meniere's disease - in detail definition, pathophysiology, investigations , management
TRANSCRIPT
Meniere's DiseaseDR. GIRISH. S
DEFINITIONA disease of membranous inner ear characterized by
EPISODIC VERTIGO FLUCTUANT SNHL TINNITUS AURAL FULLNESS
Which has its pathologic correlate-
HYDROPIC DISTENSION OF THE ENDOLYMPHATIC SYSTEM
HISTORY
The existence of peripheral vestibular disorders was proposed by Meniere in 1861.
PROSPER MENIERE, as director of a large deaf-mute institution in Paris, saw patients develop both vertigo and deafness immediately after trauma to the ear.
He concluded that both symptoms have a common inner ear origin.
HISTORY MENIERE - Autopsy of a young girl who
developed sudden hearing loss and acute vertigo.
On autopsy, found her brain was normal but the inner ear was filled with blood.
It was commonly believed well into the 20th century that Meniere's disease was caused by hemorrhage.
MENIERE'S DISEASE Prior to 1940,
"Meniere's disease" was used as a generic term for any peripheral vertigo, especially if associated with hearing loss.
HISTORY
In 1926 PORTMAN, believing Meniere’s disease was secondary to Endolymphatic hypertension, performed the first drainage operation of the endolymphatic sac
HISTORY In 1938 Hallpike and Cairns described the
underlying pathology of Meniere’s disease as being endolymphatic hydrops, but the precise etiology still remains elusive.
HISTORY
In 1985 AAO-HNS
updated the term MD should be restrictive and include only those cases with complement of classic symptoms and findings of the disease persumed to result from idiopathic EL hydrops .
ANATOMY OF COCHLEA
Fluid spaces in the cochlea are Perilymphatic space – Scala Vestibuli & Scala
Tympani Endolymphatic space – Scala media
Contd… Perilymphatic space
surrounds the membranous labyrinth and opens to CSF by cochlear aqueduct
The endolymphatic space as well as continuing throughout the membranous labyrinth is joined to the endolymphatic sac by endolymphatic duct
INNER EAR FLUIDS AND THEIR CIRCULATION
ENDOLYMPH Located in the scala media Principally secreted by
STRIA VASCULARIS PLANUM SEMILUNATUM DARK VESTIBULAR CELLS PERILYMPH ACROSS THE MEMBRANOUS LABYRINTH
Low Na+ High K+ There are two views regarding its flow
Longitudinal Radial
LONGITUDINAL PATTERN (slow process) Endolymph from the cochlea reaches saccule,
utricle & ELD and gets absorbed through endolymphatic sac which lies in the subdural space
RADIAL (rapid process) Results from production of endolymph in the dark
vestibular cells and planum semi lunatum with local absorption .
PATHOGENESIS EL hydrops occurs through over production or inadequate
absorption. ENDOLYMPH VEST. AQ. END SAC
OBSTRUCTION
Normal
Hydrops
LONGITUDINAL FLOW.Fundamental problem is ENDOLYMPHATIC MALABSORPTIVE
DYSFUNCTION
HOW THE DYSFUNCTION OCCURS?
Various explanations
Hypoplasia of the vestibular aqueduct
Narrowing of the endolymphatic duct Perisaccular fibrosis Loss of epithelial integrity and
atrophy of the sac Positive immunofluorescent staining
for Igs of the sac wall
Vascular pathology – walls of EL sac in MD shows fewer and small blood vessels than normal
Accumulation of cellular and proteinaceous debri within the sac lumen INFECTIONS
Tightly adherent dura in the region of the endolymphatic sac local sac pressure and resistance to flow malabsorption
ENDOLYMPHATIC MALABSORPTIVE DYSFUNCTION
PATHOLOGIC FINDINGS
A. ENDOLYMPHATIC HYDROPS
B. CHANGES IN PARS SUPERIOR
C. CHANGES IN HAIR CELLS
ENDOLYMPHATIC HYDROPS Physical distortion of the membraneous labyrinth.
Most consistently
found in the PARS
INFERIOR (cochlea
and saccule).
ENDOLYMPHATIC HYDROPS It is typified by bowing
of Reissner’s membrane into the scala vestibuli and the distention of the saccule
Enlargement of EL space occur at the expense of perilymphatic space.
ENDOLYMPHATIC HYDROPS Degree of endolymphatic space expansion is
variable
Endolymphatic space bulged in the region of helicotrema in 50% of cases
Saccule bulges against foot plate in 60%
Saccule bulges into SCC (in 1/3 cases)
CHANGES IN THE PARS SUPERIORUTRICLE AND SEMICIRCULAR CANALS
Less frequent Utricular dilatation and
herniation into crus commune Ampullary distorsion and
displacement of cupulae from the ampullary wall
Hair cells, along with the innervating nerves are spared.
Only in most severe cases –decrease in hair cells.
CHANGES IN HAIR CELLS
EM - fusion of cilia, disruption of cuticular bodies & basalward displacement of some OHC with loss of contact with cuticular plate .
THEORIES REGARDING GENESIS OF SYMPTOMS
I. MEMBRANE RUPTURE THEORY
Ruptures in the membranous labyrinth pathophysiology of MD.
Found in nearly all parts of the inner ear
RUPTURE
Leakage of this neurotoxic endolymph into the
perilymph
Sustained depolarization
Inactivation of the hair cells and neurons of the 8th
nerve
• Subsequent healing return of normal inner ear
function and resolution of the symptoms of
Meniere’s attack
• C/c exposure progressive irreversible
deterioration of the auditory and vestibular
functions
PHASES OF ATTACK IRRITATIVE PHASE- Increased K+ around the basal
surface of hair cells activation of vestibular nuclei PARETIC PHASE- Prolonged activation blockade of
NT release peripheral hypofunction decreased activity of vestibular nucleus
RECOVERY PHASE- Restitution of chemical composition
II. High endolymphatic pressure
Causes cochlear damage and hearing loss in MD TONNDORF – suggested mechanical distorsion and
tension in the membrane of inner ear
III. Saccular hydrops
Severe cases extend into the SCC and alter function of crista ampullaris vertigo.
Presence of such distension can also explain the positional vertigo in patients with MD
IV. Mechanical factors
Tonndorf (1968) Hydrops can mechanically alter the travelling
waves
explain certain aspects of cochlear dysfunction.
PATHOGENESIS
Excess production of endolymph
Poor absorption ofendolymph
Endolymphatic hydrops
Distension of scala media, saccule and
endolymphatic duct with marked bulging
of Riessner’s membraneRupture of Riessner’s membrane
Capillary sludging/ low perfusion
Anoxia of stria vascularis
Transudation of fluid
STRESS
Sympathetic overactivity
Internal auditory artery spasm
Inadequate vascularity of sac
Damage to neuroepithelium
Obstruction to flow
Contd…..Mixture of endo & perilymph
Increase in K+ level in perilymph
ACUTE EFFECTS Aural fullness Vertigo Temporary SN loss
CHRONIC EFFECTS Residual hearing
loss Tinnitus
CONSTITUTIONAL SECONDARY FACTORS
Meniere’s diseaseVascular
MetabolicHypothyroidism’
InfectiousSyphilis, Mumps, Herpes infection,CSOM
Allergic50% associationInner ear acting as shock organ
Psychogenicpsychological vulnarability and obscession
NeurogenicCogan’s syndrome(Hearing loss vertigo
AutoimmuneCONTRALATERAL DELAYED HYDROPS- development of Abs to inner ear antigens
Genetic (chr 6)
TERMS The triad of hearing loss, tinnitus and vertigo constitute
MENIERE’S SYNDROME If cause is unknown it is defined as MENIERE’S DISEASE. However, if a disease entity that is known to cause
endolymphatic hydrops is associated with the syndrome, the diagnosis is one of SECONDARY ENDOLYMPHATIC HYDROPS
MENIERE’S DISEASE GENETIC ANATOMICAL TRAUMATIC VIRAL INFECTION ALLERGY AUTOIMMUNITY PSYCHOSOMATIC AND PERSONALITY FEATURES
GENETIC FACTORS
Familial tendency 14-20% AD transmission Sporadic and familial cases of MD HLA-C and
HLA-A on short arm of chromosome-6 Mutation predispose to MD
ANATOMICAL Small vestibular aqueduct
TRAUMATIC Physical or acoustic trauma Trauma
Biochemical dysfunction of cells in memb labyrinth or
Simply release debri into the endolymph obstruct ELD and sac
VIRAL INFECTION Neurotropic virus Higher antibody reactivity to Herpes simplex type
I Polypeptides Herpes simplex viral DNA in ELS tissue
ALLERGY
Proposed etiologic factors
Both food and inhalants allergy
AUTOIMMUNITY
The ELS contain Ig and lymphocytes capable of generating humoral or cellular immune response
Circulating immune complexes in the serum direct cause of damage
Antibodies Vs Type II collagen found in serum of MD patients
PSYCHOSOMATIC AND PERSONALITY FACTORS
A basic disorder of personality occur in MD Emotion acts as a precipitating factor Most have an elevated obsessionality score Psychic stress in childhood Overt neurosis
MORE COMMON
SECONDARY EL HYDROPS Developmental insults ABNL metabolic and endocrine status Syphilis C/c OM Viral infection Autoimmunity Otosclerosis Leukemia
Etiological factors in 20 ELH Developmental insults like Mondini Dysplasia Abnormal metabolic and endocrine status
Metabolic states – hypoglycemia, hyperglycemia and hyperlipoproteinemia
Endocrinological associations
Hypothyroidism Adrenal pituitary insufficiency symptoms in females during premenstrual period
SYPHILIS Known cause of ELH &
Meniere’s triad of symptoms
Syphilitic osteitis of the otic capsule
Syphilitic endolymphatic
duct obstruction
Progressive over accumulation of endolymph and
subsequent rupture
C/c Otitis Media Infectious products, toxins and associated
enzymes migrating through the RW membrane in to fluids of inner ear
Osteitis from mastoiditis can affect adjacent developing sac and blood supply in Trautman’s triangle
VIRAL INFECTION as a delayed sequelae during attacks of
subclinical viral labyrinthitis
OTOSCLEROSIS When envelops vestibular aqueduct malfunction of the
ELD and sac
Otosclerosis can invade the endosteum, altering chemical characteristics of perilymph and endolymph and thus affect radial and longitudinal flow of endolymph
SYMPTOMS
Characteristics of vertigoSYMPTOMS Sudden onset Preceded by aural
fullness Feeling of to and fro
or up and down movement- Ship wrecked in storm feeling
Episodic- lasting from 20 mins to 24 hrs
Associated vomiting, anxiety
Tullio phenomenon Tumarkin drop
attacks
SIGNS Nystagmus - depending
on phase Associated
Documentable hearing loss
Spontaneous complete recovery
Absence of loss of consciousness, neurological deficits, persistant imbalance after the episode
Vertigo in Meniere’s disease IRRITATIVE PHASE- activation of vestibular nuclei
Nystagmus on same side of lesion PARETIC PHASE- blockade of NT release decreased
activity of vestibular nucleus Nystagmus on opposite side (As neuronal activity in normal side is relatively more)
RECOVERY PHASE- Restitution of chemical composition-Recovery of peripheral vestibular function after remission
Acute attacks of MD – rarely seen
Horizontal nystagmus is the cardinal finding Irritative nystagmus – towards affected ear Paralytic nystagmus – towards the normal ear Hours after attack, auditory and vestibular
symptoms subsides and nystagmus reversed towards the affected ear – recovery nystagmus
TUMARKIN CRISIS DROP ATTACKS in later stages. Occur as a result of Acute Otolithic Dysfunction Pt simply drops to the ground without warning
& can sustain # / other serious injury. There is no associated vertigo / loss of
consciousness
Existence of an EL hydrops with contact of the
saccular wall up to the internal face of the
footplate. (internal sacculostapedopexy).
This also explains the TULLIO PHENOMENON
HENNEBERT’S SIGN
HEARING LOSS
Repeated pressure trauma
Direct damage due to poor vascularityDamage to vestibular and
cochlear neuroepithelial cells
Hearing loss(lower frequencies affected first)
Clinical features
SYMPTOMS Fluctuating hearing loss More during the episode of
vertigo DYPLAUCUSIS - distorted
appearance of music Intolerability to loud sound
SIGNS Tuning fork tests s/o SNHL
PTA – low freq HL
SDS - 55-85%
Recruitment test - positive
SISI test score- >70%
Tone decay test < 20dB
SP/ AP >30%
Caloric test decreased response on affected side
Oral glycerol test
SNHL Typically fluctuant and progressive Over time, the hearing loss flattens and becomes
less variable 5-10 YEARS
SNHL
A pattern of low frequency fluctuating loss and a coincident, non changing, high frequency loss is described, a
“PEAKED” OR “TENT LIKE” AUDIOGRAM This peak classically occurs at 2KHz .
TINNITUS Subjective tinnitus Low pitched and roaring May even persist during the periods of
remissions Continuous or intermittent
TINNITUS Non pulsatile Tinnitus often begins, gets louder, or
changes pitch as an attack approaches
Later tinnitus is constant and more distracting between attacks
Mechanism of tinnitus+K Ion intoxication of outer hair cells
Contraction of outer hair cells
Tectorial membrane irritates the steriocilia of the inner hair cells
Generation of abnormal spontaneous desynchronised impulses in inner hair cells (summating potential)
TINNITUS
AAO-HNS 1995
POSSIBLE MENIERE'S DISEASE Episodic vertigo of the Meniere's type
without documented hearing loss, or
SNHL , fluctuating or fixed, with dysequilibrium but without definitive episodes
Other causes excluded
AAO-HNS 1995
PROBABLE MENIERE'S DISEASE One definitive episode of vertigo
Audiometrically documented hearing loss on at least one occasion
Tinnitus or aural fullness in the treated ear
Other causes excluded
AAO-HNS 1995 DEFINITE MENIERE'S DISEASE
Two or more definitive spontaneous episodes of vertigo 20 minutes or longer
Audiometrically documented hearing loss on at least one occasion
Tinnitus or aural fullness in the treated ear
Other cases excluded
CERTAIN MENIERE'S DISEASE Definite Meniere's disease, plus
histopathologic confirmation
Stage PTA
1 <=25
2 26-40
3 41-70
4 >70
EXAMINATION & INVESTIGATIONS
Romberg test significant instability and worsening
when the eyes are closed.
Weber tuning fork test lateralizes away from the
affected ear.
Rinne test positive.
ABC reduced .
Physical Examination
MRI • Rule out abnormal anatomy or mass lesions. • Acoustic neuromas, other CPA lesions.• MS or Arnold-Chiari malformations
CT scans• Dehiscent superior semicircular canals • Widened cochlear and vestibular aqueducts
IMAGING STUDIES
OTHER TESTS PTA SPEECH AUDIOMETRY SPECIAL AUDIOMETRY TESTS ENG ECoG CALORIC TESTS GLYCEROL TEST
Low-frequency or mixed low and high-frequency
insufficiency may be observed.
Typically, the lower frequencies are affected
more severely. This is due to preferential sensitivity of
the apex to the hydrops.
PTA
SPEECH AUDIOMETRY Discrimination score is usually 55 – 85% between the
attacks.
But it is much impaired during and immediately
following an attack.
SPECIAL AUDIOMETRY TESTS
RECRUITMENT TEST POSITIVE
SISI SCORE better than 70% in 2/3rds of
patients.
TONE DECAY TEST normally there is decay
of less than 20dB.
LOUDNESS RECRUITMENT
1. This is abnormal growth in the perceived intensity of sound
2. ABLB
3. This test is really time consuming
Detects distortion of the neural membranes of the
inner ear.
Due to perilymph pressure fluctuations and can show
evidence of cochlear involvement.
Ratio of the SP and the nerve AP in response to
auditory stimuli.
ELECTRO COCHLEOGRAPHY
ELECTRO COCHLEOGRAPHY1. Increased summating potential / action potential
ratio. 1:3 is normal
2. Widened summating potential / action potential complex. A widening of greater than 2 ms is significant
3. Small distorted cochlear microphonics
Typically causes a reduced vestibular response in the
affected ear
The direction of the spontaneous nystagmus during or
after an attack of Meniere is not a reliable indicator of the
site of the lesion.
ELECTRONYSTAGMOGRAPHY (ENG)
VESTIBULAR TESTS
1. Caloric test
2. It is low frequency stimulation (0.003 Hz) of lateral canal
3. Caloric asymmetry will point to the diseased ear
4. 20% difference between the two ears ( JONGKEE’S FORMULA ) is significant
VEMP
Measures the relaxation of sternomastoid muscle in response to ipsilateral click stimulus
This test is due to the presence of vestibulo collic reflex
Normal responses are composed of biphasic (positive-negative) waves
VEMP reveals saccular dysfunction
DEHYDRATION TESTS
1. GLYCEROL
2. FRUSEMIDE
3. ISOSORBIDE
4. UREA
5. SORBITOL
Tests are positive if there is pure tone improvement of 10dB or more at two / more frequencies between 200-2000Hz
One of the most important & commonly used
diagnostic test
Glycerol is administered orally in doses of 1.5
mg/kg in the fasting state
GLYCEROL DEHYDRATION TEST
Test is only considered positive if there is an
increase in serum osmolality of 10 mos/kg.
PTA is performed 2-3 hours after administration
A rise in threshold of at least 10db in three
consecutive octave bands were considered
diagnostic of Meniere’s disease.
GLYCEROL DEHYDRATION TEST
MANAGEMENT NON INTERVENTIONAL TREATMENT
LIFE STYLE MODIFICATIONS MEDICAL MANAGEMENT REHABILITATION
INTERVENTIONAL TREATMENT NON DESTRUCTIVE SURGICAL PROCEDURES DESTRUCTIVE SURGICAL PROCEDURES
GENERAL MEASURES REASSUARANCE CESSATION OF SMOKING (nicotine vasospasm) LOW SALT DIET AVOID EXCESS INTAKE OF WATER AVOID OVER-INDULGENCE IN COFFEE,TEA,ALCOHOL AVOID ACTIVITIES REQUIRING GOOD BODY BALANCE AVOID STRESS
ACUTE ATTACKSevere vertigo n nausea, apprehensive, head movts -> giddiness REASSUARANCE BED REST VESTIBULAR SEDATIVES
Oral/ im / iv Prochlorperazine / Promethazine Diazepam / Atropine
VASODILATORS Inhalation of Carbogen Histamine drip
VASODILATORS INHALATION OF CARBOGEN
5% CO2 + 95% O2
cerebral vasodilator, improves labyrinthine circulation
HISTAMINE DRIP Histamine diphosphate, 2.75 mg dissolved in 500
ml of glucose, given as iv drip at a slow rate good vasodilator and helps to control acute
attacks.
CHRONIC PHASE VESTIBULAR SEDATIVES VASODILATORS DIURETICS PROPANTHALINE BROMIDE ELIMINATION OF ALLERGEN HORMONES
SURGICAL TREATMENTSUsed only when medical treatment fails
SURGICAL OPTIONS Aims to achieve one or both of the two possible goals.
1. ABOLISH OR ALTER FUNCTION OF THE LABYRINTH may cause vertigo until vestibular compensation
has re-established symmetric, resting neural activity in the central pathways.
also carry the risk of hearing loss.
SURGICAL OPTIONS2. MODIFICATION OF THE UNDERLYING PATHOPHYSIOLOGY.
harder to achieve since the underlying physiology is still not well understood
SURGICAL OPTIONS
1. NONABALTIVE PROCEDURES
2. PARTIALLY ABLATIVE PROCEDURES
3. LOCAL OVERPRESSURE THERAPY
4. ENDOLYMPHIC DECOMPRESSION
5. VESTIBULAR NEURECTOMY
6. LABYRINTHECTOMY
INTRATYMPANIC DELIVERY TECHNIQUES
Direct injection through the tympanic membrane.
Injection through an inserted ventilation tube. Injection through an indwelling catheter
inserted into the middle ear. Placing a sponge through the tympanic
membrane. Injection directly into the round window niche. Minipumps.
INTRATYMPANIC DRUG DELIVERY
Direct intratympanic injection can be done in the office and is probably the easiest method.
Prior to injection, the tympanic membrane should be anesthetized.
Topical Phenol Applied Injection Of The External Auditory Canal With Lidocaine Topical Emla™ Cream (Lidocaine 2.5%, Prilocaine 2.5%)
25-gauge needle superior port to allow air to exit the middle ear and an inferior port for injection.
The middle ear generally holds 0.5 to 0.8 mL of fluid.
A brief episode of vertigo typically follows the injection
Patient should lie in a slight Trendelenberg position with the treated ear up for 30 min
INTRATYMPANIC DRUG DELIVERY
NONABALTIVE PROCEDURESINTRATYMPANIC INJECTION OF CORTICOSTEROID Corticosteroids have an anti-inflammatory effect
on the labyrinth in conditions of likely immune origin.
Steroids have been shown to influence ion transport in the labyrinth.
More helpful in the early stages of MD
INTRATYMPANIC INJECTION OF CORTICOSTEROID
Dexamethasone is now a standard therapy Repeat injections are frequently required for
recurrent symptoms. Repeat dosing at 3 months is a reasonable starting
point. Concentrations used have varied from 2 to 24
mg/mL. The risk of hearing loss is low.
PARTIALLY ABLATIVE PROCEDURES INTRATYMANIC INJECTION OF GENTAMYCIN
Gentamicin has a high vestibulotoxicity relative to its cochleotoxicity; thus, it can be used to control vestibular symptoms while sparing hearing.
Current trend single injection regimen, with additional doses only if needed to control symptoms ("titration therapy").
PARTIALLY ABLATIVE PROCEDURES GENTAMICIN diffusion through the RW
Access maybe impaired by inflammation causing
increased membrane thickness, or obstruction with fat
or fibrous tissue.
When gentamicin reaches the endolymph, it is
selectively concentrated in hair cells and supporting
cells.
Aminoglycosides destroy hair cell function by a variety of mechanisms.
They block ion currents through the stereocilia, cause adhesion of stereocilia, and ultimately, cause the hair cells to degenerate or become extruded.
Gentamicin has a greater effect on type I than on type II hair cells.
PARTIALLY ABLATIVE PROCEDURES
TRANSTYMPANIC GENTAMYCIN
Gentamycin (4mg/ml)
buffered with NaHCO3 until
pH is 6.4
Through T tube 1ml
3 injections/ day
(7am-1pm-7pm)
Lies half hour supine
with ear facing up.
LOCAL OVERPRESSURE THERAPY
Application of external pressure to the middle ear to encourage endolymphatic flow into the EL sac.
Increased endolymph pressure facilitates absorption.
MENIETT DEVICE
MENIETT DEVICE The device is a handheld air pressure generator that
the patient self-administers three times daily. The pressure is delivered in complex pulses of up to
20 cm of water over a 5-min period. The device requires ventilation tube placement in
the tympanic membrane prior to starting therapy.
ENDOLYMPHIC DECOMPRESSION
Benefits include Release of external compression on the sac Neovascularization of the perisaccular
region, allowing passive diffusion of endolymph
Creation of an osmotic gradient out of the sac
INTERNAL SHUNTS FICK ’S SACCULOTOMY CODY TACK OPERATION COCHLEOSACCULOTOMY OF SCHUKNECHT
( LABYRINTHOTOMY ) OTIC PERIOTIC SHUNT OF HOUSE & PULEC
OLD TECHNIQUES
OLD TECHNIQUES
SACCULOTOMY WAS PROPOSED BY FICK in 1964 and consisted of using a needle to puncture the saccule through the stapes footplate.
CODY TACK OPERATION Leaving a sharp prosthesis in the footplate that ruptured the saccule each time it expanded.
OLD TECHNIQUES
The OTIC-PERIOTIC SHUNT is a tube placed through the round window membrane that perforates the basilar membrane.
COCHLEOSACCULOTOMY aims to create a fracture
dislocation of the osseous
spiral lamina
(permanent fistulization of the
endolymph-containing cochlear
duct)
VARIATIONS IN EL SAC SURGERY
Simple decompression Wide decompression including the sigmoid sinus Cannulation of the endolymphatic duct EL drainage to the subarachnoid space EL drainage to the mastoid Removal of the extraosseus portion of the sac
ENDOLYMPHATIC SAC SURGERY
Simple mastoidectomy Horizontal and posterior canals
should be skeletonized and the bone over the posterior fossa thinned .
Only a thin covering of bone should be left over the facial nerve and the sigmoid sinus to allow adequate exposure of the posterior fossa dura.
The bone over the posterior fossa should be completely removed using a diamond burr .
The EL sac lies on the dura medial to the vertical segment of the facial nerve and the retrofacial air cells.
The superior aspect of the EL sac should be identified, and often lies just below a line (Donaldson's line)
Decompression of the sac requires only that the bone of the posterior fossa plate be removed.
EL SHUNTING EXTERNAL SHUNTS ( mastoid / subarachnoid )
EL SHUNTING Performed by incising the exposed sac and placing
a stent to keep the incision open. PAPARELLA AND HANSON TECHNIQUE involves
opening the edge of the sac, lysing any intraluminal adhesions, and probing the duct to insure that it is patent.
A piece of SILASTIC is placed through the incision in the sac allowing long-term drainage.
DRAINAGE TO SUBARACHNOID SPACE
More elaborate since it requires making a second incision in the posterior wall of the EL sac into the posterior fossa and a specially designed shunt tube.
DRAINAGE TO SUBARACHNOID SPACE
After the initial, lateral incision is made in the sac, a small medial incision is made to allow a shunt to be placed into the basal cistern creating a passage into the subarachnoid space .
The resulting CSF leak is controlled by placing a fascia graft over the lateral incision in the sac.
Patients can usually return to work within a week.
Although the procedure is intended to be a hearing-sparing procedure with minimal morbidity, the risk of hearing loss may be as high as 5%.
A small risk of facial nerve damage associated with the procedure.
Vestibular nerve section has a complete vertigo control rate of about 85 to 95%
80 to 90% of patients maintain their preoperative hearing.
The procedure offers much greater vertigo control rates than EL shunt procedures.
More invasive. Technically challenging procedure.
VESTIBULAR NEURECTOMY
VESTIBULAR NEURECTOMY APPROACHES TO VESTIBULAR NERVE
RETROSIGMOID / SUBOCCIPETAL MIDDLE CRANIAL FOSSA RETROLABYRINTHINE TRANSMEATAL COCHLEOVESTIBULAR
NEURECTOMY
RETROSIGMOID APPROACH Advantage of a generous exposure and a direct
view of the seventh and eighth cranial nerves. Standard suboccipital craniotomy having the
sigmoid sinus as the anterior limit of exposure. The posterior fossa dura is opened, and the
cerebellum is retracted to expose the cerebellopontine angle and petrous ridge.
The vestibular, cochlear, and facial nerves are identified, and then the superior and inferior vestibular nerves can be sectioned.
Afterward the dura is reapproximated, and the bone flap is replaced and covered as the wound is closed.
RETROSIGMOID APPROACH
MIDDLE FOSSA APPROACH Advantage - require only minimal dural violation. A vertical incision is made above the auricle and the
temporalis muscle is freed from squamous portion of the temporal bone.
A small craniotomy is made in the squamous portion of the temporal bone.
The middle fossa dura is elevated and a Fisch or House-Urban retractor is used to maintain temporal lobe elevation.
The superior SCC and geniculate ganglion are identified on the floor of the middle fossa as landmarks.
IAC is unroofed using a diamond burr. The dissection is carried out to the lateral extent
of the canal to identify "Bill's bar," which divides the facial nerve from the superior vestibular nerve.
MIDDLE FOSSA APPROACH
The dura of the posterior aspect of the canal is incised and the superior vestibular nerve is identified.
As the superior vestibular nerve is retracted, the inferior vestibular nerve can be identified, taking care to avoid the internal auditory artery and cochlear nerve.
MIDDLE FOSSA APPROACH
Often it is difficult to definitively separate the inferior vestibular nerve from the cochlear nerve, which can lead to remaining vestibular symptoms after surgery or hearing loss.
Upon nerve sectioning, the internal auditory canal can be covered with fascia, the bone flap replaced, and the incision closed.
MIDDLE FOSSA APPROACH
LABYRINTHECTOMY most destructive procedure in the treatment of
Meniere's as it destroys both hearing and vestibular
function.
Ideal candidates are those who have no hearing and
have failed more conservative treatments
Higher rate of vertigo control than vestibular
neurectomy and improves quality of life in 98% of
patients.
APPROACHES
LEMPERT’S TRANSCANAL
TRANSMASTOID (better exposure / more
popular )
LABYRINTHECTOMY
LEMPERT’S TRANSCANAL LABYRINTHECTOMY
Posterior annulus curetted for exposure
Ampullary ends of SCC probed to ensure destruction of neuroepithelium.
TRANSCANAL APPROACH
A variation on this basic technique involves drilling out the promontory to connect the OW and RW.
Posterior ampullary nerve is sectioned
Vestibule filled with absorbable gelatin sponge/fat graft
The limitation is the poor access it yields to the posterior canal, located medial to the facial nerve; thus, complete ablation may not be achieved.
The limited exposure also makes the procedure more technically difficult than the transmastoid approach.
TRANSCANAL APPROACH
TRANSMASTOID APPROACH Advantage of allowing direct visualization of the vestibular
end organs as they are removed. Standard mastoidectomy Identification of the SCC. The canals can then be blue-lined and followed medially to
the vestibule while removing the neuroepithelium under direct vision.
Complete loss of hearing is an expected
outcome.
Can preserve hearing by packing the SCC with
bone wax & using a diamond burr to remove the
canal while preserving the vestibule.
LABYRINTHECTOMY
REHABILITATION
HEARING AIDS
VESTIBULAR REHABILITATION
For patients who responded to medical or
surgical treatment for vertigo but have
some remaining disequilibrium.
THANK YOU…!