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160 Cards in this Set

  • Front
  • Back
neuron
nerve cell
receptor cell
receives stimulation from sensory cell
stimulates another neuron
interneuron
relay bipolar
communicates between 2 neurons
receives stimulation from one and excites the next
what do interneurons do in the pns
provide connection between sensory and motor neurons
and interneuron to interneuron
motor neuron
receives stimulation from neuron
stimulates a muscle
efferent stimulation
what are the 3 parts of a neuron?
cell body
dendrites
axon
cell body
soma
contains nucleus
surrounded by cell membrane
has many dendrites
dendrites
branched projections of a neuron
conduct electrical stimulation received from other cells to cell body
brings information to cell
axon
nerve fiber
long slender projection
conducts electrical impulses away from cell body
ends in presynaptic/axon terminals
transmit info from cell
axons 2 coverings
neurilemma
myelin sheath
neurilemma
first outer covering of axon
aids in regeneration of axon after damage
myelin sheath
fatty substance
insulates axon
protection
nodes of ranvier
spaces on axon without myelin sheath
speed transmission of neural impulses
ganglion/ganglia
collection of cell bodies in periphery
where are spiral ganglion located?
modiolus
modiolus
central
cone shaped
perforated
bony core
encompasses nerve fibers from hair cells and blood vessels
nucleus
collection of cell bodies in cns
nerve
a collection of axons in the pns
where is the cn viii located?
internal auditory meatus
tract
collection of axons in the cns
synapse
chemical event- the release of a neurotransmitter
what triggers the release of a neurotransmitter
arrival of a nerve impulse (action potential)
how does action potential travel?
down axon to presynaptic terminal (spike)
where does the neurotransmitter go after released?
synaptic cleft
what is a synaptic cleft?
tiny space between 2 nerve cells where the neurotransmitter passes
what happens to neurotransmitter after it reaches synaptic cleft?
it is absorbed by the post-synaptic membrane
what are the 2 neurotransmitters in the auditory system?
glutamate and acetylcholine
glutamate
afferent neurons- leads to cortex (sensory)
acetylcholine
efferent neurons- leads away from cortex (motor)
cranial nerve VIII
auditory nerve
where is CN VIII located?
connects cochlea to brainstem
what does CN VIII do?
relays info about
intensity
frequency
timing
of sound after cochlea has completed initial processing of incoming stimulus
2 divisions of CN VIII
auditory branch
vestibular branch
auditory branch
to cochlea
vestibular branch
to semicircular canals, utricle, saccule
how long is the CN VIII
ranges in length from 22-26 mm
where do the branches meet?
join in the internal auditory meatus and runs parallel with vestibular branch and facial nerve CN VII
where does the auditory nerve originate?
fibers originate at the base of the cochlear hair cells- terminal buttons, it is a fragile connection
how do the auditory nerve fibers connect to the hair cells?
habenula perforata
what is the habenula perforata?
bony structure of osseous spiral lamina
small opening where auditory fibers pass
afferent and efferent nerve fibers
where are dendrites located?
under hair cells
how many dendritic fibers pass through each habenula perforata?
about 30
what do the cell bodies form? where are they located?
spiral ganglion in modiolus
in the periphery
where do the axon terminals synapse occur?
cochlear nucleus, first synapse point in auditory brainstem
2 distinct kinds of fibers in the auditory system
type 1- afferent
type 2- efferent
type 1 fiber in the auditory system
afferent
90-95% of all auditory nerve fibers
80-85% of these are from the inner hair cells
type 2 fiber in the auditory system
efferent
5-10% of auditory nerve fibers
inner hair cells- what type of fibers? ratio? how does it look? how many contacts?
largely innervated by type 1 fibers
each cell is innervated by many different afferent fibers
"many-to-one"
gives radical appearance
10-30 afferent contacts
outer hair cells- what type of fibers? ratio?
primarily innervated by type 2 fibers
more outer hair cells than type 2 fibers
each nerve fiber goes to many outer hair cells
"one-to-many"
each outer hair cell has multiple fiber connections
origin of efferent innervation
superior olivary compleax in brainstem
what are the efferent innervation fibers called?
olivocochlear bundle(OCB)
where do OCB fibers go?
most cross to the opposite (contralateral) side- crossed
small number stay on same (ipsilateral) side- uncrossed
where do efferent to outer hair cells terminate?
directly on outer hair cells
where do efferent to inner hair cells terminate?
on afferent fiber
what fibers make up the core of the afferent branch of CN VIII
fibers from apical region of cochlea
what fibers wrap around these core fibers?
fibers from the medial region of cochlea
what fibers make up the surface?
fibers from the basal region of the cochlea
SO where are the highest frequencies represented on CN VIII?
on the circumference
what does the composition of the afferent branch of the CN VIII do?
preserves the tonotopic organization of the basilar membrane
when a cell is at resting potential, does the neuron have a charge?
yes, voltage stored in cell
source of neurons charge
-properties of cell membrane under rest
-sodium potassium pump
-since membrane is more permeable to potassium than sodium, it pumps out sodium
-the resulting distribution of ions creates a charge
what is the cells resting potential
-80mV (millivolts)
what happens to the action potential when a neurotransmitter is received by dendrites
action potential will propagate down the receiving neuron
how does the cell membrane change when a neurotransmitter is received by dendrites?
the cell membrane becomes permeable to sodium and pumps out potassium
how does the cells charge change when a neurotransmitter is received by dendrites?
the charge becomes depolarized, it goes from -80 mV to 40 mV
where does the depolarization process go?
it travels down the neuron
what happens when the charge reaches 40 mV?
there is a rapid reversal, the charge goes back to resting state of -80mV
what happens when action potential reaches the end of an axon?
it causes a synapse with the next neurons dendrites, this leads to sequential excitation from one neuron to the next
what type of an event is action potential?
all or nothing
what happens if the synapse is weak?
the neuron returns to resting state without depolarizing
how many action potential spikes are there per second?
the maximum is about 500 spikes/second
refractory period
time needed for neuron to recover before it can fire again, lasts about 1 ms
if the refractory period is 1 ms then theoretically the max spike rate is...
1000 spikes/sec but this has never been observed
2 types of neural activities
evoked potentials and single-unit recordings
evoked potentials
observe the simultaneous discharge of many neural units from a distance (ECochG, ABR, whole nerve action potential)
single unit recordings
measure response of one neuron at a time, tiny electrode not usually done on humans
what is a spontaneous rate?
neurons always fire even without acoustic stimulation
why does this happen?
currently unsure
spontaneous rates tend to be...
low or high
low= less than 20/sec
high= 60-80/sec
you must know the spontaneous rate to determine what?
when nerve is responding to stimulus
what is the neural response to an acoustic stimulus?
increase in spike rate (firing rate) above spontaneous rate, greater stimulus intensity the greater the spike rate
what changes during a stimulus response?
spike rate, size and shape of spike do not
PST histogram
post-stimulus time histogram
a way of recording neural activity
records spike rate as a function of time (spike rate/time)
in a PST histogram describe what happens before tone, tone on, tone off
before tone- spontaneous rate
tone on- slight delay, large increase in spike rate, decreases slightly, then sustained through duration of tone
tone off- sharp decline, refractory period which is less than spontaneous rate, then back to spontaneous rate
this shows that we are most sensitive to a stimulus when?
the beginning
PST histograms reflect what type of neuron activity?
afferent neuron activity, and therefore primarily the inner hair cells
how to measure a neurons threshold across frequencies
-find spontaneous rate
-start with low level signal
-change level until there is an increase in spike rate (>SR)
-look for 5-30 spike increase over SR
-perform same analysis and plot results across frequencies
what is the result of this measurement?
a tuning curve, an audigram for a neuron
each neuron has one frequency to which it is most sensitive (has lowest threshold) what is this called?
characteristic frequency
tuning curves for neurons with low characteristic frequencies are...
more symmetric
tuning curves for neurons with high characteristic frequencies are...
more asymetric, sharply tuned tip, broadly tuned tail
for a single neuron, what happens as intensity increases
spike rate increases
what is the dynamic range for intensity for a single neuron?
about 20-50 dB, after 50 spike rate plateaus
what happens when there are multiple neurons?
at first only those tuned to that characteristic frequency will fire, but then as intensity increases more and more surrounding neurons will fire
what is that effect called?
spread of excitation
acoustic tumor of the auditory nerve- incidence? age?
tumor on CN VIII nerve
8.7 persons per 1000
onset of acoustic tumor of the auditory nerve
age 30-50
may take several years to recognize depending on symptoms
what are the acoustic tumor of the auditory nerve symptoms a result of?
the tumor is pressing on anatomical regions within the auditory and surrounding systems
acoustic tumors of the auditory nerve account for what percent of intracranial tumors? cerebellopontine (within the brainstem) tumors?
intracranial tumors- 8-10%
cerebellopontine tumors- 78%
where is the auditory nerve unmyelinated?
region between endings on hair cells and the habenula perforata
when does the auditory nerve become myelinated?
as it passes through the internal auditory meatus
schwann cells
once auditory nerve is myelinated
what happens to the nerves as they leave the internal auditory meatus?
the auditory, facial, and vestibular nerves go through a recess known as the CPA in the brainstem
vestibular schwannoma
tumors most often arise from vestibular nerve in the internal auditory meatus (>90%) and encroaches on the auditory nerve
cause of vestibular schwannoma
-neoplasm arises from schwann sheath cells to form neurilemma
-sudden growth of schwann sheath cells becomes encapsulated which leads to a tumor
describe the tumors that result from vestibular schwannoma
benign
start small
usually slow growing
small- round and firm
large- lobulated
why can vestibular schwannoma tumors be especially dangerous
they are very close to the brainstem
where can vestibular schwannoma develop outside the internal auditory meatus
into the cerebellopontine angle (CPA)
into cochlea
what happens if the tumor grows into the cerebellopontine angle?
can erode bone
push on brainstem and cerebellum
what happens if the tumor grows into the cochlea?
-destroy vestibular and auditory nerve fibers
-push on cochlear branch of labyrinthine artery and cut off blood supply which leads to hair cell death and sudden hl
-destroy structures of cochlea
-push on facial nerve and cause paresis/paralysis
because most tumors affecting the auditory nerve approach the outside of the nerve fist, the _____ fibers are initially compromised, resulting in a ____ sersorineural hearing loss.
-basal
-high frequency
auditory symptoms of vestibular schwannoma
usually occur first
75% high frequency hearing loss is first symptom
usually gradual, abrupt in about 40%
tinnitus in about 80%
possible aural fullness
difficulty sustaining perception of continuous tone
audiogram configuration of someone with vestibular schwannoma
variable in degree
sloping
high frequency
sensorineural
speech recognition poorer than predicted
vestibular symptoms of vestibular schwannoma
-disequilibrium- constant and prolonged
-vertigo
-nausea
-nystagmus
-headaches (pressure)- schwannoma has invaded frontal/occipital region
cerebellar symptoms of vestibular schwannoma
uncoordinated movement- drunk like, involves lower body
tumor pushing on cerebellum
involvement CN V for vestibular schwannoma
trigeminal- tingling on face
involvement CN VII for vestibular schwannoma
facial- facial paralysis (partial or complete)
involvement CN IX and X for vestibular schwannoma
glossopharyngeal and vagus- late is disease pharyngeal and laryngeal problems, dysphonia
why is diagnosis for vestibular schwannoma difficult?
small tumors are usually asymptomatic
first symptom is usually hl
how do they diagnose vestibular schwannoma?
case history
audiologic evaluation (ABR)
otologic evaluation (by otologist)
neurologic evaluation
definitive diagnosis- radiological imaging exam
red flags for vestibular schwannoma in audiologic tests
-pure tone thresholds- unilateral/asymmetrical SNHL (90-95% of cases)
-speech recognition-poorer than predicted for HL
-tone decay
red flags for vestibular schwannoma in electrophysiologic test
-acoustic reflex threshold elevated or absent regardless of pure tone average thresholds- about 84% sensitivity
-reflex decay
-auditory brainstem response (ABR) absolute and interwave latencies
auditory brainstem response for some one with vestibular schwannoma
-may only see wave 1
-wave V may be delayed
- about 92% sensitivity
what do they do at a otoneurologic exam when looking for vestibular schwannoma?
-physical exam- review audiological findings
-doctor order MRI which is definitive
-CT if cant have MRI
MRI
magnetic resonance imaging
CT
computed tomography
3 stages of treatment for vestibular schwannoma
monitor- periodic audiological assessments, MRIs
gamma knife irradiation- ~25% increasingly used
surgery- ~50% several strategies
surgical approach for vestibular schwannoma is determined by? whos role is this?
size and location of tumor
audiologist's
what are the 3 types of surgical approaches for vestibular schwannoma?
-middle fossa approach
-translabyrinthine approach
-suboccipital/retrosigmoid approach
which is the least invasive approach?
middle fossa approach
describe the middle fossa surgical approach (tumors, where is surgery?, how does it affect hearing?)
-tumor is within internal auditory canal
-tumor is less than 3/4 inch
- surgical incision near squamous portion of temporal bone to access internal auditory meatus (don't need to go through labyrinth)
- hearing preservation possible (~60%)
describe the translabyrinthine approach (tumors, where is surgery? how does it affect hearing?)
-tumors outside of the internal auditory canal esp. if no hearing on that side
-surgical incision behind pinna
-mastoidectomy and labyrinthectomy
- 100% sacrifice of vestibular and auditory function on that side
describe the suboccipital/retrosigmoid approach (tumors, where is surgery? how does it affect hearing?)
-very large tumors
-gain access to all cranial nerves, expose brainstem structures, internal auditory meatus
- possible to preserve hearing (~40%) increased risk secondary to increased exposure
what type of disorder is neurofibromatosis type 2?
-genetic disorder
-autosomal dominant (chromosome 22)
-defective tumor suppressing genes
-50% cases inherited, 50% are de novo (new)
incidence of neurofibromatosis type 2? when does it appear?
1/33,000-50,000
appears in teens/young adulthood
diagnosis of neurofibromatosis type 2
-bilateral CN VIII tumors
-other tumors of the CNS can develop as well, additional phenotypic (observable) features
symptoms of neurofibromatosis type 2
-same as vestibular schwannoma but bilateral
-tumors tend to grow aster and be more aggressive
treatment for neurofibromatosis type 2
-depends on individual
-monitor one or both tumors
- surgical decompression
-surgical removal
-complete removal of CN VIII bilaterally in most cases
surgical removal for neurofibromatosis type 2
- harder than traditional vestibular schwannoma bc tumor is more integrated among nerve fibers
- likely to recur
removal of CN VIII bilaterally results
-will destroy hearing
- auditory brainstem implant (ABI)
ABI
auditory brainstem implant
cypass CN VIII
stimulates the cochlear nucleus
ABI v cochlear implant
cochlear implants bypass hair cells and have electrode array
what is presbycusis?
hl due to aging
4 general changes in the auditory system associated with age
(Not My First Concert- neurons, muscles, fluids, cartilage)
- loss of neurons (not replaced)
- changes in composition of intercellular fluids (endolymph and perilymph)
-changes in composition of muscles/ligaments (stapedius/tensor tympani)
-changes in cartilage (pinna and outer 1/3 of canal)
age and incidence of presbycusis
-30-40% people over 65 have significant age related hearing impairment
-50% over 80
- 2nd most common chronic health condition people report
why is it difficult to measure pure presbycusis
- noise effects- cumulative over time
- disease- meniere's otosclerosis, progressive genetic disorders, ototoxicity
- some age related declines in all populations, just more in westernized societies
4 auditory system changes with age
-conductive mechanism
-cochlear function
-CN VIII function
-CANS processing
effect of presbycusis on hearing process
-elevated thresholds
-poor speech understanding
how does presbycusis affect speech understanding
-phonemic regression- decrease in intelligibility of speech out of proportion to pure tone hearing loss associated with aging
-poorer speech recognition than predicted by audiogram
issues the older population faces
-comorbidity- presence of more than one disorder or disease
-HL may be superimposed on other age related communication issues- changes in speech comprehension and processing
5 types of presbycusis
middle ear/conductive
sensory
neural
strial/metabolic
central
typically don't occur in isolation, occur together
physical effects of middle ear/conductive presbycusis
-tympanic membrane thickens, loosens, looses elasticity
-ossicles become fixated
- arthritic changes to joints/ligaments
-cartilage softens leads to collapsing canals
not a large effect so there is not much, if any of a conductive component in presbycusis
sensory presbycusis- physical effects, onset, audiogram, speech
-changes in inner ear: atrophy of organ of corti, degeneration of neurons in organ of corti/spiral ganglion
-gradual onset
-audiogram- sloping/sharply sloping SNHL
-speech discrimination will depend on amount of impairment
neural presbycusis- physical effects, onset, HL, audiogram, speech
-loss of neurons innervating cochlea
-hair cells intact
-gradually cumulative over time
-starts in young adults
- mild HL
-gradually sloping or flat
-phonemic regression is a big problem
strial/metabolic presbycusis- physical effects, HL, audiogram, speech, treatment
-atrophy of stria vascularis
-mild to moderate HL
-flat SNHL
good speech recognition
-hearing aids very helpful
central presbycusis- physical effects, hl, speech
- degeneration of neural tissue throughout CANS
-slight HL
-behavioral thresholds attributed to peripheral fx
- speech recognition in quiet is usually good
- degraded speech tasks very difficult
- discrimination judgments are poorer (need 2x as long to detect difference)
challenge for researcher in presbycusis is...
determining underlying bases for pathology (genetic, environmental, additive, etc.)
for clinicians, findings on a thorough audiologic evaluation of someone with presbycusis will reflect the sum of...
various presbycusis types
vestibular changes with aging
-deterioration of sensory end organs for balance
-cristae in ampullae- rotary movement
-macule in saccule and utricle- linear acceleration
what do these vestibular changes cause?
disequilibrium
dizziness
falling easily
cerebral changes
comorbidity