Facial (nerve) palsy is a neurological condition in which function of the facial nerve (cranial nerve VII) is partially or completely lost. It is often idiopathic but in some cases, specific causes such as trauma, infections, or metabolic disorders can be identified. Two major types are distinguished: central facial palsy (lesion occurs between cortex and nuclei in the brainstem) and peripheral facial palsy (lesion occurs between nuclei in the brainstem and peripheral organs). Central facial palsy manifests with impairment of the lower contralateral mimic musculature. In contrast, peripheral facial palsy leads to impairment of the ipsilateral mimic muscles and also affects the eyelids and forehead. Additionally, peripheral facial palsy can cause various sensory and autonomic disorders (depending on the exact location of the lesion). Diagnosis can usually be made clinically while patient history often helps in evaluating the underlying etiology. Idiopathic facial nerve palsy is treated with oral glucocorticoids and, in severe cases, antivirals. Treatment of the other types depends on the underlying cause. Most cases of idiopathic facial palsy heal completely within 3 weeks.
- 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.
- 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.
Central vs peripheral facial nerve 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)|
|Inability to frown|| || |
|Inability 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
- Synkinetic involuntary movements of the facial muscles; (e.g., facial spasms while closing the eyes)
- Bell palsy
- Secondary facial nerve palsy: management of the underlying cause
- 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)
- Ask about symptom onset and duration, recent infections, and outdoor trips
- Ask patient to perform facial movements ; (e.g., frown, whistle, inflate cheeks, smile, show teeth/grimace, close eyes tightly, blink) and observe inabilities and asymmetries of the face.
- Additional studies to investigate for potential causes (e.g., serology for Lyme disease)
- Nerve conduction studies: can be performed to assess recovery prognosis