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Year 2 Courses > Tinnitus Midterm > Flashcards

Tinnitus Midterm Flashcards

1
Q

What is considered a key mechanism contributing to the perception of tinnitus following hearing loss?

A

Increase in spontaneous activity due to heightened neural response gain.

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2
Q

In Jastreboff’s tiger analogy, what does the tiger represent?

A

The patient’s tinnitus perception

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3
Q

What is the primary goal of Tinnitus Retraining Therapy (TRT) as suggested by Jastreboff’s model?

A

To reduce the perception and emotional distress of tinnitus through habituation.

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4
Q

Which statement best describes the relationship between tinnitus and other psychological conditions?

A

Tinnitus, anxiety, depression, and insomnia are interconnected, with each potentially exacerbating the others.

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5
Q

According to Hallam’s Model, which of the following factors can impede the habituation process to tinnitus?

A

Emotional significance attached to tinnitus

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6
Q

What is a key hypothesis regarding the role of the medial olivocochlear (MOC) system in tinnitus generation?

A

Decreased neural efferent input to the cochlear amplifier, potentially increasing spontaneous activity

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7
Q

What role does the autonomic nervous system play in the habituation process to tinnitus according to Hallam’s Model?

A

High levels of autonomic nervous system arousal can impede the habituation process by enhancing tinnitus awareness.

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8
Q

What is a key limitation of the discordant damage theory in explaining tinnitus generation?

A

It fails to explain why some individuals with profound hearing loss do not experience tinnitus

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9
Q

Increase in neural activity within the central auditory system as a compensatory response to decreased peripheral input, typically due to cochlear damage, which can manifest as tinnitus and hyperacusis.

A

Central Gain

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10
Q

What is the role of excessive intracellular calcium in noise-induced hearing loss and tinnitus?

A

It leads to overactivation of cells, oxidative stress, and eventual cell death, contributing to hearing loss and tinnitus.

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11
Q

Unfavorable alteration in the central nervous system’s function and structure in response to injury or disruption, such as hearing loss, leading to detrimental conditions like tinnitus.

A

Maladaptive Plasticity

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12
Q

The process where psychological changes or shifts in a person’s mental state cause them to become re-aware of tinnitus sounds to which they had previously adapted.

A

Dishabituation

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13
Q

Tinnitus arises from increased spontaneous neural activity at the boundary between normally functioning and damaged outer hair cells in the cochlea.

A

Edge Theory

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14
Q

A neural process that prevents tinnitus signals from reaching the auditory cortex by potentially blocking them at the thalamic level, with its failure resulting in the perception of tinnitus.

A

Inhibiting gating mechanism

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15
Q

Tinnitus can result from abnormal interactions between adjacent nerve fibers, particularly when damage or compression causes ephaptic coupling, leading to synchronized firing patterns in auditory neurons that are interpreted by the brain as sound alternatives

A

Crosstalk Theory

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16
Q

What is 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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17
Q

what are tinnitus models & their examples?

A

neurophysiological : jasterboff, maladaptive plasticity, role of Hl in tinnitus perception, & central gain

psychological/cognitive (hallam and cognitive behavior models)

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18
Q

what is a tinnitus model?

A

conceptual frameworks that aim to explain the overall phenomenon of tinnitus including its generation, perception and associated distress

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19
Q

what is a neurophysiological model?

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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20
Q

what are the 3 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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21
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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22
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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23
Q

what is 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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24
Q

what is 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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25
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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26
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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27
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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28
Q

what are limitations of the neurophysiological models

A

it is experimental evidence, the models can explain how HL could lead to tinnitus but cannot explain patients whose tinnitus was resolved after the nerve was cut

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29
Q

what is the psychological/cognitive model 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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30
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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31
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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32
Q

explain the vicious cycle of tinnitus

A

First notice the sound of tinnitus, brain interprets this new or unusual sound as significant causing you to pay more attention to it. This increased attention makes it seem louder or more intrusive causing negative emotions (anxiety, frustration, fear etc.). This emotional stress activates the limbic (emotional) and autonomic (fight or flight) systems leading to increase in arousal/stress which leads to more intense tinnitus perception.

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33
Q

what is 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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34
Q

tinnitus perception vs. tinnitus reaction

A

perception is the characteristics of the tinnitus sound itself (how it sounds) whereas reaction is the impact of tinnitus on an individual (their reaction to the sound)

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35
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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36
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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37
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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38
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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39
Q

what is the 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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40
Q

McKenna Cognitive behavioral model of tinnitus

A

tinnitus distress often stems more from an individual’s reactions and perceptions of the sound rather than the auditory signal itself. How the person thinks about their tinnitus is the primary driver of their stress

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41
Q

explanation of the cognitive behavioral model

A

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

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42
Q

under the cognitive model, how do people try and help their tinnitus

A

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)

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43
Q

how does the cognitive behavioral model differ from other models

A

-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

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44
Q

what model is the foundation for cognitive behavioral therapy (CBT)

A

McKenna et. al cognitive behavioral model
-aims at breaking the cycle of distress through therapeutic techniques

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45
Q

implications of management with the psychological and cognitive tinnitus models

A

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

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46
Q

the historically viewed origin of tinnitus and why it is being challenged

A

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

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47
Q

the favored site of origin for tinnitus

A

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

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48
Q

Functions → emotion, long-term memory, and other aspects of behavior

A

limbic system

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49
Q

important in a person’s emotional response to sounds

A

Amygdala

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50
Q

what is the autonomic system

A

controls bodily functions like homeostasis & is activated when we hear a potentially dangerous sound

51
Q

maintenance of bodily stability

A

homeostasis

52
Q

what is central gain

A

compensatory increase in CNS activity in reponse to the loss of sensory input, tinnitus occurs due to central gain which is the brain’s reaction to audiotry deprivation. It explains why you can cut the auditory nerve and the brain still hears the tinnitus

limitation : this theory only works if the patient has hearing loss.

53
Q

what is habituation

A

learning process where the brain treats constant presence of tinnitus as a non-threatening stimulus leading to gradual decrease in both awareness and distress caused by the noise

54
Q

what factors prevent habituation?

A

high levels of arousal (stress/anxiety), sudden onset of tinnitus, intense or unpredictable tinnitus, emotional significance, neural pathway damage

55
Q

Key Difference B/W Neurophysiological & Psychological Models

A

Neurophysiological models view tinnitus mainly as an issue of brain and auditory system dysfunction, whereas psychological models focus on the way tinnitus is perceived, processed, and reacted to psychologically and emotionally.

56
Q

peripheral mechanisms associated with tinnitus

A

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

57
Q

peripheral cellular mechanisms

A

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

58
Q

discordant damage of the IHCs and OHCs

A

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

59
Q

tectorial membrane displacement

A

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. 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

60
Q

what are the primary NTs within the auditory system

A

glutamate and GABA

61
Q

what receptors mediate the NTs

A

AMPA and NMDA receptors

62
Q

what should occur within the organ of corti for the transduction

A

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

63
Q

AMPA receptor process with tinnitus (associated with damage)

A

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

64
Q

NMDA receptor process with tinnitus (associated with damage)

A

noise → glutamate overstimulation → receptor activation → excessive calcium influx → disrupted neural activity → enhanced spontaneous firing (too much of it) → auditory nerve hyperactivity → tinnitus perception

65
Q

why is there an influx of calcium

A

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

66
Q

within the NTs and its impact on tinnitus, where is the damage at

A

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

67
Q

central mechanisms associated with tinnitus

A

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

68
Q

how does auditory deprivation lead to tinnitus

A

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 lasting

69
Q

inhibitory gating mechanisms

A

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

70
Q

crosstalk

A

formation between auditory nerve fibers when auditory nerve fibers are intact but other cranial nerves are damaged
-caused by nerve compression or demyelination

71
Q

how can crosstalk cause tinnitus

A

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

72
Q

how does the MOC play a role in tinnitus

A

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

73
Q

medial olivocochlear bundle

A

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

74
Q

basics of contralateral OAE suppression

A

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

75
Q

somatosensory mechanisms associated with tinnitus

A

the only non auditory sensory system that appears to be related to tinnitus
-physical structure that is involved in the tinnitus

76
Q

what are the two somatosensory aspects

A

disinhibition of the ipsilateral DCN and crosstalk

77
Q

disinhibition of the ipsilateral DCN

A

this has interaction with different pathways including the somatosensory input, so they think that it may inhibit the DCN

78
Q

objective tinnitus

A

describes sounds that are generated within the body and can be audible to another person
-mostly due to vascular disturbances

79
Q

subjective tinnitus

A

describes sounds that are perceived by the patient only
-the most common type

80
Q

acute tinnitus

A

anything occurring for less than 3 months

81
Q

chronic tinnitus

A

anything lasting for 3 to 6 months or longer

82
Q

recent onset tinnitus

A

lasting few weeks to a few months resulting from certain conditions

83
Q

delayed onset tinnitus

A

can be onset delayed after a triggering event such as noise exposure or a TBI

84
Q

primary tinnitus

A

idiopathic and may or may not be associated with SNHL
-unknown source

85
Q

secondary tinnitus

A

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

86
Q

the three main classifying factors of tinnitus

A

temporal, duration and impact

87
Q

Edge Theory (contrast theory)

A

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

88
Q

reorganization of cortical tonotopic maps

A

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

89
Q

hyperactivity and tinnitus

A

damage to the cochlea can lead to an increased spontaneous firing rate of neurons in the auditory structures
-hyperactivity is the increased spontaneous activity

90
Q

hypersynchrony and tinnitus

A

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

91
Q

why do we do a tinnitus assessment

A

improved patient provider communication, tinnitus patient reassurance, establishing a reference point, basis for treatment and documentation

92
Q

goals of initial tinnitus assessment

A

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

93
Q

tinnitus psychoacoustic assessments

A

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

94
Q

how do we find loudness levels and thresholds as part of the tinnitus assessment

A

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

95
Q

what is the most common cause of tinnitus

A

hearing loss
-this causes a deprivation of sensory input to the CANS
-cerumen can also cause this deprivation

96
Q

characteristics of tinnitus associated with meniere’s disease

A

low frequency tone
-could be due to increased endolymph pressure, rupture of reissner’s membrane and loss of hair cells

97
Q

characteristics of vestibular schwannoma associated tinnitus

A

patients complain of unilateral tinnitus and HL
-higher severity and higher annoyance tinnitus

98
Q

characteristics of otosclerosis associated tinnitus

A

high pitched or resembling white noise
-can be initially pulsatile

99
Q

characteristics of ototoxicity associated tinnitus

A

tinnitus emerges as a continuous high pitched sound and is a common side effect of various drugs

100
Q

somatic tinnitus

A

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

101
Q

causes of somatic tinnitus

A

muscle tension, TMJ/jaw problems, dental disorder, head injuries, cervical spine issues and chronic stress

102
Q

diagnosis criteria for somatic tinnitus

A

tinnitus and pain occurs simultaneously, tinnitus is preceded by trauma, tinnitus increases during bad posture, tinnitus pitch varies

103
Q

tinnitus red flags

A

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

104
Q

why do we do a tinnitus assessment

A

improved patient provider communication, tinnitus patient reassurance, establishing a reference point, basis for treatment and documentation

105
Q

goals of initial tinnitus assessment

A

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

106
Q

what has imaging studies shown within tinnitus patients

A

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

107
Q

dysfunction within the limbic system would result in …

A

failure of inhibiting the tinnitus signal, potentially causing the tinnitus

108
Q

factors related to the prevalence of tinnitus

A

hearing loss, noise exposure, head/neck injury, diseases or health conditions, medications, lifestyle factors and unknow etiology

109
Q

spontaneous tinnitus

A

sudden sound, usually unilateral and lasting 2-3 minutes
-accompanies with ear fullness

110
Q

temporary tinnitus

A

lasts minutes to days, often after noise exposure or medications
-may accompany TTS
-triggering events prior to the tinnitus

111
Q

occasional tinnitus

A

occurs less than weekly and lasts at least 5 minutes
-every few weeks, monthly or every few months

112
Q

intermittent tinnitus

A

occurring regularly and lasts at least 5 minutes
-daily or weekly

113
Q

constant tinnitus

A

continuous sound

114
Q

duration characteristics

A

how long the condition has been experienced
-recent/acute or persistent/chronic

115
Q

impact characteristics of tinnitus

A

how the tinnitus impacts the life of the patient, how much does it interfere
-non bothersome and bothesome

116
Q

non-bothersome tinnitus

A

little or no impact on quality of life or health status
-does not impact the persons daily activities

117
Q

bothersome tinnitus

A

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

118
Q

pulsating tinnitus

A

noise that usually has the same beat as the heart, pulses synchronal with the heart beat

119
Q

possible causes for pulsatile tinnitus

A

venous hums, stenosis of the carotid arteries, heart murmur, hypertension, hyperthyroidism, vascular stenosis, aneurysms and coronary artery disease

120
Q

examination symptoms for pulsatile tinnitus

A

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

121
Q

evaluation of pulsatile tinnitus

A

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

122
Q

clicking tinnitus

A

appears to be due to contractions of tensor tympani or the nasopharyngeal (middle ear) muscles controlling the patency of the ET,

123
Q

clicking tinnitus can be a symptoms of ….

A

ME myoclonus
-jerking of a muscle group

124
Q

evaluation of clicking tinnitus

A

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

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