Bell’s palsy is acute weakness of the facial muscles associated with compression of cranial nerve VII. The annual incidence is 20 to 30 per 100,000. Diagnosis is based on a thorough history and physical examination, with careful attention to exclude other causes of facial weakness, such as stroke or Lyme disease. Oral corticosteroids improve recovery rates and antiviral medications reduce synkinesis. Most patients will recover completely. Physical therapy and Botox injections can help patients with persistent symptoms. The roles of surgery and acupuncture remain unclear. Close follow-up is warranted and patients without improvement should be referred to a specialist.
Key points
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Bell’s palsy is a common, idiopathic condition causing acute onset of unilateral facial paralysis in the distribution of peripheral cranial nerve VII.
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Diagnose Bell’s palsy based on a careful history and physical examination.
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Treat all adult patients with Bell’s palsy with oral corticosteroids to increase rates of complete recovery.
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Treat all adult patients with Bell’s palsy with antiviral agents to reduce rates of synkinesis.
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Refer patients with incomplete recovery to physical therapy and to an appropriate specialist.
Introduction
Bell’s palsy, also referred to as idiopathic facial paralysis, is an acute weakness or paralysis of the facial muscles related to swelling of the facial nerve and has no apparent cause. Primary care physicians play a pivotal in the clinical evaluation, diagnosis, treatment, and follow-up of patients with Bell’s palsy, and can manage most patients with Bell’s palsy in the primary care setting. This review will provide an evidence-based approach to the diagnosis and management of Bell’s palsy.
Epidemiology
The estimated annual incidence of Bell’s palsy is 20 to 30 per 100,000 people. Although the highest incidence occurs in individuals between 15 and 45 years of age, it can occur at any age. Women and men are equally affected, , and both sides of the face are equally affected. , Conditions associated with increased risk of Bell’s Palsy include diabetes, , pregnancy, , hypertension, immunosuppression, influenza A, and other upper respiratory illnesses. ,
Pathogenesis
While Bell’s palsy has no apparent cause, the pathophysiology is associated with nerve edema and subsequent mechanical compression of the facial nerve, leading to weakness or paralysis in the distribution of the facial nerve ( Fig. 1 ). Bell’s palsy may also affect the sensory and autonomic function of the facial nerve. The facial nerve carries sensation from the external auditory canal, pinna, mastoid, and the palatal mucosa. Impaired function of the chorda tympani branch can affect taste and cause abnormal salivation. Damage to the petrosal nerve branch, which innervates the lacrimal glands, leads to decreased lacrimation. As fibers from the facial nerve also innervate the stapedius, some patients may have hyperacusis. , Potential etiologies include ischemic neuritis or reactivation of Herpes Simplex Virus Type 1 in the geniculate ganglion.
Coronavirus disease 2019 and Bell’s palsy
With the onset of the coronavirus disease 2019 (COVID-19) pandemic, questions arose regarding the relationship between Bell’s palsy, COVID-19 infection, and vaccinations against COVID-19. A systematic review and meta-analyses analyzed randomized controlled trial data and observational data. There was an increased incidence of Bell’s palsy among individuals receiving either a messenger-RNA (m-RNA) vaccine or a viral vector vaccine in randomized placebo controlled-trials of both vaccine types (odds ratio [OR] 3.0, 95% confidence of interval [CI], 1.1–8.18). A pooled analysis of observational studies of m-RNA vaccines, which included 13,518,026 observed doses and 13,510,701 unvaccinated individuals showed no association between vaccine administration and Bell’s palsy (OR 0.7, 95% CI, 0.42–1.16). This data suggest an association between COVID vaccination and incident Bell’s palsy, but does not prove a causal relationship. Furthermore, Bell’s palsy was observed to be more common following infection with COVID-19 than following vaccination (OR 3.23; 95% CI, 1.57–6.62).
Clinical presentation
Bell’s palsy presents acutely with unilateral facial weakness or paralysis involving the forehead developing over 24 to 48 h. , Rarely, Bell’s palsy can be bilateral. The palsy most noticeably affects the motor function of the facial nerve but affects the autonomic and sensory function as well. Patients may complain of alteration in taste, sensation, or hearing on the affected side. The history and physical examination are essential to the diagnosis of Bell’s palsy and can reliably lead to the diagnosis, as well as identify findings that raise concern for an alternative and potentially more serious diagnosis. The examiner should find no other neurologic abnormalities in addition to findings consistent with peripheral facial nerve involvement. ,
Examination
Bell’s palsy presents with drooping of the mouth, flattening of the nasolabial fold, inability to close the affected eye, and smoothing of the brow on the affected side. , (see Figs. 1 and 2 ) The provider should perform complete neurologic and otolaryngologic examinations with the primary goal of differentiating between an upper, or central, and lower, or peripheral, motor neuron lesion affecting the facial nerve. By definition, Bell’s palsy is a peripheral lesion, which causes weakness of all the muscles involved in facial expression on the affected side. This includes the frontalis muscle which raises the eyebrow; orbicularis oculi muscle which closes the eyelids and is involved in tear production and the corneal reflex; the orbicularis oris muscle which closes and protracts the lips, is involved with speech, and is essential to swallowing, chewing, and sucking; the buccinator muscle which pulls the corners of the mouth laterally; and the platysma muscle which pulls down the mandible and pulls the corners of the lips out to the side and down. ,
If the patient can raise their eyebrow on the affected side, suggesting that the frontalis muscle is not affected, consider a central lesion, particularly a stroke. Additionally, consider an alternative diagnosis if the initial examination reveals any neurologic findings in addition to those associated with the facial muscles described earlier as these findings would indicate a lesion affecting structures other than just cranial nerve VII. , (see Fig. 1 ) If the patient presents with ipsilateral recurrent Bell’s palsy, symptoms continue to progress beyond the initial 72 h after onset, the symptoms fluctuate, or there is bilateral involvement at initial presentation, additional evaluation is required.
While Bell’s palsy is defined as idiopathic facial nerve palsy, there are many conditions that cause peripheral facial nerve palsy or central processes that cause facial weakness. Findings that suggest an alternative diagnosis include gradual symptom onset, recent tick or vaccine exposure, tinnitus, hearing loss or vertigo, signs of infection, head and neck cancer, and limb or bulbar weakness. , Central causes will typically spare the forehead. Gradual onset and mental status changes suggest brain tumor, either primary, or if a history of cancer, metastatic. Abrupt onset associated with ipsilateral extremity weakness or other neurologic symptoms indicate a stroke. Multiple sclerosis causing facial weakness is also associated with other neurologic symptoms. Viral diseases that cause peripheral nerve palsy include COVID-19, cytomegalovirus, Epstein-Barr virus, herpes simplex, human immunodeficiency virus (HIV), influenza, mumps, and rubella—weakness associated with these infections will typically be preceded or accompanied by the associated viral syndrome. Ramsay Hunt syndrome, due to herpes zoster, is characterized by prodromal pain and a vesicular eruption in the ear canal and/or palate. Otitis media can cause peripheral nerve palsy of gradual onset, associated with pain, fever, and conductive hearing loss. Suspect Lyme disease if there is a history of tick exposure, residence in or travel to endemic areas, rash and/or arthralgias or bilateral facial weakness. Autoimmune or granulomatous conditions such as sarcoidosis, myasthenia gravis, or Guillain-Barre syndrome are more often bilateral at presentation. Cholesteatoma and head and neck cancers will typically have a gradual onset and associated findings on physical examination. Weakness associated with tinnitus and hearing loss suggests the diagnosis of acoustic neuroma. , ,
Diagnostic testing
Laboratory testing is not required to diagnose Bell’s palsy. The provider should consider laboratory testing if the patient’s history suggests an identifiable cause of peripheral facial nerve palsy, such as Lyme disease, HIV, or sarcoidosis. One guideline suggests obtaining a complete blood count with differential as an increased neutrophil-to-lymphocyte ratio has been associated with poor prognosis. However, the review upon which this recommendation is based demonstrated evidence of publication bias and was unable to provide a clear cut-off separating patients with poor prognosis from those with good prognosis. ,
Imaging is not required to diagnose Bell’s palsy if the physical examination findings are consistent with the diagnosis. There is a small risk of lacunar infarct affecting the lower pons that presents as a peripheral palsy; this is exceedingly rare. Imaging is indicated if the patient presents with recurrent ipsilateral Bell’s palsy, symptom progression beyond the initial 72 h following onset, fluctuate, or are bilateral. MRI head or MRI orbits/face/neck with and without intravenous contrast are the 2 recommended studies to evaluate for suspected tumor.
Clinical assessment tools
Patients can experience a spectrum of symptom severity. Two grading scales are commonly used to classify severity, the House-Brackmann ( Fig. 3 ) and Sunnybrook ( Fig. 4 ) scales. Classifying severity can help provide appropriate anticipatory guidance, and aid in treatment recommendations, particularly early physical therapy for individuals with scores indicating higher severity.
