Introduction
Background
The eye cannot close and constantly weeps. The mouth dribbles, the speech is interfered with and mastication impaired. The delicate shades of continence are lost. Joy, happiness, sorrow, shock, surprise, all the emotions have for their common expression the same blank stare.1
Speech, mastication, and expression of moods and emotions are based on the ability to move facial musculature—be it voluntary or involuntary. This article informs the reader about extracranial etiology of facial nerve paralysis and its current reconstructive options. The keystone of successful surgical treatment, anatomy, is recapitulated briefly to both review topographic anatomy of the facial nerve and enable the physician to localize the suspected site of injury. Clinical and technical diagnostic possibilities as well as guidelines in certain clinical scenarios are outlined in the decision-making and patient treatment sections. The patient treatment/operative technique section is subdivided further into acute and chronic stage facial nerve paralysis due to the different reconstructive strategies in these situations.
For more information, see eMedicine Plastic Surgery articles Facial Nerve Paralysis, Dynamic Reconstruction and Facial Nerve Paralysis, Static Reconstruction.
Historical review
As early as 1821, Sir Charles Bell discovered that the facial nerve is responsible for facial muscle movement.2 Soon thereafter, the recognition of the anatomic basis of facial nerve injury gave way to reconstructive strategies. For example, the first facial nerve repair was performed in 1879 by Drobnick.3 Drobnick coapted the facial nerve to the spinal accessory nerve. Alternative reconstructive options such as myoneurotization were explored with limited success by Lexer and Eden as well as Owens in 1911.4,5 In 1927, Bunnell was the first to attempt intratemporal repair of the facial nerve in its fallopian canal course.1
In 1971, Thompson became one of the pioneers in free muscle transplantation without vascular microanastomosis.6 He discovered that the best results were achieved when the graft had been denervated 2-3 weeks before transplantation. Because these methods did not yield good results in terms of postoperative muscle strength and contraction ability, they seldom are performed presently.7
Investigation into the anatomy and pathophysiology of facial nerves was undertaken concomitantly with the surgical advances in treatment of facial nerve paralysis. In 1973, May and Miehlke successfully conducted the fascicular spatial orientation (motor, secretory, afferent) of the facial nerve.8,9 With the advent of refined microsurgical techniques advocated by Millesi, Berger, and others, the suture repair of peripheral nerves underwent a renaissance in the 1970s. Concurrently, Scaramella pioneered cross-facial nerve grafts as a technique of coapting contralateral intact facial nerves to injured facial nerve.10
Harii et al broached the idea of microneurovascular free muscle transplantation for the reconstruction of the paralyzed face in 1976. This group performed a free gracilis muscle transfer for the reconstruction of a smile with excellent results.11 Microneurovascular free muscle transfer remains one of the basic methods for reanimation of the paralyzed face. Moreover, free tissue transfer obtains predictable results, since an overall survival rate of 90% is reported in the literature.
Anatomy
The facial nerve (cranial nerve VII) carries motor, secretory, and afferent fibers from the anterior two thirds of the tongue. (See Image 2 for an illustration of facial nerve anatomy.) It originates in the facial nucleus, which is located at the caudal pontine area. Corticobulbar fibers from the precentral gyrus (frontal lobe) project to the facial nucleus, with most crossing to the contralateral side. As a result, both crossed and uncrossed fibers are found in the nucleus. Moreover, the facial nucleus can be divided into two parts: (1) the upper part receiving corticobulbar projections bilaterally and later coursing to the upper parts of the face, including the forehead, and (2) the lower part, the predominantly crossed projections of which supply innervation to lower facial muscles (stylohyoid; posterior belly of digastric, buccinator, and platysma).12
In terms of topography, both the facial and intermedius nerves course from the posterior pontine area ventral passing through the facial canal together with the vestibulocochlear nerve. All 3 nerves are surrounded by pia mater through their subarachnoid course, thus becoming a common sheath at the internal auditory canal.13 Both the inferior anterior cerebellar artery and venous drainage enter the auditory canal together with the facial nerve.
Intratemporally, the facial and vestibular cochlear nerves split, entering the fallopian canal of the temporal bone. Topographically, the further course of the facial nerve is subdivided in 3 segments. The labyrinthine segment, measuring approximately 4 mm, extends perpendicular to the temporal bone axis. Initially, the facial nerve runs anterior obliquely, remaining separate from the intermedius nerve and unifying at the next level, the geniculate ganglion. Afferent fibers from the anterior two thirds of the tongue enter the geniculate ganglion with the chorda tympani, as the greater and lesser petrosal nerve emerge from the superior part.
The tympanic segment of the fallopian canal extends approximately 1 cm.14 Here, the facial nerve runs horizontally at the medial wall of the cavum tympani. The third or mastoidal segment extends directly vertical approximately 1.5 cm. The stylomastoid branch of the posterior auricular artery provides vascular supply to the facial nerve during its intrafallopian course.
Especially considering susceptibility to nerve injury, the bony canal-facial nerve diameter is an important clinical ratio. Most often, the facial nerve takes up approximately 25-50% of the canal diameter. The facial nerve exits the fallopian canal through the stylomastoid foramen, afterward taking its extratemporal course anteriorly, inferiorly, and laterally.
The posterior auricular nerve (innervating both postauricular and occipital muscles) branches posteriorly cranial just below the foramen, as do two smaller ones to the stylohyoideus and posterior belly of the digastric muscle. The facial nerve runs laterally to the styloid process. The facial nerve then enters the parotid gland between the stylohyoid and digastric muscle. The nerve gives off branches lateral to the external jugular vein, constituting the zygomatic-temporal and the cervicofacial trunks.
A diverse number of classifications of the extratemporal course of the facial nerve are found in literature. One was proposed in 1956 by Davis et al, who investigated the different course patterns of the infratemporal facial nerve in 350 cervicofacial halves.
The temporal trunk innervates the frontalis, orbicularis oculi, corrugator supercilii, and pyramidalis muscles. Zygomaticus major as well as minor, elevator ala nasi, levator labii superioris, caninus, depressor septi, compressor nasi, and dilatator naris muscles are innervated by the zygomatic division. The buccal division gives off fibers to innervate the buccinator and superior part of the orbicularis oris muscle.
Mandibular division innervations consist of risorius, quadratus labii inferioris, triangularis, mentalis, and lower parts of the orbicularis oris muscle. The cervical division provides platysma innervation. A "facial danger zone" is known to follow an imaginary line drawn from the lateral canthus to the lateral corner of the mouth and from the zygomatic arch down to the angle of the mandible. The plastic surgeon should keep in mind that the more distal the injury to the facial nerve, the better the chances for spontaneous recovery.
Generally, good reconstructive results of facial nerve repair have been yielded by Terzis et al even when a comparatively small number of axons is regenerated.15 Terzis has found a higher nerve-to-muscle fiber ratio than in other skeletal muscles (1:8 compared to 1:50 in other skeletal muscles).
For more information on the anatomy of the facial nerve and surrounding nerves, see eMedicine article Facial Nerve Anatomy.
Pathophysiology
Facial nerve injury can be complete or partial. Generally, partial disruption of axonoplasmal flow reveals a greater chance of complete functional recovery. Loss of motor function can be observed immediately after facial nerve injury. Depending on the affected trunk and localization (proximal or distal), various patterns of motor function loss can be seen and used for primary diagnosis of the lesion site. Significant muscle fiber decay has been demonstrated when denervation has been present for more than 3 years.16 Early changes at cellular level (approximately 1 wk after denervation) include chromatin changes and increased mitochondria number, DNA, and satellite cells, thus reflecting the plastic state of denervated muscle.
In addition to clinical and Histopathologic Findings, parasympathetic functions such as salivation, lacrimation, and taste sensation also may be impaired.
Clinical
History
Clinical diagnosis is based on 3 steps, identification of the affected site, underlying etiology (trauma, infectious, neoplastic), and finally, clinical staging (eg, with use of the House-Brackmann scale).
Careful delineation of the history should include onset of symptoms, an evaluation of the quality of associated symptoms, and prior infections and systemic diseases (eg, herpes simplex virus, varicella-zoster virus, neoplasms).
Physical
- A thorough head and neck examination is paramount, with occasional use of tests for salivation, tearing, and taste; these are the first steps in determining the site of injury.
- Physical examination findings reveal affected facial musculature movement.
- Tests for facial innervation include the following:
- Forehead wrinkling (frontalis muscle)
- Eye closure (orbicularis oculi muscle)
- Wide smile
- Whistling
- Blowing (eg, buccinator muscle, orbicularis oris muscle, zygomatic muscle)
- During the patient's initial consultation, evaluate general muscle status (latissimus muscle, rectus abdominis muscle) for eventual reconstruction.
- Clinically, injury to the infratemporal facial nerve can be subclassified into several degrees. Multiple classifications of facial nerve injury are found in the literature; the most frequently used is the House-Brackmann scale.17 Table 1. House-Brackmann Classification of Facial Function17
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[ CLOSE WINDOW ]Table
Grade Characteristics I. Normal Normal facial function in all areas II. Mild dysfunction Gross
Slight weakness noticeable on close inspection
May have slight synkinesis
At rest, normal symmetry and tone
Motion
Forehead - Moderate-to-good function
Eye - Complete closure with minimal effort
Mouth - Slight asymmetryIII. Moderate dysfunction Gross
Obvious but not disfiguring difference between sides
Noticeable but not severe synkinesis, contracture, or hemifacial spasm
At rest, normal symmetry and tone
Motion
Forehead - Slight-to-moderate movement
Eye - Complete closure with effort
Mouth - Slightly weak with maximum effortIV. Moderately severe dysfunction Gross
Obvious weakness and/or disfiguring asymmetry
At rest, normal symmetry and tone
Motion
Forehead - None
Eye - Incomplete closure
Mouth - Asymmetric with maximum effortV. Severe dysfunction Gross
Only barely perceptible motion
At rest, asymmetry
Motion
Forehead - None
Eye - Incomplete closure
Mouth - Slight movementVI. Total paralysis No movement Grade Characteristics I. Normal Normal facial function in all areas II. Mild dysfunction Gross
Slight weakness noticeable on close inspection
May have slight synkinesis
At rest, normal symmetry and tone
Motion
Forehead - Moderate-to-good function
Eye - Complete closure with minimal effort
Mouth - Slight asymmetryIII. Moderate dysfunction Gross
Obvious but not disfiguring difference between sides
Noticeable but not severe synkinesis, contracture, or hemifacial spasm
At rest, normal symmetry and tone
Motion
Forehead - Slight-to-moderate movement
Eye - Complete closure with effort
Mouth - Slightly weak with maximum effortIV. Moderately severe dysfunction Gross
Obvious weakness and/or disfiguring asymmetry
At rest, normal symmetry and tone
Motion
Forehead - None
Eye - Incomplete closure
Mouth - Asymmetric with maximum effortV. Severe dysfunction Gross
Only barely perceptible motion
At rest, asymmetry
Motion
Forehead - None
Eye - Incomplete closure
Mouth - Slight movementVI. Total paralysis No movement - House and Brackmann ranged injury from stage 1-6 with different chances of spontaneous recovery. These stages correspond with the pathologic findings of neurapraxia, axonotmesis, neurotmesis, and partial and complete transection of the facial nerve.
- A clinical House-Brackmann grade 1 refers to neurapraxia, which is the most likely stage for spontaneous recovery.
- Secondly, axonotmesis is the term for longer compression of the nerve, clinically a House-Brackmann level 2-3, with temporary axonoplasmal flow interruption and subsequent Wallerian anterograde degeneration. Degeneration in axonotmesis is most often incomplete with more or less axons surviving, thus clinically often a partial facial weakness results.
- Neurotmesis is a state of permanent loss of axons further characterized by (partial) demyelinization leading to moderate-to-severe facial musculature dysfunction. Regenerative impulses may end in facial synkinetic movements, mass movements, or contracture.
- Finally, clinical findings in House-Brackmann stages 5 and 6 (partial or complete transection of the facial nerve) are either minimal facial musculature movements or complete loss of function (grade 6).
Causes
Table 2. Causes of Facial Nerve Palsy in a Review of Medical Literature (1900-1990)*
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Table
| Birth | Molding Forceps delivery Dystrophia myotonica Möbius syndrome (facial diplegia associated with other cranial nerve deficits) |
| Trauma | Basal skull fractures Facial injuries Penetrating injury to middle ear Altitude paralysis (barotrauma) Scuba diving (barotrauma) Lightning |
| Neurologic | Opercular syndrome (cortical lesion in facial motor area) Millard-Gubler syndrome (abducens palsy with contralateral hemiplegia caused by lesion in base of pons involving corticospinal tract) |
| Infection | External otitis Otitis media Mastoiditis Chickenpox Herpes zoster cephalicus (Ramsay Hunt syndrome) Encephalitis Poliomyelitis (type 1) Mumps Mononucleosis Leprosy Influenza Coxsackievirus Malaria Syphilis Scleroma Tuberculosis Botulism Acute hemorrhagic conjunctivitis (enterovirus 70) Gnathostomiasis Mucormycosis Lyme disease Cat scratch AIDS |
| Metabolic | Diabetes mellitus Hyperthyroidism Pregnancy Hypertension Acute porphyria Vitamin A deficiency |
| Neoplastic | Benign lesions of parotid Cholesteatoma Seventh nerve tumor Glomus jugulare tumor Leukemia Meningioma Hemangioblastoma Sarcoma Carcinoma (invading or metastatic) Anomalous sigmoid sinus Carotid artery aneurysm Hemangioma of tympanum Hydradenoma (external canal) Facial nerve tumor (cylindroma) Schwannoma Teratoma Hand-Schüller-Christian disease Fibrous dysplasia Neurofibromatosis II |
| Toxic | Thalidomide (Miehlke syndrome, cranial nerves VI and VII with congenital malformed external ears and deafness) Ethylene glycol Alcoholism Arsenic intoxication Tetanus Diphtheria Carbon monoxide |
| Iatrogenic | Mandibular block anesthesia Antitetanus serum Vaccine treatment for rabies Postimmunization Parotid surgery Mastoid surgery Post-tonsillectomy and adenoidectomy Iontophoresis (local anesthesia) Embolization Dental |
| Idiopathic | Familial Bell palsy Melkersson-Rosenthal syndrome (recurrent alternating facial palsy, furrowed tongue, faciolabial edema) Hereditary hypertrophic neuropathy (Charcot-Marie-Tooth disease, Dejerine-Sottas disease) Autoimmune syndrome Amyloidosis Temporal arteritis Thrombotic thrombocytopenic purpura Periarteritis nodosa Landry-Guillain-Barré syndrome (ascending paralysis) Multiple sclerosis Myasthenia gravis Sarcoidosis (Heerfordt syndrome, uveoparotid fever) Osteopetrosis |
| Birth | Molding Forceps delivery Dystrophia myotonica Möbius syndrome (facial diplegia associated with other cranial nerve deficits) |
| Trauma | Basal skull fractures Facial injuries Penetrating injury to middle ear Altitude paralysis (barotrauma) Scuba diving (barotrauma) Lightning |
| Neurologic | Opercular syndrome (cortical lesion in facial motor area) Millard-Gubler syndrome (abducens palsy with contralateral hemiplegia caused by lesion in base of pons involving corticospinal tract) |
| Infection | External otitis Otitis media Mastoiditis Chickenpox Herpes zoster cephalicus (Ramsay Hunt syndrome) Encephalitis Poliomyelitis (type 1) Mumps Mononucleosis Leprosy Influenza Coxsackievirus Malaria Syphilis Scleroma Tuberculosis Botulism Acute hemorrhagic conjunctivitis (enterovirus 70) Gnathostomiasis Mucormycosis Lyme disease Cat scratch AIDS |
| Metabolic | Diabetes mellitus Hyperthyroidism Pregnancy Hypertension Acute porphyria Vitamin A deficiency |
| Neoplastic | Benign lesions of parotid Cholesteatoma Seventh nerve tumor Glomus jugulare tumor Leukemia Meningioma Hemangioblastoma Sarcoma Carcinoma (invading or metastatic) Anomalous sigmoid sinus Carotid artery aneurysm Hemangioma of tympanum Hydradenoma (external canal) Facial nerve tumor (cylindroma) Schwannoma Teratoma Hand-Schüller-Christian disease Fibrous dysplasia Neurofibromatosis II |
| Toxic | Thalidomide (Miehlke syndrome, cranial nerves VI and VII with congenital malformed external ears and deafness) Ethylene glycol Alcoholism Arsenic intoxication Tetanus Diphtheria Carbon monoxide |
| Iatrogenic | Mandibular block anesthesia Antitetanus serum Vaccine treatment for rabies Postimmunization Parotid surgery Mastoid surgery Post-tonsillectomy and adenoidectomy Iontophoresis (local anesthesia) Embolization Dental |
| Idiopathic | Familial Bell palsy Melkersson-Rosenthal syndrome (recurrent alternating facial palsy, furrowed tongue, faciolabial edema) Hereditary hypertrophic neuropathy (Charcot-Marie-Tooth disease, Dejerine-Sottas disease) Autoimmune syndrome Amyloidosis Temporal arteritis Thrombotic thrombocytopenic purpura Periarteritis nodosa Landry-Guillain-Barré syndrome (ascending paralysis) Multiple sclerosis Myasthenia gravis Sarcoidosis (Heerfordt syndrome, uveoparotid fever) Osteopetrosis |
* Adapted from May and Klein
- A common entity of facial nerve paralysis is Bell palsy, a form that is unilateral and considered of idiopathic etiology. The incidence of Bell palsy is approximately 20 cases per 100,000 per annum.18
- A viral etiology (ie, herpes simplex virus and others) has been suspected as precursor inciting factors.19
- Bell palsy normally has a sudden onset often preceded by facial dysesthesia, epiphora, pain, hyperacusis, dysgeusia, and decreased function of the lacrimal gland.20
- Ramsay Hunt described a syndromic occurrence of facial paralysis, herpetiform vesicular eruptions, and vestibulocochlear dysfunction.21
- Patients presenting with Ramsay Hunt syndrome generally have a greater risk of hearing loss than patients with Bell palsy, and the course of disease is more painful. Moreover, a lower recovery rate is observed in these patients.22
- Medical treatment is equivalent to Bell palsy; most often a combination of steroids and antiviral agents is used.23,24
- Infection with Borrelia burgdorferi via tick bites reveals another etiology of facial paralysis, thereby presenting along with all the symptoms of Lyme disease. Of patients affected with Lyme disease, 10% develop facial paralysis, 25% of whom present with bilateral palsy.25
- Bacterial infection also may lead to facial nerve paralysis, most often correlated to acute otitis media or externa. Slow-onset facial nerve palsy is observed in patients with cholesteatoma.
- Noninfectious causes of facial nerve palsy include head trauma affecting the intracranial intratemporal course of the facial nerve or, less commonly, the infratemporal cause as seen in facial blunt or sharp injury.
- Iatrogenic injury to the facial nerve most often is seen after cervicofacial rhytidectomies, surgery of the parotid gland, acoustic neuroma resection, or tumor resection at any point along the course of the facial nerve. Therefore, when facial paralysis occurs after surgery, operative exploration must follow if uncertainty exists concerning the intactness of the facial nerve. Due to topographic relations and/or tumor extension, the facial nerve occasionally must be sacrificed voluntarily as part of sound oncologic management.
- Tumor of the facial nerve (eg, hemangioma, neuroma) or tumors in the direct vicinity of the facial nerve often are concomitant with facial nerve palsy. In general, gradual onset of paralysis may lead to suspected tumor cause; however, several authors have demonstrated a sudden onset of facial nerve palsy in patients with tumors (20-27%).26,27
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| References |
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Further Reading
Keywords
facial nerve paralysis, facial nerve, facial paralysis, facial muscles, facial musculature, Bell palsy, Bell’s palsy, facial palsy, facial paralysis treatment, facial muscle movement, facial nerve injury, facial nerve reconstruction, facial nerve repair, facial movement, free muscle transplant, vascular microanastomosis, microsurgery, facial microsurgery, peripheral nerve repair, injured facial nerve, cranial nerve VII
