TUTORIAL WEEK 2
Mengapa kotoran telinga mengeras?
Apa bahaya dari make cotton bud?
Kotoran telinga yang normal kaya apa?
Mekanisme mendengar
Mekanisme keseimbangan
Tuli, kenapa bisa?
Hub. Tuli dan keseimbangan
Transmission of Sound to the Inner
Ear
What happens when sound waves reach
the ear? The auricle funnels sound waves
into the auditory canal, a task at which it
excels because of its shape, providing a
good example of the
Structure-Function Core Principle (p. 65). As
you can see in step 1 , the sound waves
strike the tympanic membrane
and cause it to vibrate at the same
frequency. This in turn causes the auditory
ossicles in the middle ear to vibrate, and
these vibra- tions are transmitted to the
oval window.
The oval window vibrates at the same
frequency as the tym- panic membrane.
However, when the ossicles transmit the
force from the larger tympanic membrane
to the smaller oval window, the force is
concentrated in a smaller area and for this
reason it
increases significantly. The ossicles also act
as a lever system to amplify the vibration
of the oval window.
Why is this important? The answer lies in
what is found on the other side of the oval
window in the inner ear: fluid, in particular
the perilymph in the vestibule and the scala
vestibuli. 2 Vibration of the oval window
produces pressure waves in the fluid that
are just like those in the air. However, more
force is needed to generate motion in fluid
than in air (think about the effort required
to move your cupped hand through water
as opposed to air). So, increased force on
the oval window is necessary to move the
fluid.
Processing of Sound in the
Inner Ear
The pressure waves generated at the oval
window travel through the perilymph of the
vestibule to the scala vestibuli of the
cochlea.
High-frequency vibrations (such as those
produced by squealing brakes on a train)
take a shortcut through the cochlear duct
(scala media) to reach the scala tympani,
which is shown in step 3a of Figure 15.31a.
As they pass through the cochlear duct to
the scala tympani, they cause the
endolymph and basilar membrane to
vibrate. These vibrations occur close to the
base of the cochlea, where the basilar
membrane is narrow and stiff (Figure
15.31b).
Notice in step 3b that low-frequency
vibrations (like those of the rumble of the
train) travel farther into the cochlea and
make the basilar membrane vibrate where
it is wider and more flexible. For very low-
frequency sounds that we cannot hear, the
waves travel all the way to the tip of the
cochlea, where the scala vestib- uli
connects with the scala tympani at an
opening called the hel- icotrema (hel′-ih-
koh-TREE-mah). The waves then travel
back to the vestibule via the scala tympani,
where they cause corre- sponding
movement of the round window.
The presence of the round window is
essential, as without it the fluid would not
move. Fluid cannot be compressed; if it is
pushed from one area, it must move into
another area (squeez- ing a water balloon
at one end forces it to bulge at the other
end). In the same way, as the oval window
is pushed into the inner ear, the round
window bulges outward, and vice versa.
Pitch is determined by which area of the
basilar membrane vibrates, whereas
loudness is determined by how much the
basi- lar membrane vibrates at that area. A
loud noise produces sound waves with
more energy, which in turn cause greater
movement of the tympanic membrane,
middle ear ossicles, and the peri- lymph
and endolymph. Increased movement of
these fluids pro- duces greater vibration of
the basilar membrane and stronger
stimulation of nearby receptor cells.
Regardless of which portion of the basilar
membrane vibrates, the movement causes
changes in the spiral organ, which rests on
the basilar membrane. To understand these
changes, we need to look at the structure
of the spiral organ in more detail (Figure
15.32).
The spiral organ contains receptor cells
called hair cells. They are grouped into a
single row of inner hair cells and three
rows of outer hair cells. The 3500 inner
hair cells are primar- ily responsible for
detecting sound. Each hair cell has
microvilli, known as stereocilia (stare′-ee-
oh-SILL-ee-ah), which project from the cell
into the endolymph of the cochlear duct.
The ste- reocilia vary in length and are
arranged from tallest to shortest. The
stereocilia themselves are stiff but “bend”
by flexing at the junction with the cell body
(like a joystick).
What makes the stereocilia bend? A stiff
membrane, called the tectorial
membrane (teck-TORE-ee-al), extends
over the hair cells and “sandwiches” them
between the basilar and tecto- rial
membranes. The stereocilia on the outer
hair cells contact the tectorial membrane,
but the stereocilia in the inner hair cells do
not. When the basilar membrane vibrates
up and down in response to sound waves,
the hair cells move with it toward and away
from the tectorial membrane.
Each stereocilium is connected to its
neighbor by an elastic filament called a tip
link (Figure 15.33a). When the tallest stereo-
cilium bends in one direction, the other
stereocilia are pulled in the same direction.
The sequence of events that takes place
when sound is transmitted to the inner ear
is shown in Figure 15.33b and proceeds as
follows:
1The basilar membrane moves up
toward the tectorial membrane,
bending the stereocilia toward the
tallest
stereocilium. As the basilar membrane
moves toward the tectorial membrane, the
stereocilia on the outer hair cells bend
against it. Stereocilia of inner hair cells also
bend due to movement of the endolymph
between the two mem- branes. When the
basilar membrane moves away from the
tectorial membrane, the stereocilia bend in
the opposite direction.
2 Bending the stereocilia opens
potassium ion chan- nels that
depolarize the hair cell. As the
stereocilia bend toward the tallest one, the
tip links stretch and pull open a potassium
ion channel in the tip of each stereocilium.
In typical neurons, opening potassium ion
channels would
hyperpolarize the cell, but the endo- lymph
contains such a high con- centration of
potassium ions that they flow into the hair
cells, causing depolarization and a local
potential.
3The depolarized hair cell releases
neurotransmitters, triggering action
potentials in the axon of the cochlear
nerve. The neurotransmitter is likely
glutamate, and it triggers an action
potential in the neuron of the cochlear
nerve innervating the hair cell.
When the basilar membrane moves back,
away from the tec- torial membrane, the
stereocilia bend in the opposite direction.
The tip links are no longer stretched and
the potassium ion chan- nels close. The hair
cells hyperpolarize, which stops the release
of neurotransmitters.
Each inner hair cell is contacted by multiple
neurons; approx- imately 90% of auditory
neurons contact the inner hair cells. In
contrast, only one neuron contacts multiple
outer hair cells. The inner hair cells perform
most of the work of detecting sound, but
destruction of the outer hair cells by certain
drugs—such as the antibiotic kanamycin—
can result in nearly complete deaf- ness.
This is because the outer hair cells play an
essential role
in increasing the sensitivity of the inner hair important for processing combinations of
cells and amplify- ing the vibration of the sounds according to their fre- quency and
basilar membrane. The outer hair cells are time interval.
capable of rapidly changing their length in
an oscillating fashion (in other words, they 5  The thalamus sends signals to the
jiggle), which enhances the move- ment of primary auditory cortex in the superior
the basilar membrane as much as a portion of the temporal lobe. As with
hundred-fold. The movement of the outer other sensory cortices, the primary
hair cells can send vibrations backward auditory cortex is where our first
through the inner ear and middle ear to the conscious awareness of sound begins, as
tympanic membrane and cause it to move. well as analysis of its location, pitch, and
A very sensitive microphone placed next to loudness.
the tympanic membrane can actually
detect sounds produced by the ear, called
otoacoustic emissions. The lack of such
sounds indicates damage in the auditory
pathway. To see how damage to hair cells
or other structures of the ear can interfere
with hearing, read A&P in the Real World:
Tinnitus.

The Auditory Pathway

After the hair cells transduce the energy
from sound waves into neural signals, these
signals travel into the CNS along the path-
way
1  Auditory signals travel through
axons of the cochlear por- tion of the
vestibulocochlear nerve to the
cochlear nuclei at the medulla-pons
junction. Axons of the cochlear nerve
synapse in the cochlear nuclei, which are
located at the junction of the pons and
medulla.
2  Axons from the cochlear nuclei
contact the superior oli- vary nucleus
in the pons. Neurons in the superior oli-
vary nucleus (ALL-ih-vair-ee) compare
information from both ears to determine
the location of the sound.
3  Auditory stimuli are then sent to the
inferior colliculus of the midbrain. The
stimuli are coordinated with head and trunk
movement to produce the startle reflex.
This reflex, a response to unexpected
sounds, causes you to turn your head and
body toward the sound to investigate it. If
you have ever “jumped out of your skin” in
response to a loud clap of thunder, you are
familiar with the startle reflex.
4  Theauditory stimuli are relayed to
the medial genicu- late nucleus of the
thalamus. The role of the thalamus in
human hearing is not clear, but it may be
EAR WAX
The external auditory canal is lined with
modified sweat glands called ceruminous
glands (seh-ROO-meh-nus) that secrete
yellow- ish-brown to gray cerumen (seh-
ROO-men), or ear wax. Ear wax lubricates
and waterproofs the external auditory canal
and the tympanic membrane; it also traps
debris before it reaches the tympanic
membrane and sweeps it out of the
auditory canal.
VESTIBULAR SENSASTION
The sense of equilibrium depends on input
from three sources: (1) the visual system;
(2) the proprioceptors in muscles and joints
that provide feedback about body position;
and (3) the vestibular system (vestibule
and semicircular canals) in the inner ear,
which provides information about head
position and move- ment, known as
vestibular sensation.
The meaning of each term can be gleaned
from its name: static means stationary or
unmov- ing, and dynamic means changing
or moving. Static equilib- rium therefore
refers to maintaining balance when the
head and body are not moving but the
head is tilted. Dynamic equilib- rium, on
the other hand, refers to maintaining
balance when the head or body is
undergoing rotational or angular motions
(such as spinning in a rotating chair) or
linear acceleration (such as riding in a car).
UTRICULE, SACCULE
Static equilibrium is monitored by the
utricle and the saccule. When you tilt your
head, how do the hair cells respond? In the
utricle, the stereocilia point vertically when
your head is upright and stationary, and
they bend when the head tilts to either side
or to the front or back. In the saccule, the
stereocilia are oriented horizontally when
your head is upright and stationary, and
bend in response to up-and-down
movements (such as when you sit up
straight from a slouched position). When
the head tilts, grav- ity pulls on the otolithic
membrane, which bends the stereocilia,
When the stereocilia bend toward the
kinocilium, the hair cells experience a local
potential and depolarize. They then release
more glutamate, increasing the number of
action potentials produced in the axons of
the vestibular nerve. Bending of the
stereocilia away from the kinocilium hyper-
polarizes the hair cells and they release
less glutamate, reducing the number of
action potentials in the axons of the
vestibular nerve
The utricle and saccule are also important
in detecting linear acceleration, a form of
dynamic equilibrium, such as riding in a car
or elevator.
SEMICIRCULAR DUCT
dynamic equilibrium includes angular or
rotational movements, such as turning your
head or spinning in a chair. The three
ducts, which con- tain endolymph, are
oriented to detect rotation in all three
planes. The semicircular ducts are
connected to the utricle; near this con-
nection, each duct has a swelling, the
ampulla. For example, when you
turn your head, the endolymph lags
behind and pushes on the cupula,
as shown in Figure 15.38b. This
bends the stereocilia, which either
increases or decreases glutamate release
from the hair cells and causes a
corresponding change in the activity of
neurons in the vestibular nerve. Your brain
interprets the change in nerve activity as
the start of head rotation (acceleration).
The endolymph “catches up” quickly during
continued rotation. When you stop turning
your head, the endolymph continues to
move and bends the cupula in the direction
opposite to that when you started turning
your head. This has the opposite effect on
glu- tamate release and the activity of the
vestibular nerve, and your brain interprets
the change to mean that head rotation has
stopped.
The Vestibular Sensation
Pathway
Detecting head movement and position is
only part of the bat- tle to maintain
equilibrium; the brain must receive and
analyze the stimuli and then coordinate a
response. The responses can be grouped
into three categories: (1) muscle movement
to produce changes in posture (for
example, flailing your arms to avoid fall- ing
when you trip), (2) cognitive awareness of
head position and/ or movement, and (3)
compensatory eye movements for some
types of head movement.
To produce these responses, the vestibular
signals need to reach various regions of the
central nervous system, as shown in Figure
15.39:
1  Vestibularsignals travel to the
vestibular nuclei located at the
medulla-pons junction.
2  Thevestibular nuclei forward the
signals simultane- ously to the
following areas of the CNS:
-The thalamus and then the inferior
parietal lobe, for conscious awareness
of head position and movement.
The inferior parietal lobe integrates the
signals so you are aware of the direction in
which your head is moving (for example,
knowing that your head is turning to the
right and not the left). Several regions of
the parietal lobe receive vestibular signals,
but their locations have not been
determined with the same accuracy as in
the visual and auditory pathways.

-The cranial nerve nuclei, to coordinate

eye movement in response to head
movement. Axons from the vestib- ular
nuclei terminate in the oculomotor,
trochlear, and abducens nuclei which give
rise to the cranial nerves that control eye
movement. One example of coordinated
eye movement is the vestibulo-ocular
reflex, which enables us to keep our eyes
fixed on an object while our head is mov-
ing. This happens when we walk or run
toward an object; as our head moves up,
our eyes move inferiorly and vice versa. We Hearing Loss
can choose to override the reflex if we want
to turn our heads without fixing our gaze.
Hearing loss or deafness can be classified
into two broad cate- gories: conduction and
-The cerebellum and spinal cord, to
sensorineural. Conduction hearing loss is
coordinate muscle movement that
due to a problem in the outer or middle ear
maintains balance in response to head
that prevents sound waves from reaching
movement. For example, tilting your head
the inner ear. Examples include excessive
back to look at the sky requires contracting
buildup of ear wax, a middle ear infection, a
muscles in your torso and lower limbs so
perforated tympanic membrane, or fusion
you don’t fall over backward.
of the auditory ossicles. Vibrations can
reach the fluid of the inner ear through the
temporal bone (bone

conduction), but with much less accuracy

than conduction through air. Many forms of
conduction hearing loss are tempo- rary
and can be corrected, for example, by
removing excess ear wax or repairing a
perforated tympanic membrane.

Sensorineural hearing loss refers to a

deficit in the cochlea or any of the neural
pathways in the cochlear nerve or CNS.
There are actually two types of
sensorineural hearing loss, and they dif- fer
significantly in terms of cause and
treatment:

1. Sensory hearing loss occurs when action

potentials cannot be generated in the
cochlea, usually due to dysfunction of the
hair cells. Exposure to loud sounds or
certain medications may damage hair cells.
We also lose stereocilia as we age,
especially those in the proximal part of the
cochlea that are responsible for detecting
high-frequency sounds. Hearing aids can
help mild to moderate cases of sensory
hearing loss. A cochlear implant may also
be an option (see A&P in the Real World:
Cochlear Implants).
2. Neural hearing loss occurs when the
signals fail to travel through the cochlear
branch of the vestibulocochlear nerve or
CNS pathways. Typical causes include
strokes or tumors such as an acoustic
neuroma, a benign tumor outside the brain-
stem at the junction of the medulla and
pons. Cochlear im- plants are not effective
for neural hearing loss.
Ceruminous glands (seh-ROO-mih-nus) are
found only in the auditory (ear) canal, where
their secretion combines with sebum and dead
epidermal cells to form ear- wax, or cerumen.21
They are simple, coiled, tubular glands with
ducts leading to the skin surface. Cerumen
keeps the eardrum pliable, waterproofs the
auditory canal, and has a bactericidal effect.
(SALADIN)

(PHYSIOLOGY ANERMAN 2016)

EAR WAX

Ear wax is more likely to accumulate and cause a

hearing impairment when normal extrusion is
prevented (for example, by hearing aids or by the
use of cotton buds to clean the ears).
In the outer part of the canal are modified sweat
glands (ceruminous glands), which secrete a
modified sweat that has bacteriocidal and
fungicidal properties, and sebaceous glands that
produce an oily material and usually discharge in
the hair follicles at the outside of the canal. Wax is
a mixture of all three components, with keratin
being predominant. Overall wax is sticky,
waterproof, and protective, and there should be a
thin coating of wax near the external opening of
the canal.
When wax gets wet, the keratin swells and can
lead to the sudden onset of complete occlusion of
the canal and a hearing loss. The wet, dead keratin
can become infected and an otitis externa develop.
Wax may obscure the view of the tympanic
membrane and may need to be removed for
diagnostic reasons.
Since the deep ear canal may be wider than the
opening, a large plug of dry, hard wax deep in the
canal can be particularly difficult to remove. If
wax needs to be removed, then various options are
available: irrigation (syringing with unregulated
manual syringes should no longer be used), wax
softeners/solvents, irrigation following wax
softeners, mechanical removal, or microsuction.

BMJ Clin Evid.

Published online 2015 Jul 27. 
Ear wax
Professor Tony Wright

Ceruminous Glands