Facial paralysis (FP) has an estimated annual incidence of approximately 70 cases per 100,000 population.1,2 Furthermore, it is estimated that approximately 127,000 cases of permanent FP occur annually.3
The most common causes of FP are Bell’s palsy, trauma, herpes zoster oticus and neoplasia.2 FP, which results from injury to the facial nerve, can appear suddenly or develop gradually over time. This condition can take many forms, including facial drooping, involuntary movements or facial tightening.
It has devastating functional and social consequences, which include loss of self-expression and personal identity, an inability to protect the eye and inabilities in eating, drinking and speaking. Patients with FP are also perceived as less attractive and intelligent by social observers.4,5 These disruptions lead to increased social isolation, higher rates of depression and poorer performance on quality of life measures.6-9
Signs and symptoms of facial paralysis can include:
- An inability to raise the eyebrow
- Lagophthalmos (inability to close the eyelids completely)
- Eye irritation and dryness
- Facial droop
- Inability to smile, pucker or frown
- Eating difficulty
- Oral incompetence
- Cheek biting
- Facial tightness and spasm
The facial nerve is the seventh cranial nerve, which originates in the brainstem and then exits the base of the skull to ultimately supply the facial muscles. Neuronal insult along the course of the nerve will result in loss of neural transmission, causing loss of muscular function.
Depending on the type of insult, recovery can range on a spectrum from complete to no recovery. Complete recovery results in no residual deficits. Partial recovery may result in a hypertonic muscular state with involuntary co-contraction of unintended muscle groups known as synkinesis. This state represents incomplete axonal loss with aberrant reinnervation. No recovery results in a flaccid state with complete loss of all muscular tone and movement. This state represents a complete loss of axonal input to the target facial muscles. Both forms of incomplete recovery impart significant morbidity secondary to loss of those aforementioned functions.
The type of neural insult, time from injury onset and degree of clinical recovery dictate the type of clinical intervention indicated. For those patients with no recovery (e.g. flaccid paralysis) resulting from known nerve transection, there is a limited time window to intervene to salvage the denervated muscles.
After 24-36 months of denervation, the muscles undergo irreversible fibrosis and atrophy, rendering them nonfunctional and nonreceptive to reinnervation. It is therefore critical to attempt to rescue the muscles from this irreversible fate by supplying alternative neural input during the reinnervation window. These procedures include cranial nerve transfers (e.g. masseteric, hypoglossal) and cross facial nerve grafts.
Those patients beyond the reinnervation window require free neurovascular muscle transfers (e.g. gracilis muscle transfer) to replace the atrophied native musculature. For those patients with partial recovery and synkinesis, the treatment plan is dependent on their symptomatology. However, the first-line non-surgical treatments are facial physiotherapy and botulism toxin injections. Surgical options include selective facial neurectomy and myectomy.
COMMON CAUSES OF FP
Bell’s Palsy. Bell’s palsy (BP) is the most common cause of facial paralysis. Often referred to as idiopathic or viral FP, this disorder leads to acute-onset FP that can be temporary and reversible, but in some cases it can lead to permanent facial synkinesis and tightness.
Typically, it affects just one side of the face. Viral etiologies have been suggested as the cause of BP. Oral steroids should be administered within 72 hours of symptom onset for patients 16 years and older, and clinicians may offer oral antiviral therapy in addition to oral steroids.10
It is very important to note that Bell’s palsy is a diagnosis of exclusion. Patients with an initial diagnosis of BP with no return of tone or movement at 6 months must be further evaluated for possible malignant FP etiology.11
Ramsay Hunt Syndrome. Herpes zoster oticus, also called Ramsay Hunt Syndrome, is characterized by the reactivation of latent varicella-zoster virus (VZV), which causes acute facial palsy, inner ear dysfunction, ear pain and herpetiform vesicles on ear. Other symptoms may include hearing loss, vertigo (abnormal sensation of movement) and tinnitus (abnormal sounds). Taste loss in the tongue and dry mouth and eyes may also occur. Recommended initial treatment for this syndrome includes antivirals and steroids.
Facial Nerve Damage. Facial nerve damage can be caused by several things, including a penetrating or blunt trauma to the facial nerve or temporal bone. It can also be caused by an:
- Injury to the facial nerve as the result of surgery such as vestibular schwannoma resection, parotidectomy, facelift, etc.
- Benign or malignant tumors within or near the facial nerve, such as vestibular schwannoma, parotid tumors etc.
- Eurological conditions, such as a cerebrovascular accidents, can also cause facial nerve damage.
A multi-disciplinary approach is necessary to manage facial paralysis. The Emory Facial Nerve Center team consists of specialists from facial physiotherapy, microneurovascular surgery, neurotology, facial plastic surgery, oculoplastic surgery, neurology, neurosurgery and neuroradiology.
Once the cause of facial paralysis is identified, the following treatments may be offered depending on the etiology of FP:
- Botulism toxin (Botox) for facial synkinesis and spasm
- Facial neuromuscular retraining to improve muscle strength, coordination and movement
- Eyelid weights and tightening procedures to protect the paralytic eye
- Nerve transfers using nearby functioning motor cranial nerves to restore facial tone and movement
- Cross facial nerve grafting using facial nerve branches from the nonparalyzed side of the face to reinnervate facial muscles on the paralyzed side
- Gracilis muscle transfer transplanting nerve and muscle from the inner thigh to the face for smile restoration
- Selective neurectomy (nerve cutting) and myectomy (muscle cutting) to relieve synkinesis and improve the ability to smile
- Static slings using the muscular lining from the thigh to balance the look of the lips, corner of the mouth and laugh line
A multi-disciplinary approach to facial paralysis is critical to improve outcomes in this challenging population. It is crucial to have these patients evaluated by a facial nerve specialist promptly following known nerve injury to assess the need for reinnervation procedures as soon as feasible. Eye care is paramount in the acute setting to protect from corneal damage and potential vision loss. Bell’s palsy is a diagnosis of exclusion and malignant etiologies must be excluded if flaccid facial paralysis persists longer than 6 months.
Physician referrals to the Emory Facial Nerve Center can be made by calling 404.778.0278.
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