Bell's palsy is a condition primarily characterized by paralysis of the facial expression muscles. It manifests as isolated peripheral facial paralysis without other signs or symptoms.
Incidence Rate
The annual incidence of Bell's palsy ranges between 11.5 to 53.3 cases per 100,000 people.
Etiology
The exact cause of Bell's palsy remains unclear. Possible associations include viral infections, inflammatory responses, or autoimmune reactions. Many researchers suggest that Bell's palsy is linked to herpes simplex virus (HSV) infection. Herpes simplex virus type 1 (HSV-1) is believed to induce facial nerve edema in the region of the geniculate ganglion, leading to facial dysfunction. HSV-1 can enter the human body via mucocutaneous contact and remains dormant in peripheral nerve ganglia until reactivated. Risk factors for Bell's palsy include pregnancy, severe preeclampsia, diabetes, upper respiratory infections, hypertension, and obesity.
Among all cases of facial nerve paralysis, 0.3% to 2% may involve bilateral paralysis. Bilateral facial nerve paralysis is more likely to reflect a manifestation of systemic diseases. Lyme disease accounts for a significant portion of bilateral facial paralysis cases, approximately 35%. Other important differential diagnoses include Guillain-Barré syndrome, diabetes, and sarcoidosis. Neurological causes of bilateral facial paralysis include Parkinson's disease, multiple sclerosis, and pseudobulbar palsy.
Pathology and Pathogenesis
The pathological changes of Bell's palsy involve facial nerve edema caused by various etiologic factors. Due to the limited volume of the facial nerve canal, increased intraneural pressure leads to impaired neural conduction and results in facial paralysis. Prolonged edema can cause ischemia, degeneration, and, in severe cases, necrosis of the facial nerve. Additionally, demyelinating lesions caused by viral infections may result in chronic or permanent facial paralysis.
Clinical Manifestations
The onset is acute, with clinical symptoms typically becoming evident within three days. Symptoms predominantly include unilateral peripheral facial paralysis, without identifiable secondary causes.
Symptoms
Symptoms include:
- Facial asymmetry and difficulty closing the eye: Patients may exhibit a deviation of the mouth commissure and an inability to fully close the affected eyelid.
- Abnormal lacrimal gland secretion: Conditions include epiphora (excessive tearing), alacrima (lack of tears), or crocodile tears (paradoxical tearing during eating).
- Taste abnormalities: involvement of the chorda tympani nerve leads to altered taste sensation on the affected side of the tongue.
- Hyperacusis: involvement of the stapedius muscle renders patients sensitive to loud sounds, a condition termed hyperacusis.
Signs
The affected side shows loss of forehead wrinkles, flattening or disappearance of the nasolabial fold, and a widened palpebral fissure.
The affected eyebrow demonstrates an inability to elevate. The affected eyelid cannot close, and during attempted eye closure, the eyeball exhibits upward and outward movement with exposure of the sclera, a phenomenon known as the "Bell's phenomenon." When smiling or showing teeth, the mouth commissure deviates towards the healthy side.
Most patients begin to exhibit signs of facial nerve function recovery within three weeks, and nearly all patients experience varying degrees of recovery by six months.
Diagnosis and Differential Diagnosis
The diagnosis of Bell's palsy is primarily based on the patient's medical history and physical examination. Electroneurography and electromyography are valuable for assessing prognosis and determining the timing of surgical intervention in patients with Bell's palsy. When the medical history and clinical presentation strongly suggest Bell's palsy, CT and MRI are not generally recommended. However, some experts consider timely imaging studies essential to exclude other conditions, such as facial nerve and internal auditory canal tumors, otitis media, or cholesteatoma of the middle ear and mastoid, especially when patients present with associated symptoms like otorrhea, vestibular symptoms, or hearing loss. Imaging is also valuable when surgical decompression is planned or in cases of persistent severe paralysis beyond six months.
In the majority of cases, MRI conducted within 10 days of the onset of facial paralysis can reveal classic signs of facial neuritis. Typical MRI findings include diffuse thickening of the affected segment of the facial nerve, increased signal intensity on T2-weighted imaging compared to the contralateral side, and enhancement following contrast administration.
Treatment
The management of Bell's palsy involves a multidisciplinary approach, emphasizing a combination of treatments, including corticosteroids or corticosteroids combined with antiviral drugs. The role of surgical intervention remains a subject of debate.
Medication Treatment
Eye Care
Proper eye protection is necessary. Incomplete eyelid closure and impaired blinking may reduce tear secretion and increase the risk of corneal exposure and ulceration, particularly at night. Eye drops or ointments, along with the use of protective eye patches, are advisable.
Corticosteroid Therapy
Corticosteroids should be administered orally within 72 hours after the onset of facial paralysis. Suggested regimens include prednisone at 25 mg, twice daily for 10 days, or prednisone at 60 mg, once daily for 5 days, followed by a gradual taper starting on day 6, reducing the dose by 10 mg per day.
Antiviral Drugs
Antiviral medications, such as acyclovir or valacyclovir, may be administered in combination with corticosteroids. Suggested dosages include oral acyclovir at 0.2–0.4 g, three to five times daily, or oral valacyclovir at 0.5–1.0 g, two to three times daily, for 7–10 days. Monotherapy with antiviral drugs is not generally recommended.
Neurotrophic and Vasodilator Medications
Supplements that support nerve health or improve microcirculation may help reduce edema and promote recovery.
Early Use of Mannitol
The use of 20% mannitol during the early stages may help reduce facial nerve edema.
Surgical Treatment
Facial nerve decompression surgery was first proposed by Ballance et al. in 1932. Facial nerve decompression has been described as a surgical approach for treating Bell's palsy. However, due to a lack of large-scale randomized, double-blind, controlled clinical studies, the timing and clinical efficacy of such surgical interventions remain controversial. High-quality clinical research is needed to further validate these outcomes.
Neuromuscular Rehabilitation
Early rehabilitation therapy during the acute phase of Bell's palsy is not generally supported by international literature. For patients with persistent facial paralysis and suboptimal treatment outcomes, facial muscle and nerve rehabilitation therapy may be considered.
Recommendations for Comprehensive Treatment
Early initiation of corticosteroid therapy is highly recommended, with the optional addition of antiviral drugs. If there is no improvement in facial paralysis after one week of treatment, or if it progresses to complete facial nerve paralysis, an assessment with electroneurography is necessary. If degeneration of the facial nerve exceeds 90% within two weeks of onset or exceeds 95% at three weeks, patients and their families should be informed of the current treatment options and prognosis, both domestically and internationally. With informed consent, facial nerve decompression surgery may be considered.