19. C. Via facial nerve:
Herpes zoster oticus, vestibular schwannoma
D. Via vagus nerve:
Larynx + hypopharynx: neoplasm, infection,
tuberculosis, trauma,
foreign body
E. Via second & third cervical nerves:
Herpes zoster, cervical spondylosis & arthritis
21. Introduction
• 30% of head trauma cases result in skull fracture
• Temporal bone # comprises 15-25% of all skull #
• Classification of temporal bone fracture:
1. Longitudinal (80%)
2. Transverse (20%)
• Recent view: > 90% are mixed or oblique fractures
especially in severe trauma
22.
23. Longitudinal fracture
• 80% of all temporal bone fractures
• Caused by lateral blows over temporal bone
• Fracture line parallels long axis of petrous pyramid
• Starts in pars squamosa, extends through postero-
superior bony external canal, continues across roof
of middle ear space (anterior to labyrinth), ends
antero-medially in middle cranial fossa in close
proximity to foramen lacerum & ovale
25. Clinical features
• Bleeding into ear canal from skin & TM laceration
• External auditory canal fracture, hemotympanum
• Conductive deafness: due to ossicular disruption
• Facial nerve paralysis (20%): late onset, involves
tympanic segment, usually temporary
• CSF otorhinorrhea: common, usually temporary
• Sensori-neural hearing loss & vertigo are rare
26. Transverse fracture
• 20% of all temporal bone fractures
• Caused by frontal or occipital blows
• Fracture line at 900 to long axis of petrous pyramid
• Starts in middle cranial fossa (close to foramen
lacerum), crosses petrous pyramid transversely &
ends at foramen magnum. May extend through
internal auditory canal & injure nerves directly.
28. Clinical features
• Profound sensori-neural hearing loss
• Severe ablative vertigo
• Third degree nystagmus present with fast
component beating away from fracture site
• Facial nerve paralysis (50%): early onset, permanent
• Intensity of vertigo + nystagmus es after 7-10
days, continues to decrease steadily until
compensation finally occurs after 3-6 months
29. Examination for temporal #
• Complete neurologic + ENT examination
• Otoscopy: EAC & TM lacerations, fracture lines
• Siegalization: for presence of fistula
• Eyes for nystagmus (direction + degree)
• Tuning fork tests: type of hearing loss
• Battle sign (ecchymosis of postauricular skin)
• Raccoon sign (ecchymosis of periorbital area)
• Kernig’s & Brudzinski’s test: for meningitis
30. Features Longitudinal Transverse
Incidence 80% 20%
Trauma site Temporal or parietal Frontal / occipital
CSF leak Otorrhea Oto-rhinorrhea
Hemotympanum Occasional Common
EAC lacerations Common Occasional
TM perforation Common Occasional
Otorrhagia Common Occasional
Hearing loss Conductive Sensori-neural
Facial palsy 20%, temporary,
delayed onset
50%, permanent,
early onset
Vertigo + nystagmus Occasional Common, severe
32. Treatment of facial nerve palsy
A. Delayed onset & incomplete facial paralysis:
oral Prednisolone for 2 weeks + observation
B. Immediate onset or complete paralysis Nerve
stimulation done b/w days 3 to 7 of trauma:
• no loss of stimulability occurs: observation
• loss of stimulability within 1 week or >90%
degeneration on ENOG within 2 wks: surgical
exploration
34. Introduction
Abnormal communication between subarachnoid
space & tympano-mastoid space leading to
discharge of cerebrospinal fluid through external
auditory canal or via Eustachian tube into
nasopharynx
35. Etiology
A. Acquired (more common)
• Operative trauma: mastoidectomy, stapedectomy,
vestibular schwannoma excision, skull base surgery
• Accidental trauma
• Non-traumatic: infection, neoplasm
B. Spontaneous
• Bony defect theory
• Arachnoid villi granulation theory
36. • Congenital defect theory: SNHL present
– enlarged petrosal facial nerve canal
– patent Hyrtl’s fissure (congenital fusion plane
found b/w otic capsule & jugular bulb)
– wide vestibular aqueduct (Mondini’s dysplasia)
– annular ring of stapes footplate
– Dehiscent tegmen plate
• Arachnoid villi granulation theory: SNHL absent
– Enlargement of arachnoid villi due to congenital
entrapments / large pressure variations
41. Clinical features
• H/o surgery / accidental trauma
• Clear watery discharge from ear or nose:
appears during straining or leaning forward (Dandy
maneuver); salty taste
• Unilateral hearing loss:
– Sensori-neural: abnormality of inner ear
– Conductive: leak elsewhere in temporal bone
• Unexplained episode of meningitis
42. Investigations
• Confirmatory test for CSF: glucose level > 30
mg/dL; presence of beta 2 transferrin
• High-resolution CT scan with contrast
– Abnormality of otic capsule: Mondini deformity
– Wide vestibular & cochlear aqueducts
– Tegmen plate defect
– Localization of leak with intrathecal Iohexol
– Presence & location of pneumocephalus
43. Medical treatment
1. Compressive dressing + bed rest (head elevation)
2. Prophylactic antibiotics indicated in:
• post-traumatic CSF leakage
• immuno-suppressed patient
• obvious soilage of central nervous system
• postoperative & spontaneous leaks (controversial)
44. 3. Medications to decrease production of CSF
a. Diuretics ( Frusemide, hydrochlorothiazide)
b. Carbonic anhydrase inhibitors (Acetazolamide)
4. Steroids (to reduce inflammation)
Hydrocortisone, dexamethasone
5. Continuous lumbar CSF drainage
Allows natural healing
45. Surgical treatment
• Primary closure with multi-layer technique using
cartilage + muscle + fascia + fat + bone wax
• Approaches: Trans-canal, Trans-mastoid, Middle
cranial fossa, Combined (middle fossa + trans-
mastoid). Combined approach for large defect (>2cm),
multiple defects, or defects that extend anteriorly.
• Refractory cases: obliteration + closure of EAC
47. Definition
Tendency of certain therapeutic agents & other
chemical substances to cause functional
impairment + cellular degeneration of tissues of
inner ear (especially end organs) & neurons of
cochlear + vestibular division of the eighth
cranial nerve (Hawkins, 1976)
48. American Speech-Language-
Hearing Association definition
Pure tone audiometry:
• 20db or greater decrease in pure-tone threshold at
one frequency
• 10db or greater decrease at 2 adjacent frequencies
Otoacoustic Emissions or BERA:
• loss of response at 3 consecutive test frequencies
where responses were previously obtained
51. Clinical features
• Hearing loss: B/L, symmetrical, high frequency,
sensori-neural; temporary / permanent; may
not manifest until several weeks or months
after completion of ototoxic agent therapy.
• Tinnitus
• Vestibular toxicity: positional nystagmus,
oscillopsia & dysequilibrium
52. Mechanisms of ototoxicity
• Direct hair cell damage: outer hair cells affected
first. Begins at basal turn of cochlea (high-
frequency sloping SNHL) & proceeds toward apex
(involvement of lower frequencies too)
• Direct vestibular injury
• Direct damage to stria vascularis
• Metabolic (non-morphologic) damage
53. Acetyl salicylic acid
• Tinnitus: main symptom
• Hearing loss: sensori-neural, reversible (within 72
hours of withdrawal), flat curve on audiogram
• Etiology: multi-factorial due to metabolic rather
than morphological damage to cochlea
54. Aminoglycosides
• Ototoxicity first with Streptomycin (1944)
• Streptomycin, Gentamicin, Netilmicin: primarily
vestibulotoxic; destroy type 1 hair cells of crista ampullaris
• Kanamycin, Amikacin, Neomycin: primarily cochleo-
toxic; damage outer hair cells at basal turn of cochlea
• Tobramycin: vestibulotoxic + cochleo-toxic
55. Aminoglycoside clearance
Aminoglycosides cleared more slowly from inner
ear fluids than from serum latency exists to
ototoxic affects of aminoglycoside progression
of hearing loss or onset of hearing loss after
cessation of aminoglycoside treatment + prolonged
susceptibility to noise-induced hearing loss
56. Macrolides
• Drugs: Erythromycin, Azithromycin, Clindamycin,
Vancomycin
• Cause reversible ototoxicity
• Onset generally within 3 days of starting treatment
• Speech frequencies affected rather than higher
frequencies
58. Anti-neoplastic agents
• Drugs: cisplatin, carboplatin, bleomycin, 5-fluorouracil
• Mechanism: Multi-factorial, partially mediated by
free-radical production. Damage stria vascularis +
outer hair cells at basal turn of cochlea.
• Hearing loss bilateral, sensori-neural, progressive
& irreversible
59. • Quinine
• Toxicity produces tinnitus, hearing loss, vertigo,
headache, nausea & vision loss
• Hearing loss usually sensori-neural & reversible
• Characteristic notch often present at 4000 Hz
• Oto-topical agent:
• Rare
• Only possible if mastoid cavity is open or
tympanic membrane perforated
60. Brock’s grading of ototoxicity
• Grade 0: threshold < 40 dB HL at all frequencies
• Grade 1: threshold > 40 dB at 8000 Hz
• Grade 2: threshold > 40 dB at 4000 - 8000 Hz
• Grade 3: threshold > 40 dB at 2000 - 8000 Hz
• Grade 4: threshold > at 40 dB at 1000 - 8000 Hz
61. High Risk Patients
• Larger doses of ototoxic agent
• Higher blood levels of ototoxic agent
• Longer duration of therapy with ototoxic agent
• Receiving other ototoxic or nephrotoxic agent
• Elderly patients
• Renal insufficiency
• Preexisting hearing problems
• Family history of ototoxicity
62. Management
• No therapy available to reverse ototoxic damage.
• Awareness of ototoxic agents & drug monitoring
during treatment. Prompt reporting of tinnitus, hearing
loss, oscillopsia & vertigo.
• Alternative therapy for high-risk patients.
• Avoid noisy environments for 6 months after treatment
completion. Avoid co-prescription of ototoxic agents.
• Amplification with hearing aid or cochlear implant.
