Subject: Medicine Topic: ENT- Hearing Loss, Vertigo and Tinnitus Lecturer: Dr. Ramos Date of Lecture:Aug.

1, 2011 Transcriptionist: pinkyred Pages: 16

REVIEW REVIEW ON ANATOMY

The otoscope may be held like a gun. . . (he was about to say more, but was distracted by the attendance.) THE TYMPANIC MEMBRANE (TM)

External ear: y anything lateral to the tympanic membrane Middle ear: y anything within the middle ear space including the Eustachian tube External ear: y cochlea, vestibule The 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

*Note the structures: y cone of light y handle of malleus y short process of the malleus y long process of the malleus y maleolar-incunal joint y malleus y incus y parstensa (major portion of tympanic membrane) y parsflaccida *Note the laterality PATHWAY OF HEARING MIDDLE EAR y converts sound energy into mechanical energy Tympanic membrane y area is 15x that of the oval window and stapes y very sound-senstive y 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 of the size of the tympanic membrane to the stapes y however, one cannot have a good and functioning eardrum (tympanic membrane) without a normal functioning Eustachian tube Eustachian tube y maintains the health of the middle ear y provides drainage: ear mucosa is respiratory. Without the Eustachian tube, mucous secretions will be a very good

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.

SY 2011-2012

y y y

y y

culture media for microorganisms to grow into aerates protects: closes when one blows hard, protecting the tympanic membrane If one does not have a Eustachian tube and he blows his nose, the tympanic membrane will fly off the ear. regulates pressure: opens in high altitudes and during descent to equalize pressure opened and closed by velo-pharyngeal muscles (tensor velipalatini, levatorvelipalatini, palatoglossus, palatopharyngeus muscle, muscles of the soft palate)

y y y y y

tectorial plate Reissner smembrane(where endolymph and perilymph are) Rosenthal s canal is where the modiolus becomes the spiral ganglion, spiral ganglion aggregates to form the cochlear nerve Basilar membrane becomes progressively thicker 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 become the cochlear nerve. Lower portion (base) is for high frequency sound; the apex is for low frequency sound.

Organ of Corti

Soft palate y opens and closes the Eustachian tube y provides a means of sealing the nasopharynx and oropharynx y allowing one to drink without having the fluids go into one s nose y allows one to pronounce K and Q y 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 corti y modiolus (midline) Bony center of the Cochlear Spiral y basilar membrane

CONDUCTIVE HEARING LOSS y Impaired conduction of sound to the inner ear. y Caused by disease of the external auditory canal and middle ear. EXTERNAL EAR PATHOLOGY External canal swelling/inflammation (e.g. furuncle/pimple, swimmer s ear: acquired by swimming in contaminated water) Foreign body(various objects including nits, usually from pets) Impacted cerumen Tumor Bony exostosis Congenital abnormalities (e.g. microtia)

y y y y y

inner and outer hair cells y depolarize and send their signals to the cochlear nerve fibers y mechanical energy becomes neurotransmitters y very low electrical energy going to the nerve y shearing the forces towards the kinocilium: excitatory y shearing the forces away from the kinocilium: inhibitory Pathway of hearing

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 its surroundings, 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 out if this happens, don t manipulate the roach, drown it in oil.) y if there are vesicles, herpes zoster oticus External ear canal y localized swelling in circumscribed otitisexterna(furuncle) y swelling in the entire ear canal in diffuse otitisexternaor swimmer s ear y hemorrhagicotorrhea in bullousotitisexternaor luga y mucopurulentotorrhea in chronic otitis media with tympanic membrane perforation Chronic inflammatory change (itching, scaling) Absent signs of otitis media y thickened and scaly skin in chronic eczema of the ear canal y ulcer in necrotizing otitisexterna y granulations (appear like raw tocino) in fungal infections, granulomatousotitisexterna, tumors Present signs of otitis media y purulentotorrhea in otitisexterna accompanying otitis media with tympanic membrane perforation

remember COLIMA: y cochlea will transmit the impulses to the cochlear nerve y to the cochlear nucleus y superiorolivary nucleus y laterallemniscus y inferiorcolliculus y medialgeniculate body y auditory cortex

HEARING LOSS, VERTIGO, DIZZINESS HEARING LOSS conductive o problem with transferring sound to the nerve sensorineural o damage to the nerve mixed o damage to both tympanic membrane and nerve

y y

mucosal polyp and crusts in bony ear canal in suspected cholesteatoma

*Do not clamp, roll it out gently with a pick under magnification. Don t jab at the skin, it s very very painful

Diffuse otitisexterna/eczema y Inflammation of the canal skin due to mechanical injury, toxicity or allergy. y Mixed bacterial infection of the skin that include G(-) organisms(Pseudomonas aeruginosa, Proteus mirabilis) anaerobes and fungi y swimmer s ear y 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 (anaerobic inflammation), crusting y Cleansing, antibiotics, keep dry, analgesia y topical steroids in patients with very inflamed ear, but should be chosen carefully steroids impair hearing and wound healing, and aggravates infection Foreign body y common in children, insert play objects into the 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

Cerumen y ear wax y ear is self cleansing epithelial migration from TM to meatus y Ceruminous/sebaceous galnds o Protective film of fatty acids, lysozymes and is acidic. o Protection y only the outer half of the ear canal produces wax (only the hair-bearing structures) y contain enzymes that kill germs and fungi y acidic to be fungicidal and fungistatic y waterproofs the ear y natural protective mechanism of the ear do not remove everyday, clean ears once every two weeks (only the outer half, with circular motions) y soften the ear wax first before irrigation y irrigate when the wax is soft and lysed with drops y hard, dry impacted wax would only absorb the 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 of the ear canal y EAC tumors are rare it commonly associated with auricular tumors (malignancy). y Frequently mistaken for otitisexterna. y Most common is skin cancer y Painful, ulcerated, non healing lesion or the EAC, bleeding, 2ndary infection, otorrhea. y BIOPSY under microscopy

y y y y

Surgery, irradiation (unfavorable because radiation is not very good with bones). cutaneous horns kulugo basal cell carcinoma hyperpigmented broad-based lesion squamous cell carcinoma non-healing ulcer

y y

Tympanic membrane sclerosis Traumatic TM perforations

Exostoses and hyperostoses abnormal bone formations in the ear canal Exostoses y True osteomas commonly located near the annulus (superomedial canal wall). y Develop from ossification centers y Pale rounded bony prominences Hyperostoses y Appositional growth of the bony EAC usually induced by periosteal irritation eg. Frequent contact with cold water

Otitis media Based largely on 2 functional disturbances y Impaired middle ear ventilation o Eustachian tube dysfunction o mucosal swelling o negative middle ear pressure o obstruction o deficient opening o 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 inflammation o U.R.T.I. adenoiditis o allergy, acid reflux. o viral/bacterial middle ear infection

Malformations of the auricle Auricular dysplasia y GRADE I structural subunits of the auricle are present .But, malformed. (macrotia, prominent ears). Simple or even no correction necessary. y GRADE IIauricle is small, severely misshapen and lacks sub units. Anomaly of the EAC often present. Meticulous corrective surgery. y GRADE III normal auricular structures are absent and EAC is almost always atretic. Audiologic testing, bone conduction hearing aids, reconstruction.

The above is a very busy slide, but, he wants us to remember: y any Eustachian tube dysfunction that causes o impaired middle ear ventilation o negative middle ear pressure o edema and mucosal inflammation y are caused by o palatal deformity o muscular dysfunction o ciliary dysfunction HISTORY There are no specific complaints for middle ear dis. Otalgia, discharge, pressure or hearing loss are non specific. Hx of chronic inflammatory ear disease usually signify otitis media.

y y MIDDLE EAR PATHOLOGY Infection: Otitis media Middle ear effusion y

y y

y y

Can lead to scarring and poor middle ear ventilation (ET) Ask for Hx of TM perforation, trauma or previous surgery.

EXAMINATION Otoscopy y mainstay of middle investigation

ear

disease

Function tests: TM mobility y passive mobility o pneumaticotoscopy y active mobility o movement of the post. Superior quadrant in reaponse to introduced air pressure. o Valsalva, Toynbee. (do not use in acute inflammation of the M.E. and N.P.) TUNING FORK TESTS 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.

y y y

Weber test

Compares air and bone conduction in the same ear. strike the tuning fork and place the base on the patient s mastoid. when patient stops hearing the tune, place it 1cm from patient s ear with the fork facing the examiner. POSITIVE RINNE air conducted sound is perceived louder and longer duration. (normal) NEGATIVE RINNE sound is perceived louder and of longer duration at the mastoid than at the ear canal. (conductive hearing loss)

y y y y

strike the tuning fork, and place on patient s forehead NORMAL sound is perceived equally in both ears. S.N.H.L. sound lateralizes to the better ear. C.H.L. sound lateralizes to the poorer ear.

OTITIS MEDIA Otitis media with effusion y One of the most common disorder in pre school children. y Eustachian tube dysfunction leads to negative pressure in the middle ear and effusion. (sniffing) y Major symptom is hearing loss. y Diagnosis: otoscopy y Decongestants, topical steroids, antibiotics y Persistence of 3wks. nasal endoscopy to r/o tumor (adults) y myringotomy

Rinne s test

Acute otitis media y Generally caused by ascending infection to the 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)

Chronic otitis media with cholesteatoma y Osteoclastic inflammation of the mucosal spaces of the middle ear. y Acquired cholesteatoma keratinizing squamousepitheliumcauses bone destruction. y Infection usually G(-) and anaerobic bacteria. Fetid discharge, hearing loss, facial paralysis, disequilibrium fistula test. y Tx Surgery eradicate disease -1st priority, hearing rehabilitation-2nd priority y when extracted, there are thick cheesy white materials that smell like feces

y y

Spontaneous TM perforation may occur NSAIDs, decongestants (<nasal obstruction), antipyretic, antibiotics

Chronic suppurativeotitis media y Chronic tympanic membrane perforation with cholesteatoma ruled out. y Active/wet drainage present (pus) culture y Inactive/dry no active inflammation, pain, discharge, swelling. y Valsalva patency y Systemic antibiotics, cleansing, antibiotic ear drops, keep dry. y avoid eardrops with aminoglycosides (ototoxic) y Surgery when dry tympanoplasty

The tympanic membrane has 3 layers: y outer epithelial, middle fibrous and inner mucosal respiratory y only the outer and inner regenerate after injury and/or infection y no fibrous layer results to a thin, transparent TM INJURIES TO THE TYMPANIC MEMBRANE and MIDDLE EAR y Either by directtrauma with a pointed object or indirectlyby pressure changes. y Ossicles can dislocate even fracture. y Facial nerve can be damaged. y Pain, bleeding, clogged sensation. y Disequilibrium, vertigo, nausea or facial nerve damage is highly suspicious of more severe injury

y y

2ndary protection, transfer, screening 02, steroids, improve microcirculation and metabolic conditions in acute exposure

y y

T.M. has a strong capacity for self healing. Most heal by themselves. Keep ears dry. Surgery for more complicated cases.

SENSORINEURAL HEARING LOSS y Noise induced hearing loss y Labyrinthitis y Ototoxicity y Sudden SNHL y Presbycusis due to aging Noise induced hearing loss y Excessive noise exposure can cause direct mechanical trauma and metabolic injury to the cochlea. y The nature and extent of damage depend on the acoustic energy and duration of noise exposure. Labyrynthitis y Infectious, inflammatory process affecting the labyrinth and its surroundings. y Tympanogenic from the middle ear to the round or oval window.( toxic, suppurative, chronic) y Meningeal infection from intracranial source (Strep.) y Hematogenous mumps, measles, HIV, CMV, syphilis y Cochlear hearing loss, tinnitus, vestibular symptoms. y Rule out fistula y Myringotomy for decompresssion, culture y Mastoidectomy y High dose antibiotics that can cross the B.B.B. y Steroids try to avoid unless absolutely necessary

y y y y y y y y y y y

if noise level is <85 dB, no problem with working 8 hrs. per day, 40 hrs. a week as noise level gets more intense, at 90 dB, one may only work 10 hrs. a week at 100 dB, one may only work 1 hr. a week at 105 dB, one may only work 30 min. a week at 120 dB, one should not even stay for a minute Acute acoustic trauma fireworks, > 140dB of short duration. Blast injury presence of a ruptured TM Acute noise induced hearing loss Often reversible concert, impact noise, power tools, engine noise Chronic noise induced hearing loss Irreversible cochlear hearing loss. Severity depends on noise level, exposure time and individual factors. * tinnitus

y y y y

Diagnosis y NO KNOWN TREATMENT y Prevention is paramount y Primary reduce noise

Damage can affect cochlear and vestibular functions Can be reversible or otherwise Symmetrical Hearing loss, tinnitus, disequilibrium

y y

Affect hair cells, striavascularis (provides nutrients to the organ of Corti) can be reversible, if drug is stopped on time

Sudden Sensorineural Hearing Loss y Immediate unilateral hearing loss of sensorineural origin that has no apparent external cause. y Idiopathic believed to be of viral, vascular or auto immune cause. Symptoms occur in seconds to hours. y Hearing loss is variable in frequencies and degree, from mild loss to sudden deafness. y Otoscopy is normal y Weber is to the better ear y REFER TO AN ENT ASAP y Steroids, oxygenation NO PROVEN THERAPY IS EFFECTIVE y 50% spontaneously resolve y herpes zoster oticus y psychogenic (e.g. shell shock)

men are more affected with presbycusis

normal hearing should not go beyond 25 dB

Presbycusis y Age related apparently idiopathic and symmetrical 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 to exogenous sources. y Progressive and no specific medical nor surgical treatment. But, hearing aids.

A is normal: the bone conduction and air conduction have no gap, at the same intensity B has conductive hearing loss: the bone and air conduction has a gap of more than 10 intensity. Also, the air conduction is at a high intensity, while bone conduction is normal C has sensorineural hearing loss: the bone conduction and air conduction have no gap, but as the frequency increases, both decrease in intensity D has mixed hearing loss: the bone conduction and air conduction has a gap of more than 10 dB, and both decrease in intensity as the frequency increases

LABYRYNTHINE ANATOMY

Utricle, saccule and semicircular canals

Note structures: y semicircular canals y utricle y saccule y ampulla y endolymphatic sac y cochlea Inner ear circulation y The different parts of the inner ear are supplied with blood through the internal auditory artery (that forms 3 branches in the inner ear) which originates from the basilar artery in the base of the skull. y three branches: o Cochlear artery supplies blood to most of the cochlea. o Vestibular artery supplies the semicircular canals and part of the vestibule. o Cochleo-vestibular artery supplies the remainder of the inner ear.

Utricle and saccule y horizontal (forward/back) and vertical (up/down), respectively y linear acceleration (up and down, forward and backward) Semicircular canals y angular acceleration (tilting, rotation)

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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. Motion sensing VESTIBULAR SYSTEM Five components ( VERY IMPORTANT! ) 1. PERIPHERAL RECEPTOR APPARATUS resides 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-OCULAR NETWORK arises from 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 orientation

movement

and

spatial

Vestibular function y Vestibulo-Ocular Reflex o Fixation of visual horizon for spatial orientation during rapid head movements. Allows a fixated object to stay within the visual field o 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 Reflex o 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 arms y trunk y spinal cord y ear y eyes y cerebellum y brain [sic]

CLINICAL PRESENTATION OF VESTIBULAR DISORDERS y DIZZINESS may mean any non painful discomfort related to the head. (cerebral, visual, vestibular etc.) y VERTIGO hallucination of movement of the patient or his environment. y UNSTEADINESS loss of equilibrium in relation to one s environment. y LIGHTHEADEDNESS loss of equilibrium within one s head. (poorly described by patient) APPROACH TO A DIZZY PATIENT Medical history Physical examination Basic laboratory exam Physiologic diagnostic tools Radiologic diagnostic tools

y y y y y

Patient evaluation y history o 1.ONSET o 2.DURATION o 3.SEVERITY

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o o o

4.AGGRAVATING FACTORS 5.RELIEVING FACTORS include:  past illness  family  allergy  medication  dietary  smoking, etc.

y y

complete ear, nose throat and neurologic exam include: o observation for nystagmus  any rhythmical eye movement either spontaneous, provoked or induced. May be physiologic or pathologic.

Clinical examination y Spinal motor function and coordination o Standard vestibular test battery:  Romberg s test.  Unterberger test.  Finger to nose test. y Oculomotor testing o Ocular motility o Smooth pursuit o Screening for oscillopsia y Nystagmus testing o Any rhythmical eye movement either spontaneous, provoked or induced. May be physiologic or pathologic Physical exam 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 component o determines direction o the reticular formation corrects the slow phase to return eyes to the last field of gaze. y slow component o is the direction of the flow of endolymph o vestibular in origin.

Classification y SPONTANEOUS NYSTAGMUS present w/o positional or other labyrinthine stimulation. y POSITIONAL NYSTAGMUS elicited by assuming a specific position as during positional testing. (Dix-Hallpike test) y INDUCED NYSTAGMUS elicited by stimulation. (ex. Caloric) y GAZE evoked nystagmus - always at direction of gaze. Dix-Hallpike Maneuver y diagnostic test for benign paroxysmal positional vertigo y frenzeled glasses highly magnifies the ocular movement y patient is asked to lie down and tilt the head, check nystagmus y 10-15% nystagmus is central (from the brain), 85% peripheral

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within the brain

Central Nystagmus y y y y y y y No Latency Lasts > 1 minute Repeatable Present in Multiple Head Positions Occassionally Absent Multidirectional / Bizarre 10 - 15 % of Vertigo Cases y if vertigo is rotatory, with motion components with otologic components, cause is otologic if no otologic symptoms, it is vestibular 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 if without neurologic symptoms, it is a medical problem (e.g. diabetes, hypertension, electrolyte imbalance)

Peripheral Nystagmus y 5 - 15 Second Latency y Disappears within 90 Seconds y Present in only 1 Head Position y Chronically Present y Unidirectional y 85 % of Vertigo Cases

y y

y y

VERTIGO/DIZZINESS Most common symptoms of vestibular dysfunction Subjective disturbance of integrity caused by contradictory sensory information processing.

Peripheral vertigo y Function of a sensory system is impaired y outside the brain Central vertigo y Central processing is impaired

if vertigo lasts seconds o during head movements, it is peripheral vestibular disorder o at rest, it is central vestibular disorder or psychogenic minutes

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with position dependence, it is benign paroxymal positional vertigo or arterial hypertension o if position independent, central vestibular disorder or drug induced hours or days o diminishing intensity, peripheral vestibular disorder o increasing intensity, central vestibular disorder or multisensory vertigo o

Fatigability (i.e., a reduction in vertigo and nystagmus if the Dix-Hallpike test is repeated)

Epley s Maneuver y magic y upon diagnosis of BPPV

Clinical entities presenting with vertigo or disequilibrium y Acoustic neuroma tumor of the CNVIII y Cardiovascular disorders - arrhythmias y BPPV precipitated by head movements y Meniere s disease fluctuating hearing loss, tinnitus, vertigo, fullness y Otitis media y Perilymph fistula y Ototoxic drugs aminoglycosides, diuretics, aspirin, chemotherapeutics y Trauma/Temporal bone fracture y Vestibular neuronitis y Otosclerosis Vestibular disorders y Vestibular neuronitis o Sudden unilateral impairment of peripheral vestibular function. o 2 wks after viral URTI o Exact site involved is vestibular nerve. o Sudden severe continuous vertigo with no apparent cause. Nausea, disequilibrium o Bed rest, steroids, anti vertigo meds. o self-limiting, but takes months y Benign Paroxysmal Positional Vertigo (BPPV) o Head trauma o Vertigo provoked by movements o Dix-Hallpike maneuver diagnosis o TxEpley s, Brandt Daroff maneuvers Criteria for BPPV y Vertigo associated with a characteristic mixed torsional and vertical nystagmus provoked by the Dix-Hallpike test y A latency (typically of 1 to 2 seconds) between the completion of the Dix-Hallpike test and the onset of vertigo and nystagmus y Paroxysmal nature of the provoked vertigo and nystagmus (i.e., an increase and then a decline over a period of 10 to 20 seconds)

y y

Epley maneuver. The patient sits on the examination table, with eyes open and head turned 45 degrees to the right (A). The physician supports the patient's head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table (B). The physician turns the patient's head 90 degrees to the left side. The patient remains in this position for 30 seconds (C). The physician turns the patient's head an additional 90 degrees to the left while the patient rotates his or her body 90 degrees in the same direction. The patient remains in this position for 30 seconds (D). The patient sits up on the left side of the examination table. (E) The procedure may be repeated on either side until the patient experiences relief of symptoms.

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y y

principle: calcium crystals are floating in the posterior semicircular canal just like in a snow globe, crystals fall on the hair cells, giving a sensation of movement in the absence of it (benign vertigo) theEpley maneuver repositions the crystals the various twists makes them exit the posterior semicircular canals

patient has acoustic neuroma (tumor of the vestibulocochlear nerve at the cerebello-pontine angle) this will manifest as hearing loss, dizziness and disequilibrium APPROACH TO MANAGEMENT VERTIGO Symptomatic relief Eliminate the underlying cause Rehabilitation TINNITUS Represents perception of sound without external stimulus Auditory sensation that occurs in the absence of an external stimuli or electrical stimuli and has no subjective information content. Mostly caused by disturbance of peripheral sensorineural structures. Noise exposure, cranial trauma, COM, family history, ototoxic drugs. Normal otoscopy

Meniere s disease y Triad of vertigo, tinnitus and fluctuating hearing loss. * ear fullness. y Most cases idiopathic y Endolymphatic cochlear hydrops o Lermoyez phenomenon o Tumarkin crisis y Low frequency hearing loss audiometry y Bed rest, anti emetics, anti vertigo meds. Differential basis of vertigo

y y y

y y

y y y

the cause of this patient s dizziness is vascular, in figure B, there is damage on the basilar artery

Classification y Subjective tinnitus perceived by the patient only. o Conductive o Sensorineural o Central y Objective tinnitus examiner is able to perceive the tinnitus. o Vascular o Myogenic y Pulsatile tinnitus coincident with the pulse. 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 bone y Non-pulsatile tinnitus o typically subjective. o Most common form of tinnitus o Most associated with hearing loss o examples:  Meniere s disease  ototoxicity  noise exposure 16

Diagnosis 1.History: y Describe sound y Duration y Other otologic symptoms (hearing loss, vertigo, otalgia, otorrhea) y Severity y Precipitating factors (noise, ototoxic drugs, trauma, infection etc.) 2. PE: y Full head and neck exam y Neuro-otologic exam y Auscultation of ear canal, peri-auricular area, orbits, neck bruits. y Palatal or TM rhythmic contractions. y additional tests: o audiometry o US o CT o MRI/MRA/MRV o angiography Management y Treatment designed to eliminate tinnitus. (anatomic or systemic causes) ex. Surgery. y Treatment designed to reduce the severity of tinnitus. (insult to inner ear) ex. Acoustic therapy, lifestyle change.

____________END OF TRANSCRIPTION__________ HI to reych, arabels, ana, quennie, eloh, jez, gem Happy studying!

IMY

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