Facial Nerve Palsy : Facial Nerve Palsy Dr. SHOUVIK CHOWDHURY SEMINAR CONTENTS : CONTENTS INTRODUCTION OF FACIAL NERVE
BELL’S PALSY Facial nerve : Facial nerve VII cranial nerve
Supplies muscles of facial expression
Some treated as intermediofacial nerve
Soummering seperated 2 and numbered seperately Embryology : Embryology Nerve of 2nd branchial arch
Facial nuclei are derived from neural crest
Ventrolateral aspect of hindbrain
Motor fibres are axons of cells in ventrolateral lamina of midbrain & grows outwards to muscle fibres of their distribution Slide 5: Facial nucleus-
special visceral/branchial efferent
Superior salivatory nucleus-general visceral efferent
Lacrimatory n- GVE & GSA fibres Nucleus Slide 6: SVA nuclei
supply Nucleus of Tractus Solitarius Slide 7: Facial nerve is a mixed nerve, having a motor root and a sensory root.
Sensory root “nervus
intermedius of Wrisberg” carries taste fibers from the anterior 2/3 of the tongue, lacrimal, palatine mucosa and general sensation from the concha and retroauricular skin,submandibular & sublingual salivary gland
Motor root supplies the muscles of the face, auricle, stapedius, stylohyoid,digastric(post.belly) Branches : Branches Branches on face : Branches on face Neurones : Neurones 1- Upper motor neuron: Primary motor cortex (Precentral gyrus)
The axons of these neurons enter the Corticonuclear fiber bundle to reach the second lower motor neuron in the Pons.
2- Lower motor neuron: Facial motor nucleus.
The facial nucleus is divided into two parts:
The upper part receives bilateral innervations, and supplies the muscles of the forehead and eyebrows (temporal branches).
The lower part receives innervations mainly from the contra lateral hemisphere, and supplies the muscles of the lower part of the face through the facial nerve. Ganglion : Ganglion Blood supply to facial nerve – clinical relevance : Blood supply to facial nerve – clinical relevance Courses between the epineurium and periosteum – making the blood supply at risk when mobilizing at the first genu
Stylomastoid artery (branch of the postauricular artery of external carotid artery)
Greater petrosal artery (branch of middle meningeal artery)
Labyrinthe segment - lacks anastomosing arterial cascades thereby making the area vulnerable to ischemia
* Parhizkar N, Hiltzik DH and Selesnick SH. Facial nerve rerouting in skull base surgery. Otol Clin N Am. 2005; 38(4): 685-710 variation : variation Facial nerve
(leave main trunk proximal to stylomastoid foramen) Site of lesion & manifestations : Site of lesion & manifestations Applied anatomy : Applied anatomy Facial paralysis
Cerebral stroke- paralysis of lower m. of face
occlusion of blood vessels
Reflexes-tectobulbar fibres from superior colliculus-eyelid closure
Fibres from trigeminal sensory n.- corneal reflex, suckling, chewing
Fibres from superior olivary nucleus on auditory pathway-reflex contraction of stepedius Herpes Zoster Oticus (Ramsay Hunt syndrome) : Herpes Zoster Oticus (Ramsay Hunt syndrome) 10-15% of acute facial palsy cases
Lesions may involve the external ear, the skin of EAC or soft palate
Associated symptoms – hearing loss, dysacusis and vertigo
Additional involvement of CN V, IX and X.
Pathogenesis – Neural injury due to edema at point between the meatal foramen and the geniculate fossa.
Shooting pain in auditory canal, soft palate
Trigger zone-pinna Melkersson-Rosenthal syndrome : Melkersson-Rosenthal syndrome Triad
Recurrent orofacial edema
Recurrent facial palsy (50-90%)
Lingua plicata (fissure tongue) – 25%
Lips become chapped, fissured and red-brown in appearance
Facial nerve decompression may be indicated if facial paralysis is severe and recurrent Superficial musculoaponeurotic system : Superficial musculoaponeurotic system Support mechanism for various soft tissue envelope
Continuous with posterior frontalis & platysma inferiorly
Anterior-inv.fascia of orbicularis oculi, zygomaticus, levator labii superioris
Dissection should be sub SMAS at level of zygomatic arch
Above arch-dissection-s.c or in loose areolar plane deep to temporoparietal fascia. Slide 23: Frey’s syndrme/gustatory sweating/crocodile tear syndrome-
Hystronic spasm-constant twitching of some/all facial muscles.
tonic contraction of orbicularis oculi m.with constant blinking of eye. Red zone of webster : Red zone of webster Slide 25: Facial palsy Facial palsy : Facial palsy Total flaccidity of facial muscles to perform motor function. Slide 27: Etiology –
Over 40 causes; broadly classified into three major groups
Central or intracranial region
Central nervous system degenerative diseases
Guillain Barre syndrome Slide 28: Tumors of the intracranial cavity-
Glomus tumour Intratemporal : Intratemporal Bacterial (e.g., otitis media; malignant otitis externa) and viral (e.g., herpes zoster) infections, diptheria, TB, mumps, infectious mononucleosis.
Longitudinal and horizontal fractures of the temporal bone
Tumors invading the middle ear, mastoid, and FN
Iatrogenic causes (surgical injury)
Congenitial – osteopetrosis (hereditary) Extracranial : Extracranial Parotid gland region
Malignant tumors of the parotid gland
Trauma (lacerations and gunshot wounds)
Parotid – main trunk, branches
TMJ – frontal
Tumor excision – cystic hygroma; hemangioma
At birth – use of suction or forceps Slide 32: Upper motor neuron-
controls- extraocular, masticatory, lingual, palatal, pharyngeal & facial group of muscles
cerebral cortex-neurons travelled in crossed & uncrossed fibres-terminates at various level of brainstem-LMN sends cranial n.to skeletal m. Slide 33: Supranuclear facial paralysis-
Lower part of face chiefly affected.
paralysis of nerve in petrous temporal
bone & motor nucleus-loss of taste in
anterior 2/3 of tongue.
Paralysis due to fracture base of skull-
involvement of auditory & petrosal n.
most common cause of injury at or after
exit from stylomastoid foramen Slide 34: Injury Symptoms Slide 35: CLASSIFICATIONS OF
FACIAL PALSY Rainer schmelzeisen classification(1999) : Rainer schmelzeisen classification(1999) Congenital-
congenital nuclear aplasia(mobius syn)
Melkersson Rosenthal syndrome
Guillan-Barre syndrome Slide 37: Neoplastic-
Temporal/external acoustic canal tumours
otitis media, viral (e.g., herpes zoster) infections, diptheria, TB, mumps, infectious mononucleosis. Slide 38: Iatrogenic-
lateral skull base surgery
Temporal bone #
facial lacerations Slide 39: Other causes-
Brainstem infarction Slide 40: Seddon (1943) classification of nerve injury
Only the myelin sheath is affected
The conduction of impulses is blocked but axoplasmic transport continues
The nerve distal to the site of the lesion has abnormal voluntary motor function but retains normal electrical stimulability
This usually occurs for several days after trauma and disappears spontaneously and completely Slide 41: Seddon (1943) classification of nerve injury
Axonal continuity is lost
Wallerian degeneration distally (3-5 days)
Although the neural element is separated and damaged, the myelin sheath remains intact
Spontaneous but incomplete recovery may be expected
If the endoneural tube is also disrupted, aberrant regeneration of axonal sprouts may randomly enter distal endoneural tubes Slide 42: Seddon (1943) classification of nerve injury
All components of the peripheral nerve are transected
Wallerian degeneration distally (3-5 days)
The epineural sheath is disrupted, allowing axon sprouts outside the nerve sheath to produce neuromas Slide 43: Seddon (1943) classification of nerve injury
Axonotomesis & neurotmesis
Axons begin to regenerate about 3 weeks after injury
Axon may regenerate at a rate of 1 mm/day
Recovery begins within 2-4 months Slide 44: Sunderland Classification(1978)
Sunderland expanded Seddon's system by subdividing type 3 injuries and proposed the following classification types:
Sunderland I (Neuropraxia) - as in Seddon.
Sunderland II (Axonotmesis) - as in Seddon.
Sunderland III (Neurotmesis) - loss of continuity of endoneurial tubes, with intact perineurium, distal Wallerian degeneration occurs.
Sunderland IV (Neurotmesis) - loss of continuity of perineurium, distal Wallerian degeneration occurs.
Sunderland V (Neurotmesis) - loss of continuity of epineurium, distal Wallerian degeneration occurs. Evaluation of acute facial paralysis : Evaluation of acute facial paralysis House-Brackman grade system(1985)
I, Normal: Normal facial functioning all areas
II, Mild dysfunction: slight weakness noticeable only on close inspection
At rest: normal symmetry and tone
Motion: some to normal movement of forehead
Ability to close eye with minimal effort
Ability to move corners of mouth with minimal effort and slight asymmetry
Mild synkinesis, contracture, or hemifacial spasm Evaluation of acute facial paralysis : Evaluation of acute facial paralysis House-Brackman grade system
III, moderate dysfunction:
obvious but not disfiguring difference between two side
No function impairment
Noticeable but not severe synkinesis, contracture, and hemifacial spasm
At rest: normal symmetry and tone
slight to no movement of forehead
Ability to close eye with maximal effort and obvious asymmetry
Ability to move corners of mouth with maximal effort and obvious asymemetry Evaluation of acute facial paralysis : Evaluation of acute facial paralysis House-Brackman grade system
IV, moderate severe dysfunction:
Obvious weakness and disfiguring asymmetry
At rest: normal symmetry and tone
no movement of forehead
Inability to close eye completely with maximal effort
Asymmetrical movement of corners of mouth with maximal effort Evaluation of acute facial paralysis : Evaluation of acute facial paralysis House-Brackman grade system
V, severe dysfunction:
Only barely perceptible motion
At rest: possible asymmetry with droop of corner of mouth and decreased or absent nasolabial fold
No movement of forehead
Incomplete closure of eye
Slight movement of corner of mouth
VI, total paralysis: no movement Slide 49: Diagnostic Evaluation of Facial Palsy
Physical examination Evaluation of facial paralysis : Evaluation of facial paralysis A careful history of the patients illness
Sudden in onset and frequently evolve over 2-3 weeks after onset-infl/infctn
Any palsy progression over 3 weeks should be evaluated for a neoplasm
Any palsy persist for 6 month without any recovery should be considered for a neoplasm.
Patients may also mention otalgia or aural fullness and facial or retroauricular pain, Physical examination : Physical examination Physical exam: : 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 Slide 53: Diagnostic Evaluation of Facial Palsy
Hearing and balance tests-stapedial reflex
Submandibular flow test
As the quality of radiographic studies, primarily high resolution CT scan, has improved, the importance of topognostic testing has fallen off Topognostic Testing : Topognostic Testing Schirmer test for lacrimation
Stapedial reflex test (stapedial branch)
Taste testing (chorda tympani nerve)
Salivary flow rates and pH (chorda tympani) Topognostic Testing : Topognostic Testing Schirmer Test
Greater superficial petrosal nerve
Filter paper is placed in the lower conjunctival fornix bilaterally
3- 5 minutes
Value of 25% or less on the involved side or total lacrimation less than 25 mm is considered abnormal. Topognostic Testing : Topognostic Testing Stapedial Reflex
Stapedius branch of the facial nerve
Most objective and reproducible
A loud tone is presented to either the ipsilateral or contralateral ear ? evokes a reflex movement of the stapedius muscle ? changes the tension on the TM (which must be intact for a valid test) resulting in a change in the impedance of the ossicular chain
If intact stapedial reflex, complete recovery can be expected to begin within six weeks Topognostic Testing : Topognostic Testing Taste Testing
Papillae generally disappear within 10 days post injury - middle 1/3 of the tongue is most indicative, because the anterior 1/3 may receive bilateral input. Topognostic Testing : Topognostic Testing Salivary flow rates
Cannulation of Wharton's ducts bilaterally
5 minute measurement of output
Significant if 25% reduction in flow of the involved side as compared to the normal side
Salivary pH ? Flow Rate Electrodiagnostic testing : Electrodiagnostic testing Conduction test:
F.nerve is stimulated at angle of mandible
Recording electrode- frontalis & o.oculi m.
Latency of muscle measured from onset of stimulus on both sides
latency>3.8 msec considered abnormal Nerve Excitability Test (NET) : Nerve Excitability Test (NET) Most predictive prognostic factor for recovery of facial nerve function*
Hilger nerve stimulator over stylomastoid foramen
Reflects elevated thresholds for neuromuscular stimulation due to degeneration / disruption of axons (comparison to contralateral side)
Difference > 3.5 milliamps - poor prognosis
* Ikeda M et. al. Clinical factors that influence the prognosis of facial nerve paralysis and the magnitudes of influence. Laryngoscope. 2005; 115:855-860. Nerve Excitability Test (NET) : Nerve Excitability Test (NET) Benefits:
Easy to perform
More comfortable for patient
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) : Maximal Stimulation Test (MST) Electrical impulse administered to depolarize the nerve with current and to compare it to contralateral side
Test is repeated periodically until definitive response
Equivalent to contralateral side
Minimally diminished (50%)
Markedly diminished (< 25% of normal)
Symmetric response within first ten days – complete recovery in > 90%
No response within first ten days – incomplete recovery with significant sequelae Electroneuronography (EnoG) : Electroneuronography (EnoG) Records compound muscle action potential (CMAP) with surface electrodes placed transcutaneously in the nasolabial fold (response) and stylomastoid foramen (stimulus)
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 Electroneuronography (EnoG) : Electroneuronography (EnoG) Most reliable in first 2-3 weeks post event (as neuropraxic fibers recover or regenerate, they discharge asynchronously and the response is subsequently diminished)
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
Test-retest variability due to position of electrodes Electromyography (EMG) : Electromyography (EMG) Assesses reinnervation potential of muscles two weeks after onset
Limited value early in evaluation because fibrillation potentials indicating axonal degeneration do not appear until 10 – 14 days post onset
Detection of motor units in 2 of 3 muscle groups – 87% satisfactory outcome
Detection of motor units in 1 muscle group – 11% satisfactory Slide 66: Trigeminal-facial reflex testing (Blink reflex)
Stimulate the supraorbital division of the ophthalmic branch of trigeminal nerve
Record EMG from orbicularis oculi muscle Slide 67: Diagnostic Evaluation of Facial Palsy
CT scans (brain stem, cerebellopontine angle, temporal bone, skull base)
Sialography of parotid
Chest radiographic survey to detect sarcoidosis, lymphoma, carcinoma Slide 68: Treatment plan Goals : Goals Normal appearance at rest.
Symmetry at involuntary motion
Restoration of oral, ocular & nasal sphincter
No loss of other significant functions Repair : Repair Immediate(0-3 weeks)
Delayed(3 wk-2 yr)
Late(over 2 yrs) Requirement of innervation : Requirement of innervation Viable ipsilateral facial nucleus
Proximal nerve segment capable of supporting axonal regeneration
Distal nerve segment through which the axon may regenerate into facial muscles Direct nerve repair : Direct nerve repair In primary repair, careful realignment of fascicles, epineural vessels & other identifying landmarks are attempted to re-establish original relationship to nerve ends.
Epineural sutures are used for small distal branches
Avoidence of tension at suture line
Use of fine caliber suture
In nerve coaptation, fibrous tissue proliferation at sutured area may endanger axon arising from central nerve stumps Slide 73: Fibrous tissue formation initiated by trauma of nerve, interpositioning of blood clots between nerve stumps & application of tension. Extratemporal nerve grafting : Extratemporal nerve grafting Baker & Conley(1979)
to reconstruct the defect to reconstitute the system without tension
Loss of main trunk or peripheral division secondary to trauma, scarring or resection Frequently use donor site : Frequently use donor site Great auricular n.
Lateral femoral n. Neurorrhaphy : Neurorrhaphy Graft should lie in healthy, well vascularized recipient area
At least 2 mm. thickness is identified
Great auricular n- below auricle at extn.surface of sternomastoid m.
Sural n.-incision behind lateral malleolus
Resection of fibrotic tissue in long standing paralysis Results : Results 3-12 cm
Facial tone-movement of middle 3rd of face
Improvement continues upto 2 years Reanimation or cross nerve grafting : Reanimation or cross nerve grafting Scaramella(1971), smith(1971), Andrel(1973),Fisch(1974), Frellinger(1975),
Principle- cross innervation from non paralyzed side by sural n. graft that connects reservoir of healthy peripheral facial nerve. Slide 80: Cross-facial nerve grafting
Identify branches on normal side
Two-four sural nerve grafts
At 9-12 mos surgery performed to coapt distal ends with selected branches of FN or facial muscles on paralyzed side Slide 82: Disadvatages- surgical intrusion to normal side of the face with sacrifice of axonal input
Highly specialized technique
Longer operating time
Suture line for each graft increasing probability of greater loss of sprouting axon
Longer time for re innervation
Technical difficulties Nerve crossover : Nerve crossover Criteria:
intact peripheral facial n.
intact mimetic muscle system
inaccessible locus of lesion
hypoglossal, spinal accessory & phrenic nerves are used Slide 84: Hypoglossal Nerve Crossover
The criteria for use of the hypoglossal nerve for facial paralysis
Intact extracranial part of the facial nerve
Some ipsilateral facial musculature
A direct VII-to- VII repair of the facial nerve injury or ipsilateral nerve grafting (VII-graft-VII) is not possible
Facial paralysis is irreversible Slide 85: Hypoglossal Nerve Crossover
Patients with denervation of less than 18 months' duration are suitable for this procedure.
When the denervation is more prolonged, fibrosis of the facial musculature prevents resuscitation, even if powerful ipsilateral motors are used. Indications of hypoglossal anastomosis : Indications of hypoglossal anastomosis F.paralysis from radical resection temporal bone
Direct & uncomplicate technique
Greater function of tongue movement
Rapid movt.& better balance
No discomfort from loss of hypoglossal n.
Little functional disability
Inapplicable in mild to moderate paresis
Regional/segmental nerve paresis Slide 88: Hypoglossal Nerve Crossover
Another chief complaints: Overactivity and mass movements.
Synkinesis and mass movements are seen in almost all patients, especially during talking and eating.
Involuntary movements of one portion of the face typically occur while another part of the face moves voluntarily.
Method to overcome problems: Reeducation; physical therapy is used to teach the patient to control facial muscles Slide 89: Hypoglossal Nerve Crossover
Another chief complaints: overactivity and mass movements.
Other methods attempted are injection of botulinum toxin, which prevents acetylcholine release at the neuromuscular end-plate, magnetic stimulation, and selective myectomy
Rubin et al. (1984) advised a Z-plasty technique to restore tongue function.
The aim of this technique is to provide muscular neurotization from the normal side across the midline into the atrophic side. Slide 90: Hypoglossal Nerve Crossover
Disadvantage – if entire hypoglossal nerve transferred to the ipsilateral facial nerve
Various degrees of tongue atrophy and difficulty in speaking and swallowing Slide 91: “Baby-sitter” Procedure
Partial hypoglossal transfer to ipsilateral FN during first stage of cross-FN grafting to help maintain the bulk and tone of facial muscles
If paralysis >6mos
Cross-facial nerve grafting must be supplemented by baby-sitter because the grafts are relatively weak motor donors. Slide 92: “Baby-sitter” Procedure
40% splitting of XII (preserves tongue muscles)
Second stage operation
Needed for coaptation with contralateral facial nerve branches for direct neurontization of the facial muscles, or to supply the muscle transfers. Slide 93: Spinal Accessory Nerve
Transfer of the spinal accessory nerve can provide good resting tonus
However, shoulder disabilities are experienced by almost all patients if the entire accessory nerve is used.
Loss of the ability to elevate the abducted arm, increased shoulder pain during activity, and frozen shoulder are the main forms of morbidity associated with this transfer. Slide 94: Spinal Accessory Nerve
Transposition of sternocleidomastoid branch of the accessory nerve avoids shoulder paralysis
Example of a partial accessory transfer - 50% of the branch to the sternocleidomastoid and 40% of the branch to the trapezius.
After these delicate splitting procedures, paralysis does not develop in the sternocleidomastoid or trapezius muscle. Advantage : Advantage Direct & uncomplicated technique
Greater function as most facial muscles are associated with conscious or unconscious tongue movement
Better facial balance
During speech movement of mouth is more natural Slide 97: Trigeminal Nerve
The masseter branch of the trigeminal nerve can be used as a motor source for local transposition or free-muscle transfers instead of a cross-facial nerve graft if it is not involved in the developmental mishap.
As with other transfers of chewing muscles, the patient is retrained by biting for smile. Regional muscle transposition : Regional muscle transposition Baker & conley(1979)
Indications- absence of mimetic muscles from long standing atropy
Need for additional muscle bulk.
Complementary to nerve grafting or crossover Slide 99: Transposition of Local Muscles
Most common: masseter and temporalis muscles
Their innervation remains the trigeminal nerve
Therefore, patient must be reeducated after transposition
Disadvantage of the use of chewing muscles: lack of synchronization with the healthy side of the face.
This is lessened by placing a cross-facial nerve graft and coapting the cross-facial nerve graft to the motor nerve of these muscles. Slide 100: Masseter Muscle-Owens(1951), Conway(1958), Lexer & Eden(1911)
A powerful chewing muscle that can be used to reanimate the mouth
Lateral and posterior displacement of the muscle because of its deeper location.
Involuntary facial movements during eating and talking
Therefore, poor symmetry and coordination. Slide 102: Temporalis Muscle
The most commonly used muscle for transposition
Used to reanimate both oral and eye sphincters simultaneously, Slide 104: Temporalis Muscle
Transposition of this muscle empties the entire temporal fossa and causes a concave deformity.
Currently, alloplastic materials that can be reshaped have been used in an attempt to address this problem.
Another cosmetic sequela of temporalis transfer is swelling over the zygomatic arch.
Other complications: involuntary facial movements during biting, chewing, and talking and a lack of symmetrical and coordinated facial movement. Advantage : Advantage Elimination of nonvascularized unit that carries risk of necrosis, breakage, atropy
Direct insertion of muscle to the area to br reanimated
Augmentation of atropic face in long standing paralysis Slide 106: Platysma and Digastric Muscles
Depression of the paralyzed lower lip must be included in the overall treatment plan.
Lack of depression of the lower lip leads to an unfavorable aesthetic and functional result.
Pedicled platysma and digastric muscles are beneficial for providing depression to the lower lip. Slide 107: Platysma and Digastric Muscles
Platysma is the first choice for depressor reanimation of the lower lip
it is innervated by the facial nerve
When the platysma is absent or paralyzed
Use the digastric muscle
A lower cross-facial nerve graft is usually coapted with the nerve to the anterior belly of the digastric muscle.
Allows for coordinated and symmetrical depression Slide 108: Transfer of Free Muscles
Indication - when facial muscles are absent or their function is substantially diminished.
Muscle atrophy should be proved with needle EMG
If the ipsilateral facial nerve is available, the nerve of the muscle transplant is coapted directly to it.
In the absence of an available ipsilateral facial nerve, cross.:facial nerve grafting from the healthy side is preferred. Slide 109: Transfer of Free Muscles
The results with cross-facial nerve grafting are always superior to those obtained with other motor sources
cross-facial nerve grafts offer the possibility of coordinated facial movement.
If the facial nerves are absent bilaterally
ipsilateral hypoglossal, trigeminal, accessory, or other motor nerves may be used as donors for the transplanted muscle. Slide 110: Transfer of Free Muscles
When the donor muscle is selected, the factors to be considered are
The strength, bulk, and excursion of the transplanted muscle should be appropriate for the muscle being substituted.
The neurovascular pedicle must be reliable.
Donor site morbidity must be minimal. Slide 111: Transfer of Free Muscles
Smile restoration procedure
Preoperative measurements and videotapes of the patient are needed to assess the excursion and force vectors.
Direction and degree of pull
Required at the level of the alar base, upper lip, commissure, and nasolabial fold should be considered carefully
place free-muscle unit accordingly. Slide 112: Transfer of Free Muscles
Muscles used as free-tissue transfers include
Gracilis, pectoralis minor, rectus abdominis, latissimus dorsi, and serratus anterior
To reconstruct two functions, eye closure and upper lip elevation, with a single muscle flap usually produce unsatisfactory results
Except in the case of the pectoralis minor (because of its dual innervation). Slide 113: Gracilis
The first choice for free-muscle transplantation to reanimate the paralyzed face in adults
Advantages: easy access, rare anatomical variations of the pedicle, easy shaping and debulking, and appropriate excursion to mimic the zygomaticus, major muscle during smiling
Strong adductor muscle, but its absence results in no functional loss. Slide 114: Gracilis
A single direction of pull
easily prevented by meticulous shaping
Secondary revision is always needed; e.g., inadequate pulling force of the free muscle
a minitemporalis muscle flap Slide 116: Pectoralis Minor
Main indication - developmental facial paralysis in young children
The length and width of the muscle at this age are ideal to fit the involved face
Bulk at this age is optimal (no sculpting needed ) Slide 117: Pectoralis Minor
Main advantage - can be transplanted as a whole
Integrity of each muscle fiber remains intact
Minimal donor site morbidity
Another important advantage: Dual innervation
Upper third is by a branch of the lateral pectoral nerve
The lower two thirds by the medial pectoral nerve.
Allows independent movement of the upper and lowerparts of the muscle: separate reanimation of the eye and mouth is possible Slide 118: Pectoralis Minor
Deep position and the short and complex neurovascular pedicle - difficult to harvest.
Brachial plexus injury in the infraclavicular region.
The pedicle - much shorter than that of the gracilis and is variable.
If debulking necessary, do after muscle is harvested
Prolongs the ischemia time.
If necessary, debulking is performed during the revision stage. Slide 119: Pectoralis Minor
Estimate percentage of bulk loss before the planned free-muscle flap is transferred
Despite accurate preoperative planning, free muscles usually require revision.
Muscle tension - an important factor in free-muscle transplantation
Mark tension in situ so that it can be reproduced following transfer. Slide 120: Muscle tension
Mark muscle every 1 cm along its longitudinal axis.
Rule of thumb in adjusting the tension of the transferred muscle:
For facial reanimation, the tension of the muscle should be the same as the tension in site, or slightly less.
In contrast, for extremity reconstruction, the tension of the free muscle should be greater than the tension in site. Slide 121: Pos-op care
External immobilization to maintain the position, e.g., of commissure
Inadvertent jaw movements do not affect the in setting of the free muscle.
Check patency of the vascular anastomosis every hour with a Doppler flowmeter.
Diet: NPO, liquid or soft for 2 to 3 weeks
Speak without opening the mouth. Slide 122: Pos-op care
After the onset of muscle contraction
Perform facial exercises in front of a mirror, goal: coordinated animation of both sides of the face
At 6 weeks
Ultrasound therapy and manual massage
To minimize scar formation on the operated side
To help to avoid scar adhesions between the skin envelope and the free-muscle unit. Slide 123: Factors correlated with the onset of functional return after free-muscle transplantation for facial paralysis (Terzis and Noah 1997)
Key factors: age, sex, and ischemia time in free-flap transplantation
No correlation between ischemia time (0 to 3 hours) and the onset of muscle contraction.
The onset of contraction was slightly earlier in women than in men, and the return of function was earlier in young than in older patients. Slide 124: Eye management
Denervation of the orbicularis oculi muscle - insufficient eyelid closure
Gravity pulls the upper and lower eyelids downward (i.e., lagophthalmos and ectropion, respectively) with loss of orbicularis oculi tonus
The ectropion everts the margin of the lower lid and the punctum lacrimalis
Tear flow and the lacrimal drainage system are disturbed. Slide 125: Eye management
Constant exposure of cornea gives rise to loss of the tear film, dryness of cornea, conjunctivitis and keratitis
If the condition progresses, corneal ulceration and blindness can develop.
The age of the patient, presence of the blink reflex and corneal sensation, the degree of lagophthalmos, and the experience of the surgeon are critical factors in determining the method of treatment. Slide 126: Nonsurgical Methods
In the early period, the following nonsurgical methods protect the eye from the detrimental effects of chronic exposure:
Eye glasses or contact lenses
Artificial tears and ophthalmic ointments
Occlusive moisture chambers
When lagophthalmos is permanent, seek surgical treatment
If the orbicularis oculi muscle is not yet atrophied, cross-facial nerve grafting or direct neurotization of the muscle can relieve the lagophthalmos. Slide 127: Tarsorrhaphy
Lateral overlapping tarsorrhaphy tightens and shortens the upper and lower eyelids
adequate functional results, but cosmetic results are unsatisfactory
The lateral tarsal strip procedure can be used as an alternative
No lid notching is required, baseline tear production is preserved, tarsal plate is not sacrificed; less morbidity than the classic technique
Neither provides equally sized eyes or coordinated movement; they limit vision, provide poor corneal protection. Slide 128: Eye Spring
For patients w/o normal blink reflex or those with intact corenal reflex and trigeminal nerve.
Inserted through two or three small incisions between the skin and tarsal plate
Complications: spring breakage and extrusion through the skin, uncommon
Reduction in tension is a more common complication, can be corrected under sedation.
If lower eyelid drooping also present - specialized upper and lower eyelid springs Slide 130: Lid Loading
Lagophthalmos - Gold weight
Choose gold weights pre-op in upright position
At insertion, pocket must be large enough to anchor to the tarsal plate
Complications: displacement, implant infection, entropion, inflammatory reaction to gold, poor eyelid contour, corneal ulceration and scarring, asYmmetrical closure, residual lagophthalmos, and thickening of eyelid tissue over the prosthesis
If complication encountered, remove implant, consider alternative reconstructive method. Slide 131: Minitendon Graft for Lower Eyelid
Treatment of choice for paralytic ectropion
Helps decrease lagophthalmos
it raises the lower eyelid
A palmaris longus tendon graft (from the nondominant hand)
Longitudinal split of the tendon is performed before it is transferred to the eye
Punctum is canalized to prevent injury
Retighten if the lower lid is still lax, symmetry with the normal eye is insufficient, and tearing cannot be controlled. Slide 132: Physiological methods of eye reanimation
Eye sphincter substitution in patients with unilateral, long-duration paralysis
Transplantation of free platysma muscle
Transfer of pedicled contralateral frontalis m.
Both muscles have thin flat bellies and have comparable density of innervation to that of orbicularis oculi. Slide 133: Physiological Methods of eye reanimation
Harvest the platysma muscle - through a submandibular incision
Isolation of the frontalis is carried out through a bicoronal incision
Risk: webbing at the medial canthus level
invariably requires Z-plasty revision Slide 134: Mild weakness may develop during the immediate postoperative period, but this weakness resolves typically in 3 months
Postoperative care is very important:
limit motions of the mouth and jaw to protect the coaptation sites.
A fluffy cotton roll dressing and elastic bandages is placed around the patient's head to protect the repairs.
During the first 24 hours, a plaster of Paris wrap is also utilized and subsequently removed.
Antiemetics are given to prevent vomiting in the early postoperative period.
Diet - fluids or a soft diet and speaks only through the teeth for 2 to 3 weeks. Slide 135: 6 weeks post-op –
Start massage and ultrasound treatments over the coaptation sites to prevent formation of scars around the nerves and adhesions with overlapping cheek skin flap.
Start intensive slow-pulse stimulation of the denervated muscles to prevent further atrophy while the facial fibers are elongating across the face.
Facial exercises, biofeedback, and physical therapy are important in restoring coordinated facial movements bilaterally. Slide 136: Terzia, JK & Mersa, B. Facial Reanimation. 2001. In The Unfavorable Result in Plastic Surgery, Avoidance and Treatment.
Goldwyn R.M. & Cohen, M.N., Lippincott, Williams & Wilkins; pp. 597-610. PRACTICE USING FACIALMUSCLES SELECTIVELY INFRONT OF MIRROR : PRACTICE USING FACIALMUSCLES SELECTIVELY INFRONT OF MIRROR Bell’s Palsy : Bell’s Palsy Background:
one of the most common neurologic disorders affecting the cranial nerves.
abrupt, unilateral, peripheral facial paresis or paralysis without a detectable cause. Background: : 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. Incidence: : Incidence: The incidence of Bell palsy is approximately 23 cases per 100,000 persons. Demographics: : 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. ETIOLOGY : ETIOLOGY HYPOTHESIS-
RHEUMATIC HYPOTHESIS- Berard (1936) rheumatic swellings may press the nerve (obsolete)
COLD HYPOTHESIS – Charles bell. Exposure to extreme cold or cold draught
ISCHAEMIC HYPOTHESIS – factors like cold, CO2 excess, vasomotor instability, injury toxic allergic hormonal influence
IMMUNOLOGICAL HYPOTHESIS - sensitization of lymphocytes to the peripheral mylin gives rise to cell mediated autoimmune response
VIRAL HYPOTHESIS – viral infections such as herpes zoster or herpes simplex Pathophysiology: : 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. Pathophysiology: : 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 History: : 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. History: : 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. History: : 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 Physical exam: : 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. Physical exam: : Physical exam: Bell's phenomenon—upward diversion of the eye on attempted closure of the lid—is seen when eye closure is incomplete. Physical exam: : 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 Physical exam: : 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. Investigations: : 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. Investigations: : Investigations: MRI has revolutionised the detection of tumours. Investigations: : Investigations: Topognostic tests and electroneurography may give useful prognostic information but remain research tools. Diagnosis: : Diagnosis: Bell palsy is a diagnosis of exclusion.
Other disease states or conditions that present with facial palsies are often misdiagnosed as idiopathic. Management: : 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. Management, Eye care : 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. Management, Steroid : 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. Management, Steroid : Management, Steroid Usual regimen is 1mg/kg/day for 1 week. Management, Steroid : 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. Management, Antivirals : 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. Management, Antivirals : Management, Antivirals Usual regimen is 400mg/24hrs divided into 5 doses for 7 to 10 days Bell’s palsy: : Bell’s palsy: Antivirals:
“More evidence is needed to show whether the antiviral drugs acyclovir or valacyclovir are effective in aiding recovery from Bell's palsy.”
* Allen D, Dunn L. Acyclovir or valaciclovir for Bell's palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD001869. Bad Prognostic Factor: : Bad Prognostic Factor: Complete facial palsy
No recovery by three weeks
Age over 60 years
Ramsay Hunt syndrome (herpes zoster virus)
Associated conditions—hypertension, diabetes, pregnancy
Severe degeneration of the facial nerve shown by electrophysiological testing References : References Gray’s anatomy
Anatomy: B.D Chaurasia
Maxillofacial surgery: Peter Ward Booth
(Vol I, II)
Maxillofacial surgery:Mc carthy
Internet sources Slide 166: Thank you! ???????????