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The Facial Nerve : The Anatomical and Surgical important

Gulam Hasan, Ashfaqul Hasan,Kulbeer Kaur, Muzaffar Ahmad, Mohd. Shafi

Authors’ affiliations :
Prof. Gulam Hasan
King Saud University
Saudi Arabia
Prof. Kulbeer Kaur
Muzaffar Ahmad
Ashfaqul Hassan
Mohd. Shafi
Dept. of Anatomy GMC,
Srinagar
Accepted for publication :
June 2004
Correspondence to :
Prof. Kulbeer Kaur
Prof. and Head,
Deptt. of Anatomy,
Govt. Medical College,
Srinagar-Kashmir, India

JK-Practitioner2005;12(1):53-57

53

Introduction:
The facial nerve is the seventh
cranial nerve .It is one of the most
important mixed nerves in the human
body and more important as a motor
nerve than as a sensory nerve and
carries a great significance for the
Anatomist, the surgeon and a clinician’
The facial nerve is formed from
elements of the second (hyoid)
branchial arch, which supplies its
motor and sensory components. The
migration of the abducens nucleus
rostrally, coupled with the movement
of the facial nucleus caudally and
laterally, gives rise to the uniquely
curved brain stem course of this nerve.
It has three nuclei two motor and
one sensory.
Motor Nuclei: Superior salivatory
nucleus and facial Motor Nucleus.
Sensory : Solitary Nucleus
Anatomy:
This is discussed in terms of the
nerve’s supranuclear, nuclear, and,
infranuclear segments.
The facial nerve is more important
as a motor nerve than as a sensory
nerve. The motor nuclei are Facial
Motor nucleus and the Superior
Salivary nucleus. The sensory nucleus
is the solitary nucleus.
The Facial Nerve is motor to :
All muscles of face
To Platysma
To Posterior belly of Digastric
and stylohyoid
To Stapedius
To three glands: Lacrimal,
Sublingual, sub mandibular Glands.
The Facial Nerve is sensory to
Lacrimal, Sublingual, Sub
mandible Glands.
Taste from ant 2/3 rd of tongue
The facial Nerve has two parts:
The facial nerve proper which is
motor to facial muscles
Nervus intermedius which is the
sensory and parasympathetic part of
facial nerve.
Course of the facial nerve
After its origin from the brain stem
The motor nerve then turns posteriorly
at a sharp angle, forming the external

Vol.12, No. 1, January-March 2005

genu. After the genu, the nerve enters
the facial canal. At the posterior aspect
of the middle ear, the nerve curves
downward at which point a branch
innervates the stapedius muscle. This
minute muscle acts to dampen wide
acoustic input surges from the delicate
bony transmission system. The
downward course takes it into the
anterior wall of the mastoid process of
the temporal bone. It is within this
segment that the chorda tympani
arises and marks the final separation of
fibers that form the nervus
intermedius. The chorda tympani
transmits afferent taste sensation and
efferent parasympathetic fibers to the
submandibular ganglion. The motor
nerve continues in the temporal bone
until it exits at the base through the
stylomastoid foramen. Three
branches immediately diverge to
innervate the posterior auricular,
posterior belly of the digastric, and
stylohyoid muscles. Running
anteriorly approximately 2 cm from
the stylomastoid foramen the nerve
divides into upper and lower
divisions, which traverse the
superficial portion of the parotid
gland .Pathology of the parotid may
impair facial nerve function.
Eventually the nerve divides further
into its five major branches (Pes
Anserinus): temporal, zygomatic,
buccal, mandibular, and cervical.
All of the muscles of facial expression
are supplied by the facial nerve, with
the exception of the levator palpebrae
superioris, which is supplied by the
oculomotor nerve.
NERVUS INTERMEDIUS
The nervus intermedius of
Wrisberg is made up of all the
components of the facial nerve except
the somatic motor component, The
superior salivatory nucleus is the
origin of the visceral motor
preganglionic parasympathetic nerve
destined for both the submandibular
and sublingual glands via
postganglionic fibers from the
submandibular ganglion. Along its
downward course within the temporal

when positive. and via the nervus intermedius to the brain stem. Nuclear agenesis of nerves VI and VII is considered the classic Syndrome. MOBIUS’ SYNDROME Peripheral facial weakness and abduction deficits are central features of this syndrome. infections. ipsilateral conjugate horizontal gaze paresis. respectively. MILLARD-GUBLER SYNDROME In Millard-Gubler syndrome there is a combination of contralateral hemiparesis. glossopharyngeal. Drooping of the angle of mouth SENSORY FUNCTION Although it is a function of overlapping sensory fibers from the trigeminal. As a result. including other cranial nerve palsies ptosis. Furthermore. nuclear. 1. and form the greater superficial petrosal nerve. and variable facial nerve palsy. and greater auricular nerves. supranuclear lesions involving the face will spare the functions of forehead wrinkling and eye closure. Visceral sensory fibers may take two routes on their way back to synapse in the nucleus solitarius. and mental retardation. DISORDERS OF UNDERACTIVITY Supranuclear Lesions Motor function of the upper face derives from both hemispheres. and pharynx runs with the maxillary nerve to the sphenopalatine ganglion. which is also a branch of the external carotid. vasculopathies. Lesions associated with these clinical features extend from the facial nucleus to the abducens nucleus and paramedian pontine reticular formation dorsomedially. Stasis of food in the mouth 3. abnormal sensation along the posterior aspect of the external auditory canal and tympanic membrane may be an early indication of facial nerve dysfunction. neuronal degeneration andmuscular dystrophy. Imaging studies in nuclear cases. and they cause an infranuclear abducens palsy rather than a nuclear disruption. often considered part of the superior salivatory nucleus. COMPLICATIONS OF AIDS Supranuclear. Flattening of nasolabial fold 11. Further supply of the middle portion of the nerve comes from the petrosal artery via the middle meningeal artery of the external carotid. Loss of wrinkling of the forehead 9. have shown brain stem atrophy and caudal pontine calcifications. Postganglionic fibers travel with the zygomaticotemporal branch of cranial nerve V to the lacrimal gland. infranuclear lesions . Difficulty in closure of the eyes 6. Portions through the facial canal. No. Loss of frowning of the forehead 8. The considerable overlap of the arterial supply. The major categories of causes are vascular. traverse the geniculate ganglion. the etiologies postulated to date include congenital hypoplasias. The posterior vertebrobasilar circulation supplies the proximal and middle portions of the nerve via the anterior inferior cerebellar artery and the internal auditory artery. Taste from the anterior two thirds of the tongue runs with the lingual nerve. Taste is most reliably tested by electrogustometry. chorda tympani. musculoskeletal abnormalities.12. Dribbling of saliva through the angle of mouth 5. computerized tomographic (CT) and magnetic resonance imaging (MRI) scans allow prompt identification of these lesions. abducens palsy. Examples of tests of these autonomic functions are the salivary flow test and Schirmer’s test of lacrimal . Depending on the clinical location of disease. and into the corticospinal tracts ventrally. genetics. These fibers run in the nervus intermedius.JK-PRACTITIONER bone. CT/MRI. Sensation from the palate. Loss of whistling l0. Cerebrospinal fluid analysis. make it unlikely that occlusion of any single artery will compromise facial nerve function. which ends in the sphenopalatine ganglion.. infectious. demyelinating and tumorous. In addition to the physical examination. and via the nervus intermedius to the brain stem.. dysfunction of the facial nerve can be due to disorders of under activity or over activity. especially in the middle. The lacrimal nucleus. vagus. Assymetry of the face 2.can also be found in AIDS patients. or infranuclear segments. Abolishion of involuntary blinking 7. nuclear. Inability to close the eyes 4. and in the majority of cases these findings are bilateral. AUTONOMIC FUNCTION Salivary and lacrimal function can be quantified and evaluated through comparison to normal controls as well as to the contralateral side. The meningeal space is a common site of infranuclear involvement. these can be further localized anatomically to the supranuclear. Finally these parasympathetic fibers reach their destination in the submandibular ganglion. cardiac anomalies. FACIAL NERVE DISORDERS Clinically. January-March 2005 54 . the preganglionic fibers separate to run with the chorda tympani. Distal segments receive blood from the stylomastoid artery. craniofacial defects. VASCULAR SUPPLY The vascular supply of the facial nerve is complex. FOVILLE’S SYNDROME Foville’s syndrome is characterized by peripheral facial weakness. which compares the amounts of electrical current applied to the anterolateral aspect of the tongue necessary to produce taste Perception. through the facial canal to the geniculate ganglion. CLINICAL EVALUATION OF INTEGRITY AND FACIAL NERVE FUNCTION MOTOR FUNCTION The majority of facial nerve functions can be readily assessed by observation: 1. A host of associated features have been described. On its course the greater superficial petrosal nerve joins the deep petrosal nerve carrying sympathetic information from the carotid plexus to form the vidian nerve. is the origin of the visceral motor preganglionic parasympathetic nerve destined for the lacrimal gland via postganglionic fibers from the sphenopalatine ganglion. nose. and contra lateral hemi paresis . vidian nerve greater superficial petrosal nerve to the geniculate ganglion. and serologic tests are very important ways of differentiating Vol. Lesions associated with these clinical features lie more ventrally in the brain stem than those of Foville’s syndrome.function respectively. The list of possible causes of supranuclear facial paresis is large.

It is often surprising to find cranial nerve signs. and lingua plicata but all three features need not be present. lesions along the course of the facial nerve must be considered.patients frequently give a history of a recent viral syndrome and auricular pain that preceded the facial weakness and vesicular eruption. autoimmunity. parotitis. Longitudinal fractures are more cornmon than transverse and seem to have a better prognosis. The extent of the herpetic involvement may not be limited to the distribution of the facial nerve. Infranuclear Lesions when facial weakness is progressive and of a peripheral nature. this might not cause alarm if one considers Bell’s palsy to be a viral disease. orofacial edema (predominately of the lips). Initial workup may also include an audiogram and brain stem auditory evoked Potentials’ BELL’S PALSY (IDIOPATHIC. The most common tumors are acoustic neuroma. dizziness. MELKERSSON-ROSENTHAL SYNDROME Classically Melkersson Rosenthal syndrome comprises a triad of recurrent infranuclear facial paralysis. Electrodiagnostic studies can be helpful. The pain associated with this viral eruption is typically severe and often persists for weeks. Thus. only very rarely do they appear in combination. an infectious process probably accounts for the majority of cases.12. The swelling may be biateral. there are several variants that involve the cranial nerves to a greater extent. No. Several causes have been put forth. with the edema antedating the weakness by months to years. and allergic reaction. and it is affected in 50%of cases of uveoparotid fever. and identifiable inflammatory or infectious causes.JK-PRACTITIONER possible causes. ACUTE IDIOPATHIC POLYNEURITIS (GUILLAIN BARRE SYNDROME) Although the typical presentation of Guillain Barre Guillain-Barre syndrome is an ascending paresis with depressed tendon reflexes. Steroids are the mainstay of treatment. lymphoma (intraparenchymal and meningeal). such as altered facial sensation. and periorbital dysesthesias (trigeminal nerve involvement) should alert the clinician to a lesion in this area. Idiopathic cranial polyneuritis should be distinguished from Guillain Barre Guillain-Barre syndrome. infection. but any combination is possible with the exception of the olfactory nerve. The advent of MRI has made evaluation of the cerebellopontine angle simple. and thus capable of causing a mononeuritis multiprex. Although controversial surgical exploration in cases of immediate-onset total paralysis together with a transverse fracture should be seriously considered. and mild pyrexia. FACIAL PALSY) Since Sir Charles Bell’s classic descriptions of peripheral facial weakness Bell’s palsy. such as clofazimine and steroids. although the 55 delayed group probably fares a little better CT scanning to look for temporal bone fractures should be performed. these lesions can be clinically localized and specific neuroradiologic techniques can be used to define further the extent of involvement and suggest a cause’ CEREBELLOPONTINE ANGLE LESIONS The cranial nerves VII and VIII are enclosed in a common sheath as they leave the brain stem in the Cerebellopontine angle on their way to the internal auditory canal. and in one case this finding preceded any nerve deficits by more than 3 months. which can often be hard to detect if accompanied by facial swelling. Vesicles can involve any aspect of the ipsilateral face indicating trigeminal nerve involvement. tinnitus. hearing loss. Tumors of the cerebellopontine angle generally of a benign histologic character. or it may occur independent of the facial paresis. As the name suggests. as well as the surgical reduction of granulomatous tissue UVEOPAROTID FEVER (HEERFORDT’S DISEASE) As the name suggests. but it tends to recur. Onset can be at any age. The acute or subacute onset of any combination of these signs should alert the clinician to this potentially fatal disorder. motor nerve conduction studies reveal slow responses. Treatment includes several drugs. although it can be anywhere along its course as demonstrated by some patients with parageusia and reduced lairimation. but persons of any age are susceptible’ Men and women are equally affected. Classically. in its full presentation uveoparotid fever is characterized by uveitis. multiple cranial nerve palasies are present at the same time in this condition. Broadly defined. By testing the various facial nerve functions. Although the cause of Bell’s palsy is unknown. The cause is probably nerve infiltration with noncaseating granulomatous material. January-March 2005 . cases of both immediate and delayed paresis are seen. corneal hypesthesia. a Combination of progressive facial weakness. tuberculosis fungus (especially Cryptococcus). It is characterized by an acute unilateral infranuclear facial palsy. The site of facial nerve inflammation is often within its path through the parotid gland.(GENICULATE HERPES’ OTITIC HERPES) The association of facial paresis with herpetic eruptions along the ipsilateral external auditory meatus constitutes the Ramsay Hunt syndrome . An elevated serum angiotensin converting enzyme (ACE) level can be helpful. meningioma. Face or head pain was almost invariable. TRAUMATIC FACIAL NERVE PALSY Trauma to the head may result in facial paresis. Consideration should be given to the presence of toxoplasmosis. A subjective feeling of diminished taste or perverted taste (parageusia) on the involved side is reported by 30o/o of patients. and auditory and vestibular symptoms are frequent. is a disease that typically affects adults 20 to 40 years. Cheilitis granulomatosis is seen on lip biopsy and helps confirm the diagnosis. The disease is self-limited. or tongue deviation in a case that is otherwise typical of Bell’s Palsy. carcinomatous meningitis.. Another less common variant is facial diplegia with distal paresthesias. such as inheritance. vascular and genetic causes account for some cases. as in some cases of Bell’s palsy RAMSAY HUNT SYNDROME. and epidermal cyst. since respiratory and autonomic involvement may occur. by far the most common type of facial palsy. The abducens nerve is most frequently affected.despite unilateral facial paresis. and cerebrospinal fluid examination Vol. The facial nerve is the most commonly involved cranial nerve in sarcoidosis. Other cranial nerve palsies in a mononeuritis multiplex fashion can be seen. The natural history is for both groups to do well. 1. cytomegalovirus’ and progressive multifocal leukoencephalopathy). nurosyphilis. IDIOPATHIC CRANIAL POLYNEURITIS. and viruses (HIV.

g. including brain stem tumors. levodopa. kindling incorporates the concepts of both ephaptic transmission and nuclear reorganization. Fuchs’s heterochromic cyclitis.. pontine tuberculoma . timber rattle snake envenomation. which then coordinates facial muscle contraction. subarachnoid hemorrhage. jaw opening or closing. and electrophysiologic studies provide support for each theory. antichorinergics. The complex nature of synkinesis is best explained by a nuclear origin. Excessive blinking is the usuaI first symptom. encephalitis lethargica. syringobulbia. and dentate nuclei. carcinomatous meningitis. including facial nuclear reorganization. and bony defects of the inferior orbital rim and floor. such as tricyclic antidepressants. All explain some components of involuntary facial movements. Several different medications have been tried. Aberrant regeneration refers to the resprouting of axons down incorrect myelin sheaths after nerve disruption. and dementia as well as the ophthalmologic manifestations of enophthalmos. cerebellopontine angle tumors. Satisfactory treatment for blepharospasm is best accomplished with botulinum. Synkinetic Movements Synkinesis is defined as an unintentional movement following the initiation of volitional movement. Supranuclear Disorders: HABIT SPASM OF THE FACE (NERVOUS TWITCH. involuntary movement of the facial muscles involving predominantly the periocular and orbicularis oris musculature . January-March 2005 56 . are seen to involve contiguous cortical areas that serve a distribution beyond the facial nerve. whereby anantidromic impulse from the ephapse of the nerve activates the facial nucleus. Nuclear Disorders FACIAL MYOKYMIA Myokymia is a continuous. aberrant regeneration. Motor tics can occur as an isolated disorder. These patients should be considered to have focal cortical disease. Todd’s paresis). As the disease progresses. A toxin injected into the muscles around the eye. or as a component of Tourettets syndrome. multiple sclerosis. insidiously becoming a spasm of the eyelid that is not under volitional control Although involvement may appear unilateral in early stages or far into the disease course. bilateral impairment is always found eventually. ESSENTIAL BLEPHAROSPASM Essential blepharospasm is a form of cranial dystonia limited to the orbicularis oculi muscles.One reason why such a varied number of drugs have been used in an attempt to treat cranial dystonia is that this disorder was initially considered a psychiatric illness. vocal cords. The presumed cause of cranial dystonia in an upset in the normal dopamine balance in the basal ganglia and brain stem. and prompt neuroanatomic studies should be carried out to direct the appropriate treatment course. This blinking gradually intensifies in character. causing some diagnostic confusion with habit spasm hemi facial spasm. and levodopa or neuroleptic use. sarcoidosis. and (4) pathologic reports of cases in which abnormalities when evident have inconsistently found gliosis and cell loss in the caudate. tetrabenazine). neck. misdirected neural firing leads to the synchronous contraction of unassociated muscle groups.12. surgical options include orbicularis myectomy. and Cardiopulmonary arrest Vol. substantia nigra. and lithium . the synkinetic movements seen after aberrant regeneration and the reflex grimacing movements created by trigeminal irritation must be considered first. neuroeeptics(including clozapine) dopamine depleters (reserpine. MEIGE’S SYNDROME (BLEPHAROSPASMOROMANDIBULAR DYSTONIA. (spastic dysphonia). the eye closure may become so frequent and prolonged that the patients functionally blind and may withdraw from all social contact. Several theories have been put forth. P R O G R E S S I V E H E M I FA C I A L AT R O P H Y (PARRYROMBERG SYNDROME) Progressive hemifacial atrophy is clearly a syndrome.JK-PRACTITIONER shows cytoalbuminologic dissociation. cysticercosis.The pathophysiology of facial myokymia needs to incorporate the variety of conditions known to be associated with it. extra ocular muscle imbalance and palsies. hypoparathyroidism. and kindling. These studies have reported on (l) different responses to pharmacologic agents that exert their effect on the basal ganglia. FOCAL CORTICAL SEIZURES Epileptiform discharges arising from the facial cortex of the motor homunculus can manifest as gross clonic movements of the contra lateral face. and limbs is often referred to as Meige’s syndrome. trigeminal anesthesia. No. Finally.BRUEGHEL’S SYNDROME) Dystonic involvement of the lower cranial muscles (mouth retraction. 1. midbrain tectum. locus ceruleus. sclera melting. Additional manifestations have included hyporeflexia seizures. Guillain-Barre syndrome. Treatment may be as simple as reassurance. retinal vascular abnormalities. or it may require more aggressive drug therapy. Postictally there can be a supranuclear type of paresis (e. peripheral facial nerve avulsion. when closely inspected. facial grimacing). Axonal compression or disruption along the course of the facial nerve may lead to involuntary or synkinetic movements. clonazepam baclofen. The unifying characteristic of all cases is acquired hemi facial atrophy. and peripheral facial neurectomy. cholinergics. DISORDERS OF OVERACTIVITY In any evaluation of unusual facial movements. which must distinguished from congenital forms and bilateral lipodystrophy. FACIAL TIC) This disorder typically occurs in childhood and is characterized by stereotypical.OROFACIALCERICAL DYSTONIA. For the few patients who do not respond to pharmacotherapy. representing exhaustion of the cortical tonic input. undulating. ephaptic (fatse synapse) transmission. Ultimately. These movements. repetitive facial movements that are reproducible and can be promptly inhibited on command. Horner’s syndrome. (2) associated conditions that affect the basal ganglia and can produce secondary dystonia including Wilson’s-disease. Iid atrophy tonic or irregular pupils. putamen. rather than a specific disease. (3) associated conditions that affect the upper brain stem including strokes and multiple sclerosis.

1991 Juncos JL. Ann Allergy 69:187.The nervous system. N Engl J Med 326:1 130. Plast Reconstr Surg 85:669.T.1994 K’L’Moore The Facial nerve . Towfighi J. Thiese SM et al: Facial dystonia. No. Palmer E et al: Mobius syndrome: Neuropathologic observations.Holds JB. destruction. voluntary movements such as smiling. ischemia. is characteristic of hemifacial spasm These bursts of clonic activity may last only seconds or eventually may become tonic and continue for periods of minutes to hours. Treatment of this condition should be aimed at the underlying pathology. 13. Ferrante R: Effects of repeated botulinum toxin injections on orbicularis oculi muscle . eating.1987 Kiriyanthan G. botulinum toxin. Scheide A et al: Incidence. Borodic GE.Krauss JK. pathologic.JK-PRACTITIONER Unknown specific changes in the micro environment of the motor neuron or its axon due to edema.23. 19.1990 Vol. unilateral facial twitching. 15. References 1.Surg Neurol 41:498. Sakuraoka K. Symptomatic pharmacologic treatment options include carbamazepine. l992 ‘ Ropper AH: The Guillain Barre Guillain -Barre syndrome. 1. Laryngoscope 99. 5. 21. The prolonged. Jaradeh S et al: Mobius Mobius syndrome: Evidence for a vascular etiology. clonazepam. or raising the eyebrows may precipitate involuntary spasms. Mulliken JB: Clinical and ultrastructural studies of Romberg’s hemifacial atrophy. 1990 Pensler M. Neouro Anatomy for Medical Students M. Riggio E. Holds JB White GL. severe contractions of facial musculature lead to annoying and frequently socially disfiguring. 20. which are effective 25% of the time. Anderson RL: Auditory brain stem responses in blepharospasm. Schumacher T. phenytoin.1973 Morgenlander JC. Text book of Neuro Anatomy. 1990 Facial Nerve . baclofen. Text Book of Anatomy. J child Neurol 8:260. Neurology 41:1800. 3.Chap The Cranial Nerves. 4. which begins insidiously around the orbicularis oculi and spreads slowly over 1 to 5 years to involve all the muscles of facial expression. Non surgical management is most successful with botulinum toxin’ Alternative drug trials. 9. 8. 11.1992 Creel DJ holds JB. grimacing appearance with partial eyelid closure This is usually painless. essential blepharospasm and hemifacial spasm. Marks K.Text of Anatomy. and anticholinergics.Tajima S. Post grad Med 88(5 ):157 . talking. 12. 22.J Clin Neuro Ophthalmol 12:121. Int J oral Maxillofac Surg 2l:115. Infranuclear Disorders HEMIFACIAL SPASM Rhyhmic.1992 Sussman GL. l994 Sabistons text book of surgery. include carbamazepine.Glocker Fx et al: Facial myokymia due to acoustic neurinoma. 57 Alderson K.Neurology Grays Anatomy 38 TH edn Grants Anatomy. January-March 2005 17. demyelination. 6. Acta Neuropathol 48:11. Massey EW: Bell’s palsy: Ensuring the best possible outcome. Dermatology 185:196. is the only permanent treatment and has an 85% success rate. Beal MF: Idiopathic cranial polyneuropathy: A fifteen-year experience. The Cranial nerves Detail of The Seventh Cranial Nerve. toxins.12. Deluke DM: MelkerssonRosenthal syndrome: Review of literature and case report. Liston SL. 1992 .The seventh Cranial Nerve. 1993 Devriese PP. The Seventh cranial Nerve. Brain 110: 197. 10. phenytoin and most recently.Laryngoscope 83:1311.Nishikawa T: Progressive facial hemiatrophy : Report of five cases and biochemical analysis of connective tissue. prognosis and recovery of Bell’s palsy: A survey of about 1000 patients^ (1974 1983). Kleid MS: Histopathology of Bell’s palsy. The Cranial Nerves :Richard Snell. and therapeutic considerations. Swisher CN. 1993 D’Cruz OF. 14. Am Fam Physician 43:2113. intermittent. Mutphy GF. Gilbert PM et al: Progressive hemifacial ahophy in a patient with lupus erythematosus.I 989 May M: Anatomy of the facial nerve (the spatial relations of the peripheral fibers in the temporal bone). Yang WH.EI Rakhawy.1991 Berkowitz and Moxham. Anderson RL: Botulinum-induced alteration of nervemuscle interactions in the human orbicularis oculi following treatment for blepharospasm.1979 Winnie R. 23.. 1992 . Steinberg S: Melkersson Rosenthal syndrome: Clinical. or metabolic alterations are proposed. Surgical decompression of the facial nerve. 18. Often. Electroencephalogre Clin Neurophysiol 86:138. Roddi R. Clin Otolaryngol 15:15. 16. 7. 2. Plast Reconstr Surg 93:1067.