The Journal for Nurse Practitioners 18 (2022) 159e163

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The Journal for Nurse Practitioners

journal homepage: www.npjournal.org

Diagnosis and Management of Bell’s Palsy in Primary Care

Jimmy Ho, Ashley Markowsky

a b s t r a c t
Keywords: Bell’s palsy is characterized by rapid, unilateral paralysis of cranial nerve VII and is the most common cause of
antivirals acute facial paralysis, although the pathogenesis of the condition is poorly understood. Bell’s palsy can be
Bell’s palsy
managed by the nurse practitioner in primary care, and the majority of clients achieve full recovery.
corticosteroids
facial palsy
Appropriate diagnosis through history and physical examination to exclude other causes allows for timely
facial synkinesis diagnosis, intervention, and patient reassurance. Pharmacologic and adjunctive treatment is available to
shorten the duration and improve symptoms. Nurse practitioners should be able to identify circumstances in
which referral to a specialist for intervention and follow-up may be appropriate.
© 2021 Elsevier Inc. All rights reserved.

Bell’s palsy, also referred to as idiopathic facial paralysis, is the the NP. The facial nerve (CNVII) innervates facial muscles, the sta-
most common cause of unilateral peripheral facial paralysis. The pedius muscle, taste to the anterior two thirds of the tongue, salivary
onset of Bell’s palsy is acute and affects the lower motor neuron tract and lacrimal gland secretion, and general sensory fibres from the
of the face, resulting in facial paralysis that resolves gradually over a posterior ear canal and tympanic membrane.1,4 The facial nerve has 3
few months.1,2 Additional associated symptoms include post- portions: the intracranial, intratemporal, and extratemporal por-
auricular pain, hyperacusis, dry eye, dry mouth, and altered sense of tions. Sensory and parasympathetic fibers of the facial nerve arise
taste.2 Facial paralysis can be challenging to diagnose in the primary from the nervus intermedius, and the motor branch of the facial
care setting because there are many differential diagnoses to be nerve originates from the facial nerve nucleus in the pons.9 The facial
considered including Ramsay Hunt syndrome type 2, Lyme disease, nerve exits the brainstem and enters the internal auditory canal of
viral infections, trauma, tumors, and neurologic causes, such as a the temporal bone and is joined by the vestibulocochlear nerve
cerebrovascular accident (CVA).3,4 The nurse practitioner (NP) needs (CNVIII) in the internal auditory canal. After exiting the internal
to be aware of how to differentiate Bell’s palsy from other more auditory canal, the facial nerve runs consecutively through the
concerning disease processes in order to appropriately manage the labyrinthine, tympanic, and mastoid segments, with the labyrinthine
patient and improve positive outcomes for symptom resolution. segment extending to the geniculate ganglion. Here the first branch
of the facial nerve, the greater petrosal nerve, emerges from the
Background geniculate ganglion and innervates the lacrimal gland. The tympanic
segment runs from the geniculate ganglion to the mastoid segment
Bell’s palsy is named after Sir Charles Bell, who detailed and and then to the stylomastoid foramen.10 In the mastoid segment, the
outlined idiopathic facial paralysis. Bell’s palsy affects the facial nerve innervates the stapedius muscle and chorda tympani. The
nerve (ie, cranial nerve VII [CNVII]).1 Bell’s palsy affects both males chorda tympani is responsible for taste to the anterior two thirds of
and females equally and occurs across the life span with increased the tongue and supplies secretomotor fibers to the sublingual and
incidence in ages 15 to 45 years.5 Approximately 25 to 30 people submandibular glands.5 As the nerve exits the stylomastoid foramen
per 100,000 are diagnosed annually in the United States with Bell’s into the extratemporal region, it gives rise to the posterior auricular
palsy, comprising up to 70% of acute unilateral facial paralysis nerve branch and further extends into the parotid gland, forming the
complaints.1,6 Risk factors include pregnancy, preeclampsia, parotid plexuses that consist of 5 major branches: the frontal,
immunocompromise, hypertension, obesity, recent upper respira- zygomatic, buccal, marginal mandibular, and cervical branches.
tory tract infection, diabetes, and birth trauma in infants.5,7,8 These branches innervate the muscles for facial expression.11

Anatomy of the Facial Nerve Etiology and Pathophysiology

To understand the pathophysiology of Bell’s palsy, knowledge of The etiology of Bell’s palsy remains unclear, and diagnosis is
the anatomy of the facial nerve and its pathways is important for based on exclusion. Proposed causes include infection, anatomic

https://doi.org/10.1016/j.nurpra.2021.10.019
1555-4155/© 2021 Elsevier Inc. All rights reserved.
160 J. Ho, A. Markowsky / The Journal for Nurse Practitioners 18 (2022) 159e163

anomalies, inflammatory disorders, cold stimulation, and required and include the presence of unilateral versus bilateral
ischemia.12 The most accepted cause of Bell’s palsy is a viral facial paralysis, dry eye, posterior auricular pain, altered taste,
infection from herpes simplex virus 1 (HSV-1).5 HSV-1 is a double- decreased tearing, and questions specific to red flag conditions.2
stranded, linear DNA that enters the body through mucous mem- The top differential diagnoses to consider include Ramsay Hunt
branes and lays dormant in the ganglia of the peripheral nerves syndrome type 2, also known as herpes zoster oticus, which is
until it is reactivated. The labyrinthine segment, the narrowest characterized by facial paralysis; otalgia and retro-orbital pain; the
portion of the facial canal, is believed to be the most probable spot presence of vesicles or a rash near the ear or external auditory
for facial nerve inflammation.12 HSV-1 reactivation results in canal, tinnitus, vertigo, hearing loss, and involvement of CNVIII; and
inflammation of the facial nerve, causing edema, compression, Lyme diseaseeassociated facial paralysis, which is associated with
ischemia, and degeneration of the nerve, which is apparent in the an environment endemic to ticks, systemic symptoms, and the
symptoms of facial motor weakness and paralysis.6,13 presence of erythema migrans.2,17 Red flag conditions include CVA
with acute-onset symptoms of unilateral facial droop, slurred
Clinical Presentation speech and hemiplegia, and neoplasm, which may present as
recurrent history of facial paralysis with no improvement.11,13
Bell’s palsy presents as acute, unilateral, lower motor facial pa-
ralysis with onset occurring over 48 to 72 hours. Associated
symptoms include hyperacusis, dry eye, posterior auricular pain,
altered taste, and decreased tearing. Recovery begins within 4 Physical Examination
weeks.2 Facial nerve paralysis causes weakness in the orbicularis
oculi, resulting in blink dysfunction and ectropion. Consequences of The NP needs to distinguish between a peripheral or central
this dysfunction are decreased tear production and lid retraction cause of facial nerve palsy with a physical examination. The mus-
with associated symptoms of dry eye, tearing, lagophthalmos, and cles of the forehead are innervated by both motor cortexes. Find-
keratitis.6,14,15 Red flag findings that are not consistent with Bell’s ings for peripheral facial palsy include both the upper and lower
palsy and warrant further investigation include severe pain, sys- portions of the face. Bell’s palsy causes paralysis of the forehead, so,
temic symptoms, a history of cancer, a history of Lyme disease if the forehead is spared, this would point to a possible red flag
exposure, or a rash on the external ear.2 diagnosis of CVA.18 Testing of cranial nerves is essential in the
diagnosis of Bell’s palsy, which should yield normal findings aside
Diagnosis from an abnormal facial nerve. The focus of the examination should
be on CNVII with the ability to smile and close both eyes, noting
Differentials unilateral involvement resulting in asymmetry of the face and
including the forehead on the affected side.18 The eye should be
There are a multitude of differentials for the diagnosis of facial evaluated for any palsy deficits such as lagophthalmos, ptosis,
nerve paralysis. The most common cause of facial palsy is Bell’s conjunctival injection, corneal abrasion, and keratitis.14,19 Otologic
palsy, which is generally considered idiopathic, although it is also and tuning fork examination should be conducted to rule out oto-
hypothesized to be caused by a viral infection of HSV-1. Differential logic causes such as cholesteatoma, otitis media, or Ramsay Hunt
diagnoses of facial nerve palsy are infectious causes, including most syndrome type 2.16 The NP should examine the affected side of the
commonly herpes simplex virus, varicella zoster virus resulting in mouth for oral incompetence and the oral mucosa for a fissured
Ramsay Hunt syndrome type 2, Lyme disease, and human immu- tongue, which is consistent with Melkersson-Rosenthal syndrome,
nodeficiency virus.5 Differential diagnoses that are related to and the nasolabial fold for effacement, which is consistent with
neurologic causes include most commonly CVA, multiple sclerosis, facial paralysis.2,6 The NP should palpate the neck and mastoid
pontine malformations, mononeuritis multiplex, and benign or process for masses and conduct a skin examination for rashes,
malignant neoplastic tumors. Inflammatory causes include nodules, or vesicles to rule out Lyme disease and Ramsay Hunt
sarcoidosis, amyloidosis, Melkersson-Rosenthal syndrome, Guil- syndrome type 2.6 A more general neurologic examination should
 syndrome, systemic lupus erythematosus, Behcet dis-
lain-Barre be performed, including an assessment of limbs for unilateral
ease, and Sjogren syndrome.6,15,16 Otologic causes for facial palsy weakness and pronator drift, as well as symptoms of ataxia,
include otitis media, cholesteatoma, and malignant otitis externa. confusion, aphasia, pupils, and visual deficits to aid in ruling out
Lastly, additional causes of facial nerve palsy can be related to CVA.11
traumatic causes, such as trauma to the temporal bone or trauma to If the history and physical examination are consistent with Bell’s
the facial nerve from previous surgeries.4 palsy, noting the extent of deficits should be considered. The most
common grading criteria for evaluating the severity of Bell’s palsy
History deficits is the House-Brackmann facial paralysis scale and can be
used to predict rates of recovery in the patient at 6 to 12 months.19
Bell’s palsy is a diagnosis of exclusion and requires a concise This scale grades the degree of symmetry or asymmetry of the face
history and physical. The practitioner should inquire about acute and gross motor function of the forehead, mouth, and eyes on a
symptom onset within the last 48 to 72 hours and if there was a scale from 1 to 6 indicating the severity of the symptoms exhibited.
presence of a viral prodrome before symptom onset. The NP should Grades of 1 to 2 are mild symptoms with a great prognosis, whereas
ask the patient if they have had any recent trauma, infection, or a score of 3 to 4 suggests a moderate severity of symptoms, and
facial surgeries to assess any underlying etiology for the facial nerve grades of 5 to 6 encompass severe deficits that are more likely to
palsy.7 Past medical history such as autoimmune disorders may result in poorer prognosis for the patient.1,4 The House-Brackmann
indicate an alternate cause of facial paralysis.16 The NP should scale is subjective and relies on the clinician’s interpretation of
assess risk factors for Bell’s palsy, including pregnancy, history of deficits and is prone to misinterpretation and interobserver vari-
diabetes, recent upper respiratory tract infections, and if the patient ability; however, it is still a fixture in clinical practice to assess facial
is immunocompromised.5,8 The NP should carefully attempt to rule paralysis severity.1 A benefit to NPs in practice is that this scale is
out differential diagnoses and red flag conditions for facial nerve easily accessible for free online through a simple search on the
palsy. A detailed history of symptoms related to facial nerve palsy is Internet.
 J. Ho, A. Markowsky / The Journal for Nurse Practitioners 18 (2022) 159e163 161

Diagnostics such as dexamethasone, that can cross the placenta. There is

minimal available evidence linking prednisone to teratogenicity in
Bell’s palsy diagnosis is based on exclusion, and diagnostics are pregnancy, thus standard dosing of prednisone can be used for
not necessary unless required to rule out other differential di- Bell’s palsy in pregnancy. Antivirals have limited evidence for use
agnoses based on history and physical examination. This may and effectiveness in pregnancy and are not recommended.7
include Lyme serology, human immunodeficiency virus, antinu-
clear antibody, complete blood count, erythrocyte sedimentation Adjunctive Care
rate, C-reactive protein, and rheumatoid factor to rule out an
alternative cause.3,6,16,18 The use of electroneuronography or elec- Bell’s palsy involves paralysis of the eyelid. This leads to the
tromyography is indicated if the patient presents with Bell’s palsy inability of the affected eye to blink, resulting in dry eye symptoms
with complete facial paralysis or with a nondisplaced temporal that could develop into corneal ulcerations, keratitis, tearing, and
bone fracture. This helps the practitioner in determining whether possible vision loss.14,19 Artificial tears to prevent dry eye may be
the patient requires facial nerve decompression and a surgical administered up to 4 times per day if the drops contain pre-
consult.6 Normally, imaging for Bell’s palsy is not required; how- servatives or more frequently if the drops are preservative free to
ever, when a diagnosis is unclear or a central cause cannot be ruled protect the cornea due to the patient’s inability to blink.14,15,18,19 The
out, a computed tomographic scan or magnetic resonance imaging patient should be instructed to manually close their affected eye at
can be performed.11 If symptoms have not improved in 4 months or regular intervals to simulate blinking. A lubricating ointment
there is recurrent facial paralysis, imaging is indicated to look for an should be applied at night because this is the most crucial time for
alternative etiology.13 corneal drying to occur.15 Taping the eye closed at night helps
protect the cornea while sleeping; however, applying a patch at
Treatment night over the eye is not recommended because of the possibility of
the eyelid opening under the patch, resulting in corneal abra-
Treatment for Bell’s palsy involves the use of corticosteroids and sion.15,18,19 Additional but less common options for ophthalmic
antivirals. Additional treatment involves the management of treatment for Bell’s palsy include surgical intervention or botuli-
ophthalmic and oral symptoms, physiotherapy, surgical consider- num neurotoxin injections depending on the length of time and the
ation, and the management of sequelae such as facial synkinesis severity of the symptoms exhibited by the patient.6,14
and depression. Flaccid facial paralysis and decreased function of the orbicularis
oris muscle leads to difficulty with mastication, speech, and swal-
Pharmacologic Treatment lowing. This can cause leakage of food or liquids from 1 side of the
mouth or pocketing of food.14 The treatment for oral insufficiency
Corticosteroids are first-line treatment for Bell’s palsy and are includes physiotherapy through facial muscle retraining, the use of
indicated for improving recovery, shortening the duration of soft foods that are easier to chew, and the use of straws for
symptoms, and limiting the development of facial sequelae.18 Cor- liquids.14,22
ticosteroids are believed to have an anti-inflammatory effect, Physiotherapy for rehabilitation of the facial muscles includes
reducing edema and inflammation of the facial nerve.8 There are 2 soft tissue mobilization, retraining of the functional use of the oral
options for corticosteroid dosing: the first is oral prednisone 60 mg muscle, and facial expression. Facial neuromuscular retraining is
daily for 5 days and then tapering the dose by 10 mg each day for 5 the most common physiotherapy technique for Bell’s palsy and
days, and the second is oral prednisone 50 mg for 10 days.1 Recent helps increase facial muscle control and function.6,15 The tech-
studies suggest the use of corticosteroids demonstrated improve- niques are dependent on the degree and deficits of facial palsy. The
ment in facial function compared with a control group.7 Possible use of biofeedback and electromyography along with neuromus-
adverse effects of high-dose corticosteroids include hypertension, cular training helps the patient reinforce and increase the control of
confusion, exacerbated diabetes, fluid retention, an increased risk muscle movements of the face.15 Physiotherapy is not curative for
of infection, osteoporosis, and peptic ulcers.20 Antivirals in combi- facial nerve paralysis but can be beneficial for improving the ability
nation with corticosteroids have demonstrated superior effective- to smile, eat, speak, and blink, which improves both psychological
ness in the treatment of symptoms compared with placebo or no and physical effects on the patient.22 Physical therapy has an
treatment and have shown some benefit in decreasing sequelae increased benefit in chronic compared with acute facial palsy.6
when used in conjunction with corticosteroids, but antivirals have The development of Bell’s palsy can result in psychological
not shown great benefit for treatment as monotherapy for Bell’s distress to patients due to a change in their appearance and their
palsy.20 Dosing for antivirals is valacyclovir 1000 mg 3 times a day inability to perform facial movements related to a decline in facial
for 7 days. Alternatively, acyclovir can be used but has less motor function, speech, and the ability to eat and drink.23 This can
bioavailability compared with valacyclovir.1 Antiviral treatment lead to feelings of depression and anxiety in the patient. Screening
should be initiated within 72 hours of symptom onset.15 Similarly, for depression, suicidality, and anxiety is warranted in every pa-
treatment for pediatric clients includes weight-based prednisone tient with Bell’s palsy due to the drastic and acute change in
or prednisolone in combination with antivirals; however, the appearance affecting the patient’s self-esteem.19,24 Referral for
spontaneous recovery rate without treatment is 97%, so no treat- counseling is recommended for clients demonstrating a need for
ment may be less detrimental in the pediatric versus the adult support to manage psychological distress.
population.21 Facial nerve decompression is the most common surgical mo-
Corticosteroids are effective for the treatment of Bell’s palsy in dality for Bell’s palsy. Facial nerve decompression involves the
pregnancy.7 Pregnancy is a risk factor for the development of Bell’s removal of the bony surroundings of the nerve, taking a middle
palsy and incomplete recovery of facial paralysis. Corticosteroids fossa approach for access to the labyrinthine segment, which is the
pose the same side effects to the mother as any adult. Fetal risks of most common site of compression.25 Indications for surgery are
corticosteroid use include low birth weight, risk of developmental acute facial palsy with complete paralysis, greater than 90%
defects if used in the first trimester, and adrenal suppression.7 degeneration on electroneurography testing, and absent electro-
Prednisone is converted to an inactive form by the placenta, so it myographic activity within 14 days of symptom onset.5,25 Addi-
has a limited effect on the fetus compared with alternative steroids, tional surgical options for Bell’s palsy include facial static
162 J. Ho, A. Markowsky / The Journal for Nurse Practitioners 18 (2022) 159e163

reanimation, nerve grafting, tarsorrhaphy, and dynamic References

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24. Cuenca-Martínez F, Zapardiel-S anchez E, Carrasco-Gonza lez E, La Touche R,
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presentation of facial nerve paralysis. Pharmacologic treatment MOO.0000000000000478
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27. Azizzadeh B, Frisenda J. Surgical management of postparalysis facial palsy and
manage specific problematic symptoms. The NP should be cogni- synkinesis. Otolaryngol Clin North Am. 2018;51(6):1169-1178. https://doi.org/
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most often results in complete resolution of symptoms, and 28. Bylund N, Jensson D, Enghag S, et al. Synkinesis in Bell’s palsy in a randomised
appropriately communicate expected outcomes with the patient to controlled trial. Clin Otolaryngol. 2017;42(3):673-680. https://doi.org/10.1111/
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reduce client anxiety. Lastly, the NP should be able to identify cir- 29. Shinn JR, Nwabueze NN, Du L, et al. Treatment patterns and outcomes in
cumstances in which referral to a specialist for intervention and botulinum therapy for patients with facial synkinesis. JAMA Facial Plast Surg.
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30. Baek S, Kim YH, Kwon Y, et al. The utility of facial nerve ultrasonography in Neck Surg. 2020;146(3):256-263. https://doi.org/10.1001/
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31. Cai Z, Li H, Wang X, et al. Prognostic factors of Bell’s palsy and Ramsay Hunt
syndrome. Medicine (Baltimore). 2017;96(2):e5898. https://doi.org/10.1097/ Jimmy Ho, MN, RN, is a graduate student at the College of Nursing, Rady Faculty of Health
MD.0000000000005898 Sciences, University of Manitoba in Winnipeg, Manitoba, Canada, and can be contacted at
32. Choi SA, Shim HS, Jung JY, et al. Association between recovery from Bell’s palsy [email protected]. Ashley Markowsky, MN, NP, is an instructor II at the
and body mass index. Clin Otolaryngol. 2017;42(3):687-692. https://doi.org/ College of Nursing, Rady Faculty of Health Sciences, University of Manitoba.
10.1111/coa.12801
33. Yoo MC, Soh Y, Chon J, et al. Evaluation of factors associated with In compliance with standard ethical guidelines, the authors report no relationships
favorable outcomes in Adults with Bell Palsy. JAMA Otolaryngol Head with business or industry that would pose a conflict of interest.