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Advanced Diagnostic Audiology > W11 > Flashcards

W11 Flashcards

1
Q

What are the 3 management strategies for APD?

A
  1. Compensatory Strategies
  2. Environmental Modifications (EMs)
  3. Assistive Technologies and Hearing Aids

like a hierarchy

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2
Q

What are compensatory strategies?

A

− Strategies to improve the learning environment without making physical alterations.

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3
Q

Examples of compensatory strategies:

A

– Improving self-advocacy and speaking up about communication difficulties
‒ Practicing in mock settings
‒ Using visual aids and lip-reading to enhance understanding.
‒ Providing notes ahead of the class to help the child prepare and reduce reliance on auditory information.
‒ Using recording devices, reduced-speed playback, captions, and note-taking aids
‒ Using alternative methods to take exams.

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4
Q

What are EMs?

A

They refer to physical changes in the environment

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5
Q

What 4 thing do EMs overcome?

A

̶ Low SNR
̶ High reverberation
̶ Poor insulation
̶ A low teacher voice level

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6
Q

Classroom ANSI standards: The maximum allowed noise is ____ dB with ____ dB SNR.

A

35, +15

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7
Q

Classroom ANSI standards: ̶ The speaker-to-listener distance should ideally be less than ____ feet.

A

3

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8
Q

Classroom ANSI standards: RT (reverberation time) should not exceed ____ sec at frequencies of 500 Hz, 1000 Hz, and 2000 Hz

A

0.6

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9
Q

Classroom ANSI standards: RT (reverberation time) should not exceed no more than ____ sec for classrooms between 10,000 and 20,000 cubic feet

A

0.7

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10
Q

Classroom ANSI standards: RT (reverberation time) should be as short as ____ sec for primary schools

A

0.3

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11
Q

̶Overall, an RT of ____sec for hearing-impaired children/APD and ____sec for hearing peers is recommended.

A

0.3, 0.6

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12
Q

What is reverberation?

A

Reverberation is the persistence of sound in a room after the sound source has stopped. Reverberation can interfere
with speech intelligibility.

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13
Q

What 4 reasons is Improving the SNR Important?

A

̶ Children’s ability to hear in noise doesn’t reach adult-like levels until adolescence.
̶ Children with normal hearing require higher SNR than adults (+10dB vs. +6dB).
̶ Children with hearing loss and APD require higher SNRs than hearing peers (+12 to +20dB vs. +10dB).
̶ While current classrooms often have SNRs ranging from -7 to +5dB, which is concerning.

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14
Q

What are 3 Negative Consequences of Poor Classroom Acoustics (long RTs and low SNRS):

A

̶ Reduced speech perception, leading to mishearing and spelling errors.
̶ Reduced reading ability
̶ Poor academic achievements

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15
Q

When are the ALDs recommended?

A

Once EMs can not meet the SNR needs of children with APD,
hearing loss, or learning disability.

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16
Q

4 Types of ALDs:

A

̶ Personal FM or ear-level FM systems
̶ Sound-field FM systems (placing speakers in the classroom)
̶ Infrared induction loops
̶ Hardwired systems

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17
Q
  • The ideal SNR in a classroom is ≥ ____
A

+15dB.

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18
Q
  • FM systems provide an average SNR advantage of ____ dB.
A

8.3

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19
Q

To determine if a child needs an FM unit for sound enhancement, the following factors should be
considered:

A

̶ Poor speech-in-noise discrimination
̶ Ability to wear and adapt to the unit
̶ Support of the school or district
̶ Compatibility with the child’s personal aids or other FM units in the classroom
̶ Child‘s willingness to wear without feeling stigmatized
̶ Teacher’s willingness to wear the microphone and transmitter and learn how to troubleshoot
̶ Teacher’s acceptance and willingness to introduce the device to the class
̶ Having solutions for potential interferences from external sources: radio stations, computers, and pagers
̶ Costs for the family and/or the school

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20
Q

Should the FM Be Fitted for One or both Ears?

A
  • Bilateral fitting is generally recommended to improve SNR and sound localization.
  • The decision should be individualized, based on the child’s needs.
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21
Q
A
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22
Q

How can you use sound field amplification systems to improve SNR?

A

Involving a microphone to capture the teacher’s voice and speakers to amplify and project it throughout the classroom.

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23
Q

What are the benefits of sound field amplification?

A

− Improved speech perception
− Improved academic achievement
− Enhanced eye contact, attending skills, reduced listening difficulties, and listener fatigue.
− They are not expensive, almost equal to the price of 1 personal amplification system

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24
Q

What are the limitations of sound field amplification?

A

− They can not overcome the effects of excessive reverberation.
− They increase the overall classroom sound levels, causing distractions for neighboring rooms

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25
Q

The following 5 Hearing aid features can be used to improve SNRs:

A

̶ Using a hearing aid with a mild gain
̶ Directional microphones
̶ Noise reduction algorithms
̶ Conservative nonlinear processing options (NPO)
̶ Wide dynamic range compression (WDRC) circuits

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26
Q

Define stroke

A

A neurological deficit caused by vascular damage in the CNS.

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27
Q

What are the 2 types of strokes?

A

hemorrhagic
ischemic

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28
Q

What is a hemorrhagic stroke?

A

When bleeding in the brain damages nearby cells.

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29
Q

What is an ischemic stroke?

A

Blockage of a blood vessel supplying the brain by a blood clot. It is called:
̶ Thrombotic stroke/atherosclerotic stroke, when the clot forms in an artery supplying the brain.
̶ Embolic stroke, when the clot forms somewhere else in the body and travels through the bloodstream to the brain.

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30
Q

What is a Mini-stroke/TIA (transient ischemic attack)?

A

̶ Due to a temporary blockage
̶ Symptoms usually last for just a few minutes or < 24 hours.

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31
Q

stroke symptoms vary based on the what?

A

place and extent of brain damage

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32
Q

What are the 3 common symptoms of stroke?

A

̶ Sudden weakness or numbness on one side of the body
̶ Confusion
̶ Headache

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33
Q

How do you differentiate between a hemorrhagic and ischemic stroke?

A

To differentiate between the 2 you need imaging

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34
Q

Are there hearing deficits associated with stroke?

A

– Hearing thresholds are mostly preserved.
‒ HL may occur by disrupted vascular supply to the inner ear or nerve.

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35
Q

Are there auditory processing deficits with stroke?

A

̶APD reported: Depending on the lesion site and time elapsed since stroke onset:
‒ Deficits in sound localization
‒ Deficits in sound recognition
o Auditory agnosia: Deficits in word, music, or environmental sound recognition (refer to session 7)
o Temporal and spectral perceptual disorders
̶Central deafness is rare.
̶ It may occur due to bilateral impaired auditory cortices or extensive brainstem damage

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36
Q

When does central deafness occur?

A

Severe head injury affecting the brainstem
OR is both auditory cortices are involved

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37
Q

What were the 4 deficits observed in a 10-year-old child with acquired APD due to severe left hemorrhagic
stroke at 13 months of age?

A

̶ Sound localization
̶ Speech perception, particularly in background noise.
̶ Speech and language development
̶ Short-term memory and attention (visual and auditory)

  • Acceptable performance at school using special education needs strategies.
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38
Q

How does sound get to the brain?

A

The majority of the
auditory nerve fibers take
a contralateral pathway
from each ear, which
assists in sound
localization and speech
perception

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39
Q

Why were most issues with this child in the right ear?

A

Most issues are in the right ear, but a stroke on the left side (why? Crossing to the contralateral side)
- If the deficit is in the LEFT ear, the damage is in the RIGHT hemisphere
Not limited to stroke

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40
Q

What test did Jafari et al. (2017) use in their study?

A

The Musical Emotional Bursts (MEB) Test
was used to assess basic emotions in music
(happiness, sadness, and fear) and neutrality

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41
Q

What were the results of the Jafari et al. (2017) study?

A

̶ MEB total scores were significantly lower in the stroke groups than in the NC group (p < 0.001).
̶ The RBD group showed lower scores than the LBD group in recognizing sadness (p = 0.047) and neutrality (p = 0.015).
̶ In support of the “valence hypothesis” of right hemisphere dominance in processing negative emotions

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42
Q

What was the conclusion of the Jafari et al. (2017) study?

A

Conclusion: The stroke affecting the auditory cerebrum can cause acquired amusia with greater severity in RBD than in LBD.

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43
Q

Define TBI

A

̶ TBI is a disturbance of brain function caused by a bump, blow, or jolt to the head, penetrating head injury, or
explosive blast.
̶ The Glasgow Coma Scale (GCS) is commonly used to classify TBI severity.

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44
Q

Glasgow Come Scale

A
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45
Q

What are the 2 types of TBI?

A

contusion
concussion

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46
Q

What is contusion TBI?

A

‒ When the brain collides with the skull due to direct trauma, leading to tissue damage and hemorrhage.

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47
Q

What is contussion TBI characterized by?

A

‒ Characterized by localized bruising or bleeding, & neurological deficits (brain structural damage).

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48
Q

what does a contusion TBI commonly affect?

A

‒ Characterized by localized bruising or bleeding, & neurological deficits (brain structural damage).

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49
Q

What problems are associated with a contusion TBI

A

‒ Impaired cognitive functions depending on the lesion site (brain functional disruption).

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50
Q

What is concussion TBI?

A

‒ Is the result of a sudden, jarring movement or blow to the head.

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51
Q

What does concussion TBI not involve?

A

‒ Does not involve visible structural brain damage or bleeding.

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52
Q

What is contusion TBI characterized by?

A

‒ It is characterized by a brain functional disruption.

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53
Q

What problems are associated with concussion TBI?

A

‒ Temporary alteration in brain function, leading to a range of symptoms, such as headache, dizziness, confusion,
memory problems, and changes in behavior or mood.

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54
Q

What is the prevalence of APD in TBI?

A

16 to 58 percent

55
Q

What does prevalence of APD in TBI depend on?

A

Depends on parts of involvement, place of involvement, and which hemisphere of the brain is affected.

56
Q

TBI APD has deficits in?

A

‒ SIN performance
‒ Temporal sequencing ability (e.g., DPT)
‒ Frequency pattern recognition ability (e.g., FPT)

These aren’t the only tests that can be used, but they have normative data and good psychometric properties

57
Q

There are deficits in AEPs with TBI that are at different levels including:

A

Deficits in AEPs at different levels, including:
‒ The brainstem
‒ Auditory cortex
‒ Higher-order processing areas

Depending on place of involvement

58
Q

What are the 2 types of abnormal cell masses (location?

A

̶ Primary brain tumors developed in the brain tissue itself.
̶ Secondary or metastatic brain tumors spread to the brain from other parts of the body.

59
Q

What are the 2 BT types based on cell type?

A

̶ Malignant
̶ Benign

60
Q

What is the incidence of BT?

A

Average estimate of 3.4 new cases per 100,000 individuals per year.
* Varies among different ethnic populations.

61
Q

What is the clinical presentation of BT?

A

̶ Neurological Symptoms can be focal or general.
̶ Common presentations include:
̶ Seizures
̶ Loss of consciousness
̶ Symptoms reflecting increased pressure within the skull:
̶ Blurred vision, vomiting, headache, feeling less alert than usual, lack of energy, problems with moving or talking.

62
Q

What is an acoustic neuroma?

A
  • Acoustic neuroma/vestibular schwannoma, is usually a slow-growing tumor
    that develops on the auditory-vestibular nerve
63
Q

What are some common audiological signs and symptoms of acoustic neuroma?

A

̶ Facial numbness and weakness or loss of muscle movement
̶ Predominantly unilateral or asymmetrical hearing loss
̶ Rarely sudden hearing loss
̶ Tinnitus in the affected ear
̶ Unsteadiness or loss of balance
̶ Dizziness (vertigo)
̶ Changes in ABR (Hain, 2023)
̶ Impaired speech perception, dichotic listening
̶ Impaired sound localization

64
Q

What are the main signs of acoustic neuroma that should be reported?

A

̶ Tinnitus in the affected ear
̶ Unsteadiness or loss of balance
̶ Dizziness (vertigo)
̶ Changes in ABR (Hain, 2023)
̶ Impaired speech perception, dichotic listening
̶ Impaired sound localization

65
Q

What are the changes in ABR associated with acoustic neuroma?

A
  • Increased IPI of waves I-III is common.
  • Wave V delay (40-60%)
  • Only wave I (10-20%)
  • Sensitivity and specificity:
  • Sensitivity: 37-91%
  • Specificity: 57-97%
  • 1/3 of patients with small tumors (on MRI) have normal ABR
66
Q

Depending on the tumor size (acoustic neuroma), its removal can result in:

A

̶ Temporary or permanent hearing loss to severe to profound hearing loss.

67
Q

What can help identify smaller tumours?

A

Stacked ABR can help identify smaller tumours

68
Q

Define epilepsy

A
  • Definition: Epileptic seizures can be classified as:
69
Q

What are the 2 types of epilepsy?

A

̶ Generalized: Involving both brain hemispheres.
̶ Focal/partial: Arising within one hemisphere but potentially involving the other

70
Q

Epilepsy patients vary in what 4 things:

A

̶ Age at onset
̶ Cognitive, developmental, motor, and sensory signs
̶ EEG characteristics
̶ Triggers

71
Q

What are the 3 types of epilepsy with APD?

A
  1. Autosomal-Dominant Lateral Temporal Epilepsy (ADLTE):
  2. Temporal Lobe Epilepsy: APDs reported:
  3. Landau-Kleffner Syndrome (LKS)
72
Q

What is Autosomal-Dominant Lateral Temporal Epilepsy (ADLTE) characterized by?

A

‒ Auditory auras, buzzing, ringing, humming sounds, and perception of voices.
‒ Stimulated by some environmental sounds (a ringing telephone) or speech in a few cases.

73
Q

What are the deficits with temporal lobe epilepsy?

A

‒ Deficits in temporal processing:
‒ Temporal resolution (GIN test) and sequencing (DPT) deficits
‒ In individuals with mesial temporal sclerosis
‒ Deficits in IID (interaural intensity differences)
‒ Impaired dichotic listening & abnormal P3 latency and amplitude
‒ In the left temporal lobe epilepsy

74
Q

Landau-Kleffner Syndrome (LKS) Involves the ____ and manifests as ____

A

temporoparietal cortices, childhood epileptic seizures.

75
Q

Landau-Kleffner Syndrome (LKS) APD difficulties:

A

– Auditory verbal and nonverbal agnosia and language difficulties
‒ Impaired auditory working memory and attention in the chronic phase of LKS

76
Q

Define MS

A

MS is a demyelinating disease characterized by:
* Chronic damage to the CNS
* Episodes of neurological dysfunction in different brain areas over time.

77
Q

What is APD like in MS?

A
  • Deficits primarily at the brainstem level:
    ‒ Impaired localization
    ‒ Reduced MLD (Masking Level Difference)
    ‒ Abnormal ABR and MLR results
    ‒ Reduced temporal resolution (e.g., GIN test)
    ‒ Impaired temporal ordering (e.g., DPT)
78
Q

What is impaired in progressive MS?

A
  • Impaired DL:
    ‒ In progressive MS due to the corpus callosum (CC) atrophy (isthmus(6)/splenium(7) involvement
79
Q

People with MS have difficulties with all types of ____ tests

A

auditory fusion (MLD)

80
Q

Where might the place of involvement for MS be?

A

The place of involvement might be in upper levels (like the CC)

81
Q

If you see difficulties in dichotic test with MS, place of involvement = ____

A

corpus callosum

82
Q

If you see difficulties in MLD with MS, place of involvement = ____

A

brainstem

83
Q

If you see difficulties in MLD AND dichotic test with MS, place of involvement = ____

A

both CC and brainstem

84
Q

What are other causes of APD?

A
  • Long-term noise exposure can affect various levels of the auditory pathway (shipyard workers, in pilots)
  • Solvent Exposure
    ̶ APD at the brainstem and midbrain levels
  • Infections
    ̶ E.g., bacterial meningitis: impaired auditory figure-ground skills, and localization
  • Neurodegenerative diseases
    ̶ Alzheimer’s disease and Parkinson’s disease: Deficits in speech processing
85
Q

What are 3 ways to manage neurological disorders?

A
  • Regular assessments to guide appropriate management:
  • The use of FM systems/remote microphones
  • Customized auditory training programs (deficit-specific)
86
Q

Why are regular Ax important with the mgmt of neurological disorders?

A

̶ Because of the likely disease progression
̶ Patients may not spontaneously share information about their auditory difficulties.

87
Q

SSNHL is a ____ emergency

A

medical

88
Q

Define SSNHL

A

Is defined as a drop in hearing, 30 dB or greater SNHL, over at least three contiguous audiometric frequencies
within 72 hours.

89
Q

SSNHL typically affects ____

A

only 1 ear

90
Q

What is the peak incidence of SSNHL?

A

̶ The peak incidence between the fifth and sixth decades

91
Q

Who does SSNHL affect?

A

̶ Equal incidence in men and women

92
Q

SSNHL affects ____ to ____ per 100,000 people annually

A

5-27

93
Q

What are the causes of SSNHL?

A
  • 90% of cases are idiopathic.
    ̶ Idiopathic causes are mostly reversible (spontaneously or with medication)
  • It can result from a variety of identifiable causes, e.g.:
    ̶ SSNHL due to identifiable causes may be unreversible.
    ̶ Infections
    ̶ Head trauma
    ̶ Cochlear trauma with tearing or rupture of delicate inner ear membranes (Reissner’s membrane), an
    explanation for a “pop” sound before hearing loss in some cases.
    ̶ Autoimmune diseases
    ̶ Exposure to certain drugs that treat cancer or severe infections
    ̶ Vascular etiology (a sudden issue in the blood supply to the cochlea)
    ̶ Disorders of the inner ear, such as Ménière’s disease (fluctuating HL)
    ̶ Neurological disorders, such as multiple sclerosis (MS)
94
Q
  • Necessity and options for treating idiopathic SSNHL are ____.
A

controversial

95
Q

SSNHL Spontaneous recovery in ____ to ____ of cases.

A

45-65%

96
Q

With SSNHL what impacts a lower prognosis for hearing recovery?

A

̶ The severity of hearing loss (greater hearing loss)
̶ With tinnitus
̶ Higher ages
̶ Presence of vertigo or imbalance
̶ Shape of the audiogram

97
Q

SSNHL - Higher rates of recovery for ____
compared with ____

A

low-frequency or mid-frequency hearing losses, flat or down-sloping hearing losses

98
Q

What is the treatment for idiopathic SSNHL?

A

̶ Corticosteroids
̶ Steroids can reduce inflammation, decrease swelling, and help the body fight illness.

99
Q

What is the does of steroids for SSNHL?

A

Dose: Prednisone, 1 mg/kg/d, to a maximum of 60 mg, for 10 to 14 days (Kuhn et al. 2011).

100
Q

What are the types of steroids for SSNHL?

A
  1. Using pills
  2. Or intratympanic injection into the middle ear in the ENT office.
    ̶ For those who cannot take oral steroids
    ̶ Or to avoid steroids’ side effects
    • Increased appetite leading to weight gain, acne, rapid mood changes, thin skin that bruises easily, and muscle weakness
101
Q

Steroids should be used ____ for the best effect

A

ASAP

102
Q

What is normal cognitive aging?

A

includes brain structural/ functional changes that are non-pathological, within
normative age limits

103
Q

What is mild cognitive impairment (MCI)?

A

a syndrome characterized by cognitive decline greater than age-, sex, and education level-matched limits, but not notably interfering with daily activities

104
Q

What is the prevalence of MCI?

A

The prevalence of MCI ranges between 3-19% over 65yr

105
Q

What are the 2 subtypes of MCI?

A

amnestic (aMCI) and non-amnestic MCI

106
Q

What is the primary distinction between aMCI and MCI?

A

the area of episodic memory, the ability to learn and retain new information

Amnestic refers to if it is associated with memory

107
Q

Roughly ____% of MCI cases progress to developing dementia within ____ of diagnosis

A

60, 5yr

108
Q

What is subjective cognitive decline?

A

(when an individual starts to feel the cognitive decline. We may tell them that their assessments are WNL, but they may still be concerned regarding their cognitive abilities)

109
Q

If you are able to delay the ability of cognitive decline through cognitive training, this is called ____

A

“healthy aging”

110
Q

What is dementia?

A

Dementia is a progressive neurodegenerative disorder characterized by cognitive impairment, neuropsychiatric
symptoms, sensory and physical disabilities, dependency, caregiver burden, substantial health care expenditures, and
premature death

111
Q

Alzheimer’s disease (AD) dementia accounts for ____ of cases

A

60–80%

112
Q

What are the subtypes of AD?

A

Familial (5-10%) & sporadic (90-95%) over 65yr

113
Q

What are the neuropathological hallmarks of AD?

A

− Brain atrophy: Progressive neuronal and synaptic
loss in the limbic system, neocortical regions, and
the basal forebrain.
− Extracellular deposition of amyloid-beta (Aβ)
peptide
− Intracellular deposition of neurofibrillary tangles
(NFTs)
− Microgliosis and astrogliosis: an abnormal
increase in the number of activated microglia and
astrocytes at the site of neurodegeneration.

114
Q

Why is there a gender disparity in dementia statistics?

A

The reasons for this disparity are multifaceted and involve biological, social, and demographic factors

115
Q

What 8 reasons explain the gender disparity in dementia statistics?

A

− Longer Life Expectancy: Women generally live longer than men, and age is the most significant risk factor for
dementia. R36503
− Hormonal Differences: The decline in estrogen levels during menopause.
− Genetic Susceptibility: Higher risk of the APOE ε4 allele, a genetic risk factor for AD, in women.
− Gender Differences in Brain Structure and Function: Women may have distinct brain aging patterns.
− Diagnosis Bias: Women are more likely to look for assessment and diagnosis.
− Social and Lifestyle Factors: Historically, women in many societies have had less access to education and
cognitive engagement opportunities.
− Higher risk of Stroke and Cardiovascular in Women: e.g.: due to anemia, early menopause, and inactivity.
− Caregiving Burden: Caregiving roles may increase stress and reduce opportunities for cognitive and physical self-care.

116
Q

____ precede the cognitive symptoms of AD by several years and can increase the risk of the disease

A

Sensory impairments

117
Q

The prevalence of sensory impairments in dementia is higher than those who are ____

A

cognitively intact

118
Q

What types of sensory impairments occur in older adults with AD?

A

− Olfactory Impairment
− Vision impairments
− Age-related hearing Loss (ARHL/presbycusis)

119
Q

____ is a strong indicator of early dementia

A

olfactory impairment

120
Q

Explain age related hearing loss (ARHL) as it preceded cognitive symptoms of AD?

A
  • ARHL/presbycusis is a mild to moderate progressive
    bilateral sensory-neural hearing loss (SNHL).
  • It has a prevalence of 50-75% at the age 70yr or
    older
  • Its prevalence increases from 5–10% at age 40 to
    about 80–90% at age 85
  • ARHL is characterized by difficulty in speech
    perception in adverse listening conditions such as
    reverberant and noisy environments
121
Q

Central vs. Peripheral HL and AD

A
  • Central HL or APD is characterized by more difficulty understanding SIN that is not explained
    by cochlear (peripheral) HL and may not improve with hearing amplification
  • Central HL is less frequent than peripheral HL.
  • Thus, it may not have a noticeable contribution to dementia risk
122
Q

Explain ARHL and dementia

A
  • ARHL precedes the cognitive symptoms of dementia by several years (5-10yr) and can increase the risk of the disease
  • The prevalence of ARHL in patients with dementia
    is higher than those who are cognitively intact
  • For every 10 dB increase in ARHL over 25 dB, there
    is a 20% increased risk of developing dementia
  • typically this is associated with more severe levels of HL
123
Q

ARHL accounts for up to ____ of global dementia cases

A

9.1%

124
Q

Why is the ARHL a significant contributor to
AD?

A
  • The onset of ARHL may trigger a need for
    increased cognitive resources during speech
    comprehension, which can lead to auditory and cognitive-related cortical reorganization
  • This process leads to the reduction of
    cognitive resources available for other cognitive functions and subsequently to the
    decline of cognitive reserve
125
Q

Explain using up your cognitive resources with ARHL and how that can lead to AD

A
  • When you are struggling for information processing, you are using your cognitive resources more than you should be (this drains that part of the brain from cognitive resources)
    • What should be used for challenging things is being used for simple tasks (maladaptive neuroplasticity)
  • This isn’t just for ARHL; when you put any stress on the brain to process information this can happen
126
Q

What are the 2 hypothesis underlying the Link between ARHL and AD?

A

sensory hypothesis
common cause hypothesis

127
Q

Explain modifiable risk factors for dementia

A
128
Q

____ Is Linked to Cognitive Decline and AD

A

Chronic Tinnitus

129
Q

Why is tinnitus linked to cognitive decline and AD?

A

It is likely resulting from:
* Large-scale brain plasticity (pathological
plasticity) in various cortical and limbic
brain regions.
* Which is associated with behavioral
changes, such as:
̶ Frustration
̶ Inability to relax
̶ Difficulty in concentration
̶ Impaired executive control of attention
and working memory

130
Q

____ can Prevent/Decrease the Risk for cognitive Decline

A

Hearing Aids

131
Q

According to cohort studies, long-term hearing aid usage can lead to what 6 things:

A

− Auditory plasticity
− Improved cortical auditory evoked potentials (CAEPs)
− Improved working memory function
− Enhanced overall cognitive performance
− Improved mental health and quality of life
− Reduction self-perceived hearing handicap

132
Q

Clinical effectiveness of CI in ARHL:

A

− Speech understanding
− Cognition
− Working memory and sustained attention
− Improved mental health and quality of life

133
Q

Addressing modifiable risk factors of dementia

A

Advanced Diagnostic Audiology (11 decks)

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