) plus oral prednisolone or placebo plus oral prednisolone [14].

● The rate of complete recovery was significantly higher in the combined valacyclovir plus
prednisolone group than in the placebo plus prednisolone group (97 versus 90 percent).

● A subgroup analysis found that the benefit of combined therapy correlated with increasing severity
of baseline facial palsy.

The strength of these results is limited by methodologic issues, including lack of blinding among
outcome assessors and a relatively high dropout rate of 25 percent [20].

Eye care — In severe cases of Bell's palsy, the cornea may be at risk because of poor eyelid closure
and reduced tearing. This may result in corneal drying and abrasion, with an associated risk of visual
loss [21]. The presence of corneal sensory loss due to concomitant fifth cranial neuropathy, although
unusual, increases the risk of corneal trauma and visual loss. Therefore, we recommend protective
measures for patients with inadequate eye closure [4].

Artificial tears are available without a prescription in liquid, gel, and ointment forms (see "Dry eye
disease", section on 'Artificial tears'). Liquid or gel formulations of artificial tears should be applied every
hour while the patient is awake, and ointment formulations (eg, Soothe), which contain mineral oil and
white petrolatum, should be used at night [22]. Protective glasses or goggles should be prescribed.
Patches can be used at night, but tape should not be placed directly on the eyelid since the patch could
slip and abrade the cornea. Rarely, tarsorrhaphy or temporary implantation of a gold weight into the
upper lid is required.

Other interventions — There is a lack of high-quality evidence to support interventions such as


physical therapies or surgical facial nerve decompression for the treatment of Bell's palsy. Nevertheless,
physical therapy is often incorporated into multimodal interventions for patients with incomplete
recovery. (See 'Management of incomplete recovery' below.)
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Physical therapy — Physical therapy encompasses a host of different interventions for Bell's palsy,
including but not limited to exercises, mime therapy, massage, electrical stimulation, acupuncture, heat
therapy, biofeedback, and combinations. A systematic review of physical therapy for Bell’' palsy updated
in 2011 identified 12 controlled trials with 872 subjects, including four trials of electrical stimulation, three
of exercises, and five of acupuncture compared or combined with another form of physical therapy [23].
The methodologic quality of the trials ranged from low to moderate; none were high. The following
observations were reported:

● 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 (ie, involuntary
movement of the ipsilateral face during volitional movement of another area of the face, which is
caused by aberrant regeneration of facial nerve fibers) 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.

● No significant benefit or harm was found from electrical stimulation or acupuncture.

Surgical decompression — The issue of surgical decompression of the facial nerve is mentioned
only for discussion, as it is not a currently recommended treatment. A systematic review updated in
2013 found only two small randomized trials comparing surgery and nonsurgical control groups [24].
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 or harmful. 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 [25].

Permanent unilateral hearing loss is the most common serious side effect among patients undergoing
facial nerve decompression [24,25]. Other risks reported with middle cranial fossa craniectomy include
seizures, leakage of cerebrospinal fluid, and facial nerve injury [22].

An uncontrolled study suggested that decompression may be of benefit in patients with profound facial
nerve dysfunction [26], and surgical middle cranial fossa decompression of the labyrinthine segment of
the facial nerve has been advocated in patients with motor nerve conduction studies (NCS) that show at
least 90 percent degeneration of the facial nerve. (See "Bell's palsy: Pathogenesis, clinical features, and
diagnosis in adults", section on 'Electrodiagnostic studies'.)

However, the results of motor NCS cannot dictate when to operate since test results begin to show
abnormalities 72 hours after neural degeneration, a time too late for treatment [27]. In addition, surgical
decompression should not be undertaken if facial paralysis has been present for 14 or more days, since
severe degeneration of the facial nerve is probably irreversible after two to three weeks [28].

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PROGNOSIS

The prognosis of Bell's palsy is related to the severity of the lesion [29]. A simple rule is that clinically
incomplete lesions tend to recover. The House-Brackmann grading system (table 1) was devised both
as a clinical indicator of severity and also an objective record of progress [30]. On this scale, grades I
and II have good outcomes, grades III and IV characterize moderate dysfunction, and grades V and VI
portend a poor result. Other grading systems (eg, the Sunnybrook facial grading system [31]) are similar
and sometimes favored [32-35].

Statistically, the natural history without treatment was described in a study of 1011 patients in 1982 [36].
One-third had an incomplete paralysis, and two-thirds had complete paralysis. Overall, 85 percent
showed signs of recovery within three weeks, 71 percent had complete recovery, 13 percent had slight
sequelae, and 16 percent had residual weakness, synkinesis, and/or contracture. Patients with
incomplete lesions had a 94 percent rate of return to normal function, while only 60 percent of those
with clinically complete lesions returned to normal function. In one report, herpes zoster was associated
with more severe paresis and a worse prognosis compared with "idiopathic" Bell's palsy [37].

The prognosis is favorable if some recovery is seen within the first 21 days of onset [38]. A diagnosis of
Bell's palsy is doubtful if some facial function, however small, has not returned within three to four
months. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on
'Diagnosis'.)

In severe lesions that recover, the outgrowth of new axons from the injury site is not discretely directed
but is disorganized and misdirected; on volitional activation of the facial nerve, a mass action of facial
musculature or synkinesis ensues. Thus, on blinking there is twitching of the angle of the mouth, and on
smiling the eye may close or wink. Similarly, with misdirected autonomic fibers, a salivary stimulus may
result in excess lacrimation, the syndrome of "crocodile tears."

Recurrence — Recurrent attacks of idiopathic facial palsy on either the ipsilateral or contralateral side
have been observed in 7 to 15 percent of patients [39-42]. In one of the largest series, which followed
1980 patients with Bell's palsy, the following observations were reported [42]:

● The recurrence rate was 7 percent, and the mean time to recurrence was approximately 10 years.

● A third or fourth attack was unusual, occurring in 3 and 1.5 percent of cases, respectively.

● Recurrence did not portend a worse prognosis for recovery. None of the patients with recurrent
Bell's palsy who were imaged by head computed tomography (CT) had a facial nerve neuroma. In
addition, 77 patients were followed for a mean of 33 years (range 2.8 to 60 years) after the initial
episode, and none developed signs of a tumor or showed progressive facial nerve dysfunction.

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Pregnancy may be a risk factor for recurrence of Bell's palsy [43]. 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'.)

The differential diagnosis of recurrent facial nerve palsy includes the Melkersson-Rosenthal syndrome,
characterized by facial paralysis, episodic facial swelling, and a fissured tongue. (See "Bell's palsy:
Pathogenesis, clinical features, and diagnosis in adults", section on 'Melkersson-Rosenthal syndrome'.)

MANAGEMENT OF INCOMPLETE RECOVERY

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 [44]. Follow-up is essential (algorithm 1) for eye care, psychologic
support, and management of long-term sequelae related to Bell's palsy [44].

As discussed separately, neuroimaging is warranted if there is slow progression of facial weakness


beyond three weeks, or if there is no improvement at four months. (See "Bell's palsy: Pathogenesis,
clinical features, and diagnosis in adults", section on 'Imaging studies'.)

A multidisciplinary approach may be helpful for patients with persistent severe deficits by incorporating
chemodenervation with botulinum toxin injections and selective surgical procedures [45]. Specific
interventions include the following:

● Botulinum toxin injections may benefit patients with synkinesis, facial spasm, or hyperlacrimation
("crocodile tears") [44,46,47].

● Brow ptosis correction may enhance facial symmetry and cosmetic appearance [44].

● Weight insertion into the upper eyelid and suspension of the lower eyelid or tarsorrhaphy can
improve eye closure [44].

Cosmetic and functional improvement may be possible with facial reanimation surgery, although it is
rarely done [44,48-50].

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


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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 5th to 6th 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 10th to 12th 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

● In severe cases of Bell's palsy, the cornea may be at risk because of poor eyelid closure and
reduced tearing. For patients with inadequate eye closure, we recommend proper eye protection
measures (Grade 1C). (See 'Eye care' above.)

● For all patients with idiopathic facial nerve palsy (Bell's palsy) or facial nerve palsy of suspected
viral etiology, we recommend early treatment with oral glucocorticoids (Grade 1A). Treatment
should preferably begin within three days of symptom onset. Our suggested regimen is prednisone
(60 to 80 mg/day) for one week. (See 'Glucocorticoid and antiviral therapy' above.)

● For the subgroup of patients with severe facial palsy at presentation, defined as House-Brackmann
grade IV or higher (table 1), we suggest early combined therapy with prednisone (60 to 80 mg per
day) plus valacyclovir (1000 mg three times daily) for one week rather than glucocorticoids alone
(Grade 2B). Acyclovir (400 mg five times daily for 10 days) is an alternative to valacyclovir but is
less convenient and has inferior bioavailability. (See 'Glucocorticoid and antiviral therapy' above.)

● The treatment of facial nerve palsy related to Lyme disease (neuroborreliosis) is discussed
elsewhere.

● The prognosis of Bell's palsy is related to the severity of the lesion. A simple rule is that clinically
incomplete lesions tend to recover. The prognosis is favorable if some recovery is seen within the
first 21 days of onset. (See 'Prognosis' above.)

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● Follow-up is essential for eye care, psychologic support, and management of long-term sequelae
related to Bell's palsy. Botulinum toxin injections may be helpful for patients with incomplete
recovery. (See 'Management of incomplete recovery' above.)

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42. Pitts DB, Adour KK, Hilsinger RL Jr. Recurrent Bell's palsy: analysis of 140 patients. Laryngoscope
1988; 98:535.
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43. McGregor JA, Guberman A, Amer J, Goodlin R. Idiopathic facial nerve paralysis (Bell's palsy) in
late pregnancy and the early puerperium. Obstet Gynecol 1987; 69:435.

44. Eviston TJ, Croxson GR, Kennedy PG, et al. Bell's palsy: aetiology, clinical features and
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management of the paralyzed face. Laryngoscope 2006; 116:1385.

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facial synkinesis and hyperlacrimation. Acta Neurol Scand 2007; 115:271.

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treatment of crocodile tears. Ophthal Plast Reconstr Surg 2006; 22:453.

48. Douglas RS, Gausas RE. A systematic comprehensive approach to management of irreversible
facial paralysis. Facial Plast Surg 2003; 19:107.

49. Labbé D, Bénateau H, Bardot J. [Surgical procedures for labial reanimation in facial paralysis].
Ann Chir Plast Esthet 2002; 47:580.

50. Jowett N, Hadlock TA. Contemporary management of Bell palsy. Facial Plast Surg 2015; 31:93.

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GRAPHICS

Management of Bell's palsy

* House-Brackmann classification of facial nerve dysfunction (refer to UpToDate text for complete description):
1. Normal
2. Mild dysfunction
3. Moderate dysfunction
4. Moderately severe dysfunction
5. Severe dysfunction
6. Total paralysis
¶ Acyclovir (400 mg 5 times daily for 10 days) is an alternative to valacyclovir but is less convenient and has inferior bioavailability.

Adapted from: de Almeida JR, Guyatt GH, Sud S, et al. Management of Bell palsy: clinical practice guideline. CMAJ 2014; 186:917.

Graphic 109357 Version 2.0

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House-Brackmann classification of facial nerve dysfunction

Grade Characteristics

I. Normal Normal function in all areas

II. Mild dysfunction Gross


Slight weakness noticeable on close inspection
May have slight synkinesis
Normal symmetry and tone at rest

Motion
Forehead: Moderate to good function
Eye: Complete closure with minimal effort
Mouth: Slight asymmetry

III. Moderate dysfunction Gross


Obvious but not disfiguring difference between the two sides
Noticeable but not severe synkinesis, contracture, or hemifacial spasm
Normal symmetry and tone at rest

Motion
Forehead: Slight to moderate movement
Eye: Complete closure with effort
Mouth: Slightly weak with maximum effort

IV. Moderately severe dysfunction Gross


Obvious weakness and/or disfiguring asymmetry
Normal symmetry and tone at rest

Motion
Forehead: None
Eye: Incomplete closure
Mouth: Asymmetric with maximum effort

V. Severe dysfunction Gross


Only barely perceptible motion
Asymmetry at rest

Motion
Forehead: None
Eye: Incomplete closure
Mouth: Slight movement

VI. Total paralysis No movement

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Contributor Disclosures
Michael Ronthal, MD Nothing to disclose Jeremy M Shefner, MD, PhD Grant/Research/Clinical Trial Support:
Biogen Idec; Cytokinetics; Amylyx; Orphazyme; Brainstorm; MT Pharma America; Medicinova [ALS].
Consultant/Advisory Boards: Cytokinetics; Mitsubishi Tanabe Pharma America; AveXis; Pinteon; Neurosense
[ALS]. April F Eichler, MD, MPH Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be provided
to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate
standards of evidence.

Conflict of interest policy

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