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REVIEW

REVIEW ON ANATOMY

External ear:

y anything lateral to the tympanic membraneMiddle ear:

y anything within the middle ear spaceincluding the Eustachian tube

External ear:

y cochlea, vestibuleThe mainstay for any diagnosis is a good physical

examination, of course, and the mainstay of any

general practitioner that wishes to examine the ear

is an otoscope.

USING THE OTOSCOPE

1. Pull the ear upward and backward to

straighten the ear canal.

2. Inspect the whole auricle and the back of

the ear (the post-auricular area). Choose the right

size of speculum.

3. Insert gently into the ear. Do not jab

because the ear is very pain sensitive. Also, do not

torque the handle while examining.

4. Roll gently with fingertips touching the

otoscope. Please be very very gentle.

The otoscope may be held like a gun. . . (he was

about to say more, but was distracted by the

attendance.)

THE TYMPANIC MEMBRANE (TM)

*Note the structures:

y cone of lighty handle of malleusy short process of the malleusy long process of the malleusy maleolar-incunal jointy malleusy incusy parstensa (major portion of tympanic

membrane)

y parsflaccida*Note the laterality

PATHWAY OF HEARING

MIDDLE EAR

y converts sound energy into mechanicalenergy

Tympanicmembrane

y area is 15x that of the oval window andstapes

y very sound-senstivey sound vibrates the tympanic membrane,

which in turn vibrates the ossicles,

eventually the footplate of the stapes.

y energy is amplified due to the proportion ofthe size of the tympanic membrane to the

stapes

y however, one cannot have a good andfunctioning eardrum (tympanic membrane)

without a normal functioning Eustachiantube

Eustachian tube

y maintains the health of the middle eary provides drainage: ear mucosa is

respiratory. Without the Eustachian tube,

mucous secretions will be a very good

Subject: MedicineTopic: ENT- Hearing Loss, Vertigo and

TinnitusLecturer: Dr. RamosDate of Lecture:Aug. 1, 2011Transcriptionist: pinkyredPages: 16

SY

2011-2012

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culture media for microorganisms to grow

into

y aeratesy protects: closes when one blows hard,

protecting the tympanic membrane

y If one does not have a Eustachian tube andhe blows his nose, the tympanic membrane

will fly off the ear.

y regulates pressure: opens in high altitudesand during descent to equalize pressure

y opened and closed by velo-pharyngealmuscles (tensor velipalatini,

levatorvelipalatini, palatoglossus, palato-

pharyngeus muscle, muscles of the soft

palate)

Soft palate

y opens and closes the Eustachian tubey provides a means of sealing the

nasopharynx and oropharynx

y allowing one to drink without having thefluids go into ones nose

y allows one to pronounce K and Qy cleft palate patients are prone to ear

infections due to the abnormal functions in

the Eustachian tube

INNER EAR

Cochlea

Note structures:

y organ of cortiy modiolus (midline)Bony center of the

Cochlear Spiral

y basilar membrane

y tectorial platey Reissnersmembrane(where endolymph

and perilymph are)

y Rosenthals canal is where the modiolusbecomes the spiral ganglion,

y spiral ganglionaggregates to form thecochlear nerve

y Basilar membrane becomes progressivelythicker as it nears the apex

The footplate of the stapes is attached to the oval

window, which is in close relationship with the

endolymph and perilymph (has higher sodium)

Vibrating the oval window vibrates the fluids

The shearing forces of the fluid vibration in the

tectorial plate rub against the hair cells in the very

sensitive basal membrane and transmit the signal to

the nerve fibers in the spiral ganglion to becomethe cochlear nerve.

Lower portion (base) is for high frequency sound;

the apex is for low frequency sound.

OrganofCorti

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inner and outer hair cells

y depolarize and send their signals to thecochlear nerve fibers

y mechanical energy becomesneurotransmitters

y very low electrical energy going to thenervey shearing the forces towards the kinocilium:

excitatory

y shearing the forces away from thekinocilium: inhibitory

Pathwayofhearing

remember COLIMA:

y cochlea will transmit the impulses to thecochlear nerve

y to the cochlear nucleusy superiorolivary nucleusy laterallemniscusy inferiorcolliculusy medialgeniculate bodyy auditory cortex

HEARING LOSS, VERTIGO, DIZZINESS

HEARING LOSSy conductive

o problem with transferring sound tothe nerve

y sensorineuralo damage to the nerve

y mixedo damage to both tympanic

membrane and nerve

CONDUCTIVEHEARING LOSS

y Impaired conduction of sound to the innerear.

y Caused by disease of the external auditorycanal and middle ear.

EXTERNAL EAR PATHOLOGY

y External canal swelling/inflammation (e.g.furuncle/pimple, swimmers ear: acquiredby swimming in contaminated water)

y Foreign body(various objects including nits,usually from pets)

y Impacted cerumeny Tumory Bony exostosisy Congenital abnormalities (e.g. microtia)

Otitisexterna

Acute inflammatory change (pain, redness, swelling,

3 weeks onset)

Auricle

y if only the cartilage is involved,perichondritis (common in physical

altercations, contact sports)

y if it also involves the earlobe and itssurroundings, cellulitis (e.g. people

reviewing, eating chips, then falling asleep,

and accidentally applying chip residue in the

ears, then a cockroach enters the ear canal,

burrowing deeper and deeper as the

patient tries to draw it outif this happens,

dont manipulate the roach, drown it in oil.)

y if there are vesicles, herpes zosteroticusExternalearcanal

y localized swelling in circumscribedotitisexterna(furuncle)

y swelling in the entire ear canal in diffuseotitisexternaor swimmers ear

y hemorrhagicotorrhea inbullousotitisexternaor luga

y mucopurulentotorrhea in chronic otitismedia with tympanic membrane

perforation

Chronic inflammatory change (itching, scaling)

Absent signs of otitis media

y thickened and scaly skin in chroniceczemaoftheearcanal

y ulcer in necrotizingotitisexternay granulations (appear like raw tocino) in

fungal infections,

granulomatousotitisexterna, tumors

Present signs of otitis media

y purulentotorrhea in otitisexternaaccompanying otitis mediawith tympanic

membraneperforation

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y mucosal polyp and crusts in bony ear canalin suspectedcholesteatoma

Diffuseotitisexterna/eczema

y Inflammation of the canal skin due tomechanical injury, toxicity or allergy.

y Mixed bacterial infection of the skin thatinclude G(-) organisms(Pseudomonas

aeruginosa, Proteus mirabilis) anaerobes

and fungi

y swimmers eary

Pain, purulent discharge, canal obstruction(due to the ear canal being bony, it cannot

swell out, it swells in) thus pain and hearing

loss.

y Diffuse swelling, fetid discharge (anaerobicinflammation), crusting

y Cleansing, antibiotics, keep dry, analgesiay topical steroids in patients with very

inflamed ear, but should be chosen

carefullysteroids impair hearing and

wound healing, and aggravates infection

Foreignbody

y common in children, insert play objects intothe ear canal.

y Ear plugs, objects used in ear manipulation,adults.

y Check for associated injuries.y DO NOT IRRIGATE!y topical anesthetics for the ear are not very

effective

*Do not clamp, roll it out gently with a pick under

magnification. Dont jab at the skin, its very very

painful

Cerumen

y ear waxy ear is self cleansing epithelial migration

from TM to meatusy Ceruminous/sebaceous galnds

o Protective film of fatty acids,lysozymes and is acidic.

o Protectiony only the outer half of the ear canal

produces wax (only the hair-bearing

structures)

y contain enzymes that kill germs and fungiy acidic to be fungicidal and fungistaticy waterproofs the eary natural protective mechanism of the eardo not remove everyday, clean ears once

every two weeks (only the outer half, with

circular motions)

y soften the ear wax first before irrigationy irrigate when the wax is soft and lysed with

drops

y hard, dry impacted wax would only absorbthe water, expand and cause even more

pain and the expansion could cause

inflammation and swelling

y soften with hydrogen peroxide, dilute drops(50%), baby oil, otosol or ducosate sodium

Tumors oftheearcanal

y EAC tumors are rare it commonlyassociated with auricular tumors(malignancy).

y Frequently mistaken for otitisexterna.y Most common is skin cancery Painful, ulcerated, non healing lesion or the

EAC, bleeding, 2ndary infection, otorrhea.

y BIOPSY under microscopy

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y Surgery, irradiation (unfavorable becauseradiation is not very good with bones).

y cutaneous horns kulugoy basal cell carcinoma hyperpigmented

broad-based lesion

y squamous cell carcinoma non-healingulcer

Exostoses and hyperostosesabnormal boneformations in the ear canal

Exostoses

y True osteomas commonly located near theannulus (superomedial canal wall).

y Develop from ossification centersy Pale rounded bony prominences

Hyperostoses

y Appositional growth of the bony EACusually induced by periosteal irritation eg.

Frequent contact with cold water

Malformations oftheauricle

Auricular dysplasia

y GRADE I structural subunits of the auricleare present .But, malformed. (macrotia,

prominent ears). Simple or even no

correction necessary.

y GRADE II- auricle is small, severelymisshapen and lacks sub units. Anomaly of

the EAC often present. Meticulous

corrective surgery.

y GRADE III normal auricular structures areabsent and EAC is almost always atretic.

Audiologic testing, bone conduction hearing

aids, reconstruction.

MIDDLE EAR PATHOLOGY

y Infection: Otitis mediay Middle ear effusion

y Tympanic membrane sclerosisy Traumatic TM perforations

Otitis media

Based largely on 2 functional disturbances

y Impaired middle ear ventilationo Eustachian tube dysfunctiono mucosal swellingo negative middle ear pressureo obstructiono deficient openingo special anatomy in

children/cleftpatients (children

have short, flat Eustachian tubes, in

contrast to adults, who have long

and angled at 45r Eustachian tubes)

y Middle ear inflammationo U.R.T.I. adenoiditiso allergy, acid reflux.o

viral/bacterial middle ear infection

The above is a very busy slide, but, he wants us toremember:

y any Eustachian tube dysfunction thatcauses

o impaired middle ear ventilationo negative middle ear pressureo edema and mucosal inflammation

y arecausedbyo palatal deformityo muscular dysfunctiono ciliary dysfunction

HISTORY

y There are no specific complaints for middleear dis.

y Otalgia, discharge, pressure or hearing lossare non specific.

y Hx of chronic inflammatory ear diseaseusually signify otitis media.

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y Can lead to scarring and poor middle earventilation (ET)

y Ask for Hx of TM perforation, trauma orprevious surgery.

EXAMINATION

Otoscopy

y mainstay of middle ear diseaseinvestigation

Function tests: TM mobility

y passive mobilityo pneumaticotoscopy

y active mobilityo movement of the post. Superior

quadrant in reaponse to introduced

air pressure.

o Valsalva, Toynbee. (do notuse in acute inflammation of the

M.E. and N.P.)

TUNING FORK TESTS

y The goal of tuning fork tests is to diff. bet.Conductive and Sensorineural hearing loss.

(hearing loss is not detected directly with

tuning forks) using 512 - 800 Hz forks.

Weber test

y strike the tuning fork, and place on patientsforehead

y NORMAL sound is perceived equally inboth ears.

y S.N.H.L. sound lateralizes to the betterear.

y C.H.L. sound lateralizes to the poorerear.

Rinnes test

y Compares air and bone conduction in thesame ear.

y strike the tuning fork and place the base onthe patients mastoid.

y when patient stops hearing the tune, placeit 1cm from patients ear with the forkfacing the examiner.

y POSITIVE RINNE air conducted sound isperceived louder and longer duration.

(normal)

y NEGATIVE RINNE sound is perceivedlouder and of longer duration at the

mastoid than at the ear canal. (conductive

hearing loss)

OTITISMEDIA

Otitis mediawitheffusion

y One of the most common disorder in preschool children.

y Eustachian tube dysfunction leads tonegative pressure in the middle ear and

effusion. (sniffing)

y Major symptom is hearing loss.y Diagnosis: otoscopyy Decongestants, topical steroids, antibioticsy Persistence of 3wks. nasal endoscopy to r/o

tumor (adults)

y myringotomy

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Acuteotitis media

y Generally caused by ascending infection tothe middle ear via the eustachian tube.

y Streptococci.,H. influenzae, B. catarrhalis,respiratory viruses.

y Adenoids- nidus for infection.y Severe ear pain, fever, ear discharge,

irritability (vomiting, diarrhea in infants)

y Spontaneous TM perforation may occury NSAIDs, decongestants (

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y T.M. has a strong capacity for self healing.Most heal by themselves. Keep ears dry.

y Surgery for more complicated cases.

SENSORINEURAL HEARING LOSS

y Noise induced hearing lossy Labyrinthitisy Ototoxicityy Sudden SNHLy Presbycusisdue to aging

Noiseinducedhearingloss

y Excessive noise exposure can cause directmechanical trauma and metabolic injury to

the cochlea.

y The nature and extent of damage dependon the acoustic energy and duration of

noise exposure.

y if noise level is 140dBof short duration.

y Blast injury presence of a ruptured TMy Acute noise induced hearing lossy Often reversible concert, impact noise,

power tools, engine noise

y Chronic noise induced hearing lossy Irreversible cochlear hearing loss. Severity

depends on noise level, exposure time and

individual factors.

* tinnitus

Diagnosis

y NO KNOWN TREATMENTy Prevention is paramounty Primary reduce noise

y 2ndary protection, transfer, screeningy 02, steroids, improve microcirculation and

metabolic conditions in acute exposure

Labyrynthitis

y Infectious, inflammatory process affectingthe labyrinth and its surroundings.

y Tympanogenic from the middle ear to theround or oval window.( toxic, suppurative,

chronic)

y Meningeal infection from intracranialsource (Strep.)

y Hematogenous mumps, measles, HIV,CMV, syphilis

y Cochlear hearing loss, tinnitus, vestibularsymptoms.

y Rule out fistulay Myringotomy for decompresssion, culturey Mastoidectomyy High dose antibiotics that can cross the

B.B.B.

y Steroids try to avoid unless absolutelynecessary

y Damage can affect cochlear and vestibularfunctions

y Can be reversible or otherwisey Symmetricaly Hearing loss, tinnitus, disequilibrium

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y Affect hair cells, striavascularis (providesnutrients to the organ of Corti)

y can be reversible, if drug is stopped on timeSuddenSensorineuralHearing Loss

y Immediate unilateral hearing loss ofsensorineural origin that has no apparent

external cause.

y Idiopathic believed to be of viral, vascularor auto immune cause. Symptoms occur in

seconds to hours.

y Hearing loss is variable in frequencies anddegree, from mild loss to sudden deafness.

y Otoscopy is normaly Weber is to the better eary REFER TO AN ENT ASAPy Steroids, oxygenation NO PROVEN

THERAPY IS EFFECTIVE

y 50% spontaneously resolvey herpes zoster oticusy psychogenic (e.g. shell shock)

y normal hearing should not go beyond 25 dBPresbycusis

y Age related apparently idiopathic andsymmetrical S.N.H.L that affects persons 50

y/o and above.

y High frequencies more affected.y Speech recognition is impaired, tinnitus,

hearing loss

y Aging, genetics, cummulative exposure toexogenous sources.

y Progressive and no specific medical norsurgical treatment. But, hearing aids.

y men are more affected with presbycusis

y A is normal: the bone conduction and airconduction have no gap, at the same

intensity

y B has conductive hearing loss: the bone andair conduction has a gap of more than 10

intensity. Also, the air conduction is at ahigh intensity, while bone conduction is

normal

y C has sensorineural hearing loss: the boneconduction and air conduction have no gap,

but as the frequency increases, both

decrease in intensity

y D has mixed hearing loss: the boneconduction and air conduction has a gap of

more than 10 dB, and both decrease in

intensity as the frequency increases

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LABYRYNTHINE ANATOMY

Note structures:

y semicircular canalsy utricley

sacculey ampullay endolymphatic sacy cochlea

Innerearcirculation

y The different parts of the inner ear aresupplied with blood through the internal

auditory artery (that forms 3 branches in

the inner ear) which originates from the

basilararteryin the base of the skull.

y three branches:o Cochlear artery supplies blood to

most of the cochlea.

o Vestibular artery supplies thesemicircular canals and part of the

vestibule.

o Cochleo-vestibular artery suppliesthe remainder of the inner ear.

Utricle, sacculeand semicircularcanals

Utricleand saccule

y horizontal (forward/back) and vertical(up/down), respectively

y linear acceleration (up and down, forwardand backward)

Semicircularcanals

y angular acceleration (tilting, rotation)

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Motion sensing

deflection and reflection of the haircells move the

otholiths toward (stimulatory) and away (inhibitory)

from the kinocilium, relaying information on which

direction the body is moving.

VESTIBULAR SYSTEM

Fivecomponents (VERY IMPORTANT!)

1. PERIPHERAL RECEPTOR APPARATUSresides in the inner ear and is responsible

for transducing head motion and position

into neural information.

2. CENTRAL VESTIBULAR NUCLEI comprise

a set of neurons in the brainstem that are

responsible for receiving, integrating, and

distributing information that controls motor

activities such as eye and head movements,

postural reflexes, and gravity-dependent

autonomic reflexes and spatial orientation.

3. VESTIBULO-O

CULAR NETWO

RK arisesfrom the vestibular nuclei and is involved in

the control of eye movements.

4. VESTIBULOSPINAL NETWORK

coordinates head movements, axial

musculature, and postural reflexes.

5. VESTIBULO-THALAMO-CORTICAL

NETWORK is responsible for the conscious

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perception of movement and spatial

orientation

Vestibularfunction

y Vestibulo-Ocular Reflexo Fixation of visual horizon for spatial

orientation during rapid head

movements. Allows a fixated object

to stay within the visual fieldo Stimuli for the VOR mainly from SCC

-This is how one fixates an object on the visual field

in a lighted area. In a dark room, one cannot move

his head because there is no visual reference.

-When one walks in the dark, even if it is a clear

room, the balance system is impaired and switches

to a different mode.

y Vestibulospinal Reflexo Maintenance of posture and

equilibrium. Relies mainly on

interaction with the proprioceptive

and motor systems

This illustrates the various connections of the

vestibular nuclei

y armsy trunky spinal cordy eary eyesy cerebellumy brain [sic]

CLINICAL PRESENTATION OF VESTIBULAR

DISORDERS

y DIZZINESS may mean any non painfuldiscomfort related to the head. (cerebral,

visual, vestibular etc.)

y VERT

IGO hallucination of movement ofthe patient or his environment.

y UNSTEADINESS loss of equilibrium inrelation to ones environment.

y LIGHTHEADEDNESS loss of equilibriumwithin ones head. (poorly described by

patient)

APPROACH TO A DIZZY PATIENT

y Medical historyy Physical examinationy Basic laboratory examy Physiologic diagnostic toolsy Radiologic diagnostic tools

Patient evaluation

y historyo 1.ONSETo 2.DURATIONo 3.SEVERITY

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o 4.AGGRAVATING FACTORSo 5.RELIEVING FACTORSo include:

past illness family allergy medication dietary smoking, etc.

y complete ear, nose throat and neurologicexam

y include:o observation for nystagmus

any rhythmical eyemovement either

spontaneous, provoked or

induced. May be

physiologic or pathologic.

Clinicalexamination

y Spinal motor function and coordinationo Standard vestibular test battery:

Rombergs test. Unterberger test. Finger to nose test.

y Oculomotor testingo Ocular motilityo Smooth pursuito Screening for oscillopsia

y Nystagmus testingo Any rhythmical eye movement

either spontaneous, provoked or

induced. May be physiologic or

pathologic

Physicalexam

y Systemic (e.g. diabetes, hypertension)y Psychiatric (e.g. hysteria)y Otologic (e.g. discharge, tumor)y Ophthalmologic (e.g. blurring of vision,

diability to fixate, glaucoma)

y Neurologic (e.g. cerebrovascular problem,tumor)

Nystagmus

y fast componento determines directiono the reticular formation corrects the

slow phase to return eyes to the

last field of gaze.

y slow componento is the direction of the flow of

endolympho vestibular in origin.

Classification

y SPONTANEOUS NYSTAGMUS present w/opositional or other labyrinthine stimulation.

y POSITIONAL NYSTAGMUS elicited byassuming a specific position as during

positional testing. (Dix-Hallpike test)

y INDUCED NYSTAGMUS elicited bystimulation. (ex. Caloric)

y GAZE evoked nystagmus - always atdirection of gaze.

Dix-HallpikeManeuver

y diagnostic test for benign paroxysmalpositional vertigo

y frenzeled glasses highly magnifies theocular movement

y patient is asked to lie down and tilt thehead, check nystagmus

y 10-15% nystagmus is central (from thebrain), 85% peripheral

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Central Nystagmus

y No Latencyy Lasts > 1 minutey Repeatabley Present in Multiple Head Positionsy Occassionally Absenty Multidirectional / Bizarrey 10 - 15 % of Vertigo Cases

Peripheral Nystagmus

y 5 - 15 Second Latencyy Disappears within 90 Secondsy Present in only 1 Head Positiony Chronically Presenty Unidirectionaly 85 % of Vertigo Cases

VERTIGO/DIZZINESS

y Most common symptoms of vestibulardysfunction

y Subjective disturbance of integrity causedby contradictory sensory information

processing.

Peripheralvertigo

y Function of a sensory system is impairedy outside the brain

Centralvertigo

y Central processing is impaired

y within the brain

y if vertigo is rotatory, with motioncomponents with otologic components,

cause is otologic

y if no otologic symptoms, it is vestibulary if vertigo is with obtundation,

lightheadedness, giddiness, nonsystematic

dizziness with no motion component, with

neurologic symptoms (e.g. dysarthria,

diplopia) with impaired consciousness,

cause is neurologic

y if without neurologic symptoms, it is amedical problem (e.g. diabetes,

hypertension, electrolyte imbalance)

y if vertigo lasts secondso during head movements, it is

peripheral vestibular disorder

o at rest, it is central vestibulardisorder or psychogenic

y minutes

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y principle: calcium crystals are floating in theposterior semicircular canal

y just like in a snow globe, crystals fall on thehair cells, giving a sensation of movement in

the absence of it (benign vertigo)

y theEpley maneuver repositions thecrystalsthe various twists makes them

exit the posterior semicircular canals

Menieres disease

y Triad of vertigo, tinnitus and fluctuatinghearingloss. * ear fullness.

y Most cases idiopathicy Endolymphatic cochlear hydrops

o Lermoyez phenomenono Tumarkin crisis

y Low frequency hearing loss audiometryy Bed rest, anti emetics, anti vertigo meds.

Differentialbasis ofvertigo

the cause of this patients dizziness is vascular, in

figure B, there is damage on the basilar artery

patient has acoustic neuroma (tumor of the

vestibulocochlear nerve at the cerebello-pontine

angle) this will manifest as hearing loss, dizziness

and disequilibrium

APPROACHTOMANAGEMENT VERTIGO

y Symptomatic reliefy Eliminate the underlying causey Rehabilitation

TINNITUS

y Represents perception of sound withoutexternal stimulus

y Auditory sensation that occurs in theabsence of an external stimuli or electrical

stimuli and has no subjective information

content.

y Mostly caused by disturbance of peripheralsensorineural structures.

y Noise exposure, cranial trauma, COM,family history, ototoxic drugs.

y Normal otoscopyClassification

y Subjective tinnitus perceived by thepatient only.

o Conductiveo Sensorineuralo Central

y Objective tinnitus examiner is able toperceive the tinnitus.

o Vascularo Myogenic

y Pulsatile tinnitus coincident with thepulse.

o Arterial etiologies: 1.AVFs/AVMs 2.Glomus tumors 3.Carotid stenosis 4.Atherosclerosis 5.Persistent stapedial artery 6.Intratympanic carotid

artery

7.Increased cardiac output pregnancy, thyrotoxicosis

o Venous etiologies: 1.Venous hum 2.Pseudotumor cerebri 3.Jugular bulb anomalies

o Non-vascular etiologies 1.Palatal myoclonus 2.Stapedial myoclonus 3.Vascular neoplasms of

skull base/temporal boney Non-pulsatile tinnitus

o typically subjective.o Most common form of tinnituso Most associated with hearing losso examples:

Menieres disease ototoxicity noise exposure

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Diagnosis

1.History:

y Describe soundy Durationy Other otologic symptoms (hearing loss,

vertigo, otalgia, otorrhea)

y Severityy Precipitating factors (noise, ototoxic drugs,

trauma, infection etc.)

2. PE:

y Full head and neck examy Neuro-otologic examy Auscultation of ear canal, peri-auricular

area, orbits, neck bruits.

y Palatal or TM rhythmic contractions.y additional tests:

o audiometryo USo CTo MRI/MRA/MRVo angiography

Management

y Treatment designed to eliminate tinnitus.(anatomic or systemic causes) ex. Surgery.

y Treatment designed to reduce the severityof tinnitus. (insult to inner ear) ex. Acoustic

therapy, lifestyle change.

____________END OF TRANSCRIPTION__________

HI to reych, arabels, ana, quennie, eloh, jez,

gemHappy studying!

IMY

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