facial nerve injury jihan al maddah. anatomy facial nerve is a mixed nerve, having a motor root and...
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Facial nerve injury
Jihan AL Maddah
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Anatomy
• Facial nerve is a mixed nerve, having a motor root and a sensory root.
• Motor root supplies all the mimetic muscles of the face which develop from the 2nd brachial arch.
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Anatomy
Sensory root “nerve of Wrisberg” carries:• taste fibers from the anterior 2/3 of the
tongue• Secretomotor fibers to the lacrimal,
submandibular and sublingual glands as well as those in the nose and palate.
• General sensation from the concha and retro-auricular skin.
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Anatomy: Nucleus
Pons (motor).• Pre-central gyrus. Upper part of the nucleus:– Upper face– Involuntary emotional movements
• Thalamus
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Anatomy: Course• Motor fibers originate VII nucleus• Hooks around VI nucleus• Joined by sensory root (nerve of Wrisberg) • Facial n. leaves the brainstem at ponto-medullary
junction• Travels through post. Canal fossa• Enters the IAM.• Traverse the temporal bone through facial canal• Leaves the temporal bone through stylomastoid
foramen.• Finally divides into terminal branches.
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Anatomy: Branches
• Greater superficial petrosal nerve:• Nerve to stapedius:• Chorda tympani:• Comunicating branch:• Posterior auricular nerve:• Muscular branches:• Peripheral branches: “Pes anserinus”
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Anatomy: Parts
• Intracranial part Pons to IAM• Intratemporal part IAM to stylomastoid foramen• Extracranial part Stylomastoid foramen to peripheral branches
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Tensor tympani m.
Eustachian tube
Epitympanic recess mastoid air cells
Facial nerve
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Anatomy: Intratemporal segments
• Meatal• Labyrinthine• Tympanic, horizontal• Mastoid, vertical
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Anatomy: Structure of the nerve
• From inside outward:– Axon– Myelin sheath– Neurolimma– Endoneurium– Perineurium– Epineurium
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Anatomy: Severity of injury
• Saunderland classification:– 1°: Partial block: Neuropraxia– 2°: Loss of axons: axonotemesis– 3°: Injury to the endoneurium: neurotemesis– 4°: Injury to the perineurium: partial transection– 5°: Injury to the epineurium: complete transection
• 1 to 3 viral inflammatory disorders• 4-5 surgical, accidental trauma, neoplasms.
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History:
• Onset: Sudden vs. Gradual• Duration:• Rate of progression:• Recuurent or familial• Associated symptoms• Medical history• Previous surgeries
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Physical exam:
• Complete vs. incomplete• Segmental vs. uniform involvement• Unilateral vs. bilateral• Cranial nerves assessment• Neurologic evaluation• Cerebellar signs
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Physical exam:
• Microscopic otoscopy• Complete head and neck exam ( including
cranial n., parotid…).• Localization of facial nerve lesion:• Central vs. Peripheral.
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Physical exam:
• Localization of facial nerve lesion:Peripheral:– Level of nucleus– CPA level:– Bony canal level: Topodiagnostics– Outside the Temporal bone
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Physical exam:
• Topodiagnostics: to localize VII n lesions– Schirmer’s test: lesion proximal to the geniculate.– Stapedial reflex: lesion above n. to stapidus– Taste test: lesion above chorda tympani n.– Submandibular salivery flow test: Warton’s ducts lesion above the chorda tympani
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Causes:
• Central:– Brain abscess– Pontine glioma– Poliomyelitis– Multiple sclerosis
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Causes:
• Intacranial part:– Acoustic neuroma– Meningioma– Metastatic CA– Meningitis
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Causes:
Intratemporal part:1) Idiopathic:• Bell’s palsy• Melkersson’s syndrome ( facial paralysis, lip swelling
and fissured tongue)
2) Infections:• ASOM• CSOM• Herpes Zoster Oticus
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Causes:
Intratemporal part: cont.3) Trauma:• Surgical: Mastoidectomy, Stapedectomy• Accidental:# temporal bone
4) Neoplasms:• Glomus jugulare tumour• Facial nerve neuroma• Metastatic CA
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Causes:
• Extracranial part:– Parotid gland CA– Parotid gland surgery– Parotid gland injury– Neonatal facial nerve injury
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Causes:
• Systemic:– DM– Hypothyroidism– Uremia– Wegener’s granulomatosis– Sarcoidosis– Leprosy– Leukemia
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Labs:
• Pure-tune audiometry• Electrophysiologic tests• Imaging tests• Others
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Labs:
• Electrophysiologic tests:– Nerve Excitability Test: NET– Maximum stimulation Test: MST– Electroneurography: ENoG– Electromyography: EMG
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Labs:
• Nerve Excitability Test: NET :– Indication: complete paralysis<3wks– Interpretation: < or = 3.5 mA threshold: Prognosis
Good– Limitation: Not useful in the 1st 3 days or during
recovery.
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Labs:
• Maximum stimulation Test: MST:– Indication: complete paralysis<3wks– Interpretation: Marked weakness or no muscle
contraction: advanced degeneration with guarded prognosis
– Limitation: Not Objective.
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Labs:
• Electroneurography: ENoG :– Indication: complete paralysis<3wks– Interpretation: < 90% degeneration: prognosis is
good; > or = 90%: prognosis is question– Limitation: False-positive.
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Labs:
• Electromyography: EMG– Indication: Acute paralysis less than 1 week or chronic
paralysis longer than 2 weeks– Interpretation:
• Active mu: intact motor axons• Mu + fibrillation potentials: partial degeneration• Polyphasic mu: regenerating nerve
– Limitation: cannot assess degree of degeneration or prognosis for recovery.
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Complications:
• Incomplete recovery• Exposure keratitis• Synkinesis• Tics and spasms• Contractures• Crocodile tears• Frey’s syndrome “gustatory sweating”• Psychological and social problems
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Bell’s Palsy
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Background:
• one of the most common neurologic disorders affecting the cranial nerves.
• abrupt, unilateral, peripheral facial paresis or paralysis without a detectable cause.
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Background:
• first described more than a century ago by Sir Charles Bell,
• yet much controversy still surrounds its etiology and management.
• Bell palsy is certainly the most common cause of facial paralysis worldwide.
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Incidence:
• The incidence of Bell palsy in the United States is approximately 23 cases per 100,000 persons.
• Internationally: The incidence is the same as in the United States.
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Demographics:
• Race: slightly higher in persons of Japanese descent.
• Sex: No difference exists • Age: highest in persons aged 15-45 years. Bell
palsy is less common in those younger than 15 years and in those older than 60 years.
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Pathophysiology:
• Main cause of Bell's palsy is latent herpes viruses (herpes simplex virus type 1 and herpes zoster virus), which are reactivated from cranial nerve ganglia.
• Polymerase chain reaction techniques have isolated herpes virus DNA from the facial nerve during acute palsy.
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Pathophysiology:
• Inflammation of the nerve initially results in a reversible neurapraxia,
• Herpes zoster virus shows more aggressive biological behaviour than herpes simplex virus type 1
• Other causes: vascular ischemia, hereditary, autoimmune disorder
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History:
• The most alarming symptom of Bell's palsy is paresis
• Up to three quarters of affected patients think they have had a stroke or have an intracranial tumour.
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History:
• The palsy is often sudden in onset and evolves rapidly, with maximal facial weakness developing within two days.
• Associated symptoms may be hyperacusis, decreased production of tears, and altered taste.
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History:
• Patients may also mention otalgia or aural fullness and facial or retroauricular pain, which is typically mild and may precede the palsy.
• A slow onset progressive palsy with other cranial nerve deficits or headache raises the possibility of a neoplasm
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Physical exam:
• Bell's palsy causes a peripheral lower motor neurone palsy,
• which manifests as the unilateral impairment of movement in the facial and platysma muscles, drooping of the brow and corner of the mouth, and impaired closure of the eye and mouth.
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Physical exam:
• Bell's phenomenon—upward diversion of the eye on attempted closure of the lid—is seen when eye closure is incomplete.
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Physical exam:
• Polyposis or granulations in the ear canal may suggest cholesteatoma or malignant otitis externa.
• Vesicles in the conchal bowl, soft palate, or tongue suggest Ramsay Hunt syndrome
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Physical exam:
• The examination should exclude masses in the head and neck.
• A deep lobe parotid tumour may only be identified clinically by careful examination of the oropharynx and ipsilateral tonsil to rule out asymmetry.
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Investigations:
• Serum testing for rising antibody titres to herpes virus is not a reliable diagnostic tool for Bell's palsy.
• Salivary PCR for herpes simplex virus type 1 or herpes zoster virus is more likely to confirm virus during the replicating phase, but these tests remain research tools.
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Investigations:
• MRI has revolutionised the detection of tumours.
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Investigations:
• Topognostic tests and electroneurography may give useful prognostic information but remain research tools.
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Diagnosis:
• Bell palsy is a diagnosis of exclusion.• Other disease states or conditions that
present with facial palsies are often misdiagnosed as idiopathic.
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Management:
• The main aims of treatment in the acute phase of Bell's palsy are to speed recovery and to prevent corneal complications.
• Treatment should begin immediately to inhibit viral replication and the effect on subsequent pathophysiological processes that affect the facial nerve.
• Psychological support is also essential, and for this reason patients may require regular follow up.
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Management, Eye care
• It focuses on protecting the cornea from drying and abrasion due to problems with lid closure and the tearing mechanism.
• The patient is educated to report new findings such as pain, discharge, or change in vision.
• Lubricating drops should be applied hourly during the day and a simple eye ointment should be used at night.
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Management, Steroid
• Two systematic reviews concluded that Bell's palsy could be effectively treated with corticosteroids in the first seven days, providing up to a further 17% of patients with a good outcome in addition to the 80% that spontaneously improve.
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Management, Steroid
• Cochrane review*:“There is insufficient evidence about the effects of
corticosteroids for people with Bell's palsy, although their anti-inflammatory effect might prevent nerve damage.”
*Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis).
Cochrane Database of Systematic Reviews 2004, Issue 4. Art. No.: CD001942.
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Management, Antivirals
• It seems logical in Bell's palsy because of the probable involvement of herpes viruses.
• Acyclovir, a nucleotide analogue, interferes with herpes virus DNA polymerase and inhibits DNA replication.
Cochrane review*:“More evidence is needed to show whether the antiviral drugs acyclovir or valacyclovir are effective in aiding recovery from Bell's palsy.”
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Outcomes:
• It has a fair prognosis without treatment, with almost three quarters of patients recovering normal mimetical function and just over a tenth having minor sequelae.
• A sixth of patients are left with either moderate to severe weakness, contracture, hemifacial spasm, or synkinesis.
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Outcomes:
• Patients with a partial palsy fair better, with 94% making a full recovery.
• The outcome is worse when herpes zoster virus infection is involved in partial palsy.
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Outcomes:
• In patients who recover without treatment, major improvement occurs within three weeks in most.
• If recovery does not occur within this time, then it is unlikely to be seen until four to six months, when nerve regrowth and reinnervation have occurred.
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Bad Prognostic Factor:
• Complete facial palsy• No recovery by three weeks• Age over 60 years• Severe pain• Ramsay Hunt syndrome (herpes zoster virus)• Associated conditions—hypertension, diabetes,
pregnancy• Severe degeneration of the facial nerve shown by
electrophysiological testing