Bell Palsy

Etiology

Historically, Bell palsy has been considered a diagnosis of exclusion, to be applied when no other causes of acute-onset facial paralysis are readily apparent. If a patient with hemifacial palsy were to present in the absence of an auriculofacial rash, history of a tick bite, other neurological deficits, and imaging or laboratory abnormalities, Bell palsy would be diagnosed. Ironically, however, the term "Bell palsy" is often misused in an overly nonspecific manner to refer to any hemifacial paralysis, regardless of etiology, for example, describing the manifestations of a coronavirus infection as "upper and lower respiratory symptoms with polyneuropathy and Bell palsy."[10]

While it remains difficult to pin down the exact cause of Bell palsy for any individual patient, there is evidence to suggest that Human herpesvirus 1 is responsible for most of the cases. This virus has been identified in the epineurial fluid of 79% of the patients with Bell palsy but in none of the patients with Ramsay Hunt or other facial palsy conditions in a 1996 study performed by Murakami et al.[11] Testing epineurial fluid for herpes simplex deoxyribonucleic acid by polymerase chain reaction is clinically impractical in most patients, but because of the ubiquity of this virus and its close relatives (other herpes simplex viruses, cytomegalovirus, Epstein-Barr virus), the diagnosis of Bell palsy is now typically made clinically if the history and physical examination are consistent.

Another unsolved mystery regarding Bell palsy is its association with coronavirus disease (COVID) 2019  and the immunizations to prevent this infection. Facial paralysis, as well as other cranial neuropathies, are known to accompany SARS-CoV-2 infection, particularly affecting the olfactory, oculomotor, and abducens nerves, but also the trigeminal, auditory, vagus, glossopharyngeal, and hypoglossal nerves.[12][13][14] More controversial, however, is the potential relationship between Bell palsy and the various available COVID vaccinations. A large metanalysis published by Rafati et al in 2023 provided results determining that the risk of developing Bell palsy after messenger ribonucleic acid (mRNA) vaccination was 3.6 times higher than in the unvaccinated population, but that there was no significant increase in the risk of Bell palsy with viral vector vaccines.[15] However, results from a 2021 study that compared the incidence of Bell palsy after immunization with the Pfizer/BioNTech mRNA vaccine to that after the CoronaVac/Sinovac inactivated virus vaccine found the incidence to be over twice as high with the CoronaVac/Sinovac injection.[16] Regardless, the chance of developing facial palsy is significantly higher (relative risk of 3.23) with COVID infection than it is after COVID vaccination.[15]

Epidemiology

The annual incidence of Bell palsy is 15 to 40 per 100,000 individuals, and the lifetime risk is 1 in 60, with a recurrence rate of 8% to 12%.[1][17] There is no sex, ethnic, or laterality predilection, and Bell palsy can occur at any age; there is a bimodal distribution with incidence peaks between 20 and 30 years and between 60 and 70.[2] There are multiple known risk factors for developing Bell palsy, including diabetes, pregnancy, preeclampsia, obesity, dental procedures, and, debatably, hypertension.[18][19][20] Pregnant patients and those with diabetes are specifically at higher risk for worse outcomes and are potentially more likely to present with worse paralysis than patients without diabetes and who aren't pregnant with Bell palsy.[3][21] 

According to a 2022 paper published by Escalante et al, the most common severity of Bell palsy is House-Brackmann grade III (mild-moderate), accounting for 41.9% of patients. Grade VI palsy (total hemifacial paralysis) occurs in 20.1% of patients. House-Brackmann grades II (mild) and V (severe) each comprise 16.3% of patients, and grade IV accounts for only 5.4%. The same study also assessed the chance of recovery as a function of palsy severity and found that patients with House-Brackmann grade VI palsy had a 60% chance of recovery to grade I or II, and grade V patients had an 83% chance if provided steroids and antivirals. Patients with grade II to IV paralysis all recovered to grade I or II in this series.[2]

Pathophysiology

Bell palsy, which is a unilateral hemifacial palsy of rapid onset, results from inflammation of the facial nerve, typically originating in the labyrinthine segment (see Image. Bell Palsy). The labyrinthine segment is the second intratemporal segment of the facial nerve and the narrowest, with an average diameter of 0.7 mm and a length of 3 to 5 mm.[22] The narrowness of this portion of the facial nerve's canal through the temporal bone of the skull (the Fallopian canal) predisposes it to dysfunction, potentially due to edema and subsequent impairment of perfusion when inflammation occurs, with Bell palsy more likely to occur in patients who have narrow labyrinthine segments of the facial canal.[23] 

Proximal to the labyrinthine segment is the canalicular segment, which runs in the internal auditory canal superior to the cochlear nerve and anterior to the superior vestibular nerve. The labyrinthine segment ends distally at the geniculate ganglion, where the greater superficial petrosal nerve branches off to supply parasympathetic innervation to the lacrimal gland and the mucous glands of the nasal cavity and palate. At the distal end of the geniculate ganglion, also known as the first genu of the facial nerve, the tympanic segment enters the middle ear and courses superior to the oval window before turning inferiorly at the second genu and entering the mastoid cavity. The mastoid segment courses downwards to the stylomastoid foramen, where the nerve exits the temporal bone on its path to the parotid gland, within which it divides into the five main branches that innervate the muscles of facial expression. These branches are the frontal, zygomatic, buccal, marginal mandibular, and cervical (see Image. The Facial Nerve).[24]

Bell palsy is thought to result from compression of the seventh cranial nerve within the labyrinthine segment of the Fallopian canal. Not only is this segment the narrowest along the nerve's course within the temporal bone, but it also appears to have the most tenuous blood supply, with very fine arterioles connecting the angiosomes supplied by the internal auditory branch of the anterior inferior cerebellar artery proximally and the petrosal branch of the middle meningeal artery distally.[25] The final segment of the intratemporal facial nerve is perfused by the stylomastoid artery, a branch of the posterior auricular artery. Further implicating the labyrinthine segment as the primary site of Bell palsy inflammation is the appearance of the nerve on magnetic resonance imaging (MRI): 59% of patients with acute Bell palsy have asymmetric enhancement of the labyrinthine segment, and a further 33% have enhancement of both the labyrinthine segment and the geniculate ganglion (see Image. Left-Sided Bell Palsy, Magnetic Resonance Image).[26] 

The severity of this inflammation may depend upon several factors, including the patient's immune status, blood glucose level, blood pressure, and age.[18][19] There is a hypothesis that edema of the nerve within the Fallopian canal compromises perfusion, leading to nerve dysfunction. The extent of the dysfunction and the prognosis for recovery depend on the degree of disruption of the internal architecture of the facial nerve, in which each axon has a myelin sheath and an endoneurial membrane surrounding it, with the axons grouped together into fascicles surrounded by perineurial membranes, and the fascicles together constituting the nerve itself, which is invested in epineurium (see Image. Neurology, Nerve Fascicle, Fasciculus, Epineurium).

A mild injury may only cause a temporary conduction block with or without focal demyelination, known as neuropraxia in the Seddon grading system, or a Sunderland class I injury. Actual axonal damage occurs in a Sunderland class II injury, but all of the internal architecture of the nerve is otherwise preserved, virtually ensuring that the axons regrow correctly along their original paths. In the case of a Sunderland class III injury, the axons undergo Wallerian degeneration as they do in a class II injury. However, the endoneurial membranes that surround the damaged axons are violated, which permits mild misdirection of the regenerating axons that may result in discoordinated movements and spasms (synkinesis). A Sunderland class IV injury adds perineurial damage to the class III injury, which results in disruption of the fascicular organization of the nerve and greater potential for synkinesis. Sunderland class II to IV injuries are collectively known as axonotmesis in the Seddon grading system, and a Sunderland class V injury is known as neuronotmesis.[27][28] Neuronotmesis is a complete transection of the nerve, including the epineurium, guaranteeing severe synkinesis even if the nerve is repaired microsurgically (see Image. Seddon and Sunderland Classifications of Nerve Injury).

History and Physical

Patients with Bell palsy present with progressive hemifacial paralysis that typically reaches a peak in severity within 24 to 72 hours of onset. Most patients will also report prodromal dull pain within or behind the ipsilateral ear. Other common associated symptoms include hyperacusis due to stapedius muscle weakness, a metallic taste on the ipsilateral side of the tongue or ipsilateral tongue numbness due to chorda tympani involvement, paradoxical eye dryness with tearing due to impairment of both eye closure and the lacrimal pump function of the orbicularis oculi muscle, ipsilateral nasal obstruction due to nasalis muscle weakness, oral incompetence and dysarthria due to orbicularis oris dysfunction, aesthetic self-consciousness because of facial asymmetry, and ipsilateral facial numbness. The latter may be a mischaracterization of facial weakness by some patients but may also represent a manifestation of the poorly understood connections between branches of the facial and trigeminal nerves that have been observed in laboratory studies.[29][30] 

If the patient notes skin or mucosal rashes, an alternative diagnosis, such as Ramsay Hunt syndrome or Lyme disease, should be considered. Similarly, if the patient mentions significant, burning pain rather than a dull otalgia, a herpes zoster diagnosis may be appropriate even in the absence of a vesicular outbreak. Most importantly, there should not be an element of the history that implicates a specific etiology for facial paralysis, such as head trauma, otologic infection, or neoplasm.

Upon physical examination, all branches of the facial nerve are roughly equally impaired on the affected side of the face in patients with Bell palsy. In contrast, a cortical stroke will typically leave forehead movement intact on the affected side due to bilateral upper motor neuron contributions to the facial nucleus. A stroke will typically also present with other neurological signs or cranial neuropathies, while Bell palsy will not. Like Bell palsy though, a brainstem stroke will cause hemifacial weakness that does not preserve forehead movement; this too will most often present with other neurological symptoms as expected with a cortical stroke.

The unilaterality of Bell palsy is an important feature that helps to differentiate it from other facial paralyses, such as Lyme disease and Guillain-Barré syndrome, which often present with bilateral, albeit asymmetric, facial paralysis. Similarly, the presence of a cutaneous or mucosal rash of the head or face along with hemifacial palsy should shift focus to a diagnosis of Ramsay Hunt syndrome; a targetoid rash anywhere on the body may indicate Lyme disease. Patients presenting with chronic facial movement dysfunction from Bell palsy rather than acute, flaccid paralysis may report facial tension, fatigue, and pain instead of frank weakness, although they may mistake this synkinetic dyscoordination and asymmetry of facial expression for persistent paralysis. Another phenomenon that may accompany facial synkinesis is Bogorad syndrome, or "crocodile tears," in which aberrant reinnervation of the lacrimal gland leads to tearing that accompanies salivation.

An assessment of facial nerve function should be performed in a systematic fashion to ensure no findings are overlooked (see Video. Acute Bell Palsy with a Severe Presentation). Evaluating each extratemporal branch of the facial nerve individually is critical, both at rest and with movement. Resting forehead rhytid and brow symmetry, as well as symmetry with elevation, should be assessed; the examiner's thumb may be used to hold the glabella still to prevent transmission of movement from the normal side to the paralyzed brow if there is any doubt about the presence of movement on the affected side. The resting appearance of the palpebral fissures should be compared, and any increased opening on the affected side should be noted, as well as whether the increased opening is due to upper eyelid retraction or lower eyelid laxity. There may be asymmetry of the lateral periocular rhytids (crow's feet) as well, with the affected side having fewer or shallower wrinkles. Gentle eye closure (with a normal blink) and eye closure with full effort should be assessed, although it is not necessary to attempt to pry open the patient's eyes manually, as this maneuver has no prognostic or diagnostic value.

If eye closure is incomplete, the Bell phenomenon should be assessed to help determine the risk of corneal exposure. The Bell phenomenon is the reflex by which the globe rolls superolaterally to protect the cornea when the eye closes; this reflex may serve to protect the cornea even if eye closure is incomplete (see Image. Bell Phenomenon). The reflex is present in 70% to 80% of the population and tends to diminish with age.[31] If, on the other hand, eye closure is complete, the finding should be considered in the context of the rest of the history and physical examination. If several days have passed since the onset of paralysis and the rest of the hemiface also demonstrates some movement, the paralysis is likely only of mild to moderate severity. If there is slow but complete eye closure and no discernable movement in the rest of the hemiface with paralysis of recent onset, the eye closure is likely due to gravity rather than volitional movement and does not indicate any retained facial nerve function. Paralytic lagophthalmos in this situation will likely develop over the ensuing 24 to 48 hours.

Evaluation of midfacial motor function begins with a comparison of the nasolabial folds at rest. The affected side's fold may be shallower and/or more vertically oriented than the unaffected side. There may also be unilaterally diminished contraction of the nasalis muscle, although, like the eyebrows, this may be difficult to discern without placing a thumb in the center of the nose to prevent transmitted movement. A Cottle maneuver, in which the examiner's thumb is used to suspend the nasal base by retracting the cheek laterally, will identify any nasal valve collapse.

In the lower face, the oral commissure may be inferiorly malpositioned, and the philtrum may be pulled towards the unaffected side due to a lack of resting muscle tone on the affected side. The smile may be asymmetric, with decreased oral commissure excursion, upper lip elevation, and lower lip depression on the affected side. Lastly, there may be asymmetric platysmal contraction or even loss of resting platysmal banding on the affected side in an older patient.

The overall function can then be categorized using the House-Brackmann scale, which was published in 1985 as a means of describing acute otologic facial paralysis, although it also works well for documenting the severity of acute Bell palsy (see Table. House-Brackmann Facial Nerve Grading System). For patients with chronic facial movement disorders due to incompletely recovered Bell palsy, the use of a more detailed scale, such as the House-Brackmann 2.0, Sunnybrook, Yanagihara, or eFace, is appropriate and conveys additional useful information (see Staging section). These patients require a more detailed physical examination; after assessing resting symmetry and voluntary movement as described above, the location and degree of synkinesis should be evaluated. Doing so requires the same facial movements previously detailed, but the examiner directs attention to the regions of the face that are not requested to move. For example, with eye closure, the clinician will look for zygomaticus muscle and platysmal contraction, or with lip pucker, there may be involuntary winking (see Video. Post-Bell Palsy Synkinesis). Other common areas in which synkinesis is seen are the mentalis, depressor anguli oris, and frontalis muscles.

Table. House-Brackmann Facial Nerve Grading System 

*In the first 1 to 2 days after paralysis onset, eye closure on the affected side may remain complete due to gravity even if there is a severe facial nerve dysfunction. Lagophthalmos may present in a delayed fashion even if the rest of the face is paralyzed, and this preserved eye closure should not be considered in the overall House-Brackmann assessment.

Additional physical examination techniques may be employed to assess ocular health, such as slit-lamp evaluation with fluorescein to identify corneal defects and Schirmer testing to evaluate tear production. The Schirmer test involves placing a strip of filter paper in the fornix of the lower eyelid for 5 minutes and measuring how far the moisture has diffused at the end of that period; 10 mm or more is considered normal. Photographs, videos, and patient-reported quality-of-life instruments should also be completed in order to facilitate objective tracking of recovery.

The Sir Charles Bell Society of International Facial Paralysis Experts recommends obtaining the following photographs of every facial paralysis patient at every visit: in repose, elevation of eyebrows, gentle eye closure, tight eye closure, wrinkling the nose, small closed-mouth smile, large smile showing teeth, lip puckering, depressing the lower lip to show the bottom teeth, and a nasal base "worm's eye" view.[33] The same movements should be recorded on video as well. Lastly, an outcomes survey, such as the Facial Clinimetric Evaluation scale (FaCE), should be documented at each visit to track the effect of any interventions performed and monitor the patient's progress over time.[34]

Patients who present with incomplete paralysis less than 72 hours after palsy onset should have a follow-up visit within 1 week to determine whether the paralysis progresses to House-Brackmann grade VI and requires evaluation with electrodiagnostic testing (see Evaluation section). Patients should also be advised to follow up immediately if eye pain, photophobia, or a foreign body sensation develops, which can indicate a corneal abrasion and necessitate ophthalmological evaluation. Vesicles ipsilateral to the paralysis appearing on the ear, scalp, face, or in the mouth within a few days after initial presentation should trigger the diagnosis of Ramsay Hunt syndrome, which necessitates a higher dose of antivirals than Bell palsy and a prolonged steroid course.[35]

Evaluation

The history and physical examination determine the need for additional evaluation, which is not required in typical cases of Bell palsy. There is some evidence to suggest that a neutrophil-to-lymphocyte ratio higher than 3.53:1 is a reliable predictor of poor recovery, but this has not achieved widespread acceptance as a standard part of the evaluation of patients with Bell palsy, given the high spontaneous recovery rate and the cost of drawing blood.[36]

When a patient presents with House-Brackmann grade VI paralysis, some surgeons will offer facial nerve decompression under specific circumstances. While the outcomes of the operation are somewhat variable and the practice controversial, the most widely adopted candidacy criteria require electroneuronography (ENoG) and electromyography (EMG). ENoG is a form of evoked EMG in which a transcutaneous stimulator is placed over the stylomastoid foramen, and cutaneous electrodes on the face record the compound muscle action potentials that result from facial nerve stimulation. The muscles typically monitored are the orbicularis oculi and the zygomaticus major. The ENoG requires an unaffected side to act as a control for comparison with the affected side, and the test, therefore, works best when only 1 side of the face is weak, as is generally the case for Bell palsy. If the compound muscle action potential amplitude is reduced by 90% or more on the paralyzed side relative to the unaffected side, the ENoG is considered positive, and the EMG is then performed.[37]

The EMG following a positive ENoG is performed by placing percutaneous needle electrodes into the same muscles monitored with the ENoG and looking for motor units that contract when the patient attempts voluntary facial movement. If motor units are identified, the nerve injury is considered incomplete, but if no motor units are present, the patient meets the criteria for operative facial nerve decompression.[38] The procedure, depending on how it is performed, requires a craniotomy or, at the very least, a mastoidectomy, and many patients are either reluctant to proceed or are not good candidates due to medical comorbidities. For these patients, performing an ENoG can still be useful because of its prognostic value.[39] When treated medically, patients with House-Brackmann grade VI paralysis who meet decompression criteria are essentially guaranteed to develop synkinesis without surgery, whereas patients with House-Brackmann grade VI paralysis who do not meet decompression criteria have a roughly 60% chance of developing synkinesis.[2] 

Laboratory investigations and imaging are more commonly performed in patients whose diagnosis of Bell palsy is questionable due to the presence of skin or mucosal lesions, other neurological symptoms, insidious paralysis onset, or repeated episodes of paralysis. Magnetic resonance imaging (MRI) can rule out space-occupying lesions, such as meningiomas or schwannomas, and contrast-enhanced computed tomography effectively assesses for geniculate ganglion vascular malformations, otologic pathology, and extratemporal masses.[40] Enhancement in the labyrinthine segment of the facial nerve, the cerebellopontine angle, the internal auditory canal, or the parotid gland is abnormal, while enhancement when limited to the geniculate ganglion and the tympanic and mastoid segments of the nerve is mostly likely normal "physiological" enhancement.[40][41] More recently, there has been increasing interest in using ultrasound to identify the location and severity of edema within the facial nerve, thereby providing prognostic information.[42] For patients with a history of travel to an endemic area, Lyme titers may be drawn, and numerous other conditions can cause facial paralysis as well, including human immunodeficiency virus infection, syphilis, West Nile virus, tuberculosis, leprosy, COVID, polio, and myriad autoimmune diseases.[1][43]

Historically, the maximal stimulation test (MST) and the nerve excitability test (NET) have been used to assess facial nerve function, but both have been largely supplanted by ENoG, which, despite the variability of its results, remains more objective and consistent than either the MST or NET. The NET involves stimulation of the face with an increasing electrical current and determining the difference between the lowest current amplitudes that produce visible contraction on each side. The MST is similar in that it requires a cooperative patient and the examiner's subjective evaluation of movement, but it involves stimulating the unaffected side with increasing electrical current until no additional contraction is achieved and then recording how much contraction is produced on the affected side with the same stimulation.[44] Various other studies may also be employed to evaluate the autonomic and sensory functions of the facial nerve, including saliva flow, taste testing, and stapedial reflex testing.

Treatment / Management

Acute Bell Palsy

Once Bell palsy is diagnosed, management is very straightforward and follows a predictable algorithm (see Image. Management of Acute Bell Palsy). Steroids and antiviral medications are prescribed, with antihyperglycemic medications added or adjusted as necessary for patients with diabetes. Corneal protection is provided, and electrodiagnostic studies are performed if a House-Brackmann grade VI paralysis is present, with surgery offered if candidacy criteria are met. Patients at high risk for exposure keratopathy are given a scleral contact lens or undergo minor surgery, such as upper eyelid loading, tarsorrhaphy, or lateral tarsal strip canthopexy. Electrical stimulation has also been shown to improve outcomes when combined with medical management, expediting recovery and enhancing facial function.[45][46] Acupuncture, on the other hand, provides questionable benefits to patients with Bell palsy according to the poor quality studies conducted thus far; it does appear to be safe for those who wish to receive the treatment.[47][48](A1)

Medical management

Ideally, patients with acute Bell palsy should be seen as soon as possible and given corticosteroids within 72 hours of paralysis onset.[49] A common regimen is 1 mg/kg daily up to 60 mg of prednisone or an equivalent dose of prednisolone for 5 to 7 days with or without a taper. There is strong evidence that steroids alone improve Bell palsy outcomes, but there is some controversy regarding the addition of antivirals. A 2007 paper published by Sullivan et al reported that patients receiving prednisolone alone had a 94.4% chance of recovery to House-Brackmann grade I or II function by 9 months post-paralysis, but that the addition of acyclovir actually decreased the chance of a similar recovery to 92.7%. On the other hand, results from a study published that same year by Hato et al found that adding valacyclovir to a course of prednisolone improved the recovery rate to 96.5%.[50](A1)

In addition to steroids and antivirals, corneal protection during recovery is a critical intervention for patients without complete eye closure. Depending upon the severity, this may be an ocular lubricant at night only or periocular surgery. Most patients are well served with artificial tear drops to use throughout the day and lubricant ointment to use at night, with or without eyelid taping (see Video. Taping the Eyelid). Upper eyelid stretching 2 to 3 times per day is also very helpful for alleviating the unopposed contraction of the levator palpebrae superioris muscle that further hinders eye closure in the absence of a strong orbicularis oculi muscle (see Video. Stretching the Upper Eyelid). For patients who continue to have ocular discomfort despite these conservative measures or who are at high risk for exposure keratopathy (corneal anesthesia, absent Bell phenomenon, slow or prolonged recovery, only seeing eye), placement of a scleral contact lens or minor surgical procedures may be required to protect the cornea until a spontaneous eye blink is restored.

Periocular procedures

Due to the expense and time required to manufacture a custom scleral contact lens, periocular procedures are more often employed for patients with long-term flaccid facial paralysis due to nerve trauma or resection; scleral contact lenses can be very useful in cases of acute Bell palsy to prevent or treat exposure keratopathy.[51] Surgical options for improving eye closure include placement of a weight or a spring into the upper eyelid, tightening of the lower eyelid with medial or lateral canthopexy and tarsal strip, and tarsorrhaphy or tarsoconjunctival flap transfer (see Image. Interventions for Corneal Protection).(B3)

Of these options, the most common is upper eyelid loading, often performed with a gold or platinum weight. The weight can be placed onto the tarsal plate (pretarsal placement) via a supratarsal crease incision, as for blepharoplasty, or the weight can be located on the levator aponeurosis (postseptal placement), again via a supratarsal crease incision. The latter approach keeps the weight hidden behind the preaponeurotic fat so that its contour is not visible externally, but because the weight sits higher than the equator of the globe, it may paradoxically cause the eyelid to open when the patient is supine.[52] A pretarsal placement, approximately 2 mm superior to the lash line, provides a greater mechanical advantage and, therefore, employs a smaller weight, but the thin skin in this location usually renders the outline of the weight visible. In either case, the implant is typically centered over the medial limbus, which is the point of maximum lagophthalmos in most cases of facial paralysis (see Image. Pretarsal Upper Eyelid Weight Placement).[53] 

The appropriate mass for the implant can be determined by trying a set of different adhesive weights on the patient's upper eyelid and identifying the one that provides the best eye closure while causing minimal blepharoptosis. For patients who are surgery-averse, the use of a skin color-matched adhesive weight is an alternative to surgical implantation, but the adhesive may be irritating to the thin skin of the upper eyelid, and weights often fall off and are lost due to their small size. For pretarsal placement, 1.2 g is a common size, while postseptal weights usually need to be slightly heavier. Heavier weights, particularly in a pretarsal location, can cause blepharoptosis even if complete eye closure is not achieved; patients should be informed of this lack of "Goldilocks" size preoperatively, ie, there is rarely an implant of just the right weight to produce complete eye closure without adverse effects.

Another common adverse event is astigmatism, which results from the mass pressing downward on the globe and distorting it. Fortunately, most astigmatism tends to correct itself spontaneously once the weight is removed. One way to minimize the astigmatism is to place an articulated chain rather than a solid weight, although doing so increases the risk of implant extrusion over time, and the thickness of a chain relative to that of a solid weight makes its contour more visible.[54] Material is also an important consideration, as, despite its inert characteristics, gold can still cause tissue reactions in 3.2% to 9.5% of the population; platinum is less reactive (<1%) and slightly denser, therefore possessing a thinner profile and potentially being less apparent under the skin.[53][55][56][57] 

When lower eyelid laxity produces paralytic ectropion, loading the upper eyelid will not be sufficient to provide complete eye closure, and repositioning the lower eyelid will be required. This can be accomplished by tightening the eyelid at the medial canthus, the lateral canthus, or both, with the lateral tarsal strip procedure most commonly performed (see Image. Tarsal Strip-Lateral Canthopexy). Some degree of overcorrection is required with this technique, as the lower eyelid begins to loosen fairly quickly, and the overcorrected appearance will not last long. As a caveat, if the cornea protrudes substantially beyond the infraorbital rim, tightening the lower lid may cause a paradoxical retraction; therefore, this "negative vector" configuration must be identified preoperatively. When addressing paralytic lagophthalmos, some surgeons prefer to address the upper and lower eyelids simultaneously, and this can be accomplished by means of a tarsorrhaphy, either with a temporary suture or with a reversible surgical procedure that adheres the upper and lower eyelids together along the grey line (see Image. Interventions for Corneal Protection). In either case, the aesthetic implications of a tarsorrhaphy are significant, and many patients decline this option for that reason. A more cosmetically acceptable means of linking the upper and lower eyelids together, thereby decreasing the height of the palpebral fissure, is the tarsoconjunctival flap, which preserves the separation of the upper and lower lash lines and does not obstruct vision (see Image. Interventions for Corneal Protection).

Facial nerve decompression

Surgery on the facial nerve itself, such as grafting or transfer, is not commonly performed in cases of acute Bell palsy; decompression of the facial nerve may be offered to patients who meet the electrodiagnostic criteria enumerated above and who are both willing and able to undergo the operation.[49] Decompression of the tympanic through the mastoid segments of the facial nerve may be accomplished via a postauricular mastoidectomy approach (see Image. Transmastoid Facial Nerve Decompression), although some surgeons do not consider this to be a thorough decompression because the neuritis in Bell palsy usually involves the labyrinthine segment, which may be best accessed via a middle fossa craniotomy. Accessing the labyrinthine segment of the facial nerve via a transmastoid approach may require removal of the incus and subsequent ossicular chain reconstruction in some cases, which can adversely impact postoperative hearing. Nevertheless, some authors do stand by the transmastoid technique because it spares the patient a craniotomy and intensive care unit admission; outcomes of this procedure are not consistently better than those after non-operative management, however.[58][59][60] (A1)

More recently, some surgeons have begun to employ a transcanal endoscopic approach to facial nerve decompression; this minimally invasive procedure provides somewhat limited access to the facial nerve, although the geniculate ganglion can be exposed effectively. Large studies with consistent resulting data are lacking with this technique, however.[61] To access the more proximal facial nerve, ie, the meatal foramen and canalicular portions, a middle fossa decompression approach is often employed or added to the transmastoid operation (see Image. Middle Fossa Craniotomy Approach to Facial Nerve Decompression).[62][63] Regardless of the approach selected, the earlier intervention appears to result in better outcomes.[38][59][60] Patients who meet criteria for facial nerve decompression but are not willing or able to undergo surgery may be offered alternative medical management, including ultra-high-dose oral corticosteroids (up to 200 mg of prednisone per day), intratympanic dexamethasone injections, and operative electrical stimulation to improve chances of satisfactory recovery.[64][65][66](A1)

Chronic facial nerve dysfunction

While every patient with true Bell palsy recovers facial motor function to some extent, many will develop synkinesis, particularly if presenting with severe or total hemifacial paralysis. The clinician is responsible for identifying these aberrant facial movements, as patients may not recognize the difference between the initial flaccid weakness and the hypertonicity that follows it, characterizing the chronic movement disorder as a continuation of the acute palsy rather than as a different, but related, clinical entity. Nevertheless, persistent facial asymmetry and mimetic dysfunction can have major adverse impacts on quality of life, causing patients to seek care. Physiotherapy and chemodenervation are sufficient for most individuals, although operative options do exist for patients who are dissatisfied with the results of conservative measures or who would prefer to avoid a prolonged course of regular botulinum toxin injections.

Physiotherapy

Facial rehabilitation therapy comprises a wide range of techniques, including neuromuscular reeducation, surface EMG biofeedback, mime therapy, video self-modeling, massage, stretching, and relaxation.[67][68][69] Neuromuscular reeducation (NMR) consists of exercises to produce small but controlled movements on the affected side of the face while concentrating on symmetry and avoiding synkinetic muscle contraction.[70] This can be performed with a mirror or EMG biofeedback that provides an audible tone when contraction is detected in the desired muscle, such as the zygomaticus major. Patients with more severe synkinesis may need to begin the course of therapy with relaxation, stretching, massage, and meditation before progressing to a point at which beginning NMR is even feasible. Exercises, such as NMR, require dozens of repetitions a few times a day to help build the neural pathways that will improve mimetic muscle coordination and symmetry of movement. These same techniques are also applied to patients who undergo nerve or muscle transfer for facial reanimation, as they need to learn to use the transferred nerve or muscle to produce the desired movement, typically biting down to smile.[71](B2)

Chemodenervation

The use of botulinum toxin injection to alleviate spasms and dyscoordinated or asymmetric movement due to facial palsy has been well-documented and found to be effective in both pediatric and adult populations.[72][73][74] There are currently several commercially available botulinum toxin preparations, but the most commonly used one is onabotulinumtoxinA, which is also the best studied, although any can be used effectively.[75] Several muscles typically become problematic with the development of synkinesis, and these are, therefore, most often the primary targets for chemodenervation. The orbicularis oculi is often injected to alleviate involuntary eye closure, particularly with mouth movement. Injections into this muscle are usually performed laterally, just deep to the skin, close to—but not medial to—the lateral orbital rim to prevent inadvertent weakening of the lateral rectus muscle and ensuing diplopia. A good starting dose is 2 aliquots of 5 units of onabotulinumtoxinA, or its equivalent in a different botulinum toxin preparation. When lower eyelid spasms persist despite lateral orbicularis oculi injections, small aliquots of 1 to 2 units may also be placed in the pretarsal portion of the inferior orbicularis oculi muscle (see Image. Injection of Botulinum Toxin for Facial Synkinesis). Care should be taken to avoid causing lower lid laxity that may result in lagophthalmos or blepharoptosis from medial injection of the upper eyelid that weakens the levator palpebrae superioris muscle. When injecting the orbicularis oculi muscle in addition to other facial muscles, it may be helpful to inject the orbicularis oculi first, while the needle is sharpest, because the thin skin in this region of the face is sensitive and prone to bruising. A fine, short needle on a small syringe is best for ensuring precise doses of toxin are administered to the desired targets; a 30- or 33-gauge needle is recommended on a 1 cc syringe. For onabotulinumtoxinA, diluting a 100-unit vial with 2 ccs of sterile, normal saline with preservatives provides 50 units in each 1 cc syringe, or 5 units per 0.1 cc, which makes keeping track of doses during injections comparatively straightforward. The preservatives in the saline improve comfort during injection, as they have a mild local anesthetic effect.(A1)

Other targets frequently injected include the platysma muscle, which, along with the depressor anguli oris muscle, can pull the oral commissure downwards when a patient is trying to smile, thus turning the expression into an unpleasant sneer. Twenty units, 4 injections of 5 units each, make a good starting point for treating the platysma. The mentalis, treated with 5 units, is also a common injection site because it tends to wrinkle with eye closure or brow elevation in patients with synkinesis (see Image. Botulinum Toxin Injection for Facial Synkinesis). Injecting the midface can be challenging, with some clinicians treating the zygomaticus major or upper lip elevators if they contract involuntarily or are hyperactive at rest and others electing to forego these injections because of the risk of causing an upper lip or oral commissure droop. Some clinicians prefer instead to treat the buccinator muscle to alleviate some midfacial tension as well as accidental cheek biting during mastication; this injection is typically performed via an intraoral approach.[76][77] While not strictly for synkinesis, injection of the depressor labii inferioris muscle on the unaffected side, also with 5 units, may improve smiling symmetry by correcting the crooked appearance of the lower lip caused by unilateral depression. Other less common targets include the posterior belly of the digastric muscle, which can cause pain when hypertonic, and the lacrimal gland, which helps to alleviate Bogorad syndrome.[78][79][80][81](B3)

Before injection of onabotulinumtoxinA, patients should be counseled that effects will not be appreciable immediately as it may take 3 to 5 days for any improvement to occur and 1 to 2 weeks to reach maximum effect. The duration of the improvement is 3 to 4 months, and patients, therefore, typically schedule injection appointments at that interval to avoid significant recurrence of synkinesis between treatments. These intervals are, however, somewhat variable among individual patients and may be shorter or longer if a different botulinum toxin preparation is used. Over time, typically several years, repeat injections of large doses of botulinum toxin may lead to neutralizing antibody development that generally manifests as a shorter duration of effect after an injection.[82] This can be addressed by increasing the doses up to a point or by switching to a different preparation of the toxin. Many patients are satisfied with the symptom improvement they achieve with chemodenervation with or without physiotherapy and do not proceed to surgical intervention. To maximize the effect of these nonsurgical interventions, however, it is imperative to start physiotherapy prior to botulinum toxin treatments so that patients have the opportunity to practice their facial exercises before the injections additionally impair muscle movement.

Myomectomy

Patients who have undergone botulinum toxin injections with good results but who desire a longer-term solution or who are losing the effectiveness of the injections due to antibody development may be candidates for myomectomy procedures, in which a segment of muscle is removed to reduce synkinetic contraction. Common targets include the platysma and the depressor anguli oris, in which diminished function will improve smile excursion, and the orbicularis oculi, whose myomectomy will reduce involuntary eye closure and squinting. A full-thickness horizontal strip of platysma muscle may be excised under local anesthesia through a 2 cm lateral transverse cervical incision, interrupting visible platysmal bands and the abnormal contraction that pulls down on the corner of the mouth.[83] The platysma is a large muscle, however, and over the course of several months, it will often restore its continuity, leading to the return of some of its synkinetic activity. Resection of a portion of the depressor anguli oris muscle, also to permit greater movement of the oral commissure during smiling, is performed via an intraoral approach. This procedure involves a 3 cm vertical incision made along the lateral margin of the orbicularis oris muscle, with dissection proceeding through the buccinator, a portion of which is also excised, before reaching the depressor anguli oris, the majority of which is then resected as a strip perpendicular to the vector of contraction.[84] Less commonly performed is resection of a strip of orbicularis oculi muscle from the lower eyelid, with or without its innervating branches of the facial nerve, via a skin-muscle flap lower blepharoplasty approach.[85]

Selective neurectomy

Like removing portions of abnormally-contracting muscles, resection of segments of nerve branches that innervate these muscles can supplement or replace long-term botulinum toxin injections, or be performed as an adjunct to myomectomy. As with myomectomy, selective neurectomy is often performed to limit involuntary eye closure or improve the symmetry of the smile, but unlike myomectomy, an extraparotid facial nerve dissection is required, and thus general anesthesia is necessary (see Image. Selective Neurectomy for Facial Synkinesis). A 2-step highly selective neurectomy is a technique that identifies zygomatic branches of the facial nerve that innervate the orbicularis oculi muscle, employing a facial nerve exploration under general anesthesia. Loops of the identified branches are then externalized via percutaneous stab incisions for resection after the patient has emerged from anesthesia, thus permitting precise titration of the number of neurectomies required to balance reduction of involuntary eyelid contraction against creating lagophthalmos.[86] (B2)

Patients report early symptomatic improvement with this technique, but nerve branches to the orbicularis oculi muscle tend to regenerate after a few months, thereby negating the effects of the surgery.[87] In the lower face, however, longer-term results appear more achievable with modified selective neurectomy of the branches that control the lower facial depressor muscles, as described by Azzizadeh et al.[88] When performing selective neurectomy, it is important to maintain excellent communication between the surgeon and the anesthesia provider, as identification of nerve branches requires not only that the patient remain still, but also that the patient remain still in the absence of paralytic drugs, the use of which would prevent electronic nerve stimulators from facilitating nerve branch identification via muscle contraction. Additionally, it may be prudent to inject the surgical field preoperatively with epinephrine only, rather than lidocaine and epinephrine, as local anesthetic medications occasionally diffuse deeply enough to block action potential conduction of the motor nerves in question and, therefore, prevent their identification with an electronic stimulator. Selective neurectomy may be combined with myomectomy to maximize relief of synkinesis and may also be combined with nerve or muscle transfer.[89]

Nerve transfer

While historically employed for restoring function in cases of flaccid facial paralysis, typically either traumatic or iatrogenic, nerve transfer may also be used to improve coordination of a particular muscle or muscle group by "disconnecting" it from the synkinetic control of the facial nerve and reinnervating it with a different motor nerve, such as the hypoglossal or masseteric nerve (the latter being a branch of the mandibular division of the trigeminal nerve). For reanimation of the flaccid face, nerve transfer is ideally performed within the first 6 to 12 months after the onset of paralysis to ensure that viable muscle remains to reinnervate, as irreversible muscle atrophy and fibrosis occur with prolonged denervation. In the case of synkinesis, however, the muscles are not denervated but rather aberrantly reinnervated, and therefore, there is no time constraint for surgical intervention.

Nerve transfer for smile rehabilitation most often involves rerouting the nerve to the masseter into the facial nerve's buccal branch that controls the zygomaticus major muscle.[90] This procedure may be performed independently or in combination with selective neurectomy or myomectomy.[89] The procedure is performed via a modified Blair incision, as one might use for a parotidectomy or facelift, and as with selective neurectomy, long-acting paralytics and preoperative injection of lidocaine should be avoided (see Image. Masseteric Nerve Transfer). The masseteric nerve is reliably located at a point 3 cm anterior to the tragus, 1 cm inferior to the zygomatic arch, and 1.5 cm deep to the parotidomasseteric fascia.[91][92] Once exposed, it is transected as distally (inferiorly) as possible, just proximal to its branch point, to provide as much length as possible to reflect the cut end of the proximal segment out of the masseter muscle to facilitate the neurorrhaphy; proximal circumferential dissection of the nerve up to the zygomatic arch will further improve its mobility.(B2)

The buccal branch that innervates the zygomaticus major muscle is consistently found at Zuker point, located halfway along a line between the root of the helix and the oral commissure.[93] This buccal branch courses deep to the parotid fascia but is superficial and just superior to the masseteric nerve, in the same plane as the parotid duct and the transverse facial vessels, which are located inferior to it. The buccal branch is transected as proximally as possible without including branches to other muscles. The use of a nerve stimulator will verify the correct receiving buccal branch for the nerve transfer. Provided the masseteric nerve is mobilized adequately, it should reach the distal segment of the buccal branch without tension. Both nerves are roughly 2 mm in diameter. The neurorrhaphy is generally performed under an operating microscope, using 9-0 or 10-0 interrupted nylon sutures on a cutting or spatula-tip needle. Several weeks to months may pass before seeing any improvement in the patient's smile, and the patient may not notice anything until the surgeon points out the movement. Initially, contraction of the zygomaticus major muscle will require intentional biting to trigger an action potential in the masseteric nerve, but over time, most patients can smile without the need to clench the jaw if they comply with the postoperative physiotherapy regimen.[94] Significant improvements in smile symmetry and oral commissure excursion (approximately 5 mm) are expected with a successful nerve transfer.[89][90]

Muscle transfer

For patients in whom nerve transfer has failed or who desire greater smile excursion than is anticipated with nerve transfer, muscle transfer techniques, such as those used for smile reanimation in a flaccidly paralyzed face, may be employed.[95] Of these, the best studied is the gracilis free muscle transfer, which takes a portion of the gracilis muscle from the medial thigh and transfers it into the face between the modiolus of the oral commissure and the temporalis fascia. This location and vector allow the gracilis to assume the function of the zygomaticus major muscle, thus permitting the patient to produce a close-lipped smile (see Image. Gracilis Free Flap for Facial Reanimation).

The adductor artery and vena comitans in the gracilis' vascular pedicle are typically anastomosed to the facial artery and vein, while the obturator nerve to the gracilis is usually coapted to the masseteric nerve, although a cross-face nerve graft may be used instead of the masseteric nerve or added via an end-to-side neurorrhaphy.[96] The monitoring of flap perfusion may be achieved with an implantable Doppler sensor, duplex ultrasound the day after surgery, or a handheld Doppler probe.[97] As with a masseteric nerve transfer, postoperative physiotherapy is critical, and the patient will initially have to bite down to smile, although this movement may not be required in the long term.(B2)

More recently, the use of dual-vector cervical strap muscle-free flaps has been described for smile restoration and, like the gracilis, has been applied to the reanimation of the flaccid face and smile rehabilitation in the context of synkinesis.[98] The advantage of the sterno-omohyoid flap over the gracilis is that it introduces less bulk into the face, thereby minimizing postoperative volume asymmetry, and it also provides 2 contractile muscle bellies that can be used to produce a smile with the dental show, replacing both the zygomaticus major and the levator labii superioris muscles' functions (see Image. Sterno-Omohyoid Flap for Facial Reanimation). This flap also relies upon the facial vessels for blood supply, although the flap's vessels, the superior thyroid artery and vein, are less reliable than the gracilis' adductor vessels, making the strap muscle flap potentially more challenging. The ansa cervicalis provides the innervation for the strap flap, and because there are 2 ends to this loop of nerve, both the masseteric nerve and a cross-face nerve graft may be coapted simultaneously in an end-to-end fashion.[99] As with nerve transfers, muscle transfer may be combined with myomectomy and selective neurectomy.(B2)

Differential Diagnosis

The differential diagnosis for acute hemifacial palsy is broad and includes infectious, neoplastic, vascular, traumatic, toxic, and metabolic etiologies.[1] In most cases, however, a patient presenting with rapid-onset, hemifacial weakness without other neurological or dermatological signs or symptoms and without a history of trauma, chemical exposure, or severe metabolic derangement will be experiencing Bell palsy.

The most common condition that may be mistaken for Bell palsy is Ramsay Hunt syndrome, particularly when it presents as zoster sine herpete, ie, hemifacial palsy without a rash but still with significant pain.[100] Lyme disease is another fairly common cause of acute facial paralysis, although it can usually be identified by the pathognomonic targetoid rash, a history of tick bite or travel to an endemic area, and potentially bilateral facial weakness. Other viral infections, such as Epstein-Barr virus, cytomegalovirus, and human immunodeficiency virus, may also present with unilateral facial paralysis but often also cause vague systemic symptoms, such as fevers, fatigue, and malaise. Tuberculosis and COVID may also cause facial paralysis, but typically with accompanying respiratory symptoms. Neoplasms, such as facial nerve schwannoma and parotid gland mucoepidermoid carcinoma, as well as autoimmune disorders, such as Sjögren syndrome, are more likely to cause an insidious onset of facial paralysis but may nevertheless present acutely.[101][102]

Cerebrovascular accident is often considered high on the differential diagnosis when a patient presents with Bell palsy, leading to unnecessary imaging. A patient with acute onset hemifacial weakness in the absence of other neurological symptoms or vital sign instability is unlikely to be experiencing cerebral ischemia, particularly if the forehead is paralyzed. A brainstem stroke, unlike a cortical stroke, will cause hemifacial weakness that includes the forehead but will typically also cause other cranial neuropathies as well as vertigo, nausea, and vomiting. Recurrent episodes of hemifacial paralysis may represent Bell palsy, which recurs in 8% to 12% of affected patients. Still, patients with more than 2 episodes without other risk factors should be evaluated further with imaging and laboratory studies, as facial nerve schwannomas and autoimmune diseases, such as Melkersson-Rosenthal syndrome, may present this way.[1]

Sometimes, risk factors may not be apparent, even with a detailed history and physical examination. For example, a patient may deny a history of head trauma but fail to mention self-contained underwater breathing apparatus (scuba) diving or air travel, either of which can result in otic barotrauma and subsequent facial paralysis.[103][104] Similarly, a patient with a distant cancer may suffer facial paralysis as a result of brain metastasis or chemotherapy. Misadventures with botulinum toxin injections can cause facial paralysis as well, which some patients may be reluctant to disclose. Last, otologic disease should not be overlooked, whether in the context of acute otitis media or a chronic cholesteatoma.

Staging

The original House-Brackmann scale is simple and easy to use for surgeons, emergency medicine providers, and primary care clinicians, but it provides very little detail, particularly concerning the function of individual zones of the face or synkinetic movement. While it is a sound staging system for acute Bell palsy, there are a number of more detailed classification systems that are better suited to describing the chronic facial movement dysfunction that may follow Bell palsy or other forms of facial paralysis that may affect different zones of the face differently, such as facial nerve trauma, iatrogenic injury, congenital anomalies, poliomyelitis, and multiple sclerosis.

The first facial paralysis grading scheme published was that of Naoaki Yanagihara in 1976, requiring patients to perform 9 facial movements and a resting evaluation. The strength of each is graded as 4 points (normal or nearly normal), 2 points (weak), or 0 points (no movement).[105] Thus, a score of 40 is normal, and a score of 0 corresponds to a House-Brackmann grade of VI. The 9 movements are eyebrow elevation, gentle eye closure, forceful eye closure, closure of the affected eye only, wrinkling the nose, puffing out the cheek, whistling, smiling, and depressing the lower lip. Scoring Bell palsy with this system requires a thorough facial nerve examination. This scale is still commonly used in Asia.

In 1996, Ross and her colleagues published the Sunnybrook Facial Grading System, named for the Sunnybrook Health Science Center in Toronto, Canada.[106] This scale goes 1 step beyond that of Yanagihara, evaluating resting asymmetry, voluntary movement, and synkinetic movement separately for each facial zone, thus providing a very detailed assessment of a patient's facial function, but at the expense of the rapidity and convenience of the House-Brackmann scale. For resting asymmetry, the Sunnybrook system individually scores the palpebral fissure height, nasolabial fold depth, and oral commissure position, with a maximum of 15 points for asymmetry across all 3 zones. For voluntary movement, eyebrow elevation, gentle eye closure, open mouth smile, snarl, and lip pucker are evaluated, with 100 points indicating normal function. Synkinetic movement is evaluated with the same facial expressions, with 15 points for severe synkinesis in all zones. The resting asymmetry and synkinesis scores are subtracted from the voluntary movement score to determine the composite Sunnybrook score.

An update to the House-Brackmann Facial Nerve Grading System with the "Facial Nerve Grading System 2.0" was devised by Vrabec et al in 2009.[107] This scale, like the Sunnybrook system, assesses the eyebrow, the eye, the nasolabial fold, and the oral commissure separately, assigning a score between 1 (normal symmetry) and 6 (no movement) for each region's function that takes into account both movement and resting symmetry. Up to 3 more points can be added to the total for disfiguring synkinesis, with 2 points indicating obvious synkinesis and 1 point signifying slight synkinesis. Because no synkinesis points can be scored when there is no movement, the maximum score is 24 points, which equates to a House-Brackmann grade VI on the original scale.

More recently, technology has been leveraged to improve the granularity and the convenience of grading facial functions. Massachusetts Eye & Ear Infirmary's eFACE application was released in 2015 and validated by a group of international facial nerve experts in 2017.[108][109] This app-based approach to evaluating facial paralysis uses multiple Likert scales to assess resting symmetry, voluntary movement, and synkinetic movement. Then, it provides a set of scores that reproducibly quantify function in terms of static symmetry, dynamic symmetry, and synkinesis, as well as regional function for the periocular area, lower face and neck, midface and smile, and smile alone (see Image. The eFACE Software Application). Further development of the software grading concept resulted in the auto-eFACE, which analyzes a set of standardized photographs to evaluate the severity of facial dysfunction using the eFACE scale.[110]

Numerous other facial nerve grading scales, such as the FAME, MoReSS, Sydney, and Toronto systems, have been developed and compared with the original House-Brackmann Facial Nerve Grading System, with many of them providing good interrater reliability and correlation with the House-Brackmann scale.[111][112][113][114][115] However, the Sir Charles Bell Society recommends using the Sunnybrook scale because of its high reliability and ability to evaluate resting asymmetry, flaccid palsy, and synkinesis.[116]

Prognosis

Bell palsy resolves completely without treatment in approximately 80% of cases, with the remaining patients developing synkinesis to some degree.[6] Oral corticosteroids with or without antivirals increase the chance of recovery from 90% to 97%.[2][7] Recurrence does occur in 8% to 12% of affected individuals, with a mean latency of 10 years between episodes.[1][17][117] Cases of multiple recurrent Bell palsy may be due to narrow Fallopian canals that exacerbate vascular insufficiency caused by nerve inflammation and edema within the enclosed space of the canal. 

Risk factors associated with the development of synkinesis include complete paralysis, age 60 years or older, and decreased salivation or taste on the ipsilateral side. While some patients are typically young and healthy with incomplete palsy and may exhibit complete recovery in as few as 2 weeks, most patients will take several months to a year to recover. The longer it takes for clinical recovery to begin and the slower the recovery once it does, the more likely synkinesis will occur. Similarly, patients who present with more severe paralysis are more likely to have worse outcomes. Escalante et al reported that House-Brackmann grade V paralysis evolves into synkinesis in 17% of patients and House-Brackmann grade VI paralysis does so in 40% of patients; conversely, no patients with a severity of House-Brackmann grade II developed synkinesis in their series.[2] Other factors that adversely affect outcomes include diabetes, pregnancy, history of a recent dental procedure, progression to complete paralysis within 24 hours of onset, and loss of more than 90% of the compound muscle action potential amplitude on electroneuronography, ENoG.[3][20][21][38][39] Debate remains regarding the impact of hypertension on recovery from Bell palsy, with some studies reporting worse outcomes and others no difference between hypertensive and non-hypertensive patients.[19][118][119] Regardless of risk factors, the mean time to development of synkinesis is roughly 5 months for patients who fail to recover completely.[2]

Complications

Despite its high spontaneous recovery rate, Bell palsy may cause synkinesis in approximately 15% of patients and corneal exposure keratopathy in about 40% of patients.[2][120] Beyond physical sequelae, psychological distress and quality-of-life decrements are known to occur with facial paralysis, particularly for women, older patients, and in cases of long-standing paralysis.[121] Fortunately, keratopathy and decreased quality of life tend to resolve as facial function recovers.