Disorders of vestibular system 04.04.16-dr.davis
-
Upload
ophthalmgmcri -
Category
Healthcare
-
view
377 -
download
1
Transcript of Disorders of vestibular system 04.04.16-dr.davis
DISORDERS OF VESTIBULAR
SYSTEM DR. DAVIS THOMAS
DR. DAVIS THOMAS
2
Introduction Basic inputs - vision, proprioception, and
vestibular system Provide ocular stability, gait control, and
balance Disorders of vestibular system are major
disruptors causing spatial disorientation Many causes of dizziness, vertigo when
caused by a loss of vestibular function Management strategies for vestibular
disorders has continued to evolve
3
Pathophysiology Balance requires –
Normal functioning vestibular systemInput from visual system (vestibulo-ocular)Input from proprioceptive system (vestibulo-spinal)
Central causes compromise central circuits that mediate vestibular influences on posture, gaze control, autonomic fx
Disruption of balance between inputs results in vertigo
Goal of treatment: restore balance between different inputs
4
Pathophysiology Vestibular system influences autonomic
system Intimate linkage in brainstem pathways
between vestibular and visceral inputs Alteration of vestibular inputs results in:
nausea, vomitingPallorRespiratory/circulatory changes
5
Vestibular Neuritis Sudden onset of peripheral vertigo Usually without hearing loss Period of several hours - severe Lasts a few days, resolves over weeks Inflammation of vestibular nerve -
presumably of viral origin Spontaneous, complete symptomatic
recovery with supportive treatment Treatment aimed at stopping inflammation
6
BPPV Most common cause Dysfunction of posterior SCC Cupulolithiasis vs. Canalithiasis Cupulolithiasis
Calcium deposits embedded on cupulaPSCC becomes dependent on gravity
CanalithiasisCalcium debris (otoconia) displaced into PSCCDoes not adhere to cupula
7
BPPV Head movements
Looking upLying downRolling onto affected ear
Result in displacement of “sludge” / otoconia Vertigo lasting a few seconds Treatment approaches
Liberatory maneuversParticle repositioningHabituation exercises
8
BPPV Epley Canalithiasis Canalith repositioning Move into vestibule Cure rates
80% - one treatment100% - multiple
9
BPPV - Epley
10
Vertebrobasilar insufficiency Vertigo, diplopia, dysarthria, gait ataxia
and bilateral sensory & motor disturbance
Transient ischemia - low stroke risk Antiplatelet therapy - aspirin 325mg qD Ticlid
Platelet aggregate inhibitorRisk of life-threatening neutropeniaOnly in patients unable to tolerate aspirin
11
Migraine Concomitant vertigo and disequilibrium Headache control improves vertigo Diagnostic criteria
Personal/family historyMotion intoleranceVestibular symptoms - do not fit other
causes Theories - vascular origin, abnormal
neural activity (brainstem), abnormal voltage-gated calcium channel genes
Meniere’s Disease
History 1861 – Prosper Meniere describes classic symptoms
and attributes to labyrinth
1871 – Knappin theorizes dilatation of membranous Labyrinth
1938 – Hallpike and Portman confirm endolymphatic hydrops via temporal bone histology
1972 – AAOO defines the disease criteria
1985 – AAO-HNS revises the definition and establishes reporting protocols
1995 – AAO-HNS revises the definition and reporting protocols again
Definition: A disease of the membranous inner ear
characterised by deafness, vertigo and usually tinnitus , which has as its pathologic correlate hydropic distension of the endolymphatic system.
Meniere’s disease Synonym – endolymphatic hydrops Idiopathic Menier’s syndrome – secondary Trauma Viral infections Syphilis Cogan’s syndrome Otosclerosis Autoimmune diseases
AAO-HNS CHE 1995 Meniere’s is diagnosed by
Episodic Vertigo○ Spontaneous, lasting minutes to hours○ Recurrent, must have 2 episodes > 20 min.○ Nystagmus during episodes
Fluctuating Hearing loss○ Avg (250, 500, 1000) 15 dB < Avg (1000, 2000, 3000)
or○ Avg (500, 1000, 2000, 3000) 20 dB > than other ear ○ For bilateral disease Avg (500, 1000, 2000, 3000) > 25
dB in the studied earRoaring Tinnitus
Aural pressure
Lermoyez syndrome Variant of meniere`s Reversed meniere`s Initially hearing loss and tinnitus develop which
persist for prolonged periods. Then vertigo develops with improvement of
hearing and tinnitus TUMARKIN CRISES: sudden unexplained fall
without loss of consciousness or associated vertigo.
deformation of otolithic membrane of utricle or saccule
Cochlear hydrops - only features of cochlear
involvement - vertigo is absent - block at the level of ductus reunionsVestibular hydrops - typical episodic vertigo - cochlear functions are normal
CLASSIFICATION OF ENDOLYMPHATIC HYDROPS
I. 1.PRIMARY 2.SECONDARY(SYPHILIS)
II. 1.EARLY ONSET 2.DELAYED ONSET
III. 1.TYPICAL 2.ATYPICAL
IV. 1.VESTIBULAR 2.COCHLEAR
AAO-HNS CHE 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 causes excluded See staging chart
Certain Meniere's disease Definite Meniere's disease, plus histopathologic confirmation
See staging chart Stage PTA 1 <=25 2 26-40 3 41-70 4 >70
AAO-HNS CHE 1995 Possible Meniere's disease
Episodic vertigo of the Meniere's type without documented hearing loss, or
Sensorineural hearing loss, fluctuating or fixed, with dysequilibrium but without definitive episodes
Other causes excluded
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
Stage PTA1 <=252 26-403 41-704 >70
Aetiology Genetic Anatomical Traumatic Viral infection Allergy Autoimmune Psychosomatic
Pathophysiology Endolymphatic hydrops leads to distortion of membranous
labyrinth
Reisner’s membrane can be seen bulging into the scala vestibuli in some histologic studies
Microruptures may lead to episodic attacks which resolve when the tears heal
Pathophysiology Theories behind endolymphatic hydrops
Obstruction of endolymphatic duct/sacHypoplasia of endolymphatic duct/sacAlteration of absorption of endolymphAlteration in production of endolymphAutoimmune insult Vascular originViral etiology
PathophysiologyProdromal stage of gradual distension of endolymphatic system
Distension progress leading to thinning & atrophy of Reissner’s membrane &saccular wall
Rupture &sudden release of large volume of endolymph in small perilymph space
Sensory & neural structure exposed to K + rich endolymph
Sudden HL & vertigo
When perilymphatic compartment is restored to normal, symptoms subside
Aided by the collapse, the rupture heals & the process is repeated.
DIAGNOSIS
AAO-HNS CHE 1985 Meniere’s is diagnosed by
Vertigo○ Spontaneous, lasting minutes to hours○ Recurrent, must have more than 1 episode○ Associated with nystagmus
Hearing loss○ Fluctuating sensorineural ○ Low-frequency or flat
Tinnitus Vertigo treatment reporting standard
0 = Complete control 1-40 = Substantial control 41-80 = Limited control 81-120 = Insignificant control > 120 = Worse
Hearing treatment reporting standard PTA reported 500, 1000, 2000, 3000 kHz If multiple pre and post levels are available, the worst is always used PTA is considered improved / worse if a 10 dB difference is noted SDS is considered improved / worse if a 15% difference is noted
Avg spells/month post-treatment (24 mon recommended)
x 100 = Control LevelAvg spells/month pre-treatment
(6 mon recommended)
AUDIOLOGICAL INVESTIGATION
TFT – Reveals SN loss PTA – Early disease - low frequency SN
loss – Late disease - high frequency SN loss
0102030405060708090
100110
500 1000 2000 4000 8000
0102030405060708090
100110
500 1000 2000 4000 80000
102030405060708090
100110
500 1000 2000 4000 8000
Early Stage Later Stage
AUDIOLOGICAL INVESTIGATION Speech reception threshold very closely
matching PTT in over 90% Speech discrimination score
Between attacks – 55 – 85 %During attacks – Low
Test for RecruitmentSISI – better than 70 %Stapedial replex +ve
Tone Decay Test – less than 20 dB Bekesy Audiometry – Type II curve
AUDIOLOGICAL INVESTIGATION ElectrocochleographyIt’s a diagnostic and prognostic test
Summating Potential (SP) is larger and more negative
SP/AP Ratio more than 30 % (Normal – 20%)
Normal M.D
GLYCEROL TEST To confirm the diagnosis and useful mainly on
prognosis Procedure 1.5 ml / kg glycerol with equal amounts of water +ve Test – 10 dB or more @ 2 or more frequency or
speech discrimination improves 12% or more -ve Test – Do not reach +ve criteria Decremental – Threshold worse by 10 dB +Ve Glycerol Test – C.I for Labyrinthectomy
ASSESMENT OF VESTIBULAR FUNCTION Caloric Test
30 – 50 % of M.D shows canal paresis on the affected side
Electronystagmography
RADIOLOGICAL INVESTIGATION X-Ray temporal bone
Hypocellularty, sigmoid sinus placed more medially and anteriorly
CT Scan To see the size, position of VA and see the size and location of
Endolympotic sac or dehiscent sup semi circular canal. To see peri aqueduct and perilabyrithine penumatization.
MRI Scan (With and without contrast)Evaluation of skull base tumours / C.P. angle
lesions / vascular lesions / multiple sclerosis / vascular compression of 8th N / acoustic neuroma
(with Gadolinium)
Special Tests Vascular imaging
Non invasive : a) Doppler Ultra Sonography b) Colour Doppler c) M.R. Angiogram (M.R.A)
Invasive : a) Conventional Angiogram b) C.T. Angiogram
Estimation of the followings
Full Blood CountESRT3, T4 & TSHUrea, ElectrolytesCholesterol & TriglyceridesGlucose & GTTVDRL & FTA-ABS
TREATMENT General measures Medical treatment Surgical treatment
General measures Dietary restriction of salt, caffeine,
alcohol, nicotine Cessation of smoking Intermittent dehydration Avoid activities requiring body balance Reassurance Bed rest
Medical Therapy Diuretics - Frusemide Vasodilators– Carbogen, Histamine, Betahistine, Nicotinic acid Labyrinthine sedative– Promethazine,
Dimenhydrinate, Prochlorperazine
SYMPTOMATIC RELIEF DURING ACUTE EPISODES
VESTIBULAR SUPPRESSANTS:i. Phenothiazines-
prochlorperazine,perphenazineii. Antihistamine-cinnarizine,
cyclizine,dimenhydrinate,promethazine,meclizine
iii. Benzodiazepines-reduce activity in vestibular nuclei & relieve anxiety associated with the attack- diazepam,lorazepam
iv. Transdermal scopalamine hydrochloride, an anticholinergic agent
PROPHYLAXIS BETWEEN ACUTE EPISODES
TO REDUCE ENDOLYMPHATIC ACCUMULATION
SALT RESTRICTION DIURETIC THERAPY(hydrochlorthiazide,
chlorthalidone,acetazolamide) HYPEROSMOLAR DEHYDRATION
Intratympanic Ablation Fowler (1948) and Schuknecht (1957)
established role of aminoglycoside therapy.Streptomicin used initiallyVertigo eliminated in all patientsProfound hearing loss in all patients
Gentamicin treatment now preferredTheoretical targets of therapy are
○ Dark cells of the stria vascularis○ Planum semilunatum of the semicircular canals
Higher doses destroy the hair cells of the cochlea
Meniett Device Transtympanic “Micropressure”
TreatmentFDA approved in 1999 as a class II
deviceTreatment self-administered TIDEach treatment is three 1-minute
cyclesApplies intermittent, alternating
pressure 0-20 cm H20Requires a tympanostomy tube
Meniett Device
Criteria: “active symptoms of vestibular or cochleovestibular hydrops”
Improvement in tinnitus, vertigo & ear fullnessImprovement in hearingRequires tympanotomy tubeProblems
○ Tube otorrhea, blockage, extrusion○ Recurrence of disease after therapy cessation
Precautions & Prerequisites for Surgery
Accurate diagnosis Failed medical management Risks Vs Benefits Bilaterality of the disease Health status
Meniere’s Disease. Classification
Conservative Ablative Miscellaneous
Conservative surgery for Meniere’s Residual hearing preserved-50dB SRT,50%SDS 1) Sac surgery :
a) Endolymphatic sac decompression b) Endolymphatic mastoid
shunt(shea,Arenberg.morrison) c) Endolymphatico subarachnoid shunt(austin)
2) Selective vestibular nerve section 3) Sacculotomy
4) Cody Tack procedure 5) Otic periotic shunt 6) Cochleosacculotomy
Meniere’s
Ablative Residual hearing sacrificed
1)Labyrinthectomy2) Labyrinthectomy with cochleo vestibular neurectomy
Meniere’s
Unilateral Disease1. Serviceable hearing
Conservative surgery-Sac surgery2. Poor hearing
Ablative surgery-Labyrinthectomy/Nerve section
Bilateral Disease1. Both ears good hearing Sac surgery-Uni/Bilateral2. Only Hearing Ear Sac surgery3. Both poor Rehabilitation exercise/Nerve section
Meniere’s
Meniere’s Endolymphatic Sac Surgery
AimTo preserve both auditory & vestibular functionPrincipleDecompress or open SacIncrease drainage & ResorptionEliminate hydropsDecrease sequelae & symptoms
Meniere’s Endolymphatic Sac Surgery Indications
Failed medical treatment with serviceable hearing
Only hearing earFluctuating hearing loss 2-3yrs with medical
treatment Contraindications
Poor hearingDecrimental glycerol test
Meniere’sProcedure
•Cortical mastoidectomy done•Identify -Lateral & post semicircular canal -Vertical segment of 7th nerve -Posterior fossa dural plate•Donaldsons line drawn•Sac identified and opened
Advantages of Sac Surgery Better hearing No post op disequilibrium Less risk Preserves both components
Complications Facial nerve injury Hearing loss CSF leak Meningitis
Final surgical option for control of vertigo 1904 described Transcanal, transmastoid PTA 70, discrim 20% Indications
- Unilateral poor hearing - Negative Glycerol test
Labyrinthectomy
Overview Acute Therapy
Long-Term Stabilization Non-invastive medical
treatments Alternative options
Non-Destructive Therapy Medical: IT Steroids Surgical: Mastoid shunt
Destructive Therapy Medical: IT Gentamicin Surgical
○ Nerve section○ Labyrinthectomy
58
Conclusions Vestibular complaints common to ENT Thorough evaluation and understanding Dx and treat acute symptoms Wean vestibular suppressants Specific pharmacotherapy instituted Chronic, uncompensated disease
benefits from early VRT
THANK U