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Facial paralysis has profound functional and psychosocial consequences, affecting expression, speech, eye protection, and quality of life. This course reviews the pathophysiology and clinical features of acute facial paralysis, which commonly presents with facial asymmetry, impaired eye closure, oral incompetence, and reduced social confidence, with most cases attributed to Bell’s palsy, though the differential diagnosis is broad and includes stroke, trauma, infection, neoplasm, and autoimmune disease. Participants will also gain an understanding of timely evaluation involving distinguishing benign, self-limited conditions from life-threatening etiologies such as cerebrovascular events, as well as facial nerve anatomy, red flags, and appropriate management, including eye protection, pharmacologic therapy, and specialist referral. This activity for healthcare professionals is designed to enhance the learner's competence in identifying facial paralysis, performing the recommended evaluation, and implementing an appropriate interprofessional approach when managing this condition, ultimately improving patient outcomes and reducing complications. Objectives: Differentiate peripheral facial nerve palsy from central causes based on diagnostic findings. Identify key red flags indicating causes of facial paralysis that require urgent evaluation. Apply evidence-based treatment strategies in patients with acute facial paralysis. Collaborate with the interprofessional team to provide holistic care and optimize recovery for patients with facial paralysis. Access free multiple choice questions on this topic.

The facial nerve's myriad functions make it critical for eating, speaking, taste, communication, cosmesis, and even the sense of self. Additionally, the facial nerve provides sensation to a portion of the external auditory canal, innervates the stapedius muscle of the middle ear, and regulates the secretion of tears and nasal mucus (see Image. The Facial Nerve). When all or part of this nerve loses its ability to conduct signals, the consequences can be devastating for the patient, affecting both physical and mental health.[1][2] The most common presenting complaints of patients with acute facial nerve palsy are facial asymmetry, particularly of the smile, eye dryness with or without excess tearing, oral incompetence, and decreased social confidence. When flaccid paralysis evolves into chronic spastic paralysis, decreased self-esteem, eye dryness, and smile asymmetry often persist, but oral incompetence may be replaced by facial tension, cramping, or twitching. Fortunately, the majority of acute facial palsy cases resolve spontaneously or with minimal pharmacological treatment. Bell's palsy is certainly the most common facial paralysis, but the list of pathologies that can present similarly is extensive, including traumatic, iatrogenic, neoplastic, autoimmune, infectious, ischemic, metabolic, toxic, and congenital causes. The broad differential diagnosis of facial paralysis makes it a condition that presents to clinicians across the interprofessional team, from emergency medicine to primary care, as well as countless specialties and subspecialties.[3][4] For this reason, the ability to take a pertinent history, perform a systematic physical examination, rule out dangerous conditions, and either provide appropriate interventions (eg, eye care, oral steroids, and antivirals) or refer to an appropriate specialist is essential for clinicians in most fields of practice.

Bell Palsy Numerous studies have examined the frequency with which different pathologies cause peripheral facial paralysis, and while the proportions differ from paper to paper, Bell palsy consistently emerges as the most common, accounting for 38% to 83% of cases (see Image. Acute Bell Palsy with a Severe Presentation).[3][4][5] Bell palsy, named for Sir Charles Bell, the Scottish neurologist who described the condition in 1821, is commonly thought to result from reactivation of herpes simplex virus (HSV) within the geniculate ganglion.[6][7][8] The exact nature of the pathology remains elusive, however, with different theories pointing to ischemic, autoimmune, and other etiologies.[9] While Bell palsy is clearly the most common peripheral facial palsy, stroke may actually account for more occurrences of acute facial paralysis overall, given that the condition affects 1 in 4 adults worldwide.[10] Ischemic strokes make up 87% of cases in the United States, 45% of which present with facial weakness.[11][12] Cortical strokes, most often from middle cerebral artery occlusion, cause an upper motor neuron deficit that characteristically results in contralateral weakness of the lower two-thirds of the face, with preservation of forehead and eyelid function in about 75% of patients.[13] Pontine strokes, on the other hand, produce an ipsilateral hemifacial palsy by affecting the lower motor neurons in the facial nucleus of the pons, thereby mimicking a peripheral facial palsy. Cerebral strokes are likely to be accompanied by limb weakness ipsilateral to the facial weakness, while brainstem strokes will often present with vertigo, ataxia, nystagmus, and diplopia. A headache may feature in either condition. Trauma

While Bell palsy is clearly the most common peripheral facial palsy, stroke may actually account for more occurrences of acute facial paralysis overall, given that the condition affects 1 in 4 adults worldwide.[10] Ischemic strokes make up 87% of cases in the United States, 45% of which present with facial weakness.[11][12] Cortical strokes, most often from middle cerebral artery occlusion, cause an upper motor neuron deficit that characteristically results in contralateral weakness of the lower two-thirds of the face, with preservation of forehead and eyelid function in about 75% of patients.[13] Pontine strokes, on the other hand, produce an ipsilateral hemifacial palsy by affecting the lower motor neurons in the facial nucleus of the pons, thereby mimicking a peripheral facial palsy. Cerebral strokes are likely to be accompanied by limb weakness ipsilateral to the facial weakness, while brainstem strokes will often present with vertigo, ataxia, nystagmus, and diplopia. A headache may feature in either condition. Trauma Trauma is the next most common cause of facial paralysis (10%-27%), which includes iatrogenic injuries from both oncologic resection and surgical misadventure, as well as temporal bone and soft tissue trauma.[14][3][15] Please see StatPearls' companion resource, "Facial Nerve Intratemporal Trauma," for further information. Within the traumatic category, iatrogenic error causes about 7% of cases, while temporal bone trauma accounts for 3%, and treatment of tumors 15%, according to a 2014 Massachusetts Eye and Ear Infirmary study. A supplementary study by the same group further investigated the epidemiology of iatrogenic facial nerve injury, finding that the most common procedure resulting in facial nerve injury, other than tumor resection, was temporomandibular joint reconstruction, which accounted for 37% of injuries.

Trauma is the next most common cause of facial paralysis (10%-27%), which includes iatrogenic injuries from both oncologic resection and surgical misadventure, as well as temporal bone and soft tissue trauma.[14][3][15] Please see StatPearls' companion resource, "Facial Nerve Intratemporal Trauma," for further information. Within the traumatic category, iatrogenic error causes about 7% of cases, while temporal bone trauma accounts for 3%, and treatment of tumors 15%, according to a 2014 Massachusetts Eye and Ear Infirmary study. A supplementary study by the same group further investigated the epidemiology of iatrogenic facial nerve injury, finding that the most common procedure resulting in facial nerve injury, other than tumor resection, was temporomandibular joint reconstruction, which accounted for 37% of injuries. The next most common was mastoidectomy (18%), and then facelift procedures (9%). Injuries at the main trunk of the facial nerve were most common, with the most frequently injured individual branches being the frontal and marginal mandibular (see Image. Rhytidectomy Complications).[16] Iatrogenic etiologies include inadvertent transection of the facial nerve, thermal or traction injury, embolization of arteries feeding the nerve, misplacement of botulinum toxin, prolonged duration of local anesthetic action, and others.[16] Temporal bone fractures, which occur with less than half the frequency of iatrogenic injuries, are most often caused by motor vehicle collisions (55%), followed by falls (25%), industrial accidents (16%), and interpersonal violence (4%).[17] Neoplasms

The next most common was mastoidectomy (18%), and then facelift procedures (9%). Injuries at the main trunk of the facial nerve were most common, with the most frequently injured individual branches being the frontal and marginal mandibular (see Image. Rhytidectomy Complications).[16] Iatrogenic etiologies include inadvertent transection of the facial nerve, thermal or traction injury, embolization of arteries feeding the nerve, misplacement of botulinum toxin, prolonged duration of local anesthetic action, and others.[16] Temporal bone fractures, which occur with less than half the frequency of iatrogenic injuries, are most often caused by motor vehicle collisions (55%), followed by falls (25%), industrial accidents (16%), and interpersonal violence (4%).[17] Neoplasms Although treatment of tumors within the temporal bone and parotid gland is a common cause of facial nerve injury, 5% of patients with neoplasms in the Massachusetts Eye and Ear study experienced facial paralysis after radiation or chemotherapy without undergoing an operation. In fact, tumors are an important cause of facial paralysis in their own right, causing 8% of facial paralysis cases even in the absence of any intervention; benign lesions accounted for twice as many cases as malignancies. The most common were skull base tumors, eg, facial nerve schwannomas, geniculate ganglion vascular malformations, cavernous brainstem hemangiomas, acoustic neuromas, and meningiomas (see Image. Acoustic Neuroma). Benign parotid tumors were also responsible for some paralyzes, although malignant parotid tumors were more likely to cause facial palsy.[3] Varicella Zoster

Although treatment of tumors within the temporal bone and parotid gland is a common cause of facial nerve injury, 5% of patients with neoplasms in the Massachusetts Eye and Ear study experienced facial paralysis after radiation or chemotherapy without undergoing an operation. In fact, tumors are an important cause of facial paralysis in their own right, causing 8% of facial paralysis cases even in the absence of any intervention; benign lesions accounted for twice as many cases as malignancies. The most common were skull base tumors, eg, facial nerve schwannomas, geniculate ganglion vascular malformations, cavernous brainstem hemangiomas, acoustic neuromas, and meningiomas (see Image. Acoustic Neuroma). Benign parotid tumors were also responsible for some paralyzes, although malignant parotid tumors were more likely to cause facial palsy.[3] Varicella Zoster Varicella zoster follows in frequency after the previously mentioned causes of facial paralysis, accounting for approximately 6% of cases. Roughly 90% of patients present with a papular eruption (Ramsay Hunt syndrome), and 10% present without one (zoster sine herpete). Varicella zoster in the absence of a rash can present very similarly to Bell palsy and is differentiated clinically by reports of greater pain and additional cranial neuropathies causing hearing loss, vertigo, or hoarseness, any of which can occur with classic Ramsay Hunt syndrome as well.[3] The varicella zoster virus remains dormant in the geniculate ganglion after a chickenpox infection, and because the geniculate ganglion also receives innervation from the glossopharyngeal nerve, the reactivated virus can produce a prodromal period of otalgia and vesicular eruptions within the external auditory canal as well as the soft palate. Additionally, up to 40% of patients with Ramsay Hunt syndrome develop vertigo with or without hearing loss due to involvement of the vestibulocochlear nerve.[18] In some cases, the recurrent laryngeal nerve may also be affected, leading to vocal fold weakness and potential hoarseness. Within the traumatic category, iatrogenic error causes about 7% of cases, while temporal bone trauma accounts for 3%, and treatment.[19] Please see StatPearls' companion resource, "Ramsay Hunt Syndrome," for further information. Congenital Facial Paralysis

Varicella zoster follows in frequency after the previously mentioned causes of facial paralysis, accounting for approximately 6% of cases. Roughly 90% of patients present with a papular eruption (Ramsay Hunt syndrome), and 10% present without one (zoster sine herpete). Varicella zoster in the absence of a rash can present very similarly to Bell palsy and is differentiated clinically by reports of greater pain and additional cranial neuropathies causing hearing loss, vertigo, or hoarseness, any of which can occur with classic Ramsay Hunt syndrome as well.[3] The varicella zoster virus remains dormant in the geniculate ganglion after a chickenpox infection, and because the geniculate ganglion also receives innervation from the glossopharyngeal nerve, the reactivated virus can produce a prodromal period of otalgia and vesicular eruptions within the external auditory canal as well as the soft palate. Additionally, up to 40% of patients with Ramsay Hunt syndrome develop vertigo with or without hearing loss due to involvement of the vestibulocochlear nerve.[18] In some cases, the recurrent laryngeal nerve may also be affected, leading to vocal fold weakness and potential hoarseness. Within the traumatic category, iatrogenic error causes about 7% of cases, while temporal bone trauma accounts for 3%, and treatment.[19] Please see StatPearls' companion resource, "Ramsay Hunt Syndrome," for further information. Congenital Facial Paralysis Congenital facial paralysis (5%) presents along a broad spectrum, with the most common manifestation being very mild congenital unilateral lower lip palsy and the most severe being bilateral Möbius syndrome (see Image. Congenital Unilateral Lower Lip Palsy).[3] The majority of congenital facial palsy cases are nonsyndromic (75%); among syndromic cases, Möbius syndrome is most common, although hemifacial microsomia syndromes, eg, auriculo-oculo-vertebral spectrum disorder (Goldenhar syndrome), are frequently involved as well. Möbius syndrome itself can vary in severity, from incomplete and asymmetric facial weakness to complete bilateral paralysis with accompanying abducens nerve palsy. Möbius has been linked to the chromosomal loci 3q21-22 and 10q21.3-22.1.[20] The incidence of this syndrome is estimated at 2 to 20 per million live births and is associated with maternal cocaine use as well as thalidomide and misoprostol administration during pregnancy.[21][22][23]

Congenital facial paralysis (5%) presents along a broad spectrum, with the most common manifestation being very mild congenital unilateral lower lip palsy and the most severe being bilateral Möbius syndrome (see Image. Congenital Unilateral Lower Lip Palsy).[3] The majority of congenital facial palsy cases are nonsyndromic (75%); among syndromic cases, Möbius syndrome is most common, although hemifacial microsomia syndromes, eg, auriculo-oculo-vertebral spectrum disorder (Goldenhar syndrome), are frequently involved as well. Möbius syndrome itself can vary in severity, from incomplete and asymmetric facial weakness to complete bilateral paralysis with accompanying abducens nerve palsy. Möbius has been linked to the chromosomal loci 3q21-22 and 10q21.3-22.1.[20] The incidence of this syndrome is estimated at 2 to 20 per million live births and is associated with maternal cocaine use as well as thalidomide and misoprostol administration during pregnancy.[21][22][23] Limb anomalies may also occur with Möbius syndrome, including clubbed feet and missing digits. When accompanied by chest wall abnormalities, the presentation is known as Poland syndrome. Less common congenital defects that may include facial paralysis are branchio-oto-renal syndrome (Melnick-Fraser), VACTERL association (vertebral, anal, cardiac, tracheal, esophageal, renal, and limb abnormalities), and CHARGE syndrome (coloboma of the eye, heart defects, atresia of the nasal choanae, retardation of growth, genital abnormalities, and ear abnormalities).[3] Importantly, congenital facial paralysis should not be confused with birth trauma to the facial nerve, which may present similarly at first but will usually result in synkinesis rather than long-term flaccid weakness. Lyme Disease

Limb anomalies may also occur with Möbius syndrome, including clubbed feet and missing digits. When accompanied by chest wall abnormalities, the presentation is known as Poland syndrome. Less common congenital defects that may include facial paralysis are branchio-oto-renal syndrome (Melnick-Fraser), VACTERL association (vertebral, anal, cardiac, tracheal, esophageal, renal, and limb abnormalities), and CHARGE syndrome (coloboma of the eye, heart defects, atresia of the nasal choanae, retardation of growth, genital abnormalities, and ear abnormalities).[3] Importantly, congenital facial paralysis should not be confused with birth trauma to the facial nerve, which may present similarly at first but will usually result in synkinesis rather than long-term flaccid weakness. Lyme Disease Lyme disease is a common cause of facial paralysis as well, and accounted for 4% of cases in the Massachusetts Eye and Ear Infirmary study.[3] Massachusetts is an area where Lyme disease is endemic, as is most of the United States, except for the Mountain West and the Pacific Northwest. In the United States, Lyme disease is caused by the spirochete Borrelia burgdorferi, which is carried by the deer tick, Ixodes scapularis. In Western Europe, Ixodes ricinus is the primary vector, with Ixodes persulcatus more common in Eastern Europe and southern Russia. In Europe and Asia, Borrelia afzelii, Borrelia garinii, and Borrelia valaisiana are the more commonly responsible bacteria.[24] Lyme disease typically presents with a targetoid rash (erythema migrans) and facial paralysis develops later, either unilaterally (92%) or bilaterally (8%).[3][25] Please see StatPearls' companion resource, "Lyme Disease," for further information. When considering Lyme disease in the differential diagnosis of a patient with facial paralysis, the likelihood that Borrelia infection is responsible is low outside endemic areas; however, a travel history should always be elicited. Central Nervous System Lesions Beyond ischemic events, other central nervous system lesions, including vascular malformations, pseudobulbar palsy, encephalitis, and Parkinson disease, account for just under 4% of facial paralysis cases.[3] Autoimmune and Other Infectious Diseases

Lyme disease typically presents with a targetoid rash (erythema migrans) and facial paralysis develops later, either unilaterally (92%) or bilaterally (8%).[3][25] Please see StatPearls' companion resource, "Lyme Disease," for further information. When considering Lyme disease in the differential diagnosis of a patient with facial paralysis, the likelihood that Borrelia infection is responsible is low outside endemic areas; however, a travel history should always be elicited. Central Nervous System Lesions Beyond ischemic events, other central nervous system lesions, including vascular malformations, pseudobulbar palsy, encephalitis, and Parkinson disease, account for just under 4% of facial paralysis cases.[3] Autoimmune and Other Infectious Diseases Autoimmune diseases and other inflammatory conditions should not be overlooked as potential causes of facial paralysis, although they are comparatively uncommon, accounting for only 2% of cases. The most common causes of facial paralysis are Guillain-Barré and Melkersson-Rosenthal syndromes, with less common causes including sarcoidosis, multiple sclerosis, amyloidosis, Behçet disease, Sjögren syndrome, giant cell arteritis, and systemic lupus erythematosus.[3][26] Other infections beyond HSV, varicella zoster virus, and Borrelia species may cause facial paralysis, including human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), mumps, West Nile virus, and many others.[3][27][28] Together, they constitute just over 1% of cases. Meningitis and encephalitis, or even cellulitis of the facial soft tissues, may uncommonly cause facial paralysis. Worldwide, poliomyelitis remains a significant cause as well.[3] More recently, severe acute respiratory syndrome COVID-19 has come under scrutiny for its association with facial paralysis. While population-level data on the overall incidence of facial paralysis after COVID-19 infection remain lacking, evidence suggests that the risk of developing facial paralysis within 2 months of infection is substantially elevated compared with that of uninfected individuals (relative risk of 1.8). The relative risk was even higher (up to 44.4) for patients who did not receive a COVID-19 vaccination and still developed an infection, compared with those who did.[29] Otologic Conditions

More recently, severe acute respiratory syndrome COVID-19 has come under scrutiny for its association with facial paralysis. While population-level data on the overall incidence of facial paralysis after COVID-19 infection remain lacking, evidence suggests that the risk of developing facial paralysis within 2 months of infection is substantially elevated compared with that of uninfected individuals (relative risk of 1.8). The relative risk was even higher (up to 44.4) for patients who did not receive a COVID-19 vaccination and still developed an infection, compared with those who did.[29] Otologic Conditions Otologic conditions may also rarely result in facial paralysis. Otologic etiologies account for about 1% of facial paralysis presentations; acute otitis media, with or without mastoiditis, accounts for the largest proportion (81% of otologic cases). Cholesteatoma, a benign collection of sloughed, keratinized squamous epithelial cells that erodes into the facial nerve and causes paralysis, is rare (10% of otologic cases), and barotrauma is rarer still (5% of otologic cases).[3] While it did not appear in the Massachusetts Eye and Ear Infirmary study, necrotizing (malignant) otitis externa is also a potential otologic cause of facial paralysis. Idiopathic Causes Ultimately, true idiopathic cases of facial paralysis are uncommon, as a thorough history and physical examination, when supplemented by imaging and laboratory studies as necessary, will provide a diagnosis in 98% of cases.[3]

The majority of large epidemiological studies on facial paralysis focus on Bell palsy, making it challenging to find reliable data that describe less common causes of facial paralysis. A 10-year retrospective study published in 2013 by Hadlock's team at the Massachusetts Eye and Ear Infirmary did, however, compile some important statistics.[3] They found that the average age of presentation with facial palsy was 44.5 ± 18.6 years, and that 65% of the patients were female. Peitersen's 2002 paper reported incidence by age in slightly more detail, indicating that the peak for presentation with Bell palsy was in the 15 to 45 year range, while that of Ramsay Hunt syndrome was highest in older patients, steadily increasing after age 45.[5] Appreciating where these studies were performed, though, is important, as the institution's patient population will affect the demographic analysis. At a military health center that provides primary through tertiary care, Escalante et al found that Bell palsy had a bimodal age predilection, with peaks at 21 to 25 and 61 to 65 years of age, and that no statistically significant differences were noted between the number of cases in males and females or between the left and right sides.[4] That said, autoimmune diseases are known to occur more commonly in women than in men, and this trend seems to persist in facial paralysis, given that twice as many females were diagnosed with autoimmune facial palsy as males in the Hadlock study. Other than as it pertains to epidemiology of individual conditions that may cause facial paralysis, eg, sarcoidosis or HIV, for example, no significant correlation has been demonstrated between race, sexual orientation, or other demographic factors and the incidence of facial paralysis.

Appreciating where these studies were performed, though, is important, as the institution's patient population will affect the demographic analysis. At a military health center that provides primary through tertiary care, Escalante et al found that Bell palsy had a bimodal age predilection, with peaks at 21 to 25 and 61 to 65 years of age, and that no statistically significant differences were noted between the number of cases in males and females or between the left and right sides.[4] That said, autoimmune diseases are known to occur more commonly in women than in men, and this trend seems to persist in facial paralysis, given that twice as many females were diagnosed with autoimmune facial palsy as males in the Hadlock study. Other than as it pertains to epidemiology of individual conditions that may cause facial paralysis, eg, sarcoidosis or HIV, for example, no significant correlation has been demonstrated between race, sexual orientation, or other demographic factors and the incidence of facial paralysis. Because Bell palsy is far and away the best studied facial paralysis, additional information is available for this condition that may or may not pertain to facial palsy as a whole. The overall incidence of Bell palsy is 10 to 40 cases per 100,000 persons per year, depending upon the study.[30] Escalante's group reported that Bell palsy most commonly presents with House-Brackmann grade III paralysis (42%), with grade VI (complete paralysis) accounting for 20% of occurrences. In 2012, Narci et al investigated the seasonality of Bell palsy incidence, finding that March to May and September produced the greatest numbers of cases; however, in 2023, Varga et al reported slightly different results: Bell palsy was most common in winter and spring (December through May) in their study.[31][32]

Because Bell palsy is far and away the best studied facial paralysis, additional information is available for this condition that may or may not pertain to facial palsy as a whole. The overall incidence of Bell palsy is 10 to 40 cases per 100,000 persons per year, depending upon the study.[30] Escalante's group reported that Bell palsy most commonly presents with House-Brackmann grade III paralysis (42%), with grade VI (complete paralysis) accounting for 20% of occurrences. In 2012, Narci et al investigated the seasonality of Bell palsy incidence, finding that March to May and September produced the greatest numbers of cases; however, in 2023, Varga et al reported slightly different results: Bell palsy was most common in winter and spring (December through May) in their study.[31][32] Other factors have been associated with the development of Bell palsy as well, including pregnancy, hypertension, hyperlipidemia, and diabetes mellitus. All of these factors tend to make the severity at presentation and the outcome after recovery worse than in patients with Bell palsy without these comorbidities.[33][34][35] Unlike Bell palsy, Ramsay Hunt syndrome tends to present with more severe paralysis (47% House-Brackmann VI and 30% House-Brackmann V) and is more likely to affect older patients, with its peak incidence in the fifth and seventh decades of life.[36] Fortunately, the shingles vaccine may also offer protection against the development of Ramsay Hunt syndrome. Temporal bone trauma has also been studied in detail, providing useful statistics on demographics and injury patterns. Approximately 70% of temporal bone fractures occur in patients 11 to 40 years of age, and males are 3 times as likely to suffer these injuries as females.[37] Facial nerve injury occurs in 7% to 12% of temporal bone fractures, with certain fracture patterns more liable to cause this complication than others.[17][37][38] Fractures that disrupt the otic capsule are highly likely to result in facial paralysis, which occurs in up to 48% of cases.[37] Fractures that spare the otic capsule cause facial paralysis less often; it happens only 6% of the time (see Image. Transverse Temporal Bone Fracture).[37]

Facial paralysis can arise from several physiological insults, including neurochemical blockade, demyelination, crush injury, traction injury, inflammation, ischemia, transection, or a lack of functional nerve and muscle. In many cases, it may not be apparent what the exact cause of the paralysis is, even if the etiology is correctly identified. Infectious pathogens, in particular, may affect facial nerve function at 1 or more sites and through several mechanisms, including invasion of the peripheral nerve itself, inflammation of the meninges or brain, immune complex deposition and demyelination, or vascular inflammation and injury.[39][40][41] For example, enteroviridae, Mycoplasma, and Mycobacteria can all cause facial palsy via otitis media or meningoencephalitis; these infections present differently and have different prognoses. Enteroviridae and CMV can cause facial paralysis during acute infection, or Guillain-Barré syndrome, which affects the facial nerve. As with other herpesviruses, eg, herpes simplex virus 1 (HSV-1), human herpesvirus 6 (HHV-6), and varicella-zoster virus (VZV), CMV can also lie latent for years and cause facial palsy upon reactivation.[42][43] CMV is also more likely to become a clinically significant infection in patients already infected with HIV, which can itself cause facial paralysis during seroconversion. Of course, the presence of antibodies to any of these microbes in a patient's serum does not necessarily indicate causality, as many may be found simultaneously. Syphilis, for example, is more common in patients with HIV, as are tuberculosis and human T-lymphotropic virus (HTLV), any of which can also cause facial paralysis. Certain infections are known to cause autoimmune reactions that result in neuropathy, but some autoimmune conditions are also associated with each other, eg, sarcoidosis and Melkersson-Rosenthal syndrome, which can also both cause facial paralysis, thus further clouding the diagnostic picture. Comorbidities may also muddy the waters, as in the case of Takayasu arteritis, which is a rare condition that has been reported to cause facial paralysis, as other vasculitides are known to do, or the palsy may occur due to the hypertension that accompanies the condition.[44] Seddon and Sunderland Classifications of Nerve Injury

Certain infections are known to cause autoimmune reactions that result in neuropathy, but some autoimmune conditions are also associated with each other, eg, sarcoidosis and Melkersson-Rosenthal syndrome, which can also both cause facial paralysis, thus further clouding the diagnostic picture. Comorbidities may also muddy the waters, as in the case of Takayasu arteritis, which is a rare condition that has been reported to cause facial paralysis, as other vasculitides are known to do, or the palsy may occur due to the hypertension that accompanies the condition.[44] Seddon and Sunderland Classifications of Nerve Injury Regardless of the exact pathophysiology, the severity of the clinical presentation will correlate with the histopathologic extent of the damage. The Sunderland classification categorizes nerve injuries based on the degree of injury to the nerve's internal architecture. The most basic element of a nerve's anatomy is the axon, which connects a nerve cell body to its end organ; in motor nerves, the axon is covered in a myelin sheath. Surrounding the myelin is the endoneurial membrane, and a perineurial membrane surrounds a bundle of axons, known as a fascicle. All of the nerve's fascicles are contained together within an epineurial membrane, which serves as the outer covering of the nerve itself (see Image. Nerve Fascicle and Connective Tissue Layers). Damage limited to the myelin sheath with disruption of signal transmission defines a Sunderland class I injury. Such injuries are typically short-lived and demonstrate complete recovery. Injury to the axons with intact endoneurial membranes corresponds to a Sunderland class II injury; recovery remains complete but occurs more slowly because axonal regrowth proceeds at approximately 1 mm/day.[45] Sunderland class III injury involves disruption of both axons and endoneurial membranes, while preservation of fascicular architecture occurs due to intact perineurial membranes. Damage extending to the perineurial membranes with preservation of the epineurium defines a Sunderland class IV injury. Disruption of the epineurium, as seen in nerve transection, characterizes a Sunderland class V injury.[46] MacKinnon later introduced a sixth category to account for mixed histopathologic patterns of varying severity, commonly observed in crush injuries.[47]

Sunderland class III injury involves disruption of both axons and endoneurial membranes, while preservation of fascicular architecture occurs due to intact perineurial membranes. Damage extending to the perineurial membranes with preservation of the epineurium defines a Sunderland class IV injury. Disruption of the epineurium, as seen in nerve transection, characterizes a Sunderland class V injury.[46] MacKinnon later introduced a sixth category to account for mixed histopathologic patterns of varying severity, commonly observed in crush injuries.[47] Accurate classification based solely on physical examination remains impractical, even when supplemented by electrodiagnostic studies. The Seddon classification system provides a more clinically applicable framework by categorizing nerve injuries into 3 groups: neuropraxia, a transient conduction block corresponding to Sunderland class I; axonotmesis, representing axonal injury with variable connective tissue disruption corresponding to Sunderland class II, III, or IV; and neurotmesis, indicating complete nerve transection equivalent to Sunderland class V (see Image. Seddon and Sunderland Classifications of Nerve Injury).[48] Wallerian Degeneration Axonal injury initiates Wallerian degeneration, a process in which the damaged axon and its surrounding myelin are dismantled and cleared to allow regeneration of a new axon. Successful regeneration requires preservation of the neuronal cell body within the facial nucleus in the ventrolateral tegmentum of the pons. Peripheral facial palsy typically involves a disruption limited to axons, allowing potential recovery. In contrast, central nervous system lesions, eg, stroke, poliomyelitis, and trauma, may destroy neuronal cell bodies, eliminating the potential for spontaneous recovery.

Axonal injury initiates Wallerian degeneration, a process in which the damaged axon and its surrounding myelin are dismantled and cleared to allow regeneration of a new axon. Successful regeneration requires preservation of the neuronal cell body within the facial nucleus in the ventrolateral tegmentum of the pons. Peripheral facial palsy typically involves a disruption limited to axons, allowing potential recovery. In contrast, central nervous system lesions, eg, stroke, poliomyelitis, and trauma, may destroy neuronal cell bodies, eliminating the potential for spontaneous recovery. The facial nerve contains approximately 9,000 motor axons, each encased in myelin produced by Schwann cells.[49] Nodes of Ranvier interrupt the myelin sheath at regular intervals, separating adjacent Schwann cell segments and exposing the axonal membrane to enable saltatory conduction, thereby accelerating signal transmission.[50] Wallerian degeneration begins at the node of Ranvier nearest the proximal side of the injury. Macrophages, fibroblasts, and Schwann cells subsequently clear axonal debris and degenerated myelin, including inhibitory proteins, eg, myelin-associated glycoprotein, to optimize the environment for regeneration.[51] The duration of this process varies with the nature of the injury. Electrodiagnostic testing may detect Wallerian degeneration as early as 72 hours after nerve transection. Crush injuries may prolong degeneration due to variable axonal damage, while temporal bone fractures may require up to 2 months for completion.[52] Clinical implications include loss of distal nerve stimulability after degeneration, limiting intraoperative identification of the distal stump beyond 3 days postinjury. Disruption of internal neural architecture during degeneration also increases the risk of misdirected regeneration, resulting in synkinesis. Synkinesis

The duration of this process varies with the nature of the injury. Electrodiagnostic testing may detect Wallerian degeneration as early as 72 hours after nerve transection. Crush injuries may prolong degeneration due to variable axonal damage, while temporal bone fractures may require up to 2 months for completion.[52] Clinical implications include loss of distal nerve stimulability after degeneration, limiting intraoperative identification of the distal stump beyond 3 days postinjury. Disruption of internal neural architecture during degeneration also increases the risk of misdirected regeneration, resulting in synkinesis. Synkinesis Spontaneous recovery occurs in the vast majority of facial nerve pathologies unless a portion of the nerve or its target muscle has been extirpated or the pons has sustained injury. Long-term flaccid paralysis from facial nerve lesions remains uncommon in inflammatory or infectious conditions, eg, Bell palsy, Ramsay Hunt syndrome, Lyme disease, and Guillain-Barré syndrome, except in cases of ongoing pathology, including nerve entrapment, eg, Eagle syndrome, or when neuronal cell bodies have been affected, as in poliomyelitis and leprosy. Injuries exceeding Sunderland class II almost invariably lead to synkinesis, with severity correlating to the extent of injury. Synkinesis manifests as involuntary muscle contractions that accompany voluntary facial movements or occur independently, including twitching or increased resting tone. Autonomic manifestations may also arise, eg, lacrimation triggered by salivation, termed Bogorod syndrome or “crocodile tears,” resulting from aberrant regeneration of fibers originally destined for the chorda tympani nerve through the greater superficial petrosal nerve. Regenerating axons form multiple growth cones that traverse residual neural architecture, with potential misdirection if structural integrity has been compromised. Persistence of multiple growth cones may result in a single neuron innervating multiple muscles. Management of synkinesis often proves more challenging than treatment of flaccid paralysis.[53] In Bell palsy, synkinesis typically emerges by approximately 5 months; persistence of flaccid paralysis beyond this period warrants consideration of an alternative diagnosis.[4] Intratemporal Facial Nerve Anatomy

Regenerating axons form multiple growth cones that traverse residual neural architecture, with potential misdirection if structural integrity has been compromised. Persistence of multiple growth cones may result in a single neuron innervating multiple muscles. Management of synkinesis often proves more challenging than treatment of flaccid paralysis.[53] In Bell palsy, synkinesis typically emerges by approximately 5 months; persistence of flaccid paralysis beyond this period warrants consideration of an alternative diagnosis.[4] Intratemporal Facial Nerve Anatomy The facial nerve's axons travel a long route through the Fallopian canal within the temporal bone and between the superficial and deep lobes of the parotid gland, and particular sites along its path are more prone to injury than others. The facial nucleus in the pons receives bilateral innervation from the cerebral motor cortex to control the upper face, and contralateral innervation for the mid- and lower face. Axons from the facial nucleus then leave the pons and travel across the cerebellopontine angle within the posterior cranial fossa to enter the temporal bone's internal auditory canal via the internal auditory meatus. The intratemporal portion of the facial nerve's course is divided into 4 segments: meatal, labyrinthine, tympanic, and mastoid. The meatal (or canalicular) segment, which runs through the internal auditory canal with the cochlear and vestibular nerves, is 8 to 10 mm in length and up to 9 mm in diameter.[54] Within the internal auditory canal, a comparatively large amount of space exists between the nerves and the bone of the canal, allowing tumors in this area, eg, schwannomas, to grow for quite some time before a functional deficit appears, unless the lesion is at the narrower lateral aspect, known as the meatal foramen. The diameter at this point, where the Fallopian canal begins, is only 0.6 mm.[55] Of note, the nerves within the internal auditory canal are not surrounded by epineurium, but the canal is lined with dura mater.

The intratemporal portion of the facial nerve's course is divided into 4 segments: meatal, labyrinthine, tympanic, and mastoid. The meatal (or canalicular) segment, which runs through the internal auditory canal with the cochlear and vestibular nerves, is 8 to 10 mm in length and up to 9 mm in diameter.[54] Within the internal auditory canal, a comparatively large amount of space exists between the nerves and the bone of the canal, allowing tumors in this area, eg, schwannomas, to grow for quite some time before a functional deficit appears, unless the lesion is at the narrower lateral aspect, known as the meatal foramen. The diameter at this point, where the Fallopian canal begins, is only 0.6 mm.[55] Of note, the nerves within the internal auditory canal are not surrounded by epineurium, but the canal is lined with dura mater. Upon passing through the meatal foramen, the facial nerve enters the labyrinthine segment, a 4 mm long leg that swings anteriorly towards the geniculate ganglion. In contrast to the generous width of the medial internal auditory canal, the labyrinthine segment is very narrow, at only 0.7 mm in diameter, which makes injury to the temporal bone in this region very likely to traumatize the facial nerve as well; the labyrinthine segment is the most common location for facial nerve injury in temporal bone fractures, which may involve development of intraneural hematoma, penetration by a bony spicule, or crushing or shearing between 2 displaced segments of the bony facial canal.[56]

Upon passing through the meatal foramen, the facial nerve enters the labyrinthine segment, a 4 mm long leg that swings anteriorly towards the geniculate ganglion. In contrast to the generous width of the medial internal auditory canal, the labyrinthine segment is very narrow, at only 0.7 mm in diameter, which makes injury to the temporal bone in this region very likely to traumatize the facial nerve as well; the labyrinthine segment is the most common location for facial nerve injury in temporal bone fractures, which may involve development of intraneural hematoma, penetration by a bony spicule, or crushing or shearing between 2 displaced segments of the bony facial canal.[56] Bell palsy most commonly affects the distal meatal and labyrinthine segments, potentially because swelling of the nerve within the narrowest portions of the canal causes pressure that subsequently occludes the vasa nervorum.[57] Another clinical entity, recurrent facial palsy, may share some of the inflammatory characteristics of Bell palsy, but is also likely caused by abnormally narrow choke points within the Fallopian canal, which results in a lower-than-usual threshold for ischemic dysfunction of the facial nerve.[58] Carrying both preganglionic, parasympathetic fibers, the greater superficial petrosal nerve departs the main trunk of the facial nerve at the geniculate ganglion, travels along the floor of the middle cranial fossa, and then joins with the deep petrosal nerve to pass through the foramen lacerum as the Vidian nerve, whence it enters the pterygopalatine fossa and ganglion. These visceral efferent axons then innervate the lacrimal gland and the mucous glands of the nasal cavity and palate. From the geniculate ganglion, the facial nerve courses posteriorly through its tympanic, or "horizontal" segment for 9 to 10 mm along the medial wall of the middle ear, just superior to the stapes and oval window. It then takes a turn inferiorly by the mastoid antrum, anterior to the horizontal semicircular canal, at the second genu. The final intratemporal segment of the Fallopian canal is the 11 to 12 mm long "vertical" segment, which passes down through the mastoid, just posterior to the external auditory canal, to exit the skull at the stylomastoid foramen.[59]

These visceral efferent axons then innervate the lacrimal gland and the mucous glands of the nasal cavity and palate. From the geniculate ganglion, the facial nerve courses posteriorly through its tympanic, or "horizontal" segment for 9 to 10 mm along the medial wall of the middle ear, just superior to the stapes and oval window. It then takes a turn inferiorly by the mastoid antrum, anterior to the horizontal semicircular canal, at the second genu. The final intratemporal segment of the Fallopian canal is the 11 to 12 mm long "vertical" segment, which passes down through the mastoid, just posterior to the external auditory canal, to exit the skull at the stylomastoid foramen.[59] Within this mastoid segment, the nerve to the stapedius muscle and the chorda tympani nerve, which provides taste sensation to the anterior two-thirds of the tongue and parasympathetic innervation to the submandibular and sublingual glands, leave the main trunk of the facial nerve, the former proximally and the latter in the midportion of the mastoid. While inflammation in Bell palsy and Ramsay Hunt syndrome can certainly extend into the horizontal and vertical segments of the Fallopian canal, the diameter here is wider (2.5 mm and 3.4 mm, respectively) and therefore, a less common location for inflammatory pathology compared to the labyrinthine, geniculate ganglion, and meatal segments of the facial nerve.[60][57] After leaving the temporal bone, the nerve courses deep to the posterior belly of the digastric muscle and superficial to the stylohyoid muscle, both of which it innervates, and then enters the posterior border of the parotid gland. Within the gland, it travels for 10 to 20 mm before dividing at the pes anserinus, typically first into superior and inferior divisions, and then into 5 major branches (frontal, zygomatic, buccal, marginal mandibular, and cervical), each of which branches several more times before innervating their target muscles of facial expression. The main midfacial branches, the zygomatic and buccal, tend to anastomose together via smaller branches, providing robust and redundant innervation of this critical area of the face (see Image. The Facial Nerve). Please see StatPearls' companion resource, "Facial Nerve Repair," for further information on extratemporal facial nerve anatomy.[61]

When attempting to elucidate the etiology of a facial paralysis, the history and physical examination will provide the answer for over 90% of patients if approached systematically and thoroughly. Once the diagnosis is established, determining the timeline and severity of the paralysis will dictate the prognosis for recovery. Clinical History The clinician should establish how long ago the paralysis began and how it was first noticed, as well as how long it took to reach its functional nadir (ie, when it was at its worst). If a patient presents early in the course of Bell palsy, for example, the paralysis may still be worsening, as less severe cases may continue to do for up to 72 to 96 hours after onset; these patients will need to be reexamined frequently until the palsy has ceased to evolve further. In some cases, the paralysis may begin insidiously, as is often the case with neoplasms, and the patient will not be able to pinpoint an exact start date. For traumatic or iatrogenic facial paralysis, the timeline may be more compressed, and the question will become a matter of whether the patient already had the paralysis immediately upon presentation, or immediately upon emergence from anesthesia in the case of an iatrogenic injury, or whether it took some time to develop after the injury or surgery. Immediate, complete hemifacial paralysis is suspicious for facial nerve transection, and thus should alert the surgeon that operative exploration and repair may be required in short order, while the distal stump of the nerve remains stimulable. If the paralysis is either incomplete or delayed, on the other hand, a transection injury can be ruled out immediately. The corollary in viral facial paralysis, eg, Bell palsy and Ramsay Hunt syndrome, is that complete, rapid-onset hemifacial palsy (that evolves over 24 hours or less) is more likely to represent a severe nerve injury and have a poorer recovery.[4] For nonacute cases, determining how long the paralysis has been stable at its nadir, whether it has already begun to recover, how long recovery has taken to begin, how long recovery has lasted, and what functional deficits persist is also useful.

If the paralysis is either incomplete or delayed, on the other hand, a transection injury can be ruled out immediately. The corollary in viral facial paralysis, eg, Bell palsy and Ramsay Hunt syndrome, is that complete, rapid-onset hemifacial palsy (that evolves over 24 hours or less) is more likely to represent a severe nerve injury and have a poorer recovery.[4] For nonacute cases, determining how long the paralysis has been stable at its nadir, whether it has already begun to recover, how long recovery has taken to begin, how long recovery has lasted, and what functional deficits persist is also useful. Other important exposures to identify include a viral prodrome, which may indicate Bell palsy, EBV, CMV, HIV, COVID-19, West Nile virus, or other infections as the etiology. A rash may indicate Lyme disease, if targetoid (see Image. Lyme Disease "Bulls-Eye" Rash), or Ramsay Hunt syndrome, if vesicular and appearing on the ear, cheek, palate, buccal mucosa, tongue, or scalp (see Image. Ramsay Hunt Syndrome). A new sexual partner or a history of multiple partners may point to HIV or neurosyphilis, while a history of arthropod bites or a travel history may make Lyme disease, West Nile virus, or even poliomyelitis or leprosy more likely. Primary tumors, metastatic disease, chemotherapy, or radiotherapy may cause facial paralysis, so an oncological history should be taken, as should a trauma and surgical history. Patients with chronic ear disease, eg, otitis media or cholesteatoma, may also develop facial paralysis, necessitating an otologic history as well. Lastly, asking patients about injections, eg, cosmetic botulinum toxin or lidocaine for dental procedures, may prove informative.

Other important exposures to identify include a viral prodrome, which may indicate Bell palsy, EBV, CMV, HIV, COVID-19, West Nile virus, or other infections as the etiology. A rash may indicate Lyme disease, if targetoid (see Image. Lyme Disease "Bulls-Eye" Rash), or Ramsay Hunt syndrome, if vesicular and appearing on the ear, cheek, palate, buccal mucosa, tongue, or scalp (see Image. Ramsay Hunt Syndrome). A new sexual partner or a history of multiple partners may point to HIV or neurosyphilis, while a history of arthropod bites or a travel history may make Lyme disease, West Nile virus, or even poliomyelitis or leprosy more likely. Primary tumors, metastatic disease, chemotherapy, or radiotherapy may cause facial paralysis, so an oncological history should be taken, as should a trauma and surgical history. Patients with chronic ear disease, eg, otitis media or cholesteatoma, may also develop facial paralysis, necessitating an otologic history as well. Lastly, asking patients about injections, eg, cosmetic botulinum toxin or lidocaine for dental procedures, may prove informative. Symptoms that may be associated with facial paralysis include hearing loss, hyperacusis, vertigo, epiphora, xerophthalmia, eye pain, nasal obstruction, dysarthria, oral incompetence, otalgia, facial pain, dysgeusia, hoarseness, dysphonia, dysphagia, and others. Determining which of these the patient is experiencing will help localize the lesion. For example, dysgeusia and hyperacusis imply an injury within or proximal to the mastoid segment, where the chorda tympani and the nerve to the stapedius muscle branch off the main trunk of the facial nerve. On the other hand, an isolated lower lip asymmetry may indicate damage to a single distal branch of the extratemporal nerve. The presence of some symptoms may also indicate involvement of cranial nerves beyond the facial nerve, including the vestibulocochlear or vagus nerves, which may be involved in Ramsay Hunt syndrome or COVID-associated cranial neuropathy. Physical Examination

Symptoms that may be associated with facial paralysis include hearing loss, hyperacusis, vertigo, epiphora, xerophthalmia, eye pain, nasal obstruction, dysarthria, oral incompetence, otalgia, facial pain, dysgeusia, hoarseness, dysphonia, dysphagia, and others. Determining which of these the patient is experiencing will help localize the lesion. For example, dysgeusia and hyperacusis imply an injury within or proximal to the mastoid segment, where the chorda tympani and the nerve to the stapedius muscle branch off the main trunk of the facial nerve. On the other hand, an isolated lower lip asymmetry may indicate damage to a single distal branch of the extratemporal nerve. The presence of some symptoms may also indicate involvement of cranial nerves beyond the facial nerve, including the vestibulocochlear or vagus nerves, which may be involved in Ramsay Hunt syndrome or COVID-associated cranial neuropathy. Physical Examination On physical examination, voluntary facial movements should be observed individually in order to assess the function of each of the major extratemporal facial nerve branches. From top to bottom, patients are asked to raise their eyebrows, gently close their eyes, forcefully close their eyes, wrinkle their noses, smile with closed lips, smile showing teeth, pucker their lips, and show their bottom teeth. The Sir Charles Bell Society of international facial paralysis experts recommends obtaining photos and videos of each of these expressions in addition to a photograph in repose and a "worm's eye" view of the nasal base.[62] Any asymmetry should be noted, as should whether the eye on the affected side can close completely with gentle effort, with full effort, or not at all, as this will affect the House-Brackmann staging of the paralysis. If the eye cannot close completely, the presence or absence of a Bell phenomenon, in which the globe elevates during attempted eye closure in order to protect the cornea, should be noted (see Image. Bell Phenomenon). Performing an examination in this manner will make the differences among hemifacial palsy, segmental weakness, and mid-lower facial upper motor neuron weakness readily apparent.

Any asymmetry should be noted, as should whether the eye on the affected side can close completely with gentle effort, with full effort, or not at all, as this will affect the House-Brackmann staging of the paralysis. If the eye cannot close completely, the presence or absence of a Bell phenomenon, in which the globe elevates during attempted eye closure in order to protect the cornea, should be noted (see Image. Bell Phenomenon). Performing an examination in this manner will make the differences among hemifacial palsy, segmental weakness, and mid-lower facial upper motor neuron weakness readily apparent. For the patient whose paralysis onset was more than a few weeks prior to the examination, the same series of expressions should be repeated, with the examiner looking for involuntary, synkinetic movements in addition to voluntary movements. The most common are oral commissure movement, mentalis contraction, and platysma tightening with eye closure, and eye closure and brow contraction with lip pucker (see Image. Post-Bell Palsy Synkinesis). The presence or absence of synkinesis will help guide the treatment plan and inform the diagnosis. A classic example is the school-aged child who presents with unilateral facial paralysis since birth: if the paralysis is flaccid, particularly if it does not involve the entire hemiface, congenital facial paralysis is most likely (see Image. Congenital Facial Paralysis). However, if synkinesis is present, the facial nerve injury most probably occurred during childbirth. In addition to examining the patient's facial movements, resting symmetry should be assessed. Significant brow ptosis, particularly with incomplete eye closure, may require an intervention in order to prevent sloughing of epidermal cells onto the unprotected cornea. Lower lid laxity, especially with ectropion, can contribute to difficulty with eye closure and may need correction. Effacement or asymmetry of the nasolabial fold, particularly with nasal base and philtrum asymmetry, is often indicative of external nasal valve collapse, which the patient may describe as nasal obstruction. Any asymmetry of the oral commissure should be documented; care should be taken with this assessment, as men may grow out facial hair in order to make this deformity less conspicuous.

In addition to examining the patient's facial movements, resting symmetry should be assessed. Significant brow ptosis, particularly with incomplete eye closure, may require an intervention in order to prevent sloughing of epidermal cells onto the unprotected cornea. Lower lid laxity, especially with ectropion, can contribute to difficulty with eye closure and may need correction. Effacement or asymmetry of the nasolabial fold, particularly with nasal base and philtrum asymmetry, is often indicative of external nasal valve collapse, which the patient may describe as nasal obstruction. Any asymmetry of the oral commissure should be documented; care should be taken with this assessment, as men may grow out facial hair in order to make this deformity less conspicuous. Beyond a detailed assessment of the face itself, the head and neck, and the rest of the patient should be examined as well, including obtaining vital signs, a cranial nerve examination with evaluation of corneal sensation, observation of gait, postural stability, and limb strength, and evaluation of the skin for rashes. The head and neck examination should particularly look for lymphadenopathy, facial edema, a fissured tongue, nasal septal perforation, and parotid swelling. Edema and tongue fissuring are pathognomonic of Melkersson-Rosenthal syndrome, while a septal perforation may indicate sarcoidosis, polyangiitis with granulomatosis (Wegener granulomatosis), or tertiary syphilis. Enlargement of the parotid may indicate mumps virus infection, abscess, or a neoplasm. Fiberoptic nasolaryngoscopy will identify involvement of the recurrent laryngeal branch of the vagus nerve if vocal fold asymmetry is noted, and an otologic examination will help to exclude otitis media or cholesteatoma as the culprit, or even uncover occult Ramsay Hunt syndrome with vesicles in the external auditory canal. Additionally, an outcome survey, eg, the Facial Clinimetric Evaluation scale (FaCE), should be completed by the patient at regular intervals to track recovery progress and evaluate the effect of any interventions performed.[63]

Imaging Studies If the cause of the paralysis remains unclear despite a thorough clinical history and physical examination, contrast-enhanced computed tomography (CT) of the parotid bed and temporal bone should be performed, with magnetic resonance imaging (MRI) of the brain and internal auditory canal to follow if the CT is negative. Interpretation of MRI in the context of Bell palsy should be performed cautiously, as a normal facial nerve will often enhance with gadolinium in the region of the geniculate ganglion or even into the tympanic and mastoid segments (see Image. Left-Sided Bell palsy, MRI).[64] When the enhancement extends proximally into the labyrinthine or meatal segments, pathology is more likely to be present.[57] Laboratory and Histologic Studies If imaging is negative and the patient's history elicits a high index of suspicion for malignancy, positron emission tomography-CT may be helpful. As a last resort, a facial nerve biopsy may be considered in cases of complete paralysis with insidious onset. If the onset of paralysis is rapid, a neoplasm may still be to blame, although tumors are more likely to cause a slowly progressive paresis.[65] A laboratory evaluation may be more appropriate for acute onset facial paralysis; however, if the CT and MRI are unremarkable. Tests to consider include autoimmune and inflammatory marker studies (ANA, cANCA, ACE, RF, ssA/ssB), genetic studies, cultures, antibody titers, or polymerase chain reaction for suspected pathogens (Lyme, HSV-1, CMV, EBV, VZV), and biopsy of suspicious lesions identified on imaging.[66][67] The differential diagnosis may inform the selection of which tests to order. Additionally, C-reactive protein, erythrocyte sedimentation rate, and lymphocyte-to-neutrophil ratio may indicate the severity of the immune response. Of note, Lyme-specific IgG and IgM will elevate in Lyme disease, although Lyme titers can also rise with the following conditions, making diagnosis less straightforward: syphilis, Toxoplasma gondii infection, EBV infection, HIV infection, rheumatoid arthritis, and systemic lupus erythematosus, among others. Additional Diagnostic Studies

Additionally, C-reactive protein, erythrocyte sedimentation rate, and lymphocyte-to-neutrophil ratio may indicate the severity of the immune response. Of note, Lyme-specific IgG and IgM will elevate in Lyme disease, although Lyme titers can also rise with the following conditions, making diagnosis less straightforward: syphilis, Toxoplasma gondii infection, EBV infection, HIV infection, rheumatoid arthritis, and systemic lupus erythematosus, among others. Additional Diagnostic Studies While a broad range of studies is available to support the diagnostic process, further testing may be performed to determine the location and severity of the injury. The most commonly performed is electroneuronography (ENoG), which is an evoked electromyogram (EMG) obtained by stimulating the facial nerve transcutaneously as it exits the stylomastoid foramen and recording the amplitude of the compound muscle action potential (CMAP) obtained at facial muscles of the examiner's choosing, often the orbicularis oculi, zygomaticus major, nasalis, or orbicularis oris. The CMAP amplitude will decrease on the paralyzed side if a Sunderland class II or worse injury is present, provided sufficient time has passed for Wallerian degeneration to occur, because even stimulation and recording downstream of the injury will be affected by this process. Using the CMAP amplitude on the normal side as a control will provide the clinician with a basis for comparison to determine how much signal amplitude has been lost, which serves as a proxy for estimating the extent of Wallerian degeneration. If more than 90% of the CMAP amplitude is lost, the injury is considered severe, and this threshold is sometimes used as an indication for decompression of the intratemporal portion of the facial nerve in cases of Bell's palsy and temporal bone fracture. Because measuring the CMAP amplitude requires that axons discharge synchronously at their neuromuscular junctions, ENoG results will often lag behind clinical findings during recovery. When movement begins to return to the face, but the CMAP amplitude remains poor, the phenomenon is known as "early deblocking."[68]

Using the CMAP amplitude on the normal side as a control will provide the clinician with a basis for comparison to determine how much signal amplitude has been lost, which serves as a proxy for estimating the extent of Wallerian degeneration. If more than 90% of the CMAP amplitude is lost, the injury is considered severe, and this threshold is sometimes used as an indication for decompression of the intratemporal portion of the facial nerve in cases of Bell's palsy and temporal bone fracture. Because measuring the CMAP amplitude requires that axons discharge synchronously at their neuromuscular junctions, ENoG results will often lag behind clinical findings during recovery. When movement begins to return to the face, but the CMAP amplitude remains poor, the phenomenon is known as "early deblocking."[68] This situation corresponds to the polyphasic potentials that may be seen on voluntary needle EMG, which is often used to supplement ENoG studies, particularly when attempting to establish candidacy for intratemporal facial nerve decompression in Bell palsy.[69] By inserting a recording electrode needle into a facial muscle and asking the patient to contract it, the examiner may gain insight into the status of the facial muscles. If the nerve and its connection to the muscle in question are intact, voluntary motor units will be seen. If the muscle has been denervated within the last 1 to 2 years, fibrillation potentials and positive sharp waves will be observed. Denervation long enough to result in muscle atrophy and fibrosis, however, will produce a flat line tracing. Ongoing nerve recovery, which may or may not be clinically apparent, will manifest as polyphasic action potentials.[70]

This situation corresponds to the polyphasic potentials that may be seen on voluntary needle EMG, which is often used to supplement ENoG studies, particularly when attempting to establish candidacy for intratemporal facial nerve decompression in Bell palsy.[69] By inserting a recording electrode needle into a facial muscle and asking the patient to contract it, the examiner may gain insight into the status of the facial muscles. If the nerve and its connection to the muscle in question are intact, voluntary motor units will be seen. If the muscle has been denervated within the last 1 to 2 years, fibrillation potentials and positive sharp waves will be observed. Denervation long enough to result in muscle atrophy and fibrosis, however, will produce a flat line tracing. Ongoing nerve recovery, which may or may not be clinically apparent, will manifest as polyphasic action potentials.[70] Other facial electrodiagnostic studies include the nerve excitability test (NET) and the maximal stimulation test (MST), but these are largely of historic interest. During the NET, both sides of the face are stimulated to compare the lowest amplitude required to produce visibly apparent motion on the affected side to that on the normal side.[71] Performing the MST requires stimulating the normal side with progressively stronger electrical currents until no additional contraction is appreciated on examination. This same current level is then applied to the paralyzed side, and the resulting muscle contraction is subjectively compared between the 2 sides.[72] Importantly, the ENoG, NET, and MST all require a normal side for comparison with findings on the paralyzed side, thereby limiting their utility in cases of bilateral facial paralysis. Beyond electrodiagnostic studies, the following physiological tests may be used to evaluate the involuntary motor and special sensory functions of the facial nerve, which can, in turn, help to pinpoint the location of the lesion:

Other facial electrodiagnostic studies include the nerve excitability test (NET) and the maximal stimulation test (MST), but these are largely of historic interest. During the NET, both sides of the face are stimulated to compare the lowest amplitude required to produce visibly apparent motion on the affected side to that on the normal side.[71] Performing the MST requires stimulating the normal side with progressively stronger electrical currents until no additional contraction is appreciated on examination. This same current level is then applied to the paralyzed side, and the resulting muscle contraction is subjectively compared between the 2 sides.[72] Importantly, the ENoG, NET, and MST all require a normal side for comparison with findings on the paralyzed side, thereby limiting their utility in cases of bilateral facial paralysis. Beyond electrodiagnostic studies, the following physiological tests may be used to evaluate the involuntary motor and special sensory functions of the facial nerve, which can, in turn, help to pinpoint the location of the lesion: Schirmer test (lacrimal gland function): A strip of filter paper is placed into the lower conjunctival fornix, and the extent to which moisture can wick along it in 5 minutes is measured. Less than 10 mm of moisture indicates reduced tear production.[73] Importantly, a unilateral lesion within the geniculate ganglion can produce bilateral lacrimal deficiencies. Please see StatPearls' companion resource, "Schirmer Test," for further information.[73] Stapedius reflex test Facial nerve-mediated contraction of the stapedius muscle occurs involuntarily in response to high-intensity sound stimuli. A lesion in the tympanic segment of the nerve or more proximal will be apparent on this examination. Testing of the stapedius reflex is performed during audiometric evaluation. A sound is presented either to the ear ipsilateral or contralateral to the facial weakness, and contraction of the stapedius muscle is observed, which will manifest as a decrease in tympanic membrane compliance. The facial nerve mediates the efferent limb of this reflex; thus, a facial nerve injury will result in loss of the stapedial reflex ipsilateral to the injury, regardless of whether the sound is presented to the ipsilateral or the contralateral ear.

Testing of the stapedius reflex is performed during audiometric evaluation. A sound is presented either to the ear ipsilateral or contralateral to the facial weakness, and contraction of the stapedius muscle is observed, which will manifest as a decrease in tympanic membrane compliance. The facial nerve mediates the efferent limb of this reflex; thus, a facial nerve injury will result in loss of the stapedial reflex ipsilateral to the injury, regardless of whether the sound is presented to the ipsilateral or the contralateral ear. A defect in the afferent limb of the reflex, ie, significant hearing loss, will result in loss of bilateral stapedial contraction with a sound presented to the damaged ear, although sound presented to the normal ear will still cause normal, bilateral stapedial contraction. In cases of facial nerve injury and hearing loss, particularly bilateral hearing loss, the interpretation of these test results may be more complicated. Sialometry: Salivary flow rate is assessed from the submandibular duct following stimulation with lemon juice or a 2% citric acid solution.[74] If positive, a reduction in salivation by 25% on the affected side compared to the unaffected side, which indicates a lesion at or proximal to the root of the chorda tympani nerve within the mastoid segment of the Fallopian canal.[75] Taste test: Using salty, sweet, sour, and bitter tastes along the lateral aspects of the anterior two-thirds of the tongue, decreased sensitivity on the affected side localizes the lesion proximal to the root of the chorda tympani nerve as well.

Management of facial paralysis is an interprofessional process, which may include medication, physical therapy, injections, minor procedures, and major surgical operations. The interventions selected for any individual patient will depend on the severity of the weakness, the etiology, the time elapsed since the onset of paralysis, and the patient's priorities. Acute Facial Paralysis Treatment and diagnosis of acute facial palsy should be pursued concomitantly, as the diagnosis will inform some aspects of the treatment, while others will be undertaken regardless of etiology. Patients with House-Brackmann grade IV and greater paralysis will need to take steps to avoid corneal exposure complications, eg, abrasions and ulcers, which can be uncomfortable and potentially lead to long-term vision loss. Eye care for facial paralysis patients should include artificial tear drops throughout the day, lubrication at night and as necessary during the day, eyelid stretches to help with passive closure and limit retraction of the upper eyelid, and taping at night (see Image. Stretching the Upper Eyelid). If these conservative measures prove insufficient to prevent ocular discomfort or injury, a scleral contact lens may be provided to improve moisturization and protection, or a minor procedure may be offered, eg, eyelid weight placement, tarsorrhaphy, lateral tarsal strip-canthopexy, or tarso-conjunctival flap transfer (see Image. Pretarsal Upper Eyelid Weight Placement).[76][77][78] These measures may also be appropriate for patients at higher risk of developing ocular complications, eg, those with an anticipated prolonged duration of paralytic lagophthalmos or those with corneal hypesthesia, as may occur with trigeminal nerve injury during skull base tumor resection (see Image. Management of Acute Bell Palsy).[3] Ophthalmology referral is strongly recommended.

If these conservative measures prove insufficient to prevent ocular discomfort or injury, a scleral contact lens may be provided to improve moisturization and protection, or a minor procedure may be offered, eg, eyelid weight placement, tarsorrhaphy, lateral tarsal strip-canthopexy, or tarso-conjunctival flap transfer (see Image. Pretarsal Upper Eyelid Weight Placement).[76][77][78] These measures may also be appropriate for patients at higher risk of developing ocular complications, eg, those with an anticipated prolonged duration of paralytic lagophthalmos or those with corneal hypesthesia, as may occur with trigeminal nerve injury during skull base tumor resection (see Image. Management of Acute Bell Palsy).[3] Ophthalmology referral is strongly recommended. In the case of facial paralysis brought on by otologic pathology, eg, otitis media or mastoiditis, early surgical intervention is essential. If facial paralysis occurs in the context of acute otitis media, the infection should be treated with appropriate antibiotics, and a tympanostomy tube should be placed if the eardrum is not already perforated; mastoidectomy is indicated only for concomitant mastoiditis. The pathology in these cases is typically no more than inflammation of a facial nerve that is dehiscent in its tympanic segment and is readily restored to normal function with resolution of the infection.[79] If the paralysis occurs in a patient with chronic otitis media with cholesteatoma, however, urgent tympanomastoidectomy is critical to prevent erosion of the facial nerve by the cholesteatoma, as longer delays in surgical intervention are associated with poorer outcomes.[80][81][82] In the rare case of barotraumatic facial paralysis, the goal is rapid restoration of Eustachian tube function, which is accomplished with conservative measures (eg, yawning and chewing) and oral or intranasal steroids, antihistamines, and decongestants, potentially accompanied by myringotomy.[83][84][85] Pharmacologic therapy

In the case of facial paralysis brought on by otologic pathology, eg, otitis media or mastoiditis, early surgical intervention is essential. If facial paralysis occurs in the context of acute otitis media, the infection should be treated with appropriate antibiotics, and a tympanostomy tube should be placed if the eardrum is not already perforated; mastoidectomy is indicated only for concomitant mastoiditis. The pathology in these cases is typically no more than inflammation of a facial nerve that is dehiscent in its tympanic segment and is readily restored to normal function with resolution of the infection.[79] If the paralysis occurs in a patient with chronic otitis media with cholesteatoma, however, urgent tympanomastoidectomy is critical to prevent erosion of the facial nerve by the cholesteatoma, as longer delays in surgical intervention are associated with poorer outcomes.[80][81][82] In the rare case of barotraumatic facial paralysis, the goal is rapid restoration of Eustachian tube function, which is accomplished with conservative measures (eg, yawning and chewing) and oral or intranasal steroids, antihistamines, and decongestants, potentially accompanied by myringotomy.[83][84][85] Pharmacologic therapy Once the cause of the paralysis has been elucidated, targeted pharmacological therapy can also be provided. The most common regimen prescribed for Bell palsy includes high-dose prednisone (60 mg orally daily for adults) or prednisolone with or without an antiviral (valacyclovir 500 mg orally twice a day) for 1 week, ideally initiated within 72 hours of paralysis onset.[86][87][88] For Ramsay Hunt syndrome, the valacyclovir dose is higher (1,000 mg orally 3 times daily), may be delayed by up to 5 days from onset, and the regimen lasts 3 weeks.[36] Due to the higher pain levels most patients report in Ramsay Hunt syndrome, analgesia should be strongly considered as part of the treatment regimen. High-dose steroids are also employed in cases of facial paralysis with temporal bone fracture, although outcomes seem better when the course continues for at least 2 weeks.[89][56] In the case of extratemporal facial nerve trauma, oral steroids may be considered, as well as the calcium channel blocker nimodipine, which is administered at a dose of 60 mg every 4 hours for 2 weeks, longer if recovery is prolonged.[90]

Due to the higher pain levels most patients report in Ramsay Hunt syndrome, analgesia should be strongly considered as part of the treatment regimen. High-dose steroids are also employed in cases of facial paralysis with temporal bone fracture, although outcomes seem better when the course continues for at least 2 weeks.[89][56] In the case of extratemporal facial nerve trauma, oral steroids may be considered, as well as the calcium channel blocker nimodipine, which is administered at a dose of 60 mg every 4 hours for 2 weeks, longer if recovery is prolonged.[90] For Lyme disease and Guillain-Barré syndrome, on the other hand, steroids should be avoided because they are ineffective and potentially harmful. Lyme disease is best treated with 100 mg of doxycycline orally twice daily for 3 weeks, and Guillain-Barré syndrome requires plasmapheresis.[91][92][93] The high doses of steroids provided to Bell palsy patients can be challenging for patients intolerant to such systemic therapy, due to diabetes mellitus, for example, and these patients may benefit from intratympanic steroid injections, which may be given in addition to or instead of oral steroids.[94] On the other hand, patients who meet criteria for facial nerve decompression but cannot undergo craniotomy may benefit from even higher doses of oral steroids than the standard regimen (>100 mg/day).[95] Lastly, some evidence suggests that transcutaneous electrical stimulation may improve outcomes for patients with severe Bell palsy.[96][97] Operative therapy In certain patients, operating on or around the facial nerve itself may also be an option, chiefly in cases of severe Bell palsy, recurrent facial palsy, complete hemifacial paralysis due to temporal bone fracture, or penetrating or iatrogenic facial nerve injury (see Image. Management of Traumatic Facial Paralysis Algorithm). For temporal bone fracture-associated facial paralysis and Bell palsy, ENoG has been used as a screening criterion: if the patient has no discernible movement and more than 90% of the CMAP amplitude has been lost, intratemporal decompression of the facial nerve may be offered.[55][56]

In certain patients, operating on or around the facial nerve itself may also be an option, chiefly in cases of severe Bell palsy, recurrent facial palsy, complete hemifacial paralysis due to temporal bone fracture, or penetrating or iatrogenic facial nerve injury (see Image. Management of Traumatic Facial Paralysis Algorithm). For temporal bone fracture-associated facial paralysis and Bell palsy, ENoG has been used as a screening criterion: if the patient has no discernible movement and more than 90% of the CMAP amplitude has been lost, intratemporal decompression of the facial nerve may be offered.[55][56] In Bell palsy in particular, EMG is often used as a second criterion, with surgical candidacy requiring the absence of voluntary motor units, although EMG has also been proposed to be useful for temporal bone fractures.[98] While potentially helpful for adult patients, surgical decompression of the facial nerve within the labyrinthine segment is not recommended for the pediatric population, as research has failed to demonstrate beneficial outcomes, and a significant risk of sensorineural hearing loss is present with the procedure.[99] On the other hand, even though Ramsay Hunt syndrome likely involves a pathophysiology similar to that of Bell palsy, no evidence to date indicates that facial nerve decompression has a role in its management for either adults or children. In the event of a penetrating injury to the facial nerve, the decision whether to intervene may prove easier if a known transection has occurred. In this case, repair with neurorrhaphy sutures placed into the epineurium should be performed as soon as possible, ideally within 72 hours, so that the distal stump remains stimulable and therefore easier to find intraoperatively. Nerve repair, however, may still be effective several months after the injury and can provide excellent functional recovery in certain cases, provided that the scar tissue that has accumulated at the nerve stumps is removed before neurorrhaphy.[100] Chronic Facial Paralysis

On the other hand, even though Ramsay Hunt syndrome likely involves a pathophysiology similar to that of Bell palsy, no evidence to date indicates that facial nerve decompression has a role in its management for either adults or children. In the event of a penetrating injury to the facial nerve, the decision whether to intervene may prove easier if a known transection has occurred. In this case, repair with neurorrhaphy sutures placed into the epineurium should be performed as soon as possible, ideally within 72 hours, so that the distal stump remains stimulable and therefore easier to find intraoperatively. Nerve repair, however, may still be effective several months after the injury and can provide excellent functional recovery in certain cases, provided that the scar tissue that has accumulated at the nerve stumps is removed before neurorrhaphy.[100] Chronic Facial Paralysis With conservative management, the vast majority of acute facial paralyzes will demonstrate recovery beginning in the first 2 weeks to 6 months after onset, and finishing by 9 to 12 months. In most cases, this will involve a return to normal or near-normal function, but not in all cases. The patients who fail to recover fully may either remain flaccidly paralyzed, as they were at the onset of the palsy, or they may recover with synkinesis. Synkinesis is far more common than permanent flaccid paralysis, which is fortunate because it usually results in minimal resting asymmetry or corneal exposure, although it remains potentially very distressing for affected patients. Synkinesis is ideally managed conservatively, with stretches, massages, and exercises provided by a therapist trained in facial rehabilitation. These maneuvers focus on improving symmetry in facial expressions and reducing resting facial tension and cramping.[101] In many cases, botulinum toxin injections may be added to further relax hyperactive muscles or reduce movement on the unaffected side to improve symmetry (see Image. Botulinum Toxin injection for Facial Synkinesis).[102][103][104] Surgical therapy

Synkinesis is ideally managed conservatively, with stretches, massages, and exercises provided by a therapist trained in facial rehabilitation. These maneuvers focus on improving symmetry in facial expressions and reducing resting facial tension and cramping.[101] In many cases, botulinum toxin injections may be added to further relax hyperactive muscles or reduce movement on the unaffected side to improve symmetry (see Image. Botulinum Toxin injection for Facial Synkinesis).[102][103][104] Surgical therapy If physiotherapy and chemodenervation fail to achieve the desired results, surgical intervention may be considered, including selective neurectomy of branches to the muscles most involved in synkinetic contraction, as well as partial or total resection of those muscles.[105][106][107][108] For some patients, however, these interventions do not provide adequate improvement in smile symmetry; more advanced techniques to augment facial movement, rather than reduce synkinetic contraction, may be helpful in these situations. Masseteric nerve transfer and functional gracilis muscle transfer, for example, are techniques more commonly employed to correct chronic flaccid paralysis, but both have been shown to work well either alone or in combination with neurectomy for patients with synkinesis (see Image. Masseteric Nerve Transfer).[109][110] Please see StatPearls' companion resource, "Bell Palsy," for further information regarding conservative and operative management of chronic nonflaccid facial paralysis.[111] Less commonly, patients may be left with long-term facial flaccidity, either due to a facial nerve injury that fails to recover or to a lack of facial nerve or muscle. The most likely scenarios are oncological resection, congenital facial paralysis, or penetrating trauma, eg, a gunshot or stab wound. Other causes may include temporal bone fracture, poliomyelitis, and pontine stroke. If the facial nerve or facial muscles are absent, no potential for spontaneous recovery is evident; similarly, if more than a year has passed without evidence of clinical improvement, or if EMG at this time point shows fibrillations or a flat line, the patient is also highly unlikely to regain function without intervention.

Less commonly, patients may be left with long-term facial flaccidity, either due to a facial nerve injury that fails to recover or to a lack of facial nerve or muscle. The most likely scenarios are oncological resection, congenital facial paralysis, or penetrating trauma, eg, a gunshot or stab wound. Other causes may include temporal bone fracture, poliomyelitis, and pontine stroke. If the facial nerve or facial muscles are absent, no potential for spontaneous recovery is evident; similarly, if more than a year has passed without evidence of clinical improvement, or if EMG at this time point shows fibrillations or a flat line, the patient is also highly unlikely to regain function without intervention. Patients with flaccid paralysis and no potential for spontaneous recovery are candidates for surgical reanimation as well as reinnervation, if performed early enough. Reinnervation procedures include nerve repair, grafting, and transfer options. Nerve repair results are best when performed within 6 months of the original injury, and this may mean either primary repair of the severed nerve or interposition grafting.[112] Interposition, or "cable," grafting is indicated if more than a 6 mm gap is present between the nerve ends, with segments of the great auricular, sural, or medial antebrachial cutaneous nerves most often employed.[113][114][115][116] Despite the addition of a second neurorrhaphy, which may reduce axonal growth back to the denervated muscles, interposition grafting is preferable to primary neurorrhaphy under tension, which is likely to result in significant scarring at the coaptation site, thereby further obstructing axonal growth.[117] Nerve transfer, on the other hand, may be performed as late as 1 to 2 years after the nerve injury and still produce good results.[118] The masseteric nerve has become the de facto gold standard donor for nerve transfer for smile reanimation (masseteric nerve to buccal branch of facial nerve) because of its robust axon count and high reliability, although it has a low resting firing rate, which translates to minimal resting facial tone.[119][120]

Despite the addition of a second neurorrhaphy, which may reduce axonal growth back to the denervated muscles, interposition grafting is preferable to primary neurorrhaphy under tension, which is likely to result in significant scarring at the coaptation site, thereby further obstructing axonal growth.[117] Nerve transfer, on the other hand, may be performed as late as 1 to 2 years after the nerve injury and still produce good results.[118] The masseteric nerve has become the de facto gold standard donor for nerve transfer for smile reanimation (masseteric nerve to buccal branch of facial nerve) because of its robust axon count and high reliability, although it has a low resting firing rate, which translates to minimal resting facial tone.[119][120] For improvement of resting flaccidity, the hypoglossal nerve may be a better choice. However, caution is warranted with this technique because of the high morbidity of tongue denervation and the risk of producing facial synkinesis when the hypoglossal nerve is coapted to the main trunk of the facial nerve (see Image. Hypoglossal Nerve Transfer).[121] Some authors have even used cross-face nerve grafts to connect individual small branches on the normal side to specific target branches on the paralyzed side to selectively reinnervate facial functions, eg, eye closure and smiling.[116] Cross-face nerve grafting is less reliable, however, because of the low axon counts in the small branches used as donors as well as the length of the interposition graft. The technique also requires 2 stages: the first involves placement of the grafts and connection to the donor branches, and the second involves resection of the scarring that develops at the distal tip of the graft and connection to the recipient branches after 6 to 9 months. The delay gives the donor axons a chance to grow through the graft across the face before coaptation to the recipient nerve is performed.

For improvement of resting flaccidity, the hypoglossal nerve may be a better choice. However, caution is warranted with this technique because of the high morbidity of tongue denervation and the risk of producing facial synkinesis when the hypoglossal nerve is coapted to the main trunk of the facial nerve (see Image. Hypoglossal Nerve Transfer).[121] Some authors have even used cross-face nerve grafts to connect individual small branches on the normal side to specific target branches on the paralyzed side to selectively reinnervate facial functions, eg, eye closure and smiling.[116] Cross-face nerve grafting is less reliable, however, because of the low axon counts in the small branches used as donors as well as the length of the interposition graft. The technique also requires 2 stages: the first involves placement of the grafts and connection to the donor branches, and the second involves resection of the scarring that develops at the distal tip of the graft and connection to the recipient branches after 6 to 9 months. The delay gives the donor axons a chance to grow through the graft across the face before coaptation to the recipient nerve is performed. Combining all of these techniques for targeted reinnervation with improvement of resting tone has gained popularity as well. However, the results are seldom as dramatic as the patient and surgeon would desire.[122][123] Regardless of which nerves are selected for transfer, once movement begins to return, the patient engaging with a therapist to learn how to use the reinnervated muscles effectively is imperative; the same applies to transferred muscles. The major caveat with nerve transfers is that the longer the duration of flaccid paralysis, the greater the likelihood that the target muscle has undergone some degree of irreversible atrophy and fibrosis, thus limiting its potential for recovery. Additionally, with brainstem and skull base pathologies, ensuring that the original pathology did not also affect the nerve that might be used for transfer, eg, the hypoglossal or trigeminal nerve, is essential. In cases of type 2 neurofibromatosis, cross-face nerve grafting is avoided for this reason, as the risk of developing bilateral acoustic neuromas is high, and using the contralateral facial nerve for reinnervation of the paralyzed hemiface is therefore prone to future failure. Reanimation procedures

Combining all of these techniques for targeted reinnervation with improvement of resting tone has gained popularity as well. However, the results are seldom as dramatic as the patient and surgeon would desire.[122][123] Regardless of which nerves are selected for transfer, once movement begins to return, the patient engaging with a therapist to learn how to use the reinnervated muscles effectively is imperative; the same applies to transferred muscles. The major caveat with nerve transfers is that the longer the duration of flaccid paralysis, the greater the likelihood that the target muscle has undergone some degree of irreversible atrophy and fibrosis, thus limiting its potential for recovery. Additionally, with brainstem and skull base pathologies, ensuring that the original pathology did not also affect the nerve that might be used for transfer, eg, the hypoglossal or trigeminal nerve, is essential. In cases of type 2 neurofibromatosis, cross-face nerve grafting is avoided for this reason, as the risk of developing bilateral acoustic neuromas is high, and using the contralateral facial nerve for reinnervation of the paralyzed hemiface is therefore prone to future failure. Reanimation procedures Given that reinnervation options tend to focus on restoring the smile, other areas of the face, particularly the periocular region, are often best served by reanimation procedures. In the face, reanimation is typically conceptualized as either "static" or "dynamic," depending on whether the surgery employs functional muscle to restore movement or the primary goal is to improve resting symmetry. Static reanimation procedures are comparatively simple and are often performed in the office, eg, the eyelid operations mentioned above, brow lifting, and midfacial suspension. A plethora of options exist to reposition ptotic facial features, including suture suspension brow lifting, endoscopic brow lifting, direct brow lifting, suture-based midfacial and nasal valve suspension, fascia-based midfacial and nasal valve suspension, lower lip wedge excision, and modiolar rotational cheiloplasty (see Images. Direct Brow Lift and Static Facial Suspension With Fascia Lata).[124][125][126][127]

Given that reinnervation options tend to focus on restoring the smile, other areas of the face, particularly the periocular region, are often best served by reanimation procedures. In the face, reanimation is typically conceptualized as either "static" or "dynamic," depending on whether the surgery employs functional muscle to restore movement or the primary goal is to improve resting symmetry. Static reanimation procedures are comparatively simple and are often performed in the office, eg, the eyelid operations mentioned above, brow lifting, and midfacial suspension. A plethora of options exist to reposition ptotic facial features, including suture suspension brow lifting, endoscopic brow lifting, direct brow lifting, suture-based midfacial and nasal valve suspension, fascia-based midfacial and nasal valve suspension, lower lip wedge excision, and modiolar rotational cheiloplasty (see Images. Direct Brow Lift and Static Facial Suspension With Fascia Lata).[124][125][126][127] Dynamic reanimation procedures, eg, reinnervation techniques, tend to focus on the restoration of the smile. However, muscle transfer has also been described for the rehabilitation of eyelid closure, specifically the use of a pedicled contralateral orbicularis oculi, an ipsilateral temporalis muscle, or a free gracilis transfer.[128][129] Microneurovascular free gracilis muscle transfer is the most commonly employed technique for smile reanimation due to its high reliability (>90%), particularly when innervated by the masseteric nerve.[130] The first description of gracilis muscle transfer with microsurgical coaptation of an artery, vein, and nerve was published by Harii in 1976, using the deep temporal nerve for control of the muscle.[131]

Dynamic reanimation procedures, eg, reinnervation techniques, tend to focus on the restoration of the smile. However, muscle transfer has also been described for the rehabilitation of eyelid closure, specifically the use of a pedicled contralateral orbicularis oculi, an ipsilateral temporalis muscle, or a free gracilis transfer.[128][129] Microneurovascular free gracilis muscle transfer is the most commonly employed technique for smile reanimation due to its high reliability (>90%), particularly when innervated by the masseteric nerve.[130] The first description of gracilis muscle transfer with microsurgical coaptation of an artery, vein, and nerve was published by Harii in 1976, using the deep temporal nerve for control of the muscle.[131] Subsequently, transfer of the masseteric nerve and cross-face nerve grafting have become more popular methods for innervating the transplanted muscle, depending on the patient's priorities regarding resting symmetry, the extent of smile excursion, and the spontaneity of the smile. The masseteric nerve is known for providing greater movement and higher success rates, while cross-face nerve grafting permits a spontaneous smile (without clenching the jaw to activate the masseteric nerve) and greater symmetry.[130] That said, numerous other muscles are used regularly, including the pectoralis minor and latissimus dorsi. However, technical descriptions have been published on the transfer of the rectus abdominis, sternocleidomastoid, masseter, temporalis, and abductor hallucis, among others, each with its own advantages and disadvantages in donor-site morbidity, reliability, volume, and contraction velocity.[132][133][134][135][136][137][138] In most cases, the muscle is anchored to the orbicularis oris at the oral commissure on one end and the temporalis fascia or the periosteum of the zygomatic arch at the other, after applying enough tension to the muscle to ensure that contraction will produce the desired movement. This arrangement works well for producing a close-lipped smile, but does not tend to allow the patient to show any teeth; more recent advances in surgical technique have focused on providing multiple vectors of muscle contraction to add upper lip elevation, lower lip depression, and lower eyelid contraction to create a more natural appearing smile.

In most cases, the muscle is anchored to the orbicularis oris at the oral commissure on one end and the temporalis fascia or the periosteum of the zygomatic arch at the other, after applying enough tension to the muscle to ensure that contraction will produce the desired movement. This arrangement works well for producing a close-lipped smile, but does not tend to allow the patient to show any teeth; more recent advances in surgical technique have focused on providing multiple vectors of muscle contraction to add upper lip elevation, lower lip depression, and lower eyelid contraction to create a more natural appearing smile. Some authors have described splitting the gracilis muscle longitudinally for this purpose, while others have looked to the transfer of muscles with multiple independent units, eg, the serratus anterior, or the transfer of multiple muscles en bloc, eg, the sternohyoid and omohyoid.[139][140][141][142] For isolated restoration of lower lip depression, disinsertion of the anterior belly of the digastric muscle from the hyoid bone and reimplantation into the orbicularis oris of the lower lip has been described, and this can be performed alone or added to a free muscle transfer as part of a more comprehensive reanimation plan.[143] Please see StatPearls' companion resource, "Facial Nerve Repair," and "Facial Nerve Trauma," for further information on the technical details of facial reinnervation and reanimation procedures.[61][144]

The differential diagnosis for facial paralysis is very broad, making a systematic approach essential for narrowing down potential etiologies and identifying the underlying cause. Two of the most important factors are the timeline of the paralysis, which includes whether the onset was rapid (over the course of several days) or insidious (weeks to months with no clear starting point), how long the paralysis has remained flaccid and whether a history of resolution and recurrence is present, and the extent of the paralysis, not just the House-Brackmann grade but also whether 1 or both sides of the face are affected, whether the entire hemiface is involved equally or whether a segmental or regional weakness only is present, and whether additional neurological deficits are noted. Recurrence may be seen with benign facial nerve tumors, autoimmune disease, and even Bell palsy, which has a recurrence rate of roughly 8%. Ramsay Hunt syndrome, in contrast, is unlikely to recur except in immunocompromised patients. Prolonged flaccidity, lasting a year or longer, rules out Bell's palsy, Ramsay Hunt syndrome, Lyme disease, and any other condition that does not produce either anatomical transection of the facial nerve, persistent neuritis, or death of the cell bodies within the facial nucleus. Examples of conditions that manifest with prolonged flaccid facial paralysis include congenital facial palsies, stroke, poliomyelitis, and trauma, either penetrating or iatrogenic (see Table 1). Table 1. Etiologies of Facial Paralysis Table Conditions Laterality (U) unilateral; (B) bilateral, either synchronous or asynchronous, symmetric or asymmetric; (S) segmental, unilateral, but not the entire hemiface); (R) rapid; (I) insidious; (Y) yes

The House-Brackmann facial nerve grading system (see Table 2), described in 1985, is the most commonly used facial paralysis staging system due to its simplicity.[413] It was developed by a pair of neurotologists, whose primary experience with facial paralysis was with skull base tumors and otologic pathology; for this reason, the House-Brackmann facial nerve grading system does not permit a precise description of synkinetic findings nor of segmental paralysis. The key points within each grade are in bold. Table Table 2. House-Brackmann Facial Nerve Grading System. Note that grades II, III, and IV all have no resting asymmetry, but are differentiated based on whether the eye can close completely with gentle effort, with full effort, or not at all. Grades V and VI are considered severe due to the gross resting asymmetry (subtle resting asymmetry is nearly always perceptible with grade II and above, if the clinician is an astute observer), with grade VI having no demonstrable movement. Importantly, the same degree of paralysis may appear different across patients, as younger patients are less likely to have resting asymmetry than older patients, whose heavier tissues require more baseline muscle tone to prevent ptosis. Additionally, early in cases of rapid-onset complete paralysis, eg, with a facial nerve transection or particularly fulminant Bell palsy, eye closure may be preserved due to relaxation of the orbicularis oculi muscle and the assistance of gravity. Over hours to days, however, the levator palpebrae superioris muscle will begin to contract unopposed, raising the eyelid and making closure impossible without manual assistance. Despite the popularity of the House-Brackmann system, the first facial paralysis grading scheme was actually published by Naoaki Yanagihara in 1976. Scoring patients with this system requires evaluating 9 specific facial movements and resting symmetry. The strength of each is graded as 4 points (normal or nearly normal), 2 points (weak), or 0 points (no movement).[414] Thus, a score of 40 is normal, and a score of 0 corresponds to House-Brackmann grade VI. The movements are eyebrow elevation, gentle eye closure, forceful eye closure, closure of the affected eye only, wrinkling the nose, puffing out the cheeks, whistling, smiling, and depressing the lower lip.

Despite the popularity of the House-Brackmann system, the first facial paralysis grading scheme was actually published by Naoaki Yanagihara in 1976. Scoring patients with this system requires evaluating 9 specific facial movements and resting symmetry. The strength of each is graded as 4 points (normal or nearly normal), 2 points (weak), or 0 points (no movement).[414] Thus, a score of 40 is normal, and a score of 0 corresponds to House-Brackmann grade VI. The movements are eyebrow elevation, gentle eye closure, forceful eye closure, closure of the affected eye only, wrinkling the nose, puffing out the cheeks, whistling, smiling, and depressing the lower lip. In 1996, Ross and her colleagues published the Sunnybrook Facial Grading System, named for the Sunnybrook Health Science Center in Toronto, Canada.[415] This scale goes a 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.

In 1996, Ross and her colleagues published the Sunnybrook Facial Grading System, named for the Sunnybrook Health Science Center in Toronto, Canada.[415] This scale goes a 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 schema, the "Facial Nerve Grading System 2.0," was devised by Vrabec et al in 2009.[416] This scale, like the Sunnybrook system, assesses the eyebrow, palpebral fissure, nasolabial fold, and oral commissure separately, assigning a score from 1 (normal symmetry) to 6 (no movement) for each region's function, thereby accounting for 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 no movement is noted, the maximum score is 24 points, which equates to a grade VI on the original House-Brackmann scale.

An update to the House-Brackmann schema, the "Facial Nerve Grading System 2.0," was devised by Vrabec et al in 2009.[416] This scale, like the Sunnybrook system, assesses the eyebrow, palpebral fissure, nasolabial fold, and oral commissure separately, assigning a score from 1 (normal symmetry) to 6 (no movement) for each region's function, thereby accounting for 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 no movement is noted, the maximum score is 24 points, which equates to a grade VI on the original House-Brackmann scale. More recently, technology has been leveraged to improve the granularity and the convenience of grading facial function. Massachusetts Eye and Ear Infirmary's eFACE application was released in 2015 and validated by a group of international facial nerve experts in 2017.[417][418] This app-based approach to evaluating facial paralysis uses multiple Likert scales to assess resting symmetry, voluntary movement, and synkinetic movement. The software then provides a set of scores that quantify function in terms of static symmetry, dynamic symmetry, and synkinesis, as well as regional function scores 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 led to the auto-eFACE, which analyzes a set of standardized photographs to assess the severity of facial dysfunction using the eFACE scale.[419] Numerous other facial nerve grading scales, eg, 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.[420][421][422][423][424] However, the Sir Charles Bell Society recommends using the Sunnybrook scale for its high reliability and ability to assess resting asymmetry, flaccid palsy, and synkinesis.[425]

Given that the majority of lower motor neuron facial paralyzes occur with Bell palsy, the prognosis for affected patients is generally good. All patients will eventually demonstrate at least some degree of recovery with Bell palsy, as they will with essentially any pathology that does not ablate the facial nerve or the muscles it innervates. Recovery, though, may be incomplete and synkinetic. For Bell palsy, an overall greater than 90% chance of returning to House-Brackmann I function is present after treatment with oral steroids and antivirals, with slightly lower rates without pharmacological treatment.[426][5][86] When segregated by severity of paralysis, however, the numbers change dramatically. According to the Escalante study, an estimated 100% chance of recovery to House-Brackmann I or II is reported for patients presenting with House-Brackmann II to IV paralysis, with the chance of House-Brackmann II recovery (subtle synkinesis) increasing with higher-severity paralysis at presentation. For patients with House-Brackmann V paralysis, the chance of recovery to House-Brackmann I function drops to 72%, and the chance of developing synkinesis rises to 28%, while with House-Brackmann VI paralysis, the chance of recovery to grade I is only 25%, but a 75% chance of developing synkinesis is present.[4] When Bell palsy patients meet criteria for facial nerve decompression but do not undergo surgery, the chance of a House-Brackmann III recovery with synkinesis is near 100%, whereas the chance of recovery to grade I or II function after decompression is up to 90% in some studies, with others indicating no clear difference in outcomes with or without surgery.[69][55][427] When performed for recurrent facial palsy, however, nerve decompression appears to provide an overall improvement in House-Brackmann scores and a decrease in episode frequency.[428] Beyond severity at presentation, numerous other risk factors are known to contribute to worse outcomes in Bell palsy, including hypertension, pregnancy, age older than 50 years, association with dental procedures, postauricular pain, diabetes mellitus, loss of stapedial reflex, decreased salivation, and prolonged duration of paralysis before onset of recovery (beyond 10-12 weeks).[4][33][177][5][429][5][430]

When Bell palsy patients meet criteria for facial nerve decompression but do not undergo surgery, the chance of a House-Brackmann III recovery with synkinesis is near 100%, whereas the chance of recovery to grade I or II function after decompression is up to 90% in some studies, with others indicating no clear difference in outcomes with or without surgery.[69][55][427] When performed for recurrent facial palsy, however, nerve decompression appears to provide an overall improvement in House-Brackmann scores and a decrease in episode frequency.[428] Beyond severity at presentation, numerous other risk factors are known to contribute to worse outcomes in Bell palsy, including hypertension, pregnancy, age older than 50 years, association with dental procedures, postauricular pain, diabetes mellitus, loss of stapedial reflex, decreased salivation, and prolonged duration of paralysis before onset of recovery (beyond 10-12 weeks).[4][33][177][5][429][5][430] The prognosis of facial paralyzes other than Bell palsy tends to be somewhat less optimistic, with Ramsay Hunt syndrome recovering to House-Brackmann I or II function in only 60% to 70% of cases.[431] As with Bell palsy, patients with more severe deficits at presentation are liable to have poorer functional outcomes, as are older patients.[36] With respect to Lyme disease, the prognosis is very similar to that of Ramsay Hunt syndrome, with younger patients and those who receive antibiotics but do not receive steroids recovering better than patients who are given steroids.[432][92][433] Temporal bone fractures are somewhat parallel to Bell palsy, as prognosis depends upon the severity of the lesion. Patients who present with milder injuries, such as incomplete or delayed onset palsy, have essentially a 100% chance of reaching at least House-Brackmann II function, with over 94% returning to normal.[434][37][56] In contrast, for patients who present with immediate, complete hemifacial paralysis and meet ENoG criteria for decompression, the best outcome that can be expected without surgery is House-Brackmann III function with synkinesis, which occurs in over 90% of cases. Only 23% of these patients return to grade I function even with surgery.[56][435]

The prognosis of facial paralyzes other than Bell palsy tends to be somewhat less optimistic, with Ramsay Hunt syndrome recovering to House-Brackmann I or II function in only 60% to 70% of cases.[431] As with Bell palsy, patients with more severe deficits at presentation are liable to have poorer functional outcomes, as are older patients.[36] With respect to Lyme disease, the prognosis is very similar to that of Ramsay Hunt syndrome, with younger patients and those who receive antibiotics but do not receive steroids recovering better than patients who are given steroids.[432][92][433] Temporal bone fractures are somewhat parallel to Bell palsy, as prognosis depends upon the severity of the lesion. Patients who present with milder injuries, such as incomplete or delayed onset palsy, have essentially a 100% chance of reaching at least House-Brackmann II function, with over 94% returning to normal.[434][37][56] In contrast, for patients who present with immediate, complete hemifacial paralysis and meet ENoG criteria for decompression, the best outcome that can be expected without surgery is House-Brackmann III function with synkinesis, which occurs in over 90% of cases. Only 23% of these patients return to grade I function even with surgery.[56][435] With respect to central nervous system lesions, loss of eye closure with cortical strokes has been reported as an indicator of poorer prognosis, with lower rates of independent living at 180 days after the event than patients with preserved eye closure, likely due to a more severe cerebral injury.[308] For surgically treatable pathologies, however, eg, syringobulbia in the setting of Chiari malformation, recovery of facial and other cranial nerve function may be complete after craniocervical decompression.[148][436]

While facial nerve injury can be a complication in and of itself, it may in turn produce adverse ramifications, eg, corneal injury, vision impairment, psychological distress, and chronic pain. Most cases of facial nerve palsy resolve spontaneously, but the paralytic lagophthalmos present before recovery can nevertheless produce long-term visual deficits. Inability to close the eye completely, particularly in the setting of corneal hypaesthesia or absence of the Bell phenomenon, may lead to exposure keratopathy, corneal abrasions, or even corneal scarring and vision loss if left untreated.[437] Furthermore, early involvement of an ophthalmologist may prevent ocular sequelae; should such complications occur, interventions ranging from aggressive use of ocular lubricant to scleral lens fitting to eyelid weight placement, or even corneal transplantation may be required. Beyond the inability to close the affected eye, other functional deficits may include ipsilateral nasal obstruction, dysgeusia, hyperacusis, epiphora, xerophthalmia, oral incontinence, lip or cheek biting, dysarthria, food trapping inside the cheek, difficulty whistling or drinking through a straw, unattractive facial asymmetry, and trouble expressing emotions nonverbally. Facial asymmetry and difficulty nonverbally expressing emotions have been shown to cause social anxiety both in the acute, flaccid stage of the paralysis and in the chronic, synkinetic phase.[2] Many of the other functional deficits will abate as muscle tone returns during recovery, including hyperacusis, dysgeusia, and oral incontinence. Still, others may persist, eg, xerophthalmia and the inability to whistle. The development of synkinesis may also bring additional concerns, including chronic facial and neck pain or tension, particularly towards the end of the day, occasional twitching, and Bogorad syndrome, also known as gustatory lacrimation or "crocodile tears." The latter is a particular presentation of synkinesis in which axons from the superior salivatory nucleus that are meant to course along the chorda tympani nerve instead travel through the greater superficial petrosal nerve, thus triggering tearing when salivation occurs.[438] Management of synkinetic complications involves physical therapy, chemodenervation with botulinum toxin, and occasionally, surgery, as detailed above.

Clinicians practicing in the following specialties may be involved in the care of patients with facial nerve palsy: otolaryngology, facial plastic surgery, plastic surgery, oculoplastic surgery, ophthalmology, optometry, neurology, neurotology, rheumatology, infectious disease, oncology, audiology, neuroradiology, behavioral health, physical therapy, occupational therapy, and speech-language pathology. Tertiary care teams that specialize in the management of facial paralysis are frequently directed by facial plastic or general plastic surgeons.

Many causes of facial paralysis are potentially preventable, including stroke, temporal bone fracture, Ramsay Hunt syndrome, Lyme disease, and other infectious illnesses. Others may not be, eg, Bell's palsy, skull base tumors, and autoimmune conditions. Appropriate prevention strategies depend on an individual's most relevant risk factors, and they may range from improving cardiovascular health to prevent intracranial ischemic events to avoiding exposure to infectious diseases. Disease avoidance itself may take many forms, including immunization against COVID or herpes zoster, mosquito nets and tick checks when in endemic areas, washing hands before eating or touching one's face, drinking clean water, and using condoms during sexual intercourse. While traumatic causes of facial paralysis are somewhat less predictable, the wearing of helmets during contact sports and high-speed activities, eg, lacrosse or horseback riding, has been shown to decrease the rate of skull fractures.[439][440] Intraoperatively, the risk of iatrogenic facial nerve injury can be minimized with nerve integrity monitoring, and some might contend that avoidance of inebriation and physical altercation can reduce the risk of both blunt and penetrating facial nerve trauma.[441][442][443][444] In the event that facial paralysis occurs, patients must be counseled to take meticulous care of the affected eye, using eye exercises, artificial tear drops, lubricants, and taping as necessary to prevent corneal injury. In cases of long-term facial palsy, many patients also find support groups to be immensely helpful.

Facial nerve palsy is a clinically significant condition with diverse etiologies, ranging from benign, self-limited processes such as Bell’s palsy to life-threatening causes including stroke, malignancy, and severe infection. Dysfunction of the facial nerve disrupts motor, sensory, and autonomic functions, leading to facial asymmetry, impaired eye closure, oral incompetence, and psychosocial distress. Accurate diagnosis requires a systematic history and a focused neurologic and head-and-neck examination to distinguish peripheral from central causes and identify red flags. Most acute peripheral cases improve spontaneously or with early corticosteroid therapy, with antivirals considered in select cases, while prompt eye protection is essential to prevent corneal injury. Imaging and laboratory evaluation are reserved for atypical or progressive presentations. Interprofessional collaboration is essential to optimize outcomes, as patients often require coordinated care across multiple specialties. Physicians, primary care clinicians, and advanced practitioners lead initial evaluation, initiate evidence-based treatment, and determine the need for referral. Neurologists and otolaryngologists refine diagnosis and guide complex management, while ophthalmologists prevent and treat ocular complications. Surgeons address traumatic, neoplastic, or refractory cases. Nurses monitor symptoms, reinforce education, and support adherence, while pharmacists ensure safe medication use and counsel on adverse effects. Rehabilitation specialists provide facial retraining and manage synkinesis. Effective communication, shared decision-making, and timely referral reduce complications, improve functional recovery, and enhance patient-centered care.