Evaluation & Treatment


The diagnosis of facial nerve paralysis depends upon a cogent analysis of a number of different elements. Timing of each element is important and the ultimate diagnosis may require the collaboration of a number of physicians. Depending upon the location of the injury/disorder of the nerve along its course from the brain to the face, it presents with different symptoms. The astute clinician may be able to determine the site of the problem with just a physical exam.

Options for imaging include ultrasound, magnetic resonance imaging (MRI) and computed tomography (CT). Ultrasound is very helpful in diagnosing soft tissue abnormalities of the face such as salivary gland tumors, nerve sheath tumors, and cysts. It cannot penetrate bone, so its role is limited. CT scans offer very detailed pictures of bone and can be very helpful in diagnosing temporal bone fractures, and problems with the bones of the middle and inner ear. It is a rapid test, but does not provide fine detail on the facial nerve itself. MRI is a time-consuming and expensive test and often requires the placement of an IV for contrast dye. The MRI provides fine resolution of the entire course of the facial nerve from the brain to the face. It is usually the most important test for virtually any facial nerve disorder. The contrast dye can help identify enhancement of the nerve, which is usually consistent with inflammation.

There are a number of viral, bacterial and auto-immune diseases that can lead to facial nerve disorders. These include mumps, otitis media, syphilis, chicken pox, and measles. Depending upon the circumstances, testing for these diseases may make up part of the diagnostic pathway for a facial nerve disorder.

The clinical exam of a patient with a facial nerve disorder is very important. The exam usually includes an exam of the middle ear, hearing evaluation, palpation of the face and neck, ophthalmologic and neurologic assessments. When combined with the clinical history, diagnosis may be readily made even in the absence of imaging and blood testing.


Electromyography is a neuroelectrophysiological test that evaluates the health and integrity of the facial nerve. It is usually employed greater than 6 months following the onset of facial nerve paralysis. Small needles are inserted into select facial muscles and patients are asked to contract those muscles. Nerve signals are thereby recorded which yield information about the health of the nerve and muscle. Muscles which are undergoing reinnervation demonstrate the presence of action potentials and spike and wave activity. Muscles which are not experiencing reinnervation demonstrate fibrillation potentials or baseline, random electrical noise. This means that the muscles are still alive and awaiting a signal from a nerve, but that a nerve has not yet demonstrated evidence of the onset of recovery. Electrical silence is associated with a chronically denervated muscle, which can no longer be successfully reinnervated.

Electroneuronography is a test usually performed by audiologists to assess the integrity of the facial nerve. Two electrodes are taped to one side of the face. The first is taped over the stylomastoid foramen behind and under the ear and the second is taped near the nasolabial fold. The electrode behind the ear emits an electrical pulse and the electrode at the nasolabial fold picks up the any signal that is transmitted by the facial nerve fibers. Comparing the size, speed and strength of the transmitted signal allows for the measurement of the integrity of the facial nerve. Comparison between tests performed on the different sides of the same face permit an estimation of the degree of difference between the normal and the disordered nerve. ENoG’s performed on different days permits assessment of the worsening or potential improvement in nerve health.

Facial neuromuscular retraining (FNR), also known as facial rehabilitation, is an exciting facet in the overall treatment of facial nerve disorders. When performed by an experienced physical therapist, facial rehabilitation can help patients optimize their facial muscular function. Consisting of selected and precise exercises and expression modification, FNR attempts to modify the expressions between the two sides of the face in order to realize as much symmetry as possible. In the setting of Bell’s palsy with incomplete recovery, FNR attempts to train the nerves and the brain to accommodate to the mass movements and to progressively teach the face to normalize its expressions. In the setting of reinnervation and or regional muscle transfer, NMT helps to improve the use of the new facial function and to optimize the recovery of symmetry.

Botulinum toxin therapy consists of the selective use of any of 3 commercially available preparations (Botox®, Xeomin®, Dysport®) to improve the symmetry of facial function. While “botox” is most commonly used for cosmetic reasons, when injected into muscles, it causes temporary paralysis. This usually starts 3-5 days after injection and commonly lasts for approximately 3 months. When used cosmetically, botulinum toxin therapy prevents wrinkles by temporarily paralyzing the muscle responsible for the wrinkling. This same concept of selectively paralyzing muscles of facial expression can be used with facial paralysis. For example, when only 1 side of the forehead wrinkles, causing asymmetry of the eyebrows, the normal or unparalyzed side may be treated with botulinum toxin, bringing about symmetry of the two sides. When it comes to synkinesis, botulinum treatment can eliminate some of the facial contractions and maximize smile excursion.

Facial nerve paralysis results when the signal to move the face that is sent from the brain is interrupted in its course to the muscles of facial expression. Interruption of the signal, due to brain trauma/surgery, middle ear trauma/surgery or facial soft tissue surgery leads to reversible atrophy and drooping. The number of potential causes of the interruption of the facial nerve signalling (the facial nerve is essentially just an extension cord delivering impulses from the brain to the face), is literally limitless, including everything from a stroke (hemorrhagic or ischemic cerebrovascular accident (CVA)), to a temporal bone fracture, to an inborn absence of the facial nerve (Mobius syndrome). Most importantly, the droopiness and atrophy of the face is only reversible if it is treated within the first 18-24 months after the onset of facial paralysis.

The best outcome of a facial nerve injury occurs when the nerve recovers all by itself, and no surgery is necessary. Recovery may take 6-12 months, and the EMG and/or ENoG may be helpful in detecting the onset of recovery.

If trauma or surgery led to a gap in the nerve, the best treatment is usually just to “bridge” the gap with a nerve graft. As long as both ends of a severed or injured nerve can be accessed, a nerve graft can be taken from the neck, or thigh or leg and used to restore continuity of the facial nerve and allow it to heal.

If the proximal end of the facial nerve cannot be accessed, due to the injury occurring in the brain, the best outcomes traditionally come from nerve transposition.

Nerve to Masseter transposition (5 to 7)

Nerve transposition in the treatment of facial paralysis simply means finding a locally available motor nerve and using it to delivery nerve power to the facial nerve. Locally available nerves include the nerve to the tongue (12th nerve), the nerve to the sternocleidomastoid muscle (11th nerve), and the nerve to the masseter muscle (5th nerve). While many patients undergoing nerve transposition used to undergo a 12/7 procedure (transposition of the 12th nerve to the 7th nerve), this treatment left many of them with some degree to tongue paralysis and led to synkinesis (mass movement) of the face. Contemporary treatment at high volume hospitals has therefore shifted to use of the 5/7 procedure (transposition of the nerve to masseter to the facial nerve). Use of the masseter nerve has many advantages: (1) the nerve is in close proximity to the facial nerve so the scar resulting from the operation is less noticeable (essentially a facelift scar); (2) the loss of masseter function is relatively mild when compared to loss of tongue function; (3) the amount of retraining needed to learn to smile with the nerve to masseter is much less than that needed for the other nearby motor nerves, as virtually everyone bites down somewhat with a big smile; (4) the ability to smile returns much faster using the nerve to masseter (3-4 months quicker).

Temporalis tendon transfer/Lengthening temporalis myoplasty

If nerve transposition is not an option, immediate smile restoration is possible using the temporalis muscle. This remarkable muscle is powered by a different nerve than the muscles of facial expression and can be easily detached from the mandible and inserted into the corner of the mouth to provide a smile. The more minimally invasive temporalis tendon transfer (T3) is a good option for people with a sufficiently long tendon, although it usually only provides 4 mm of lip movement. The lengthening temporalis myoplasty requires an external incision on the temple, and may lead to some flattening of the temple, but usually provides somewhat more movement and a more natural appearance of movement of the lateral lip and corner of the nose.

When neither the proximal nerve nor the distal nerve segments are available for reinnervation, or more than 2 years have passed from the time of injury, only neuromuscular tissue transfer or regional muscle transfer offer potential smile restoration. While the regional muscle transfer may be relatively simple and quick, and offer immediate dynamic smile, the neuromuscular tissue transfer offers the potential for more movement and the restoration of a potentially normal smile.

Neuromuscular Tissue Transfer, most commonly known as the gracilis free flap, is a beautiful operation that may be performed in 1 or 2 stages. When performed in 1 stage, the team collaborate in surgery. The first team performs the facial dissection, raising the facelift flap, identifying the masseteric nerve and preparing the facial vessels for anastomosis. The second team harvests the gracilis muscle from the medial thigh. The gracilis is a relatively unimportant muscle which has a large artery, vein and nerve entering it. All three of these are harvested with the muscle and are transferred to the face. Blood circulation to the muscle is restored with microsurgery, and the nerve is also hooked up to the masseter nerve. Six to 12 months after successful surgery, patients can begin to smile broadly with biting.

When performed in 2 stages, a long nerve graft is first harvested from the leg and is hooked up to a redundant nerve of smiling on the normal, fully functional side of the face. This nerve graft is brought out to the other, paralyzed side of the face. Approximately 6 months later, the second stage takes place, and the gracilis muscle can be hooked up to both the masseter nerve and the contralateral facial nerve graft, offering the potential for spontaneous smiling, as well as smiling with biting.

Dynamic facial reanimation is not always possible for our patients. Sometimes, due to time, trauma, previous surgery, age or illness, operations involving months-long recovery, nerve grafts or muscle transpositions are simply not feasible. In these cases, static suspension of the face is usually still an option. While restoration of the ability to smile is usually welcome, restoration of facial symmetry at rest is much more important. Without facial symmetry at rest, average people one encounters in life, at the mall, shopping center, church or workplace, will invariably stop and stare at people with facial paralysis. This kind of attention is usually unwanted, and while people are not intentionally rude or impolite, they often just can help staring. Autologous fascia or dermal matrices can be used below the skin to just lift up the smile lines and restore a significant degree of facial symmetry. Static slings can also be used to treat segmental paralyses, or they can be even combined with dynamic options, to reinforce the symmetry of the neutral facial expressions. At UCSF, we want our patients to be confident in going out in public and leading their normal lives.

Synkinesis, (also known as mass movement) is very challenging for our patients. Most commonly seen as over-closing of the eye with almost any facial expression, or grimacing of the mouth with eye closure, it is also associated with the inability to smile fully. There are 7 or 8 muscles that surround the mouth, like spokes emanating from the center of a wheel. When misfiring with synkinesis, these muscles can all contract at once, literally freezing the mouth in an expression of rigidity. While botulinum toxin treatment may treat one of several of these muscles, the execution of a smooth, broad, expressive smile is still very difficult to achieve. By selectively cutting small nerve branches that enable synkinesis, the preserved, positive, functional nerve branches are then able to power more normal facial expressions, such as smiling and puckering. Selective removal of hyperfunctional muscles, or muscles causing asymmetries, may permit more equal and full facial movement.