Tympanic Membrane and Ossicular System

The tympanic membrane (eardrum) transmits sound vibrations to the

ossicles in the middle ear.

Handle of malleus attached to tympanic membrane, connected to incus,

which articulates with the stapes. Faceplate of stapes lies against the oval
window of the cochlea.

Conduction of Sound

Tensor tympani muscle keeps tympanic membrane tensed. Ossicles

suspended by ligaments, malleus and incus function as a lever with a fulcrum
at the tympanic membrane border. Movement of incus and stapes transmits
vibrations to the cochlear fluid via the oval window.

Impedance Matching by Ossicular System

Amplitude of stapes movement is ¾ of malleus handle’s movement.

Lever system increases force by 1.3 times, though reduces displacement.

Tympanic membrane surface area ≈ 55 mm² vs. stapes ≈ 3.2 mm² (≈17-
fold difference).

Combined, results in ~22 times more force on cochlear fluid than on

tympanic membrane.

Provides impedance matching between air and cochlear fluid (50–75%

efficient for 300–3000 Hz frequencies).

Without ossicles, hearing sensitivity drops by 15–20 decibels.

Attenuation Reflex (Protective Mechanism)

Triggered by loud sounds via reflex within 40–80 milliseconds.

Stapedius muscle contracts pulling stapes outward; tensor tympani

contracts pulling malleus inward.

Increases ossicular rigidity, reducing low-frequency sound conduction.

Attenuation can reduce intensity by 30–40 decibels (like the difference

between a loud voice and whisper).

Functions:

Protect cochlea from loud, damaging sounds.

 Mask background low-frequency noise, improving speech perception.

Diminish hearing of one's own voice via nerve signals activating these
muscles during speech.

Transmission of Sound Through Bone

Cochlea embedded in bony labyrinth of temporal bone.

Skull vibrations can transmit sound to cochlea (e.g., via tuning fork on
mastoid process).

Requires amplification for audible perception of airborne sounds via bone.

Functional Anatomy of the Cochlea

The cochlea is a coiled structure consisting of three parallel tubes:

Scala vestibuli, Scala media, Scala tympani

Reissner’s membrane separates scala vestibuli from scala media.

Basilar membrane separates scala media from scala tympani.

The organ of Corti lies on the basilar membrane and contains hair cells — the
primary receptors for sound vibrations.

Sound Conduction through the Cochlea

Sound enters via the oval window, where the stapes footplate transmits
vibrations.

Fluid moves forward in scala vestibuli and scala media with inward stapes
movement, and backward with outward movement.

Reissner’s membrane is thin and flexible, allowing sound vibrations to pass

freely between scala vestibuli and scala media.

Its primary role is to maintain the unique ionic composition of endolymph in

the scala media.

Basilar Membrane Structure and Resonance

Made of 20,000–30,000 basilar fibers projecting from the modiolus to the

outer wall.

Fibers are stiff at the base (near oval window) and limber at the apex
(near helicotrema).
 Length increases 12-fold from base to apex (0.04 mm to 0.5 mm).

Stiffness decreases >100-fold from base to apex.

High-frequency sounds resonate near the base; low-frequency sounds

resonate near the apex.

Transmission of Sound Waves — "Traveling Wave"

Stapes footplate movement pushes fluid, displacing basilar membrane toward

the round window.

Creates a traveling wave along the basilar membrane toward the helicotrema.

Wave travels fast at the base (due to stiff fibers) and slows toward the apex.

Frequency-Specific Vibration Pattern

Each sound wave reaches a peak amplitude at its natural resonant point on
the basilar membrane:

High frequencies — vibrate near the base.

Medium frequencies — vibrate mid-cochlea.

Low frequencies — vibrate near the helicotrema.

Beyond its resonant point, the wave dissipates and stops.

Amplitude Pattern of Basilar Membrane Vibration

The amplitude pattern shows the extent of vibration at various points along
the membrane during a cycle.

Maximum displacement occurs at the region tuned to the sound’s

frequency.

Different frequencies produce different peak locations of vibration:

8000 Hz — near the base.

<200 Hz — near the apex at the helicotrema.

Frequency Discrimination

The cochlea distinguishes sound frequencies by the location of maximum

vibration along the basilar membrane.

Hair cells at the site of peak vibration activate corresponding nerve fibers.
 This place principle forms the basis of pitch perception.

Function of the Organ of Corti

Primary Role:

Receptor organ that converts basilar membrane vibrations into nerve

impulses.

Structure:

Located on the basilar membrane. Contains sensory receptors:

Inner hair cells: ~3,500, larger (12 µm), single row.

Outer hair cells: ~12,000, smaller (8 µm), 3-4 rows.

Innervation:

90–95% of cochlear nerve endings synapse with inner hair cells —

critical for sound detection.

Nerve fibers lead to the spiral ganglion of Corti in the cochlea’s

modiolus, then to the cochlear nerve, and CNS at the upper medulla.

Excitation Mechanism:

Hair cells have stereocilia projecting into the tectorial membrane.

Bending of stereocilia:

Towards longer stereocilia → depolarization.

Away → hyperpolarization.

Causes shearing against the tectorial membrane with basilar membrane

vibrations.

Vibration Transmission:

Basilar fibers, rods of Corti, and reticular lamina move as a unit.

Upward motion: rocks reticular lamina inward.

Downward motion: rocks it outward → triggers stereocilia shearing.

Auditory Signal Transmission:

 Despite fewer numbers, inner hair cells transmit ~90% of auditory
signals.

Outer hair cells modulate sensitivity and pitch tuning through

feedback from brainstem neurons (can contract/alter stiffness).

Hair Cell Receptor Potentials:

Stereocilia bending opens 200–300 cation channels → K⁺ influx from

endolymph → hair cell depolarization.

Generates alternating receptor potentials that stimulate cochlear nerve

endings.

Neurotransmitter:

Likely glutamate (not confirmed) released during depolarization to

excite auditory nerves.

Endocochlear Potential:

Endolymph (in scala media) has high K⁺, low Na⁺ (opposite of
perilymph).

Maintains a +80 mV potential inside scala media relative to

perilymph.

Hair cell intracellular potential: −70 mV (to perilymph) and −150

mV (to endolymph at stereocilia tips).

This high potential difference boosts hair cell sensitivity to faint

sounds.

Determination of Sound Frequency — The “Place” Principle

High-frequency sounds activate the basilar membrane near the base of the
cochlea.

Low-frequency sounds activate near the apex of the cochlea.

Intermediate frequencies stimulate areas between the two extremes.

There’s a spatial organization of nerve fibers from the cochlea to the

auditory cortex.

The nervous system uses the position of maximal stimulation on the basilar
membrane to detect sound frequencies — called the place principle.

Sounds below 200 Hz stimulate the entire apex, making discrimination

difficult via the place principle.
 Volley (frequency) principle helps detect frequencies from 20 to ~1500–
2000 Hz via synchronized nerve impulses (volleys).

Even with destruction of the apical cochlea, some low-frequency

discrimination remains, supporting the volley principle.

Determination of Loudness

Loudness perceived by:

Increased amplitude of basilar membrane vibration → increased

firing rate.

More hair cells stimulated on the fringes of the resonating region

(spatial summation).

Outer hair cells get stimulated at high intensities — their activation

signals loud sounds.

Power law of loudness perception:

Sensation of loudness increases with the cube root of actual sound

intensity.

Ear compresses a 1 trillion-fold range of sound energy into about a

10,000-fold perceived loudness range.

Decibel (dB) system:

Sound intensity measured logarithmically.

1 bel = 10-fold increase, 1 decibel = 0.1 bel (~1.26 times increase).

Ears detect as little as 1 dB change in intensity.

Threshold for Hearing at Different Frequencies

Most sensitive frequency: around 3000 Hz.

Lower frequencies need higher intensity to be heard.

Hearing range for a young person: 20 to 20,000 Hz.

At low sound levels (60 dB below standard) → limited to 500–5000 Hz.

With aging, the range narrows to 50–8000 Hz or less.

Central Auditory Mechanisms

Auditory Pathways:

Spiral ganglion fibers → dorsal & ventral cochlear nuclei (medulla).

Second-order neurons decussate to the contralateral superior olivary

nucleus.

Pathway ascends via lateral lemniscus → inferior colliculus → medial

geniculate nucleus (thalamus) → auditory cortex (superior temporal gyrus).

Signals transmitted to both brain sides, predominantly contralateral.

Crossovers occur at:

Trapezoid body, Commissure between lateral lemnisci,

Commissure between inferior colliculi

Collaterals reach:

Reticular activating system (alerts whole CNS to loud sounds).

Vermis of the cerebellum (for sudden noise reactions).

High spatial organization preserved from cochlea to cortex for sound

frequency mapping.

Firing Patterns:

Auditory nerve fibers: Fire up to 1000 impulses/sec, rate depending on

loudness.

Impulse synchronization with sound waves occurs up to 2000–4000 Hz.

In brainstem tracts: Synchronization persists below 200 Hz.

Above inferior colliculi, synchronization mostly lost.

Auditory processing begins at cochlear nuclei, where signals start getting

analyzed, not just relayed.

Function of the Cerebral Cortex in Hearing

Auditory Cortex Location:

Primarily on the supratemporal plane of the superior temporal gyrus

Extends onto the lateral side of the temporal lobe, insular cortex, and
lateral parietal operculum.

Subdivisions:
 Primary Auditory Cortex: Receives direct input from the medial
geniculate body.

Auditory Association (Secondary) Cortex: Receives input from the

primary cortex and nearby thalamic association areas.

Sound Frequency Perception

At least six tonotopic maps in the auditory cortex.

High frequencies activate posterior neurons, low frequencies activate

anterior neurons.

Different maps extract distinct sound features (pitch, direction, onset,

modulation, etc.).

Neurons in the auditory cortex respond to a narrower frequency range

than earlier relay centers.

Frequency sharpening occurs via lateral inhibition along the auditory

pathway.

Integration and Sound Pattern Discrimination

Some neurons associate auditory input with other sounds or sensory modalities.

The parietal auditory association area overlaps with somatosensory area II,
allowing cross-modal integration.

Complete bilateral auditory cortex destruction:

Doesn’t stop sound detection.

Abolishes discrimination of pitch and sound patterns.

Unilateral destruction:

Slightly reduces hearing in the opposite ear.

Impairs sound localization due to lack of comparative input.

Wernicke’s area (posterior superior temporal gyrus):

Lesions here impair the interpretation of word meanings, though

hearing and repetition remain intact.

Determination of Sound Direction

Two main cues:

 Time lag between sound arrival in each ear (effective <3000 Hz).

Intensity difference between ears (effective >3000 Hz).

Pinnae help determine if sound is from front, back, above, or below by

altering sound quality.

Neural Mechanisms for Sound Localization

Superior Olivary Nuclei (brainstem) crucial for initial sound direction

analysis:

Medial Superior Olivary Nucleus: Detects time lags between ears

using spatially organized neurons.

Lateral Superior Olivary Nucleus: Detects intensity differences.

Directional information sent to a distinct cortical area from that for tonal
information.

Centrifugal (Descending) Auditory Pathways

Retrograde (descending) fibers from the auditory cortex to the cochlea via the
superior olivary nucleus.

Mainly inhibitory — modulate cochlear hair cell sensitivity (reduce sound by

15–20 dB).

Allows selective attention to particular sound qualities (e.g., focusing on a

single instrument in an orchestra).

Types of Deafness

Nerve Deafness

Caused by impairment of the cochlea, auditory nerve, or central

auditory pathways.

Permanent if cochlea or auditory nerve is destroyed.

Conduction Deafness

Caused by impairment of outer or middle ear structures (tympanic

membrane, ossicles) that conduct sound to the cochlea.

Sound can still reach the cochlea via bone conduction if conduction
structures are impaired.

Audiometer
 Device to assess hearing loss across various frequencies.

Emits pure tones at calibrated zero-intensity levels (barely audible to normal

ear).

Hearing loss measured in decibels above normal.

Tests both air conduction (via earphone) and bone conduction (via mastoid
vibrator).

Results plotted on an audiogram showing hearing threshold at different

frequencies.

Audiogram in Nerve Deafness

Hearing loss evident in both air and bone conduction.

Typically affects high-frequency sounds first (damage at cochlear base).

Common in aging (presbycusis).

Other patterns:

Low-frequency deafness from prolonged loud sound exposure.

All-frequency deafness from ototoxic drugs (e.g., streptomycin,

kanamycin, chloramphenicol).

Audiogram in Middle Ear (Conduction) Deafness

Common causes:

Middle ear fibrosis after infection. Otosclerosis (hereditary ossicle

fixation).

Bone conduction remains normal; air conduction is depressed, especially

at low frequencies.

In severe cases, ankylosis of the stapes to the oval window can cause total
ossicular deafness.

Treated surgically by replacing stapes with Teflon or metal prosthesis.