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Facial Nerve Palsy Facial Nerve Palsy Dr V.RAMKUMAR Dr V.RAMKUMAR CONSULTANT DENTAL&FACIOMAXILLARY CONSULTANT DENTAL&FACIOMAXILLARY SURGEON SURGEON REG NO:4118-TAMILNADU- INDIA(ASIA) REG NO:4118-TAMILNADU- INDIA(ASIA)

Facial nerve palsy

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Page 1: Facial nerve palsy

Facial Nerve PalsyFacial Nerve Palsy

Dr V.RAMKUMARDr V.RAMKUMARCONSULTANT DENTAL&FACIOMAXILLARY CONSULTANT DENTAL&FACIOMAXILLARY

SURGEONSURGEONREG NO:4118-TAMILNADU- INDIA(ASIA)REG NO:4118-TAMILNADU- INDIA(ASIA)

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AnatomyAnatomy

Facial nerve is a mixed nerve, having Facial nerve is a mixed nerve, having a motor root and a sensory root.a motor root and a sensory root.Motor root supplies all the mimetic Motor root supplies all the mimetic muscles of the face which develop muscles of the face which develop from the 2from the 2ndnd brachial arch. brachial arch.

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AnatomyAnatomy

Sensory root Sensory root ““nerve of Wrisbergnerve of Wrisberg”” carries taste fibers from the anterior carries taste fibers from the anterior 2/3 of the tongue and general 2/3 of the tongue and general sensation from the concha and sensation from the concha and retroauricular skin.retroauricular skin.

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AnatomyAnatomy

Also it carries secretomotor fibers to Also it carries secretomotor fibers to the lacrimal, submandibular and the lacrimal, submandibular and sublingual glands as well as those in sublingual glands as well as those in the nose and palate.the nose and palate.

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Anatomy: NucleusAnatomy: Nucleus

Pons.Pons.precentral gyrus.precentral gyrus.Upper part of the nucleus:Upper part of the nucleus:– Upper faceUpper face– Involuntary emotional movements Involuntary emotional movements

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Anatomy: CourseAnatomy: CourseMotor fibers originateMotor fibers originate……Hooks aroundHooks around……Joined byJoined by……Facial n. leaves the brainstemFacial n. leaves the brainstem……Travels throughTravels through……Enters the IAC.Enters the IAC.Then traverse the temporal bone through Then traverse the temporal bone through facial n. canalfacial n. canalLeaves the temporal bone throughLeaves the temporal bone throughFinally divides into terminal branches.Finally divides into terminal branches.

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Anatomy: PartsAnatomy: Parts

Intracranial partIntracranial partIntratemporal partIntratemporal partExtracranial partExtracranial part

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Anatomy: Intratemporal segmentsAnatomy: Intratemporal segments

MeatalMeatalLabyrinthineLabyrinthineTympanic, horizontalTympanic, horizontalMastoid, verticalMastoid, vertical

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Anatomy: BranchesAnatomy: Branches

Greater superficial petrosal nerve:Greater superficial petrosal nerve:Nerve to stapedius:Nerve to stapedius:Chorda tympani:Chorda tympani:Comunicating branch:Comunicating branch:Posterior auricular nerve:Posterior auricular nerve:Muscular branches:Muscular branches:Peripheral branches: Peripheral branches: ““Pes anserinusPes anserinus””

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Anatomy: Surgical landmarksAnatomy: Surgical landmarksMiddle Ear and Mastoid Surgery:Middle Ear and Mastoid Surgery:– Processus chocleariformisProcessus chocleariformis– Oval window and horizontal canalOval window and horizontal canal– Short process of the incusShort process of the incus– PyramidPyramid

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Anatomy: Surgical landmarksAnatomy: Surgical landmarks

Parotid Surgery:Parotid Surgery:– Cartilaginous pointer:Cartilaginous pointer:– Styloid processStyloid process– Posterior belly pf digastric musclePosterior belly pf digastric muscle

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Anatomy: Structure of the nerveAnatomy: Structure of the nerve

From inside outward:From inside outward:– AxonAxon– Myelin sheathMyelin sheath– NeurolimmaNeurolimma– EndoneuriumEndoneurium– PerineuriumPerineurium– EpineuriumEpineurium

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Anatomy: Severity of injuryAnatomy: Severity of injury

Saunderland classification:Saunderland classification:– 1°: Partial block: Neuropraxia1°: Partial block: Neuropraxia– 2°: Loss of axons: axonotemesis2°: Loss of axons: axonotemesis– 3°: Injury to the endoneurium: 3°: Injury to the endoneurium:

neurotemesisneurotemesis– 4°: Injury to the perineurium: partial 4°: Injury to the perineurium: partial

transectiontransection– 5°: Injury to the epineurium: complete 5°: Injury to the epineurium: complete

transectiontransection

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History:History:

Onset: Sudden vs. GradualOnset: Sudden vs. GradualDuration:Duration:Rate of progression:Rate of progression:Recuurent or familialRecuurent or familialAssociated symptomsAssociated symptomsMedical historyMedical historyPrevious surgeriesPrevious surgeries

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Physical exam:Physical exam:

Complete vs. incompleteComplete vs. incompleteSegmental vs. uniform involvementSegmental vs. uniform involvementUnilateral vs. bilateralUnilateral vs. bilateralCranial nerves assessmentCranial nerves assessmentNeurologic evaluationNeurologic evaluationCerebellar signsCerebellar signs

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Physical exam:Physical exam:

Microscopic otoscopyMicroscopic otoscopyComplete head and neck examComplete head and neck exam

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Physical exam:Physical exam:

Localization of facial nerve lesion:Localization of facial nerve lesion:Central vs. Peripheral. Central vs. Peripheral.

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Physical exam:Physical exam:

Localization of facial nerve lesion:Localization of facial nerve lesion:Peripheral:Peripheral:

– Level of nucleusLevel of nucleus– CPA level:CPA level:– Bony canal level: TopodiagnosticsBony canal level: Topodiagnostics– Outside the Temporal boneOutside the Temporal bone

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Physical exam:Physical exam:

Topodiagnostics:Topodiagnostics:– SchirmerSchirmer’’s test:s test:– Stapedial reflex:Stapedial reflex:– Taste test:Taste test:– Submandibular salivery flow test: Submandibular salivery flow test:

WartonWarton’’s ductss ducts

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Causes:Causes:

Central:Central:Intacranial part:Intacranial part:Intratemporal part:Intratemporal part:Extracranial part:Extracranial part:Systemic:Systemic:

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Causes:Causes:

Central:Central:– Brain abscessBrain abscess– Pontine gliomaPontine glioma– PoliomyelitisPoliomyelitis– Multiple sclerosisMultiple sclerosis

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Causes:Causes:

Intacranial part:Intacranial part:– Acoustic neuromaAcoustic neuroma– MeningiomaMeningioma– Metastatic CAMetastatic CA– MeningitisMeningitis

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Causes:Causes:

Intratemporal part:Intratemporal part:– Idiopathic:Idiopathic:

BellBell’’s palsys palsyMelkerssonMelkersson’’s syndromes syndrome

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Causes:Causes:

Intratemporal part:Intratemporal part:– Trauma:Trauma:

Surgical: Mastoidectomy, StapedectomySurgical: Mastoidectomy, StapedectomyAccidental:# temporal boneAccidental:# temporal bone

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Causes:Causes:

Intratemporal part:Intratemporal part:– Neoplasms:Neoplasms:

Glomus jugulare tumourGlomus jugulare tumourFacial nerve neuromaFacial nerve neuromaMetastatic CAMetastatic CA

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Causes:Causes:

Extracranial part:Extracranial part:– Parotid gland CAParotid gland CA– Parotid gland surgeryParotid gland surgery– Parotid gland injuryParotid gland injury– Neonatal facial nerve injuryNeonatal facial nerve injury

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Causes:Causes:Systemic:Systemic:– DMDM– HypothyroidismHypothyroidism– UremiaUremia– PANPAN– WegenerWegener’’s granulomatosiss granulomatosis– SarcoidosisSarcoidosis– LeprosyLeprosy– LeukemiaLeukemia

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Labs:Labs:

Pure-tune audiometryPure-tune audiometryElectrophysiologic testsElectrophysiologic testsImaging testsImaging testsOthersOthers

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Labs:Labs:

Electrophysiologic tests:Electrophysiologic tests:– Nerve Excitability Test: NETNerve Excitability Test: NET– Maximum stimulation Test: MSTMaximum stimulation Test: MST– Electroneurography: ENoGElectroneurography: ENoG– Electromyography: EMGElectromyography: EMG

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Complications:Complications:Incomplete recoveryIncomplete recoveryExposure keratitisExposure keratitisSynkinesisSynkinesisTics and spasmsTics and spasmsContracturesContracturesCrocodile tearsCrocodile tearsFreyFrey’’s syndrome s syndrome ““gustatory sweatinggustatory sweating””Psychological and social problemsPsychological and social problems

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Bell’s PalsyBell’s Palsy

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Background:Background:

one of the most common neurologic one of the most common neurologic disorders affecting the cranial disorders affecting the cranial nerves. nerves. abrupt, unilateral, peripheral facial abrupt, unilateral, peripheral facial paresis or paralysis without a paresis or paralysis without a detectable cause.detectable cause.

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Background:Background:first described more than a first described more than a century ago by Sir Charles century ago by Sir Charles Bell,Bell,yet much controversy still yet much controversy still surrounds its etiology and surrounds its etiology and management.management.Bell palsy is certainly the Bell palsy is certainly the most common cause of most common cause of facial paralysis worldwide. facial paralysis worldwide.

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Incidence:Incidence:

United StatesUnited StatesInternationally Internationally

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Incidence:Incidence:

The incidence of Bell palsy in the The incidence of Bell palsy in the United States is approximately 23 United States is approximately 23 cases per 100,000 persons.cases per 100,000 persons.Internationally:Internationally: The incidence is the The incidence is the same as in the United States. same as in the United States.

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Demographics:Demographics:

Race:Race:Sex:Sex:Age:Age:

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Demographics:Demographics:

Race: Race: slightly higher in persons of slightly higher in persons of Japanese descent. Japanese descent. Sex: Sex: No difference exists No difference exists Age: Age: highest in persons aged 15-45 highest in persons aged 15-45 years. Bell palsy is less common in years. Bell palsy is less common in those younger than 15 years and in those younger than 15 years and in those older than 60 years. those older than 60 years.

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Pathophysiology:Pathophysiology:Main cause of Bell's palsy is latent Main cause of Bell's palsy is latent herpes viruses (herpes simplex virus herpes viruses (herpes simplex virus type 1 and herpes zoster virus), type 1 and herpes zoster virus), which are reactivated from cranial which are reactivated from cranial nerve ganglia.nerve ganglia.Polymerase chain reaction Polymerase chain reaction techniques have isolated herpes techniques have isolated herpes virus DNA from the facial nerve virus DNA from the facial nerve during acute palsy.during acute palsy.

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Pathophysiology:Pathophysiology:

Inflammation of the nerve initially Inflammation of the nerve initially results in a reversible neurapraxia,results in a reversible neurapraxia,Herpes zoster virus shows more Herpes zoster virus shows more aggressive biological behaviour than aggressive biological behaviour than herpes simplex virus type 1herpes simplex virus type 1

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BELLS SIGNBELLS SIGN

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History:History:

The most alarming symptom of Bell's The most alarming symptom of Bell's palsy is paresispalsy is paresisUp to three quarters of affected Up to three quarters of affected patients think they have had a stroke patients think they have had a stroke or have an intracranial tumour.or have an intracranial tumour.

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History:History:

The palsy is often sudden in onset The palsy is often sudden in onset and evolves rapidly, with maximal and evolves rapidly, with maximal facial weakness developing within facial weakness developing within two days.two days.Associated symptoms may be Associated symptoms may be hyperacusis, decreased production of hyperacusis, decreased production of tears, and altered taste.tears, and altered taste.

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History:History:

Patients may also mention otalgia or Patients may also mention otalgia or aural fullness and facial or aural fullness and facial or retroauricular pain, which is typically retroauricular pain, which is typically mild and may precede the palsy.mild and may precede the palsy.A slow onset progressive palsy with A slow onset progressive palsy with other cranial nerve deficits or other cranial nerve deficits or headache raises the possibility of a headache raises the possibility of a neoplasm neoplasm

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Physical exam:Physical exam:

Bell's palsy causes a peripheral lower Bell's palsy causes a peripheral lower motor neurone palsy,motor neurone palsy,which manifests as the unilateral which manifests as the unilateral impairment of movement in the impairment of movement in the facial and platysma muscles, facial and platysma muscles, drooping of the brow and corner of drooping of the brow and corner of the mouth, and impaired closure of the mouth, and impaired closure of the eye and mouth.the eye and mouth.

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Physical exam:Physical exam:

Bell's phenomenonBell's phenomenon——upward upward diversion of the eye on attempted diversion of the eye on attempted closure of the lidclosure of the lid——is seen when eye is seen when eye closure is incomplete. closure is incomplete.

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Physical exam:Physical exam:

Polyposis or granulations in the ear Polyposis or granulations in the ear canal may suggest cholesteatoma or canal may suggest cholesteatoma or malignant otitis externa.malignant otitis externa.Vesicles in the conchal bowl, soft Vesicles in the conchal bowl, soft palate, or tongue suggest Ramsay palate, or tongue suggest Ramsay Hunt syndrome Hunt syndrome

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Physical exam:Physical exam:

The examination should exclude The examination should exclude masses in the head and neck.masses in the head and neck.A deep lobe parotid tumour may only A deep lobe parotid tumour may only be identified clinically by careful be identified clinically by careful examination of the oropharynx and examination of the oropharynx and ipsilateral tonsil to rule out ipsilateral tonsil to rule out asymmetry.asymmetry.

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Investigations:Investigations:

Serum testing for rising antibody Serum testing for rising antibody titres to herpes virus is not a reliable titres to herpes virus is not a reliable diagnostic tool for Bell's palsy.diagnostic tool for Bell's palsy.Salivary PCR for herpes simplex virus Salivary PCR for herpes simplex virus type 1 or herpes zoster virus is more type 1 or herpes zoster virus is more likely to confirm virus during the likely to confirm virus during the replicating phase, but these tests replicating phase, but these tests remain research tools.remain research tools.

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Investigations:Investigations:

MRI has revolutionised the detection MRI has revolutionised the detection of tumours.of tumours.

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Investigations:Investigations:

Topognostic tests and Topognostic tests and electroneurography may give useful electroneurography may give useful prognostic information but remain prognostic information but remain research tools. research tools.

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Labs:Labs:

Nerve Excitability Test: NET :Nerve Excitability Test: NET :– Indication: complete paralysis<3wksIndication: complete paralysis<3wks– Interpretation: < or = 3.5 mA Interpretation: < or = 3.5 mA

threshold: Prognosis Goodthreshold: Prognosis Good– Limitation: Not useful in the 1Limitation: Not useful in the 1stst 3 days or 3 days or

during recovery.during recovery.

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Labs:Labs:

Electroneurography: ENoG :Electroneurography: ENoG :– Indication: complete paralysis<3wksIndication: complete paralysis<3wks– Interpretation: < 90% degeneration: Interpretation: < 90% degeneration:

prognosis is good; > or = 90%: prognosis is good; > or = 90%: prognosis is questionprognosis is question

– Limitation: False-positive results in Limitation: False-positive results in deblocking phase.deblocking phase.

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Labs:Labs:Electromyography: EMGElectromyography: EMG– Indication: Acute paralysis less than 1 week or Indication: Acute paralysis less than 1 week or

chronic paralysis longer than 2 weekschronic paralysis longer than 2 weeks– Interpretation:Interpretation:

Active mu: intact motor axonsActive mu: intact motor axonsMu + fibrillation potentials: partial degenerationMu + fibrillation potentials: partial degenerationPolyphasic mu: regenerating nervePolyphasic mu: regenerating nerve

– Limitation: cannot assess degree of Limitation: cannot assess degree of degeneration or prognosis for recovery.degeneration or prognosis for recovery.

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Diagnosis:Diagnosis:

Bell palsy is a diagnosis of exclusion.Bell palsy is a diagnosis of exclusion.Other disease states or conditions Other disease states or conditions that present with facial palsies are that present with facial palsies are often misdiagnosed as idiopathic. often misdiagnosed as idiopathic.

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Management:Management:The main aims of treatment in the acute The main aims of treatment in the acute phase of Bell's palsy are to speed recovery phase of Bell's palsy are to speed recovery and to prevent corneal complications.and to prevent corneal complications.Treatment should begin immediately to Treatment should begin immediately to inhibit viral replication and the effect on inhibit viral replication and the effect on subsequent pathophysiological processes subsequent pathophysiological processes that affect the facial nerve.that affect the facial nerve.Psychological support is also essential, and Psychological support is also essential, and for this reason patients may require for this reason patients may require regular follow up. regular follow up.

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MANAGEMENT OF EYE CAREMANAGEMENT OF EYE CARE•CORNEAL PADCORNEAL PAD

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Management, SteroidManagement, Steroid

Two systematic reviews concluded Two systematic reviews concluded that Bell's palsy could be effectively that Bell's palsy could be effectively treated with corticosteroids in the treated with corticosteroids in the first seven days, providing up to a first seven days, providing up to a further 17% of patients with a good further 17% of patients with a good outcome in addition to the 80% that outcome in addition to the 80% that spontaneously improve.spontaneously improve.

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Management, SteroidManagement, Steroid

Usual regimen is 1mg/kg/day for 1 Usual regimen is 1mg/kg/day for 1 week.week.To be tapered in the 2To be tapered in the 2ndnd week. week.

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Management, AntiviralsManagement, Antivirals

It seems logical in Bell's palsy It seems logical in Bell's palsy because of the probable involvement because of the probable involvement of herpes viruses.of herpes viruses.Aciclovir, a nucleotide analogue, Aciclovir, a nucleotide analogue, interferes with herpes virus DNA interferes with herpes virus DNA polymerase and inhibits DNA polymerase and inhibits DNA replication.replication.

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Management, AntiviralsManagement, Antivirals

Usual regimen is 4000mg/24hrs Usual regimen is 4000mg/24hrs divided into 5 doses for 7 to 10 daysdivided into 5 doses for 7 to 10 days

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SURGICAL MANAGEMENTSURGICAL MANAGEMENT

EYELID PARALYSIS-TARSORRAPHYEYELID PARALYSIS-TARSORRAPHY

NEURORRAPHY PROCEDURESNEURORRAPHY PROCEDURESNERVE ANASTAMOSISNERVE ANASTAMOSIS

SURGICAL DECOMPRESSIONSURGICAL DECOMPRESSIONFACIAL REANIMATION SURGERYFACIAL REANIMATION SURGERY

Page 64: Facial nerve palsy

Bad Prognostic Factor:Bad Prognostic Factor:Complete facial palsyComplete facial palsyNo recovery by three weeksNo recovery by three weeksAge over 60 yearsAge over 60 yearsSevere painSevere painRamsay Hunt syndrome (herpes zoster Ramsay Hunt syndrome (herpes zoster virus)virus)Associated conditionsAssociated conditions——hypertension, hypertension, diabetes, pregnancydiabetes, pregnancySevere degeneration of the facial nerve Severe degeneration of the facial nerve shown by electrophysiological testingshown by electrophysiological testing