Hearing Aids and Cognition | January 2021 Hearing Review

A recent study shows how even mild-moderate hearing loss might influence brain processing 

By Hannah Glick, AuD, PhD, and Anu Sharma, PhD

One of the most amazing abilities of the human brain is its capacity for change. The term neuroplasticity refers to the brain’s ability to adapt or change. While the brain is most amenable to change early in development (developmental neuroplasticity), neuroplastic changes may occur across the human lifespan as a result of disease, injury, dysfunction, and learning (adulthood neuroplasticity). Based on our findings, it appears that untreated hearing loss (even mild sensorineural hearing loss) is associated with neural reorganization and cognitive deficits. 

There are 466 million people worldwide living with hearing loss impacting communication, 93% of which are adults.1 Along with heart disease, hypertension, and arthritis, hearing loss is one of the leading adult chronic health conditions.2 Age-related hearing loss (ARHL), or presbycusis, is the most common type of hearing loss identified in adults. ARHL represents a great majority of the population of patients that we see in our clinics. ARHL is characterized by a bilateral, symmetrical, slowly progressive sensorineural hearing loss (SNHL). The most common symptom of ARHL is difficulty understanding speech in adverse listening scenarios. Perhaps due to the slow  progressive nature of ARHL and low rates of hearing screening and diagnostic testing, many adults are unaware they have hearing loss and therefore, treatment is often delayed almost a decade after initial hearing loss onset.3 

By the time patients with ARHL reach our clinics, many describe behavioral compensations and coping mechanisms which they’ve developed to adapt to their hearing loss, including: listening harder, focusing more intensely, “filling in the gaps,” and even avoiding adverse listening situations altogether.4 The good news is, for a large portion of patients, treatment with hearing aids will increase audibility and improve speech perception. Uptake and utilization rates of hearing aids among motivated and able groups is good, and these patients generally report high levels of satisfaction and benefit. However, for some patients, self-perceived benefit is poor, and uptake and utilization with hearing aids is a challenge. 

For those with unsatisfactory results, one must wonder if the hearing aids were appropriately fit? Did the patient wait too long prior to pursuing intervention? Are there individual patient-related factors (eg, social isolation, cognitive function, depression, etc) preventing this patient from reaching a positive outcome? Further, for every patient who chooses to pursue amplification, there are perhaps 3 to 4 candidates who do not pursue amplification for multiple reasons, including denial, expense, cosmetics, access, “hearing is not bad enough,” and more. These are the patients who keep us up at night.

As hearing care professionals (HCPs), we understand our adult patients may compensate behaviorally to adapt to untreated hearing loss. However, for those with untreated hearing loss, we wonder about the many ways their brains change and adapt to cope with and manage their hearing loss. In this article, we take you on a journey into the brain of adults with mild-moderate ARHL, describing the impact of untreated hearing loss on neurocognitive function before and after treatment with hearing aids. In addition, we discuss the implications of this research on early identification and intervention and the role that HCPs may play in cognitive screening.

Using EEG to Study the Effects of Hearing Loss on Neurocognitive Function in Clinical Populations

One of the most amazing abilities of the human brain is its capacity for change. The term neuroplasticity refers to the brain’s ability to adapt or change. While the brain is most amenable to change early in development (developmental neuroplasticity), neuroplastic changes may occur across the human lifespan as a result of disease, injury, dysfunction, and learning (adulthood neuroplasticity). 

As a profession, we are just beginning to unearth the impact of ARHL loss on neuroplasticity. Electroencephalography (EEG) provides a non-invasive, relatively inexpensive neuroimaging method which can be used to assess neuroplastic changes in clinical populations with hearing loss. 

In our laboratory, we use 128-channel, high-density EEG to evaluate how hearing loss affects the auditory cortex using cortical sensory evoked potentials. For example, we present sound (eg, speech), visual stimuli, and/or vibrotactile stimuli to participants with normal hearing (NH) and participants with hearing loss, and we measure neural activity in response to these stimuli. These recordings are referred to as cortical auditory evoked potentials (CAEPs), cortical visual evoked potentials (CVEPs), and cortical somatosensory evoked potentials (CSSEPs), respectively. 

Similar to auditory brainstem response testing (ABR), we evaluate CAEP, CVEP, and CSSEP waveforms in terms of their peak latencies and amplitudes. Because we are collecting data using many channels and topographically located electrodes, we can estimate where in the brain these responses originate from through an advanced statistical modeling approach called Current Density Source Reconstruction (CDR). CDR can be projected onto a 3D image of the brain (aka, structural MRI). While EEG lacks the fine spatial resolution of other neuroimaging methods, such as functional magnetic resonance imaging (fMRI) or positron emission tomography (PET), its superb temporal resolution (timing) and inexpensive and non-invasive nature makes it an excellent method to assess neuroplasticity in clinical populations with hearing loss.  

Effects of Mild-Moderate Untreated Hearing Loss on Neurocognitive Function

Recently, in our laboratory (see Glick and Sharma5 for full details), we studied a group of 13 adults (average age = 62.62 years, sd = 4.91) with clinically normal pure-tone hearing thresholds (average PTA = 10.58 dB HL, sd = 5.23), and a group of 28 adults (65.40 years, sd = 4.23) with early-stage, mild-moderate ARHL (average PTA = 27.08 dB HL, sd = 10.41). Many of the adults in the hearing loss group were unaware they had hearing loss prior to participating in the study, and people in both groups had no history of neurocognitive impairment. Participants in the ARHL group had not worn hearing aids previously. 

We collected baseline CVEPs from both groups in response to a visual motion stimulus (soon after hearing aid fitting) and 6 months post-hearing aid fitting. We also tested speech perception in noise using a clinical test (QuickSIN™) and cognitive function in both groups. Our cognitive test battery evaluated a variety of cognitive domains, including global cognitive function (using the Montreal Cognitive Assessment [MoCA]), executive function (using the Behavioral Dys-control Scale 2 [BDS-2]), processing speed (using the Symbol Digit Modalities Test [SDMT]), visual working memory (using the Reading Span Test [Reading Span]) and auditory working memory (using the Word Auditory Recall Response Measure [WARRM]). We assessed baseline cognitive function aided in the hearing loss group to negate the possible effects of reduced audibility on cognitive test performance (all ARHL participants were fit with the same brand of hearing aids within ±5 dB of NAL-NL2 prescriptive targets from 250-4000 Hz). 

At baseline, the NH group showed expected activation of visual processing regions of the brain in response to the visual stimulus. The untreated ARHL group exhibited visual activation plus additional activation of auditory regions of the brain, which is evidence of cross-modal reorganization.5 In addition, the ARHL group showed recruitment in the frontal cortex during this task. Recruitment of the frontal cortex has been observed in participants with ARHL and may reflect increased effort or cognitive load.6,7 Together, these findings indicate extensive cross-modal reorganization in the hearing loss group before hearing treatment—a surprising finding given that many of the participants in the ARHL group were unaware they had hearing loss. 

Speech perception and cognitive function performance for both groups at baseline are displayed in Table 1. When compared to the NH group, the untreated ARHL group exhibited poorer speech perception in noise and poorer cognitive function across all domains assessed (global cognitive function, executive function, processing speed, visual working memory, and auditory working memory). Of note, greater cross-modal re-organization by vision (earlier CVEP latencies) was associated with poorer QuickSIN performance and more high frequency hearing loss (high frequency PTA). Further, cross-modal reorganization was associated with poorer cognitive functioning at baseline. 

Table 1. Average speech perception in noise scores and cognitive performance between the normal hearing (NH, n=13) and age-related hearing loss (ARHL, n=28) groups at baseline.5 Cognitive performance in the ARHL group was assessed in an acutely aided condition to negate possible effects of audibility on test performance. Compared the NH group, the ARHL group demonstrated significantly poorer speech perception in noise performance and poorer cognitive function across the domains of global cognitive function, executive function, processing speed, visual working memory, and auditory working memory.

Effects of Treatment with Hearing Aids on Neurocognitive Function

ARHL participants fit with hearing aids at baseline were provided counseling regarding how to use the hearing aids and were instructed to wear the hearing aids for 6 months (minimum of 5 hours/day) to remain in the study. Participants returned for interim hearing aid checks and routine data logging over the course of 6 months. Of the 28 ARHL participants initially enrolled, 21 participants met minimum daily use requirements and returned for 6-month follow-up testing. Average daily hearing aid use in the ARHL group (n=21) was 9.84 hours/day (sd = 2.96). At 6-month follow-up, CVEPs, speech perception in noise (QuickSIN), and cognitive assessments (MoCA, BDS-2, SDMT, RST, WARRM) were repeated to evaluate changes during hearing aid use. 

Baseline versus 6-month follow-up CVEP results for the ARHL group are summarized in Figure 1. At baseline, analysis of the CVEPs in the ARHL group demonstrated additional extensive cross-modal recruitment in the temporal and frontal cortical regions. These baseline findings are not typical. Six months later, we observed a reduction in cross modal recruitment based on the CVEPs, demonstrating evidence of a reversal in cross-modal reorganization. While reversal in cross-modal recruitment by vision and vibrotactile processing has been reported in a previous case of pediatric single-sided deafness (SSD) following cochlear implantation,8 to our knowledge this is the first study documenting the potential for hearing aids to reverse cross-modal neuroplasticity by vision. 

Figure 1. Current Density Source Reconstructions (CDRs) for cortical visual evoked potentials (CVEPs) elicited by a visual motion stimulus in the ARHL group (n=21) at baseline and 6 months post-treatment with hearing aids.5 The graded color scale depicts the statistical likelihood of activation in each cortical region, from low statistical likelihood (red) to high statistical likelihood (yellow). At baseline, the ARHL group shows evidence of cross-modal re-organization, as evidenced by recruitment of temporal cortex and frontal cortex in addition to occipital regions typically associated with visual motion processing. At 6 month post-treatment follow-up (ie, after hearing aid use), there is a reduction in temporal and frontal cortex activity, suggestive of a cross-modal reorganization and restoration of more typical visual processing patterns.

Also worth noting, we saw significant improvements in QuickSIN scores and cognitive function in the ARHL group at 6-month follow-up (Table 2). As indicated in Table 2, significant improvements in cognitive function were observed in the domains of global cognitive function, processing speed, executive function, and visual working memory (but not auditory working memory—perhaps due to the high auditory demand of this task). Taken together, our results suggest that treatment with well-fitted hearing aids can provide neurocognitive benefit, as demonstrated in our group of adults with early-stage, mild-moderate hearing loss. 

Table 2. Average speech perception in noise scores and cognitive performance between ARHL group (n=21) at baseline and 6 months post-treatment with hearing aids.5 Cognitive performance in the ARHL group was assessed in an acutely aided condition at baseline and 6-month follow-up to negate possible effects of audibility on test performance. The ARHL group demonstrated significant improvements in speech perception in noise performance and cognitive function across the domains of global cognitive function, executive function, processing speed, visual working memory. There was no significant improvement in auditory working memory post-treatment with hearing aids.

Clinical Implications  

As HCPs, we understand the ways in which adult patients may compensate behaviorally to adapt to untreated hearing loss: listening harder, focusing more intensely, relying on visual cues, “filling in the gaps,” and avoiding adverse listening situations altogether. This study, and the emerging evidence from other neuroimaging studies, supports growing evidence that untreated hearing loss is not just linked to behavioral compensation but also neurophysiological compensation. Based on our findings, it appears that untreated hearing loss (even mild sensorineural hearing loss) is associated with neural re-organization and cognitive deficits. 

One of the important findings from this study is the correlation between cross-modal re-organization and speech perception in noise scores on the QuickSIN. Notably, poorer QuickSIN scores were associated with more extensive brain re-organization. While further research is needed, these results highlight the need for HCPs to look “beyond the audiogram” when considering the need for amplification. Routine use of the QuickSIN among audiologists has been reported as low as 10%.9 The QuickSIN test takes less than 5 minutes to administer and provides real-world pragmatic information about a patient’s speech intelligibility in noise. Beck and Benitez10 stated fewer than 15% of audiologists appear to test SIN and recently published a novel 2-minute SIN test. Of note, they reported a SIN score likely represents the single most important measure of auditory function.

According to the International Hearing Society (IHS), the American Academy of Audiology (AAA), and the American Speech Language Hearing Association (ASHA), HCPs should engage in best practices while fitting hearing aids.11-13 Specifically, probe-microphone real-ear measurements are recommended to verify the hearing aid fitting. Of note, all subjects in our study were well-fitted with regard to best practices. Nonetheless, we observed anecdotal neuroimaging evidence from long-term hearing aid users in our laboratory who were previously “underfit” per real-ear measures, which indicated cross-modal re-organization after extended periods of hearing aid use—thus reinforcing the idea that neuroplastic changes may be induced and perpetuated by auditory deprivation. As shown in this study, adults with mild-moderate ARHL who were fit within ±5 dB of NAL-NL2 prescriptive targets from 250-4000 Hz showed significant improvements in neurocognitive function. 

Earlier Intervention?

Should HCPs be recommending amplification sooner? Many HCPs delay recommendation of hearing aids until hearing loss negatively impacts communication. Many patients delay intervention until hearing loss has negatively impacted their quality of life. HCPs should remain abreast of new evidence emerging which may indicate previously unrecognized neuro-plastic cortical negative effects from mild hearing loss on the brain, and perhaps more importantly, the potential benefits of earlier treatment. Even though our ARHL group had only early-stage hearing loss, post-treatment self-reported benefit and satisfaction rates were excellent.5 This, coupled with objective benefit from amplification (neurocognitive and speech perception benefit), presents a compelling case for earlier treatment. 

Further, we urge HCPs to consider the potential value that cognitive screening may add to the lives of our patients. According to Taylor et al,14 almost 90% of Americans report they would prefer to know the cause of confusion or memory loss if the cause was Alzheimer’s disease, yet less than half of these adults have had a conversation about their cognitive function with a healthcare provider. Alarmingly, many primary care doctors do not screen for cognitive function and these deficits go undiagnosed in many adults.15 From an economic standpoint, early diagnosis of dementia would reduce healthcare costs up to an estimated $64,000/person.16 Further, many HCPs are starting to employ cognitive and dementia screening tests within the framework of listening and communication assessment.17

While more research is needed, our study revealed cognitive deficits in the ARHL group at baseline and significant improvements in cognitive function over the course of 6 months of hearing aid use. As such, the potential clinical use of cognitive screening during the hearing aid candidacy evaluation and/or to assess post-treatment outcomes was reinforced. 

Consistent with Beck et al,18 we believe screening of health conditions co-morbid with ARHL (ie, cognition, dementia, depression, social isolation, etc) is within the scope of practice of a licensed audiologist. While some audiologists feel uneasy about performing cognitive screenings, professionals should consider training opportunities such as certification courses to administer cognitive screenings (eg, the 5-minute MoCA screening tool). 

In selecting a cognitive screening tool, we recommend clinicians consider a screening sensitive to mild cognitive impairment (MCI), as many individuals with MCI are at risk for developing dementia. MCI presents itself in the form of subtle cognitive deficits compared to dementia. Before initiating a cognitive screening program, we recommend clinicians develop strong referral networks with physicians, psychologists, social workers, neuropsychologists, and others so patients who fail a screening can be referred for additional diagnostic testing, care, and professional support. While more research is needed, cognitive screenings may soon emerge as a secondary or tertiary audiological outcome measure to assess benefit from treatment with hearing aids or cochlear implants, in addition to traditional verification and validation measures.

Finally, based on our study findings and the growing body of literature linking untreated hearing loss to cognitive decline, we encourage HCPs to advocate bringing hearing loss to the forefront of the public health conversation on aging. Many professionals and the public remain unaware of the effects of hearing loss on neurocognitive, psychological, and behavioral function. Many adults dismiss hearing loss as a “normal part of aging.” Despite the great success we see in the vast majority of patients we treat in our practices, the reality is that only 29% of adults ever have their hearing tested19 and less than 15% of adults with hearing loss (<4% of Americans with mild hearing loss) who could benefit from hearing aids have them.20 

There exists great opportunity for HCPs to expand access to hearing technology. If we want to change these statistics, we have to re-imagine the ways in which we identify, treat, and manage hearing loss, and we have to rally support from allied and medical health professionals to put hearing loss higher on the health priority list. 


This review article features data from Drs Glick and Sharma’s article5 in the February 18, 2020 edition of Frontiers in Neuroscience.

Original citation for this article: Glick H, Sharma A. The brain on hearing aids: Can treatment with hearing aids improve neurocognitive function in age-related hearing loss? Hearing Review. 2021;28(1):28-32.

CORRESPONDENCE can be addressed to Dr Glick at [email protected] or Dr Sharma at [email protected]


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