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genu. After the genu, the nerve entersthe facial canal. At the posterior aspectof the middle ear, the nerve curvesdownward at which point a branchinnervates the stapedius muscle. Thisminute muscle acts to dampen wideacoustic input surges from the delicate bony transmission system. Thedownward course takes it into theanterior wall of the mastoid process ofthe temporal bone. It is within thissegment that the chorda tympaniarises and marks the final separation off ibers that form the nervusintermedius. The chorda tympanitransmits afferent taste sensation andefferent parasympathetic fibers to thesubmandibular ganglion. The motornerve continues in the temporal boneuntil it exits at the base through thestylomastoid  foramen . Three branches immediately diverge toinnervate the posterior auricular,posterior belly of the digastric, andstylohyoid muscles . Runninganteriorly approximately 2 cm fromthe stylomastoid foramen the nerve

divides into upper and lowerdivisions, which traverse thesuperficial portion of the parotidgland .Pathology of the parotid mayimpair facial nerve function.Eventually the nerve divides furtherinto its five major branches (PesAnserinus): temporal, zygomatic,buccal, mandibular, and cervical.All of the muscles of facial expressionare supplied by the facial nerve, withthe exception of the levator palpebraesuperioris, which is supplied by the

oculomotor nerve.NERVUS INTERMEDIUSThe nervus intermedius of

Wrisberg is made up of all thecomponents of the facial nerve exceptthe somatic motor component, Thesuperior salivatory nucleus is theorigin of the visceral motor preganglionic parasympathetic nervedestined for both the submandibulara n d s u b l i n g u a l g l a n d s   v i a postga ngli on ic fibe rs from thesubmandibular ganglion. Along itsdownward course within the temporal

Introduction:The facial nerve is the seventh

cranial nerve  .It is one of the mostimportant mixed nerves in the human body and more important as a motornerve than as a sensory nerve andcarries a great significance for theAnatomist, the surgeon and a clinician’The facial nerve is formed fromelements of the second (hyoid) branchial arch, which supplies itsmotor and sensory components. Themigration of the abducens nucleusrostrally, coupled with the movementof the facial nucleus caudally andlaterally, gives rise to the uniquelycurved brain stem course of this nerve.It has three nuclei two motor andone sensory.Motor Nuclei: Superior salivatorynucleus and facial Motor Nucleus.Sensory : Solitary NucleusAnatomy:

This is discussed in terms of thenerve’s supranuclear, nuclear, and,infranuclear segments.

The facial nerve is more important

as a motor nerve than as a sensorynerve. The motor nuclei are FacialMotor nucleus and the SuperiorSalivary nucleus. The sensory nucleusis the solitary nucleus.The Facial Nerve is motor to :

All muscles of faceTo PlatysmaTo Posterior belly of Digastric

and stylohyoidTo StapediusTo three glands: Lacrimal,

Sublingual, sub mandibular Glands.

The Facial Nerve is sensory toLacrimal, Sublingual, Submandible 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 offacial nerve.Course of the facial nerve

After its origin from the brain stemThe motor nerve then turns posteriorlyat a sharp angle, forming the external

Authors’ affiliations :Prof. Gulam HasanKing Saud UniversitySaudi Arabia

Prof. Kulbeer Kaur

Muzaffar Ahmad

Ashfaqul Hassan

Mohd. ShafiDept. of Anatomy GMC, Srinagar 

Accepted for publication :June 2004

Correspondence to :

Prof. Kulbeer KaurProf. and Head,Deptt. of Anatomy,Govt. Medical College,Srinagar-Kashmir, India

The Facial Nerve : The Anatomical and Surgical important

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

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membrane may be an early indication of facial nervedysfunction. Taste is most reliably tested byelectrogustometry, which compares the amounts ofelectrical current applied to the anterolateral aspect of thetongue necessary to produce taste Perception.AUTONOMIC FUNCTION

Salivary and lacrimal function can be quantified and

evaluated through comparison to normal controls as well asto the contralateral side. Examples of tests of theseautonomic functions are the salivary flow test andSchirmer’s test of lacrimal ,function respectively.FACIAL NERVE DISORDERS

Clinically, dysfunction of the facial nerve can be due todisorders of under activity or over activity; these can befurther localized anatomically to the supranuclear, nuclear,or infranuclear segments.DISORDERS OF UNDERACTIVITY

Supranuclear LesionsMotor function of the upper face derives from both

hemispheres. As a result, supranuclear lesions involving theface will spare the functions of forehead wrinkling and eye

closure. In addition to the physical examination,computerized tomographic (CT) and magnetic resonanceimaging (MRI) scans allow prompt identification of theselesions. The list of possible causes of supranuclear facial paresis is large. The major categories of causes are vascular.infectious. demyelinating and tumorous.FOVILLE’S SYNDROME

Foville’s syndrome is characterized by peripheral facialweakness, ipsilateral conjugate horizontal gaze paresis, andcontra lateral hemi paresis . Lesions associated with theseclinical features extend from the facial nucleus to theabducens nucleus and paramedian pontine reticularformation dorsomedially, and into the corticospinal tracts

ventrally.MILLARD-GUBLER SYNDROME

In Millard-Gubler syndrome there is a combination ofcontralateral hemiparesis, abducens palsy, and variablefacial nerve palsy. Lesions associated with these clinicalfeatures lie more ventrally in the brain stem than those ofFoville’s syndrome, and they cause an infranuclear abducens palsy rather than a nuclear disruption..MOBIUS’ SYNDROME

Peripheral facial weakness and abduction deficits arecentral features of this syndrome, and in the majority of casesthese findings are bilateral. A host of associated featureshave been described, including other cranial nerve palsies ptosis, musculoskeletal abnormalities, cardiac anomalies,craniofacial defects, and mental retardation. Nuclearagenesis of nerves VI and VII is considered the classicSyndrome, Furthermore, the etiologies postulated to dateinclude congenital hypoplasias, vasculopathies, genetics,infections, neuronal degeneration andmuscular dystrophy.Imaging studies in nuclear cases, when positive, have shown brain stem atrophy and caudal pontine calcifications.COMPLICATIONS OF AIDS

Supranuclear, nuclear, infranuclear lesions .can also befound in AIDS patients. The meningeal space is a commonsite of infranuclear involvement. Depending on the clinicallocation of disease, CT/MRI, Cerebrospinal fluid analysis,and serologic tests are very important ways of differentiating

 bone, the preganglionic fibers separate to run with the chordatympani.. Finally these parasympathetic fibers reach theirdestination in the submandibular ganglion. The lacrimalnucleus, often considered part of the superior salivatorynucleus, is the origin of the visceral motor preganglionic parasympathetic nerve destined for the lacrimal gland via postganglionic fibers from the sphenopalatine ganglion.

These fibers run in the nervus intermedius. traverse thegeniculate ganglion, and form the greater superficial petrosal nerve. On its course the greater superficial petrosalnerve joins the deep petrosal nerve carrying sympatheticinformation from the carotid plexus to form the vidian nerve,which ends in the sphenopalatine ganglion. Postganglionicfibers travel with the zygomaticotemporal branch of cranialnerve V to the lacrimal gland. Visceral sensory fibers maytake two routes on their way back to synapse in the nucleussolitarius, Taste from the anterior two thirds of the tongueruns with the lingual nerve, chorda tympani, through thefacial canal to the geniculate ganglion, and via the nervusintermedius to the brain stem. Sensation from the palate,nose, and pharynx runs with the maxillary nerve to the

sphenopalatine ganglion, vidian nerve greater superficial petrosal nerve to the geniculate ganglion, and via the nervusintermedius to the brain stem.VASCULAR SUPPLY

The vascular supply of the facial nerve is complex.The posterior vertebrobasilar circulation supplies

the proximal and middle portions of the nerve via theanterior inferior cerebellar artery and the internalauditory artery, respectively.

Further supply of the middle portion of the nerve comesfrom the petrosal artery via the middle meningeal artery ofthe external carotid.

Distal segments receive blood from the stylomastoid

artery, which is also a branch of the external carotid.The considerable overlap of the arterial supply. especially inthe middle. Portions through the facial canal. make itunlikely that occlusion of any single artery will compromisefacial nerve function.CLINICAL EVALUATION OF INTEGRITY ANDFACIAL NERVEFUNCTIONMOTOR FUNCTION

The majority of facial nerve functions can be readilyassessed by observation:1. Assymetry of the face2. Stasis of food in the mouth3. Inability to close the eyes4. Dribbling of saliva through the angle of mouth5. Difficulty in closure of the eyes6. Abolishion of involuntary blinking7. Loss of frowning of the forehead8. Loss of wrinkling of the forehead9. Loss of whistlingl0. Flattening of nasolabial fold11. Drooping of the angle of mouthSENSORY FUNCTION

Although it is a function of overlapping sensory fibersfrom the trigeminal, glossopharyngeal, vagus, and greaterauricular nerves, abnormal sensation along the posterioraspect of the external auditory canal and tympanic

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delayed group probably fares a little better CT scanning tolook for temporal bone fractures should be performed.Longitudinal fractures are more cornmon than transverseand seem to have a better prognosis. Although controversialsurgical exploration in cases of immediate-onset total paralysis together with a transverse fracture should beseriously considered. Electrodiagnostic studies can be

helpful, as in some cases of Bell’s palsyRAMSAY HUNT SYNDROME.(GENICULATEHERPES’ OTITIC HERPES)

The association of facial paresis with herpetic eruptionsalong the ipsilateral external auditory meatus constitutes theRamsay Hunt syndrome .patients frequently give a history ofa recent viral syndrome and auricular pain that precededthe facial weakness and vesicular eruption. The extent of theherpetic involvement may not be limited to the distributionof the facial nerve. Other cranial nerve palsies in amononeuritis multiplex fashion can be seen. Vesicles caninvolve any aspect of the ipsilateral face indicatingtrigeminal nerve involvement, and auditory and vestibularsymptoms are frequent. The pain associated with this viral

eruption is typically severe and often persists for weeks.MELKERSSON-ROSENTHAL SYNDROME

Classically Melkersson Rosenthal syndrome comprisesa triad of recurrent infranuclear facial paralysis,orofacial edema (predominately of  the lips), and linguaplicata but all three features need not be present; only veryrarely do they appear in combination. Onset can be at anyage. The swelling may be biateral- despite unilateral facial paresis, or it may occur independent of the facial paresis,with the edema antedating the weakness by months to years.Cheilitis granulomatosis is seen on lip biopsy and helpsconfirm the diagnosis. Several causes have been put forth,such as inheritance, infection, autoimmunity, and allergic

reaction. Treatment includes several drugs, such asclofazimine and steroids, as well as the surgical reductionof granulomatous tissueUVEOPAROTID FEVER (HEERFORDT’S DISEASE)

As the name suggests, in its full presentationuveoparotid fever is characterized by uveitis, parotitis, andmild pyrexia. The facial nerve is the most commonlyinvolved cranial nerve in sarcoidosis, and it is affected in50%of cases of uveoparotid fever. The site of facial nerveinflammation is often within its path through the parotidgland, although it can be anywhere along its course asdemonstrated by some patients with parageusia and reducedlairimation. The cause is probably nerve infiltration withnoncaseating granulomatous material. An elevated serumangiotensin converting enzyme (ACE) level can be helpful.ACUTE IDIOPATHIC POLYNEURITIS (GUILLAINBARRE SYNDROME)

Although the typical presentation of Guillain BarreGuillain-Barre syndrome is an ascending paresis with depressed tendon reflexes, there are several variants thatinvolve the cranial nerves to a greater extent. Another lesscommon variant is facial diplegia with distal paresthesias.The acute or subacute onset of any combination of thesesigns should alert the clinician to this potentially fataldisorder, since respiratory  and autonomic involvementmay occur.  Classically, motor nerve conduction studiesreveal slow responses, and cerebrospinal fluid examination

 possible causes. Consideration should be given to the presence of toxoplasmosis, lymphoma (intraparenchymaland meningeal), nurosyphilis, tuberculosis fungus(especially Cryptococcus) , and viruses (HIV,cytomegalovirus’ and progress ive mult i focalleukoencephalopathy). Infranuclear Lesions when facialweakness is progressive and of a peripheral nature, lesions

along the course of the facial nerve must be considered. Bytesting the various facial nerve functions, these lesions can be clinically localized and specific neuroradiologictechniques can be used to define further the extent ofinvolvement and suggest a cause’CEREBELLOPONTINE ANGLE LESIONS

The cranial nerves VII and VIII are enclosed in acommon sheath as they leave the brain stem in theCerebellopontine angle on their way to the internal auditorycanal. Thus, a Combination of progressive facial weakness,tinnitus, hearing loss, dizziness, and periorbital dysesthesias(trigeminal nerve involvement) should alert the clinician to alesion in this area.. Tumors of the cerebellopontine anglegenerally of a benign histologic character. The most

common tumors are acoustic neuroma, meningioma, andepidermal cyst. The advent of MRI has made evaluation ofthe cerebellopontine angle simple. Initial workup may alsoinclude an audiogram and brain stem auditory evokedPotentials’BELL’S PALSY (IDIOPATHIC. FACIAL PALSY)

  Since Sir Charles Bell’s classic descriptions of peripheral facial weakness Bell’s palsy, by far the mostcommon type of  facial palsy,  is a disease that typicallyaffects adults 20 to 40 years, but persons of any age aresusceptible’ Men and women are equally affected. It ischaracterized by an acute unilateral infranuclear facial palsy.A subjective feeling of diminished taste or perverted taste

(parageusia) on the involved side is reported by 30o/o of patients. It is often surprising to find cranial nerve signs,such as altered facial sensation, corneal hypesthesia, ortongue deviation in a case that is otherwise typical of Bell’sPalsy. Broadly defined, this might not cause alarm if oneconsiders Bell’s palsy to be a viral disease, and thus capableof causing a mononeuritis multiprex. Although the cause ofBell’s palsy is unknown, an infectious process probablyaccounts for the majority of cases; vascular and geneticcauses account for some cases.IDIOPATHIC CRANIAL POLYNEURITIS.

As the name suggests, multiple cranial nerve palasiesare present at the same time in this condition. The abducensnerve is most frequently affected, but any combination is possible with the exception of the olfactory nerve. Face orhead pain was almost invariable, and in one case this finding preceded any nerve deficits by more than 3 months. Thedisease is self-limited, but it tends to recur. Steroids are themainstay of treatment. Idiopathic cranial polyneuritis should be distinguished from Guillain Barre Guillain-Barresyndrome, carcinomatous meningitis, and identifiableinflammatory or infectious causes.TRAUMATIC FACIAL NERVE PALSY

Trauma to the head may result in facial paresis, whichcan often be hard to detect if accompanied by facial swelling.cases of both immediate and delayed paresis are seen. Thenatural history is for both groups to do well, although the

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course.ESSENTIAL BLEPHAROSPASM

Essential blepharospasm is a form of cranial dystonialimited to the orbicularis oculi muscles. Excessive blinking is the usuaI first symptom. This blinking graduallyintensifies in character, insidiously becoming a spasm of theeyelid that is not under volitional control Although

involvement may appear unilateral in early stages or far intothe disease course, causing some diagnostic confusion withhabit spasm hemi facial spasm, bilateral impairment isalways found eventually. As the disease progresses, the eyeclosure may become so frequent and prolonged that the patients functionally blind and may withdraw from all socialcontact.MEIGE’S SYNDROME (BLEPHAROSPASM-OROMANDIBULAR DYSTONIA,OROFACIAL-CERICAL DYSTONIA,BRUEGHEL’S SYNDROME)

Dystonic involvement of the lower cranial muscles(mouth retraction, jaw opening or closing, facialgrimacing), neck, vocal cords, (spastic dysphonia), andlimbs is often referred to as Meige’s syndrome.

The presumed cause of cranial dystonia in an upset inthe normal dopamine balance  in the basal ganglia and brain stem. These studies have reported on (l) differentresponses to pharmacologic agents that exert their effect onthe basal ganglia; (2) associated conditions that affect the basal ganglia and can produce secondary dystonia includingWilson’s-disease, encephalitis lethargica, and levodopaor neuroleptic use; (3) associated conditions that affect theupper brain stem including strokes and multiple sclerosis; and (4) pathologic reports of cases in which abnormalitieswhen evident have inconsistently found gliosis and cell lossin the caudate, putamen, substantia nigra, locusceruleus, midbrain tectum, and dentate nuclei.

Satisfactory treatment for blepharospasm is bestaccomplished with botulinum. A toxin  injected into themuscles around the eye. Several different medicationshave been tried, such as tricyclic antidepressants,antichorinergics, neuroeeptics(including clozapine)

dopamine depleters (reserpine, tetrabenazine),levodopa, cholinergics, clonazepam baclofen, andlithium .One reason why such a varied number of drugs have been used in an attempt to treat cranial dystonia is that thisdisorder was initially considered a psychiatric illness. Forthe few patients who do not respond to pharmacotherapy,surgical options include orbicularis myectomy, peripheralfacial nerve avulsion, and peripheral facial neurectomy. Nuclear DisordersFACIAL MYOKYMIA

Myokymia is a continuous, undulating, involuntarymovement of the facial muscles involving predominantly

the periocular and orbicularis oris musculature  .The pathophysiology of facial myokymia needs to incorporatethe variety of conditions known to be associated with it,including brain stem tumors, pontine tuberculoma  ,cerebellopontine angle tumors, carcinomatousmeningitis, sarcoidosis, syringobulbia, subarachnoidhemorrhage, multiple sclerosis, Guillain-Barresyndrome, cysticercosis, timber rattle snakeenvenomation, hypoparathyroidism, andCardiopulmonary arrest

shows cytoalbuminologic dissociation.P R O G R E S S I V E H E M I F A C I A L A T R O P H Y(PARRYROMBERG SYNDROME)

Progressive hemifacial atrophy is clearly a syndrome,rather than a specific disease. The unifying characteristic ofall cases is acquired hemi facial atrophy, which mustdistinguished from congenital forms and bilateral

lipodystrophy. Additional manifestations have includedhyporeflexia seizures, trigeminal anesthesia, anddementia as well as the ophthalmologic manifestations ofenophthalmos, Iid atrophy tonic or irregular pupils,Horner’s syndrome, Fuchs’s heterochromic cyclitis,retinal vascular abnormalities, sclera melting, extraocular muscle imbalance and palsies, and bony defects ofthe inferior orbital rim and floor.DISORDERS OF OVERACTIVITY

In any evaluation of unusual facial movements, thesynkinetic movements seen after aberrant regeneration andthe reflex grimacing movements created by trigeminalirritation must be considered first. Synkinetic MovementsSynkinesis is defined as an unintentional movement

following the initiation of volitional movement. Axonalcompression or disruption along the course of the facialnerve may lead to involuntary or synkinetic movements.Several theories have been put forth, including facial nuclearreorganization, aberrant regeneration, ephaptic (fatsesynapse) transmission, and kindling. All explain somecomponents of involuntary facial movements, andelectrophysiologic studies provide support for each theory.The complex nature of synkinesis is best explained by anuclear origin. Aberrant regeneration refers to theresprouting of axons down incorrect myelin sheaths afternerve disruption.. Ultimately, misdirected neural firing leadsto the synchronous contraction of unassociated muscle

groups. Finally, kindling incorporates the concepts of bothephaptic transmission and nuclear reorganization, wherebyanantidromic impulse from the ephapse of the nerveactivates the facial nucleus, which then coordinates facialmuscle contraction. Supranuclear Disorders:HABIT SPASM OF THE FACE (NERVOUS TWITCH.FACIAL TIC)

This disorder typically occurs in childhood and ischaracterized by stereotypical, repetitive facial movementsthat are reproducible and can be promptly inhibited oncommand. Motor tics can occur as an isolated disorder, or asa component of Tourettets syndrome. Treatment may be assimple as reassurance, or it may require more aggressivedrug therapy.FOCAL CORTICAL SEIZURES

Epileptiform discharges arising from the facial cortex ofthe motor homunculus can manifest as gross clonicmovements of the contra lateral face. These movements,when closely inspected, are seen to involve contiguouscortical areas that serve a distribution beyond the facialnerve.

Postictally there can be a supranuclear type of paresis(e.g. Todd’s paresis), representing exhaustion of the corticaltonic input. These patients should be considered to havefocal cortical disease, and prompt neuroanatomic studiesshould be carried out to direct the appropriate treatment

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eventually may become tonic and continue for periods ofminutes to hours. The prolonged, severe contractions offacial musculature lead to annoying and frequently sociallydisfiguring, grimacing appearance with partial eyelidclosure This is usually painless. Often, voluntarymovements such as smiling, eating, talking, or raising theeyebrows may precipitate involuntary spasms. Surgical

decompression of the facial nerve, is the only permanenttreatment and has an 85% success rate. Non surgicalmanagement is most successful with botulinum toxin’Alternative drug trials, which are effective 25% of thetime, include carbamazepine, phenytoin, baclofen,clonazepam, and anticholinergics.

Unknown specific changes in the micro environment ofthe motor neuron or its axon due to edema, demyelination,toxins, ischemia, destruction, or metabolic alterations are proposed. Treatment of this condition should be aimed at theunderlying pathology. Symptomatic pharmacologictreatment options include carbamazepine, phenytoin andmost recently, botulinum toxin.

Infranuclear DisordersHEMIFACIAL SPASMRhyhmic, intermittent, unilateral facial twitching,

which begins insidiously around the orbicularis oculi andspreads slowly over 1 to 5 years to involve all the muscles offacial expression, is characteristic of hemifacial spasmThese bursts of clonic activity may last only seconds or

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