WHAT IS FACIAL PARALYSIS?
The facial nerve is responsible for facial movement and, therefore, for facial expressions. Damage to this nerve can lead to paralysis of the facial muscles, resulting not only in impaired function but also in significant disfigurement. Facial nerve damage is relatively common, has various causes, and generally follows a benign course, although irreversible sequelae may occur. It is a condition that requires a complex, multidisciplinary approach
WHAT ARE THE CAUSES OF FACIAL PARALYSIS?
Idiopathic Peripheral Facial Paralysis (Bell’s Palsy)
This is the most common form of peripheral facial paralysis, accounting for 50–75% of cases. It typically has a sudden and unilateral onset and is more frequent in young women under 40 years old. The exact cause is unknown—hence the term “idiopathic”—but the most accepted theory is that it is due to viral neuritis caused by the herpes simplex virus (HSV), which inflames the nerve. Since the nerve is encased in bone, it cannot expand (like being in a bottleneck), resulting in a reversible nerve injury. Predisposing factors include pregnancy, diabetes, and hypertension.
Diagnosis of Bell’s palsy is made by exclusion and must be differentiated from other secondary facial paralyses.
Treatment consists of high-dose oral corticosteroids for the first five days, followed by a tapering dose. Increasingly, antiviral therapy (such as acyclovir, valacyclovir, or famciclovir) is being combined with corticosteroids. Even without treatment, Bell’s palsy has a good prognosis, with most patients experiencing spontaneous recovery, including return of facial movement within three weeks and complete recovery within three months.
Infectious Peripheral Facial Paralysis
This can be caused by bacterial agents (e.g., Borrelia burgdorferi) or viruses such as varicella-zoster, rubella, Epstein-Barr virus, and HIV.
Herpes Zoster Oticus
Infection with the varicella-zoster virus (VZV) causes Herpes Zoster Oticus. This condition is characterized by intense facial pain and the appearance of herpetic vesicles in the Ramsay-Hunt area—the skin innervated by the sensory component of the facial nerve, involving the auricle and external auditory canal. It tends to occur in immunocompromised or diabetic patients and has a poor prognosis. Treatment includes corticosteroids and antiviral therapy, ideally started within 72 hours of symptom onset.
Lyme Disease
Lyme disease is a bacterial infection caused by Borrelia burgdorferi, transmitted via tick bites and typically found in endemic rural areas. It usually presents with a characteristic rash called erythema migrans. Diagnosis is confirmed by serology (ELISA or Western Blot), and treatment involves doxycycline.
Traumatic and/or Iatrogenic Peripheral Facial Paralysis
This is the second most common type. Causes include facial trauma and temporal bone (petrous portion) fractures. These fractures may be longitudinal (along the long axis of the bone) or transverse (perpendicular to the long axis), although many are mixed. CT scans are used to evaluate the fracture line.
Obstetric trauma deserves special mention. It is the most common facial paralysis in newborns, though still rare. It is often linked to instrument-assisted deliveries (forceps). It must be differentiated from congenital facial paralysis, which is usually associated with syndromes or malformations.
Iatrogenic facial paralysis, secondary to surgery, usually results from otologic surgery, skull base surgery, or parotid gland surgery.
Tumoral Peripheral Facial Paralysis
Facial paralysis caused by tumors tends to have an insidious and progressively worsening onset and may go unnoticed initially. It is associated with head and neck cancers or cerebellopontine angle tumors, most commonly vestibular schwannoma (acoustic neuroma).
Other Causes
– Neurological (stroke, Guillain-Barré syndrome, multiple sclerosis)
– Otologic (acute or chronic otitis media, cholesteatoma, malignant external otitis, vestibular schwannoma)
– Systemic (sarcoidosis, autoimmune diseases, Paget’s disease of bone, vasculitis, porphyria, diabetes mellitus, leukemia)
– Syndromic (Melkersson-Rosenthal, Moebius syndrome)
WHAT ARE THE SYMPTOMS OF FACIAL PARALYSIS?
Facial paralysis presents as impaired facial muscle mobility, which may be unilateral or bilateral. Muscle weakness may vary in severity and location. Common signs include the disappearance of forehead wrinkles on the affected side, inability to raise the eyebrow, difficulty closing or blinking the eye, loss of the nasolabial fold, drooping of the mouth corner (which deviates to the healthy side), and difficulty blowing, whistling, or puffing out the cheeks. Bell’s phenomenon may also occur, where the eyeball moves upward and outward when the patient attempts to close the eyelid.
Symptoms may appear suddenly or gradually. The pattern of onset is crucial for determining the underlying cause.
It is important to review the patient’s medical history (e.g., hypertension, diabetes, obesity, cardiovascular risk factors, current medications) and ENT history (e.g., infections, ear surgeries, trauma, family history of hearing loss, alcohol or tobacco use).
Associated symptoms may help identify the cause and include neurological signs, vertigo, ear discharge or pain, hearing loss, dry eyes (xerophthalmia), excessive tearing (epiphora), excessive salivation (sialorrhea), retroauricular pain, and throat or neck discomfort.
WHAT IS THE TREATMENT FOR FACIAL PARALYSIS?
Treatment includes pharmacological therapy, eye care, rehabilitative therapy, and surgery.
Pharmacological Treatment
Should always be prescribed by a physician. ENT specialists are particularly well-qualified to assess and manage this condition. The choice of medication depends on the underlying cause.
Eye Care
After facial paralysis, the eye may suffer irreversible damage if the cornea remains exposed due to incomplete eyelid closure. Eye care is therefore essential. Patients should use intensive eye lubrication with artificial tears or non-antibiotic lubricating ointments if there’s no suspected superinfected ulcer. Nighttime eye patching is also important.
Rehabilitative Treatment
Rehabilitation is critical in managing facial paralysis. For long-standing paralysis, rehabilitation follows facial reanimation surgery or is used in cases of spastic facial paralysis. The goal is to reduce hypertonia and control synkinesis using botulinum toxin.
Surgical Treatment
Patients who do not regain facial movement or in whom nerve regeneration is not expected may be candidates for facial reanimation surgery. This can be dynamic (restoring movement to the paralyzed side) or static (aiming for symmetry without restoring movement), depending on the patient’s needs and expectations.
In the first 18–24 months after onset, dynamic reinnervation techniques are ideal. These may involve nerve grafts (e.g., from the greater auricular or sural nerve) or cross-facial nerve grafting using the healthy facial nerve, the masseteric nerve, or the hypoglossal nerve.
For long-standing paralysis (more than 24 months), a free muscle transfer with reinnervation is recommended, as the facial muscles atrophy from prolonged denervation.
Static techniques (which restore symmetry but not movement) include temporalis muscle transposition, fascia lata slings, and forehead lifts.
Ocular surgery aims to protect the eye and may include gold eyelid weights, hyaluronic acid or autologous fat injections in the upper eyelid, tarsorrhaphy, or canthoplasty, among others.