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AUDE 6220 > midterm > Flashcards

midterm Flashcards

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1
Q

tinnitus

A

a phantom auditory perception ; the perception of a sound without corresponding acoustic or mechanical correlates in the cochlea
-involuntary
-the site of generation is anywhere on the pathways of sound

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2
Q

breakdown of tinnitus models

A

neurophysiological (jasterboff) and psychological/cognitive (hallam and cognitive behavior models)

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3
Q

neurophysiological models

A

biological basis of tinnitus in the auditory system
-the consensus that tinnitus results from the perception of abnormal activity
-main model is jasterboff’s model

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4
Q

what are the three proposed mechanisms for how tinnitus is coded in the cortex

A

increased spontaneous activity fed by increased or decreased activity, cross fibers correlation with normal or increased spontaneous activity and more fibers with similar best frequency following HL induced plasticity

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5
Q

how does maladaptive plasticity correlate to tinnitus

A

tinnitus is thought to result from the CNS in response to HL or other causes so what happens is that the CNS is trying to fix something but it ended up becoming worse

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6
Q

explain how HL can impact tinnitus

A

HL will cause a decreased input to the auditory system, the brain them tries to maintain homeostasis by compensating however the increased neural gain causes more spontaneous neural activity
-therefore it is believed that increased spontaneous activity is proposed as a key mechanisms for tinnitus perception

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7
Q

central gain

A

a compensatory increase in central auditory activity as a response to the loss of sensory input
-a limitation to believing that central gain plays a role in tinnitus is that it requires everyone to have HL, but not everyone that has tinnitus has a HL

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8
Q

jasterboff’s neurophysiological model

A

focuses on how the auditory and non-auditory systems interact as well as it is based on general neurophysiology and behavioral neuroscience
-hypothesis is that many systems in the brain are involved in tinnitus, with the auditory system playing a secondary role

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9
Q

the main idea of jasterboff’s model

A

tinnitus should not simply be categorized into peripheral and central, meaning all levels are involved but it varies between cases

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10
Q

what does jasterboff’s model suggest

A

tinnitus becomes problematic when negative associations are formed with the tinnitus perception
-remember the concept of the tiger in the room, by perceiving it as negative or dangerous it becomes worse

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11
Q

what is involved in jasterboff’s model

A

limbic system (emotional responses), sympathetic autonomic nervous system (fight or flight) and the reticular foramen (attention and awareness)

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12
Q

jasterboff’s model suggests that tinnitus is not just a ______________ but there is also a ____________

A

sensory experience ; emotional and cognitive components

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13
Q

what are limitations of the neurophysiological models

A

it is experimental evidence, the models can explain how HL could lead to tinnitus but not how everyone with HL gets tinnitus, it cannot explain observations of patients that tinnitus was resolved after the nerve was cut

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14
Q

psychological/cognitive models of tinnitus

A

revolves around looking at how tinnitus disrupts the quality of life as well as the characteristics of tinnitus
-main models include hallam’s and the cognitive behavioral model

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15
Q

what domains can tinnitus impact

A

function impairments (thoughts/emotions, hearing, sleep and concentration) and activity limitations (socialization, physical health, work, education and economic)

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16
Q

common symptoms that are associated with impacting the quality of life due to tinnitus

A

insomnia, loss of concentration, low mood/irritability, anxiety and clinical depression

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17
Q

explain the vicious cycle of tinnitus

A

tinnitus can trigger anxiety which reinforces the tinnitus perception, creating a feedback loop leading to an increased emotional distress
-it’s the loop of negative emotional distress and increasing tinnitus that continues to go around and around

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18
Q

tinnitus perception vs. tinnitus reaction

A

perception is the characteristics of the tinnitus sound itself whereas reaction is the impact of tinnitus on an individual

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19
Q

hallam’s model

A

the thought that tinnitus might occur without auditory dysfunction and is potentially triggered by psychological factors
-hypothesis is that tinnitus is influenced by the ability of the CNS to inhibit unnecessary sensory input

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20
Q

the main idea of hallam’s model

A

bothersome tinnitus is the result of the failure to habituate, which is the decrease in response to a stimulus when it is presented repeatedly
-remember, habituation is believed to be a learning process where the brain will begin to associate with the constant presence of tinnitus as a non-threatening stimulus

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21
Q

evidence that supports hallam’s model

A

majority of people who have tinnitus do not complain about it, distress from tinnitus tends to decrease over time, no relationship between tinnitus loudness and distress levels and individuals often grow more tolerant of tinnitus

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22
Q

what are some factors that could lead to the inability to habituate

A

high levels of arousal, sudden onset of tinnitus, emotional significance, neural pathway damage and dishabituation

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23
Q

what causes dishabituation

A

changes or shifts in a persons mental state that can lead to re-awareness of the tinnitus
-some sort of change
-once this has occurred, habituation will have to occur all over again

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24
Q

treatment for hallam’s model

A

relaxation therapy (aims to lower autonomic arousal and interrupt the feedback loop) and formal cognitive therapy (alters emotional responses to tinnitus, reducing perceived distress and aiding habituation)

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25
cognitive behavioral model of tinnitus (McKenna et. al, 2014)
focuses on how the individual thinks about their tinnitus -believes that the cognitive interpretations are the primary driver of the stress associated with tinnitus
26
explanation of the cognitive behavioral model
negative interpretations of tinnitus increase the selective attention which then leads to greater awareness of tinnitus -due to the increased attention, the person notices the tinnitus more often which then creates a cycle that reinforces the negative interpretations
27
under the cognitive model, how do people try and help their tinnitus
safety seeking behaviors such as avoidance or suppression (may provide short term relief but prevents long term adaptation) and selective attention (can distort how the tinnitus is perceived)
28
how does the cognitive behavioral model differ from other models
-greater emphasis is placed on vigilance and orientation to tinnitus rather than a failure to habituate -emphasizes the impact of negative thoughts and cognitive distortions on tinnitus distress
29
what model is the foundation for cognitive behavioral therapy (CBT)
McKenna et. al cognitive behavioral model -aims at breaking the cycle of distress through therapeutic techniques
30
implications of management with the psychological and cognitive tinnitus models
correcting negative automatic thoughts, reducing sympathetic autonomic nervous activity, reducing selective attention/monitoring for tinnitus related cues, correcting distorted perceptions of tinnitus intensity and its impact on functioning and correcting inaccurate beliefs
31
the historically viewed origin of tinnitus and why it is being challenged
tinnitus has been thought to occur as a result of dysfunction of the peripheral auditory system however it has been challenged due to the main point that when the auditory nerve is severed, this does not eliminate the tinnitus in every case -the thought behind the nerve being severed is that if the connection is broken then the tinnitus will not be heard
32
the favored site of origin for tinnitus
central origin, meaning that the tinnitus perception is a brain issue -there is some underlying causes that begins tinnitus, but ultimately its the brains reaction to some change
33
peripheral mechanisms associated with tinnitus
tinnitus associated with the cochlea -cellular mechanisms, edge theory, discordant damage of hair cells, tectorial membrane displacement, NTs and their receptors, transduction in the organ of corti and cochlear synaptopathy
34
peripheral cellular mechanisms
loss of OHC electromotility, loss of synapse between IHCs and spiral ganglion neurons, damage to stereocilia bundle, rupture of the basilar membrane and death of the hair cells -remember if there is any damage it will lead to HL which eventually will cause tinnitus
35
edge theory (contrast theory)
tinnitus is induced by increased spontaneous activity in the edge areas -the edge area is the area of transition from normal OHCs on the apical side of a lesion to OHCs toward the basal side that are missing or being altered -there is spontaneous activity at this area
36
discordant damage of the IHCs and OHCs
noise and ototoxicity → imbalance of cilia damage (hair cell loss) → nerve fiber imbalance → altered higher brian centers → tinnitus -with any damage there can be an imbalance between the OHCs and IHCs due to the IHCs resilience to damage, so the OHCs will continue to become more damaged -this imbalance will then be carried into the brain causing an already messy signal to be perceived, which is the tinnitus
37
tectorial membrane displacement
this membrane should be above the hair cells however any changes in the position could potentially trigger tinnitus to occur -the change in location could occur after intense noise exposure
38
how can the tectorial membrane be displaced
the membrane may dip down onto the IHCs causing depolarization and an increased cochlear activity, contributing to the tinnitus perception by sending it to the brain
39
what are the primary NTs within the auditory system
glutamate and GABA
40
what receptors mediate the NTs
AMPA and NMDA receptors
41
what should occur within the organ of corti for the transduction
sound wave moving in will move the endolymphatic fluid, hair cells tip, potassium flows into the cell, calcium flows outward and pushes the NTs into the receptors -in order for NTs to be dumped, calcium channels open -once it has been released and have become bonded, it then becomes recycled through reuptake and at the same time the Ca will then leave the cell -the cell is then depolarized
42
AMPA receptor process with tinnitus (associated with damage)
noise exposure (or some sort of damage) →excessive glutamate release by the IHCs → AMPA receptor overactivation (because glutamate is binding, more work for the receptors) → excessive calcium influx → nerve cell damage → disrupted auditory signal transmission → tinnitus perception
43
NMDA receptor process with tinnitus (associated with damage)
noise → glutamate overstimulation → receptor activation → excessive calcium influx → disrupted neural activity → enhanced spontaneous firing (too much of it) → auditory nerve hyperactivity → tinnitus perception
44
why is there an influx of calcium
the hair cells become overstimulated, leading to overproduction of glutamate (which leads to more calcium getting into the cell) -this overstimulation, leads to an overproduction of everything -therefore it does not get cleared as it normally would
45
within the NTs and its impact on tinnitus, where is the damage at
damage at the level of the nerve fibers and damage of the hair cells -this then allows more calcium to get into the spiral ganglion leading to damage
46
cochlear synpatopathy
damage to the synapses between IHCs and the cochlear nerve fibers can cause a hidden HL which has associated tinnitus and difficulty hearing in noise -this damage can cause excessive glutamate to release
47
central mechanisms associated with tinnitus
central mechanisms are often triggered by reduced cochlear activity, but cochlear damage is not always necessary -auditory deprivation, inhibitory gating mechanisms, reorganization of cortical tonotopic maps, hyperactivity, hypersyncrhony, cross talk and MOC function
48
how does auditory deprivation lead to tinnitus
an imbalance between inhibition and excitation leads to an increased neuronal activity and a perception of sound without external stimuli -activation of neuronal plasticity occurs with the lack of sensory input, causing changes that can be temporal or long lastin
49
inhibitory gating mechanisms
there is a system that blocks the tinnitus signal from reaching the cortex, if this is compromised the tinnitus signal is not inhibited at the thalamic level and it is then related to the cortex -all resulting in a perceived tinnitus
50
reorganization of cortical tonotopic maps
abnormal auditory cortex activation is linked with reorganization of the cortical tonotopic maps -the extent of reorganization is correlated with the occurrence/severity of tinnitus in both patients
51
hyperactivity and tinnitus
damage to the cochlea can lead to an increased spontaneous firing rate of neurons in the auditory structures -hyperactivity is the increased spontaneous activity
52
hypersynchrony and tinnitus
synchronization may be initiated by increased neural activity and reorganized by cortical frequency maps -we are looking at the neurons doing the same thing at the same time
53
crosstalk
formation between auditory nerve fibers when auditory nerve fibers are intact but other cranial nerves are damaged -caused by nerve compression or demyelination
54
how can crosstalk cause tinnitus
the new connections lead to syncrhonized firing of auditory neurons, mimicking the patterns of actual sounds -the brain then interprets this as actual sounds, resulting in the tinnitus
55
how does the MOC play a role in tinnitus
there is some impairment in the system as there needs to be a reduction in the neural efferent input to the OHCs resulting in a increase in the gain of the cochlear amplifier
56
medial olivocochlear bundle (MOC)
auditory efferent pathway projecting from the MOC and innervates the OHCs -this is activated by electrical or chemical stimulation and once it is activated, the system inhibits OHC concentration therefore reducing the amplitude of OAEs
57
basics of contralateral OAE suppression
minimum suppression of 0.5-1 is needed to indicate integrity of the MOC system -once the noise is activated, it will suppress the system
58
somatosensory mechanisms associated with tinnitus
the only non auditory sensory system that appears to be related to tinnitus -physical structure that is involved in the tinnitus
59
what are the two somatosensory aspects
disinhibition of the ipsilateral DCN and crosstalk
60
disinhibition of the ipsilateral DCN
this has interaction with different pathways including the somatosensory input, so they think that it may inhibit the DCN
61
the auditory limbic system
part of the brain involved in our behavioral and emotional responses, especially when it comes to behaviors we need for survival such as feeding, reproduction and caring for young and the fight or flight responses
62
why is it believed that the limbic system plays a role in tinnitus
it mediates the emotional response to tinnitus -so patients with strong emotional responses to tinnitus often will show an enhanced sympathetic nervous system
63
what has imaging studies shown within tinnitus patients
dysregulation between the limbic and auditory system, increased connectivity between limbic and auditory, amygdala and other limbic structures become more active in people with tinnitus, greater connectivity between auditory and limbic areas correlated with higher levels of tinnitus distress
64
dysfunction within the limbic system would result in …
failure of inhibiting the tinnitus signal, potentially causing the tinnitus
65
factors related to the prevalence of tinnitus
hearing loss, noise exposure, head/neck injury, diseases or health conditions, medications, lifestyle factors and unknow etiology
66
objective tinnitus
describes sounds that are generated within the body and can be audible to another person -mostly due to vascular disturbances
67
subjective tinnitus
describes sounds that are perceived by the patient only -the most common type
68
acute tinnitus
anything occurring for less than 3 months
69
chronic tinnitus
anything lasting for 3 to 6 months or longer
70
recent onset tinnitus
lasting few weeks to a few months resulting from certain conditions
71
delayed onset tinnitus
can be onset delayed after a triggering event such as noise exposure or a TBI
72
primary tinnitus
idiopathic and may or may not be associated with SNHL -unknown source
73
secondary tinnitus
associated with a specific underlying cause or an identifiable organic condition -underlying cause other than SNHL -could be something like a muscle spasm or TMJ
74
the three main classifying factors of tinnitus
temporal, duration and impact
75
temporal characteristics of tinnitus
talking about how the tinnitus is perceived -spontaneous, temporal, occasional, intermittent and constant
76
spontaneous tinnitus
sudden sound, usually unilateral and lasting 2-3 minutes -accompanies with ear fullness
77
temporary tinnitus
lasts minutes to days, often after noise exposure or medications -may accompany TTS -triggering events prior to the tinnitus
78
occasional tinnitus
occurs less than weekly and lasts at least 5 minutes -every few weeks, monthly or every few months
79
intermittent tinnitus
occurring regularly and lasts at least 5 minutes -daily or weekly
80
constant tinnitus
continuous sound
81
duration characteristics
how long the condition has been experienced -recent/acute or persistent/chronic
82
recent/acute tinnitus
experienced for less than 6 months
83
persistent/chronic tinnitus
experienced for 6 months or longer -may require lifelong management
84
impact characteristics of tinnitus
how the tinnitus impacts the life of the patient, how much does it interfere -non bothersome and bothesome
85
non-bothersome tinnitus
little or no impact on quality of life or health status -does not impact the persons daily activities
86
bothersome tinnitus
distressing and negatively affects quality of life and/or health status -affecting sleep, concentration and they may not be able to keep up with conversations
87
pulsating tinnitus
noise that usually has the same beat as the heart, pulses synchronal with the heart beat
88
possible causes for pulsatile tinnitus
venous hums, stenosis of the carotid arteries, heart murmur, hypertension, hyperthyroidism, vascular stenosis, aneurysms and coronary artery disease
89
examination symptoms for pulsatile tinnitus
glomus jugulare (slow growth), pulsatile tinnitus, ME mass, cranial nerve involvement, vertigo otorrhea, rising sun, red tympanic membrane -look for the spikes on a tymp
90
evaluation of pulsatile tinnitus
tinnitus of this origin can be suppressed by compression of the jugular vein -find the SCM muscle and press firmly and hold for 10 seconds on the artery -ask the patient is it changed their tinnitus at all -if changed, refer out for vascular workup -if its the same, then we have confirmed pulsatile tinnitus
91
clicking tinnitus
appears to be due to contractions of tensor tympani or the nasopharyngeal (middle ear) muscles controlling the patency of the ET,
92
clicking tinnitus can be a symptom of ....
ME myoclonus -jerking of a muscle group
93
evaluation of clicking tinnitus
may be detectable with the usage of reflex testing or reflex decay (indicated by a jumpy response) -reflex decay if a longer response, so there is a better chance of seeing it on this one
94
somatic tinnitus
tinnitus caused or influenced by sensory input in the body, such as a muscle spasm -closely related to factors of the head or neck -perceived in the ear ipsilateral to the somatic event -there are no other hearing or vestibular complaints -hearing is WNL
95
causes of somatic tinnitus
muscle tension, TMJ/jaw problems, dental disorder, head injuries, cervical spine issues and chronic stress
96
diagnosis criteria for somatic tinnitus
tinnitus and pain occurs simultaneously, tinnitus is preceded by trauma, tinnitus increases during bad posture, tinnitus pitch varies
97
tinnitus red flags
pulsatile tinnitus, tinnitus in association with vertigo, unilateral tinnitus or HL, examination showing abnormalities of the ear, tinnitus in association with asymmetric HL, psychological distress, significant associated sleep/concentration problems, anxiety regarding possible underlying pathology, tinnitus is not improving
98
why do we do a tinnitus assessment
improved patient provider communication, tinnitus patient reassurance, establishing a reference point, basis for treatment and documentation
99
goals of initial tinnitus assessment
rule out or confirm disease/pathology, document health conditions influencing tinnitus perception, evaluate auditory function to identify peripheral or central auditory dysfunction associated with the mechanisms of tinnitus, describe and quantify the severity of the tinnitus, define the impact of tinnitus on the quality of life and contribute to decisions regarding an effective management plan
100
tinnitus psychoacoustic assessments
includes pitch matching, loudness matching, minimum masking level and residual inhibition -can only be completed if the patient is experiencing tinnitus at the time of assessment
101
how do we find loudness levels and thresholds as part of the tinnitus assessment
we do the typically down 10 up 5 and once the closest 5 dB level has been found, we will increase in 1 dB steps to close in on the specific level
102
what is the most common cause of tinnitus
hearing loss -this causes a deprivation of sensory input to the CANS -cerumen can also cause this deprivation
103
characteristics of tinnitus associated with meniere's disease
low frequency tone -could be due to increased endolymph pressure, rupture of reissner's membrane and loss of hair cells
104
characteristics of vestibular schwannoma associated tinnitus
patients complain of unilateral tinnitus and HL -higher severity and higher annoyance tinnitus
105
characteristics of otosclerosis associated tinnitus
high pitched or resembling white noise -can be initially pulsatile
106
characteristics of ototoxicity associated tinnitus
tinnitus emerges as a continuous high pitched sound and is a common side effect of various drugs

AUDE 6220 (2 decks)

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