Ear is composed of three parts: External ear, middle ear, and the Inner ear. Hearing tests (Rinne's and Weber's tests). Most important hearing and ear diseases are included.

1. The Ear
HAMZEH KIFAH YACOUB
REG. #: 21811020
MEDICAL STUDENT AT AQU
2021

2. DEVELOPMENT OF THE EAR
 External Ear
 1. dorsal portion of the first pharyngeal cleft forms the
external auditory meatus and tympanic membrane.
 2. Auricular hillocks form the auricle.
 Initially, the external ears are in the lower neck region, but
with development of the mandible, they ascend to the side of
the head at the level of the eyes

3. Auricular hillocks
 They are a swellings, three on each side of external auditory meatus.
 They fuse together forming the definitive auricle
 External ear starts developing at the 6th week.

4. Middle Ear
 1. The first Pharyngeal arch forms the incus, malleus, tensor
tympani muscle, and trigeminal nerve.
 2. The second Pharyngeal arch forms the stapes, stapedius
muscle, and facial nerve.
 3. The first Pharyngeal pouch forms the tympanic cavity.

5. Milestones for pediatric speech and
hearing
 0 to 3 months: startled by loud sounds, calmed by familiar voices.
 6 months: localize sounds.
 9 months: respond to name and can mimic sounds.
 12 months: say first words.
 18 months: can follow simple commands.
 2 years: say 20 or more words and put together 2-word sentences.

6. Ear Anatomy
 Ear is composed of three parts: External ear, middle ear, and
the Inner ear.
 External ear includes auricle , external auditory canal, and
tympanic membrane (drum)
 Middle ear includes middle ear cavity (tympanic cavity),
mastoid air cells, three ossicles and Eustachian tube (which
opens in nasopharynx).
 Inner ear : bony labyrinth, (cochlea, choclear nerve, vestibular
nerve) membranous labyrinth

7. Auricle Anatomy
 Auricle is composed of upper ¾ cartilaginous part and ¼ fibro fatty part
called the lobule
 Connected to the skull by ligaments and muscles and covered by skin.
 It works as a funnel for sound waves entry.
 It receives sensory innervation by auricular branch of vagus and
facial nerves, and greater auricular nerve, and auriculotemporal
branch of trigeminal nerve, and lesser occipital nerve.

8. Auricle Anatomy
 It has main structures which are :
 Helix
 Antihelix
 Concha
 Tragus
 Lobule

9. Auricle blood supply and venous
drainage
 Auricle receives blood from superficial temporal and posterior auricular
arteries.
 Superficial temporal and posterior auricular arteries are branches of ECA.
 The veins of the Auricle are analogous to the arteries of the region

10. Pinna innervation
 The sensory innervation to the skin of the auricle comes from:
1) Greater auricular nerve (branch of the cervical plexus) – innervates the
skin of the auricle.
2) Lesser occipital nerve (branch of the cervical plexus) – innervates the skin
of the auricle.
3) Auriculotemporal nerve (branch of the mandibular nerve) – innervates the
skin of the auricle and external auditory meatus.
4) Branches of the facial and vagus nerves – innervates the deeper aspect of
the auricle and external auditory meatus.

12. External Auditory meatus
 2.5 cm long, from the concha to the tympanic membrane.
 Consists of external cartilaginous 1/3 and internal bony 2/3.
 Cartilaginous 1/3 is wider than the bony 2/3, and contains hair
follicles, sebaceous and ceramen glands
 Ear wax is produced by the cartilaginous part.
 External auditory meatus has 2 narrowing areas: one between
cartilaginous and bony part, another 0.5cm lateral to tympanic
membrane.
 innervated by auriculotemporal branch of trigeminal nerve
and the auricular branch of vagus nerve.

13. Tympanic membrane (Ear drum)
 Consists of three layers: an outer (cutaneous), intermediate (fibrous), and
inner (mucous) layer.
 TM is divided into two parts depending on tightness; Pars Tensa, and Pars
Flaccida
 The difference between pars tensa and pars flaccida is that pars flaccida
doesn’t have fibrous intermediate layer.
 Also, pars tensa has a fibrocartilaginous ring which fixes the tympanic
membrane to the sulcus at the inner end of external meatus.
 The most depressed center of TM is called the Umbo.

14. Tympanic membrane (Ear drum)
 Cone of light is a triangular reflection of light, corresponds to the 5 o'clock
position in the right eardrum and the 7 o'clock position in the left
eardrum.
 Swallowing causes movement of tympanic membrane due to negative ear
pressure.
 TM external (thin skin) surface is innervated by trigeminal nerve
mandibular branch, while inner (mucus) surface is innervated by
glossopharyngeal branch

16. Middle ear
 As we said before: middle ear includes middle ear cavity (tympanic cavity),
mastoid air cells, three ossicles and Eustachian tube

17. Tympanic Cavity of middle ear
 Tympanic membrane includes tympanic cavity proper which is internal to
tympanic membrane, and epitympanic recess which is superior to
tympanic membrane and includes head of malleus and body of incus.
 Tympanic cavity communicates anteriorly with nasopharynx through
Eustachian tube. It communicates posteriorly with mastoid air cells and
mastoid antrum

18. Boundaries of Tympanic cavity
 1. Roof: tegmen tympani.
 2. Floor: jugular fossa.
 3. Anterior: carotid canal.
 4. Posterior: mastoid air cells and mastoid antrum through the aditus ad
antrum.
 5. Lateral: tympanic membrane.
 6. Medial: lateral wall of the inner ear, the promontory which is formed by
the basal turn of the cochlea, the oval window, and the round window.
 Oval window transmits vibrations of the ossicles into the perilymph of
the scala vestibuli of cochlear duct.

19. Auditory Ossicles
 They are 3 bones: Malleus, Incus, and Stapes.
 They transmit vibrations from the Tympanic membrane to inner ear.
 Malleus consists of head, neck, handle, and anterior and lateral processes, the
head articulates with incus in the epitympanic recess, while handle is fused to
TM, and makes an insertion of Tensor tympani muscle.
 Incus consists of body and two processes, Long process connects to stapes,
and short process attaches to posterior ligament of incus.

20. Auditory Ossicles
 Stapes consists of head, neck, two processes, and a base.
Its neck attaches to stapedius muscle.
Stapes has a hole through which the stapedial artery is transmitted in the
embryo; this hole is obturated by a thin membrane in the adult.
The base of stapes is attached by the annular ligament to the margin of the
oval window.

21. Persistent stapedial artery
 Postembryonic persistence of the stapedial artery is
rare. The stapedial artery may present as a pulsatile
middle ear mass or may be found incidentally during
middle ear surgery. The presence of a persistent
stapedial artery (PSA) may be recognized with plain
radiography, CT, or angiography.

22. Otosclerosis and conductive deafness
Abnormal ossification between the base and the oval
window limits the movement of the stapes, causing
conductive deafness.
 Conductive deafness is hearing impairment caused by a defect of a sound-
conducting apparatus such as the auditory meatus, eardrum, or ossicles.

23. Sensorineural deafness
 hearing impairment because of a lesion of the auditory nerve
or the central afferent neural pathway.

24. Evaluation of hearing loss, Weber and
Rinne tests
 Weber test: Place the base of a struck tuning fork on
the bridge of the forehead, nose, or teeth. In a
normal test, there is no lateralization of sound. With
unilateral conductive loss, sound lateralizes toward
affected ear.
 With unilateral sensorineural loss, sound lateralizes
to the normal or better-hearing side.

25. Rinne test
 Rinne test: Place the base of a struck tuning fork on
the mastoid bone behind the ear. Have the patient
indicate when sound is no longer heard. Move fork
(held at base) beside ear and ask if now audible. In a
normal test, AC > BC; patient can hear fork at ear.
With conductive loss, BC > AC; patient will not hear
fork at ear.

26. Weber’s and Rinne’s Tests by 512Hz fork

27. Conductive hearing loss
 Conductive hearing loss is caused by impaired sound transmission to the
inner ear.
 Abnormalities in the external canal, tympanic membrane, ossicles, and
middle ear account for this type of hearing loss.
 The maximal amount of Conductive Hearing Loss is 60 decibels, over 50
decibels is most likely caused by ossicular chain pathology.

28. Sensorineural hearing loss
 Sensorineural hearing loss is caused by inadequate sound processing by
the end organ of hearing, the cochlea (sensory), or poor transmission by
the eighth cranial nerve (neural ) to the centralnervous system.
 The function of the cochlea is to convert sound energy into electrical
impulses that are then transmitted to the auditory centers in the brain.

29. Presbycusis
 Presbycusis is age-related hearing loss. This is the most common type of
hearing loss in adults,
 Presbycusis is bilateral, symmetric, slowly progressive high-frequency loss.
 Onset is in adults over 60 years, and the exact cause is unknown.
 Hearing aids are the most effective treatment.

30. Medications can cause ototoxicity
 Antibiotics (specifically aminoglycosides and vancomycin)
 Chemotherapy drugs (cisplatin)
 Loop diuretics (furosemide, ethacrynic acid)
 NSAIDs and salicylates (aspirin)
 Others…

31. Newborn hearing screening
 The U.S. federal government mandates newborn hearing screening,
(programs are state regulated). The most commonly used test is
otoacoustic emissions (OAE), which tests the outer hair cell response to
acoustic stimulation. The other common test is auditory brainstem
response (ABR), in which the eighth nerve and central nervous system
produce sounds in response to an acoustic stimulation. In either case, if
the test is abnormal, the newborn is referred for further testing.
 Note: congenital hearing loss accounts for 1-3 infants per 1000.

32. Otitis media and Otitis externa
 Otitis media is a condition of middle ear infection that may be spread from the
nasopharynx through the auditory tube, can occur as a result of a cold, sore throat, or
respiratory infection. causing temporary or permanent deafness.
 Otitis media occurs mostly in children because their Eustachian tube is less oblique
than adults.
 Otitis externa is infection of the ear canal also known as swimmer’s ear, which is
usually caused by a bacterial organism such as pseudomonas.
 Otitis externa is an infection of the skin of the external auditory canal , which
can extend to surrounding structures such as the pinna, tragus, tympanic
membrane, and regional lymph nodes.

33. Otitis externa pathogenesis
 OE occurs when the protective mechanisms of the ear canal are disrupted.
 Cerumen is produced by glands in the cartilaginous ear canal, works as
bacteriostatic and protects the ear canal by acting as a barrier to moisture.
It is slightly acidic.
 Cotton swabs can cause OE by removing the protective cerumen and
injuring the ear canal.
 Moist and humid environments can also contribute to infections.
 Staphylococcus aureus and Pseudomonas aeruginosa are the most
 common causative organisms.

34. Cotton swabs contribute to OE by causing injury to
E.canal.

35. Sign and symptoms of acute OE
 Rapid onset of intense ear pain.
 Pain is exacerbated by palpation of the tragus and pinna.
 Ear canal inflammation (erythema, edema, and drainage).
 Plugged feeling in the affected ear.
 To be classified as acute the pain should be of less than 48 hours duration.
 Drainage from the ear canal may cause eczema of the outer ear.

36. Chronic OE
 otorrhea with symptoms of otitis externa.
 present for more than 6 weeks.
 The pain is often not as severe as acute OE.
 Chronic OE may occur after inadequate treatment of AOE.

37. Malignant OE
 Infection of the skull base that can occur after acute or chronic OE.
 Most often seen in elderly patients with diabetes and the
immunocompromised.
 The infection can spread intracranially and cause cranial nerve deficits and
is a life threatening condition.
 Symptoms include: deep stabbing ear pain (worsen with head motion),
otorrhea, fever, loss of voice, dysphagia, and facial weakness.

38. Otitis externa treatment
 Restoring the normal pH, topical antimicrobial therapy, for removal of
causative agents.
 Fluoroquinolone drops are first-line therapy.
 If any systemic symptoms are present, give the patient antibiotics covering
S.aureus.
 2 to 3 drops of a 1 : 1 solution of white vinegar and 70% ethyl alcohol can
be instilled into the ear before and after swimming for patients with
recurrent OE.

39. Ciprofloxacin ear drops

40. Acute Otitis media Diagnosis
 it is critical to be able to distinguish normal middle ear status from OME
or AOM
 otoscopy is the standard examination technique for suspected OM.
examination of the external ear and tympanic membrane is essential,
examining the entire head and neck region of patients with suspected OM
is important as well.
 normal TM is a translucent pale gray, yellow or blue TM is consistent with
middle ear effusion (MEE)
 In AOM, the TM is usually bulging; in OME, the TM is typically retracted or
in the neutral position.
 Impaired TM mobility is the most consistent finding in patients with OME

41. Otitis media management
 Most cases of AOM improve spontaneously. Cases that require treatment
may be managed with antibiotics and analgesics if needed.
 “In February 2013, the American Academy of Pediatrics (AAP) and the
American Academy of Family Physicians (AAFP) released updated
guidelines for the diagnosis and management of AOM, including recurrent
AOM, in children aged 6 months through 12 years. The recommendations
offer more rigorous diagnostic criteria to reduce unnecessary antibiotic
use. According to the guidelines, management of AOM should include an
assessment of pain. Analgesics, particularly acetaminophen and ibuprofen,
should be used to treat pain whether antibiotic therapy is or is not
prescribed’’

42. AOM Antibiotics prescribing
recommendations
 Antibiotics should be prescribed for AOM in children aged at least 6
months with severe signs or symptoms (moderate or severe otalgia,
otalgia for 48 hours or longer, or temperature 39°C or higher)
 unilateral, nonsevere AOM in children aged 6-23 months or nonsevere
AOM in older children may be managed either with antibiotics or with
close follow-up and withholding antibiotics unless the child worsens or
does not improve within 48-72 hours of symptom onset
 Amoxicillin is the antibiotic of choice (unless the child received it within 30
days, has concurrent purulent conjunctivitis, or is allergic to penicillin); in
these cases, clinicians should prescribe an antibiotic with additional beta-
lactamase coverage.

44. Otitis media subtypes
There are several subtypes of OM, as follows:
 Acute OM (AOM)
 OM with effusion (OME)
 Chronic suppurative OM
 Adhesive OM
OME often follows an episode of AOM. Symptoms that may be indicative of OME
include the following:
1. Hearing loss
2. Tinnitus
3. Vertigo
4. Otalgia

45. Otitis media with effusion
 The presence of an effusion in the middle ear without signs of acute
inflammation.
 Can occur primarily from negative middle ear pressure from eustachian
tube blockage as seen with adenoid hypertrophy, upper respiratory
infection.
 Can also occur after an episode of acute otitis media after the
inflammation has subsided.
 Can exist for several weeks with 90% resolution by three months.
 Doesn’t benefit from treatment with antibiotics.

46. Otitis media with effusion treatment
 not improved by administration of antibiotics, steroids, antihistamines or
decongestants.
 Patient with an effusion lasting for more than 3 months should undergo
testing of their hearing, Children should be tested sooner because the risk
for language delay,
 If there is a hearing loss, tympanostomy tubes are recommended.

47. Myringotomy
 Ear canal and tympanic membrane are visualized through a speculum.
 After evaluation of the ear drum and middle ear, a small incision is made in
the anterior-inferior quadrant of the tympanic membrane to avoid the
ossicles and chorda tympani.
 Any fluid is removed by suction and the ear tube is placed with gentle
pressure.

48. Chronic suppurative otitis media
 Otorrhea from a perforated tympanic membrane.
 Perforation can occur from an acute otitis media or chronic middle ear
effusion.
 Otorrhea can be the result of secretions entering the middle ear from the
eustachian tube or from water exposure of the middle ear mucosa.

49. Chronic suppurative otitis media
treatment
 You must rule out a cholesteatoma, which can also lead to chronic ear
drainage.
 In the absence of cholesteatoma the treatment include topical antibiotic
ear drops, usually ofloxacin.
 Avoid water exposure.

50. Chronic suppurative otitis media
complications
 persistent mastoid and middle ear inflammation and infection. This can
occur with or without cholesteatoma, tympanic membrane perforation, or
persistent otorrhea through ventilation tubes.

51. Acute otitis media complications
 Acute OM develops in previously healthy ears.
 Characterized by mucosal edema with exudation of fluid, bacterial
proliferation, and the.
 formation of byproducts of inflammation (pus).
 Infection then spreads contiguously into the mastoid.
 Meningitis is an example of hematogenous spread. Meningitis usually
occurs as a result of Acute OM rather than Supporaative OM,

52. Cholesteatoma
 Epidermal inclusion cysts of the temporal bone composed of squamous
epithelium and associated debris.
 The word cholesteatoma was first used to describe its light color and gross
resemblance to cholesterol crystals under microscopy. But there’s no fat in
cholesteatoma!
 Three main types of cholesteatoma: Congenital, primary acquired, and
secondary acquired.

53. How Cholesteatoma forms?
 Congenital cholesteatomas are thought to originate from keratinizing
squamous epithelium of the middle ear cleft.
 Primary acquired cholesteatomas usually arise in the setting of retraction
of the Tympanic Membrane, usually as a result of otitis media and chronic
eustachian tube dysfunction.

55. Cholesteatoma symptoms
 Usually affect one ear.
 Recurring watery, often smelly, discharge from the ear, which can be
intermittent or continuous.
 a gradual hearing loss in the affected ear.
 Vertigo.
 Tinnitus.

56. Cholesteatoma on CT scan
 Blunting or erosion of the scutum is a common finding on CT in those with
cholesteatoma.
 Scutum is a bony prominence in the lateral portion of the middle ear and
superior portion of the external auditory canal.

58. Cholesteatoma surgical approach
 There are various surgical approaches, including tympanotomy, atticotomy,
cortical mastoidectomy, canal wall up or down mastoidectomy.
 Facial nerve monitoring should also be considered, especially during
surgeries or cases with extensive disease.

59. Referred otalgia
 Ear pain most commonly comes from the external, middle or inner ear.
But it can also be referred from elsewhere in the body.
 The sensory innervation of the ear involves six nerves: two branches of the
cervical plexus, derived from the second and third cervical roots, and four
cranial nerves-trigeminal (V), facial (VII), glossopharyngeal (IX), and vagus
(X).
 stimulation of any branch of these nerves by any of the structures
receiving sensory input from these nerves can cause ear pain.
 Diagnosis of the etiology of ear pain in the absence of primary ear
pathology a challenge!

60. Referred otalgia
 Referred otalgia can be the result of problems ranging from dental issues
(e.g. temporomandibular disease) to a more serious conditions requiring
immediate diagnosis and intervention (e.g. hidden malignancy).
 The physician must use a structured, systematic approach to identify the
etiology of the patient’s pain.

61. Referred otalgia
 Ask the patient if he/she has Dental problems, Current or recent infections,
Sinus issues, Cancer risk factors, Recent trauma, Gastrointestinal history,
Dysphagia, esophagitis, reflux…
 It is important to think about imaging at some point when a diagnosis
cannot readily be made, Dental X-ray, CT for TMJ, MRI of brain, PET scan…

62. Referred otalgia nerves connections

63. Referred otalgia nerves connections

64. Middle ear muscles
 1. Stapedius Muscle:
the smallest of the skeletal muscles in the human body.
Arises from the pyramidal eminence, and its tendon emerges from the
eminence.
Inserts on the neck of the stapes.
innervated by a branch of the facial nerve.
It Pulls the head of the stapes posteriorly, thereby tilting the base of the
stapes away from the cochlea in term to prevent injury from loud noise.
Stapedius paralysis results in hyperacusis.

65. Hyperacusis (hyperacusia)
 excessive acuteness of hearing,
 May occurbecause of paralysis of the stapedius muscle (causing
uninhibited movements of the stapes).
 May results from a lesion of the facial nerve.
 Ear protection plugs can be used to decrease noise intensity.

66. Middle ear muscles
 Tensor Tympani Muscle
Arises from the cartilaginous portion of the auditory tube.
inserts on the handle of the malleus.
Tightens the tympanic membrane in response to loud noise.

68. Eustachian Tube
 Connects the middle ear to the nasopharynx.
 Allows air to enter or leave the middle ear cavity and thus balances the
pressure in the middle
 ear with atmospheric pressure, allowing free movement of the tympanic
membrane.
 Has cartilaginous portion that remains closed except during swallowing or
yawning.
 Is opened by the simultaneous contraction of the tensor veli palatini and
salpingopharyngeus muscles.

69. Eustachian tube
 Ear infections are more common in children because their eustachian
tubes are shorter, narrower, and more horizontal than in adults
 Bacteria can become trapped when the tissue of the eustachian tube
becomes swollen from colds or allergies. Bacteria trapped in the
eustachian tube may produce an ear infection

70. Middle ear innervation and blood
supply
 Middle ear is innervated by the tympanic branch of the glossopharyngeal
nerve, which forms the tympanic plexus with caroticotympanic nerves from
the internal carotid plexus of sympathetic fibers
 Receives blood from the stylomastoid branch of the posterior auricular
artery and the anterior tympanic branch of the maxillary artery.

71. Inner Ear
 The place where vibrations are transduced to nerve impulses that are
transmitted through the acoustic nerve to the central nervous system.
 Composed of outer bony labyrinth which is filled with perilymph and inner
membranous labyrinth filled with endolymph.
 Bony labyrinth consists of choclea, vestibule, and semicircular canal.
 Membranous labyrinth consists of organ of corti, utricle, and saccule and
semicircular ducts.

72. Inner Ear
 the cochlea housing the cochlear duct for auditory sense.
 the vestibule housing the utricle and saccule, and the semicircular canals.
 Semicircular canal houses the Semicircular ducts.

73. Bony Labyrinth Structures
 vestibule is a cavity of the bony labyrinth communicating with the cochlea
anteriorly and the semicircular canals posteriorly.
 Bony cochlea consists of two ducts: the upper scala vestibuli, which begins
in the vestibule and receives the vibrations at the oval window, and
contains perilymph. and the lower scala tympani which ends at the round
window, where the sound waves dissipates back into the air of middle ear.
 Perilymph of scala vestibuli and scala tympani mixes in the helicotrema
region at the apex of choclea.

74. Bony Labyrinth

75. Membranous Labyrinth
 Filled with endolymph.
 The cochlear duct between scala vestibuli and scala tympani, contains
endolymph and the Organ of corti which is composed of hair cell
receptors.
 Cochlear duct is covered by basilar membrane and tectorial membrane,
these membranes move in response to fluid movement in scala vestibuli.

76. Membranous Labyrinth
 utricle and saccule are dilated membranous sacs in the vestibule and
contain sense organs called maculae, which detect linear acceleration of
the head.
 The macula of the utricle has a horizontal orientation, and the macula of
the saccule has a vertical orientation.
 semicircular ducts consist of anterior (superior), lateral, and posterior
ducts, and their dilated ends are called ampullae, which detect rotational
or angular acceleration

77. Inner ear mechanism of hearing
 The fluid outside the ducts is perilymph, the fluid inside the ducts is
endolymph.
 The scala vestibuli and scala tympani contain perilymph, which has a high [Na+],
The scala media contains endolymph, which has a high [K+].
 The scala media is bordered by the basilar membrane, which is the site of
the organ of Corti.

78. Inner ear mechanism of hearing
 The organ of Corti is located on the basilar membrane. It contains the
receptor cells (inner and outer hair cells) for auditory stimuli.
 Cilia protrude from the hair cells and are embedded in the tectorial
membrane.
 Inner hair cells are arranged in single rows and are few in number. Outer
hair cells are arranged in parallel rows and are greater in number than the
inner hair cells.
 The spiral ganglion contains the cell bodies of the auditory nerve [CN VIII],
which synapse on the hair cells.

79. Inner ear mechanism of hearing
 The cilia of hair cells are embedded in the tectorial membrane.
 Sound waves cause vibration of the organ of Corti.
 The basilar membrane is more elastic than the tectorial membrane,
vibration of the basilar membrane causes the hair cells to bend by a
shearing force as they push against the tectorial membrane.
 Bending of the cilia causes changes in K+ conductance of the hair cell
membrane. Bending in one direction causes depolarization; bending in the
other direction causes hyperpolarization.
 The oscillating potential of the hair cells causes intermittent firing of the
cochlear nerves.

80. Inner ear mechanism of hearing
 The frequency that activates a particular hair cell depends on the location of the
hair cell along the basilar membrane.
 The base of the basilar membrane is narrow and stiff, responds best to high
frequencies.
 The apex of the basilar membrane is wide and compliant, responds best to low
frequencies.

81. Inner ear mechanism of hearing
 Fibers ascend through the lateral lemniscus to the inferior colliculus to the
medial geniculate nucleus of the thalamus to the auditory cortex.
 Fibers may be crossed or uncrossed. As a result, a mixture of ascending
auditory fibers represents both ears at all higher levels. Therefore, lesions
of the cochlea of one ear cause unilateral deafness, but more central
unilateral lesions do not.

82. Vertigo
 Vertigo is a false sensation of movement in the absence of actual
movement. It may be caused by Ménière disease, labyrinthitis, positional
vertigo, traumatic vertigo, perilymphatic fistula, and cervical vertigo.
 Other causes include vascular disease of the brain stem, arteriovenous
malformation, brain tumor, MS, drug overdose, and vertebrobasilar
migraine.

83. Vertigo
 With the dizzy patient, the first step is to determine the nature of the patient’s
complaints. “Dizziness” is a nonspecific term that provides no meaningful
information about what is occurring to the patient.
 by taking a complete history, it is possible to determine whether the patient is
experiencing vertigo or presyncope.
 Patients who experience vertigo will describe a sensation of movement without
actually moving. They describe their environment ‘spinning around them’.
 Where as Patients with presyncope will describe their symptoms as
“lightheadedness” or “feeling like I’m going to black out.” Associated
symptoms include generalized weakness, palpitations, and shortness of breath.
 Vertigo is usually a manifestation of neurologic disease, whereas presyncope is
a cardinal manifestation of cardiovascular disease.

84. Vertigo
 Vertigo could be secondary to peripheral or due to central vestibular
disease.
 Central vertigo has gradual onset, no tinnitus or hearing loss, with signs of
diplopia, cortical blindness, weakness and numbness.
 Peripheral vertigo doesn’t include the above criteria.
 Both vertigos have nystagmus, while central vertigo nystagmus does not
suppress with fixation, and peripheral vertigo does.

85. Benign paroxysmal positional vertigo
 Calcium carbonate structure in the saccule or utricle of the inner ear
(otolith/otoconia).
 Does peripheral vertigo that characteristically is exacerbated by head
movement or change in head position.
 Typically, episodes will occur in clusters that persist for several days.
 There will be a latency of several seconds after head movement before the
onset of vertigo.
 The vertigo usually lasts 10 to 60 seconds.
 treated with positional maneuvers that attempt to move the otolith out of
the circular canals.

86. Labyrinthitis vertigo
 Sudden onset of severe vertigo that lasts for several days with hearing loss
and tinnitus.
 The disease frequently follows an upper respiratory tract infection.
 treated symptomatically with meclizine, diazepam when symptoms are
severe.
 Steroids help labyrinthitis.

87. Perilymphatic fistula
 A form of peripheral vertigo related temporally to head trauma (blunt
trauma to the ear, e.g., a slap to the ear) or extreme barotrauma during air
flight.

88. Central vertigo
 Central vertigo is caused by any cerebellar or brain-stem tumor, bleed, or
ischemia. Drug toxicity or overdoses are important causes of central
vertigo.
 In the young patient with unexplained central vertigo, consider multiple
sclerosis.

89. Vertigo treatment
 Symptomatic treatment for peripheral vertigo includes meclizine.
 In severe cases, diazepam.

90. Meniere's disease
 Ménière’s disease is a condition marked by episodes of loss of balance
(vertigo) and nausea due to increased endolymph pressure inside
vestibular apparatus, it occurs due to excessive accumulation of
endolymph.
 Normal physiology is that Endolymph is secreted by epithelial cells
continuously and drains from inner ear to the venous sinus in the dura
mater of brain.

91. Ménière disease
 characterized by tinnitus, hearing loss, and episodic vertigo.
 Each episode lasts 1 to 8 hours.
 The symptoms wax and wane as the endolymphatic pressure rises and
falls.
 The two most common causes of Ménière disease are syphilis and head
trauma.

92. Ménière disease treatment
 Ménière disease is treated with a low-salt diet and diuretics.
 Patients who fail medical therapy, should undergo surgical decompression.

93. Meniere's disease

94. Meniere's disease

95. Facial Nerve (CN VII) anatomy
 Facial nerve is sensory-motor nerve.
 The nerve arises in the pons in brain stem.
 begins as two roots: a large motor root, and a small
sensory root.
 Both roots pass through the internal acoustic meatus
(in petrous part of temporal bone).
 The two roots fuse to form the facial nerve.

96. Facial Nerve (CN VII) anatomy
 Facial nerve gives rise to 3 main nerves:
1. Greater petrosal nerve gives parasympathetic fibers to
lacrimal glands.
2. Nerve to stapedius muscle in middle ear.
3. Chorda tympani: special sensation from the anterior two-
thirds of the tongue via the lingual nerve, as well,
parasympathetic fibers to submandibular and sublingual
salivary glands.

97. Facial Nerve Anatomy ( Z shaped)

98. Facial Nerve Anatomy
 At the parotid gland, facial nerve bifurcates into five motor
branches which innervate muscles of facial expression:
 1. Temporal
 2. Zygomatic
 3. Buccal
 4. Marginal Mandibular
 5. cervical – innervates platysma.

99. Facial Nerve Anatomy

100. Facial nerve intracranial lesion
 The muscles of facial expression will be paralyzed or severely
weakened.
 As well other symptoms will appear depending on the lesion
location and affected branches.
 Ipsilateral hyperacusis may occur due to Stapedius
nerve lesion!
 Ipsilateral lacrimal fluid reduction, and reduced salivation may
occur (Greater petrosal and chorda tympani respectively)

101. Facial nerve UMN and LMN lesions
 Pons is the location of facial nerve nuclei.
 Facial nucleus is splitted into 2 halves
The top half provides fibers of facial expression of the upper face, the lower
half provides fibers of facial expression of the lower face.
 Upper half receives innervation from ipsilateral and contralateral motor
cortex.
 The lower half of the nucleus is only innervated by the lower part of motor
cortex.

102. Facial nerve UMN and LMN lesions
 If there’s a facial palsy to UMN, you will see paralysis of the all contralateral
and upper face of the ipsilateral side.
 Lower motor neuron lesion affects the upper and lower ipsilateral side.

103. Facial UMN and LMN

104. Facial nerve palsy
 Inability to wrinkle brows
 Drooping eyelid
 Inability to close eyes
 Inability to puff cheek
 asymmetrical smile
 Drooping corner of mouth
 Dry mouth

105. Differential diagnosis for a facial palsy
 Bell’s palsy: as a result of viral infection, such as HSV-1, CMV, and EBV, less
common risk factors include diabetes mellitus and pregnancy.
 UMN causes: such as a stroke, subdural hematoma, or a brain tumor.
 LMN causes: Infective, such as acute otitis media, cholesteatoma, viral
infection (including HSV-1, CMV, and EBV).
 Neoplasm (parotid malignancy).
 Trauma or iatrogenic.

106. Ramsay-Hunt Syndrome
 Herpes Zoster oticus.
 There is a unilateral facial palsy caused by reactivation of varicella zoster
virus from the geniculate nucleus, the nucleus of the facial nerve.
 presents with a moderate to severe ear pain.
 Within a few days this will develop into a facial palsy, accompanied by
ipsilateral vertigo, hyperacusis, and tinnitus.
 Facial palsy from Ramsay-Hunt syndrome tend to be more severe than
Bell’s Palsy.

107. Ear embryological defects
Congenital Hearing loss
 In the most extreme cases, it is caused by the absence of the
tympanic cavity and the external meatus.
 Other causes may include abnormal membranous and bony
labyrinths, or malformation of ear ossicles or the tympanic
membrane (ear drum).

108. Congenital hearing loss causes
 It could be caused by genetic factors.
 Environmental factors also interfere with internal ear
and external ear development.
 Viruses infection such as Rubella and CMV during
pregnancy.

109. External ear defects
 Anotia and microtia are birth defects of a baby's ear.
 Anotia happens when the external ear (auricle) is missing
completely.
 Microtia happens when the external ear is small and not
formed properly.

110. Anotia and Microtia causes
 The causes of anotia/microtia among most infants are
idiopathic.
 In some cases, anotia/microtia occurs because of an
abnormality in a single gene.
 isotretinoin (a drug used for acne) during pregnancy can
lead to a pattern of birth defects, which often includes
anotia/microtia.

111. Anotia and Microtia

112. Anotia and Microtia
 Anotia/microtia are visible at birth.
 CT scan of the baby’s ear provides a detailed picture of the ear. This will
help the doctor see if the bones or other structures in the ear are affected.
 children with anotia/microtia can develop normally and have healthy lives.

113. Auditory canal Atresia
 Auditory canal atresia is partial or total failure of the ear canal to develop.
usually associated with absence of the tympanic membrane and
underdevelopment of the middle ear bones.
 Usually the inner ear (cochlea) is healthy and normally developed in these
children.
 Can be treated surgically by Canaloplasty (a procedure widens the external
auditory canal to alleviate a blockage, hearing loss or infection)

114. References:
 BRS Gross Anatomy , Kyung Won Chung
 Teach me Anatomy website
 Hearing health foundation
 Medscape
 UpToDate
 Nature
 Medline plus

115. References:
 Charlett SD, Coatesworth AP. Referred otalgia: a structured approach to
diagnosis and treatment. Int J Clin Prac 2007;61(6):1015-21.
 Li JC, Brunk J. Otalgia. Available at www.emedicine.com/ent/topic199.htm .
Accessed Jan. 17, 2008.
 NMS Medicine book.
 BRS physiology book.
 ENT secrets book.
 Kaplan Internal Medicine lecture notes for USMLE step 2.

116. Hamzeh Yacoub
4th year medical
student
AQU