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1. FACIAL NERVE
4 FUNCTIONAL COMPONENTS – Facial N. is the nerve of the 2nd
pharyngeal arch.
1. Branchial Motor
(Sp. Visceral Efferent)
(Largest portion)
Voluntary control
VII Nucleus
2. Visceral Motor
(General visceral efferent)
Superior salivary nucleus
and lacrimatory nucleus
3. Special sensory, (Special
afferent)
Genicular Ganglion
4. General sensory
(General afferent)
Genicular Ganglion
– Muscles of facial expression
– Posterior belly of diagastric
– Stylohyoid
– Stapedius
- Parasympathetic innervation of lacrimal,
submandibular and sublingual glands
- Mucous membrane of nasopharynx, hard and
soft palate.
- Taste sensation from anterior 2/3 of tongue.
- Hard and soft palate
General sensation from the skin of concha of the
auricle and a small area behind ear.
BRANCHIAL MOTOR COMPONENT
Origin and central course:
The branchial motor component originates from the motor nucleus
of CN VII in the caudal pons.
Fibres leaving the motor nucleus of CN VII initially travel medially
and dorsally to loop around the ipsilateral abducens nucleus (CN VI)
producing a bulge in the floor of 4th
ventricle – FACIAL COLLICULUS.
Fibres exit the ventrolateral aspect of the brain stem at the caudal broder
of pins in conjuction with nerves intermidius components of CN VII.

2. INTRACRANIAL COURSE
Upon emerging from the ventrolateral aspect of the caudal border
of the pons, all the components of facial nerve enter the internal auditory
meatus along with the fibres of vestibulocochlear nerve. Facial nerve
passes through the facial canal in the petrous portion of temporal bone.
The cause of the fibres is along the roof of the vestibule of inner ear,
posterior to cochlea. At the geniculate ganglion the components of the
facial nerve take different pathways. Branchial motor component passes
through the geniculate ganglion without synapsing, turn 900
posteriorly
and laterally before curving inferiorly just medial to the middle ear to exit
the skull through the STYLOMASTOID FORAMEN.
The nerve to the stapedius muscle is given off from the facial nerve
in its cause through the petrous portion of the temporal bone.
EXTRACRANIAL COURSE AND FINAL INNERVATION
The posterior auricular nerve, nerve to posterior belly of diagastric
and the nerve to stylohyoid muscle are given upon the facial nerves exit
from stylomastoid foramen. The remaining fibres enter the substance of
the parotid gland and divide to form the
- Temporal
- Zygomatic
- Buccal
- Mandibular
- And cervical branches that innervate the muscles of facial
expression.
VOLUNTARY CONTROL OF MUSCLES OF FACIAL EXPRESSION.
It originates in the motor cortex is in association with other cortical
areas) and pass via the corticobulbar tract in the posterior limb of the
internal capsule to the motor nuclei of facial nerve.

3. Fibres pass to both, the ipsilateral and contralateral motor nuclei of
facial nerve in the caudal pons.
- The portion of the nucleus that innervates the muscles of forehead
receives corticobulbar fibres from both, the contralateral and
ipsilateral motor cortex.
- The portion of the nucleus that innervates the lower muscles of
facial expression receives corticobulbar fibres from only the
contralateral motor cortex.
This is very important clinically as central (upper motor neuron)
and peripheral (lower motor neuron) lesions will present differently.
LOWER MOTOR NEURON (LMN) LESION:
It results from damage to motor nucleus of facial nerve or its
axons.
A LMN lesion results in the paralysis of all muscles of facial
expression (including those of the forehead ipsilateral to the lesion.
Clinical correlation
Bell’s Palsy- A LMN lesion occurs at or beyond the stylomastoid
foramen is commonly called – Bells Palsy.
- A LMN lesion is conjunction with deficits associated with abducens
nerve indicate a lesion in the brainstem which affects both, the
motor nucleus of facial nerve and abducens nucleus.
- A LMN lesion in conjunction with deficits associated with
vestibulocochlear nerve are characteristic of a lesion in the region of
the internal acoustic meatus. Eg. Acoustic Neuroma.
- Upper motor neuron (UMN) lesion:
Results in damage to neuronal cell bodies in the cortex or their
axons that project via the corticobulbar tract through the posterior limb
of the internal capsule to the facial nerve motor nucleus.

4. Voluntary control of only lower nucleus of facial expression on the
side control lateral to the lesion will be lost. Voluntary control of the
muscles of the forehead will be spared due to bilateral innervation of the
portion of the motor nucleus (CV VII). That innervates the upper muscles
of facial expression. UMN lesions are usually due to stroke.
Characteristics of an UMN lesion of facial nerve
- Facial asymmetry
- Atrophy of muscles of lower portion of face on affected side
- No eyebrow droop
- Intact folds on forehead
- Intact conjunctival reflex
- Smoothing of nasolabial folds on affected side.
- Lips can’t be held tightly together or pursed.
- Difficult to keep food in mouth while chewing on affected side.
- Distinguishes UMN from LMN lesion.
VISCERAL MOTOR COMPONENT
- Parasympathetic component of facial nerve. Consists of efferent
fibres which stimulate secretion from submandibular, sublingual,
and lacrimal glands as well as mucous membranes of nasopharynx
and hard and soft palates.
ORIGIN AND CENTRAL COURSE
The visceral motor component originates from a diffuse collection
of cell bodies in the caudal pons just below the facial nucleus –
SUPERIOR SALIVATORY NUCLEUS. Fibres exit the ventrolateral aspect
of the brainstem at the caudal border of the pons as part of the nervus
intermedius portion. These don’t’ loop around the abducens nucleus. The

5. nerves intermedius exists the brainstem just lateral to brachial motor
component.
INTERNCRANIAL COURSE
Upon emerging from the pons, all the components of facial nerve enter
the internal auditory meatus along with the fibres of the
vestibulocochlear nerve. Within the facial canal the visceral motor fibres
divide into 2 groups
1) Greater petrosal nerve
2) Chorda Tympani
Greater petrosal nerve- lacrimal, nasal and palatine glands chorda
tympani- Submandibular and sublingual glands.
COURSE OF GREATER PETROSAL
At the geniculate ganglion it turns anteriorly and medially exiting
the temporal bone via the petrosal foramen and enters the middle cranial
fossa. It passes deep to the trigeminal ganglion to enter the foramen
lacerum. The nerve traverses the foramen and enters a canal at the base
of the medial pterygoid plate in conjunction with sympathetic fibres (deep
petrosal nerve) branching from the plexus following the internal carotid
artery. The parasympathetic and the sympathetic fibres together make
up the nerve of the pterygoid canal. On existing the canal, preganglionic
parasympathetic fibres of facial nerve synapse in the pterygopalatine
ganglion which is suspended from the fibres of the maxillary division of
the trigeminal nerve (V2) in the pterygopalatine fossa.
COURSE OF CHORDA TYMPANI
The preganglionic fibres of the chorda tympani branch from the
other fibers of facial nerve as they pass the facial canal just posterior to

6. the middle ear. The fibres pass through the middle ear in close
relationships with the tympanic membrane and exit the base of the skull
to enter the infratemporal fossa. Here in the fossa the chorda tympani
joins the fibres of the lingual branch of mandibular division of (V3)
trigeminal N. the (CN VIII) preganglionic fibres synapse in the
submandibular ganglion suspended from the lingual nerve (V3). Post
ganglionic fibres then either enter the submandibular gland directly or
follow the lingual nerve before branching to innervate the sublingual
gland.
SPECIAL SENSORY COMPONENT:
Afferent fibres that convey taste information from anterior 2/3 of
the tongue and hard and soft palates
PERIPHERAL COURSE:
Chemoreceptors of taste buds located on anterior 2/3 of the
tongue and hard and soft palates, initiate receptor potentials in response
to chemical stimuli. The taste buds synapse with the peripheral
processes of special sensory neurons from facial nerve. These neurons
generate action potentials in response to the taste bud’s receptor
potentials. The peripheral processes of these neurons follow the lingual
N. and then chorda tympani to the petrous portion of the temporal bone
(as the path followed by efferent visceral motor fibres)
CENTRAL COURSE:
The central processes of the special sensory neurons pass from the
geniculate ganglion through the facial canal and enter the brainstem as
part of the nervous intermedium portion. The fibres then join the caudal
portion of tractus solitarius and ascend to synapse in nostral portion of
the nucleus solitarius (gustatory nucleus(. Nucleus solitarius project

7. both, ipsilaterally and contralaterally to the ventral posteromedial (VPM)
nucleus of the thalamus.
Tertiary neurons from the thalamus project via the posterior limb
of the internal cortex to the area of the cortex responsible for taste.
GENERAL SENSORY COMPONENT
- Minor component
- Afferent fibres which convey the general sensory information from
the skin of the concha of the external ear from a small area of the
skin behind the ear.
It may also supplement the mandibular division of trigeminal N in
providing sensation from the wall of the acoustic meatus and the outer
surface of tympanic membrane.
CENTRAL COURSE:
Cell bodies of these primary sensory neurons reside in the
geniculate ganglion. The peripheral processes of these neurons pans
from the skin of the external ear and small region of skin behind the ear
through the stylomastold foramen, in conjunction with the fibres of
branchial motor. They then course through the petrous portion of
temporal bone to the geniculate ganglion. From here, the central
processes of the general sensory fibres travel through the facial canal of
the petrous portion of temporal bone and exit in the internal acoustic
meatus.
The central processes then enter the brain stem as part of nervus
intermedius. These fibres then descend in the spinal tract of trigeminal
N. To synapse in the spinal tract of trigenimal nerve to synapse in the
spinal nucleus of trigeminal nerve.

8. Ascending secondary neurons originating from the spinal nucleus
of trigeminal nerve project to the contralateral VPN (ventral
posteromedial) nucleus of the thalamus via the anterolateral system.
Tertiary neurons from the thalamus project via the posterior limb
of the internal capsule to the sensory cortex of the post – central gyrus.
PERIPHERAL LESIONS
By using the knowledge of the anatomy of the facial nerve, the
location of a lesion can be determined by the presence or absence of
certain deficits.
A lesion of the facial proximal to the branching of the greater petrosal
nerve and chorda tympani is characterized by the following:
- Paralysis of all the muscles of facial expression ipsilateral to the
lesion (LMN lesion of brachial motor component).
- Loss of secretion from lacrimal gland and mucous membrane of
nasal and oral pharynx ipsilateral to the lesion (lesion of greater
petrosal N, visceral motor component).
- Loss of secretion from submandibular and sublingual glands
ipsilateral to the lesion (lesion of chorda tympani, - visceral motor
component.
- Loss of taste from anterior 2/3 of tongue ipsilateral to the lesion
(lesion of chorda tympani, special sensory component).
- Loss of general sensation from concha of external ear and small area
of skin behind the ear (general sensory component).
- Deficits in heaving and/ or vestibular functions ipsilateral to the
lesion (associated with vestibulocochlear N).
- Intact general sensation of the tongue (supplied by trigeminal N).
- If the lesion was distal to the greater petrosal nerve but proximal to
the chorda tympani the patient would present as above, except that

9. the secretory functions of lacrimal, nasal and palatine glands would
be intact.
- A lesion which affected the lingual N just distal to its junction with
chorda tympani would present as follows:
- Loss of secretion from submandibular and sublingual glands
ipsilateral to the lesion (visceral motor component).
- Loss of taste from anterior 2/3 of tongue ipsilateral to the lesion (sp.
Sensory component).
- Loss of general sensation from the tongue (general sensory
component of trigeminal N.)
FACIAL NERVE PARALYSIS
- Twitching, weakness a paralysis of the face is a symptom of same
disorders involving the facial N. It is not a disease itself. It may be
caused due to circulatory disturbances, injury, infection or tumour.
They are accompanied by heaving impairment.
DIAGNOSIS OF FACIAL NERVE DISORDERS
An extensive evaluation is often necessary to determine the cause
of the disorder and localize the area of nerve involvement.
1. Stapedius nerve test – (Hearing test)
- Determines disorders in the delicate heaving mechanism.
Impedance audiometry records the presence or absence of
stapedius muscle contraction.
Absence of reflex – Lesion proximal to stapedius N.
2. Petrosal nerve test – (Tear test)
Schirmer test- Quantitative tear production evaluation.
- Implies a lesion at a proximal to geniculate ganglion X ray.
- CT scan, with and without contrast is preferred for lesions of
internal acoustic meatus, posterior fossa and brain stem.

10. Higher resolutions for base of skull lesions
- MRI scan is best for soft tissue assessment of tumours and
infection.
3. Electrical tests
a) Nerve excitability tests
Determines the extent of nerve fiber damage in total paralysis.
Test may be normal inspite of paralysis of fare indicating better
outlook for return of function.
b) Electroneurography
Measures muscle response to electrical stimulation
c) Electromyography
For long standing cases. Determines if muscles/ Nerves
BELL’S PALSY
- The most common condition resulting in facial nerve weakness or
paralysis is Bell’s palsy, named after Sir Charles Bell who Ist
described the condition. The underlying cause of this condition is
not known but it may be due to a virus infection of the nerve. This
swelling results in presence on the nerve fibres and their blood
vessels, causing facial paralysis.
- 0.2% population is affected
- Middle aged people are more affected and a higher tendency in
women
- Diabetics have 4 times greater chance to develop Bell’s Palsy, Last
trimester of pregnancy is also a time of increased risk of Bell’s Palsy.
Bells Palsy is caused by inflammation within a small bony tube
called fallopian canal. This canal is extremely narrow. An inflammation
within it is likely to exert presence on the nerve, compressing it.
Likewise, if the nerve itself becomes inflamed within the canal it
encounters pressure with the result of compression. The nerve has yet

11. not exited the skull and divided into its several branches, resulting in
impairment of all functions controlled by the 7th
crania, nerve. If only a
part of the face is affected the condition is not “Bell’s Palsy.” E.g. If the
mouth area is weak but the forehead moves, Bells Palsy is ruled out.
Facial muscles differ from skeletal muscles is that they do not
immediately begin to atrophy from lack of use. Facial N is one of the 12
cranial nerves. Thus all the facial muscles are not affected. The muscles
that close the eyelid are controlled by facial N. but not the muscles that
control eye movements. Chewing and swallowing are other examples
which are not affected.
SIGNS AND SYMPTOMS OF BELL’S PALSY
- Bell’s Palsy begins with slight pain around one ear followed by
abrupt paralysis of the muscles of that side of the face.
The following are the characteristics indication on the affected side:
- Marked facial asymmetry
- Eyebrow droop
- Smoothing out of forehead and nasolabial folds
- Dropping of the corner of the mouth
- Uncontrolled tearing
- Unable to close eye
- Difficulty in keeping food in mouth while chewing on affected side
- Lips can’t be tightly held together or pursed.
The degree of paralysis should peak within several days of onset-
never longer than 2 weeks.
- Viral and bacterial infections and autoimmune disorders are the
common causes of Bell’s Palsy.
HERPES SIMPLEX 1.
- HSVI was suggested as a cause of Bell’s Palsy. Exposure to HSVI is
common during childhood. The active virus runs throughout its

12. course without blisters (only 15% cases develop blisters). After the
active stage, in the dormant stage it resides on the nerve tissue.
When the latent virus reactivates at the facial N. The immune
system produces antibodies which cause inflammation. If the
location of inflammation is in the fallopian canal it causes pressure
on the nerve leading to temporary paralysis.
RAMSEY HUNT SYNDROME
- Causative virus is varicella zoster virus (VZV) which is the virus that
causes chicken pox. The virus resides on the nerve tissue in
dormant state on the nerve ganglia after the initial infectious stage.
When the virus is reactivated the resulting blisters are called
“Shingles”.
In addition to the classic symptoms of Bells Palsy there are
additional symptoms.
a) Pain – Acute pain behind the ear and inside the ear which is very
severe.
b) Vertigo –
c) Hearing loss
d) Blisters – Shingles in the ear. They last for 2-5 weeks and are very
painful.
e) Swollen and tender lymph nodes near affected area.
HIV / AIDS
HIV can cause facial paralysis and increase chance of developing
Ramsey Hunt Syndrome and Bells Palsy. Early stages of HIV paralysis is
due to viral infection. Later stages paralysis is due to opportunistic
infections.
BACTERIAL TRIGGERS

13. 1) Lyme disease – Causes facial paralysis and same signs and
symptoms as Bell’s Palsy. Bacteria enter the body through the skin
at the site of thick bite. Early symptom is a red ring around the site
of the bite and flu like symptoms.
2) Otitis Media – Bacteria from acute or chronic middle ear infections
can invade the canal around the nerve through small portals.
Bilateral:
Bell’s Palsy and Ramsey Hint Syndrome can be bilateral although
extremely rare.
Mononucleosis, flu, Guillain-Basre syndrome, Lyme disease are
potential triggers for bilateral palsy.
MELKERSSON – ROSENTHAL SYNDROME-
- Can be unilateral/ bilateral palsy. It is recurrent. More ever there is
a fissured tongue and non-pitting oedema of the face.
MEDICAL TREATMENT
Although same patients recover spontaneously, the after effects in
the remaining 10% - 20% can be severe and distressing. Corticosteroids
result in 80%-90% complete recovery.
- Prednisolone 20 mg four times a day for 5 days and then tailed off is
recommended.
- Combination of oral acyclovir 400 mg 5 times a day with oral
prednisolone 1mg/ Kg daily for 10 days is more effective.
- Use of vasodilators e.g. Histamine are helpful in some cases.
SURGICAL TREATMENT
Surgical decompression aims at relieving the pressure on the facial
N. and restoring its circulation again.
1. Mastoid decompression of facial nerve

14. - It is performed when the nerve function is deteriorating.
- Incision is made behind the ridig mastoid bone around the swollen
nerve which is removed, relieving the pressure.
The degree and rapidity of facial nerve function depends upon
the amount of damage present in the nerve at the time of the
surgery.
Recovery takes 3 – 12 months and may not be complete.
2. Middle fossa facial nerve decompression
- At times deeper portions of the facial N are affected.
- The incision is made above the ear with removal of small portion of
the skull.
- Mastoid and middle fossa facial nerve decompression
- It s a combination of the above 2 procedures.
RISKS AND COMPLICATIONS OF FACIAL NERVE SURGERY
1. Hearing loss – some hearing impairment in operated ear
immediately following surgery. This is due to fluid and swelling in
mastoid and middle ear. It subsides in 2-4 weeks and hearing
returns to preoperative level.
2. Dizziness – Due to swelling of the inner ear structures. Some
unsteadiness persists for a few days post operatively.
3. Related to middle fossa approach:
a) Hematoma (collection of blood under skin incision)
b) Cerclorospinal fluid leak
c) Infection which may lead to meningitis
d) Temporary paralysis of half the body due to swelling in the
brain.
EYE CARE

15. The most complication that may develop as a result of total facial
N. paralysis is a ulcer of the cornea of the eye. Te eye or the affected side
should be protected by keeping it moist.
- Using the eye with the back of the finger is an effective way to keep
the eye moist.
- Glasses must be worn outside to prevent dust from entering the eye.
- Artificial tears are used in cases of dry eye.
- At times it is necessary to tape the eyelid
- In long standing facial paralysis cases, it may be necessary to insert
a gold weight or a spring into the eyelid to help close it.
INJURIES OF THE FACIAL NERVE
- The most common cause of an injury is a skull fracture
- May occur immediately or develop some days later due to nerve
swelling
- Facial nerve injuries may occur due to operations on the ear. This
generally occurs when the nerve is not in its normal anatomical
position or when the nerve is distorted by middle ear disease.
Treatment:
Depends on the extent of nerve damage
Medical treatment – Same as Bell’s Palsy
Surgical treatment:
a) Decompression
b) Middle fossa decompression
c) Facial nerve graft- Necessary if the damage to the nerve is extensive.
A skin sensation nerve is removed from the neck and transplanted
into ear bone, to replace diseased portion of facial nerve.
TUMORS

16. Acoustic Tumors:
The most common tumor to involve the facial nerve is a
nonmalignant fibroid tumor of the vestibulocochlear nerve, the acoustic
tumor. Although there is now weakness of the face before surgery, tumor
removal results in weakness or paralysis of the face. This subsides in
several months. It may be necessary to remove a portion of the facial N to
remove the acoustic tumor. Rarely it may be possible to sew the nerve
ends together a insert a nerve graft at the time of surgery. Later a nerve
anastomosis surgery is carried out connecting the hypoglossal N to the
facial N. the face is totally paralyzed until the nerve regrows.
FACIAL NERVE NEUROMA
A nonmalignant fibroid growth which may grow in the facial nerve
itself.
- It may or may not produce a gradual facial N paralysis. Removal of
the neuroma involves removal of affected facial nerve portion.
Usually a graft is possible at the time of surgery. (Graft taken from
skin sensation nerve). When portion of facial N nearest to the brain
is destroyed, then a facial reanimation procedure is necessary.
FACIAL REANIMATION:
1. Eyelid surgery: implantation of gold or a spring into the upper eyelid
can be helpful in counter balancing the lifting eyelid muscle.
2. Hypoglossal- Facial nerve anastomosis-
Connection of a portion or all of the tongue N to the facial N may
provide a good tone to the face. Facial movements are obtained by
attempting to move the tongue to the involved side when a smile is
desired.
3. Temporalis muscle transposition:

17. Transferring one of the jaw muscles to the corner of the mouth
improves facial symmetry. Smiling is relearned by attempting to bite
at the same side.
4. Miscellaneous
A face life or removal of excess skin at the brown or cheek can be
carried out.
- Some patients who have faulty return of facial function,
selective cutting of facial N branches facial muscles may be of
benefit.
OTHER FACIAL NERVE DISORDERS
1. Facial spasm- surgery to correct this problem may involve (a)
Intentional weakening of nerve through an incision on the face or (b)
relieving pressure on the nerve adjacent to the brain.
2. Mastoid infection:
It is due to acute or chronic middle ear infections. In acute
infections the weakness usually subsides as the infection is
controlled and the swelling around the nerve subsides.
In chronically infected ears there is pressure from a cholesteatoma
(skin lined cyst).
3. Post operative facial nerve weakness
Delayed weakness or paralysis following reconstructive middle ear
surgery is uncommon, but occurs at times due to swelling of the
nerve during healing period.
4. Hemifacial spasm – uncommon disease of unknown cause which
results in spasmodic contractions of one side of the face.
5. Brain disease- Tumors and circulatory disturbances of the nervous
system may cause facial N paralysis eg. Stroke.
NEUROMUSCULAR RETRAINING FOR FACIAL PARALYSIS

18. Neuromuscular retraining (NMR) for facial paralysis is a marriage
of neurophysiology, psychology, therapeutic sciences, earning theory and
art, it uses selective motor training to facilitate symmetrical movement
and control undesired gross motor activity (synkinesis). The patients are
instructed to perform small, specific movements on the contralateral
side.
FACIAL EXERCISES
FRO- Raise your eyebrow
COR, PRO – Bring your eyebrows down and together
OCS, OCI – Gently close eyes
OCS, OCI – Squint your lower eyelids up
OCS, OCI – Close your eyes tightly
DIN – Flare nostrils
RIS, ZYJ, ZYN, LAO, LLS – Smile evenly with lips together
RIS, ZYJ, ZYN, LAO, LLS – A big wide smile with lips apart.
LLS, LAO – Raise upper lip while wrinkling your nose
RIS – Move the corner of the mouth back towards the ear
OOS, OOI – Pucker the lips
OOS, OOI – Press lips together
OOS, OOI – Pull lips back and over the teeth
OOS, OOI – Push the lips out as far as you can
OOI, DAO, DLI – Roll lower lip out and down
DAO, DLI – Turn corner of mouth downwards
DAO, DLI – Pull lower lip down to expose lower teeth
MEN – Tighten the chin
PLA – Tighten the neck
DENTAL ASPECTS OF FACIAL PARALYSIS

19. - Results in poor soft tissue cleansing and accumulation of food
debris in the vestibules.
- Excessive plaque or the teeth an affected side
- Where there is residual palsy, saliva may leak from the affected side
and cause angular stomatitis, leading to a cosmetic defect.
- Construction of a splint to support the angle of the mouth may then
improve aesthetics.
- A facial graft or facial lypoglossal nerve anastomosis may reduce the
cosmetic deformity.
CROSS REFERENCE
1. Orofacial problems associated with bilateral VII cranial N. Palsy –
Francis ST and PM Banasik – JADA 1977 Vol 95 Pg 315- 318.
Permanent bilateral facial palsy is rate and can cause multiple
problems for the dentist. Case report:
A 35 years man developed left facial N paralysis followed by the right side
after 6 months. Dizziness, nausea and vomiting and ataxia slowly
appeared
The extraoral examination revealed classical facies of bilateral Bell’s
Palsy. Xerostomia was evident.
Oral hygiene was poor, severe caries and gen. periodontal disease.
Treatment:
- All remaining maxillary/ mandibular teeth were extracted.
Methylcellulose 1% aqueous solution was prescribed to reduce
xerostomia.
- The palsy and xerostomia would affect denture dentition.
- Conventional dentures were fabricated. Marked reduction in
xerostomia was seen as the oral cavity was sealed from the ambient
air.
- Mandibular denture had an attached lip support.

20. - Vertical grooves were placed distal to the cuspid.
A 19 gauge wire was bent to fit the groove and extended horizontally
over the lip at the right commissure. This end was affixed by cold
cure resin. The denture was then inserted and the wire was made to
follow the contour of the lower lip. It was then bent over the lip at
the left commissure and attached to the left side in the same
manner.
Treatment resulted in better esthetic, physiologic and psychological
improvement.
2. Prosthodontic Management Of A Patient With Neurological Disorder
After Resection Of Acoustic Neuroma
- H. C. Karkazis – JPD 2002; Vol 87 Pg 419-422.
The acoustic neuroma originates just inside the internal antitory
meatus, eventually causes displacement of adjacent brain tissue as
well as trigeminal, glossopharyngeal facial and vagus nerves. This
causes unilateral facial paralysis, ataxia, dysphoria, dysarthria and
dysphagia.
Prosthodontic management for an edentulous patient with severe
neurological disorders after the neuroma was resected is described.
Establishment of a neutral zone in such patients is a challenge.
Clinical report: A 85 year man had a history of a large acoustic
neuroma removed from the right side. Due to reduced pharyngeal
sensation and poor gag reflex, during impression making the excess
material was immediately removed from the PPS area. A medium
body polyether was used for the final impression due to high
viscosity. A properly fitting maxillary rim was placed in the maxilla.
During the procedure, the paralyzed lip was retracted to create
symmetry on tooth sides.

21. A thick mix of tissue conditioning material (TCM) was adapted to the
top of the mandibular rim. It was placed in the mouth with
maxillary rim and patient was asked to perform the normal
movements. After initial set, it was removed and trimmed, then
replaced in the mouth. The repeated swallowing actions guided the
mandible to close in centric relation. The second base was then
placed on the cast, buccal and lingual indices were fabricated with
silicone putty. The tem was removed and molten was wax filled in its
place. The final VDO and centric was determined in the patients
mouth.
- Teeth setting was done. Mandibular posterior teeth were positioned
in the recorded neutral zone area.
Dentures were processed in the usual manner. During finishing no
denture base acrylic was removed from the polished surface.
The neutral zone mandibular complete denture addressed the need
to maximize muscle control.
REFERENCES
1. Gray’s Anatomy.
2. human Anatomy – B. D. Chaurasia.
3. Oral Medicine, diagnosis and treatment – Burket’s.
4. Text Book on Oral Pathology – Shafer, Hine, Levy.
5. Manual of Practical Anatomy – Cunninghams.
6. JADA Vol 95 Aug 1977 Pg 315.
7. JPD 2002 Vol 87 Pg 419-422.