Facial nerve palsy is the partial (paresis) and/or total (paralysis) loss of facial nerve (cranial nerve VII) function. The most common cause is peripheral facial nerve palsy, also known as Bell palsy. Secondary causes include trauma, infections, brainstem stroke, tumors, and metabolic disorders. Clinical features include decreased or absent movement of the facial muscles, hyperacusis, alterations in taste, and dry eyes and mouth. Facial nerve palsy is a clinical diagnosis made after obtaining a thorough history and physical examination, which includes assessing for in order to differentiate between central (e.g., as a result of stroke) and peripheral (e.g., idiopathic, or caused by infection or trauma). If a secondary cause is suspected following assessment, diagnostic studies may be performed. Idiopathic peripheral facial nerve palsy is treated with oral glucocorticoids with or without antivirals and most cases resolve within three weeks. If secondary causes are identified, the underlying cause is treated. Complications include incomplete recovery of facial nerve function, facial synkinesis, and ocular complications related to incomplete eye closure.
- Idiopathic (most common cause of peripheral facial nerve palsy): Acute idiopathic peripheral facial palsy is also known as Bell palsy. 
The muscles responsible for eyelid and forehead movements are innervated by fibers from both sides.
- Central facial palsy: There is a unilateral upper motor neuron lesion between the cortex and nuclei in the pons (corticobulbar tract), but the muscles of the eyelids and forehead are still supplied by input from the other side, so function is preserved (forehead sparing).
- Peripheral facial palsy: There is a unilateral lower motor neuron lesion between the nuclei and muscles, which results in the paralysis of the ipsilateral eyelid and forehead muscles because no other input reaches these muscles.
- The lower facial muscles are only innervated by fibers from the contralateral hemisphere (via ipsilateral nuclei and the ipsilateral peripheral nerve), so they are paralyzed in both central and peripheral facial palsy.
|Motor signs in central and peripheral facial palsy|
|Clinical feature||Central (signs are contralateral to the lesion)||Peripheral (signs are ipsilateral to the lesion)|
|Ability to frown or lift eyebrows|| || |
|Ability to close the eyelids completely|| || |
|Mouth drooping|| |
Additional signs of peripheral facial palsy
- Sensory disturbances
- Dry mouth (as a result of decreased saliva production)
- Bell's phenomenon: a physiologic, reflexive movement of the eye (upward and outward) that occurs when the eyelid is actively closed
- Lagophthalmos: The patient cannot fully close the eyes (due to paralysis of the orbicular oculi muscle). 
- Decreased lacrimation
- Corneal ulceration and keratitis
- Facial synkinesis; : involuntary movements of the facial muscles; (e.g., facial spasms while closing the eyes)
Clinical evaluation 
- Ask about symptom onset and duration (e.g., acute vs. progressive).
- Assess for possible secondary causes, e.g., stroke, tumors, recent infections, and; exposure from outdoor trips.
- Evaluate for facial asymmetry at rest.
Ask the patient to perform facial movements.
- Assess for asymmetries and facial muscle strength.
- Differentiate between .
- Perform a complete neurological examination: Look for focal neurological signs.
- Evaluate for signs indicative of a secondary cause, e.g., tick bites, signs of trauma. , , ,
When an acute central cause is suspected (e.g., other acute are present), evaluate for . Consider a tumor in patients with gradual onset, or slowly progressing neurological symptoms (e.g., change in mental status, involvement of select branches of the facial nerve and/or other cranial nerves, or other subacute focal neurological deficits). 
Severity assessment 
- Determine the level of dysfunction of forehead movements, eye closure, and mouth closure.
- Consider the use of a validated severity scale.
Diagnostic studies 
Diagnostic studies are not routinely needed for acute unilateral facial nerve palsy unless a secondary cause is suspected (see “Etiology”) based on atypical symptoms and/or abnormal physical examination findings (See “Clinical features” and “Clinical evaluation”). Specialist consultation is advised.
- Laboratory studies: Consider for select infectious causes.
- Neuroimaging should be performed if neoplastic, vascular, or traumatic causes are suspected, for example:
Other neurological studies
- Consider nerve conduction studies: e.g., for patients with Bell palsy PLUS complete facial nerve paralysis, or suspected polyneuropathy (e.g., multiple sclerosis, Guillain Barré syndrome)
- Consider audiology to evaluate for sensorineural hearing loss ( ): e.g., in patients with VZV, TBI, and suspected peripheral nerve or brain tumors
Recommendations in this section are consistent with the 2013 American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) Bell palsy guidelines and the 2012 American Academy of Neurology (AAN) guideline update on steroids for Bell palsy (reaffirmed in January 2020). 
Begin central facial nerve palsy is suspected. without delay if acute
Symptomatic therapy 
Provide symptom-based treatment for all patients (regardless of the cause).
- Incomplete eye closure: Initiate eye care; (e.g., artificial tears; , eye ointment, and/or taping or patching of the eye). 
- Incomplete mouth closure: Advise the patient on proper lip and mouth care.
- Persistent facial nerve paresis (≥ 3 months): Consider physical therapy and facial reconstructive options. 
Bell palsy 
- Oral glucocorticoids: Consider for all patients (regardless of severity). 
- Surgical decompression 
Follow up with specialist consult and/or advanced studies if the patient has any of the following: 
- No signs of improvement in 2–3 weeks 
- Persistent (≥ 3 months), progressive, and/or recurrent symptoms
Initiate therapy (i.e., oral glucocorticoids with or without antivirals) within 48–72 hours of symptom onset. 
Secondary facial nerve palsy
Consider the following depending on the suspected etiology.
- Peripheral causes
- Central causes: Consult the appropriate specialist to determine the best treatment options (See “Treatment” sections in “Ischemic stroke,” “Intracerebral hemorrhage,” “Multiple sclerosis,” and “Brain tumors.”)
- Traumatic facial nerve palsy: a common complication of basilar skull fractures (e.g., temporal bone fractures) 
- Idiopathic facial palsy: complete recovery in ∼ 85% of cases (within 3 weeks)
- Misdirected regrowth of nerve fibers can lead to persistent disorders (e.g., synkinesias)