This chapter reviews the epidemiology, causes, pathogenesis, diagnosis, and treatment strategies for the most frequently encountered causes of dizziness in the elderly patient. Although a complaint of dizziness might seem enigmatic at first, rational ways exist to evaluate this sensation and establish a cause based on a number of well-recognized health problems that affect many elderly patients (i.e., cardiovascular disease, depression, cervical spondylosis, polypharmacy, deconditioning). The vestibular system encompasses sensory structures in the labyrinth of the inner ear but also integrates visual and somatosensory information in service of three essential roles of the nervous system: maintenance of upright posture during standing and locomotion, stabilizing vision during head motion, and regulation of autonomic tone in response to orthostatic changes. Because of the multitude of underlying health conditions and situations that can cause dizziness, many different physicians and health care professionals encounter patient complaints of dizziness. Internists, geriatricians, family care physicians, neurologists, otorhinolaryngologists, psychiatrists, physiatrists, emergency physicians, and physical therapists all have the opportunity to diagnose and treat many patients with dizziness. This chapter is intended to help organize the approach to the elderly dizzy patient given the latest clinical and basic research on the causes and treatments of dizziness.
EPIDEMIOLOGY OF DIZZINESS
Dizziness is reported in approximately 30% of all people over the age of 65 (19,97). In the United States, it is the most common presenting complaint to office practices among patients over the age of 75 (50). The physician consultation rate in 1981 for the symptom of dizziness in the United Kingdom was approximately 54 in 1,000 for people aged 65 to 74 years and 76 in 1,000 for people aged 75 years or older (87). One of the most serious consequences of dizziness is falls. The National Health Interview Survey Supplement on Aging in 1986 determined that more than 18% of all persons 65 to 74 years of age and more than 25% of all those 75 years of age or older had fallen in the previous year. In these groups, 15% to 23% fell because of dizziness alone (40). The same survey reported that a staggering 34% of persons 65 to 74 years old and 37% of persons older than 75 years had limited their activity because of dizziness. Smaller studies using more select populations of older people find that between 20% and 30% of falls are caused by dizziness (3,117). Some of these studies also suggest that patients who are older than 60 years have an increased incidence of potentially treatable diseases as a cause for their dizziness (3,54).
Another consequence of falling is the subsequent deterioration of function after the fall. Many elderly people who fall develop a fear of falling that limits their daily activity. This has a significant impact on mobility and can be quantified easily and reliably (78). Restriction of activities due to lack of confidence leads to more deconditioning, further increasing the risk of falling. Dynamic posturography studies of elderly people with dizziness and without dizziness show that a fear of falling is associated with an increased sway velocity and risk for fall, regardless of dizziness status (4). Clearly, with advancing age, dizziness is more common, and it represents an increasing risk for falls, as well as for syncope, functional disability, nursing home placement, stroke, and death (12,33,51,97,110).
The characteristics of dizziness in older people are different than the characteristics in younger people. In 1992, Kroenke et al. (51) studied 185 consecutive outpatients with a chief complaint of dizziness. Within a subgroup of 85 younger patients (average age, 49 years), they found that the symptoms of dizziness differed from the 100 older remaining patients (average age, 61 years). The older group was significantly more likely to have daily dizziness, limitation of function because of dizziness, fear of underlying illness, and increased use of medications for dizziness (51). These findings may mean that older individuals who experience dizziness are less able to compensate for the dizziness, have more severe dizziness, or report dizziness more often.
The presence of dizziness has a negative impact on quality of life in patients over 60 years of age and is associated with role limitations in physical and emotional spheres. When dizziness is episodic, the frequency of attacks correlates with perceived disability, resulting in additional psychological distress (43).
The differential diagnosis of dizziness in elderly patients is extensive. Studies designed to determine the cause of dizziness in geriatric patients have returned highly variable results, partly because of the different populations, criteria, and study designs used. Alternatively, dizziness is a highly variable symptom with a number of conditions that predispose to it. Tinetti et al. (112), using Drachman’s categorization of dizziness symptoms, determined the prevalence of dizziness subtypes and associated treatable factors in a population of 1,087 independent people 72 years of age and older. The study, conducted over an 11-year period, showed that 29% of individuals experienced dizziness. No single cause for dizziness was found in this study, although many factors were related to its development. The authors suggest that dizziness can occur with either severe impairment of a single system (vision, vestibular, sensory, motor, or cerebellar) or with mild to moderate impairment of several systems. They conclude that dizziness should be considered a geriatric syndrome so that physicians will regard the symptom as a complex of interrelated systems, which, when perturbed, results in the disorienting sensation (112).
In the German National Telephone Health Interview Survey of 2003, participants were asked about the type of dizziness, duration, provoking factors, impact of dizziness, health care utilization, and previous diagnoses. The prevalence of vestibular vertigo was 16% for individuals 60 years of age and older (20% of women and 11% of men) (70). The prevalence of vertigo, dizziness, and disequilibrium was determined in a longitudinal and cross-sectional study from Sweden in cohorts between 70 and 90 years old. The prevalence of balance problems at age 70 was 36% for women and 29% for men and increased to 51% of women and 45% of men in the oldest age group (44).
DESCRIPTIONS OF DIZZINESS
When a patient complains of being dizzy, the subjective experience can be described with a perplexing number of seemingly equally nebulous terms: swimming, floating, lightheadedness, whirling, fainting, disorientation, unsteadiness, rocking, giddiness, dissociation, imbalance, or spinning.
Traditionally, the patient’s description and history have guided subsequent questioning, examination, and testing. Some studies suggest that a careful history can predict the eventual diagnosis in 70% of chronically dizzy geriatric patients (97,98). However, this does not necessarily imply that what the term “dizziness” means to any given patient must be defined unequivocally in order to achieve diagnostic accuracy. Nevertheless, much of the literature assumes this premise, attempting to divide patients’ dizziness into one of four proposed subcategories (23). These dizziness subtypes include:
Vertigo: a sensation of rotational, spinning movement
Presyncope: a sensation of fainting or “passing out”
Disequilibrium: a sensation of imbalance while standing or walking with no abnormal sensation in the head
Other sensations: loosely defined as nonspecific dizziness, floating, giddiness, or other descriptions that fall outside of the previous categories
One difficulty with this type of scheme is that up to 60% of individuals fall into more than one symptom category (18,51,97,112). Alternative algorithms for anamnestic diagnosis focus not only on the type of dizziness, but also rely heavily on the timing of symptoms and the presence or absence of auditory complaints (47).
Risk factors associated with developing dizziness in old age include angina, hypertension, myocardial infarction (MI), stroke, Parkinson’s disease, arthritis, diabetes, syncope, neurosensory impairment, alcohol use, smoking, nervousness, and medication use. In terms of medication use, antihypertensive agents, anticonvulsants, anxiolytics, antidepressants, and antipsychotics carry the highest risk for causing dizziness. A population-based cross-sectional study of 1,087 independent healthy people older than 72 years of age sought predisposing characteristics and situational factors associated with dizziness (112). Seven associated characteristics were identified with significant relative risk for dizziness (Table 8-1).
When they compared the 29% of the study population who reported dizziness with those who were not dizzy, each of the four types of dizziness was associated with a significantly higher number of these characteristics (2.0 to 2.5 on average) than the nondizzy group (1.5 on average). Therefore, when assessing a geriatric patient even without a primary complaint of dizziness, recognition of one or more of these characteristics may help in uncovering an unreported problem. Also, recognition of the “syndrome” should not preclude a search for a specific cause (22).
Table 8-1.Adjusted Relative Risks for Characteristics Associated with Dizziness
Associated Characteristic
Relative Risk
Anxiety
1.69
Depression
1.36
Impaired balance
1.34
Past MI
1.31
Postural hypotension
1.31
Five or more medications
1.30
Impaired hearing
1.27
MI, myocardial infarction
Vertigo, defined as the perception of motion, has a prevalence of 25% to 54% in elderly persons complaining of dizziness (18,51,97,112). A careful history of dizziness has been shown to be 87% sensitive for vestibular disorder (51). Other symptoms often associated with vertigo include nausea, vomiting, unsteadiness, and sometimes hearing loss. The underlying mechanisms implicated include disorders of the peripheral or vestibular system and the cerebellar system. Specific diseases are discussed in the text that follows.
In elderly patients complaining of dizziness, presyncope, defined as a feeling of fainting, has a prevalence of 11% to 42% (97,112). History alone carries a sensitivity of 74% for cardiovascular (51). Associated symptoms include pallor, perspiration, palpitations, and syncope. The underlying mechanisms of presyncope stem from decreased cerebral perfusion caused by cardiovascular disease, hypovolemia, overmedication, orthostatic intolerance, dysautonomia, and hypercapnia.
Disequilibrium, as a category of dizziness, includes people with a sensation of imbalance while on their feet. The symptom of dizziness is not directly referred to as a sensation in the head and is usually dependent on standing, movement, or both. Therefore, this type of dizziness can include people suffering from gait abnormalities (e.g., disequilibrium syndrome, presbyastasis, or senile gait). In clinical studies of geriatric patients who complain of dizziness, 28% to 78% are diagnosed with disequilibrium (18,51,97,112). Extreme variability in the prevalence of this problem primarily results from the different patient populations under consideration. For example, some investigations that study nursing home residents show significantly higher numbers of a disequilibrium type of dizziness than similar outpatient community-based studies. The higher rate of disequilibrium in the nursing home population is likely because of the fact that placement in a nursing home environment is often predicated on mobility problems. Also, independent elderly outpatients with a gait abnormality are less likely to remain in the general community. A retrospective study of 116 neuro-otology clinic patients with an average age of 75 years and with the presenting complaint of dizziness showed that disequilibrium was the dizziness type most frequently reported to occur in combination with other types (55% of cases). As the primary type, it was seen in 28% of cases (97).
Because studies show that up to 50% to 60% of people with dizziness above the age of 65 years experience more than one dizziness symptom (18,96,97, 112), disequilibrium is likely a part of many geriatric causes of dizziness. The underlying mechanisms for disequilibrium vary, but disorders of the visual, vestibulospinal, proprioceptive, somatosensory, cerebellar, pyramidal, and extrapyramidal motor systems can all cause this type of dizziness.
In most studies of older people, the category of nonspecific dizziness comprises 17% to 33% of the study samples (18,26,51,97,99,112). An important reason for this variability in prevalence is the difference in how each study accounts for various psychiatric problems (e.g., panic disorders, anxiety, and obsessive-compulsive and mood disorders). It is also likely that cognitive decline in some older people makes reporting of symptoms, especially in large epidemiologic surveys, inaccurate or vague.
ANATOMY AND PHYSIOLOGY OF DIZZINESS
Before a discussion of the multiple causes of dizziness can begin, it is important to appreciate some of the anatomic and physiologic changes that occur with age in the nervous system. Age-related degeneration of the vestibular, cerebellar, visual, somatosensory, and proprioceptive systems can all have important implications for the development of different types of dizziness. Disequilibrium can result from the accumulation of mild to moderate deficits in multiple systems or from more severe deficits in one sensory system. Presyncope usually results from vascular or cardiac causes, and nonspecific light-headedness can have many causes without a clear pathophysiology. In particular, vertigo is attributable to processes that affect the peripheral and central vestibular systems. To appreciate the effects of age-related degeneration on the systems that are known to result in symptoms of vertigo and imbalance requires a familiarity with the normal anatomy and physiology of the vestibular system. Furthermore, central nervous system, visual, and somatosensory signals are as important as labyrinthine input in processing vestibular information. The sense of motion, therefore, is truly multimodal.
PERIPHERAL VESTIBULAR SYSTEM
The human vestibular system is composed of peripheral and central components. Both components function to maintain visual and postural stability during movement and provide sensory input to a perceptual mechanism subserving spatial orientation and navigation. The peripheral system begins with the end organs that transform angular and linear accelerations of the head into neural signals. These transformations occur in two endolymph-filled, paired membranous labyrinths in the petrous portion of each temporal bone. Within each labyrinth is a specialized sensory neuroepithelium arranged in two types of unique sensory receptors: (a) the three semicircular canals (SCCs)—posterior, anterior, and lateral—and (b) the two otolith organs—utricle and saccule. The three SCCs are oriented orthogonally to transduce head rotation about any axis. These function in pairs with a contralateral canal that lies in the same plane (e.g., the lateral SCC pair, the left anterior and the right posterior SCC pair). The otolith organs sense linear acceleration caused by gravity or translation, with the utricular maculae roughly in the same horizontal plane and the saccular maculae close to the midsagittal plane.
Mechanical transduction occurs at specialized projections at the apices of the hair cells. Each SCC has a patch of neuroepithelium at a widening of the canal termed the “ampulla,” where hair cells can be deflected by movement of the cupula, a structure that spans the inner diameter of each canal. When the head is at rest, primary vestibular afferents in the VIIIth nerve have a spontaneous discharge rate, so input from each side is balanced. When the head is accelerated about an axis that lies perpendicular to the plane containing an SCC pair, the cupula is pushed into the column of fluid (endolymph) contained within the canal. The cupula is deflected, exciting hair cells innervating the canal toward which the head is rotating and inhibiting the afferents from the contralateral canal in a push-pull manner. For example, rotation of the head to the right increases the firing rate of VIIIth nerve fibers on the right and decreases in the firing rate of primary vestibular afferents on the left. The brain receives more neural activity from the right compared to the left and correctly interprets this information as rightward head turning in space. This generates leftward slow-phase eye velocity and rightward quick phases of nystagmus. This is the basis for the vestibular ocular reflex (VOR), which provides stable gaze despite head movements during locomotion. The absence of the VOR leads to oscillopsia (i.e., movement of the visual image on the retina) during head movement.
The hair cell processes of the otolith organs are in contact with the otoconial membrane, a structure embedded with calcium carbonate crystals. These “ear stones” are subjected to linear accelerations when the head is tilted with respect to gravity or with changes in linear velocity, generating a shear force that deflects the hair cells. While a normal constituent of the labyrinth, otoconia may become dislodged from an otolith organ and migrate into an SCC, making the canal sensitive to gravity when it normally only responds to head rotation. This is the mechanism of benign paroxysmal positional vertigo (BPPV), discussed later.
Additional peripheral vestibular structures include the cell bodies of primary vestibular afferent neurons in the Scarpa ganglion, with their peripheral process innervating the hair cells and their central processes, which are the Schwann cell-myelinated axons of the vestibular nerve. The VIIIth nerve travels through the internal auditory canal along with the facial nerve, traverses the subarachnoid space, and enters the lateral brainstem at the pontomedullary level. Vestibular nerve axons terminate within the vestibular nuclei and the flocculonodular lobe of the cerebellum.
CENTRAL VESTIBULAR SYSTEM
The central vestibular system is composed of projections from the four vestibular nuclei (superior, inferior, medial, and lateral) and the vestibulocerebellum (flocculonodular lobe and posterior vermis). These nuclei project to brainstem, thalamic, and spinal cord targets involved in orienting and reflexive righting movements of the eyes (VOR), head and neck (vestibulocolic system), and body (vestibulospinal system). The cerebellum is crucial for adaptation through inhibition of the brainstem vestibular neurons via direct Purkinje cell projections, and it influences ocular motor function via fibers from the fastigial nucleus. The nodulus of the cerebellum and commissural brainstem connections play a role in the central velocity storage mechanism, which is responsible for the duration of nystagmus following labyrinthine stimulation. To summarize the activity of the central vestibular system is well beyond the scope of this chapter, and the reader is referred to texts devoted to this topic (56). However, central vestibular structures involved in the generation of horizontal and vertical VOR eye movements are important for clinicians caring for patients with dizziness to understand because nystagmus is a compelling and informative examination finding in many of these patients.
Movement of the head about the yaw axis of the body (horizontally, as if saying “no-no”) stimulates the lateral SCC, as mentioned earlier. To maintain fixation on a salient visual target, such as an oncoming car, the eyes are moved in a lateral conjugate fashion away from the direction of head movement. The distance and speed that the eyes move are dictated by the neural activity initiated by the magnitude and velocity of the response from the lateral SCC. Many pathways are shared with the saccadic system, which organizes a coordinated burst of activity required to move the eyes and shift gaze onto a target. The paramedian pontine reticular formation (PPRF) is the burst generator for horizontal rapid eye movements (saccades and quick phases of nystagmus), whereas another pontine nucleus, the nucleus prepositus hypoglossi (NPH), integrates the burst signal to an eye position signal. This latter function maintains final eye position achieved by the burst and allows for stabilization of the eyes in an eccentric position in the orbit. A similar midbrain system initiates and maintains eye movements in response to head movements about the pitch axis (vertically, as if saying “yes-yes”). The PPRF counterpart in the vertical system is the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), and the corresponding integrator is the interstitial nucleus of Cajal (INC). Deficits in gaze holding, caused by structural or toxic metabolic damage, compromise these neural integrators and result in direction-changing, gaze-evoked nystagmus with quick phases in the direction of attempted gaze. Cerebellar dysfunction also causes an ipsilateral deficit in gaze holding and a gaze-evoked nystagmus. This should be distinguished from nystagmus that occurs following a unilateral vestibular loss, which is a direction-fixed spontaneous nystagmus that may be observed with the eyes in the straight-ahead position (especially with fixation removed).
One important anatomic fact allows for the rapid excitation of the proper eye muscles via VOR pathways. Individual SCCs excite only the specific oculomotor nuclei necessary to move the eyes in the opposite direction of the head movement responsible for the activation of that SCC. In other words, the VOR acts to maintain stable gaze by activating the eye muscles needed to precisely counteract any three-dimensional head movement. Thus, pathologic nystagmus can reveal its vestibular origins when it occurs in a direction predicted by dysfunction of one or more SCCs. All of these reflexive movements of the eye are under the influence of the cerebellum, cortex, and sensory systems. A loss of vestibulocerebellar function alone can lead to inaccurate eye movements, nystagmus, and sensations of vertigo. A loss of cortical activity leads to a lack of saccadic eye movement necessary for rapid fixation of a visual target. A loss of visual sensation often leads to a spontaneous horizontal and vertical nystagmus and drift.
Table 8-2.Age-Dependent Changes in the Vestibular System
Labyrinths
Deformation of walls, abnormal endolymphatic flow
Cupula
Deposition of debris, inaccurate response to movements
Otoconia
Fragmentation, formation of endolymphatic debris
Hair cells
Apices accumulate lipofuscin
Cilial derangement, fusion, formation of giant cilia
Loss in cristae (40%), loss in maculae (20% to 30%)
Scarpa ganglion
Large decrease in number of neurons over 60 years
Saccular nerve
Degeneration of small and large fibers
Utricular nerve
Degeneration of small and large fibers
Vestibular nerve
Decrease in number of myelinated fibers over 40 years
Slower conduction times with age
Vestibular nucleus
Loss of neurons (3% per decade) between ages 40 and 90 years
Cerebellum
Dramatic decrease in Purkinje cell number over 60 years
Two additional basic principles are worth mentioning. First, the central vestibular system has the ability to adapt to changes in peripheral sensitivity with time. After an acute unilateral loss of labyrinthine function, for instance, the initial response to the altered input is nausea, ataxia, and a sensation of vertigo, with nystagmus beating toward the intact side. Many days later, the vertigo and associated symptoms dissipate, and only careful examination may reveal the imbalance between the two ears. This adaptive response to an acute change requires an intact central vestibular system and cerebellum, and this capacity for plasticity is reduced with age (75). Second, the central vestibular system works with cortical structures to maintain posture and a sense of position in space. This can be important in conditions that mainly affect the cortex and deep white matter projections such as multi-infarct dementia and frontotemporal atrophy.
AGE-RELATED CHANGES IN THE ANATOMY AND PHYSIOLOGY OF DIZZINESS
Peripheral and central vestibular structures degenerate with age (Table 8-2). The functional implications that are suggested by the loss of these structures are multiple. Loss of peripheral vestibular components such as hair cells (up to 40% in crista ampullaris and 30% in the maculae), Scarpa ganglion cells (especially over 60 years of age), and saccular and utricular nerve degeneration can all lead to increased neural response times (81,83,84). After the age of 40, a selective loss of large-fiber vestibular axons also results in increased conduction times (9,10). Within the labyrinths, otoconia fragmentation and deposition on the cupula have been demonstrated to occur with aging (85). The increased incidence of BPPV as a function of age may be related to this anatomic change (74). Others claim that changes, such as deformation of the labyrinthine walls, that occur with age can lead to altered endolymphatic flow and symptoms of vertigo (90).
Central vestibular structures also undergo changes with age. It is estimated that a 3% decrease occurs per decade in the number of neurons in the vestibular nuclear complex in humans (57). Ageinduced loss of cerebellar Purkinje cells can decrease the coordination of movements and visual-vestibular adaptability (36,113). In a study of 90 healthy people of widely varying ages, a 2.5% per decade decrease in Purkinje cell number from ages 0 to 100 years was found. The relationship between age and cell loss was curvilinear and showed no profound difference until the fifth or sixth decade, when a precipitous drop in cell number was noted (36). It is thought that the age-dependent atrophy of the cerebellar vermis, especially lobes 6 and 7, may also play a role in disorders of the visual-vestibular system that result in sensations of dizziness (80).
Impairment of distal somatosensory function and proprioception also occurs with age and can lead to feelings of disequilibrium or “spindle vertigo” (26,58,95). As vestibular degeneration accumulates with age, reliance on somatosensory systems for balance is increased. In a study of 30 healthy people aged 20 to 81 years, the subjective sensation of straight-ahead was demonstrated using a subject-controlled laser pointer on a blank screen. The head-fixed measurement was made with and without unilateral neck vibratory stimulation. Both young and old subjects showed that subjective straight-ahead moved toward the side of vibratory stimulation (presumably because of compensation secondary to the illusion of movement away from the side being vibrated). However, older subjects showed significantly greater changes from true straight-ahead than the younger subjects (106). This implies that compensatory systems are part of a normal sensory substitution process in the course of aging. It is already known that an increase in the gain of the cervico-ocular reflex occurs after bilateral vestibular lesions in humans (89). Thus, even a mild to moderate deficiency in visual or somatosensory systems can be an important predisposing risk factor for the development of dizziness or unsteadiness.
Degenerative changes in the vestibular system attributable to age are well known; however, the functional implications of these changes are less well understood. The VOR can be tested in humans using electronystagmography (ENG), in which eye movements are recorded using electro-oculography (EOG) or video-oculography during caloric irrigation of each ear and positional testing. Caloric testing is helpful mainly for determining the symmetry of labyrinthine responses, and results do not correlate with either age-related anatomic findings or functional imbalance (60). Rotational chair studies provide quantitative assessment of VOR gain and phase. The clinical applications of these tests are discussed later in this chapter. Vestibulospinal and vestibulocolic reflexes are also testable in humans with posturography. Normative data for elderly subjects in VOR testing demonstrate a clear decline in function with age. In a 5-year longitudinal study of 110 healthy people aged 75 or older, a decrease in central VOR responses was demonstrated as a function of age. Rotary chair data demonstrated that gain (or the size of response) of the VOR was decreased and the phase lead of the VOR was increased with age (24). Additionally, a significant drop was noted in the average gain of visual-vestibular reflexes and optokinetic nystagmus (OKN). The basis for this may be related to the rapid drop-off in Purkinje cell number after the sixth decade, as previously discussed (36). However, the neural systems responsible for OKN and visual-vestibular responses include many different structures such as the primary visual cortex, frontal and parietal visual motor centers, thalamic and brainstem nuclei, and cerebellum. The authors of this study pointed out that the abnormal visual-vestibular responses they observed could lead to deficits in VOR function with normal head movements, resulting in sensations of dizziness. Plasticity in these pathways is required with changes in spectacle correction or while using bifocals, as many elderly do, which challenges the system even more. Other studies of the VOR and visual-vestibular responses in healthy elderly volunteers show age-related functional changes such as an amplitudedependent decrease in VOR gain and a shorter dominant VOR time constant (increased phase lead) (5,26,75,77). Thus, as evidence supporting the natural aging process as a predisposing factor for dizziness develops, it is important to remember to use age-adjusted normative reference values for comparison.
Colledge et al. (18) reported such a high prevalence of asymptomatic abnormalities in healthy control subjects over the age of 65 years with routine ENG, electrocardiogram (ECG), and magnetic resonance imaging (MRI) testing that these tests had no value in screening for causes of dizziness in the elderly. They did find that posturography was sensitive for symptomatic dizziness, but it lacked specificity. In a separate study, a significant difference in dynamic posturography testing was seen between younger and older healthy people (4). A significant increase was seen in sway velocity for older people with dizziness and imbalance than for older people who were healthy. Increased sway velocity also correlated with an increased chance of falling (4). Other studies find similar results with increased sway velocity and disequilibrium (26). Thus, even if they lack specificity, abnormal sway velocities and dynamic posturography studies may help determine the elderly at risk for falling.
The caloric test, which has also been shown to be of little value in discerning age-dependent changes in healthy individuals (24,77,106), is generally useful in indicating an asymmetry between the two lateral SCC but not in quantifying the overall level of vestibular function. The exception would be in a patient with a significant bilateral peripheral weakness, which is seen following aminoglycoside (usually gentamicin) ototoxicity or with neurofibromatosis Type II. Normal caloric responses have been reported in persons with up to 25% reduction in crista ampullaris hair cells (15,67).
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