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Diseases of the External, Middle and Inner Ear August, 24, 2017
Dr. Ramon Alcira, MD
Department of Otorhinolaryngology

I. Otalgia
a. Diseases of the External Ear
i. Acute otitis externa
ii. Acute forms
iii. Chronic causes
b. Diseases of the Middle ear
i. Bullous Myringitis
ii. Acute Suppurative Otitis Media
iii. Acute Non-suppurative Otitis Media
iv. Chronic Suppurative Otitis Media
v. Chronic Non-Suppurative Otitis Media
vi. Referred Otalgia
vii. TMJ Dysfunction
II. Hearing Loss
a. Conductive
b. Sensorineural Fig. 1 Furunculosis
III. Tinnitus  Diffuse Otitis Externa
a. Objective o Entire external auditory canal narrows
b. Subjective o Swimmer’s ear – caused by pseudomonas
IV. Dizziness o Diagnostic features:
a. The vestibular system physiology  Tragal tenderness
b. Nonvestibular causes  Severe pain
c. Vestibular Basis  Canal wall swelling involving most of the canal
V. Ear Deformity  Scanty discharge
a. Congenital  Normal or slightly diminished hearing
b. Acquired  Absence of obvious fungal particles
*from 3A 2017, -18, Italicized: Doc, Boeis, Boxed: Boies  Possible presence of tender regional adenopathy
 Regardless of the difference in etiology, the treatment for both
Ear discharge: only a few, so this will be incorporated on the other symptoms circumscripta and diffuse otitis externa is the same  oral antibiotics
OTALGIA (EAR PAIN) o DOC: penicillinase resistant penicillin + topical antibiotics
 Sources of otalgia: (polymixin, neomycin + steroid)
o External ear o Steroid may be hydrocortisone, dexamethasone or flucinolone
o Middle ear acetamide
o Referred otalgia  Other drugs: quinolone (ofloxacin or ciprofloxacin) + steroid for middle
o Temporomandibular joint dysfunction (differential to otalgia - very ear problems (perforation in TM)
close proximity to the ear)
 Inflammation of the External ear – otitis externa  The external ear canal is derived from the ectodermal first branchial
 Inflammation of the Middle ear – otitis media cleft.
 Inflammation of the Inner ear – labyrinthitis (doc: there is no such thing  The TM represents the closing membrane of the first branchial cleft.
as otitis interna)  At some point during the development, the external ear canal is closed
Diseases of the External Ear completely by a meatal plug of tissue but reopens again; this may be a
Acute Otitis Externa factor in some cases of atresia or stenosis.
 The pinna is derived from the margins of the first branchial cleft and the
 Hallmark – tragal tenderness
first and second branchial arches.
 Apply slight pressure to the tragus  the patient complains of pain.
 The external ear or pinna, is composed of cartilage covered by skin. The
 If it’s a middle ear problem, even if you twist the patient’s tragus, it’s not
shape of the cartilage is unique and intreating patients with injuries to
going to hurt.
the external ear, every effort must be made to preserve this structure.
 In otoscopy, you will see a collapsed external auditory canal 
 The skin can be stripped off the underlying cartilage by hematoma or
ordinarily, the tympanic membrane would not be visible because the ear
pus and the necrosis of the underlying cartilage leads to a cosmetic
canal will not allow you to see through the swelling.
deformity of the pinna (cauliflower ear).
 In many instances, the TM may be spared.
 The external ear canal is cartilaginous laterally but bony medially.
 There may or may not be hearing loss depending on the degree of
 There is often narrowing of the external ear canal at the bone-cartilage
occlusion of the ear.
junction.
 There may or may not be discharge depending on the severity of the
 The TMJ and parotid gland are anterior to the external ear canal, while
external otitis.
the mastoid process is posterior.
 Acute otitis externa circumscripta (Furunculosis)
 The facial nerve exits the stylomastoid foramen and passes lateral to the
o “may pimple sa tenga” “ there is pointing” “may mata”
styloid process posteroinferior to the external ear canal and then runs
o Caused by staphylococcus usually
beneath the external ear canal to enter the parotid gland.
o Confined to the fibrocartilaginous portion of the external auditory
meatus.  The cartilage of the external ear canal is one of the surgical landmarks
used to find the facial nerve; the tympanomastoid suture is another
o Furunculosis begins in a pilosebaceous follicle
o Pain is marked because of limited room for expanding edema in this landmark.
anatomic area.
Other Acute Forms
o Abscess formation occurs and a “point” may form, at which time,
drainage can be established by a needle.  OTOMYCOSIS
o Topical medications, heat, and analgesics are generally prescribed. o Black, hairy stuff on the external auditory canal – Aspergillus niger
o White and cottony – Aspergillus flavus

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o Usually bilateral and may be associated with bronchiectasis and

o Pain is not the predominant symptom but itchiness  when the chronic sinusitis.
patient starts to scratch it’s going to excoriate the skin and cause o Patient presents with pain and hearing loss.
irritation  acute bacterial otitis. o Caused by an overproduction of squamous epithelium and squamous
o In this case, you need to treat the bacterial otitis first then follow up with plugs and a faulty migration of the epithelium.
anti-fungals., otherwise it will recur
o Anti-fungals are given in topical preparations  MALIGNANT OTITIS EXTERNA
 Clotrimazole o Disease of the external auditory canal that has the propensity of
destroying the temporal bone.
 HERPES ZOSTER OTICUS o Main organism involved is Pseudomonas (opportunistic infection)
o Presence of vesicles in the concha of the external auditory canal, typical o If you see a patient with malignant otitis externa, screen that
of the varicella zoster infection. patient for underlying diseases that have affected the immune
o Reactivation of chicken pox; affects a dermatomal level. system: AIDS, uncontrolled diabetes, hypercholesterolemia, etc.
o In the case of Herpes zoster oticus, the nerve affected is the geniculate o One of the few diseases where you could perform simple
ganglion of the facial nerve. mastoidectomy  you do not go deep inside the bone, you just drill
o Aside from pain, the patient may also complain of facial paralysis. of what is necrotic.
o Pain + Facial paralysis = Ramsay Hunt’s Syndrome o Treatment: Aminoglycosides + treatment of underlying cause or
o Exquisitely painful because the nerves are affected. predisposing factors + if needed, debridement of the necrotic
o Neurotrophic virus so recurrence is possible. temporal bone by simple mastoidectomy.
o Postherpetic neuralgia – pain persists even when treated with oral
steroids  RELAPSING POLYCHONDRITIS
o Contagious because the crusts and the fluid of the vesicles harbors the o Autoimmune disease
virus. o Recurrent, progressive destruction of the cartilages of the head and
o If the person who gets exposed has not had any varicella zoster infection neck.
yet, he will get chickenpox and not herpes zoster. o May include the nasal septum – saddle nose deformity
o Ear deformity – pinna is involved
 PERICHONDRITIS o May also involve the cartilage of the laryngotracheal skeleton.
o Doc: Very common among males with jealous girlfriends: ‘Walang
hiya ka! Babaero ka!’
 Two distinct entities, keratosis obturans and cholesteatoma of
o Usually due to trauma; may be seen among boxers.
the external auditory canal, may present as a keratin plug
o The skin of the pinna is closely integrated with the covering of the
occluding the external auditory canal.
cartilage, the perichondrium.
 Keratosis obturans is usaually bilateral and may be associated
o Fluid accumulating between the cartilage itself and the
with bronchiectasis and chronic sinusitis.
perichondrium  when the fluid becomes infected  diffuse
o The patient presents with pain and hearing loss.
swelling of the ear  Perichondritis
o No bony erosion is observed.
o Treated with systemic antibiotics and if needed, incision and
o Plug removal and treatment of the inflammatory process
drainage of the fluid under sterile conditions.
are the recommended therapy.
o If bacteria gains access and resides in the cartilage, it’s going to
cause permanent deformity of the cartilage  cauliflower ear.  Cholesteatoma of the external auditory canal is usually
unilateral.
o Develops when trauma or inflammation causes an effusion of serum
o Patient presents with dull pain and intermittent otorrhea
or pus between the layer of the perichondrium and the cartilage of
due to bony erosion and secondary infection.
the external ear.
o Circumscribed periostitis and faulty epithelial migration
o In most cases of trauma, the injury is in the form of a laceration, or is
have been postulated as causes.
the result of incidental damage during surgery on the ear.
o Treatment: Debridement of the bone or canalplasty and
tympanomastoidectomy where appropriate .

Furunculosis (Otitis Externa Circumscripta)

 Confined to the fibrocartilage portion of the external auditory
meatus.
 In severe cases, surrounding cellulitis may extend beyond this
area.
 Pain may be quite marked because of limited room for expanding
edema in this anatomic area.

Diffuse Otitis Externa

 Occurs during hot, humid weather and is caused by Pseudomonas
group, and less often, by S. albus, E. coli and Enterobacter
aerogenes.
Fig 2. Perichondritis  The stroma overlying the bone of the inner third of the canal is
Chronic Causes very thin, allowing minimal room for swelling.
 KERATOSIS OBTURANS  Thus, the subjective discomfort the patient experiences if often out
o Similar to impacted cerumen + ciliary dysfunction inherent to the of proportion to the extent of the disease visualized
patient
o Epithelial debris becomes very adherent to the external auditory canal
to the point that it will behave like a mass and excavate the external
auditory canal.
o Has a tendency to recur.
o Treatment of choice: manual extraction
o If there is evidence of secondary bacterial infection, treat accordingly.
o Keratin plug occluding the external auditory canal. remember me? ;P

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 Usual causes are the top 3 organisms that cause URTI: S. pneumoniae, H.
Otomycosis
influenza, Moraxella
 Several fungi may cause inflammatory reactions in the external
 Associated with URTI
auditory canal.
 Eustachian tube obstruction – primary event that triggers the development
 The two most common fungi found there are Pitysporum and
of Acute Otitis Media.
Aspergillus.
 Pathogenesis:
o The Pitysporum organism may cause only a superficial scaling
o Middle ear cavity filled with air  suddenly, you develop a disease
similar to a dandruff of the scalp, may be associated with an
causing Eustachian tube dysfunction (ET is normally closed, it only
inflammatory seborrheic dermatitis, or may form the basis on
opens when you yawn or swallow; opens by muscular action by tensor
which more uncomfortable infections develop, such as furuncles
and levator veli palatini)  it becomes closed  air in the middle ear
or eczematous changes.
cavity becomes resorbed by the blood vessels inside  pressure inside
 branch of the 7th cranial nerve, extend to the auricle, or have faded
the middle ear becomes negative (develop suction inside the middle ear
by the time the patient is seen.
cavity)  pressure inside the capillaries (hydrostatic pressure) exceeds
o Other combinations of ssx may exist owing to progressive
the pressure in the middle ear cavity  to equalize, the hydrostatic
involvement of vestibular and acoustic fibers of the 8th cranial
pressure is going to force the fluid part of the clot into the middle ear
nerve.
cavity = TRANSUDATION  transudate infected by bacteria 
 Treatment: EXUDATE
o Mainly symptomatic
 During the time that there is Eustachian tube obstruction and
o Systemic steroids (depending on the result of nerve function
transudation, there is no pain. What the patient will feel is EAR FULLNESS.
testing).
 When the patient starts building up pus or exudate, there’s going to be pus
Herpes Zoster Oticus (Ramsay Hunt Disease) under pressure.
 The onset of facial paralysis, when accompanied by otalgia and a o Negative pressure – retracted TM
herpetic eruption involving portions of the external ear, is o When fluid and pus develops – bulging TM
considered to be caused by a viral infection involving the
 If untreated, the TM may rupture and you may see fluid coming out.
geniculate ganglion.
 Treatment:
 The vesicular skin involvement may be limited to the specific area o Treat the underlying cause: events that lead to Eustachian tube
of the external canal innvervated by a small sensory branch of the obstruction  URTI, cleft palate, adenoid enlargement, tumor in the
7th cranial nerve, extend to the auricle, or have faded by the time nasopharynx, uncontrolled allergic rhinitis, and nasopharyngeal mass.
the patient is seen. o Give antibiotics for otitis media, if the patient already has a perforation,
o Other combinations of ssx may exist owing to progressive
add a topical antibiotic preparation to dry the ear faster.
involvement of vestibular and acoustic fibers of the 8th o Penicillinase-resistant penicillin
cranial nerve.
 Anatomic variations of Eustachian tube:
 Treatment: o Child – more horizontal, shorter, wider  promote stasis of fluid in the
o Mainly symptomatic middle ear.
o Systemic steroids (depending on the result of nerve function o Adult – more vertical, longer, narrower  promotes easier drainage, it
testing). is harder for fluid to get in.
Perichondritis
 This condition develops when trauma or inflammation
causes an effusion of serum or pus between the layer of
the perichondrium and the cartilage of the external ear.
 In most cases, the injury is in the form of laceration or is
the result of incidental damage during surgery to the ear.
 Diagnosis:
o Involved part of the auricle swells, becomes reddened,
feels warm and is very tender upon palpation.
 Treatment:
o Parenteral antibiotic as well as topical treatment of
any associated canal infection.
o Choice of drug is based on culture results or other
indications of organism involved.
o IND if the condition seems to be spreading and there
is evidence of fluid under the perichondrium. Fig. 3 Comparison of Eustachian Tubes
 Eustachian tube obstruction in cleft palate:
o The tensor and levator veli palatine are integrated in the soft
Diseases of the Middle Ear palate  deficient palatal musculature when the patient has cleft
Bullous Myringitis palate (ET is abnormally closed, cannot perform the ventilatory
function of the ET because the muscles lack the anchorage to open
 Isolated infection of the TM, without involvement of the middle ear cavity.
the ET).
 Blebs or bullae on the epithelial surface of the TM.
 + pain (otalgia)
 Hearing loss may be negligible in contrast with Otitis media where HL is an Acute Non - Suppurative Otitis Media (ANSOM)
outstanding symptom (main differentiating point)  Sequelae of untreated ASOM.
 Complication: Sensorineural HL (cochlear damage from invading  Aka Serous Otitis Media
organism) (external ear diseases that may cause nerve deafness)  Outstanding symptom: there is no otalgia because the infection has
been rid of bacterial toxins, (child- poor school performance)
Acute Suppurative Otitis Media (ASOM)  Treatment:
o treat underlying cause
 This is the precursor of the “luga”
o If the condition cannot be treated conservatively, you may perform
 External auditory canal is normal – no tragal tenderness. myringotomy/tympanotomy – make a surgical incision on the TM
 There is definite HL because there is fluid inside the middle ear cavity. and if needed, insert a ventilation tube/myringotomy tube to
 +/- discharge, depending on whether there is a perforation facilitate removal of fluid inside.
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Chronic Suppurative Otitis Media (CSOM)  Complications:

 Very important primary health concern in the Philippines o Hearing loss
 “Luga”, “Tulok” o Facial nerve paralysis
 There is always a tympanic membrane perforation. o Sub-periosteal abscess
 It results from a neglected acute middle ear infection.
 Can be a precursor to a host of complications, some of which are fatal. Chronic Non-Suppurative Otitis Media
 Cholesteatoma  May be a serous otitis media that persisted.
o There is no cholesterol in cholesteatoma  “Glue ear” or middle ear atelectasis.
o Primarily keratinizing epithelium that has migrated into the middle  Very hard to treat even if you put myringotomy tubes.
ear; ectopic skin in the middle ear.  May erode on the ossicles because of the pressure producing
o Ectopic skin may pile up, enlarge, and behave like a mass. permanent conductive hearing loss
o Complications will come, depending on which part of the middle ear  Tuberculous Otitis Media
has been eroded. o Hallmark: presence of multiple perforations on the TM.
 Because of this clinical appearance, CSOM has been labelled as either
safe/dangerous infection. Referred Otalgia
 Condition (eg. pharynx) that will produce pain in the ear
CSOM : SAFE DANGEROUS  Shared innervation between the pharynx and the middle ear
Area Involved Tubotympanic Attico-antral o CN V2
Perforation Central Marginal/Attic o CN IX (Jacobsen’s nerve)
Pus Mucoid/odorless o CN X (Arnold’s nerve)
Granulation - +
Polyp - + TMJ Dysfunction
Hearing Loss Conductive Mixed  Pain when you palpate the TMJ
Cholesteatoma - +  Clicking sound heard when you ask the patient to close/open mouth.
X-rays - +  There is pain whenever the patient opens his jaw or chews
 (+) Trismus/Lockjaw
 Otoscopic findings are normal

Diseases of the Tympanic Membrane

 Usually associated with pathologic changes of the middle ear and
mastoid.
 Pathologic features:
o TM may be thickened owing to inflammation.
o It may contain white thick patches or even become entirely white
and think owing to deposition of hyalinized collagen in its middle
layer as a result of previous inflammation (tympanosclerosis).
o May become thinner from loss of its middle layers (membrane
propria) – due to Eustachian tube ventilation dysfunction.
o TM may be retracted if there is a vacuum in the middle ear, or
may bulge when fluid, infection or a tissue mass such as a tumor
is present in the middle ear.
 Myringitis refers to an inflammation of the TM.
o In hemorrhagic, or bullous myringitis, the most notable
finding is bleb formations (bullae) on the TM and adjacent
canal wall.
o This appearance can occur in children, in whom it is
associated with the common bacteria that cause ASOM.
o In adults, it is usually a self-limited disease and is associated
with infections caused by Mycoplasma pneumoniae.
o Sensorinueral hearing loss has been reported as a result of
this infection.
 Treatment:
o When there are systemic manifestations. Erythromycin is the
DOC.
o For relief of pain the blebs or vesicles can be disrupted with a
fine needle or myringotomy knife.
 HUGOT #1: One who refuses to invest time on things that are
important has no right to waste time on things that aren’t.
 Doc: Next, we go to, hearing loss.
3A: BREEEEAAAAAK…..
Doc: Break? Break sa boyfriend? O sige, as a form of break, do you have any
questions? Hindi tayo pwede magbreak, mahaba lecture ko, di kayo
makakapag-quiz
3A: 
Doc: Sino daw ang apostoles na Malaki ang katawan? (Medyo irehe tong
joke na to)
Doc: Saint Machu. XD
Fig 4 Shape and Relationships of Middle Ear

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Disorders of the Eustachian Tube Acute Purulent Otitis Media

 ET connects the middle ear cavity with the nasopharynx and is  The middle ear is usually sterile; the combined actions of the
intimately related to diseases of both. cilia and mucus-secreting enzymes and antibodies acts as a
 The lateral third as it enters the middle ear is bony, whereas the defense mechanism when these microbial contaminants are
medial two-thirds is fibrocartilaginous. exposed to the middle ear space during the act of swallowing.
 Surgical repair of the cleft palate is undertaken as soon as possible for  Acute Otitis Media results when this physiologic mechanism is
functional purposes. disrupted.
 Many children require frequent placement of ventilation tubes, and  Obstruction of the ET is also a basic causative factor in acute
often, a long-lasting type tube is inserted. otitis media.
 Functions of the ET are:  Classic symptoms include pain, fever, malaise, and sometimes
o Ventilation – provides equalization of atmospheric pressure on both headache in addition to earache.
sides of the TM. o In children, anorexia and sometimes nausea and vomiting
o Drainage – secretions formed in the middle ear will drain into the are present.
nasopharynx through a normally functioning ET. o Abscess in the middle ear.
o Protection of the middle ear from contamination by nasopharyngeal  Treatment:
secretions. o Because of the increasing incidence of ampicillin
Abnormally Patent ET resistance, antibiotics are combined with clavulanic acid
 Open all the time so that air enters the middle ear with respirations. and are effective against beta-lactamase formers.
 Patient’s history reveals a significant weight loss which leads to loss o Either a cephalosporin or ampicillin combined with
of adipose tissue around the ET orifice. clavulanic acid has become the preferred medication
 The condition can produce: o Sulfisoxazole + Erythromycin is another effective
o autophony (hearing one’s respiration) substitute in penicillin-allergic patients.
o a sensation of fullness  All medications should be administered for at least 10-14 days,
o plugged-up feeling in the ear and a follow up examination is a must to ensure complete
 The TM in this patient will be atrophic and thin and will move in and resolution
out with respiration, a tell-tale diagnostic sign. Serous Otitis Media
 Treatment: insertion of a ventilation tube through the TM to  Caused by transudation of plasma from the blood vessels
decrease the disturbing effects. into the middle ear space largely due to hydrostatic pressure
Palatal Myoclonus differences..
 Fairly rare condition in which the palatal muscles undergo periodic  ET dysfunction is a major underlying factor.
rhythmic contractions.  Other causative factors include:
 Clicking sounds in the patient’s ear may be heard by examiner’s ear. o Hypertrophy of the adenoids
 Associated with vascular lesions, multiple sclerosis, aneurysms of the o Chronic adenoiditis
vertebral artery, tumors and various other lesions of the brainstem of o Cleft palate
cerebellum. o Tumors in the nasopharynx
 Usually, no treatment is needed; rarely, incision of the tensor tympani o Associated inflammation such as sinusitis/rhinitis
muscle of the middle ear can be considered. o Radiation therapy
o Immunologic/metabolic deficiency
 Middle ear effusion is the most common cause of
ET Obstruction hearing loss in school-age children.
 Can result from nasopharyngitis or adenoiditis.  PE reveals drumhead immobility as assessed with a
 When a nasopharyngeal tumor obstructs the ET, the first clinical pneumatic otoscope.
finding can be fluid in the middle ear. o Positive and negative pressures are applied to the ear
 Obstruction may also be caused by a foreign body, such as a posterior canal after obtaining an adequate seal.
pack for nasal epistaxis, or mechanical trauma from aggressive o If there is air in the tympanum, it will be compressed
adenoidectomy resulting in scarring and closure of the tube. and the drumhead will move inward with the
application of positive pressure and outward with
Cleft Palate negative pressure.
 CF deformity results to ET dysfunction due to lack of anchorage of the o Movement is damped in the presence of serous otitis
tensor palatine muscle. media
 In the unrepaired cleft palate, this prevents the muscle from exerting o The malleus appears short, retracted and chalky
sufficient contraction on the ET orifice to open it during swallowing. white.
o Results in inadequate ventilation of the middle ear, and o Fluid levels or bubbles may be seen.
inflammation ensues.  Treatment for these conditions if first medical and
 Surgical repair of the cleft palate is undertaken as soon as possible for then, surgical.
functional purposes. o Antibiotics
 Many children require frequent placement of ventilation tubes, and o Antihistamines (only used when associated with
often, a long-lasting type tube is inserted. nasal or sinus congestion)
Doc: (on a roll) why is Jesus sad? o Decongestants
3A: Why? o ET ventilation exercises
Doc: Because Jesus Cries. Why is Jesus rich? o Allergic hyposensitization (reserved for cases in
which definite allergies are demonstrated by skin
Doc: Because Jesus saves. Ano apelyido ni Jesus? testing)
3A: Ano?
Doc: Christmas. Diba, Mary Christmas?
Doc: San daw galing ung crucifix ni Kristo?
Doc: Ilocos. Ano ba ung nakalagay? INRI – Ilocos Norte Region I. XD
Doc: Oh, let’s go.

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Chronic Infection of the Middle Ear and Mastoid NIHL Acoustic Trauma
 Since the middle ear is connected to the mastoid, chronic otitis
media is accompanied by chronic mastoiditis. Low level exposure, Acute, Sudden, so loud
 Active Chronic Otitis Media – presence of infection with long period that can disrupt the ear
drainage from the ear or otorrhea resulting from underlying hair cells
pathologic changes such as cholesteatoma or granulation tissue.
o There is an aural discharge Usually IRREVERSIBLE
o Otorrhea may be purulent (thick, white) or mucoid
(watery, thin) depending on the stage of inflammation.
o A mucous discharge results from activity of secretory o Temporary threshold shift: short exposures, so ear can recover –reversible
glands in the middle ear and mastoid. o Presbycusis: (acquired HL)
o A very foul smelling, putrid discharge of dirty grayish  HL d/t old age
yellow color suggests cholesteatoma.  Stria vascularis sources of endolymph
 Inactive COM – refers to the sequalae from a previously active
infection that has burnt out, thus, otorrhea is absent.  TYPES of PRESBYCUSIS: * further read on the box part
o Patients often complain of a hearing loss.  Sensory: selective loss of hair cells
o Vertigo, tinnitus, or a sense of fullness may be felt as well.  Mechanical: Stiffening of the basilar membrane Inefficient organ of
o Dry perforation of the TM may be seen cotri
o Tympanosclerosis  Strial/ metabolic: degeneration of the stria vascularis: best prognosis,
 loss of ossicles which is sometimes visible through the discriminations are excellent. This is the one that is most favored
TM perforation from hearing aid use.
 fixation or disruption of ossicles from previous  Neural: Degeneration of the nerve cells itself; poorest prognosis
infection Tests to evaluate the hearing
 If there is sufficient disability and hearing loss, surgical - Subjective
correction or tympanoplasty can be considered. - Objective
 Conservative treatment consists essentially of advising the Even if you are just observing a patient you can tell which type of HL they
patient to keep water out of the ear and cleansing in the office have
with careful pot suctioning. - Pre-lingual Deafness (Congenital) : before the person learned to talk
o Hydrogen peroxide or alcohol can be used for cleansing o Absence of auditory milestones: More, localize sound, cannot
with a soft cotton-tipped wire applicator for removal of recognize voices, unintelligible speech, patient is dependent on
diseased tissue and inspissated suppuration. gestures
- Post-lingual Deafness: had experience to hear; they have a tendency to lip
HEARING LOSS read, speech is usually loud, they usually answer in appropriately
- Idiopathic
Types of Hearing loss:
-most common is Meniere’s Disease (see later)
- Conductive – External, middle
(Triad: HL, tinnitus, vertigo)
- Sensorineural – inner ear Sensorineural: loud speaker kasi di nila naririnig sarili nila
- Overlaps & Complication middle ear then involved inner ear
Conductive: inappropriately kasi naririnig pa din nila sarili nila unlike sa
Congenital: if you have a problem with the external ear it doesn’t follow that sensorineural kasi they can hear themselves
you will have a problem with the inner ear. So feedback is important for voice regulation
Inner ear is more stable, because it develops 1 week earlier, external and middle - Tumors
ear develop at the same time. So you may have a congenital problem with the 3A: Breaaaaak
external ear it usually follows that you have a problem with the middle ear, not Doc: tan****ng break yan :D ano break na tayo?
the inner ear. What is the common name of NaCl ? Ito ang nilalagay mo sa itlog ng mister
mo sa umaga. Answer: “talcum powder” ;P
**Bahay bata uterus diba? So how about the vagina? Bahay batuta ;P - Meds: most notorious ototoxic drug: streptomycin, aspirin (too much intake),
External Ear Sources of HL furosemide (elderly with RF, CHF) there are some drugs when withdrawn,
o Congenital, infectious, foreign bodies, trauma, Ear canal Mass but for a very long time a damage can become irreversible
o IMPACTED cerumen - just remove the offending thing there
o TRAUMA - to ext. ear: usually the external ear -> otitis Externa Medical Labyrinthectomy: injection of aminoglycoside for intractable
o MASSES - oxystosis, osteomas, polyps, (Conductive hearing loss) Meniere’s to induce deafness, done as a last resort for suicide patients.
Middle ear infection-> Middle ear polyps -> there would also be
polyps from the external but will not affect the inner ear CONGENITAL DEAFNESS OF GENETIC ORIGIN
Middle Ear Sources of HL Deafness of Genetic Origin Occurring Alone
- Congenital: vesicular aplasia/ hypoplasia (Conductive HL)
o Michel’s Deafness
Infections: Otitis Media
- Trauma: temporal Bone fracture without inner ear involvement - Total lack of development of the inner ear. Autosomal dominant
Inner Ear Sources of HL o Mondini’s Deafness
- (Sensorineural HL) (Nerve deafness) - Partial aplasia of the bony and membranous labyrinth
- Congenital: Aplasia, hypoplasia - Results in a flattened cochlea with development only of the
- Infections: meningitis, CSOM, Viral, basal turn so that instead of 2.5 turn, there are only 1.5 turns,
o Unilateral: mumps while the middle and apical turns occupy a common space
o Bilateral measles - Osseous vestibular labyrinth may also be malformed.
- Acquired (presbycusis, meds)
- Dysgenesis of the Organ of Corti → HL (AD)
- temporal bone fracture with inner ear involvement, NIHL,
Acoustic trauma.

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o Scheibe’s Deafness
- Bony labyrinth is fully developed but the pars inferior (saccule
and cochlear duct) is represented by mounds of
undifferentiated cells. This is the most common of all inherited
congenital deafness disorders and is usually transmitted as an
autosomal recessive tratit. There may be residual hearing in low
frequencies
- The organ of Corti and adjacent ganglion cells of the basal coil of
the cochlea are most severely affected -> high frequency HL
- Bony and membranous labyrinths: appear normal
Deafness Associated with Other Abnormalities
o Waardenburg’s Disease
- Dominant trait; primary features include lateral
displacement of the medial canthi and lacrimal points, a flat
nasal root, hyperpplasia of the eyebrows, partial or total
heterochromia of the irides, partial albinism in the form of a
white forelock, congenital deafness in around 1/4
o Albinism
- May be autosomal dominant/recessive, sex-linked. HL may
be bilateral and severe
o Hyperpigmentation
- Severe sensorineural deafness, pigmentary defects progress
from small spots in localized areas in childhood to larger
lesions over the entire body in adults.
o Onychodystrophy
- Congenital male dystrophy and congenital sensorineural
deafness, recessive. Affected siblings have small, short
fingernails and toenails and severe high-frequency deafness
o Pendred’s Disease (Non-endemic Goiter) Delayed or acquired genetic Deafness
- 10%; abnormal iodine metabolism → thyroid enlargement o Usually bilateral, Autosomal Dominant, can appear in
(adolescence with nodular development in adulthood; childhood or in early adulthood and will progress in severity
usually born with severe HL during the remainder of the patient’s life.
o Jervell’s Disease (Jervell & Lange-Nielsen Disease) o Genetic Progressive deafness: bilateral, generally falt, basin-
- Prolongation of QT interval, Stokes-Adams attacks, shaped sensorineural configuration on the audiogram with
congenital bilateral severe HL, usally die  during childhood fairly good discrimination.
o Usher’s Disease o There may be absence of Organ of Corti and spiral ganglion
- Main features: progressive retinitis pigmentosa and cells in the basal turn and irregular degeneration of the stria
congenital severe to moderate sensorineural HL, vascularis
recessive/sex linked/dominant, bilateral and severe HL o Otosclerosis
- AD, primarily conductive HL, may be associated with
progressive sensorineural HL
 Symptoms develop: late teens, adults
Congenital Deafness of Non-genetic Origin  CHL is the main problem but in time SHL can happen d/t
o Rubella cochlear otosclerosis
- Still one of the most common causes of nongenetic congenital -
deafness (German measles)
- If a woman contracts German measles within the 1st 3 Deafness Associated with Other Abnormalities
months of pregnancy, the pars superior is generally normal. -all of them suffer from progressive sensorineural deafness (SHL)
Pathologic examination: shows aplasia of the organ of Corti o Alport’s Disease: bilateral, symmetric, worse in higher
and of the saccule (pars inferior) frequencies HL
o Erythroblastosis Fetalis o Von Recklinghausen’s Disease: localized form of
- Rh incompatibility; characterized by a deposition of bilirubin neurofibromatosis with bilateral acoustic tumors
in the CNS, jaundice, mental retardation, cerebral palsy, and o Hurler’s Syndrome : profound SHL, fatal
deafness shortly after birth in these infants. o Klippel-Feil Syndrome: skeletal defect, profound HL
o Cretinism o Refsum’s Disease: retinitis pigementosa, ichthyosis,
- Aka endemic cretinism, generally accepted that iodine polyneuropathy, ataxia, progressive SHL
deficiency is responsible for the cretinism o Alstrom’s Disease: retinitis pigementosa, DM, obesity,
- Usually in the Alps, mixed HL (conductive, sensorineural) progressibe HL
o Paget’s disease: skeletal deformities, long bones of legs
o Richards-Rundle Syndrome: mental deficiency, ataxia,
Ototoxic Drugs
hypogonadism, (all appear in childhood) severe deafness, total
o When using these: get baseline hearing levels, test for balance, HL by 5 or 6 y/o
warn patient of the potential for toxicity
o Crouzon’s Disease: premature synostosis of the cranial suture,
exophthalmos, parrot or hook nose, short upper lip and
protruding lower lip, atresia of auditory meatus, mixed HL

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Acoustic Tumors
o Acoustic Neuroma PRESBYCUSIS
- Most common inner ear tumor causing HL - Sensory presbycusis: pathology hair cells are lost first →loss
- Benign tumors of the Schwann cells covering the CN 8, these in cochlear neurons → hair loss on the basal turn of the
schwannomas occur most often on the balance portion of CN8. cochlea and high-tone HL
- Younger ones/ family history of this: may present an early - Neuropresbycusis: primary loss of cochlear neurons with
manifestation of von Recklinghausen sydnrome (VRS) relative preservation of the hair cells: greater loss of word
- VRS causes all cases of bilateral acoustic neuromas discrimination and only gradual loss of hair cells over time.
- Usual course: patient develops unilateral SHL, mild at 1st but - Strial Presbycusis: leaves excellent words discrimination
as the tumor grows, it slowly crushes the nerves of the after the degenerative process causes moderate to severe HL
internal auditory canal, patients rarely complain of vestibular that is relatively flat in nature: stria vascularis degenerate &
symptoms shrink
- Can cause sudden HL or Meniere-like syndorms as well - Cochlear-conductive HL: leaves a normal neuronal and hair
- Any unilateral or asymmetric HL is an acoustic neuroma population without damage to the stria vascularis but shows
until proven otherwise HL that is r/t a limitation of movement in the basilar
- Small ones can be diagnosed with ABR (Auditory brainstem membrane
response) testing and radiologic conformation.
Acoustic tumors are seen only on enhanced CT scans with high
resolution thin slices. MRI may be more sensiotive that CT TINNITUS
scan  A howling sound from middle ear
o Other HL causing tumors  Ringing high pitch from inner ear – usually assoc with HL; very hard to treat
- CN 7 neuromas, meningiomas, hemangiomas, aberrant vessels
o Surgical removal: has 3 main routes: can be resected from the
Objective Tinnitus
middle fossa, from the posterior fossa, or across the labyrinth
o Surgical procedure depend on tumor size, potential for  A tinnitus the examiner and patient can both hear with use of instruments.
hearing preservation, and surgical experience  Diseases
o Glomus tumor of middle ear – pulsating sound synchronous with
pulse, soufflé
TRAUMA o Palatal myoclonus – abnormal involuntary, irregular, movement of
o Mechanical energy palate producing a clicking sound since Eustachian tube is connected
- Temporal bone fractures: temporal bone is made of some of the with the soft palate- annoying to patient
densest bone, protected by its central location, when it does Tx: anti-convulsant (Carbamazepine)
fracture it usually includes: loss of consciousness, subdural or
epidural hematoma, or concussion Subjective Tinnitus
o Longitudinal fractures 80%:
- begin at the foramen magnum, travel out to the external auditory  A tinnitus only the patient can hear
canal, ear bleeds, (Conductive) CHL  This is different from auditory hallucination (voice and words)
o Transverse Fractures 20%:  Causes of Subjective tinnitus:
-injuries to the labyrinth and CN7 d/t fracture line travels thru the o External ear
petrous apex or the labyrinth. o Middle ear (Meniere’s disease, labyrinthitis, Presbycusis)
-labyrinthine injuries: can be less severe: concussion o Inner ear
phenomenon with balance recovery and hearing, if more severe: o Systemic cause- Diabetes mellitus with hypoglycemic or
total HL hyperglycemic episodes
 Tinnitus is any abnormal ringing sound that the patient hears
 IT is common and is associated most frequently with sensorineural
hearing loss
 Must be examined for anatomical source:
o Abberant vessels
o Middle ear
 A sensorineural etiology will decrbie worsening of tinnitus in quiet
environments where competing noise is not masking. They will
complain of bothersome tinnitus surrounding time of falling asleep
or waking.
 Evaluation: Thorough audiologic evaluation.
● Meniere’s disease consist of a triad of tinnitus, vertigo and
HL (not exclusive to Meniere’s, Labyrinthritis, Fistulas also
have these)


Fig 5 transverse and longitudinal fracture

o Acoustic energy
- Blast injuries → concussion wave that does more damage to the
middle ear> inner ear → high-tone SHL (d/t loudness and length of
exposure
- Most common cause of SHL :Safe exposure: 80dB for 8hrs,
dangerous: 110dB:High tone HL occurs first d/t acoustic energy
and natural frequency of the inner ear hearing mechanism
- Noise exposure → temporary threshold shift → improve <2wks
repeated trauma →permanent threshold changes

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IDIOPATHIC CAUSES OF HL - Solid Cerumen Plug becomes wet → swell →temporary hearing
- Meniere’s disease : loss (HL)
o disorder d/t swelling of the endolymphatic space, cochlear in - Normal External Canal: narrowest in the middle, cotton swabs
nature, fluctuation in HL with a low-tone tinnitus push wax down to narrow isthmus against drum head →
o attacks can last several mins to hrs. usually involves vestibular IMPACTED CERUMEN →difficult, painful removal
changes (abangan mamaya) - Treatment : removal via: curette under direct visualization, water
- Multiple Sclerosis irrigation by special metal syringe, Hartmann Type of alligator
o A cause of varying degrees of HL, structural location of the HL forceps (for hard plugs)
is not clear - After removal: drops that may be given are: mineral oil, hydrogen
o Relatively rare; SHL peroxide, Debrox, Cerumenex
o Next to visual symptoms, the most common manifestation of
MS can be in CN 8 DIZZINESS/ VERTIGO
ISSUES OF SUDDEN HL  Can be classified as:
1. Peripheral – seat of lesion at the vestibular system
- HL may be minimal, severe, temporary, or permanent
o 3 SCC’s and 2 Otolith organs (Utricle and Sacule)
- Only a symptom complex and is not common
o Otolith organs sense linear acceleration without any angular
- Usually no cause is found </3 ; may be thromboembolic or
component (eg. Travelling forward, backward, up, or down)
immunologic cause
o SCC sense angular acceleration (eg. Ballet dancer doing a
- Prognosis is best if treatment is <24hrs, patients are put to bed pirouette)
rest, high-dose steroids, vasodilators, plasma expanders, anti- o Why 3 SCC’s? Because we are 3 dimensional beings
coagulants 2. Central – Vestibular nuclei or the brain itself
 Another classification:
1. Presyncope – on the verge of losing consciousness
BAROTRAUMA o “parang nagningitim ang paningin ko ng sandal”
- Damage to tissues d/t changes inbarometric pressure w/c occur o “para akong tutumba or mahihimatay”
during diving/ flying. 2. Disequilibrium – “para po akong lasing/ nakasakay sa barko”;
- Boyle’s Law: ↓ or ↑ in environmental pressure will expand or “para pong nakalutang ang ulo ko”
compress, respectively, a given enclosed volume of a gas. Volume 3. Psychogenic dizziness – “pag ako po ay na sa mall doon ako
of gas is inversely to pressure nahihilo”
- This can occur in gas filled parts of the body: liddle ear, sinus, 4. Vertigo – hallucination of spinning movement (refer to discussion
lungs) these become encoles spaces thru blockage of normal below)
venting pathways o Hallucination of spinning movement
- Middle ear: most common site o It may be the person or the surroundings that is spinning
- Eustachian tube: OPEN swallowing, chewing, yawning, Valsalva o May not always be an ear problem but you have to rule out ear
Manuever problems because they can only produce one type of dizziness,
- As environmental pressure ↓ , middle ear will expand and that is vertigo
passively vent thru the eustachian tube (ET) o “Why spinning? Why not up and down or to and fro? It is
- As environmental pressure ↑, air in the middle ear and w/in the because we have more SCC’s than otolith organs… so by mass
tube is compressed → collapsed ET → P becomes too great (90- effect you have more receptors for angular acceleration than
100mmHg) → cartilaginous portion of the ET firmly collpase you have for linear acceleration. So whenever the vestibular
→relative vaccuum develops w/in middle ear mucosa→ tympanic system becomes pathologic, the pathologic side will produce
membrane retract inwards →stretching of eardrum→ rupture of o
small vessels to produce an injected appearance and o more stimuli coming from the SCC which are three and the
hemorrhagic blebs w/in the drum → further pressure increase → otolith organs which are two therefore by mass effect you have
small vessels w/in middle ear mucosea will dilate and ruptre → rotatory dizziness.”
hemotympanum → rupture tympanic membrane
- Symptoms: common complaint: ascending or descending vertigo, Intermittent/Episodic Persistent
pain, feeling of fullness, ↓ hearin, Dx is confirmed by otoscopy. (+) hearing  Menier’s disease  Labyrinthitis
Severe cases: 4-6wks to resolve, mostly 2-3 days loss  Superior SCC  Temporal bone
- Persistent tinnitus, vertigo, SHL: symptoms of inner ear damage ( dehiscence fracture w/ otic
may require surgery) capsule involvement
 Labyrinthine fistula
(-) hearing  BPPV  Vestibular neuritis
CERUMEN(ear wax) loss
- Product of both sebaceous, apocrine glands at cartilaginous  Superior SCC dehiscence – dizziness whenever the person strains
portion of external auditory canal o “The most bizarre chief complaint that my colleague had was:
- Types “everytime I have sex, when I am about to cum, I become dizzy”
o Wet: Caucasians, Blacks because of the straining during the climax pressure builds up in the
o Dry: American, Indians; SCC (Bad trip diba? Kasi you are about to cum but you become dizzy…
- OLDER people: cerumen tend to be drier edi manlalambot.. -_- *insert doc’s sound effect*)”
o d/t atrophy of apocrine glands w/ subsequent lessening  Dizziness from the inner ear is fatigable ⟶ repeated Dix hallpike ⟶ may
of sweat component go away
o more prone to canal debris d/t epithelial debris build
up not to wax
 Pattern of nystagmus from peripheral is consistent from test to test
(upward, downward, or torsional) while nystagmus from central
- Protective qualities: vehicle for removing epithelial debris and
interverse (varies and non-fatigable)
contaminants away from tympanic membrane
- Lubrication prevents desiccation of epidermis with its associated
fissuring
- Fatty acid, lysozyme, immunoglobulin: inhibitory /bactericidal
- Excessive cerumen accumulation: NOT a dse

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THE VESTIBULAR SYSTEM PHYSIOLOGY  In the utricular macula, the kinocilium is located on the side of the
 Sensory signals coming from the inner ear, the retina, and the hair cell located closest to the central region, the striola
musculoskeletal system are integrated in the CNS to control gaze  Thus, during a given head tilt or linear acceleration, some of the
and the position and movement of the body in space. afferents will be excited and others will be inhibited
 Receptors are hair cells located in the cristae of the semicircular  The afferents with a given polarization may project to different
canals (SCC) and the maculae of the otolith organs. neurons in the vestibular nuclei and may sub serve different
 Those of the SCC are sensitive to rotation, specifically angular functions
acceleration while those of the otolith organs are sensitive to  Because there are different polarizations within each macula, the
linear motion, specifically linear acceleration, and to changes in CNS has information about linear motion in 3 dimensions, even
head position relative to gravity though there are only 2 maculae
Hair cells
 The individual hair cells of the SCC and the otolith organs are very
Vestibular Reflexes
similar  The afferents go to the CNS and synapse on the neurons in the
 Each has a structural polarization that is defined by the positons of vestibular nuclei in the brain stem
the stereocilia relative to the kinocilium  Neurons in the vestibular system project to other parts of the brain;
 If a movement causes the stereocilia to be bent toward the some go directly to the motoneurons and others go to the brain
kinocilium, then the hair cells are excited. stem reticular formation, cerebellum and other structures
 If the movement is in the opposite direction and causes a bending  Direct connections between the vestibular nuclei and the
away from the kinocilium, then the hair cells are inhibited. extraocular motoneurons constiture one important pathway by
 In the absence of any movement, there is some release of the which eye movements and Vestibulo-ocular-reflex (VOR) are
transmitter from the hair cells which causes the afferent nerve fibers controlled
to have a spontaneous or resting firing rate.  The VOR is an eye movement that has a “slow” component and a
 This makes it possible for the afferents to be excited or inhibited, “fast” component in the same direction as the head rotation. The
depending on the direction of the movement slow component compensates for the head movement and serves to
redirect gaze to another part of the visual field.
 This alteration in the direction of the eye movement during
Semicircular Canals (SCC) vestibular stimulation is one example of a normal nystagmus.
 The polarization is the same for all hair cells – during rotation they
are all excited or inhibited
 Three canals are approximately perpendicular to each other, and
Breaaaak: What is Nystagmus? It’s the eye Jerking off ;)
each canal of one ear is approximately coplanar with a canal from
the other ear.  Involuntary eye movements have 2 components:
 There are three pairs: 1. Fast component – compensatory of the vestibular system to re-
1. Left horizontal-right horizontal correct itself
2. Left anterior-right posterior 2. Slow component – pathologic
3. Left posterior-right anterior  Nystagmus is labeled by the fast component since it is easier to see
o During a rotation one canal of a pair will be excited while the  Usually, the direction of the nystagmus points to the direction of the
other will be inhibited lesion if you will observe in correctly
 Irritative lesion like Menier’s disease point to the side of the
offending ear
Destructive lesions like CP angle tumor usually point to the normal ear

Fig. 6 Horizontal rotation to the right – the right horizontal

canal will be excited and those of the left canal will be inhibited

 Angular rotation is the adequate stimulus for the SCC afferents

 Sudden deceleration is equivalent to a rotation in the opposite
Otolith Organs
 There are 2 otolith organs:
1. Utriculus – located in the horizontal plane
2. Saculus – located in the vertical plane
 Stimulus: Linear acceleration and Gravity
 The hair cells of the otolith organs do not all have the same
polarizations

Fig. 7 inhibition and excitation pathways

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Evaluation of Vestibular Function

 Done to assess the vestibular system, to stimulate an end-organ,
and look into the interaction among several sensory inputs Evaluation of Vestibular Function
 An important objective is to determine where the problem lies in 4. Posturography
vertigo (CN8 or CNS)  New technique for measuring upright posture
1. Caloric Stimulation  Subjects stand on a platform that measures the force exerted
 Test subject is placed with the plane of one SCC aligned with a by each foot, and the positions of the head and hips are
plane vertical to the earth measured
 A fluid that is warmer or colder than the body temp is placed  Several different conditions used: normal vision with fixed
in the external ear canal ⟶convection in the endolymph platform to stand on, no vision, no ankle movement, and visual
⟶deflection of the cupula in the canal which is aligned with conflict
the gravity and stimulation of its afferents  Subjects with impaired vestibular function: difficulty when the
 Maximum velocity of the slow component and the time course platform moves with the subject as he sways back and forth
of the nystagmus are measured when there is no vision
present
 Standard position is with the head tilted backward DIZZINESS/ VERTIGO
approximately 60 degrees so that the horizontal canal is in the  Balance depends upon four separate and interdependent systems:
vertical plane 1. The vestibular system senses accelerating movement and
 Cold fluid to the right ear causes a nystagmus with the slow perceives gravity
phase to the right and a warm fluid causes slow phase to the 2. Proprioceptive cues from joint position senses and muscle
left tone provides information concerning the relationship of the
 Response typically lasts for 2-3 mins head to the remainder of the body
 A significantly reduced response to stimulation of one ear 3. Vision gives perceptions of position sense, speed, and
compared to the other is evidence for a peripheral deficit on orientation
that side 4. All of these senses are integrated through the brainstem
2. Rotation
 Advantages: 1) quantitate the stimulus; 2) vary stimulus
parameters; and 3) information about both inner ear and CNS
3. Positional Testing
 Can be used to diagnose BPPV (rapid change in head position;
sudden in onset and short in duration
 Upon repeated testing, the nystagmus will diminish and then
disappear
 Fatigable nystagmus = BPPV
Not fatigable nystagmus = CNS


Nonvestibular Causes of Dizziness
Hyperventilation
 One of the more common causes of nonvestibular dizziness
 Symptoms of lightheadedness and paresthesia in the distal
extremeties occur with rapid ventilation
 Circumoral area is particularly prone to paresthesia
 Associated with hysterical types of personality

Hypoglycemia
 Transient reduction in blood glucose which occur in chemical
diabetics
 Often accompanied by nausea and vomiting (N/V)
 True spinning vertigo is rare
 Px complain of smptoms of unsteadiness and lightheadedness
associated with severe sweating and pallor

Fig 8 Positional testing

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Vascular Causes Labyrinthitis

 Any vascular phenomenon that compromises the blood supply to the  An inflammatory process involving the inner ear mechanism
brainstem and cerebellum can lead to symptoms of dizziness or  Different clinical and pathologic classification:
unsteadiness 1. Acute toxic labyrithitis
o Caused by vertebrobasilar spasm o Infection of nearby structures (e.g. middle ear, meninges)
 Longer-term disequilibrium and unsteadiness of similar etiologies o Resolves with some loss of hearing and vestibular
are caused by vestibroasilar artery insufficiency (must be function
significantly compromised to flows <50% of normal) o Caused by toxic products from an infection and not by the
o Often associated with atherosclerotic disease and embolic organisms
phenomena 2. Acute suppurative labyrinthitis
 Rarely is the vestibrobasilar system involved in an isolated manner, o Occurs with an acute bacterial infection that extends into
more commonly, the carotid arteries are also involved the structures of the inner ear
o Chances of complete loss of hearing and vestibular
Cervical Vertigo function are quite high
 The exact role of cervical vertigo is uncertain 3. Chronic changes
 Initially thought to be a variant of vertebrobasilar insufficiency o May lead to endolymphatic hydrops or pathologic
 Cervical position sense is thought to be lost in some of the patients changes ultimately sclerosing the labyrinth
therefore producing dizziness
 Tx: PT to restore strength of the neck Meniere’s Disease
 Disorder of swelling of the endolymphatic space
Vertigo on a Vestibular Basis  Referred to as hydrops
Benign Postional Vertigo (BPV)  When this process reaches a pinnacle, a Reissner’s membrane
 Believed to result from structural alteration of the cupula of the ruptures ⟶ mixing of endolymph and perilymph ⟶ temporary
posterior SCC, which makes it sensitive to gravity hearing loss
 Sometimes referred to as “Cupiolithiasis”  Resolves when the membrane reseals and the chemical composition
o Pathologically the calcified cupula is thought to fracture, of the endolymph and perilymph returns to normal
leading to this syndrome  Classically, the px develops a low-tone sensorineural hearing loss
 Usually seen in px who note that they have acute attacks of transient followed by a low-pitched tinnitus
dizziness with a certain position of the head – accompanied by  Px describe aural fullness and then become acutely vertiginous
nystagmus that fatigue upon repeated testing  Attacks last between 15mins and several hours
 Typically, there is a delay from the onset of change in position to the  Can be modified to involve only the vestibular portion of the
onset of vertigo labyrinth when symptoms involve only changes in balance and aural
 The first attack is usually the most severe; subsequent and repeated fullness
attacks become less sever in nature  Unpredictable disorder that can occur at any time
 Dx: Dix-hallpike Maneuver  Primarily affects middle-aged women
 Tx: symptomatic relief + reassurance that the process usually  Fluctuates in long periods of time but can progress rapidly, leading
resolves spontaneously to total hearing loss and lack of reliable vestibular function in the ear
 Etiology: Hypothyroidism and Syphilis
So what is BPPV?  Tx: low salt diet + diuretics, vestibular suppressants, and/or surgery
 You develop cupiolithiasis or canalithiasis
 How did stones get there? You have a gel-like substance you call
otoconia, these otoconia are the component of the sense organ of the
utricle ⟶ these become detached ⟶ calsify & develop inertia⟶ roam
around the fluid filled inner ear wherein it often ends up in the posterior
SCC (95% of the time) ⟶ dizziness
 Main Dx maneuver: Diz hallpike maneuver
Tx: Get rid of the particles inside the posterior canal and put it back to the
utricle through a series of Repositioning maneuvers (Eg. Epley maneuver
and Semont maneuver)
Vestibular Neuritis 
 Caused by an unknown source Fig 9 Meniere’s Disease
 Severe dizziness with intractable vomiting, nausea, and inability to
stand or walk  Due to overproduction of the endolymph
 Symptoms can go on for 3-4 days whith some px needing to be  First you have tinnitus because of the build-up of endolymph ⟶
hospitalized for symptoms of dehydration Reissner’s membrane wall rupture ⟶ mixture of the peri and
 Attacks leave the px’s with unsteadiness and imbalance for several endolymphs ⟶ dizziness and eventually hearing loss
months  Ruptured wall will heal off ⟶ endolymph will reconstitute ⟶ will go
 Repeated episodic attacks can occur back to “norma”
 Usually no hearing changes  Hallmark: Fluctuating hearing loss
 Viral sequelae of URTI
 Selectively affect the vestibular arm of CN 8 “A man who says sorry because he is wrong is honest. A
man who says sorry even if he is not sure is wise. A man
who says sorry even if he knows he is right is a husband.”

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Perilymph Fistula External Acquired

Hematoma
 Px who have sudden barotrauma in the area of the ear can
experience sensorineural hearing loss and dizziness  This condition is most frequently seen in wrestlers or boxers.
 Untreated it may result in the so called cauliflower ear.
 Seen in divers, flyers, and anyone who has sudden change in
pressure in the middle ear space  Simple needle aspiration of the hematoma has been used in the past,
but most physicians now recommend more vigorous treatment by
 These sudden changes can cause a disruption of round or oval
incision and drainage of collected blood under sterile conditions,
window membrane ⟶perilymph leak into the middle ear space
followed by application of pressure dressings, particularly in the
 Can occur without apparent pressure change
conchal area.
 Tx: fat grafts (sealing the leak)
 Localized pressure is better obtained by using through and through
 Resolution of the symptoms of dizziness occurs in only few cases
sutures over dental rolls or other similar materials.
 Treatment is best accomplished as soon as practical following injury,
Treatment before organization of the hematoma begins.
 Vestibular suppressants: Antihistamines and BDZ’s (Antivert and  Wrestlers should be reminded about wearing protective headgear,
Valium) = symptomatic relief even during practice.
 Severe and persistent cases can be treated with vestibular nerve
sections: Neoplasms
1. Middle fossa – for px under 60  A variety of skin lesions, including neoplasms, may be encountered
2. Posterior fossa – suboccipital cranioectomy on the auricle and in the external canal. Few are peculiar to this
Translabyrinthe – destruction of entire vestibular system anatomic region.
 Somewhat unusual from the standpoint off appearance is osteoma , a
benign tumor of the external canal wall which presents as a single
SOURCES OF EAR DEFORMITY firm rounded growth attached by a smaller bony pedicle to the inner
Congenital third or bony portion of the canal wall. Osteomas are carefully
chiseled from the canal wall with the aid of an operating microscope.
 A variety of congenital anomalies involving the external ear and canal  This tumor should be differentiated from an exostosis , which is more
result from the maldevelopment in both the first and second brachial common and which consists of a rounded protuberance of
arches. hypertrophic canal bone ( usually multiple and bilateral. Causes are
 Auricular deformities are most prominent, of which the most common unclear, it has been stated that these growth occurs more frequently
is lop- ear deformity in which the ears protrude excessively. Several in people who do a great deal of swimming in cold waters. Exostoses
plastic procedures have been devised for the correction of this condition. usually require no treatment, although they may result in more
frequent canal blockage by cerumen in some individuals.
 Other malformations of the auricle include an abnormally large or small
 Benign polyps from the middle ear present in the external canal.
pinna (macrotia and microtia). Careful removal under the operating microscope is indicated if they
 Congenital defects such as rudimentary ear appendages and even total are not responsive to medical treatment , in such cases, they should
absence of the ear are occasionally encountered and may be associated be examined histologically.
with partial or complete stenosis of the canal. Such conditions may  Squamous Cell Carcinoma, the most common malignancy of the
involve soft tissue and bone. In select cases surgical procedures can external auditory canal is amenable to cure if diagnosed early and
properly treated.
correct hearing loss resulting from canal stenosis.
 Chronic discharge, often serosanguinous, and free bleeding, pain and
 Another rarely seen developmental defect of the ear involves first swelling within the canal are manifestations that, singly or in
brachial cleft abnormalities. These present as cysts or sinus tracts combination, should suggest the possibility of a new growth.
involving the pinna and external auditory canal. There are two types of  A chronic external otitis that does not respond to the proceeding
the first brachial cleft abnormalities; recommendations requires a biopsy. Facial paralysis is a late
Type 1 anomalies - Contain ectodermal tissue only, are free of cartilage development.
and are of the first cleft origin only.  Malignant tumors involving the pinna are much more common than
Type 2 anomalies – Contain both epithelium of first cleft origin and
those seen in the canal itself. The two main types are squamous cell
cartilage from the first and second arches.
 The sinus tracts may be observed to drain intermittently and occasionally and basal cell carcinoma. The preferred initial treatment is surgical
become infected. excision. Regional node dissection may be indicated with the
squamous cell variety.
 Usually a tract can be identified by methylene blue injection and excised.
 In some patients, these tracts may pass medially, or lateral to the facial
nerve, the facial nerve must be identified during dissection.

Fig. 11 Keloid of lobule following ear piercing

( management- excision)
Fig10. Infected preauricular sinus
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Miscellaneous
 Sebaceous cysts occur in the post- auricular fold and are often multiple.
Large cysts may become inflamed intermittently and are more likely to be
cured by complete excision than by drainage alone.
 Nodules involving the helix may represent localized areas of chondritis,
known as chondrodermatitis nodularis chronicis helicis ( painful nodule).
They are more common in men and occur most often on the superior helix
or anthelix. While steroid injection is sometimes adequate treatment, local
excision provides both a cure and a pathologic diagnosis.
 Gouty tophi may occur in the subcutaneous tissue or cartilage of the auricle
as whitish yellow nodules containing urate or sodium biurate crystals.
Unsightly tophi may be excised.
 Pain in the area of the auricle and external canal in the absence of physical
findings certainly deserves investigation.

REVIEW QUESTIONS
1. What condition is considered upon onset of facial paralysis,
accompanied by otalgia and herpetic eruption involving portions of
the external ear?
2. What condition is considered when trauma or inflammation causes
an effusion of serum or pus between the layer of the perichondrium
and the cartilage of the external ear?
3. What rare condition results in the palatal muscles to undergo
periodic rhythmic contractions resulting in a clicking sound that can
be heard by the examiner?
4. It is manifested by congenital stenosis of the ear plus maxillofacial
dysotoses.
5. Tympanic membrane thickening that may contain white thick
patches owing to deposition of hyalinised collagen in the middle ear
due to previous inflammation.

Review Questions answers

1. Herpes Zoster Oticus ( Ramsay Hunt Disease)
2. Perichondritis
3. Palatal Myoclonus
4. Treacher – Collins Syndrome
5. Tympanosclerosis

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Diseases of the External, Middle and Inner Ear August, 24, 2017
Dr. Ramon Alcira, MD
Department of Otorhinolaryngology

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