ENT otology 2

The flashcards below were created by user Kianoosh on FreezingBlue Flashcards.

  1. Malignant otitis externa is?
    An aggressive and potentially life-threatening infection of the soft tissues of the external ear and surrounding structures, quickly spreading to involve the periostium and bone of the skullbase.
  2. Staging of Malignant otitis externa(MOE)?
    • 1) Clinical evidence of malignant otitis externa with infection of soft tissues beyond the external auditorycanal, but negative Tc-99 bone scan
    • 2) Soft tissue infection beyond external auditory canal with positiveTc-99 bone scan
    • 3) As above, but with cranial nerve paralysis
    • 3a Single
    • 3b Multiple
    • 4) Meningitis,empyema,sinus thrombosis or brain abscess
  3. Diagnosis criteriae for Malignant otitis externa(MOE)?
    In summary, the combination of pain, granulations, otorrhea and resistance to local therapy forat least eight to ten days are highly sensitive for making adiagnosis of malignant otitis externa.

    Diabetes or otherimmunocompromised state, Pseudomonas aeruginosa on culture, a positive bone scan and cranial nerve palsy are confirmatory factors that enhance the specificity of the diagnosis.
  4. Radiologic investigations for Malignant otitis externa(MOE)?
    • Technetium (TC-99): detects osteoblasts/osteoclasts : for diagnosis
    • Gallium (Ga-67): detects leukocytes: returns to normal after subsiding the infection.
  5. Current Mortality rate of Malignant otitis externa(MOE)?
    • if early detection: 10%
    • if cranial nerve palsy: 80%
  6. What is the difference between Keratosis obturans and primary EAC cholesteatoma?
    Keratosis obturans is the accumulation of a large plug of desquaminated keratin in the external auditory meatus,while primary auditory canal cholseteatoma is the invasionof squamous tissue from the ear into a localized area of bony erosion.
  7. Symptoms of Keratosis Obturans?
    Keratosis obturans occurs more commonly in younger patients. It classically presents with acute severe otalgia and a conductive hearing impairment. Infrequently the disease is bilateral. There may be an associated bronchiectasis or sinusitis.
  8. The most common presentation of EAC cholesteatoma?
    chronic otorrhoea with dull pain or itching. It is not associated with hearing impairment.
  9. Definition of otitis externa?
    a generalized condition of the skin of the external auditory canal that is characterized by general oedema and erythema associated with itchy discomfort and usually an ear discharge.
  10. Definition of perichondritis of external ear?
    • infection or inflammation involving the perichondrium of the external ear, auricle and external auditory canal. it is usually secondary to trauma.
    • DD: repalsing perichondritis, NHL
  11. classification of perichondritis of external ear?
    • erysipelas of external ear
    • cellulitis of external ear
    • perichondritis
    • chondritis.
  12. Clinical management of perichondritis of external ear?
    • Consider broad-spectrum (including anti pseudomonas)antibiotic prophylaxis in severely traumatized or burnt pinnas
    • Early use of local and systemic broad-spectrum, antipseudomonal antibiotic if perichondritis issuspected
    • In resistant cases, add effective local antibiotic delivery by irrigation
    • Conservative surgery for drainage of abscesses,creation of irrigation and excision of necroticcartilage, with preservation of the perichondrium wherever possible.
  13. What is relapsing perichondritis?
    • a rare systemic autoimmune? disease involving multiple cartilages and joints causing atrophy with cyctic spaces in cartilage.
    • No reliable tests
    • Tx: steroids, immunosuppressants
  14. What is Tympanic sulcus?
    the groove on the inner aspect of the tympanic part of the temporal bone in which the tympanic membrane is fixed.
  15. Greisinger's sign is due to?
    • Mastoid pain due to thrombophlebitis of mastoid emissary vein in lateral sinus thrombosis (LST)
    • Definition of Herpes zoster oticus?
    • Herpes zoster oticus or Ramsay Hunt syndrome is defined as a herpetic vesicular rash on the concha, external auditory canal or pinna with a lower motor neurone palsy of the ipsilateral facial nerve.
  16. Management options for Ramsay hunt syndrome?
    acyclovir 80mmg 5/day and prednisolone within 3 days of the onset of symptoms. Better recovery with early treatment, compared to only poor results when treatment is started on or after day 8.
  17. Definition of OME?
    chronic accumulation of mucus within the middle ear and sometimes the mastoid air cell system. The time that the fluid has to be present for the condition to be chronic isusually taken as 12 weeks.
  18. Tos staging of attic retraction ?
    Image Upload 1
  19. Triad of signs of temporal bone TB:
    • regional lymphadenopathy in the absence of typical systemic features of tuberculosis
    • delayed onset of presentation
    • refractory otitis unresponsive to conventional antimicrobial agents.
  20. Characteristic finding of temporal bone TB otitis media?
    • Abundant,pale granulations appear to be characteristic of tuberculous otitis media.
    • Image Upload 2
  21. Definition of otosclerosis?
    • Otosclerosis is a localized hereditary disorder (autosomal dominant with variant penetration) affecting endochondral bone of the otic capsule.
    • characterized by disordered resorption and deposition of bone. An otosclerotic lesion consists of areas of bone resorption, new bone formation, vascular proliferation and a connective tissue stroma.
    • Otosclerosis occurs at certain sites of predilection within the otic capsule: fisula antefenestrum the commonest
  22. What is the first histologic change of otic capsule in otoscerosis?
    Blue mantel: they stain more basophilic in otic capsule specimen
  23. Why otosclesis causes bone deformity?
    An otosclerosis focus is usually a little larger in volume than the bone that it replaces, and thus, otosclerosis causes thickening of the structures affected.
  24. Types of otosclerosis lesion?
    • active: spongiotic
    • inactive: sclerotic
  25. Aetiological agents of otosclerosis?
    • genetic mutaions
    • measles viral infection
    • autoimmunity disorder
  26. True or false?
    Complete obstruction of the round window membrane means that stapes surgery in such an ear will not be successful.
  27. What is the mechanism of SNHL in otosclerosis?
    SNHL occurs when an otosclerotic focus reaches the endosteum of the cochlea, causing atrophy of the subjacent spiral ligament with impairment of fibrocytes and replacement by an amorphous eosinophilic substance (hyalinization of the spiral ligament) and also disturbing the normal homeostasis of cochlea.
  28. incidence and cause of vestibular symptoms in otosclerosis?
    • 10-30%
    • degeneration of Scarpa's ganglion from soluble toxic substances liberated by otosclerotic bone or to changes in biochemistry of the inner ear fluids or both.
  29. Is otosclerosis gendere related?
    Incidence of otosclerotic Bony changes are equal in men/women (3.5%). It is only when the air-bone gap is 30 dB or greater are women (x 3) more likely to have otosclerosis than men. The incidence increases with age.
  30. What is The 'gold' reference standard of diagnosis of otosclerosis?
    surgery, when it should be possible to exclude the considerably rarer causes of such an impairment, e.g. congenital ossicular chain abnormalities.A 'flamingo flush' or Schwartz sign, a red blush of the tympanic membrane over the promontory,is said to be due to the vascularity of an active otosclerotic focus but is rarely seen.
  31. What frequencies are better to be checked for air-bone gap in otosclerosis? What resultes are important?
    the American Academy of Otolaryngology and Head and Neck Surgery hasrecommended that a four frequency average over 0.5, I, 2 and 3 kHz be taken. >10dB AB gap: CHL, >20dB: required surgery ( even between 10-20dB)
  32. what is Carhart's notch?
    when the skull is vibrated by bone-conduction sound, the sound is detected by the cochlea via 3 routes.Route (a) is by direct vibration within the skull, route (b) is by vibration of the ossicular chain which is suspended within the skull and route (c) is by vibrations emanating into the external auditory canal as sound and being heard by the normal air-conduction route. In a conductive hearing impairment the latter two routes are deficient but are regained by successful reconstruction surgery. Hence the bone-conduction thresholds improve following surgery.The reason that there is a Carhart notch at 2 kHz before the surgery is that the Carhart effect is greatest around that frequency.
  33. Is there any role for flouride in controlling otosclerosis?
    There is no evidence at present that the level of fluoride in water has an impact on the natural progression of clinical otosclerosis.There is no evidence to support the use of oral sodium fluoride in otosclerosis.
  34. What activicites are cautioned or banned after stapedotomy?
    Flying as a Military pilot,Commercial air travel, snorkelling, scuba-diving, strenuousactivities and parachuting.
  35. Do tympanometry and radiography in general aid the diagnosis of clinical otosclerosis?
  36. postoperative complications of stapedotomy?
    • CHL: (eraly, late: the main cause of revision surgery)
    • SNHL:(early, late, due to surgical trauma: more common in revisoin surgery)
    • FN injury: (early: LA injection, late: unknown) 0.1-0.5%
    • Vertigo: if persistant: BPPV, perilymph fistula, overlong prosthesis
    • Perilymph fistula: (primary: at the end of op, secondary: late) 1.5-12%
    • Reparative granuloma: granulation around prosthsis, 1-2 weeks post-op, 0.1%
    • Discomfort ot loud noise
    • Alteration in taste: damage to CT, 30%
    • Cholesteatoma
    • Meningitis
  37. Symptoms/signs of perilymph fistula after stapedotomy?
    persistent or fluctuating hearing impairment in 71-87% of cases, which may be sensorineural, mixed orconductive in nature; vertigo in approximately 1/3 of patients and dysequilibrium in a further third; tinnitusin 28-45%; and sometimes a sense of fullness in the ear. Some patients with a fistula have presented with meningitis. A positive fistula test may be present in 2/3 of cases.
  38. The main 3 causes of failure in stapedotomy?
    • Prosthsis displacement
    • Incus erosion
    • Bony growth over the fenestration
  39. What is the 2nd most common bone disease in the world?
    Most common in?
    Relation to ENT?
    • Paget's diease or osteitis deformas
    • In whites, m/f=3:2
    • unknown
    • increased bone turnover
    • monostotic, polyostotic
    • HFSNHL, LF AB gap
    • X-ray
    • Pysiotherapy, antiresorptive, analgesics, surgery
    • Osteosarcoma, frontal bossing, pain, deformity
  40. What is otitic barotrauma?
    • an injury produced by mechanical forces caused by a change of pressure in the gas-filled space of ear.
    • Both midle and inner ear can be involved.

    • general mechanism: oedema or rupture of middle ear vessels due to negative pressure of midle ear (difference > 60mmHg), locking ET tube (difference >90mmHG), severe TM retraction or rupture. Unilateral TM rupture in diving can cause caloric vertigo due to influx of cold water into middle ear.
    • pressing stapes to OW due to TM retraction and bulging of RW due to negative pressure of middle ear,plus positive intrecranial pressure during diving or Valsava's menouvre can cause rupture in RW and perilympg fistula.(diference >120-300mmHg)
  41. Variants of otitic barotrauma?
    • Compression injuries (descent)
    • Injuries at stable pressure (high-pressure nervous syn in divers exposed to extremely high pressures, they muts inhale Trimix which is combination of hydrogen-helium-oxygen,
    • Decompression injuries ( Ascent)
  42. What is the cause of Barotraumatic facial palsy in ascent?
    The most widely accepted explanation for atransient unilateral facial palsy occurring during, or soon after ascent is that of a pressure-induced neuropraxia throught the Dehiscence of the facial nerve in its intramastoid portion, which occurs in 0.5 to 57% of all temporal bones.
  43. Types of presbycusis?
    • sensory: loss of hair cells at the basal turn of organ of corti. (the most common)
    • neural: degeneration of cochlear nerve.
    • vascular (metabolic): atriphy of Steria vascularis
    • Cochlear conductive (mechanical): stiffness of cochlear basilar membrane.
    • Cochlear duct changes: submicrospcopic changes in intracellular organelles, and endolymphatic composition
    • mixed: some combination of the other 5 types
  44. Binaural hearing has been shown to produce an approximate, additional, 10dB sensory advantage.
  45. What is ototoxicity?
    Ototoxicity is chemical injury to the labyrinth occurring as a side effect of pharmacotherapy.
  46. Risk factors of ototoxicity?
    • Risk factors for ototoxicity include the cumulative drug dose, the duration of treatment, bacteraemia and renal or liver failure.
    • Also: genetic susceptibility, seriously ill patients, foetus at around 18-20 weeks of gestation.
  47. What is the pattern of hearing loss in ototoxicity of cisplatin?
    bilateral, symmetric, progressive, high frequency sensorineural loss, caused by a loss of cochlear outer, and to a lesser extent inner hair cells
  48. What is the mechanism and pattern of hearing loss in ototoxicity of Loop Diuretics?
    oedema of the stria vascularis which causes a loss of the endocochlear potential (battery of hair cells)

    Reversible, flat sensorineural hearing loss, but a permanent profound loss can occur. The auditory symptoms may beassociated with ataxia.
  49. What is the mechanism and pattern of hearing loss in ototoxicity of Aspirin and Quinine?
    Impairment of ionic conductances through outer hair cells.

    reversible tinnitus, hearingimpairment, nausea and transient vomiting. The auditorysymptoms correspond with a flat, reversible sensorineuralhearing,
  50. postulated causes of sudden SNHL?
    • Viral infection
    • Other infection: syphilis, encephalitis
    • Vascular
    • Autoimmune
    • Hypoxia
    • Labyrinthine membranerupture
    • Barotrauma
    • Ototoxic drugs
    • Multiple sclerosis
    • Cogan's disease
    • Haematological: sickle cell, hyperviscosity
    • Meniere's disease
    • Vestibular schwannoma: vascular compromise
  51. Tests to do in sudden sensoryneural hearing loss (SSNHL)?
    • full blood count and erythrocyte sedimentation rate(ESR)
    • urea and electrolytes
    • lipid profile
    • glucose
    • thyroid function
    • syphilitic serology
    • auto-antibodies
    • ± MRI (depending on availability).
  52. What is recovery types of sudden sensoryneural hearing loss (SSNHL)?
    • complete, <10 db (about 50% of untreated cases)
    • partial,~ 50 percent
    • none, <50 percent of deficit
  53. Definition of Tinnitus?
    a sound perceived for more than five minutes at a time, in the absence of any external acoustical or electrical stimulation of the ear and not occurring immediately after exposure to loud noise.
  54. Definition of hyperacusis?
    Possible causes?
    • reduced tolerance to noise, or an increased sensitivity to sounds in levels that would not cause discomfort in a normal individual. patients with hyperacusis complain of excessively loud perception of ordinary environmental sounds.
    • disinhibition of the efferent feedback control: Facial/ bell's palsy, Ramsay Hunt syn, after stapedectomy, myasthenia gravis.
  55. Definition of paracusis?
    Paracusis refers to auditory dysfunction, in which the perception of volume, pitch, timbre or other quality of sound may be altered. In the majority of cases, paracuses are attributed to abnormalities at the auditory periphery.
  56. Definition of diplacusis?
    • Diplacusis or double hearing is a phenomenon of altered sound perception, which differs from that of a presented sound.
    • It can be binuaral or monoaural.
    • In binaural diplacusis, the same tone is perceived differently in each ear. It is most frequently reported in Meniere's disease.
  57. Is tinnitus related to hearing impairment?
    Yes. 74 % of patients complaining of hearing loss (of unspecified type) have tinnitus.
  58. What is the mechanism of tinitus after being exposed to loud noise?
    Glutamate is the main excitatory neurotransmitter, which is highly neurotoxic. Excessive noise exposure leads to excessive glutamate release and excitotoxic intracellular Ca++ overload, which could be a basis for tinnitus.
  59. What could be the mechanism of tinnitus in noise iduced HL or ototoxicity or ageing?
    They alter inhibitory amino acid neurotransmitter receptors in the central auditory pathways, most notably in the cochlear nucleus and the inferior colliculus. A down regulation of GABA, resulting from noise-induced damage in the auditory periphery, may reduce inhibitory function of the efferent system and, thus, may provide a basis for tinnitus.
  60. What is the eligibility criteria for BAHA?
    the bone-conduction averaged over 0.5, 1, 2 and 3 kHz should be equal to or better than 45 dB HL for an ear-level aid and better than 58 dB HL for a body-level aid.
  61. Exclusion criteriae for cochlear implant?
    • Medical: life treatening disease, Major psychological/ psychiatric disorder
    • Otological: Active middle ear disease, either acute or chronic
    • Cochlear obliteration: after meningitis or cochlear otosclerosis
  62. Who are the classical patients for middle ear implants?
    Middle ear implants are classically indicated for patients with mild to severe SNHL as an alternative to a conventional amplification aid.
  63. What is the indication of VIBRANT SOUNDBRIDGE implant?
    It has been applied tostimulate the round window membrane directly and in various types of conductive and mixed hearing loss.
  64. Describe a clinical case of vestibular neuronitis:
    The typical clinical case of vestibular neuronitis is an adult patient who suddenly experiences quite violent rotatory vertigo. The patients are usually able to describe the exact moment when the vertigo occurred and the feeling of disequilibrium or dizziness is often so pronounced that the patient cannot remain upright, but has to stay in a supine position. There is also a typical absence of auditory symptoms such as hearing loss or tinnitus as well as other neurological symptoms and signs.The vertigo or feeling of disequilibrium slowly recedes over the following days and the patient is usually able to sustain him or herself within a week
  65. What is the proposed cause for vestibular neuronitis?
    Neurotropic viruses, especially herpes simplex
  66. What is the common pathologic finding in vestibular nerve of a known case of vestibular neuronitis?
    A common finding is a diffuse lymphocytic infiltration with areas of gliosis in the vestibular nerve. The number of fibres in the vestibular nerve is also diminished on the affected side and there are marked signs of degeneration in the remaining fibres.
  67. What is the most common cause of peripherally induced vertigo?
  68. Clinical features of BPPV?
    rapid onset vertigo when turning over in bed or when extending the neck. After the positional change, there is usually a short latency of up 8 seconds before the vertigo appears. In the typical situation, the vertigo only lasts for a few seconds (five to ten) and then gradually disappears.There are no concomitant auditory symptoms such as hearing loss and/or tinnitus. The condition is normally self-limiting
    • The most common symptoms are vertigo or dizziness that may be elicited by a number of stimuli, such as sudden increase in pressure within the external auditory canal (Hennebert's sign), loud sounds (Tullio phenomenon) and by a Valsalva manoeuvre.
    • Some patients also complain of hearing loss of a mild to moderate character. Thus there may be a low frequency air-bone gap at two or more frequencies and Weber's test lateralizes to the diseased ear.
  70. where are the most common areas of dehiscence in SUPERIOR SEMICIRCULAR CANAL DEHISCENCE (SSCD)?
    The dehiscence is normally found at one or two defined sites, i.e. over the vertex or superior most part of the semicircular canal in the vicinity of the arcuate eminence or in the posterior portion of the canal in close relation to the superior petrosal sinus.
  71. Inner ear malformations in CHARGE syn?
    absent oval window, hypoplastic endolymphatic sac,absent bony and membranous semicircular canals and ampullae as well as a reduced number of Scarpa's ganglion cells.
  72. Vestibular abnormalities in DOWN's syn?
    large vestibule, changes in the otolithic organs as well as in the semicircular canals and their ampullae.
  73. Vestibular malformations in ALPORT syn? (a genetic disorder characterized by glomerulonephritis, end stage kidney disease, and hearing loss)
    underdeveloped or hypopoplastic endolymphatic sac and vestibular aqueduct.
  74. Vestibular malformations in Arnold-Chiari syn? (a defect in the formation of the cerebellum and brainstem)
    various portions of the semicircular canal system may be hypoplastic or even absent.
  75. What is large vestibular aqueduct syndrome?
    One of the most common malformations in the inner ear associated with sensorineural deafness. It may manifest as a mild to profound, fluctuating, stepwise progressive or sudden sensorineural hearing loss that begins in infancy or childhood. It is also associated with vestibular abnormalities.
  76. Symptoms of intralabyrinthine schwannomas
    How to diagnose?
    • long lastin dysequilibrium and hearing loss, sometimes mimicking meniere's sysmptoms (atypical Meniere's disease)
    • MRI: high intensity T1, low intensity T2, shine after contrast.
  77. Vestibular symptoms of Leukemia?
    acute profound sensorineural hearing loss as well as dizzinessand/or sudden loss of peripheral vestibular function, usually together with local symptoms such as ear bleeding/discharge, ear ache and with thickening of the tympanic membrane and the pneumatized region of the temporal bone.
  78. What is the most common tumor of cranial nerve VIII? which is also the most common neoplasm in CPA?
    Brief info?
    • Vestibular schwannoma
    • it accounts for 8-10% of intracranial tumours.
    • Benign, nonencapsulated, mostly arises form superior division of the vestibular nerve. It grows medially toward CPA, forming a mushroom appearance. It erodes posterior bony wall of IAC.
    • Clinical picture: slowly progressive unilateral HFSNHL, tinnitus, imbalance, with Meniere like symptoms in 30%.
  79. What is the gold standard test to diagnose vestibular schwannoma?
    Gadolinium enhanced MRI
  80. Definition of neurofibromatosis?
    a group of diseases characterized by the development of multiple benign tumours(neurofibroma/schwannoma) along neural roots, peripheral nerves and/or their terminal ramifications.
  81. Types of Neurofibromatosis?
    • Type 1: NF + multiple skin cafe au lait spots
    • Type 2: Bilateral vestibular tumours and meningiomas along spinal nerve roots.
  82. Describe NF type 2
    • Bilateral vestibular tumours and meningiomas along spinal nerve roots.
    • Originated form scwann cells, meningeal and glial cells.
    • autosomal dominant,50%penetration.
    • symptoms: bilateral SNHL, tinnitus, imbalance, muscular weakness, visual disturbances, skin manifestations. ,mostly starting after age of 10.
    • 11% asymptomatic.
    • MRI: bilateral vestibular schwannoma is typical
  83. prevalence of dizziness?
    • dizziness,vertigo and unsteadiness accounts for 1/4 of referrals to ENT and neurology clinics.
    • Approximately 1/4 of people experience dizziness at some time in their life and in 80 percent of cases this is severe enough to see a doctor.
    • Dizziness occurs in almost 50% of people above the age of 7S years.
  84. Definition fo vertigo?
    illusion ofeither oneself or the environment rotating.
  85. objective, visible balance problem is more likely to be a neurological gait disorder.
  86. nonvestibular causes of dizziness?
    • endocrine
    • Cardiovascular
    • haematological
    • psychological
  87. Main causes of acute episode of vertigo?
    • No hearin symptoms: vestibular neuronitis
    • Hearing loss: labyrinthitis
    • CNS symptoms: brainstem stroke

    ALL of them may have nausea/vomiting/sweating/ malaise, and vertigo exacerbation with head movement.
  88. What are the oculomotor examinations?
    • search for:
    • spontaneous and gaze-evoked nystagmus (latent nystagmus is due to congenital problem, shown by covering one eye) (all the nystagmuses without any vestibular symptoms are central)
    • convergence (+ above 60 y, midbrain lesions)
    • smooth pursuit (normal: rules out centralvestibular disorder, abnormal + imbalance=central lesion)
    • saccades ( hypermetric: cerebellar injury)
    • vestibulo-ocular reflexes (slow doll's eye, Halmagyi,check for vestibular acute problems, VOR suppression to check central lesions)
    • positional manoeuvres (Dix-hallpike for BPPV)
  89. possible causes of a nystagmus of peripheral vestibular origin, observable by the naked eye in primary gaze?
    vestibular neuritis, Meniere'sattack, recent labyrinthine surgery or trauma
  90. A large, horizontal nystagmus in a patient with no significant vestibular or neurological symptoms is mainly due to?
    congenital nystagmus
  91. Classification of nystagmus?
    • First degree nystagmus is a nystagmus only visible on gaze deviation in the direction of the fast phase
    • Second degree when present in primary gaze
    • Third degree when it is also visible when the eyes are deviated in the opposite direction to that of the fast phase.
  92. What is Alexander's law?
    A second or third degree nystagmus will enhance on gaze deviation in the direction of the fast phase.
  93. properties of eye saccade movements?
    • velocity(normal, slow or absent saccades, i.e. a gaze palsy)
    • accuracy (normo, hypo or hypermetric)
    • binocular conjugacy (conjugate or dysconjugate, for instance as ininternuclear ophthalmoplegia).
  94. what does hypermetric eye saccade movement mean?
    (travelling passed the new targeted point during saccade movement and need to correct) Cerebellar lesion
  95. What is the most common SSC incolved in BPPV? what is the type of related nystagmus?
    • Posterior SSC
    • Rotary nystagmus
  96. Describe a peripheral vestibular nystagmus.
    a typical peripheral vestibular nystagmus is small in the light but increases in the dark and it has a linear slow phase velocity in the horizontal (or horizontotorsional) direction. It normally follows Alexander's law of increasing in magnitude when looking in the direction of the fast phase.
  97. What is Caloric test?
    • The principle of the caloric test is that changes in temperature in the external auditory canal influence the level of activity of the vestibular labyrinth. Irrigation of EAC with water or air, 7 degrees over or below 37.
    • COWS (cold=opposite, warm=same side fast phase horizontal nystagmus)
  98. Causes of bilateral caloric nystagmus?
    • aminoglycoside ototoxicity
    • post meningitis
  99. How can body posture help in dagnosis?
    There are abnormal tilts or rotations in dystonia, flexed posture in Parkinson's disease, hyperextension in progressive supra nuclear palsy(PSP) and titubation in cerebellar disease. In lesions of the vestibular nuclei, as in the lateral medullary (Wallenberg) syndrome, there can be an ipsilesional ear-down head tilt, together with a skew eye deviation (ipsilesional lower eye) and ipsilesional body pulsion.
  100. How Romberg test can be used in detecting vestibular disorder?
    Only in the acute phase of a peripheral vestibular disorder will the Romberg test be positive, usually with an ipsilesional fall. In a patient with either cerebellar degeneration or polyneuropathy, a high level of unsteadiness on eyeclosure may indicate the presence of additional bilateral vestibular failure
  101. What is Unterberger test?
    Image Upload 3
    In the Unterberger test, instead of walking along, the patient is asked to walk on the spot with the eyes closed. In unilateral vestibular lesions the patient turns towards the hypoactive side.
Card Set
ENT otology 2
Flashcards for ENT otology part 2 Disclaimer: These flashcards are designed to help ENT residents/master's student in their preparations for final exams. The sources are different textbooks, lecture notes, and pictures uploaded in internet. Please send suggestions/feedbacks to dr.kian@ymail.com
Show Answers