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43. Rubinstein JT, Bierer S, Kaneko C, etal. Implantation of the semicircular canals with preservation of hearing and rotational sensitivity. Otol Neurotol. 2012;33(5):789. https://doi.
org/10.1097/MAO.0b013e318254ec24.
44. van de Berg R, Lucieer F, Guinand N, etal. The vestibular implant: hearing preservation during intralabyrinthine electrode insertion-a case report. Front Neurol. 2017;8:137. https://doi.
org/10.3389/fneur.2017.00137.
E. Loos et al.
Chapter 16
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Aging andtheVestibular System
AdamThompson-Harvey andYuriAgrawal
Introduction
By 2030, one in ve US residents and almost 30% of all patients seen by an otolaryngologist will be over the age of 65 [1, 2]. Annually, one in ve older adults in the
United States experiences dizziness or imbalance [3]. Two-thirds of older adults,
specically those aged 65years and older, experience two or more sensory decits
[4], and nearly 50% of individuals over age 60 have some form of physiologic vestibular loss [5]. Age-related decline in vestibular function has important consequences for older adults, notably postural imbalance, gait impairment, and
falls [6, 7].
The majority of older adults with dizziness or imbalance see at least one physician and more than one-third see three or more providers [3]. Underlying vestibular
loss in older adults leads to an estimated individual lifetime economic burden of
$64,929 and total lifetime societal burden of $227 billion [8]. Even after adjusting
for age-related variables, such as hearing and vision loss and cardiovascular risk
factors, older adults with vestibular loss experience a signicant reduction in their
quality of life [8]. Further, there is increasing evidence demonstrating worse cognitive function in older patients with dizziness and imbalance compared to those without [9, 10].
A. Thompson-Harvey (*)
Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: athompharvey@mcw.edu
Y. Agrawal
Division of Otology, Neurotology, and Skull Base Surgery, Department of OtolaryngologyHead and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
e-mail: yagrawa1@jhmi.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
B. T. Crane et al. (eds.), Disorders of the Vestibular System,
https://doi.org/10.1007/978-3-031-40524-2_16
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In this chapter, we will discuss age-related changes in the vestibular system and
how these changes present in older adults. We will explore the essentials behind
evaluating older adults with dizziness, with the goal of maintaining long-term health
and well-being. Lastly, this chapter will focus on special considerations in the rehabilitation of older adults with vestibular loss. Ultimately, at the end of this chapter,
the reader should feel comfortable taking a comprehensive and evidence-based
approach to the diagnosis and treatment of vestibular disorders in the older adult.
A. Thompson-Harvey and Y. Agrawal
Epidemiology ofAge-Related Vestibular Loss
Dizziness and imbalance are common among older adults, with the prevalence estimated to be 20–30%, increasing to 50% in those above age 80, although measurable
vestibular loss does not appear to be universal [11–14]. Thus, vestibular loss in the
older population may be considered “age-concomitant” rather than an “age dependent” condition.
Sex-related differences in vestibular function in older adults remain unclear.
Some studies show a preponderance for females, while others show no signicant
difference in prevalence [5, 14]. Although males tend to have larger semicircular
canal diameter and utricular and saccular surface area [15], Li and colleagues found
that older females maintained a higher vestibulo-ocular reex (VOR) gain on video
head impulse testing (VHIT) [16]. Alternatively, studies on cervical vestibular
evoked myogenic potential (cVEMP) testing in older adults yielded no signicant
sex-related differences [17].
Studies focused on differences in racial/ethnic susceptibility to presbyvestibulopathy are lacking. As it stands, no signicant racial/ethnic differences in vestibular function among older adults have been demonstrated in large US population
studies [5, 6, 16, 18]. In Meniere’s disease, a vestibular disorder that tends to
increase in prevalence with age [19], studies have shown a higher prevalence among
patients of European ancestry and a disproportionately low prevalence among
patients of African ancestry [20, 21]. Temporal bone histologic research by Li and
colleagues suggested that melanin may be protective against age-related declines in
utricular function, provided larger ocular vestibular evoked myogenic potentials
(oVEMP) amplitudes and longer negative wave latencies in those identied as
Black than Whites [22]. It is unclear if paucity of racial/ethnic data related to presbyvestibulopathy is due to intrinsic health care inequities or differential burden of a
disease based on genetic, demographic, or environmental factors.
GainTc
Age
rman, 2001
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Pathophysiologic Changes intheAging Vestibular System
Vestibular loss in older adults or “presbyvestibulopathy” is a progressive, bilateral
disorder that reects structural and physiological age-related degradation of vestibular function. Decits to the peripheral and central vestibular systems may be due
to the combination of endogenous factors (e.g., genetic) and cumulative exposure to
vestibulotoxic agents including metabolic, infectious, inammatory, ischemic,
pharmacologic, and traumatic factors. Although the VOR, a frequently used physiologic measure of vestibular function, has been shown to remain steady up to age 70
or 80years, total vestibular reserve declines slowly with age, which can be estimated by the Gain-Time constant (GainTc) proposed by Hain etal. (Fig.16.1) [16,
23–25]. Increased sensitivities of afferent vestibular nerve bers and central mecha-
nisms compensate for earlier-onset hair cell loss yet remain vulnerable to neuropathologic degradation after age 60 [26–29]. After age 70, signicant functional
declines in angular (aVOR) and linear acceleration (otolith organs) can translate to
gaze and postural instability, contributing to in an increased risk for falls [30]. Akin
to the natural course of presbycusis, presbyvestibulopathy may exhibit highfrequency- specic functional changes within the vestibular system. As a result, the
clinician should interpret vestibular function testing with age-related changes in
mind (Table16.1).
GainTc Product vs age
14.00
12.00
10.00
8.00
6.00
4.00
2.00
0.00
020406080 100
Fig. 16.1 Total vestibular reserve declines slowly with age, based on estimates from Paige etal.,
1992, Baloh etal., 1993, and Furman etal., 2001, using Gain-Time Constant (Gain TC) product
calculation described in Hain TC, Cherchi M, Perez-Fernandez N. The Gain-Time Constant
Product Quanties Total Vestibular Output in Bilateral Vestibular Loss. Front Neurol. 2018 Jun
11;(9):396
Paige, 1992
Baloh, 1993
Fu
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A. Thompson-Harvey and Y. Agrawal
Table 16.1
diagnostic manifestations and vestibular test ndings
Pathological changes Diagnostic manifestations Clinical test ndings
Peripheral vestibular system
Otolith:
• Scarpa’s ganglion degeneration
and hair cell loss [89–91] [Park,
2001 #3254]
• Otoconia degeneration
(saccule>utricle) and reduction in
mass [92–95]
Semicircular canals:
• Selective loss of Type I hair
cells (crista>macula) [98, 99]
Central vestibular system
Brainstem:
• Loss of vestibular ganglion,
afferent, and vestibular nuclear
complex nuclei cells [106, 107]
Cerebellum:
• Global volume loss [112]
• Decreases in Purkinje cell
density white vermis and occular
nodular lobe [113] [Andersen, 2003
#3260]
Cerebral cortex:
• Breakdown of central
processing mechanisms for
vestibular compensation (by age
60) [114]
• Hippocampal atrophy (temporal
parietal junction) [115]
Age-related changes to the peripheral and central vestibular system and associated
• Benign paroxysmal
positional vertigo (BPPV)
• Decline in highfrequency VOR processing
mechanism (e.g., velocity
storage)
• Impairment in gaze
stabilization
• Possible postural
instability
• Impaired VOR
adaptation
• Impaired perceptual
function (e.g., sensation of
self-motion)
• Possible impairment in
spatial orientation
• Possible role in
dementia
• Positive Dix–Hallpike
• oVEMP and cVEMP [30,
96, 97]:
↓ Amplitude
↑ Latency
• Rotatory Chair:
↓ Gain and time constant
[100]
↑ Phase lead [101]
↓ Response amplitude and
compensatory response
phase [102]
• Caloric testing:
No signicant changes [102]
• Dynamic Visual Acuity
Test (DVAT): [30]
↑ LogMAR scores in each
canal plane
• Gaze Stabilization Test
(GST): [103]
↓ Maximal achieved head
velocity
• Video Head Impulse Test
(VHIT) changes: [24, 104]
↓ Slight VOR gain [105]
↓ Overt saccadic amplitude
↑ Overt saccadic latency and
covert saccadic amplitude
• Dynamic posturography:
↑ Sway velocity [108–110]
• Optokinetic testing:
[111]
↓ Smooth pursuit gain for
moderate to high target
velocities
↓ Saccadic velocity and
accuracy
↑ Saccadic latency
• Torsional nystagmus in
response to galvanic
vestibular stimulation
(GVS) [116]
• Mechanoreceptor decline
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321
Impact ofVestibular Loss onOlder Adults
Older adults are particularly vulnerable to postural imbalance, gait impairment, and
falls, as the vestibular system serves as an integral component of a multisensory unit
(Fig.16.2) [6, 31–34]. Agrawal etal. reported a 50% prevalence of abnormal horizontal head impulse testing (HIT) among their cohort of community-dwelling older
adults, which was positively correlated with fall risk after controlling for visual
acuity, somatosensory function and muscle strength [6]. Additionally, measurable
reductions in vestibular function may serve as an independent predictor of reduced
gait kinematics in older adults [6, 35]. Variations in gait are predictive of fall risk,
wherein older adults may manifest more careful control over foot placement by taking longer, slower steps as vestibular function declines [36]. Indeed, an estimated
50,000 excess falls per year among older adults can be attributed to vestibular loss,
the leading cause of injury-related death among this group [37, 38]. While vestibular loss may be a key mediator between age and declining activities of daily living
(ADLs) [39], older adults may show increased social isolation and decreased physical mobility due to fear and anxiety of falling [40, 41].
There is increasing evidence demonstrating worse cognitive function in older
patients with dizziness and imbalance compared to those without [9, 10]. In one
prospective longitudinal study, cognitive function among older adults with imbalance was found to worsen in the fth year of follow-up when compared to controls.
Recent studies in mice suggest the importance of otolith input in spatial cognition
[42]. In humans, saccular function and cognition may be linked (Fig.16.3). Reduced
Vestibular
• Hair cell loss
• Neuronal loss
• Otoconia degeneration
Visual
• Presbyopia
• Cataracts
• Macular degeneration
• Glaucoma
Somatosensory
• Neuropathy
Fig. 16.2 Postural stability is maintained by the integration of somatosensory, visual and vestibular inputs to the central nervous system, followed by outputs to the musculoskeletal system.
Function of all the components deteriorates as the age advances. (Modied from Iwasaki S,
Yamasoba T.Dizziness and Imbalance in the Elderly: Age-related Decline in the Vestibular System.
Aging Dis. 2014 Feb 9;6(1):38–47)
Central Nervous
System
• Brain atrophy
• Increased cognitive load
Musculoskeletal
System
• Sarcopenia
• Osteopenia/osteoporosis
• Arthritis
322
Exec. Function Attention
Language
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Aging
Vestibular
Loss
Thalamus
Hippocampus
Basal ganglia
A. Thompson-Harvey and Y. Agrawal
Prefrontal
cortex
Saccule
Other risk
factors:
ototoxicity
antibiotics
Neurodegeneration of
vestibular cortex and
neural circuits involved
in spatial processing
Spatial
Memory
NORMAL
COGNITION
MCI
AD
Fig. 16.3 Conceptual model of impact of aging on vestibular function (notably saccular function),
which contributes to neurodegeneration of neural circuits involved in vestibular processing and
deterioration specically in spatial cognitive ability. (With permissions from Agrawal Y, Smith PF,
Rosenberg PB.Vestibular impairment, cognitive decline and Alzheimer’s disease: balancing the
evidence. Aging & Mental Health. 2020;24(5):705–708)
saccular function was found to have the strongest association with spatial ability in
healthy older adults [31]. Patients with Alzheimer’s disease were noted to have specically worse saccular and utricular function relative to age-matched controls [43].
As vestibular loss may represent a modiable risk factor for cognitive decline and
dementia [44, 45], the effect of presbyvestibulopathy on cognition and subsequent
impact of vestibular rehabilitation among older adults should be considered a critical new area of investigation.
Evaluation ofVestibular Loss inOlder Adults
As all forms of dizziness and/or disequilibrium can occur in older adults, one should
perform a complete history and physical examination with special attention to the
peripheral vestibular assessment. Bedside balance function tests that can be easily
performed with older patients include looking for spontaneous nystagmus, head
impulse testing, clinical dynamic visual acuity testing, head-shake testing, Dix–
Hallpike maneuvers, foam and dome, and Timed Up and Go testing [46]. However,
clinicians should remember that the geriatric patient typically has a multifactorial
aspect to his or her symptoms, and mainstays of management rely on appropriate
identication of vestibular and nonvestibular contributors.
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Table 16.2
Polypharmacy
Medications that can produce or exacerbate dizziness or imbalance:
Alcohol
Sedatives, anxiolytics
Antihypertensives
Antiepileptics
Aminoglycosides
Concomitant systemic disease that is often more prevalent in older adults:
Cardiovascular disease (e.g., hypertension, arrhythmias)
Diabetes
Eye disorders (e.g., presbyopia, cataracts, or macular degeneration)
Musculoskeletal weakness
Arthritis
Peripheral sensory loss (e.g., neuropathy)
Psychiatric disease (e.g., depression, anxiety)
History of hearing loss
Home modications/home environments
A screening questionnaire may be useful to direct specialty referrals (e.g., to neurology,
ophthalmology, cardiology)
Nonvestibular contributors to dizziness to assess in older adults
In addition to a thorough review of nonvestibular contributors (Table16.2), clinicians should obtain orthostatic vital signs, perform a mini-mental status examination, and check for extremity and postural tremor to rule out autonomic or central
pathology when appropriate.
Sensitive communication is key. Older adults with vestibular loss may describe
feeling “off-balance or unsteady” (~70%), and/or “like fainting” (~30%), and/or
another 30% report “spinning or vertigo sensation” [14]. Provided two-thirds of
adults over the age of 70 have bilateral hearing loss [47], clinicians should be aware
of concomitant presbycusis and may need to adjust their speech to ensure clarity.
The most common form of dizziness in the older adult is Benign Paroxysmal
Positional Vertigo (BPPV) [48], yet older patients may not specically complain of
vertigo even when manifesting BPPV-related nystagmus. Indeed, 9% of older adults
are thought to have unrecognized BPPV [49]. Because BPPV can be readily treated
with rehabilitative therapy, the clinician should be sure to screen for vestibular loss
when treating older adults with a history of imbalance or falls. Additionally, studies
have shown an increasing prevalence of Meniere’s disease with age [19, 21, 50, 51].
Considering the increased recognition of age-related vestibular loss, the
Classication Committee of Barany Society recently developed the following diagnostic criteria for presbyvestibulopathy (PVP) [52]:
• Each of the criteria A through D have to be fullled
A. Chronic vestibular syndrome (at least 3months duration) with at least two of
the following symptoms:
1. Postural imbalance or unsteadiness
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A. Thompson-Harvey and Y. Agrawal
2. Gait disturbance
3. Chronic dizziness
4. Recurrent falls
B. Mild bilateral peripheral vestibular hypofunction documented by at least one
of the following
1. VOR gain measured by video-HIT between 0.6 and 0.8 bilaterally
2. VOR gain between 0.1 and 0.3 upon sinusoidal stimulation on a rotatory
chair (0.1Hz, V
=50–60°/s)
max
3. Reduced caloric response (sum of bithermal maximum peak SPV on each
side between 6 and 25°/s)
C. Age ≥60years
D. Not better accounted for by another disease or disorder
The decision to obtain vestibular laboratory testing should be based on the nature
of the patient’s condition, the clinician’s expertise, and the availability of laboratory
testing. Unfortunately, evidence-based guidelines directing the use of specic vestibular function tests for patients with dizziness are lacking [53], especially as it
pertains to older adults.
Management oftheOlder Adult with Vestibular Loss
The practicing otolaryngologist should readily recognize BPPV and feel comfortable treating older adults with a canalith repositioning maneuver (e.g., Epley) at the
time of diagnosis. If clinic space cannot allow for such maneuver, the patient is
intolerant, or returns with recurrent spells, referral to a vestibular physical therapist
is appropriate. Considering the increased risk of falls in older adults, referrals to
multidisciplinary falls prevention clinics should be integral part of treatment, if
available at one’s institution.
Pharmacological therapies for dizziness should be used judiciously and sparingly in older individuals. Vestibular suppressants (e.g., meclizine, scopolamine,
lorazepam) are effective at reducing acute symptoms of vertigo and motion sickness
but are not recommended in the geriatric population. They have sedating effects and
are metabolized/cleared more slowly in older adults and are therefore not indicated
in the setting of chronic, progressive vestibular loss [54]. Even more, these medications can blunt the error signal that drives vestibular compensation [55]. Nonetheless,
the prevalence of prescription drug use for dizziness or imbalance in older adults is
estimated to be 62% [3].
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Vestibular Rehabilitation intheOlder Adult
Current practice guidelines recommend the use of vestibular rehabilitation therapy
(VRT) for vestibular dysfunction [56], and in older adults with dizziness, gaze stability exercises reduce the risk of falls [57]. The majority of older adults perform
VRT at home, typically using the Cawthorne and Cooksey protocol [58]. This protocol promotes visual stabilization of head movements, improves postural stability
in situations where sensory conicts arise, minimizes sensitivity to head movements
and improves static and dynamic body balance [59, 60]. Those more likely to drop
out of rehabilitation tend to be very elderly males with stability decits and poor
center of gravity balancing on computerized dynamic posturography (CDP) [61];
thus, successful rehabilitation must include targeted techniques that specically
increase self-efcacy [62].
However, direct measurements of home gaze stability exercise behavior, such as
the head velocity, range of motion, and frequency of head movements, often rely on
camera-based systems, including video and motion cameras [63, 64
prototyped custom sensors [65–68], and there are no current FDA-approved mobile
applications for home VOR monitoring. To this extent, mobile applications have
been developed that utilize the gyroscopes and accelerometers native to existing
smartphones to track postural balance remotely via vibrotactile feedback [69, 70].
Huang and colleagues looked to obtain information on home gaze stabilization
excise progress by developing an iPod-based mobile application that measured
user’s head velocity in the yaw and pitch planes; however, this required users to
secure the device to a hat and mostly interact with the application without direct
visualization [71]. Future research into smartphone based assessments of the VOR
may ultimately aid clinicians in providing effective and resourceful rehabilitation
remotely to older adult patients with balance disorders.
] or lab-
Considerations inVestibular Compensation intheOlder Adult
The role of prophylactic VPT for presbyvestibulopathy is unclear. Older patients
with vestibular loss should be aware that therapy may need to be augmented by a
multimodal approach and goals may not be total resolution of symptoms. This is
because, at present, it is challenging to disambiguate whether clinical symptoms are
due to physiologic or compensation decits. For example, reactive postural tasks
may be impaired due to VOR and vestibulo-spinal reex (VSR) decits, while
anticipatory postural adjustments that guide navigation may be affected by vestibular perceptual decits [72]. Age-related changes in neuronal plasticity/reweighting
mechanisms compromise vestibular compensation, which can occur due to central
pathology or medications [73, 74]. Although a standardized, comprehensive
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