FACIAL NERVE PARALYSIS

Dr. Vikas

NERVE FIBER COMPONENTS

Axon Myelin sheath Endoneurium Perineurium Epineurium

It has no perineurium from brainstem to IAC

NERVE FIBER COMPONENTS

Endoneurium Surrounds each axon Adherent to Schwann cell

layer Vital for regeneration

Perineurium Encases endoneural

tubules Tensile strength Barrier to infection

Epineurium (nerve sheath) Outermost layer Houses vasa nervorum for

nutrition

NEUROPATHOPHYSIOLOGY OF NERVE INJURYSEDDON CLASSIFICATION(1943)

Neuropraxia – A low severity injury that typically leads to

complete recovery.  The structure of the nerve remains intact but electrical conduction down the axon is interrupted, typically by ischemia or compression injury, additionally secondary injuries can be caused by vascular damage leading to intrafascicular edema.

Complete recovery of function with no distal Wallerian degeneration

Axonotmesis Disruption of the neuronal axon takes place but the

myelin sheath is still intact. Endoneural tubules are preserved but Wallerian

degeneration occurs Typically this is caused by a crush based injury.  Depending on the severity of the injury,

regeneration may occur over the timescale of weeks to years.

Neurotmesis – Complete nerve transsection occurs Commonly a neuroma forms over the proximal

stump of the nerve, preventing normal continued regeneration to occur.

SEDDON CLASSIFICATION

SUNDERLAND CLASSIFICATION

1°: Partial block: Neuropraxia 2°: Loss of axons, endoneurial tubes remain

intact: axonotmesis 3°: Injury to the endoneurium: neurotemesis 4°: Injury to the perineurium in addition to

above: partial transection 5°: Injury to the epineurium in addition to

above: complete transection The first three degrees are seen in viral and

inflammatory disorders while 4th and 5th are seen in surgical or accidental trauma

HOUSE-BRACKMANN FACIAL NERVE GRADING SYSTEM

HOUSE-BRACKMANN FACIAL NERVE GRADING SYSTEM

Not a perfect Grading system because of –

1. the problems of inter & intraobserver variations

2. applicable only to disorders of nerve proximal to pes anserinus

3. not appropriate for single branch injuries

EVALUATION OF FACIAL PARALYSIS

Clinical feature Central v/s Peripheral facial paralysis Complete head and neck examination Cranial nerve evaluation

Topographic diagnosis

Electro-diagnostic testing

Central v/s Peripheral facial paralysis

UMN LESIONS LMN LESIONS

Paralysis of inferior ¼ of the face Contralateral to the lesion

Upper part of face is innervated bilaterally by the UMN

Inferior half have only contralateral innervation

Seen mostly in intracranial lesions (stroke)

Paralysis of the lateral half of the face Ipsilateral to the lesion

The fibers carrying LMN (that are supplying the

entire lateral half of face) are all within within the fascial nerve

Seen in Fascial nerve lesions(Bell’s Palsy)

PERIPHERAL PARALYSIS

Lower motor neuron lesion - At rest –

less prominent wrinkles on forehead of affected side, eyebrow drop, flattened nasolabial fold, corner of mouth turned down

Unable to – wrinkle forehead, raise eyebrow, wrinkle nasolabial fold, purse lips, show teeth, completely close eye

TOPOGNOSTIC TESTING

1. Schirmer test for lacrimation (Geniculate ganglion)

2. Stapedial reflex test (stapedial branch)

3. Taste testing (chorda tympani nerve)

4. Salivary flow rates and pH (chorda tympani)

SCHIRMER TEST

Greater superficial petrosal nerve,Geniculate ganglion Filter paper strip is placed in the lower conjunctival fornix

bilaterally Rate of tear production of the two side is compared after ~5

minutes Normally the portion of the filter paper in contact with the

conjunctiva acts as an irritant, stimulating an increased flow of tears, which are then wicked along the filter paper strip by capillary action

SCHIRMER TEST

SCHIRMER TEST

The reflex is consensual; that is, the irritating stimulus in either eye causes tearing in both eyes, and a unilateral sensory (trigeminal) deficit will reduce tearing bilaterally. However, unilateral corneal anesthesia reduces tearing asymmetrically, with a greater reduction on the anesthetized side. (Crabtree and Dobie, 1989);

when a sensory deficit is present, one should consider bilateral corneal anesthesia and stimulation of lacrimation by other noxious stimuli (for example, inhalation of ammonia)

SCHIRMER TEST

Schirmer's test is usually considered positive if the affected side shows less than half the amount of

lacrimation seen on the normal side. Fisch (1977) pointed out that tearing is often inexplicably

reduced bilaterally in Bell's palsy, and this bilateral reduction even persists after unilateral resection of the geniculate ganglion.

Thus, judging not only the symmetry of the response but also its absolute magnitude is important: a total response (sum of the lengths of wetter filter paper for both eyes) of less than 25 mm is considered abnormal.

STAPEDIAL REFLEX

Stapedius branch of the facial nerve A loud (supra threshold) tone is presented to

either the ipsilateral or contralateral ear evokes a reflex movement of the stapedius muscle changes the tension on the Tympanic Membrane (which

must be intact for a valid test) resulting in a change in the impedance of the ossicular chain.

An absent reflex or a reflex that is less than half the amplitude of the contralateral side is considered abnormal

STAPEDIAL REFLEX

The reflex can be elicited by either ipsilateral or contralateral acoustic stimulation, or in cases of bilateral severe hearing loss, by tactile or electrical stimulation.

It is absent in 69% of cases of Bell's palsy (84% when the paralysis is complete) at the time of presentation (Koike et al, 1977);

the reflex recovers at about the same time as clinically observed movements do. The prognostic value of this test therefore seems limited.

TASTE TESTING (ELECTROGUSTOMETRY)

Psychophysical assessment can be performed with natural stimuli, such as aqueous solutions of salt, sugar, citrate, and quinine, or with electrical stimulation of the tongue.

Electirical stimulation (electrogustometry), has the advantages of speed and ease of quantification

The tongue is stimulated electrically to produce a metallic taste & Threshold of the test is compared between two sides

ELECTROGUSTOMETER

TASTE TESTING (ELECTROGUSTOMETRY)

In normal subjects, the two sides of the tongue have similar thresholds for electrical stimulation, rarely differing by more than 25%

thresholds difference of more than 25% is abnormal Taste function apparently recovers before visible

movement in some cases, so if the results of electrogustometry are normal in the second week or later, clinical recovery is imminent.

Total lack of Chorda tympani : No response at 300 uAmp

Disadvantage : False +ve in acute phase of Bell’s palsy The major problem with taste testing is that the results of

this test will be abnormal in almost all patients who are in the acute phase of Bell's palsy (Tomita et al, 1972); thus this test cannot be used to select patients with a poor prognosis.

SALIVARY FLOW TESTING

For Chorda tympani The patient is advised to refrain from intake of any food or

beverage (water exempted) one hour before the test session. Smoking, chewing gum and intake of coffee also are prohibited during this hour. The subject is advised to rinse his or her mouth several times with deionized (distilled) water.

Cannulation of Wharton's ducts bilaterally Gustatory stimulus – 6% citric acid on antr. Part of tongue Output is measured after 5 minutes. Significant if 25% reduction in flow of the involved side as

compared to the normal side Salivary pH Flow Rate Submandibular salivary pH of 6.1 or less predicts incomplete

recovery in cases of Bell's palsy (Saito et al, 1977)

SALIVARY FLOW TESTING

ELECTRO-PHYSIOLOGICAL TESTING

When a conduction block exists, the patient is unable to move his face voluntarily, but a facial twitch can still be elicited by percutaneous electrical stimulation of the nerve distal to the lesion.

The electrical response of the facial muscles to voluntary, mechanical, or electrical activation of the nerve may also be recorded. Tests based on these two principles – electrical stimulation and recording of the electromyographic (EMG) response

are useful in prognosis and in the selection of patients for different treatments.

ELECTRO-PHYSIOLOGICAL TESTS

Nerve excitability test (NET) Maximal stimulation test (MST) Electromyography (EMG) Electroneuronography (evoked

electromyography) (ENoG)

NERVE EXCITABILITY TEST (NET)

Compares transcutaneous current threshold required to elicit minimal muscle contraction between two sides

The stimulating electrode is placed on the skin over the stylomastoid foramen with a return electrode taped to the forearm.

Beginning with the normal side, electrical pulses (0.3 msec in duration) are delivered, steadily increasing current levels until a facial twitch is just noticeable.

The lowest current eliciting a twitch is the threshold of excitation.

NERVE EXCITABILITY TEST (NET)

Next, the process is repeated on the paralyzed side, and the difference in thresholds between the two sides is calculated.

In a simple conduction block, such as occurs after infiltration of the perineural tissues with lidocaine (Xylocaine), no difference exists between the two sides; the paralyzed nerve is as easy to stimulate (distal to the point of the conduction block) as is the normal nerve.

After a more severe injury (Sunderland class II to V), in which distal axonal degeneration occurs, electrical excitability is gradually lost

this takes 3 to 4 days, even after a total section of the nerve. This means that the findings of the NET always lag several days behind the biologic events themselves

NERVE EXCITABILITY TEST (NET)

A difference of 3.5 milliamperes (mA) or more in thresholds between the two sides has been proposed as a reliable indicator of progressive degeneration and has been used as an indicator for surgical decompression

The NET is useful only during the first 2 to 3 weeks of complete paralysis before complete degeneration has occurred.

It is unnecessary in cases of incomplete paralysis, in which the prognosis is always excellent .

If the paralysis becomes total, the test can determine whether a pure conduction block exists or whether degeneration is occurring, as indicated by progressive loss of excitability.

NERVE EXCITABILITY TEST (NET)

Once excitability is lost and that result is confirmed by repeat testing, further excitability tests are pointless because clinically evident recovery always begins before any apparent electrical excitability returns.

Electrical stimulation is generally relatively ineffective in eliciting a synchronous and thus observable twitch in the early stages of regeneration. Similarly, if a paralysis that has become complete begins to recover clinically before any degeneration is noted, continuing stimulation is unnecessary because recovery will be rapid and complete.

NERVE EXCITABILITY TEST (NET)

Benefits Easy to perform More comfortable for patient

Drawbacks Subjectivity (relies on operator’s visual

detection of response) May exclude smaller fibers (current

thresholds are likely to selectively activate larger fibers with lower thresholds and not those smaller fibers closer to stimulating electrode)

MAXIMAL STIMULATION TEST (MST) Instead of measuring threshold, however, maximal stimuli

(current levels at which the greatest amplitude of facial movement is seen) is employed.

The electrode type and placement and the nerve-stimulating equipment are the same as in the NET.

Increasing current levels are used until maximal movement is seen, and the paralyzed side is compared to the normal side (maximal nevre stimulation(~5mA)

Movements on the paralyzed side are subjectively expressed as a percentage (0%, 25%, 50%, 75%, 100%) of the movement on the normal side.

Symmetric response within first ten days – complete recovery in > 90%

No response within first ten days – incomplete recovery with significant sequelae

ELECTROMYOGRAPHY

The recording of spontaneous and voluntary muscle potentials by needles introduced into the muscle is called electromyography (EMG).

Records motor unit potentials of the orbicularis oculi & orbicularis oris muscle during rest & voluntary contraction

In a normal resting muscle biphasic / triphasic potentials are seen every 30-50msec.

EMG can be used to determine:-1.If a nerve in question is in fact in

continuity(volitional activity recorded)2.Evidence of degenration ( fibrillation after 10-14

days)3.If there are early sign of reinnervation

(polyphasic innervation potentials after 4-6 weeks)

Fibrillation potentials typically arises 2-3 weeks following injury

With regenration of nerve after injury, polyphasic reinnervation potential replaces fibrillation patential

Reinnervation potentials may precede clinical signs of recovery by 6-12 weeks

Polyphasic potential indicate regenrative process & surgical intervention is therefore not indicated

Fibrillation indicate lower motor neuron denervation but viable motor end plates, so surgical intervention needed(to achieve nerve continuity)

Electrical silence indicates atrophy of motor end plates & need for muscle transfer procedure

EVOKED ELECTROMYOGRAPHY (EEMG) OR EVOKED ELECTRONEURONOGRAPHY (ENOG)

Records compound muscle action potential (CMAP) with surface electrodes placed transcutaneously in the nasolabial fold (response) and stylomastoid foramen (stimulus)

Responses to maximal electrical stimulation of the two sides are compared

Responses are recorded electrically by a bipolar electrode pair placed in the nasolabial groove.

EVOKED ELECTROMYOGRAPHY (EEMG) OR EVOKED ELECTRONEURONOGRAPHY (ENOG)

Waveform responses are analyzed to compare peak-to-peak amplitudes between normal and uninvolved sides where the peak amplitude is proportional to the number of intact axons.

Most valuable prognostic indicator---Its main indicaion acute onset complete facial paralysis

This method offers the potential advantage of an objective registration of electrically evoked responses, and the amplitude of response of the paralyzed side (in mV) can be expressed as a precise percentage of the normal side's response.

EVOKED ELECTROMYOGRAPHY (EEMG) OR EVOKED ELECTRONEURONOGRAPHY (ENOG)

ELECTRONEURONOGRAPHY (ENOG)

)

Response <10% of normal in first 3 weeks-poor prognosis

Response >90% of normal within 3 weeks of onset- 80-100% probability of recovery Testing every other day Not useful until 4th day of paralysis as it takes about 3

days for degeneration to reach completion Also of less value after three weeks bcoz of nerve fibre

desynchronization Advantages: Reliable Disadvantages:

Uncomfortable Cost Test-retest variability due to position of

electrodes

LIMITATION OF ELECTOPHYSIOLOGICAL TESTING

Electric impulse can stimulate only normal/ neuropraxic fibres and can’t distinguish b/w axonotemesis or neurotemesis

Provides no useful information in cases of incomplete facial paralysis

It fails to provide information on the immediate post paralysis pariod( first 72 hours)

FACIAL PARALYSIS

CAUSES:

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

CAUSES:

Central: Brain abscess Pontine glioma Poliomyelitis Multiple sclerosis

Intacranial part: Acoustic neuroma Meningioma, congenital cholesteatoma Metastatic CA Meningitis

CAUSES: Intratemporal part:

Idiopathic: Bell’s palsy Melkersson’s syndrome

Infections: ASOM,CSOM Herpes Zoster Oticus

Trauma: Surgical: Mastoidectomy, Stapedectomy Accidental:# temporal bone

Neoplasms: Glomus jugulare tumour,Facial nerve

neuroma,Metastatic CA

CAUSES:

Extracranial part:1.Malignancy of parotid2.Surgery of parotid3.Accidental injury in parotid region4.Neonatal facial injury(forceps delivery)

Systemic diseases: diabetes, uraemia,hypothyroidism, leprosy,sarcoidosis, demyelinating disease

BELL’S PALSY

Bell palsy is certainly the most common cause of facial paralysis worldwide.

Paralysis of all muscle groups on one side of the face, sudden onset,absence of signs of CNS disease; absence of signs of ear or cerebello-pontine angle disease.

first described by Sir Charles Bell, controversy still surrounds its etiology

and management.

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.

Recurrence rate 4-15% Familial incidence 4.1% Less comman in pregnancy but prognosis is

significantly worse in pregnant women

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.

Herpes zoster virus shows more aggressive biological behaviour than herpes simplex virus type 1

PCR techniques have isolated herpes virus DNA from the facial nerve during acute palsy.

Inflammation of the nerve initially results in a reversible neurapraxia,

HISTORY:

Sudden in onset and evolves rapidly, with maximal facial weakness developing within two days.

A slow onset progressive palsy with other cranial nerve deficits or headache raises the possibility of a neoplasm

Associated symptoms may be hyperacusis, decreased production of tears, and altered taste.

otalgia or aural fullness and facial or retroauricular pain, which is typically mild and may precede the palsy.

PHYSICAL EXAM:

Bell's palsy causes a peripheral LMN palsy,

U/L impairment of movement in the facial & platysma muscles, drooping of the brow & corner of the mouth, & impaired closure of the eye and mouth.

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

PHYSICAL EXAM:

Polyposis or granulations in EAC suggest cholesteatoma or malignant otitis externa.

Vesicles in the conchal bowl, soft palate, or tongue suggest Ramsay Hunt syndrome

A deep lobe parotid tumour may only be identified clinically by careful examination of the oropharynx and ipsilateral tonsil to rule out asymmetry.

MANAGEMENT, STEROID

Usual regimen is 1mg/kg/day for 1 week.

To be tapered in the 2nd week. 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.”

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.

Usual regimen 200 mg – 400 mg,5 times a day for 10 days

Cochrane review*:“More evidence is needed to show whether the antiviral drugs

acyclovir or valacyclovir are effective in aiding recovery from Bell's palsy.”

.

WHEN TO DO DECOMPRESSION

If the pt either progresses to complete paralysis or present with complete paralysis, an ENOG is obtained 3 days after occurance of complete paralysis

If degeneration <90% -conservative Repeat ENOG every 1-3 day If degeneration >90% -surgical decompression is

an option However, if >90% degeneration occur after the 2-

week, surgical decompresion does not alter outcome

OUTCOMES:

It has a fair prognosis without treatment, with almost 3/4 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.

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.

Patients with a partial palsy fair better, with 94% making a full recovery.

The outcome is worse when herpes zoster virus infection is involved

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

MELKERSSON-ROSENTHAL SYNDROME

Acute episodes of facial paralysis Facial swelling Fissured tongue

“Scrotal” tongue Very rare Familial but sporadic

Usually begins in adolescence

Leads to facial disfigurement No definite therapy

ALTERNATIVE CAUSES OF ACUTE FACIAL NERVE PARALYSIS

Atypical signs & symptoms which suggest etiology other than Bell’s palsy require imaging

Clinical history is crucial in distinguishing etiologies

Choice of imaging technique depends on clinical suspicion

LYME DISEASE

Lyme disease (borreliosis) Endemic areas (Northeast USA, central

Europe, Scandinavia, Canada) Consider in children w/atypical facial palsy

Imaging: small white matter lesions similar to multiple sclerosis, enhancement of facial & other cranial nerves

Bilateral facial paralysis: 25% Important to make diagnosis early

because it is curable early w/antibiotics

RAMSAY HUNT SYNDROME

Caused by reactivation varicella zoster virus (herpes virus type 3)

Facial paralysis + hearing loss +/- vertigo Herpes zoster oticus

Two-thirds of patients have rash around ear Other cranial nerves, particularly trigeminal

nerves (5th CN) often involved Worse prognosis than Bell’s (complete recovery:

50%) Important cause of facial paralysis in children

6-15 years old

INFECTIOUS CAUSES

Acute facial paralysis may result from bacterial or tuberculous infection of middle ear, mastoid & necrotizing otitis externa

Incidence of facial paralysis with otitis media: 0.16%◦ Infection extends via bone dehiscences to nerve

in fallopian canal leading to swelling, compression & eventually vascular compromise & ischemia

Immune compromised patients are at risk for pseudomona infection

Poor prognosis (complete recovery is < 50%)

NEOPLASMS

27% of patients with tumors involving the facial nerve develop acute facial paralysis

Most common causes: schwannomas, hemangiomas (usually near geniculate ganglion) & perineural spread such as with head and neck carcinoma, lymphoma & leukemia

Other neoplasms can also involve the facial nerve◦ Adults: metatstatic disease, glomus tumors,

vestibular schwannomas & meningiomas◦ Children: eosinophilic granuloma & sarcomas

GLOMUS TUMOR

Glomus tumors arising from jugular bulb (jugulare) and/or middle ear (tympanicum) may involve the facial nerve

VESTIBULAR SCHWANNOMA

Common tumor

However, facial nerve is resistant to compression Therefore, tends to produce facial paralysis

mostly when they attain a large size

OTHER CAUSES

Guillain-Barre Syndrome Ascending paralysis

Iatrogenic Temporal bone surgery

Excision of vestibular schwannoma has <10% chance of paralysis

Middle ear surgeries Babies who required forceps delivery

>90% recovery

Rcurrent facial palsy: seen in Bell’s palsy, Melkersson’s syndrome, diabetes, sarcoidosis tumuors

Bilateral facial paralysis: simultaneous bilateral facial paralysis may be seen in GBS, sarcoidosis, sickle cell anaemia, acute leukemia, bulbar palsy leprosy

FACIAL NERVE TRAUMA - OVERVIEW

- Second most common cause of FN paralysis

- Represents 15% of all cases of FN paralysis

- Most common cause of traumatic facial nerve injury is temporal bone fracture

TEMPORAL BONE FRACTURE– 5% of trauma patients sustain a temporal bone

fracture– 3 types

» Longitudinal Most common type – 70-80% Fracture line parallel to long axis of petrous

pyramid Secondary to temporopartietal blunt force facial nerve paralysis in 25% of

cases(delayed)» Transverse

10-20% of fractures Fracture line perpendicular to long axis of

petrous pyramid Secondary to occipital blow facial N. paralysis in 50% of

cases(immediate)» Mixed

10% of temporal bone fractures

IATROGENIC TRAUMA

– Surgical• Most common overall surgery with FN injury is

parotidectomy• Most common otologic procedures with FN

paralysis– Mastoidectomy – 55% of surgical related FN

paralysis– Tympanoplasty – 14%– Mechanism - direct mechanical injury or heat

generated from drilling– Most common area of injury – distal tympanic

segment including the 2nd genu, followed by mastoid segment

• Unrecognized injury during surgery in nearly 80% of cases

SURGICAL TREATMENT FOR FACIAL NERVE INJURY

A. Facial nerve decompressionB. Neurorrhaphy(nerve repair)

1.direct end to end anastomosis 2. interposition cable grafting: sural / great auricular

C. Nerve transposition: hypoglossal-facialD. Muscle transposition: temporalis, masseterE. Micro-neuro-vascular muscle flapF. Static procedure: eyelid implant, facial sling

TREATMENT PROTOCOL

A.Upto 3 weeks: nerve decompression or nerve repairB. 3 weeks- 2 years: nerve repair or nerve transpositionC. >2yrs with fibrillation in EMG nerve repair or nerve transpositionD. >2yrs with electrical silence in EMG muscle transposition/ eyelid implant/ facial

sling

APPROACH TO TREATMENT AND TREATMENT OPTIONS - IATROGENIC INJURY

• If transected during surgery– Explore 5-10mm of the involved segment– Stimulate both proximally and distally• Response with 0.05mA = good prognosis; further

exploration not required• If only responds distally = poor prognosis, and further

exploration is warranted

• If loss of function is noted following surgery, wait 4 hours and then re-evaluate the patient. This should be ample time for an anesthetic to wear off

– Waited time and still paralysis• Unsure of nerve integrity – re-explore as soon as possible

APPROACH TO TREATMENT AND TREATMENT OPTIONS - IATROGENIC INJURY

• Integrity of nerve known to be intact– High dose steroids – prednisolone at 1mg/kg/day x

10 days and then taper– 72 hours – ENoG to assess degree of degeneration» >90% degeneration – re-explore» <90% degeneration – monitor

if worsening paralysis occurs re-explore if no regeneration, but no worsening, timing

of exploration or whether to is controversial

If more than 50% of the circumferance has been disrupted it should be repaired with either direct epineural suture or inlay graft

INTRATEMPORAL APPROACHES TO DECOMPRESSION• Nerve may be injured along multiple segments

– localize injured site pre-operatively– Full exposure of the nerve from IAC to the stylomastoid foramen if

can’t localize• Approach to full exposure is based on patient’s auditory and

vestibular status– Intact - Transmastoid/Middle cranial fossa approach– Absent – Transmastoid/Translabyrinthine approach

• Diamond burs and copious irrigation is utilized to prevent thermal injury

• Thin layer of bone overlying the nerve is bluntly removed• Whether to perform neurolysis or not to open the nerve

sheath is debateable – Recommended to drain hematoma if identified

ACUTE VS. LATE DECOMPRESSION - CONTROVERSIAL

Quaranta et al (2001) examined results of 9 patients undergoing late nerve decompression (27-90 days post injury) who all had >90% degeneration 7 patients achieved HB grade 1-2 after 1 year 2 achieved HB grade 3 Concluded that patients may still have a benefit of

decompression up to 3 months out Shapira et all (2006) performed a retrospective review looking

at 33 patients who underwent nerve decompression. They found no significant difference in overall results between those undergoing early (<30 days post-injury) vs. late (>30 days post-injury) decompression

Most studies like these have been very small, and lack control groups. Some studies have shown improvements with decompression occurring 6-12 months post-injury, but further evidence is needed

FACIAL REANIMATION

Facial reanimation is a family of different surgical techniques to make one's paralyzed face move more normally.

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GENERAL PRINCIPLES

Reinnervation of facial muscles should occur ASAP

Upper and lower face should be reanimated separately Avoids mass movement

Both static and dynamic procedures can be employed

Procedure tailored to patient’s needs

ASSESSMENT AND PLANNING

Cause of facial paralysis Functional deficit/extent of paralysis Time course/duration of paralysis

Likelihood of recovery Other cranial nerve deficits Patient’s life expectancy Patient’s needs/expectations

PRIMARY NERVE REPAIR

End-to-end anastomosis preferred

Can be performed with defect < 17 mm

Extratemporal repair performed < 72 hrs of injury

Most common methods Group fascicular repair Epineural repair

Group fascicular repair

PRIMARY NERVE REPAIR Severed ends of nerve

exposed Devitalized tissue/debris

removed with fine scalpel Small bites of epineurium

Epineural sheath approximated with 9-0 nonabsorbable suture Epineural repair

recommended for injury proximal to pes anserinus and intratemporal Horizontal segment rarely

accessible to suture repair

Epineural repair technique

NERVE REPAIR - OVERVIEW

• Recovery of function begins around 4-6 months and can last up to 2 years following repair

• Nerve regrowth occurs at 1mm/day• Goal is tension free, healthy anastomosis• Rule is to repair earlier than later - – After 12-18 months, muscle reinnervation becomes less efficient

even with good neural anastomosis – Some authors have reported improvement with repairs as far out

as 18-36 months– May and Bienstock recommend repair within 30 days, but others

have found superior results if done up to 12 months out

• 2 weeks following injury -> collagen and scar tissue replace axons and myelin

– Nerve endings must be excised prior to anastomosis for this reason if this far out

NERVE REPAIR - OVERVIEW

Rule is to repair earlier than later

PRIMARY ANASTOMOSIS

• Best overall results of any surgical intervention• Done if defect is less than < 17mm

– Mobilization of the nerve can give nearly 2cm of length

– With more mobilization comes devascularization• Endoneurial segments must match - promotes

regeneration• Ends should be sutured together using three 9-0/10-

0 monofilament sutures to bring the epineurium or perineurium together

• It is best to freshen the end of both the nerve & graft by making an oblique(45 degree) cut, increasing the surface area

GRAFTING AND NERVE TRANSFER - OVERVIEW

Approach is based on availability of proximal nerve ending

Performed for defects > 17mm Results in partial or complete loss of donor nerve

function Best functional results are obtained with cable grafting

when a segment of the facial n. is disrupted Also recommended if there is tension at the

anastomotic site of a primary nerve repair Graft should be aprox. 25% longer than needed

to allow for a tension free anastomosis

INTERPOSITION GRAFTING

Cable grafts Used when defect > 17mm; nerve cannot

be reapproximated w/o tension Most common

Greater Auricular Nerve Sensory nerves from superficial cervical plexus Sural nerve Medial antebrachial cutaneous nerve

INTERPOSITION GRAFTING

Recovery Movement first noticed 6 months after

surgery Tinel’s sign heralds recovery Muscle tone preceeds voluntary movement Mid 1/3 of face usually recovers first, then

spreads superiorly toward eye Expect 12-18 months Variable degree of synkinesis Majority of cases reach House-Brackmann III

INTERPOSITION GRAFTINGGREATER AURICULAR NERVE

Harvesting Located on lateral

surface of SCM at the midpoint of a line drawn between mastoid tip and mandibular angle

May extend postauricular incision or use separate neck incision

INTERPOSITION GRAFTINGGREATER AURICULAR NERVE

Useful features Proximity to facial nerve Cross-sectional area (~equal) Limited morbidity

Limitations Reconstruction of long defects and/or

branching nerve gaps Ideal for defects < 6cm in length

SURAL NERVE Anatomy

Formed by union of medial sural cutaneous nerve and lateral sural cutaneous branch of peroneal nerve.

Pierces fascia of gastrocnemius and runs in lateral compartment in association w/ saphenous vein

Distally, located between lateral malleolus and tendon of the calcaneus.

SURAL NERVE

Harvesting Multiple transverse

incisions v. longitudinal incision are made.

Longitudinal incision made posterior to the lateral malleolus and then extended upwards depending on length needed Nerve dissected

proximally to desired length

SURAL NERVE Pros:

Length (40cm) Accessibility Low morbidity associated with sacrifice Two team approach

Reduced surgical time

Cons: Variable caliber

Often too large Difficult to make graft approximation

Unsightly scar

MEDIAL ANTEBRACHIAL CUTANEOUS NERVE (MACN)

Anatomy Arises from medial cord of brachial plexus,

adjacent to ulnar nerve Medial to axillary artery Anterior and medial to brachial artery Distally, it is closely associated with basilic

vein

MACN

Harvest Important landmarks:

Medial epicondyle of humerus Biceps tendon Basilic and medial cubital veins Fascial plane separating bicep from tricep

Tips Use of sterile, proximal tourniquet

Facilitates basilic vein identification Upper extremity can be prepped from axilla to

wrist or continuous with the head/neck. May employ 2-team approach

CROSSOVER TECHNIQUES

Scenarios for use: Irreversible facial nerve injury Intact facial musculature/distal facial

nerve Intact motor endplates Intact proximal donor nerve

Ideal if performed within a year of facial paralysis Prior to distal muscle/facial nerve atrophy

Pros Low level of difficulty Time interval until movement

4-6 months Avoid multiple sites of anastomosis Mimetic-like function achievable with practice

Cons Donor site morbidity Some degree of synkinesis

CROSSOVER TECHNIQUES

HYPOGLOSSAL-FACIAL

Technique modification aka partial XII-VII transfer Donor nerve harvested One end of donor nerve is sutured to severed main trunk

of CN VII; other end hooked up to proximal segment of partially severed CN XII

The procedure has been modified by only partially sectioning the hypoglossal nerve and interposing, by end to-side anastomoses,by a greater auricular nerve graft between the hypoglossal and facial nerves.

Since the hypoglossal nerve is transected only halfway, tongue function can be preserved.

Limits tongue dysfunction and atrophy

CN XII-CN VII anastomosis contraindicated with ipsilateral vagal paralysis Swallow dysfunction

Improved facial tone/symmetry in ~ 6 months

Pt learns to smile by moving the tongue Exercise/biofeedback training

Adjunctive lid procedures usually required

CROSS-FACIAL NERVE GRAFTING

Contralateral CN VII used to reinnervate paralyzed side using a nerve graft◦ Sural nerve often employed◦ ~25-30cm of graft needed

Restitution of smile and eye blinking when successful

Disadvantage◦ 2nd surgical site◦ Violation of the normal facial nerve

CROSS-FACIAL NERVE GRAFTING

4 techniques1. Sural nerve graft routed from

buccal branch of normal CN VII to stump of paralyzed CN VII

2. Zygomaticus and buccal branch of normal CN VII used to reinnervate zygomatic and marginal mandibular portions respectively

3. 4 separate grafts from temporal, zygomatic, buccal and marginal mandibular divisions of normal CN VII to corresponding divisions on paralyzed side.

4. Entire lower division of normal side grafted to main trunk on paralyzed side.

MUSCLE TRANSPOSITION (AKA “DYNAMIC SLING”)

When to use: Facial neuromuscular system absent

Neural techniques unsuitable i.e. congenital facial paralysis

Facial nerve interruption of at least 3 years Loss of motor endplates

Crossover techniques not possible due to donor nerve sacrifice

Muscle transposition most commonly employs the temporalis muscle because of its good location, length,contractility, and vector of pull.

good for reanimation of the mouth in patients with long-standing (at least 1 year in length) paralysis.

Allows patients to have a voluntary smile.

TEMPORALIS

TEMPORALIS

Overcorrection at oral commissure is critical 2nd or 3rd molar of upper dental

arch should be exposed when procedure is finished

Harvest and placement of temporoparietal facial flap recommended to fill donor site

Oral support possible within 6 weeks Movement achieved by clenching

the jaws Unnatural contraction requiring

rehabilitation/Physiotherapy

MASSETER

Used when temporalis muscle is not available

May be preferred due to avoidance of large facial incision

Disadvantage: Less available muscle compared to

temporalis Vector of pull on oral commisure is more

horizontal than superior/oblique like temporalis

MICRONEUROVASCULAR TRANSFERFREE MUSCLE FLAPS

Created based on the potential of achieving individual segmental contractions Reduction of mass movement/synkinesis

Numerous muscle flaps used thus far: Gracilis Latissimus dorsi Inferior rectus abdominus

ADDRESSING PARALYTIC EYELIDS

Pre-op assessment by ophthalmology Complete eye exam including:

Visual acuity assessment Lower lip laxity (snap test) Tear production (Schirmer test) Lacrimal system integrity (Jones test) Measurement of the distance btwn upper

and lower eyelids upon closure (margin gap)

STATIC FACIAL SLING TECHNIQUE

1. Preauricular, temporal or nasolabial fold incision may be used

2. Additional incisions made adjacent to oral commisure at vermillion border of upper and lower lip

3. Subcutaneous tunnel dissected to connect temporal to oral commisure incisions

4. Dissection may be carried out in midface adjacent to nasal ala, if needed (for alar collapse)

5. Implant strip is split distally to connect to the upper/lower lips

6. Implant secured to orbicularis oris/commisure using permanent suture

7. Implant is suspended and anchored superiorly to superficial layer of deep temporal fascia, or zygomatic arch periosteum, using permanent suture.

8. May also secure to malar eminence using small miniplate or bone anchoring screw

Facial Paralysis

(Acute < 3 wks) Intermediate(3 wks-2 years)

Chronic (>2 years)

CN VII decompression

Nerve repair

Primary Cable graft -G. auricular -Sural -MACN

Nerve transfer -hypoglossal -masseteric -spinal acc.

Cross-facialGraft

RegionalMuscleTransfer -Temporalis -Masseter -Digastric

Free MuscleTransfer -Gracilis -serratus -L. dorsi -Pec minor

+/-Static Techniques: Slings, Gold weight/Lid procedures, etc

Reanimation

Summary

Thanks

PROXIMAL AND DISTAL SEGMENTS AVAILABLE

• Great auricular nerve– Usually in surgical field– Located by drawing a line perpendicular to a line drawn b/w

mastoid tip to the angle of the mandible– Can only harvest 12cm of this nerve– Loss of sensation to lower auricle with use

• Sural nerve– Located 1 cm posterior to the lateral malleolus– Can provide 35cm of length– Very useful in cross facial anastomosis– Loss of sensation to lateral calf and foot

• Ansa Cervicalis – only utilized if neck dissection has been performed

• 92-95% of these patients have some return of facial function– 72-75% have good results (HB 3 or above)

ONLY DISTAL SEGMENT AVAILABLE

• Requires that the patient have an intact distal nerve segment and facial musculature suitable for reinnervation – Determined by EMG and/or muscle biopsy

• Hypoglossal nerve– Direct hypoglossal-to-facial graft

• Distal branch of facial nerve is attached to hypoglossal nerve• 42-65% of patient’s expected to experience decent symmetry and tone• Complications – atrophy of ipsilateral tongue, difficulties with chewing,

speaking, and swallowing– Partial hypoglossal-to-facial jump graft

• Uses a nerve cable graft, usually the great auricular nerve, to connect the distal end of the facial nerve to a notch in the hypoglossal nerve

• Much fewer complications, but increased time• May compared the results of direct VII-XII graft to the VII-XII jump graft

COMPARISON OF DIRECT HYPOGLOSSAL GRAFTING VS. JUMP GRAFTING

• Jump graft – 8% of patients experienced permanent

complications– 41% obtained good movement with less synkinesis– Longer recovery time (9-12 months prior to some

function)• Direct graft

– 100% permanent complications– Stronger motor function– Less recovery time

MUSCULAR TRANSPOSITION

If there is no functional neuromuscular system, surgical reconstruction involve muscular transposition

Pedicaled muscle graft: temporalis, masseter

Free muscle graft: gracillis, rectus abdominis abductor hallucis, pectoralis minor , latissimus dorsi

In adults, the pedicled grafts are most commonly used

Free muscle transfer with a neurovascular anastomosis(using the contralateral facial nerve for innervation) is the mainstay of treatmentof children with congenital disorder ( moebius syndrome)

Free muscle transfer procedure are of limited effectiveness

Muscle transposition most commonly employes the temporalis muscle bcoz of its good location, length & contractility

It is a proven & useful technique for facial reanimation in who nerve grafting or cranial nerve substitution procedure are not poissible

Temporalis transposition is a dynamic technique that allows the patients to have a voluntary smile

COMPLICATION OF FACIAL PARALYSIS

1. incomplete recovery: facial asymmetry persists, eye can’t be closed resulting in epiphora. A weak oral sphinctor causes drooling & difficulty in taking food

2.exposure keratitis: eye can’t be closed, tear film from the cornea evaporates causing dryness, exposure keratitis and corneal ulcer

3. synkinesis(mass movement): when the pt. wishes to close eye corner of mouth also twiches or vice versa

4.tics and spasm: result of faulty regeneration of fibres. Involuntary movements are seen on the affected side of face

5. contractures: results from fibrosis of atrophied or fixed cotraction of a group of muscles

6. Crocodile tears(gustatory lacrimation): unilateral lacrimation with mastication. Due to faulty regeneration of parasympathetic fibres which now supply lacrimal gland instead of the salivary glands. It can be treated by section of GSPN or tympanic neuractomy

7. Frey’ syndrome(gustatory sweating): there is sweating and flushing of skin over the parotid during mastication. It results from parotid surgery

8. psychological and social problems

THANK YOU