Facial nerve palsy

Weakness or paralysis of the facial muscles due to dysfunction of CN VII (facial nerve); peripheral lesions (e.g., Bell's palsy) cause ipsilateral complete facial paralysis (forehead included), while central lesions (e.g., stroke) spare the forehead.

• Facial nerve palsy is common (Bell's palsy accounts for most cases) and can significantly affect eye protection, speech, and appearance. Importantly, it must be differentiated from serious causes like stroke. Early recognition of Bell's palsy allows timely treatment (steroids) for better recovery, and prompt identification of other etiologies (e.g., Lyme, Ramsay Hunt) can prevent complications.

• Peripheral (LMN) facial palsy classically presents with acute unilateral facial weakness: patients wake up unable to close one eye, with drooping of the mouth and inability to raise the eyebrow on the affected side. There may be retroauricular pain, altered taste (anterior 2/3 tongue), or hyperacusis (due to stapedius muscle paralysis).
• Common causes of peripheral facial palsy include idiopathic Bell's palsy (often preceded by a viral prodrome), Ramsay Hunt syndrome (facial paralysis with ear pain and vesicular rash from VZV), Lyme disease (especially if bilateral palsies, in endemic areas), otitis media (in children), and tumors (e.g., a parotid gland neoplasm or acoustic neuroma).
• Central (UMN) facial palsy is most often due to a stroke (usually an ischemic infarct in the contralateral motor cortex or internal capsule); it presents with lower face weakness but forehead sparing, and often other neurologic deficits (arm/leg weakness, dysarthria).

1. First, distinguish central vs peripheral: examine forehead muscle function. If the patient can wrinkle the forehead on the weak side, the lesion is likely central (UMN); if the forehead is weak, it's a peripheral (LMN) palsy.
2. If peripheral, look for clues to cause: check the ear for vesicular rash (zoster), examine for bilateral involvement (Lyme or Guillain-Barré), palpate the parotid region for a mass (tumor), and ask about tick bites or systemic symptoms. Absence of such clues with a typical presentation suggests Bell's palsy (idiopathic).
3. Imaging (MRI) is generally not needed for straightforward Bell's palsy, but obtain MRI if the presentation is atypical (gradual onset, additional cranial nerve deficits, hearing loss, or no improvement over time) to exclude structural lesions (tumor, brainstem lesion).
4. Initiate treatment promptly if Bell's palsy is suspected. Protect the eye from drying (artificial tears, tape at night) while blink is impaired. Arrange follow-up to monitor recovery; most Bell's palsy cases begin to improve within a few weeks. If no improvement by ~3 months, refer to neurology/ENT for further evaluation.

1. For Bell's palsy, start high-dose corticosteroids (e.g., prednisone 60 mg/day) within 72 hours of onset – this significantly improves the chance of complete recovery. Antivirals (e.g., valacyclovir) are often added, especially for severe paralysis or Ramsay Hunt, although their benefit is less clear.
2. Eye care is critical: use lubricating drops and tape the eyelid shut at night to prevent corneal drying and injury (since the eye doesn't fully close).
3. Treat specific causes accordingly: e.g., acyclovir for Ramsay Hunt (with steroids), doxycycline for Lyme disease, surgical removal for tumors, and standard stroke management if central. Refer to neurology or ENT if facial palsy is atypical or not improving in expected time.

• Forehead test: stroke spares the forehead (patient can raise eyebrows) unlike Bell's palsy. Forehead involvement = LMN lesion.
• Only a few conditions cause bilateral facial palsy – think Lyme disease or Guillain-Barré syndrome if both sides are affected.
• Bell's palsy often causes hyperacusis (stapedius paralysis) and taste loss (chorda tympani involvement) – these do not occur in a central facial palsy.

• Facial weakness with forehead sparing plus other acute neurologic deficits (e.g., limb weakness, aphasia) → suspect stroke (urgent brain imaging is indicated).
• Gradually progressive facial paralysis over weeks/months, or facial weakness with a parotid mass or other cranial nerve deficits → concern for a tumor (obtain imaging).
• Bilateral or recurrent facial palsy should prompt evaluation for systemic causes (e.g., Lyme disease, sarcoidosis, Guillain-Barré) rather than idiopathic Bell's palsy.

1. Facial droop → check forehead: if forehead is weak → LMN palsy; if forehead intact → UMN palsy (likely stroke).
2. If UMN (central) palsy → urgent neuroimaging and appropriate stroke management.
3. If LMN palsy → assess for secondary causes: look for herpes zoster (ear rash), tick exposure (Lyme), otitis (middle ear infection), trauma, or tumor signs. Perform directed tests (Lyme serology, MRI if tumor suspected).
4. If Bell's palsy likely (acute isolated CN VII palsy with no red flags) → start steroids promptly (within 72 hours) and provide eye protection; antivirals may be added if severe. No immediate imaging is required in typical cases.
5. Follow up to monitor recovery; if no improvement by ~3 months or atypical features present, obtain MRI and refer to specialist (neurology/ENT).

• A 30‑year‑old with diabetes develops sudden left facial droop with inability to close the left eye or raise the left eyebrow (forehead is weak). No arm or leg weakness → Bell's palsy (peripheral CN VII palsy).
• An elderly patient with right facial droop who can still wrinkle the right forehead, accompanied by right arm weakness and slurred speech → stroke causing central facial palsy (left UMN lesion).
• A patient with severe ear pain and vesicular eruption in the external ear followed by facial paralysis → Ramsay Hunt syndrome (herpes zoster of CN VII).