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Bell’s palsy
Bell’s palsy

Bell’s palsy

Pathophysiology

Bell’s palsy is an idiopathic, acute, unilateral paralysis of the facial nerve → unilateral paralysis of the face.

Before, we discuss Bell’s palsy further, let’s review what we know about the 7th cranial nerve:

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The facial nerve arises from the pons and courses through the internal acoustic meatus before entering the facial canal. It then exits the cranium via the stylomastoid foramen.

CN7 has many functions:

  • Sensory function - provides taste sensation to the anterior 2/3rds of the tongue via the chorda tympani branch. It also provides a small region of sensation to the ear.
  • Motor function - muscles of facial expression, stylohyoid, stapedius and posterior belly of digastric muscles.
  • PSNS function - lacrimal glands, and submandibular and sublingual salivary glands.

Within the facial canal, the facial nerve gives rise to 3 branches:

  1. Greater petrosal nerve - carries PSNS fibres.
  2. Chorda tympani - carries information from taste buds to the pons.
  3. Nerve to stapedius - provides innervation to the stapedius muscle to prevent hearing damage by allowing reflexive contraction.
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As it exits the stylomastoid foramen and the cranium (extracranially) it gives off the posterior auricular nerve and 5 other branches as it passes through the parotid gland:

  1. Temporal
  2. Zygomatic
  3. Buccal
  4. Marginal mandibular
  5. Cervical
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🚗
Branches of CN7: “To Zanzibar By Motor Car” To - temporal Zanzibar - zygomatic By - buccal Motor - marginal mandibular Car - cervical
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😷 Presentation

  • ⭐️ LMN ipsilateral facial paralysis
    • Inability to close eyelid due to paralysis of orbicularis oculi as this is innervated by the temporal and zygomatic branches (one is still able to open eyes normally as this is controlled by the oculomotor nerve and the levator palpebrae muscle).
    • Hyperacusis - this is when everyday sounds are much louder. This is because the stapedius muscle is paralysed.
    • Metallic taste in anterior 2/3rds of tongue - due to paralysis of the chorda tympani.
    • Reduced lacrimation - due to greater petrosal nerve paralysis.
🧠
Bell’s palsy vs. Stroke If the face were to be divided into 4 quadrants, each upper quadrant would be innervated by both the ipsilateral and contralateral facial nerve. The lower quadrants are innervated by solely the ipsilateral facial nerve. What implication does this have on differentiating stroke from Bell’s palsy?
  • Bell’s palsy is non forehead-sparing - as it is a LMN facial nerve paralysis → paralyses the entirety of the affected side. Therefore the occipitofrontalis muscle which wrinkles the forehead is not spared and one is unable to wrinkle the forehead.
  • Stroke is forehead-sparing - this is because strokes are supranuclear lesions (UMN) causing contralateral facial paralysis, yet there is still the ipsilateral innervation to the upper quadrant → we can still wrinkle the forehead.
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⚠️ Risk factors

  • We are still unsure of the causes of Bell’s palsy but it is associated with herpes viridae infections:
    • HSV-1
    • VZV
    • CMV
    • EBV
  • It most commonly occurs in younger people (20-40 years old).
  • It is also more common in pregnant women.
  • Diabetics are also more prone.

🔢 Classification

The House-Brackmann classification is used to stage the severity of a facial palsy (not exclusive to Bell’s):

Grade
Description
Characteristics
I
Normal
Normal facial function in all areas.
II
Mild dysfunction
Slight weakness noticeable on close inspection. May have slight synkinesis (unwanted contractions when attempting to move facial muscles).
III
Moderate dysfunction
Obvious, but not disfiguring differences between both sides. Noticeable, but not severe synkinesis/hemifacial spasm. Complete eye closure with effort.
IV
Moderately severe dysfunction
Obvious weakness of disfiguring asymmetry, normal symmetry and tone at rest but unable to complete eye closure.
V
Severe dysfunction
Only barely perceptible facial muscle motion. Asymmetry at rest.
VI
Complete paralysis
No movement.

📝 Differential diagnosis

LMN causes of facial palsy

  • Infective causes - AOM, cholesteatoma, HSV-1, CMV, EBV.
  • Neoplasm
  • Trauma
  • Iatrogenic

UMN causes of facial palsy

  • Stroke
  • Subdural haematoma
  • Brain tumour

🔍 Investigations

It is usually clinically diagnosed a is a diagnosis of exclusion.

🧪 Serology for HSV-1 and VZV can also be done but this won’t change the management.

🧰 Management

Most of the time it will spontaneously return to full function.

💊
Medical management:
  • Oral corticosteroids within 72 hours of presentation:
    • Prednisolone - 25mg BD for 10 days.

      • or

    • Prednisolone - 60mg OD for 5 days → reduce to 10mg OD.
👁️
Eye care: Since the eyes are unable to close on their own, we need to take care of them to prevent exposure keratopathy → damage to the cornea. We use eye drops and artificial tears. The eye also needs to be taped closed at night with microporous tape.
🔪
Surgical management: Surgery is indicated in patients with facial weakness or synkinesis. Botox may be given for synkinesis.

✍️ Referral

Referral to ENT surgeon should be made if:

  • There is a doubt of diagnosis.
  • Bilateral Bell’s palsy.
  • No sign of improvement after 3 weeks.

Referral to ophthalmology should be made if:

  • Cornea remains exposed after attempting to close eye (House-Brackmann IV or more).