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- 0-15 normal
- 16-25 slight
- 26-40 mild
- 41-55 moderate
- 56-70 moderately severe
- 71-90 severe
- 90+ profound
What are the landmarks for mastoid antrum in mastoidectomy?
- spine of henle
- cribriform bone
- McEwen's triangle
Free field voice test estimated thresholds?
- whisper 2 feet: 12dB
- whisper 6 inches: 34 dB
- Conversation 2 feet: 48 dB
- Conversation 6 inch: 56 dB
- Loud 2 feet: 76 dB
Resonance of external and middle ear parts?
- EAC: 3000 Hz
- TM: 800-1600HZ
- Middle ear: 800Hz
- Ossicles: 500-2000Hz
Main causes of crocodile tear syn?
- After Bell's palsy
- Syphilitic lesion of geniculate ganglion
- Section of greator superficial petrosal nerve
Types of grommet?
- Kurz ( metal tube)
- Goodie T.tube
- Reuter Bobbin
- Collar button
- Linderman- Silverstein
Types of OAE? (otoacoustic emissions)
- spontaneous (SOAE)
- transient (TOAE)
- distortion product (DPOAE)
- Stimulus frequency (SFOAE)
What is TOAE?
In humans, a delay between stimulus offset and onset of the evoked emissions varies between 4 ms, for high frequencies, and 20 ms for low frequencies. This temporal separation helps in visual identification and separation of the transient-evoked emissions from the stimulus that evoked them, that is also recorded. Thus, TEOAEs are typically presented as an amplitude/time plot of the acoustic waveform recorded from the ear canal.
How to evoke TOAE?
With a tone burst in the mid-frequencies.
What is DPOAE?
- DPOAEs are generated in the cochlea in response to two simultaneous pure-tone stimuli (primary tones). This tonal response is not present in the eliciting stimuli, and is therefore referred to as a distortion.
- DPOAEs are attributed to nonlinearity of motion of the outer haircells, particularly at low stimlus levels.
Methods of placing microphone for recording ECoG?
- On the TM
- in EAC
What is ABEP?
Auditory nerve and brainstem evoked potentials, same as ABR or BSER
waves of ABEP: normal latencies, and relations?
- wave I: 1.5ms after stimulus onset: Cohclea
- Wave II: 1 ms: proximal CNVIII
- Wave III: same: brainstem (cochlear nucleus, Sup.Olivary complex)
- Wave IV, V: same: upper pons (lat.lemniscus, Inf. colliculus)
What is SSRs?
The major peaks of AMEPs (auditory middle-latency potentials) are approximately 25 ms apart, stimulation (with clicks or tone pips) at a rate of 40 persecond results in the summation of non corresponding components to consecutive stimuli, creating a periodic sinusoidal waveform.
Definition of tympanometric acoustic reflex?
Tympanometry is the continuous measurement of middle ear impedance as air pressure in the sealed external ear canal is varied.
- A: clear peak of compliance between 0 and -100mm of water
- As: short peak in the same zone (Otosclerosis)
- AR: very tall peak (ossicular disruption)
- B: flat, fluid in middle ear
- C: peak at pressure more negative than -100cm H2O
What are the most widely used hearing screening tests?
How to use ABEP (ABR) as audiogram estimation?
When frequency-specific stimuli are used, the most prominent component of ABEPs is a slow negativity following peak V, at approximately 10 ms,other wisecalled SN10 (slow negativity at 10ms). This slow nagativity, or the preceding peak V, can be detected down to approximately 10-15 dB above the subject'shearing threshold for the stimulus used to evoke SN10.
ABEPs with prolonged peak I latency, but normal latencies of the subsequent peaks, are also compatible with high-frequency sensorineural hearing loss.
TOAE related numbers?
- click 80 dB
- 700-4000 Hz
- (-)ve if HL more than 25-30dB
DPOAE related numbers?
- 2 primary sounds F1, F2, 1.2 difference
- If (-)ve in normal middle ear: hearing threshold less than 30-35dB
- Normal OAE
- Abnormal ABR
- Poor speech discrimination
- Missing ART
- normal imaging
What is EcoG?
What are its components?
Short latency evoked potential that reflects the summed activity of a large number of peripheral auditory nerve fibers and cochlea
- SP/AP normally 0.16-0.31%
- it is not suitable in HL>70dB
How ABR can detect hearing threshold?
- Lowest level of sound intensity at which wave V is present is ABR threshold and can predict hearing sensitivity within 5-20dB
- What happens if one labyrinth is destroyed?
- a complete or, more often, partial ocular tilt reaction that is always towards the side of the lesion. Owing to semicircular canal deafferentation, there is also a spontaneous horizontal torsional nystagmus, with the fast phases away from the side of the lesion, as well as vomiting.
Hyposthesia of posterior wall of EAC plus SNHL ( vestibular schwannoma)
Cohen-Friedman criteria for Malignant otitis externa?
- - pain
- - exudate
- - not responding to locat treatment for 1 week
- - oedema
- - microabscess
- - granulation tissue
- - Pseudomona +ve
- - positive TC-99 scan
- - old age
- - DM
- - Lower CN palsy
- -Positive CT finding
Definition of Malignant otitis externa?
Malignant otitis externa is an aggressive and potentially fatal infection originating in the external canal, with progressive spread along the soft tissues and bone of the skull base, ultimately involving intracranial structures
Types and examples of some ototoxic drugs?
- -cochleotoxic: neomycin
- -vestibulotoxic: gentamicin
- Loop diuretics
- Cytotoxic: cisplatin
- Beta blockers
What happens if both labyrinths are destroyed?
the patient will not experience vertigo, since there is no left-right asymmetry in vestibular nucleus activity.
What is Bechterew effect?
Unilateral labyrinth destruction has symptoms. but if the other labyrinth is destroyed after the first one, the vestibular symptoms will subside.
What happens if one labyrinth is stimulated?
A stereotyped reflex rotation of the head and eyes in the plane of the stimulated SCC. For example, stimulation of the left lateral scc or its nerve produces predominantly horizontal left beating nystagmus, corresponding to the orientation of the lateral scc within the temporal bone.
How to define the location of otoconia in Dix-hallpike test by looking at the nystagmus?
If the nystagmus is predominantly horizontal, then the otoconia are in the lateral scc. If the nystagmus is upbeat and torsional, then the otoconia are in the posterior scc.
What semicircular canal is usally tested by Caloric test?
Lateral. as it is the nearest one to thermal stimulus.
What is the management option for vertigo due to acute relapsing Multiple Sclerosis?
What is Stemetil?
- (Prochlorperazine) a dopamine (D2) receptor antagonist that belongs to the phenothiazine class of antipsychotic agents that are used for the treatment of vertigo. It is a stong antiemetic, and is also a highly potent typical antipsychotic. It is also used to treat migraine headaches.
- Side effects: akathisia (restless leg syn), dystonia, extrapyramidal symptoms in elderly.
What are the vestibular neurotransmitters?
- Peripheral vestibular: Glutamate, Glycine
- Central vestibular modulators: histamine (excitory), dopamine (inhibitory), noradrenaline , serotonine
- VOR pathways: GABA ( inhibitory)
Mechanysms of drugs which control Vertigo?
They suppress integration of sensory stimuli by targeting acetylcholine, histamine and y-GABA neurotransmitter action at the level of primary to secondary vestibular neurons and the vestibular nuclei.
What is the mechanism of antiemetic drugs?
- the chemoreceptor zone in the area postrema: blocked by dopamine agonists
- the gastrointestinal tract: blocked by serotonin 5-hydroxytryptamine (HT)
- from the labyrinth leading to stimulation of the vestibular nuclei: blocked by antihistamine and glutamate antagonists.
Vestibular suppressant drugs categories?
- Anticholinergics: SC Hyoscine, Scopolamine nasal spray
- Antihistamines: Promethazine, IV Prochloprazine (Stemetil), Piperazines (Cyclizine, Dimenhydrinate)
- Ca++ channel antagonists: Cinnarizine (Stugeron)
- Others: Diazepam, steroids, Metoclopramide (Ach,Dopa, 5HT3 antagonist),
What is the mechanysm of Betahistine in controlling the vertigo in Meniere's?
- It is a histamine analogue with weak agonistic H1,H2 and strong antagonistic H3.
- -Reduction of asymmetric function of vestibular end organs.
- -Improved microvascular circulation of Stria Vascularis
- -Inhibition of activity in vestibular nuclei.
- -Less specific effect on alertness through Cerebral H1 receptors.
What is the mechanism of action of intratympanic injection of gentamicin for Meniere's?
- It is a vestibulotoxic drug which destroys the dark cells of secretory epithelium of vestibule and reduces the endolymph production.
- profound SNHL in 3%
what is your diagnosis? what is its definition?
- The patient (young child) can detect sounds better than speech, worse hearing in noisy area or by phone. Normal OAE, better PTA than expected, poor ABR or Speech Detection result, normal imaging.
- Causes: prematurity, perinatal events, LBW, hyperbilirubinema, ototoxicity, CP, neonatal ventilation dependency.
Why intracranial portion of facial nerve is vulnerable in CPA surgery?
Lack of covering. It only has piamatter and not covered by perineurium.
Is facial recess lateral or medial to facial nerve?
What is the thinnest and shortest part of facial nereve?
What is the most important landmark of second genu of facial nerve?
Seddon types of nerve injury?
Why after nerve injury, the distal nerve excitability is maintained for 3-4 days?
Because wallerian degeneration takes place over a 3-4 days period following injury.
Describe nerve coating layers:
Sunderland types of nerve injury?
Definition of Grade II House-Brackmann staging system for facial nerve palsy?
- Slight weakness noticeable only on close inspection
- Complete eye closure with minimum effort
- Slight asymmetry of smile with maximal effort
- Synkinesis barely noticeable, contracture or spasm absent
Definition of Grade III House-Brackmann staging system for facial nerve palsy?
- Obvious weakness, but not disfiguring
- May not be able to lift eyebrow
- Complete eye closure and strong but asymmetric mouth movement with maximal effort
- Obvious, but not disfiguring synkinesis, mass movement or spasm
Definition of Grade IV House-Brackmann staging system for facial nerve palsy?
- Obvious disfiguring weakness
- Inability to lift eyebrow
- Incomplete eye closure and asymmetry of the mouth with maximal effort
- Severe synkinesis, mass movement, spasm
Definition of Grade V House-Brackmann staging system for facial nerve palsy?
- Motion barely perceptible
- Incomplete eye closure, slight movement corner mouth
- Synkinesis, contracture and spasm usually absent
Topodiagnostic tests of facial nerve?
- Schirmer ( >75% unilat decrease)
- Stapediall reflex
- Electrogustometry (comparison)
- Salivary flow testing (>25% reduction of submandibular gland secretion)
What is the window period to perform ENG in FN palsy?
Electronystagmography(ENG) is not useful until the fourth day of facial nerve paralysis as it takes about three days for Wallerian degeneration to reach completion. It is also of less value after three weeks because of nerve fibre desynchronization (concurrent degeneration and regeneration).
What is the most valuable prognostic test among electrophysiological tests of FN palsy?
EnoG, which detects compound muscle action potential CMAP after stimulus of nerve at SM foramen through surface electrodes.
In Bell's palsy, degeneration of >90 percent developing within 14 days of complete paralysis indicates probable poor recovery in >50 percent of cases.
Can EnoG be used in Ramsay Hunt syn? why?
- because of multiple sites of nerve involvement.
Fisch's recommendation for surgical intervention in traumatic facial nerve injrury?
Fisch has recommended surgical intervention within three weeks in patients where traumatic injury has resulted in >90 percent amplitude reduction by ENG within six days of the injury.
What is electromyography of facial nerve?
Electromyography records active motor unit potentials of the orbicularis oculi and orbicularis oris muscles during rest and voluntary contraction.
When EMG is valuable to perform after facial nerve injury?
EMG has no value in the first twoweeks after the onset of paralysis because fibrillation potentials indicating nerve degeneration do not appear until after eight to ten days.
Types of muscle response in EMG?
- polyphasic: regenerative processes. surgery not required.
- Fibrilation: lower motor neuron injury, viable motor end plates. surgery required for anastomosis.
- Silent: long term denervation. Facial re-animation required (Static, dynamic)
Limitations of EMG?
- It only stimulates normal or neurapraxic fibres and cannot distinguish between second- and third-degree injuries which have different prognoses.
- It provides no useful information in cases of incomplete facial paralysis.
- It fails to provide information on the immediate post -paralysis period (first 72 hours).
Causes of facial palsy?
- Birth related
- trauma (fracture, injury, barotrauma...)
- Neurological (obercular syn, Millard Gubler syn)
- Infection (bacterial, viral,TB, fungus, lyme)
- Metabolic (DM,HBP, hyperthyroidism)
- Neoplastic (cholesteatoma, leukemia, glomus, schwannoma, NF,..)
- Toxic (tetanus, CO)
- Iatrogenic (mastoid surgery, tonsillectomy, post-immunization..)
- Idiopathic (Bell's, Melkerson, autoimmune, PAN, MS,MG, sarcoidosis)
What is the major aetiologic agent in Bell's palsy?
Poor prognosis is Bell's palsy recovery?
The majority of patients with Bell's palsy recover completely. However, poor prognosis has been related to complete paralysis at onset or incomplete paralysis with late onset of recovery, old age, a dry eye, abolished taste, absent stapedius reflex and postauricular pain.
What is the mainstay of treament for facial palsy associated with AOM?
- Antibiotic therapy. If no TM perforation: M&G
- Mastoid exploration and facial nerve decompression
What is the antibiotic of choice in Malignant otitis externa?
Ciprofloxacin 750mg/BD x 6 weeks
Parts of temporal bone?
- I. squamous;
- 2. petromastoid;
- 3. styloid;
- 4. zygomatic.
causes of granular myringitis?
- High-ambienttemperature, swimming, lack of hygiene, local irritants and foreign bodies have all been suggested as causative factors.
- Granular myringitis is also occasionally seen as apostoperative complication of tympanic membrane grafting.
What is benign necrotizing otitis externa?
Benign necrotizing otitis extern a is the clinical condition of idiopathic necrosis of a localized area of bone of thetympanic ring, with secondary inflammation of the overlying soft tissue and skin.
Boundaries of infratemporal fossa?
- The infratemporal fossa lies below the middle cranial fossa, between the ramus of the mandible and the lateral wall of the pharynx.
- The 'roof' is the infratemporal area of the skull base,which comprises the greater wing of the sphenoid with a small triangular contribution posteriorly from the squamous temporal bone.
Contents of infratemporal fossa?
- Pterygoid muscles
- Maxillary artery and its branches
- Pterygoid venous plexus and maxillary veins
- branches of mandibular nerve.
What are the parts of maxillary artery?
3 parts, proximal, on and distal to the lateral ptreygoid muscle, having 5 branches each.
Branches of first part of maxillary artery?
- inferior alveolar artery
- middle meningeal artery
- accessory meningeal artery
- deep auricular artery
- anterior tympanic artery.
Branches of the second part of maxillary artery?
- Masseteric artery
- Pterygoid branches
- Deep temporal arteries (anterior and posterior)
- Buccal artery
Branches of the third part of maxillary artery?
- Sphenopalatine artery (Nasopalatine artery is the terminal branch of the Maxillary artery)
- Descending palatine artery
- Infraorbital artery
- Posterior superior alveolar artery
- Artery of pterygoid canal
- Pharyngeal artery
- Middle superior alveolar
- Anterior Superior Alveolar
Main symptoms of lateral skull base lesions (CPA tumors, VS,memningiomas, paragangliomas...)?
- Hearing loss (81% of all cases), SNHL,CHL, MHL
- Otorrhea, especially persistantly tinged with blood
- Tinnitus (Subjective or objective)
- Vertigo & imbalance (up to 50% cases)
- Headache, otalgia, facial pain
- Ophtalmic symptoms
- Facial palsy (30% of cases)
- Lower cranial nerve symptoms (jugular formamen area)
Why is it advised to do MRI for BBPVs which do not respond to Epley's maneuvre?
There have been a number of reports in the literatureof patients with skull base and intracranial tumours that have presented with symptoms and signs of BPPV, e.g. meningiomas,VS, gliomas, lipomas and CPA cholesteatomas.
Investigations for suspected CPA lesions?
- Bilateral otoscopy
- H&N examination
- neurological examination ( CN palsy)
- Vestibular examination (nystagmus, Rhomberg, Unterberger)
- Audiology + speech audiometry
- Vestibular function tests (Caloric tests, nystagmography)
- Facial function tests (ENoG)
- Radiology (MRI)
What is the enzymatic activity of progression of otosclerosis related to?
Alpha 1 antitripsin which can be detected in perilymph of patients with progressive otosclerosis.
Skin abscesses related to mastoid abscess?
- citelli (behind mastoid)
- Bezold (on the sternocleidomastoid muscle)
Congenital inner ear dysplasia?
- Mondini: lack of upper turn of cochlea (50%)
- Shiebe: cochleosaccular dysplasia
- Common cavity
- Alexander: Lack of basal turn
- Bing-Siebman: Lack of membraneous labyrinth
- Michel: total aplasia
Variants of Meniere's disease?
- Cochlear hydrops
- Vestibular hydrops
- Drop attacks (Tumarkin crisis)
- Lermoyes Syn ( HL, then vertigo while HL improves)
WHat is Glycerol test in Meniere's disease?
- Oral Glycerol 1.5mg/kg
- then PTA after 1-2 h
(+)ve If >10dB improvement in more than 2 frequencies or SDS improve more than 10%
Types of Stapedial otosclerosis?
- biscuit type
Van der Hoeve syn?
- osteogenesis imperfecta
- blue sclera
contraindication of stapedotomy?
- The only hearing ear
- Associated with Meniere's disease
- Young children
- Professional athletes
- Work in noisy surroundings
- otitis externa
5 causes of SNHL after stapedotomy?
- Immediate: direct trauma to labyrinth/rupture of cochlear duct
- contamination of perylymph fluid
- repairative granuloma
- Acoustic trauma by excessive manipulation of foot plate
- Perlilymph fistula
5 Causes of CHL post stapedotomy?
- Malfunction of prosthesis
- Fibrous adhesion
- TM perforation/retraction
- Failure to recognise malleus fixation
- Failure to recognise RW obliteration
Criteria for tympanoplasty?
- CHL > 30 dB
- Good cochlear function
Contraindication for tympanoplasty?
- Dead ear
- poor cochlear function
- Epidermization of middle ear
- an only hearing ear
- much better hearing ear
Indications of labyrinthine neurectomy?
- Vestibular MD
- Refractory BPPV
- Recurrent vestibular neuronitis
- Traumatic labyrinthis
Relapse and mortality rate of malignant otitis externa?
advantages of binaural hearing?
- locating the direction of sound
- Binaural squelch (cocktail party effect) (ability of focusing on a sound in a noisy area)
- Binaural summating (improving sound/noise ratio)
- vestibulo-ocular reflex (eye movement control)
- vestibulocollic reflex (Neck movement control)
- vestibulospinal reflex (body posture control)
- Olivocochlear reflex (stiffening BM in cochlea)
maskin methods for FFVT?
- paper rubbing (30dB)
- tragal rubbing (50dB)
- barany box (90-100dB)
Rules of masking in PTA?
- AC difference:
- >40dB (headphone)
- >55dB (earphone)
BC difference >15dB
BC of better ear in better by 40,55 dB than the not masked AC of worse ear
Numbers in tympanometry?
- probe tone 226Hz
- Altering presure: +200 to -200 daPa
- Normal ear canal volume: 0.6-1.5ml
- ME pressure: +-100daPa
- Static admittance: 03-1.4 (least reflected SPL)
Numbers in Acoustic reflex?
- The lowest intensity level at which the acoustic reflex can be detected at 0.5, 1,2,4k
- Normal: 70-100dB
- not more than 110dB
Acoustic reflex decay is (+)ve when?
Test for 10 secs, when acoustic reflex decreases by >50% in the first 5 seconds of testing
- When BCs are normal, and AC thresholds exceed intraural attenuation:
- If not masking: reflect the response from non test ear
- If masking: worse results on test due to overmasking
Audiometric criteria for acoustic neuroma?
- asymmetric hearing loss in HF at > 2 adjacent frequencies
- poor SDS
- Absent ARTS
- Positive acoustic reflex decay
Fluctuating HL, diplacusis, recruitment, recurent vertigo
Congenital / aquired (Barotrauma, trauma, heavy lifting, middle ear surgery)
RW,OW (Mondini). labyrinth (Cholesteatoma), SCDS
Ix: exploration, HRCT
Tx: Packing the defect
Patsonic staging for cholesteatoma?
- 1: limited to 1 quadrant
- 2: multiple quadrant without ossicular involvement
- 3: ossicular involvement without mastoid involvement
- 4: mastoid involvement: 67% risk of residual disease
Basic theories of choleteatoma?
- Invagination of TM (attic retraction pocket) (witmaack-tumarkin)
- Basal cell hyperplasia (papillary projection) (Lange)
- Migration through perforation (Habermann,Weiss)
- Squamous metaplasia of middle ear epithelium (Wendt, sade)
- Congenital cell rest in ant.epithympanum (Michael)
Definition of cholesteatoma?
Epidermal inclusion cyst of middle ear or mastoid, containing desquamated debris (keratin)
Indications of OAE?
- - Noise induced SNHL
- - Ototoxic drugs
- - Congenital HL
- - Hypoxia
Examples of MHL?
- Ototoxicity in TM perforation
- Congenital anomaly of inner and outer ear
Types of Presbycusis?
- Sensory : Organ of corti, HFSNHL
- Neural: Spiral g: HFSNHL, poor speech descrimination score
- Strial (metabolic): Flat PTA
- Cochlear conductive: BM stiffnes (sloping PTA)
- The triad of hearing loss, tinnitus, and vertigo constitutes Meniere's syndrome. If the cause is
- unknown, it is defined as Meniere's disease.
The main causes of Meniere's syn:
- Infections: otosyphilis, viral (late onset of endolymphatic hydrops)
- auto-immune: Cogan
- Neoplastic: Schwannoma
- otosclerotic foci causing mechanical endolymphatic blockage
Definition of sudden SNHL?
- HL> 30dB
- In > 3 consequtive frequencies
- In less than 72 hours
possible etiologies of otosclerosis?
- Humoral autoantibody to collagen type 2
- genetic mutation in collagen metabolism
- measles viral infection in otic capsule
Otologic manifestations of Paget's disease?
Clinical manifestations include hearing loss, tinnitus, and mild vestibular dysfunction. The facial nerve is spared. Hearing loss occurs in 5% to 44% of patients
the most common cause of progressive conductive hearing loss in adults?
The pathologic changes of otosclerosis?
It begins as spongification of the bone of the otic capsule.
In what situation, otosclerosis is manifested with isolated SNHL?
Occasionally, the lesion may involve only the cochlea, causing an isolated sensorineural hearing loss
what is ART in otoclerosis?
- early OS: diphasic
- Late OS: absent
Complications of stapedotomy?
- Total SNHL 0.2%
- HL 2%
- Serous labyrintitis
- Damage to chorda Tympani 30%
- TM perforation
- positive fistula test due to long prosthesis
- facial nerve palsy
- perilymph fistula
Types of tympanoplasty?
I: like myringoplasty
II: prosthesis between malleus and stapes
- a: myringostapedopexy
- b: prosthesis between remnant of malleus or TM and stapes (Minor collumella)
- c: prosthesis between TM and footplate (Minor comullea)
IV: Cavum minor
(TM attached to footplate)
- V: (in case of fixed footplate)
- a: Third window (fenestration of LSCC)
- b: removal of footplate and attachment of TM to the fat graft in oval window)
Indications of Hyperbarric chamber?
- mucormycosis (fungal rhinosinusitis)
- FN palsy
- radiosensitization in radioresistance in RT
Mechanism of bone erosion in cholesteatoma?
- Increase osteoclastic activity:
- -katepsin like protease
- Keratin debris:
- -reduce pH
- --direct mineral bone resorption
- --increase activity of catepsin like protease
- -FB granuloma
- Activated monocytes:
- -increase PG production, Leukotriens, Cytokines (increase osteoclastic activity)
- Direct pressue
- -resistance to antibiotic
- -increase lipopolysaccaridase (increase osteoclastic activity)
symptoms/signs of superior semi-circular canal dehiscence?
- hyperacusis of bone conduction
- dizziness in loud noise (tulio's), increase pressure in middle ear or intracranium (Hennebert)
- vertical nystagmus
- PTA: conductive hearing gain
- reduced threshold in VEMPs