Key words
age related hearing loss - presbycusis - central auditory processing disorder - neurocognitive disorder - Alzheimer disease - Parkinson syndrome - hearing rehabilitation
1. Introduction
Successful communication in complex listening situations requires not only the
detection of the target signal and the segregation of the scenario into different
sound sources. The listener must also track who is speaking, grasp the meaning of
the statement, memorize and compare it with already existing knowledge, suppress
irrelevant interfering signals, formulate an own response in parallel and execute it
at the right time. Longer conversations in groups require the integration of new
information with already expressed contents of each speaker while again and again
the attention switches between the persons involved.
This means that in order to assess and use the information contained in spoken
language, a fluent and swiftly functioning integrative system of perceptual and
cognitive processes is required. Both the auditory and cognitive systems are subject
to typical aging processes; and with higher age, the incidence of neurodegenerative
diseases increases, sometimes having a considerable influence on the ability to
communicate. In recent years, hearing disorders have increasingly become the focus
of scientific research as a potentially modifiable risk factor for neurocognitive
impairment in an aging society. In this review, hypotheses on the causal
relationship will be presented as well as specific auditory impairments in the
context of the most common neurodegenerative disorders of the elderly. Finally the
effect of hearing rehabilitation will be discussed.
2. Cognition and speech understanding
2. Cognition and speech understanding
2.1 Definition and domains
Cognition (Latin: cognoscere=to recognize, to experience, to
perceive) is a collective term for processes of reception, processing, storage,
and retrieval of information as well as their results (knowledge, attitudes,
beliefs, expectations). These processes can take place consciously,
e. g. when solving tasks, or unconsciously, e. g. when forming
opinions [1]. Human cognitive skills
include, among others, processes of perception, attention, learning and memory,
thinking, but also recognition of emotions, and control of one’s own
behavior. The ability to use these skills to solve problems, adapt to new
situations, and interact effectively with the environment is referred to in
psychology as “intelligence” (Latin
intelligentia=cognition, intellect). While Cattell’s
intelligence model distinguished only between fluid intelligence (innate,
experience-independent ability to reason and solve problems) and crystalline
intelligence (predominantly culture-dependent ability to apply acquired
knowledge), nowadays the Cattell-Horn-Carroll (CHC) model is considered the one
that most comprehensively describes the structure of intelligence [2]. It includes 16 factors from the areas
of acquired knowledge, thinking ability, processing speed, memory, sensory
processing, psychomotor skills, and kinesthetics and serves as the basis for the
most widely used intelligence tests.
For the diagnosis of neurocognitive disorders, the “Diagnostic and
Statistical Manual of Mental Disorders – DSM-5” [3] defines 6 cognitive domains on which the
diagnostic criteria are based and which can be assessed in standardized
neuropsychological testing ([Table
1]).
|
Cognitive domain
|
Subdomains
|
|
Complex attention
|
Permanent attention
|
Didived attention
|
Selective attention
|
Processing rate
|
|
Executive functions
|
Planning
|
Decision making
|
Working memory
|
Exploiting feedback/correting errors
|
Acting against habits/behavioral inhibition
|
Mental flexibility
|
|
Learning and memory
|
Immediate memory*
|
Short-term memory (including free recall, recall with cue
stimuli, and recognition)
|
Ultra long-term memory (semantic and autobiographical)
|
Implicit (procedural) learning
|
|
Speech
|
Speech production (including naming, word finding, word
fluency, grammar and syntax)
|
Speech comprehension
|
|
Perceptive-motor
|
Visuo perception
|
Visuo construction
|
Perceptive-motor
|
Practice
|
Gnosis
|
|
Social cognition
|
Recognizing emotions
|
Theory of mind (ability to observe the Erkennen von Emotionen
Theory of Mind (ability to pay attention to another
person's state of mind or experience)
|
*is sometimes included in the term of working memory.
2.3 Normal cognitive aging
Cognitive processes are subject to
chronological aging processes to varying degrees and are highly associated with
the loss of everyday functioning, onset of dementia, and general mortality [4]
[5]. It is well known that basal, knowledge-independent
“fluid” functions show a greater age decline than lifelong
acquired “crystalline” knowledge, which can still show growth
into old age [6]. A persons’
intelligence is seen as the result of function or knowledge build-up, loss, and
compensation mechanisms. This means in order to maintain cognitive performance
as fluid abilities are lost, we rely more and more on already established,
automated crystalline processes to accomplish tasks [6]
[7]. Research continues to address the extent to which training can
counteract functional loss and the importance of individual cognitive domains in
this process. In a large cross-sectional study on 48,537 subjects and evaluation
of normative values of standardized IQ and memory tests, Hartsthorne and Germine
were able to show that there is greater heterogeneity with regard to the time of
maximum functional capacity between the individual domains than previously
assumed [8]: short-term memory and
processing speed reach maximum values already in the teenage years, working
memory peaks in young adulthood with the onset of decline in the 30ies. Peak
performance in e. g. vocabulary and emotion recognition, on the other
hand, is reached only in the middle age and maintained over a much longer period
of several years. As an explanation for individual performance differences,
however, non-specific age effects, such as a general slowing, must be considered
in addition to these domain- and function-specific changes. Recent long-term
studies indicate that approximately 30-50% of individual differences in
age progression are due to a “general factor” [9].
In addition to significantly
reduced general processing speed and working memory compared to younger people,
loss of executive functions and episodic memory occur in older age [10]
[11]. Morphologically, changes are seen in the middle temporal lobe
(episodic memory) and the prefrontal/striatal system (executive
functions) [12]. Neurodegenerative
diseases such as Alzheimer’s disease or Parkinson’s syndrome
affect these areas to varying degrees and lead to specific functional
deficits.
2.4 Cognitive reserve
People of about the same age with similar central changes, e. g., in the
context of a neurodegenerative disease but also in the course of normal aging,
may nevertheless vary considerably in their clinical symptoms and cognitive
performance. To explain this observation, the concept of cognitive reserve was
introduced [13]. It refers to the ability
to compensate for newly occurred damage and to maintain existing functions by
using alternative neuronal networks [14].
Both congenital and acquired or environmental factors (e. g.,
intelligence, educational level, physical activity, recreational and social
activities) play a role. Differences in cognitive reserve are also considered as
an explanation for the individual impact of sensory impairment (e. g.,
hearing loss) in higher age [15].
2.5 Information processing model and cognitive concepts in relation with
hearing and speech comprehension
From a cognition-psychology perspective, spoken communication can be understood
as a process of information processing: The incoming stimulus is perceived by
the sensory system, processed, and finally leads to a reaction ([Fig 1], adapted from [16]). This complex process depends the
properties of the incoming stimulus (bottom-up) and is also influenced by
cognitive processes (top-down). In the theoretical model of Wingfield and Tun
[17] ([Fig 2]), the interactive roles of
peripheral, central, cognitive, and linguistic factors to speech understanding
are illustrated in more detail: In the periphery, the sensory system must
receive the spectral and temporal cues of the speech signal and pass them on to
the central auditory pathway for further processing with as little interference
as possible. In the next stage of central auditory processing (perceptual
system), binaural information is encoded in addition to spectral and temporal
features of the speech signal (especially signal onset and duration). The
so-called “object formation”, i. e. the ability to
recognize a target signal and to follow it in the presence of competing
background noise or speakers, also occurs at this level. This is followed by the
linguistic operations of sound analysis and lexical recognition at the word
level. Based on syntactic (position of a word in a sentence) and semantic (word
meaning) prior knowledge, sentences are captured. The comparison with contextual
information (speaker, situation, object, time, etc.) finally enables
comprehension within the conversation [18]. The single processing steps are influenced by cognitive abilities or
processes such as memory functions (prior knowledge, working memory) and general
processing speed, attention, and executive functions (top-down). At the same
time, the characteristics of the stimulus (e. g., speech rate, accent,
type and number of noise sources, reverberation etc.) determine subsequent
processing (bottom-up). Auditory and cognitive processes are so closely
intertwined that a sharp separation of “peripheral” and
“central” auditory functions does not adequately capture the
complexity of speech processing [19]. The
typical complaint of the elderly – to hear but to understand poorly
– is merely a clinical symptom of normal age-related changes in all
sections of this system from the periphery to the cortex, which may be
additionally impaired by neurodegenerative diseases.
Fig 1 Generalized model for bottom-up and top-down processing of
auditory information (adapted from [16]). The stimulus is first coded
into neural information in the periphery, relevant information is
selected and then interpreted in the next step. Finally, it is stored in
memory while the answer is formulated at the same time. The quality and
content of the stimulus influence further processing (bottom-up),
information that has already been extracted or recorded content can lead
to changes in the processing of subsequent stimuli (top-down).
Fig 2 Wingfield and Tun's information processing model
[17]. Sensory, perceptual and cognitive systems interact when processing
auditory information. The mixed input signal must first be broken down
into relevant (target signal) and irrelevant information (interfering
signal). The attention filter determines the extent to which the
individual signal components are further processed. Word recognition is
first achieved via several intermediate steps, and finally, after
further linguistic operations, discourse comprehension. The information
processing process can be influenced at all levels by both cognitive and
acoustic factors.
3. Age-related hearing loss
3. Age-related hearing loss
3.1 Prevalence and socio-economic consequences
In 2019, according to the WHO, about 1.5 billion people worldwide were affected
by hearing loss [20], and 430 million
(about 5.5% of the world population) had at least moderate hearing
impairment. The WHO expects this number to increase to 700 million people with
moderate or higher levels of hearing loss in the better hearing ear by 2050, out
of a projected total of 2.5 billion people affected. The individual development
of hearing throughout the life span depends on various protective and damaging
factors [21]. In addition to genetic,
biological, and environmental influences, individual lifestyle (nicotine abuse,
diet, noise exposure) also plays a role. Age-related hearing loss (ARHL)
represents the greatest socio-economic burden over a lifetime due to its high
prevalence in the population. According to current estimates, in 2019
approximately 42% of all people affected by hearing loss were at least
60 years old [20], and the proportion of
moderate or higher levels of hearing loss increases exponentially with higher
age (prevalence at 60-69 years: 15.4%; more than 90 years:
58.2%). WHO estimates the annual costs due to hearing loss to be
approximately $ 980 billion. In recent years, age-related hearing loss
has been increasingly identified as a potential risk factor for neurocognitive
disorders [22]
[23]
[24]
[25]. Positive effects of
audiological rehabilitation with hearing aids for the course of these disorders
[26]
[27]
[28] as well as
health-related quality of life [29] are
seen. Nevertheleess, in Europe, hearing aids are used by only about 33%
of the approximately 57 million people with hearing loss in need of care,
although they are widely available [20]
[30].
3.2 Age-related changes of the peripheral auditory system
Age-related degenerative processes affect both outer and inner hair cells,
supporting cells, stria vascularis, and spiral ganglion cells [31]
[32]
[33]
[34]
[35]
[36]. The pure-tone
audiogram typically shows a loss of high frequency hearing [36]
[37]
[38]. For medical expert
reports, DIN EN ISO 7029:2017 should be consulted, which allows estimation of
normal hearing for ages between 20 and 80+ years [39] ([Fig
3]). The current 3rd version is based on data from healthy
men and women published after 2000. Compared with previous versions, the average
hearing loss is lower for all age groups, reflecting changes in living and
working conditions.
Fig 3 Average hearing threshold progression for men and women aged
20-80+ according to DIN EN ISO 7029:2017:06 (according to [39]).
The 50th percentile of the respective age group is shown.
Based on experience from animal models regarding the underlying etiology, Dubno
et al. [37] classified audiometric
phenotypes of age-related hearing loss. A low-grade hearing loss up to
1 kHz and rather flat high-frequency hearing loss in indicative of
metabolically-induced atrophy and degeneration of the stria vascularis, whereas
a steeply declining hearing threshold between 2 and 8 kHz with normal
low-frequency hearing indicates a sensory disorder (hair or supporting cell
damage).
In the same study [37], approximately
11% of pure-tone audiograms were classified as “older
normal”, with an average hearing loss of no more than 20 dB HL
in the high-frequency range. Nevertheless, elderlies with normal pure-tone
audiograms also report hearing difficulties and tinnitus [40]
[41]. For this hidden hearing loss (HHL), different pathophysiological
mechanisms have been discussed in recent years [42]
[43]
[44]. In addition to disturbances of the
afferent synapse of the inner hair cells (cochlear synaptopathy [35]
[42]
[43]
[45]
[46]), demyelination processes (temporary loss of cochlear Schwann
cells [47] or in the context of
demyelinating neuropathy [48]), and
persistent dysfunction of the outer hair cells [49]
[50] have been described.
These changes lead to impaired transmission of temporal and spectral fine
structure [51], especially of rapid signal
changes as well as signal duration. The phonetic contrasts necessary for
accurate word recognition decrease, which manifests in reduced speech
understanding, especially in noisy environments, even before high-frequency
hearing loss is detected in the puretone audiogram.
Amplitude changes of wave I of the early auditory evoked potential elicited by
suprathreshold stimulation [34]
[46]
[51] or an altered SP/AP amplitude ratio in
electrocochleography [52] are discussed as
electrophysiologic markers of the disturbed cochlear function.
Age-related changes of the central auditory system
3.2.1 Structural-morphological as well as neurochemical changes
Aging processes affect the entire central auditory pathway from the cochlear
nucleus to the auditory cortex (see [53]
[54] for a comprehensive
overview). Throughout the lifespan, the human cortex is subject to
remodeling processes that become visible and measurable due to modern
imaging techniques such as magnetic resonance imaging. MR spectroscopy also
allows metabolic and neurochemical changes to be detected. In healthy
adults, there is a general brain volume reduction with increasing age [55]
[56]
[57]. Volume changes in
gray matter [58]
[59]
[60] and white matter [60]
[61]
[62] as well as cortex thickness [58]
[63] have been discribed. Regions particularly affected include
the temporal lobe, hippocampus [60]
[64]
[65] and prefrontal cortex [59]
[61]
[66]
[67]. Lin et al. [68] demonstrated that hearing loss
accelerates volume decline in both the total volume and the right temporal
lobe. Further studies showed gray matter reductions beyond the age norm in
the superior and medial temporal gyrus [69] and superior and medial frontal gyrus [69]
[70]
[71], primary auditory
cortex [72]
[73], and occipital lobe and
hypothalamus [70]. Diffusion-weighted
MR images also showed changes in myelination, fiber density, and axonal
parameters in the superior olive complex, lemniscus lateralis, and inferior
colliculus [69]
[74]. MR spectroscopy has demonstrated
dysfunction of GABAergic neurotransmission in the central auditory system of
patients with presbycusis [54]
[75]
[76].
This means that, on one hand, structural changes in the central auditory
pathway already occur in the course of normal aging, which can have a
negative effect on speech understanding; on the other hand, age-related
hearing loss additionally leads to impairment of further areas in the
association cortex [77].
3.2.2 Changes of central-auditory processing and perception
Structural and neurochemical changes in the central hearing pathway lead to
impaired encoding of temporal characteristics of speech. As part of normal
aging processes, there are changes in neural timing and precision in speech
processing [18] with implications for
comprehension of speech both in quiet and in noise. In general, the ability
to perceive rapid temporal changes in the speech signal decreases. That is,
older people need larger differences or temporally longer features (voice
onset time, vowel duration, pauses etc.) to distinguish individual speech
sounds [78]. If the speech signal is
additionally spectrally altered, these difficulties increase, as several
studies with vocoded speech have shown [79]
[80]. This is
particularly relevant with regard to cochlear implant fitting. Impaired
neural encoding of signal onset is also thought to be the cause of greater
difficulty for elders to understand speech with altered speed, stress, or
rhythm. For example, research by Gordon-Salant et al. demonstrated that
older normal-hearing subjects have significantly greater problems with
understanding fast speakers or speech with a foreign accent [81]
[82].
The ability to separate single speech streams, i. e. to follow a
speaker in the presence of noise or competing speakers, also declines with
age and has been demonstrated in a multitude of studies [83]
[84]
[85]
[86]. This has been attributed to
impaired processing of temporal fine structure as well as perception of
brief amplitude changes in the envelope of the speech signal
(“listen to the dips”) [87]. In addition, age effects have been demonstrated in the
binaural processing of speech signals [88]
[89]
[90].
A comprehensive review of age-related electrophysiological changes in the
central auditory pathway can be found in [91]. Early auditory evoked potentials, especially the so-called
frequency following response (FFR) after stimulation with both tone and
speech signals, objectify impaired temporal processing at the brainstem
level. Depending on the experimental design, late auditory evoked potentials
allow both the differential detection of disturbed temporal processing of
auditory stimuli at the cortical level, independent of attention and
cognition (N1-P2) and the assessment of cognitive processes if the
potentials are measured in an event-related manner (P300, N200). Therefore,
the latter can also be used to distinguish between normal aging processes,
mild cognitive impairment, and Alzheimer’s dementia [92].
3.2.3 Central presbycusis
In English-speaking countries, the described age-related disorders of central
processing and perception of auditory information with age-appropriate
pure-tone hearing threshold are summarized under the term of central
auditory processing disorder (CAPD) or central presbycusis [93]
[94]. The disorder is considered to have multifactorial causes,
correlations with age-related cognitive disorders are seen, clinically, a
sharp separation between cognitive and auditory processing is hardly
possible.
The German Society of Phoniatrics and Pediatric Audiology defines auditory
processing and perception disorders in more detail: According to the current
guideline, the diagnosis of auditory processing and perception disorders
should only be made if, at age-appropriate pure-tone hearing thresholds,
there are deficits in analysis, differentiation, and identification of time,
frequency, and intensity changes of acoustic or auditory speech signals as
well as processes of binaural interaction (e. g., for sound
localization, lateralization, noise suppression, and summation) and dichotic
processing that cannot be better explained by other disorders, such as
attention deficits, general cognitive deficits, cross-modality mnestic
disorders [95]. The deficits in the
auditory domain must be significant compared to language-independent
cognitive performance. At the same time, there is a high comorbidity to
e. g. disorders of attention. Clinically, it must then be decided,
taking into account all findings, which disorder is leading. With regard to
differentiation from infantile auditory processing and perception disorder
and in view of the usually modality-spanning aging processes, it seems to
make sense to rather use the term of “central presbycusis”
for disorders of central auditory processing newly occurring in older
age.
3.3 Influence of cognitive processes on speech comprehension
In order to follow a conversation successfully and participate in it, listeners
and speakers must not only perceive what is being said and understand the single
words even under unfavorable complex conditions (background noise,
reverberation, high speech rate, accent, etc.), but also grasp the content in
context, compare it with their own prior knowledge, and formulate a response. On
the cognitive level, this requires, among other things, keeping one’s
attention on the target signal, storing it in working memory, and matching it
with long-term memory – as quickly as possible in order to be able to
follow the rest of the conversation. Working memory, executive functions, and
processing speed are therefore seen as the most important cognitive factors for
speech comprehension, especially in noise [96], and a large number of studies have investigated them
(e. g., executive functions and attention [97]
[98], processing rate and working memory [87]). The importance of auditory and
cognitive factors and their interaction for the quality of speech comprehension
has been increasingly taken into account in the last 10-20 years, so that the
term of “cognitive hearing science” has been established [99].
3.3.1 Inhibition control
In the information processing model by Wingfield and Tun [17] ([Fig 2]), the “attention filter” symbolizes the
ability to selectively follow a single signal in the presence of noise or
competing speakers and thus to suppress further processing of the
non-selected speech streams very early in the process. Disruption of
inhibition control, e. g., in the course of normal aging, limits
this ability and may thereby impair speech comprehension.
At the word level, perceived phonemes must be matched with the mental
lexicon. The success of this lexical process depends on the frequency of
occurrence of a word within a language as well as the number of words, with
overlapping phonemes (neighborhood density). The Neighborhood Activation
Model [100] theorizes that the more
frequently a word occurs within a language (high frequency) and the fewer
words with overlapping phonemes (low neighborhood density), the easier it is
to recognize the word correctly. Accordingly, words with high neighborhood
density have more competitors that must be suppressed by the listener to
enable correct word retrieval. Research on the neighborhood density effect
has shown that in older adults, there is a significant relationship between
measures of inhibition control and speech comprehension in noise
(e. g., [101]). In addition,
with increasing age, frequently occurring competing words are more
intrusive, i. e. they are more often misidentified as a target
signal [102]
[103].
3.3.2 Working memory
In cognition psychology, working memory is understood as limited resource
that allows information to be kept and processed in immediate memory [104]. In phonological analysis, working
memory is considered to play a significant role as an interface to long-term
memory. To explain why in some situations speech understanding is effortless
while in others increased listening effort is required, Rönnberg et
al. developed the Ease of Language Understanding (ELU) model (see [105] for a comprehensive review). The
incoming multimodal signal is quickly and automatically matched (within
180-200 ms [16]) with the mental
lexicon. If a minimum number of matching phonological attributes is found,
the implicit lexical process proceeds rapidly, and the signal is understood.
If no match is found, semantic and episodic long-term memory must be
explicitly accessed with the aid of working memory to enable language
processing. If the input signal is difficult to understand –
e. g., due to hearing impairment or unfavorable acoustic environment
– it must be held longer in working memory and more cognitive
resources must be expended to understand what is being said. Listening
effort increases [106]. In particular,
a significant dependence on working memory capacity has been shown for
speech comprehension in noise, independent of age [107]
[108].
3.3.3 Significance of the context
Phonological matching can be facilitated by the aid of contextual
information, allowing partial compensation for the deficits caused by
hearing impairment. Benichow et al. [109], for example, demonstrated that although hearing loss had a
significant effect on speech understanding in noise, it decreased with
increasing probability of the target word to occur in the context of the
sentence. At the same time, both age and cognitive performance (especially
working memory as well as processing speed) were significant predictors of
speech understanding independent of the amount of contextual
information.
Increasing deficits in inhibition control with age may, in turn, contribute
to wrongly identify acoustically unintelligible words as utterances that are
probable within context [110]
[111]
[112]. A recent study by van Os et al. [113] revealed that older subjects are
also able to rationally adjust their response behavior within a trial and,
for example, rely more on the acoustic information than the context when the
context offered is misleading.
3.3.4 Listening effort
If cognitive resources must be used to understand disturbed speech signal,
they are lacking for other processes such as encoding what is heard into
memory. The so-called “Framework for Understanding Effortful
Listening” (FUEL) [114]
describes successful speech comprehension as dependent on the quality of the
acoustic stimulus, the demand of the task, and the listener’s
motivation to exert the effort necessary to achieve it. Increased listening
effort may not only deplete available cognitive resources more rapidly, but
also reduce the listener’s motivation to exert that effort at all
– even if the utterance itself was correctly understood.
4. Hearing disorders in frequent neurodegnerative diseases in higher ages
4. Hearing disorders in frequent neurodegnerative diseases in higher ages
4.1 Neurocognitive disorders
Neurocognitive disorders (NCD) are disorders that are associated with a
subjective or objective loss of previously existing cognitive abilities in at
least one of the 6 cognitive domains of complex attention, executive function,
learning and memory, language, perceptual-motor, social cognition (cf. [Table 1)] and do not only occur
exclusively in the context of delirium or can be explained by another existing
mental disorder (such as major depression, schizophrenia) [3]. The DSM-5 distinguished between mild
(minor) and severe (major) forms, which are seen on a continuum of cognitive and
functional impairment. In minor NCD, moderate cognitive performance impairments
are present but do not affect the ability to perform activities of daily living
independently, although greater effort or compensatory strategies may be
required. In major NCD cognitive performance has significantly declined and
impairs independence in performing activities of daily living. The impairment in
everyday activities can me mild (only instrumental activities such as household,
handling money), moderate (limitations in basic activities of daily life like
eating, dressing), or severe (complete dependence). The major NCD is intended to
replace the widely used, and sometimes stigmatizing, term of dementia. Specific
pathophysiological processes are known for the majority of neurocognitive
disorders, allowing further specification of both minor and major NCD ([Table 2]).
|
Minor/major NCD due to
|
|
Alzheimer’s disease
|
|
Fronto-temporal lobe degeneration
|
|
Lewy body dementia
|
|
Vascular disease
|
|
Cranio-cerebral trauma
|
|
Substance/drug consumption
|
|
HIV infection
|
|
Prion disease
|
|
Parkinson’s syndrome
|
|
Huntington disease
|
|
Other medical factors
|
|
Multiple etiologies
|
|
Not specified
|
4.1.1 Socio-economic relevance
Neurocognitive disorders predominantly affect older age, so a global increase
in the number of cases is expected with demographic change. Based on data
from the Global Burden of Disease Study of 2019 [115], the number of dementia patients
worldwide was estimated to 55.4 million in 2019, and projections expect and
increase to 152.8 million affected people in 2050 [116]. In some regions, however,
decreases in new cases were observed: A recent analysis of the incidence
rate over the last 25 years for Europe and North America showed a decrease
in the incidence of dementia 13% per decade [252]. According to the German Alzheimer
Society, approximately 1.8 million people in Germany were affected by
dementia at the end of 2021, the vast majority (1.7 million) were over 65
years of age [117], and women were
twice as likely to develop the disease than men. The number of newly
diagnosed cases in the 65+ age group was estimated at 430,000 [117]. It is expected to increase to 2.8
million affected persons by 2050. At the same time, due to demographic
change, the number of working-age individuals caring or paying for the care
of dementia patients will decrease significantly [118].
In view of this major social challenge, prevention is of particular
importance. An expert consortium recently identified 12 potentially
modifiable risk factors, which together explain almost 40% of all
dementias ([Table 3]). Hearing loss
is the most important risk factor in middle age.
|
Time
|
Risk factor
|
Relative risk
|
Attributable risk
|
|
Younger age (<45 years)
|
Education
|
1.6
|
7.1%
|
|
Middle age (45-65 years)
|
Hearing loss
|
1.9
|
8.2%
|
|
Cranio-cerebral trauma
|
1.8
|
3.4%
|
|
Hypertension
|
1.6
|
1.9%
|
|
Excessive alcohol consumption
(>24g/d)
|
1.2
|
0.8%
|
|
Obesity (BMI ≥ 30)
|
1.6
|
0.7%
|
|
Higher age ( 65 Jahre)
|
Smoking
|
1.6
|
5.2%
|
|
Depression
|
1.9
|
3.9%
|
|
Social isolation
|
1.6
|
3.5%
|
|
Physical inactivity
|
1.4
|
1.6%
|
|
Air pollution
|
1.1
|
2.3%
|
|
Diabetes
|
1.5
|
1.1%
|
*the attributable risk indicates the percentage by which one
can reduce the incidence of disease if one completely eliminates the
risk factor; BMI = Body-Mass-Index.
Societal changes such as improved education as well as adjustments in
individual lifestyles could therefore contribute to a significant reduction
in the risk of dementia and thus improve the quality of life in older age.
For example, Norton et al. [119]
estimated that even a prevalence reduction of 10-20% of each risk
factor per decade could reduce the number of global Alzheimer patients by
8.8-16.2 million in 2050.
The national dementia strategy paper, adopted in 2020, seeks to address the
increasing societal demands of dementia and aims to improve the lives and
care of people with dementia in Germany. However, a concrete package of
measures for the implementation of prevention strategies based on the
above-mentioned risk factors is missing to date [120].
4.2 Alzheimer’s disease
Alzheimer’s disease (AD) is the most common cause of major NCD,
accounting for an estimated 2/3 of all cases [121]. It is a progressive neurodegenerative
disease with characteristic biological changes, primarily associated with memory
impairment, leading to dementia [121]. The
biological feature is the increasing deposit of β-amyloid and tau
proteins in the brain of affected individuals. Approximately, 95% of the
cases occur sporadically and usually after the age of 65 years (“late
onset Alzheimer’s disease”, LOAD), in less than 5% of
the cases, the first symptoms appear before the age of 60 years (“early
onset Alzheimer’s disease”, EOAD) [122]. The sporadic form usually progresses
slowly over years to decades, whereas more rapid courses are often observed in
EOAD. The most important genetic risk factor for the sporadic disease is the
so-called ApoE-4 allele of the gene for apolipoprotein E, which is involved in
lipid metabolism and plays a role in amyloid deposit. For the early onset of the
disease, 3 genes (presenilin-1, presenilin-2, amyloid precursor protein) have
been identified so far as risk factors [121], which occur in a familial cluster in about 1% of all AD
patients. In the course of the disease, β-amyloid accumulates between
the nerve cells, initially in the form of oligomers, later as amyloid plaques,
leading to a disturbance of nerve cell function and the associated development
of clinical symptoms. Since about 20 years, subtypes of β-amyloid can be
detected in CSF and used as biomarkers for AD (Aβ42 and
Aβ42/Aβ40 ratio). In addition
to extracellular amyloid deposits, intracellular deposits of defective tau
proteins are typically found as neurofibrillary bundles or
“tangles”. Total tau and phosphor-tau concentrations can be
determined in the CSF. The first one indicates nonspecific nerve cell damage and
may also be elevated in other neurodegenerative diseases or strokes. Phospho-tau
(pTau), on the other hand, is significantly elevated exclusively in AD. The
German S3 Dementia Guideline therefore recommends the combined measurement of
Aβ42, total tau, and pTau to differentiate
neurodegenerative and other causes in unclear dementias [123].
The amyloid deposits can also be visualized by positron emission tomography
(amyloid PET).
The leading clinical symptom is slowly progressive disturbances primarily of
learning and memory, but also of attention as well as spatial and temporal
orientation [121]
[122]. Radiologically, in addition to a
general brain volume reduction, atrophy of the medial temporal lobe, especially
the hippocampus, is typically found [124].
In approximately 10% of the cases, the disease manifests with atypical
symptoms such as loss of visuospatial abilities (posterior parietal atrophy,
Benson syndrome) [125] or as frontal or
logopenic variants [126]
[127], both of which resemble typical
fronto-temporal dementias. Parieto-temporal metabolic disorders can be
visualized by fluorodeoxyglucose PET (FDG-PET) and assist in confirming the
diagnosis. Cognitive function loss is usually accompanied by neuropsychiatric
symptoms, such as apathy, agitation, anxiety, sleep disturbances, and
depression.
Alzheimer’s disease is nowadays understood as a continuum, as the
biological processes begin years to decades before the onset of the first
symptoms and result in cognitive changes as the disease progresses. Based on the
biological markers, it is possible to identify patients as affected by
Alzheimer’s disease already at the preclinical stage or at the stage of
mild cognitive impairment (minor NCD or mild cognitive impairment, MCI).
4.2.1 Hearing loss and Alzheimer’s disease
Already in 1993, Sinha et al. [128]
reported the involvement of the auditory system in Alzheimer’s
disease. Amyloid plaques and intracellular neurofibrils were detected in the
medial geniculate corpus and inferior colliculus, primary auditory cortex,
and auditory association areas. A functional feature of temporo-parietal
changes in AD is considered to be a disturbance in auditory scene analysis,
i. e., the ability to identify auditory objects –
e. g., a speaker – and to follow them even in the presence
of noise [129]
[130]
[131]
[132]
[133]. For example, Goll et al. [129] demonstrated that Alzheimer
patients were significantly worse at discriminating spectrally and
temporally altered environmental sounds compared to healthy individuals with
comparable peripheral auditory thresholds when non-verbal working memory was
taken into account, while the ability to perceive pitch and timbre remained
the same. Coeberg et al. [134] also
found significantly more auditory agnosia for environmental sounds in
patients with mild Alzheimer’s disease compared to healthy
individuals, with 37% of patients showing impairment in recognition
and 57% in naming test sounds. The mean hearing threshold of the
patients affected by agnosia was significantly higher, independent of age.
This means, peripheral hearing loss in combination with Alzheimer’s
pathology increases the likelihood of the occurrence of further central
auditory deficits (in this study, an odds ratio of 13.75 versus healthy
subjects).
Already in 1986, Uhlmann et al. [135]
described a correlation between peripheral hearing and significantly faster
cognitive performance loss in AD. In a long-term study of 639 cognitively
healthy individuals at study inclusion [136], an increase in dementia risk of 20% was shown for
each 10 dB increase in mean hearing threshold. Broken down by degree
of hearing loss, the hazard ratios were 1.89 for low, 3.00 for moderate, and
4.94 for severe hearing loss. A meta-analysis of 33 studies confirmed the
association of peripheral hearing and cognitive function [137]. The cognitive performance of
patients with hearing loss was lower than that of hearing healthy
individuals, regardless of whether the hearing loss was treated or not.
Nevertheless, the difference between individuals with treated hearing loss
and hearing healthy individuals was more than half. Hearing loss had a
negative effect on all cognitive domains investigated (attention, processing
speed, working memory, long-term memory, executive functions, semantic and
lexical knowledge), but the effect size was small (accounting for
4-6% of variance).
A similar relationship has been shown for central hearing impairment. As
early as 1996, Gates et al. [138]
reported a 6-fold higher risk of dementia for patients with central hearing
impairment, and further large longitudinal and cross-sectional studies came
to similar conclusions [139]
[140]
[141]
[142]
[143]. Central hearing impairment in
particular has therefore been discussed as a possible harbinger of later
dementia [133]
[138]
[140]
[144]. A recent
meta-analysis [145] concluded that
although a number of subjective audiometric methods for assessing central
auditory processing (including speech in noise, dichotic
hearing/binaural processing, time-compressed speech) can
discriminate well between normal cognitive aging and mild cognitive
impairment or AD, a reliable differentiation between MCI and AD has not yet
been possible. Moreover, whether in the preclinical phase of AD without
cognitive impairment these investigations can contribute to an earlier
diagnosis than by the currently known neurological and biological markers
remains open [146].
Auditory, event-related potentials could potentially close this gap. In a
study of 26 patients with a positive family history of AD, it was shown that
carriers of mutations in the presenilin-1 and APP genes already show
significant changes in central auditory potentials even before cognitive
deficits become clinically manifest [147]. The latency delay of late auditory-evoked potentials N100,
P200, N200, and P300 demonstrated in this study was taken as an
electrophysiological sign of slower cortical information processing. A later
meta-analysis by Morrison et al. [92],
evaluating studies published between 2005 and 2017 on auditory-evoked
potentials in patients over 60 years of age, concluded that P300 and N200
are appropriate electrophysiological markers for distinguishing normal
cognitive aging, mild cognitive impairment, and AD.
4.3 Parkinson’s syndrome (PS)
Parkinson’s syndrome is the most common neurodegenerative disease after
Alzheimer’s disease [148]
[149]. According to a recent epidemiological
estimate based on health insurance data of 3.7 million insured persons,
approximately 420,000 people in Germany were affected in 2015 [150], the standardized prevalence amounted
to 511.4/100,000.
The incidence increases with higher age: while about 50/100,000 of the
65-year-old people are affected, about 400/100,000 patients are found in
the age group of 85 years and older [151].
Due to demographic change, but also earlier detection, the number of people
affected by PS in the EU is expected to increase to about 4.25 million by 2050
[152]. Parkinson’s syndrome
(PS) comprises an etiologically and phenotypically heterogeneous group of
disorders. In addition to idiopathic Parkinson’s syndrome (IPS, about
75% of all cases), a distinction is made between genetic forms as well
as Parkinson’s syndromes in the context of other neurodegenerative
diseases (atypical PS, multisystem atrophy, Lewy body-type dementia, progressive
supranuclear gaze palsy, corticobasal degeneration) and symptomatic (secondary)
Parkinson’s syndrome (drug-induced, posttraumatic, toxic, metabolic,
inflammatory, tumor-related) [153]
[154]
[155]
[156]. In addition to the
cardinal motor symptoms (akinesia/bradykinesia, resting tremor, rigor,
and postural instability), a wide variety of accompanying sensory, autonomic,
psychological, and cognitive symptoms may occur and significantly impair quality
of life [157]
[158]. Cognitive disorders mainly affect
executive functions, such as planning, anticipatory thinking, working memory,
and difficulties in switching attention between different tasks.
The incidence of so-called Parkinson’s dementia is estimated in
international cross-sectional studies to be between 20-44%, which
corresponds to a 3-6-fold higher risk of disease for Parkinson patients compared
to non-affected individuals [159]
[160]. In a German cross-sectional study of
873 patients with idiopathic Parkinson’s syndrome, 28.6% of the
patients met the diagnostic criteria for dementia according to DSM-5, with the
frequency increasing significantly with higher age as well as disease stage
[158]. The British CamPalGN study
followed 142 patients newly diagnosed with IPS between 2000 and 2002 [161], 46% of this population
developed dementia within the 10-year follow-up period, again including age at
diagnosis and disease stage as significant prognostic factors.
4.3.1 Hearing loss and Parkinson’s syndrome
Hearing loss is discussed as another non-motor accompanying symptom of PS
[162]
[163]
[164]
[165]
[166]. Several studies have shown that
hearing impaired people suffer more frequently from PS [162]
[167]. In pure-tone audiometry, predominantly high-frequency
losses [168]
[169]
[170]
[171] are found that
exceed the extent of merely presbycusis [169]
[172]
[173]
[174]
[175]. A British
case-control study of 55 patients with PS and early onset (≤55
years) found unilateral or bilateral hearing thresholds deviating from the
age norm in 64.7% of patients and 28% of the age- and
sex-matched control group [169]. No
difference was found in brainstem audiometry between the two groups in this
study, so the authors assumed pure cochlear involvement. The suggestion of
dopamine-dependent cochlear dysfunction is supported by evidence of reduced
DPOAE amplitudes that improved with levodopa substitution [172]; in this study, DPOAE dysfunction
correlated with the clinical severity of Parkinson’s syndrome.
Another study group found additional significant lateral differences.
Cochlear function measured by DPOAE and pure-tone audiometry was not only
worse in Parkinson patients than in the control group of the same age, but
also significantly more pronounced on the ipsilateral ear of motor symptoms
[176].
Beyond tone audiometric changes, difficulties in the perception of rhythms
and tonal differences [177]
[178] have been reported.
A number of studies have demonstrated changes in the morphology, latency, and
interpeak intervals of early auditory brainstem response (ABR) in PS
patients [168]
[179]
[180]. Similarly, reduced amplitudes and prolonged latencies of
vestibular evoked potentials (VEMP) were found [179]
[181]
[182]. The
event-related potential P3 is suitable to detect stage and progression of
Parkinson’s syndrome. The subject is offered sequences of repetitive
standard stimuli that are rarely interrupted by a deviant stimulus
(so-called oddball paradigm). The evoked potential (P300, P3a, P3b) is
dependent on attention and working memory and therefore seems to be suitable
to assess the impairment of executive functions in PS [183]
[184]
[185]
[186]
[187]. With increasing severity, there is a reduction in amplitude
as well as prolongation of latency, so that patients with and without
Parkinson’s dementia can be distinguished electrophysiologically
[188]
[189].
Although auditory stimuli and music are used for the treatment of
Parkinson-related gait disorders and postural instability [190]
[191]
[192], the importance
of auditory rehabilitation for Parkinson patients is not discussed in
therapy studies.
5. Correlation of hearing loss and cognitive impairment
5. Correlation of hearing loss and cognitive impairment
The importance of cognitive processes for speech comprehension, especially in
challenging listening situations, is well established. Age-related deficits lead to
restrictions in communication ability, social isolation and, associated with this,
to psychological stress and reduced quality of life. The question of a possible
causal relationship between hearing loss and reduced cognitive abilities up to
manifest dementia has increasingly become the focus of scientific research in recent
years (see comprehensive reviews in e. g. [53]
[146]
[166]
[193]
[194]
[195]
[196]). The analysis of already published study results is complicated by the
great heterogeneity of the collected data, both in terms of audiological and
cognitive parameters, as well as in terms of the studied groups, recorded
influencing factors, and duration of follow-up.
Usually, the pure-tone hearing threshold is used for the assessment of (peripheral)
hearing loss, but already here, there are differences in the grouping of the
included subjects, depending on the method used to differentiate between subjects
with and without hearing loss.
On the basis of 3 long-term studies [136]
[197]
[198]
(at least 5 years of follow-up) of subjects without cognitive impairment with tone
audiometrically determined hearing threshold, the Lancet Commission [24]
[25]
calculated a relative risk of 1.9 for developing dementia in the presence of hearing
impairment (defined as hearing loss greater than 25 dB HL in the pure-tone
audiogram) in middle age (55 years and older) compared with normal hearing subjects.
Hearing loss in middle age has been identified as the most important modifiable risk
factor for developing dementia.
Few studies explicitly address the relationship between central auditory disorders
and dementia or cognitive deficits in old age. A meta-analysis by Dryden et al.
[199] identified 25 studies that
investigated the relationship between cognitive performance and speech understanding
in noise as a measure of central hearing impairment. For both the subset of studies
that included only peripherally normal hearing subjects (16 articles) and studies
that also included subjects with at most moderate hearing loss (up to 70 dB
HL, 9 studies), the overall correlation (r=0.31 [normal hearing],
r=0.32 [up to moderate hearing loss]) of cognitive function and speech
understanding in noise was weak. Broken down by cognitive domains, the strongest
correlation was seen for processing speed (r=0.39), followed by inhibition
control (r=0.34), working memory (r=0.28), and episodic memory
(r=0.26), whereas global measures of crystalline intelligence showed a
significantly weaker correlation (r=0.18).
Wayne and Johnsrude [194] state that the use of
global cognitive screening tests such as the Montreal Cognitive Assessment (MoCa
[200]), the Mini-Mental State Test (MMST
[201]), and the Modified Mini-Mental State
Test (3MS [202]) in normal aging individuals
shows little variability, and thus may underestimate the impact of hearing loss on
cognitive function.
At the same time, the presence of hearing impairment may interfere with the
performance in cognitive tests and lead to an overestimation of the cognitive
deficit present, especially when instructions are given verbally, as shown by
several studies in normal-hearing, cognitively healthy subjects with simulated
hearing loss [203]
[204]
[205]. Therefore, special versions of cognitive screening instruments for
hearing-impaired people have been developed, which should be used preferentially in
the future (refer to Völter et al. [206] for a comprehensive overview).
5.1 Explanatory models for the interaction of hearing and cognition
In order to explain the relationship between (age-related) hearing loss and
cognitive decline, a number of models are discussed, which will be briefly
described below. A comprehensive review is provided by Wayne and Johnsrude [194].
5.1.1 Model 1: Cognitive load on perception hypothesis
Declining cognitive capacity places increasing load on perception so that no
longer sufficient resources are available for the processing of sensory
information. This leads to an audiometrically measurable hearing impairment
[207]
[208]. A study by Kiely et al. [209] seems to confirm this theory.
After analyzing longitudinal data from a total of 4221 subjects, the authors
concluded that, in addition to age and hypertension, a score of less than 24
on the Mini-Mental State Test was among the independent predictors of annual
hearing threshold deterioration. Ex post, it remains unclear to what extent
the hearing impairment itself affected the test result, because the test
used was presented verbally ([Fig
4a]).
Fig 4 Explanatory models for the connection between
age-related hearing loss and cognitive function loss: A) Cognitve
load on perception hypothesis: Loss of cognitive function leads to a
measurable hearing impairment via the disturbed processing of
sensory information B) Information degradation hypothesis:
Age-related hearing loss degrades the information available for
further processing. Temporarily cognitive resources are used to
compensate, which are then no longer available for other cognitive
processes. This process is potentially reversible by providing
hearing aids which improve the information available. C) Sensory
deprivation hypothesis: The sensory deprivation associated with
presbycusis leads to permanent structural brain changes and
permanent loss of cognitive function D) Common cause hypothesis:
Common endogenous and exogenous causes lead to both a loss of
cognitive function and presbycusis.
5.1.2. Model 2: Information degradation hypothesis
This model assumes that reduced or impaired peripheral hearing triggers an
upward cascade in which cognitive resources are applied to compensate for
the hearing impairment, rendering them unavailable for other cognitive
processes [207]
[210]. Evidence for this assumption is
high; for example, several studies have shown that the ability to recall
words or sentences deteriorates during a demanding perceptual experiment in
elderly subjects [17]
[211]. The associated increased
listening effort has negative effects on working memory and inhibition
control [17]. The cognitive loss in
this model is reversible – it is assumed that if peripheral input is
improved, e. g., by compensating for hearing loss with hearing aids,
at least partial recovery of cognitive performance is possible ([Fig 4b]).
5.1.3 Model 3: Sensory deprivation hypothesis
This model assumes that a lasting shift in resources to compensate for
perceptual deficits leads to a permanent loss of cognitive function.
Neuroplastic remodeling in central auditory areas and neurovascular and
neurophysiological changes similar to those seen in dementia are postulated
as possible mechanisms [106]
[212]
[213]
[214]. For congenital
or early acquired hearing loss, the associated neuroplastic changes are
already well established [215]
[216], but cognitive performance is
little affected [217]. Sensory
deprivation alone is thus insufficient as an explanatory model for cognitive
loss in old age ([Fig 4c]).
5.1.4 Model 4: Common cause hypothesis
General age-related neurodegeneration processes could have negative
consequences for both cognitive performance and sensory perception [207]
[208]. For example, the decrease in processing speed is discussed
as one such common factor [218]. In
addition to genetic causes [219],
cerebrovascular disease [220] and
general loss of physical functioning have been considered as possible
mechanisms ([Fig 4d]).
5.1.5 Multifactorial model
None of the above assumptions alone can explain all observed changes in older
age; a combination of several effects is most likely. Wayne and Johnsrude
[194] therefore postulated a
multifactorial model illustrating the interdependence of sensory and
cognitive processes ([Fig 5]).
Fig 5 Multifactorial model of the connection between
age-related hearing loss and cognitive function loss (adapted and
expanded from [194]. Aging processes affect both the sensory and the
cognitive system. Age-related hearing loss leads to a sensory
deficit with impaired perception. Compensatory mechanisms increase
access to cognitive resources which are already reduced by aging.
The communication disorder resulting from the perceptual disorder
promotes loneliness and social isolation, which has negative
psychosocial consequences (e.g. depression) and potentially
increases frailty. Cognitive performance decreases due to multiple
loads.
Age-related neurodegenerative changes increase cognitive demands and, in
combination with sensory deficits, lead to impaired perception. Compensation
for perceptual deficits increases cognitive load, which can lead to declines
in mental performance. Other sensory deficits (e. g., impaired
vision or balance) amplify the impairment. The communication disorder caused
by the hearing loss promotes social isolation and loneliness and with it
depression and frailty – the latter being further risk factors for
cognitive decline independent of hearing loss [53]
[221].
6. Can treatment of hearing loss reduce cognitive impairment?
6. Can treatment of hearing loss reduce cognitive impairment?
Due to the widespread availability of hearing aids, treatment of age-related hearing
loss is perceived as an achievable target for dementia prevention. However, testing
the effectiveness of such an intervention presents unique challenges. For example,
in the context of an observational study, it is difficult to monitor the quality of
hearing aid fitting as well as the duration of daily use. The latter is now
facilitated by the possibility of data logging by the hearing aid. A recent study on
datasets of more than 15,000 hearing aid users was able to objectify the
considerable inter- but also intraindividual variance in daily hearing aid use [222]. At the same time, factors such as
socio-economic status, education level, social environment, communication behavior,
and access to health care play a role in both hearing aid use and risk of cognitive
decline, making independent assessment of the impact of hearing rehabilitation
difficult. Large epidemiologic aging studies in the past have partially included
hearing threshold but not systematic hearing aid use (e. g., for the
German-speaking countries [223]).
A multicenter, randomized-controlled longitudinal intervention study initiated in
2018 in the USA including more than 800 70-84-year-old individuals without dementia
with low to moderate hearing loss comparing the efficacy of hearing aid provision
with health education alone with parallel collection of audiologic data as well as
cognitive performance over a 3-year period (ACHIEVE study, [224]) intends to address the issue, but
completion is not expected until late 2022 at the earliest.
Regarding the different intervention options, currently most data are found on
conventional hearing aid fitting, in recent years increasingly also on cochlear
implantation.
6.1 Provision of hearing aids
The Lancet Commission [24] cites 3 recent
studies to support the possible preventive effect of hearing aid use. A
prospective study demonstrated a correlation between increased incidence of
dementia in subjects with self-reported hearing loss within the 25-year
observation period only if they did not use hearing aids [225]. The cross-sectional study of Ray et
al. [226] also found cognitive deficits
only in the subgroup of hearing impaired subjects who did not use their hearing
aids, but the groups studied varied considerably in age and severity of hearing
loss. The long-term study by Maharani et al. [227] found a slowing of age-related functional loss in episodic
memory after the onset of hearing aid use.
In a comprehensive systematic analysis of long-term studies published between
1990 and 2020 on the relationship between hearing aid use and cognitive function
[228], the authors concluded that to
date, based on the current body of studies, no definitive conclusion on the
preventive effect of hearing aid use can be drawn. The methodology of the
existing studies is extremely heterogeneous, of particular importance is the
generally short follow-up period with regard to the rather slow age-related
cognitive function loss. In addition to the aforementioned study by Maharani et
al. [227], the authors were able to
identify only 1 other study in which subjects were followed-up for at least 10
years, which did not reveal any differences between intervention group (with
hearing aids) and control group for any cognitive measures [229]. In addition, a common problem in
comparative studies was large hearing threshold differences between intervention
and control groups. Furthermore, hearing aid compliance was poorly reported or
not reported at all in 9/17 studies, leaving it unclear to what extent
subjects used the hearing aid adequately. The greatest potential benefit of
hearing aid provision appeared to be in the area of executive function –
after all, 6/11 studies found improvement [228]. Two out of 4 studies found
significant improvement with hearing aid use on screening tests (MMST). However,
it was not reported whether the hearing impaired version was used, so it cannot
be excluded that due to hearing impairment in baseline testing, cognitive
function loss was overestimated and the improvement found by using the hearing
aids was only due to a better understanding of the verbally presented tasks.
6.2 Cochlear implantation
It is well established that elderly patients with severe hearing loss or deafness
benefit from cochlear implantation in terms of speech understanding and quality
of life (e. g., [230]
[231]
[232]
[233]
[234]). Compared to normal-hearing
individuals, the incoming signal is already highly degraded by the signal
processing of the cochlear implant, which requires a greater input of cognitive
resources to understand speech in the first place. Assuming that aging processes
of the central auditory pathway affect CI recipients to the same extent as
normal-hearing individuals, older CI users are at an even greater disadvantage
because impaired temporal processing further deteriorates the already degraded
signal [235]. As in normal-hearing
individuals, working memory function affects speech comprehension [236]
[237], and linguistic context can be used to some extent to improve
speech comprehension [238].
In recent years, a number of studies have been published explicitly addressing
the alteration of (global) cognitive functions by cochlear implantation [239]
[240]
[241]
[242]
[243]
[244]
[245]
[246]
[247]
[248]
[249]
[250]
[251]. Similar to studies on hearing aid
users, the neurocognitive test batteries chosen varied widely, although tests
suitable for hearing impaired people were increasingly used [244]
[245]
[246]
[247]
[248]
[251]
[252]. The follow-up period was relatively
short (12 months) in most studies, probably because the long-term studies in
questions were initiated only in recent years. Four research groups reported
results after 18 [251], 24 [246], at least 25 [242], and 60 months [240]. Positive effects, especially on
executive functions, were already reported within the short follow-up period. A
limiting factor is the small number of cases – mostly<20
patients have been included [241]
[242]
[243]
[244]
[252]. The largest number of participants
with simultaneous use of a neurocognitive test battery adapted for hearing
impaired subjects has been studied so far by Völter et al. [246]
[247]
[248]. During a follow-up
period of at least 24 months, 71 elderly CI patients (mean age at implantation
66.03 years) showed significant improvements in executive functions (attention,
working memory, inhibition) already after 6 months compared to preoperative
performance, and after 12 months, memory and word fluency had also significantly
improved. After 24 months, there was an improvement in processing speed;
inhibition control (flanker) was no longer significantly better, and there were
no changes in mental flexibility throughout the study period. Preoperatively,
the performance of 12 of the 71 subjects was below 68% confidence
interval in 3 or more subtests; after 12 months, this was the case in only
3/71 subjects. By the end of the study, 5/71 subjects had
deteriorated in more than 2 subtests. Cognitive performance had no significant
effect on speech comprehension at rest.
A similar result was already reported by Mosnier et al. [239] in their investigation of 94 CI users
aged 65-85 years: Of 37 subjects with preoperatively worse cognitive function,
81% improved within the first 12 months, and performance remained stable
in 19%. Regarding dementia development, the follow-up study by the same
research group is particularly interesting [240]. 80 subjects of the original 94 included were still alive 5
years after implantation, 70 of whom could be followed-up. Before cochlear
implantation, 31 subjects had cognitive performance in the range of mild
cognitive impairment. Of these, 32% recovered to normal function,
6% developed dementia, and 61% remained stable. Of the 38
subjects with preoperatively normal function, none developed dementia during the
follow-up period, but in 32% of the cases, cognitive performance was in
the range of mild cognitive impairment after 5 years. A correlation with the
achieved speech comprehension could not be proven.
Overall, all studies published so far show a clear positive, at least
stabilizing, mostly even improving effect of cochlear implantation.
7. Outlook
Sensory and cognitive deficits are closely linked via complex bottom-up and top-down
processes. The consequences of both normal and pathological aging processes will
inevitably pose major challenges to our society in the future. The realization that
a number of risk factors can be modified already in young and middle ages offers
opportunities for prevention. In particular, the consistent treatment of hearing
loss must become an even greater focus of health education, also in view of the
threat of social isolation and depression as further risk factors for cognitive
decline, in order to increase the alarmingly low rate of care, even in
industrialized countries. It is essential to take into account the special needs of
the elderly, both with regard to the operation of hearing systems (fine motor
requirements when changing batteries vs. using rechargeable batteries, simple
operating structure/coupling with external systems) and the fitting process
(possibly longer habituation phase, slower processing speed, lower differentiation
acuity when comparing different settings). Appropriate compensation for the
increased time required for consultation and repeated adjustment would increase the
incentive for providers to devote the necessary attention to this patient group. The
higher costs of care would be offset by a significantly improved quality of life and
longer cognitive function preservation in the case of successful adaptation, which
could lead to a reduction in the costs of care and thus to a reduction in the burden
on society as a whole. To validate the success of the fitting, further long-term
studies are required that record in detail both cognitive function and hearing
performance as well as the type and extent of use of hearing systems and apply
measurement methods that are methodologically adapted to possible cognitive and
sensory deficits.
