Bells palsy

Bell’s palsy is an acute, idiopathic facial nerve paralysis that typically affects one side of the face. It is the most common cause of sudden facial weakness and can significantly impact quality of life. Early recognition and management are essential to optimize recovery and reduce complications.

Definition and Classification

Definition

Bell’s palsy is defined as a sudden, unilateral weakness or paralysis of the facial muscles due to dysfunction of the seventh cranial nerve (facial nerve), without an identifiable cause. The onset is usually rapid, and symptoms may reach maximum severity within 48 hours.

Types

• Idiopathic Bell’s Palsy: Facial nerve paralysis with no identifiable cause, accounting for the majority of cases.
• Secondary Facial Nerve Palsy: Facial paralysis resulting from known causes such as infections, trauma, neoplasms, or systemic diseases.

Etiology

Viral Infections

• Herpes Simplex Virus: Reactivation of latent HSV-1 in the geniculate ganglion is the most commonly implicated factor in idiopathic Bell’s palsy.
• Varicella-Zoster Virus: Can cause facial nerve inflammation, sometimes presenting as Ramsay Hunt syndrome if vesicular eruptions are present.
• Other Viral Agents: Cytomegalovirus and Epstein-Barr virus have also been associated in some cases.

Non-Viral Causes

• Trauma: Temporal bone fractures or surgical injury can damage the facial nerve.
• Neoplasms: Tumors such as parotid gland neoplasms or cerebellopontine angle tumors can compress the nerve.
• Autoimmune Disorders: Conditions like Guillain-Barre syndrome may involve facial nerve dysfunction.
• Ischemic Neuropathy: Vascular compromise of the facial nerve may contribute in some patients, especially those with comorbidities like diabetes.

Anatomy of the Facial Nerve

Cranial Nerve VII Overview

The facial nerve is the seventh cranial nerve responsible for motor control of facial expression, as well as carrying taste sensation from the anterior two-thirds of the tongue and parasympathetic fibers to salivary and lacrimal glands.

Course and Branches

• Intracranial Segment: Emerges from the brainstem and travels through the internal auditory canal.
• Intratemporal Segment: Passes through the facial canal within the temporal bone, giving off branches to the stapedius muscle and chorda tympani.
• Extratemporal Segment: Exits the stylomastoid foramen and divides into five major branches to innervate the muscles of facial expression.

Functional Components

• Motor: Controls muscles of facial expression, eyelid closure, and stapedius muscle function.
• Sensory: Conveys taste from the anterior two-thirds of the tongue and sensation from part of the ear.
• Parasympathetic Fibers: Innervates lacrimal, submandibular, and sublingual glands for tear and saliva production.

Pathophysiology

• Inflammation and Edema of the Facial Nerve: Viral reactivation or immune-mediated processes lead to swelling within the narrow facial canal, causing nerve compression and dysfunction.
• Compression within the Facial Canal: Edema and inflammation increase intraneural pressure, impairing blood flow and axonal conduction, resulting in muscle weakness or paralysis.
• Immune-Mediated Mechanisms: Autoimmune responses triggered by viral infections may contribute to demyelination and nerve injury.

Clinical Features

Motor Manifestations

• Unilateral Facial Weakness: Sudden onset of drooping on one side of the face affecting the forehead, eyelid, and mouth.
• Drooping of Mouth and Eyelid: Inability to smile or close the eye completely, leading to asymmetry.
• Inability to Close Eye: Lagophthalmos may result in exposure keratitis if not managed appropriately.

Associated Symptoms

• Altered Taste Sensation: Loss of taste in the anterior two-thirds of the tongue.
• Hyperacusis: Increased sensitivity to sound due to stapedius muscle paralysis.
• Facial Pain or Discomfort: Aching around the jaw or ear on the affected side.

Diagnosis

Clinical Evaluation

• History and Symptom Onset: Rapid onset of unilateral facial weakness, typically reaching maximum severity within 48 hours.
• Physical Examination: Assessment of facial symmetry, ability to raise eyebrows, close eyes, smile, and frown.
• Grading of Facial Nerve Function: Use of standardized scales such as the House-Brackmann scale to quantify severity and monitor recovery.

Laboratory and Imaging Studies

• Blood Tests: To rule out infections, autoimmune disorders, or metabolic causes if secondary facial palsy is suspected.
• MRI or CT: Imaging may be indicated to exclude structural lesions, tumors, or demyelinating diseases affecting the facial nerve.

Differential Diagnosis

• Stroke: Central facial palsy with sparing of the forehead and associated neurological deficits.
• Lyme Disease: Facial nerve involvement secondary to Borrelia infection.
• Ramsay Hunt Syndrome: Facial palsy associated with vesicular rash due to varicella-zoster virus.
• Parotid Tumors: May compress the extratemporal facial nerve causing progressive weakness.
• Otitis Media: Middle ear infections can lead to secondary facial nerve paralysis.

Management

Pharmacologic Treatment

• Corticosteroids: Prednisone or equivalent is the mainstay therapy to reduce inflammation and edema of the facial nerve, ideally initiated within 72 hours of symptom onset.
• Antiviral Therapy: Acyclovir or valacyclovir may be considered in cases with suspected viral involvement, particularly when combined with corticosteroids.

Supportive Care

• Eye Protection: Use of artificial tears, lubricating ointments, or eye patching to prevent corneal drying and injury due to incomplete eyelid closure.
• Physical Therapy and Facial Exercises: Gentle exercises to maintain muscle tone and prevent contractures, aiding in functional recovery.

Surgical and Interventional Options

• Decompression Surgery: Rarely indicated, reserved for severe, progressive cases with poor prognosis despite medical therapy.
• Botulinum Toxin for Synkinesis: Used in long-term management to treat abnormal facial movements that may develop during recovery.

Prognosis

• Typical Recovery Timeline: Most patients begin to recover within 2 to 3 weeks, with substantial improvement by 3 to 6 months.
• Factors Affecting Recovery: Age, severity at onset, comorbid conditions, and prompt initiation of therapy influence outcomes.
• Complications: Incomplete recovery, facial synkinesis, contractures, and persistent asymmetry may occur in a subset of patients.

Prevention and Risk Reduction

• Prompt Treatment of Viral Infections: Early management of herpes simplex or other viral illnesses may reduce the risk of Bell’s palsy development.
• Management of Comorbid Conditions: Controlling diabetes, hypertension, and other systemic illnesses can lower susceptibility to facial nerve complications.
• Awareness of Early Symptoms: Recognizing initial signs such as facial drooping or numbness allows for rapid medical intervention and improves outcomes.

References

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2. Evans OM, Grogan PM. Bell’s palsy: diagnosis and management. Am Fam Physician. 2020;101(4):213-219.
3. Gilden DH. Clinical practice. Bell’s palsy. N Engl J Med. 2004;351:1323-1331.
4. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985;93(2):146-147.
5. Lockhart P, Dooley J. Bell’s palsy. BMJ. 2018;360:k513.
6. Peitersen E. The natural history of Bell’s palsy. Acta Otolaryngol. 1972;73(3-6):123-135.
7. Baugh RF, Basura GJ, Ishii LE, et al. Clinical practice guideline: Bell’s palsy. Otolaryngol Head Neck Surg. 2013;149(3_suppl):S1-S27.