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Facial nerve




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Facial nerve Document Transcript

  • 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.