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Afferent Auditory Pathway

The cochlear branch of the vestibulocochlear nerve


merges with the vestibular branch that has bundled
from the nerve fi bers of the ampullae, saccule, and
utricle.
The two branches maintain their separate identities
but combine to become cranial nerve VIII. Cranial
nerve VIII meets cranial nerve VII (the facial nerve) to
travel through the internal auditory canal (IAC). The
cochlear branch occupies a position beneath the
facial
nerve and to the side of the vestibular nerve.

A lesion along the auditory pathway (e.g.,


a Schwannoma or acoustic neuroma)
creates a retrocochlear hearing loss.
Audiometrically, a retrocochlear hearing
loss will look the same as a sensorineural
hearing loss (i.e., air and bone conduction
loss). A lesion on the cochlear nerve will
cause a loss in the detection of sound and
a loss in the recognition of words.

Cranial nerve VIII enters the brainstem at the


junction of the pons and medulla. The cochlear nerve
travels through the different levels of the brainstem
to terminate at the auditory cortex, Heschls gyrus
of the temporal lobe of the cerebrum. The nerve fi bers
synapse with at least four different nuclei along the
way
to the cortex. The fi rst-order neurons originate from
the cochlear hair cells (mostly the IHCs) and terminate
at the cochlear nuclei.

All fi bers terminate at either the ventral cochlear


nucleus or the dorsal cochlear nucleus, where they
synapse with the second-order
neurons. It is at this level that the neurons pass
through
the trapezoid body to be distributed to the ipsilateral
and contralateral superior olivary complex. Each
superior olivary complex and the nuclei above will
have information from both ears. This is referred to as
binaural representation and is important for localization
of a sound source.

Third-order neurons continue upward from


the superior olivary complex along a tract called
the lateral lemniscus. These third-order neurons
are joined by some second-order neurons that
arosefrom the cochlear nucleus but bypassed the
superior
olivary complex. The second- and third-order neurons
may terminate at the lateral lemniscus or continue
to the inferior colliculus at the dorsal midbrain.
The majority of neurons will synapse at the inferior
colliculus.

The inferior colliculus has a large bundle


of nerve fi bers that cross to communicate with the
nucleus on the opposite side. A commissural tract
allows the two inferior colliculi to communicate with
each other. Interaural time and intensity differences
occur at this level, playing a role in auditory
localization.
Fourth-order neurons leave the inferior colliculus
to terminate at the medial geniculate body of the
thalamus.

The third-order neurons that bypassed the


inferior colliculus will terminate here. In other words,
all ascending (i.e., afferent or sensory) neurons will have a fi nal
synapse at this subcortical level before proceeding to the auditory
cortex. The fi nal destination of afferent fi bers is Heschls gyrus
(also referred to as the anterior and posterior transverse gyri),
which is
found within the superior temporal gyrus along the
temporal lobe of the cerebrum (Brodmann areas 41
and 42) in both hemispheres. The frequency organization
of the cochlea is preserved along the pathway
and in bands across the cortical surface of the superior
temporal gyrus. The orderly representation is
known as tonotopic organization.

Researchers (e.g.,
Troost & Waller, 1998) have demonstrated the
tonotopic
organization of the medial geniculate body in
which low frequencies are represented laterally and
high frequencies are located medially in the principal
division. The peripheral auditory mechanism is the
site for the detection of sound but it is the central
cortical
level that is the location for conscious processing
of sound that we refer to as hearing.

Binaural representation is critical in the processing


of acoustic information. It is used for localization as in
detecting the origin of a sound. The interaural acoustic
information is processed for time, intensity, and
frequency characteristics. The differences are conveyed
throughout the pathway to the auditory cortex.
Damage to the pathway, after the point of binaural
representation, usually has no effect on the detection
of sound, thanks to the redundancy of information
being sent to the brain

. Hearing loss (a detection of


impaired frequency and intensity of sound) is
theoretically only caused by damage to the
outer and middle ear, cochlea, or cochlear
nerve. Auditory processing is
the brain using the frequency, intensity, and
pattern
of sounds (speech in particular) that our ears
detect
(the brain using what the ear hears

A lesion along
the auditory cortex interferes with the processing of
speech creating a central hearing loss. This is most
obvious when the speech signal is in competition with
or imbedded in background noise. The individual has
an inability to fi lter out competing auditory signals.
A central auditory processing disorder (CAPD) is
the result of a central hearing loss. For the most part,
auditory processing works fi ne in simple face-to-face
conversation in a quiet environment.

However, when
the system is stressed, as when trying to converse
in the presence of background noise or listening to
instruction while the teacher walks around a large
reverberant classroom, a lesion in the system will
become apparent and the auditory information will
be misunderstood or missed altogether. Many sites
can be at fault for a central hearing loss: a defi cit in the
interpretation of the signal; disruption in the redundant
auditory pathway; or lack of communication
between the two auditory cortices

The prevalence of
CAPD in children is estimated to be between 2% and
3% (Chermak & Musiek, 1997) with it being twice as
prevalent in males than females. It often coexists with
other disabilities. These include speech and language
disorders or delays, learning disabilities or dyslexia,
attention defi cit disorders with or without
hyperactivity,
and social and/or emotional problems. Testing
for CAPD is complicated and time-consuming.

Due
to neuromaturation of the central auditory nervous
system, assessment of children under age 7 is not
recommended due to the high degree of variability
in their performance. After an extensive case history
and assessment is completed, specifi c suggestions for
management will be shared. Keep in mind this is not a
peripheral loss so traditional amplifi cation is not the
treatment. CAPD management is usually in the form
of an auditory training program and phonological
awareness training, therapy for any existing language

and/or behavior defi cits, and methods for


improving
the quality of the incoming signal. This can be
accomplished
with the use of a personal auditory trainer to
enhance the signal (e.g., the teachers voice)
over the
random background (e.g., other sounds in the
classroom),
thereby improving the signal-to-noise ratio.

Efferent Auditory Pathway


Efferent Auditory Pathway
All the information from the peripheral hearing
mechanism is carried along the afferent pathway to
the cortex for processing. The efferent pathway is the
way the brain communicates information down to
the peripheral structures. The olivocochlear pathway
(refer back to Figure 12-17) carries efferent information
from the olivocochlear bundle (OCB) in the superior
olivary complex in the brainstem to the hearing
mechanism.

Guinan, Warr, and Norris (1983) described two main


olivocochlear pathways, one crossed and the other
uncrossed. The uncrossed pathway originates from the
lateral superior olivary complex (LSOC) and consists
of unmyelinated fi bers that terminate on the afferent
fi bers of the IHCs. The OHCs receive few of these
same uncrossed fibers.
The crossed pathway originates from the medial
superior olivary complex (MSOC).
.

These fi bers are myelinated and terminate directly


on the OHCs. The role of the efferent pathways (both
crossed and uncrossed) is believed to be the
production
of inhibitory effects. Information along the efferent
pathway seems to inhibit the OHCs ability to amplify
the BM motion. It is believed that this function
further
facilitates the active tuning effect of the hair cells.

Why You Need to Know


The IAC is a site for the growth of a benign Schwannoma
neuroma that tends to arise from the vestibular
nerve but with time will encroach on the
cochlear nerve. The neuroma is contained within
the narrow meatus and therefore quickly compresses
on the nerve causing unilateral symptoms
such as balance disturbances, tinnitus, and hearing
loss. Remembering the tonotopic organization
of the cochlear nerve, a lesion will initially result
in a high-frequency hearing loss. An undiagnosed
neuroma may grow large enough to affect the mid
to low frequencies and compress on the facial nerve
(cranial nerve VII) causing facial paresis.

Why You Need to Know


Auditory brainstem response (ABR) audiometry
refers to the measurement of the electrical potential
of the auditory pathway as it passes through
the different levels of the brainstem. The responses
are elicited by an auditory stimulus. Test
administration
and interpretation are performed by an
audiologist. The signal travels along the auditory
pathway from the cochlear nucleus to the inferior
colliculus. The elicited response can be measured
by surface electrodes. The response normally
occurs
within a 15-millisecond time period after a stimulus
is presented. ABR audiometry is considered an

Neural Pathways
All cochlear hair cells receive both afferent (i.e.,
sensory)
and efferent (i.e., motor) innervation; however,
the majority of fi bers are afferent. This section will
provide a discussion of the afferent and efferent
auditory
pathways as they relate to the process of hearing.
The central processing of auditory information within
and between the two cerebral hemispheres

Neurotransmission
Neurotransmission
The hair cells are innervated by no less than 30,000
nerve fi bers. Before joining with the fi bers of the
IHCs, the nerve fi bers that connect to the OHCs
course through the tunnel of Corti. Together they move
through the habenula perforata. The nerve fi bers carry
information along their peripheral processes to the
spiral ganglia. The nerve fi bers are
unmyelinated in
the region between their endings on the hair cells

and the habenula perforata but become myelinated


as they pass through the internal auditory canal (IAC).
For the OHCs, the neural information is a product of
the shearing action of the tectorial membrane. For the
IHCs, the neural information is a product of the
turbulence
created in the fl ow of the endolymph. Although
there are approximately three times as many OHCs as
IHCs, the OHCs send only 5% of the afferent
information
along the cochlear nerve

The IHCs send 95% of


the afferent information. Each IHC communicates
with as many as 10 to 18 ganglion cells (see Figure
12-17). The remaining 5% of peripheral nerve fi bers
branch with as many as 10 to 50 OHCs (this is a
relatively
small number of afferent nerve fi bers spread out
over a relatively large number of OHCs) (Spoendlin

).
The process known as transduction, the changing
(i.e., transforming) of mechanical vibrations from the
BM into neural information, occurs at the level of the
hair cells. Endolymph is rich with the positively
charged ions potassium and calcium. Endolymph has
a resting potential (the voltage potential present with
no stimulation) of 100 millivolts (mV) to 80 mV
(Tasaki & Spiropoulis, 1959). Therefore, the scala
media has a strong positive potential called the endocochlear
potential (EP). Transduction is dependent
on the intracellular resting potential of the hair cells,
which are about 40 mV for the IHCs and 70 mV for
the OHCs

The
positive resting potential of endolymph and the negative
resting potential of the hair cells yield a very large
voltage potential difference of 120 to 150 mV depending
on the cell type. As described by Hudspeth (1989),
when a stimulus is delivered a mechanical gate on the
stereocilia is opened, the tip
links reach up from the top of the shorter cilia to the
side of the adjacent taller cilia. This arrangement
allows them to be stretched much like a spring to open
a gate (Pickles, Comis, & Osborne, 1984). With the gate
now open, a route is provided for the higher concentration
of potassium (K) in the endolymph to fl ow
toward the lower concentration within the hair cells

As a result of the fl ow of potassium, the EP shifts


negatively
from its highly positive charge (the opposite
positive and negative charge differences want to
balance).
The EP shifting of a positive charge is termed
depolarization. Depolarization activates channel
opening along the lateral cell membrane. These
channels
allow for the infl ux of calcium and the effl ux
of potassium from the hair cell. The infl ux of

calcium triggers the release of the


neurotransmitter
glutamate into the nerve terminals in contact with
the hair cell base. The diffusion of the
neurotransmitter
across the terminal triggers an action potential to
be propagated down the nerve fi bers. For a split
moment, the shifting of the ion concentrations
within
the hair cells causes the cell to be hyperpolarized

When a cell is in a state of hyperpolarization, it is


unable to be stimulated. It is not until it regains its
resting potential that it is again ready to respond.
During
the action of transduction, the ion balance within
the endolymph is shifted dramatically. It is the
function
of the stria vascularis to return the endolymph to
its resting (potassium, sodium, and calcium)
balance