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A New Perspective on Vestibular Assessment

Wyngaerde, Kelly Van De, AuD

doi: 10.1097/01.HJ.0000557745.35776.af
Hearing and Balance
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Dr. Van De Wyngaerde is an audiologist completing a vestibular fellowship at Vanderbilt University Medical Center. She is mentored by Gary Jacobson, PhD, and Richard Roberts, PhD.

Research shows that increased severity of hearing loss results in greater brain atrophy and risk for dementia.1 It stands to reason that vestibular loss might also impact brain volume and impair cognitive function. The peripheral vestibular system is responsible for our ability to detect angular and linear head acceleration and deceleration as well as transmit information that is used to control eye movement and maintain posture. The assessment of the vestibular system has been limited to the peripheral end organs and brainstem reflexes (i.e., vestibulo-ocular reflex and vestibulo-colic reflex), which have been carried out through caloric irrigation, vHIT, rotary chair, and VEMP testing. However, recent attention has been directed toward the effects of vestibular system loss and its upstream effect on cortical areas of the brain, including centers that mediate spatial memory and motion perception. Results of these studies support the contention that vestibular loss does, in fact, alter brain function at the cellular level, and that these changes have an effect on behavior.

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IMPACT ON SPATIAL AWARENESS

Much of the data concerning peripheral vestibular impairment and its effects on the brain and cognition stem from research involving rodents. These animal studies have indicated anatomical connections between the vestibular nucleus and the hippocampus, an area of the brain that has long been known to play a vital role in learning, memory, and spatial awareness.2 Complete loss of peripheral vestibular function has been associated with decreased performance in spatial memory tests that are sensitive to the integrity of the hippocampus. For example, rodents whose vestibular systems were destroyed showed permanent deficits in creating spatial maps, resulting in poor performance during navigational tasks.3 It has been proposed that the vestibular system provides a neural substrate for spatial representation that is necessary for successful navigation of an environment.

Evidence from human studies also implicate both the vestibular system and hippocampus as core structures involved in spatial awareness. Brandt, et al.,4 evaluated 10 individuals with complete vestibular loss following bilateral vestibular neurectomies. Performance was measured for non-spatial and spatial memory tasks using the Wechsler memory test (WMT) and the virtual Morris water maze test (vMWMT). All subjects demonstrated normal performance on the general memory tasks; however, performance was significantly poorer in the spatial memory task. Further, review of subsequent MRI studies revealed that these subjects showed, on average, a 17 percent reduction in the hippocampal mass compared to the control subjects. Each of the subjects with hippocampal atrophy were unable to create spatial representation or cognitive maps to navigate the maze. These data support the notion that the hippocampus is involved in spatial aspects of memory processing and this function requires a bilaterally intact peripheral vestibular system. A real-world example of spatial memory in humans would be the inability to locate a car in a large mall parking lot because we have lost the ability to use external landmarks (e.g., the relationship between where we parked and the nearby stores that enable us to locate our parking spot).

The results of subsequent research have supported the contention that chronic loss of vestibular function results in hippocampal atrophy, and thus, spatial memory impairment. In another study similar to that conducted by Brandt, et al., Kremmyda and colleagues5 evaluated 15 individuals with partial bilateral vestibulopathy. Performance was recorded for the vMWMT and hippocampal volume derived from MRI testing was measured. Study results revealed that individuals with partial bilateral vestibulopathy showed hippocampal atrophy and performed worse on the spatial memory task compared to the controls. Interestingly, the deficits seen on the spatial memory task for these patients with a partial loss of peripheral vestibular function were not as severe as those found in the study completed by Brandt, et al. Further, a similar study involving patients with unilateral vestibular dysfunction showed no spatial memory impairment or hippocampal atrophy. Together, these data suggest that the degree of peripheral end-organ impairment is indexed to the severity of spatial memory impairment and that these upstream effects must be both severe and bilateral for anatomical and functional changes to occur.

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FOCUS ON COGNITIVE IMPAIRMENT

Impairments in vestibular projections to the central nervous system have also been associated with health conditions that affect cognition (i.e., dementia or Alzheimer's Disease). One of the earliest biomarkers for these diseases is hippocampal atrophy. Thus, it has been speculated that vestibular deafferentation may also increase the risk of dementia and play a role in the clinical presentations of spatial disorientation and “wandering.” For example, Harun, et al.,7 showed that abnormal otolith function was more prevalent in individuals with mild cognitive impairment and Alzheimer's Disease as compared to their controls. Individuals with bilaterally absent cVEMPS (i.e., a measurement of the functional status of the saccule and the inferior vestibular nerve) had a more than three-fold increased risk for developing Alzheimer's Disease. The authors hypothesized that disruption of the pathway from the otolith end organs to the cortical reception areas are involved in cognitive processing and could underlie the association between vestibular dysfunction and cognition.

Cognitive impairments beyond spatial memory and spatial navigation have also been observed. Popp, et al.,8 compared various domains of cognition such as short-term memory, executive function, processing speed, and visuospatial abilities between individuals with bilateral vestibular loss, unilateral vestibular loss, and healthy controls. Individuals with bilateral vestibular loss performed significantly poorer in all domains as compared to the other two groups. Individuals with unilateral loss were also impaired in several domains and their performance was worse than healthy controls. As had been reported previously, there was a correlation observed between the degree of vestibular impairment and cognitive deficits. These findings once again add support to the hypothesis that having some residual level of input into the central vestibular system was enough to maintain (i.e., protect) cognitive function.

These investigations highlight the upstream effects of severe to profound vestibular end-organ impairment on brain volume and cognition as it relates to spatial and non-spatial memory. However, other aspects of cognitive function are also associated with the vestibular system such as bodily self-consciousness and self-motion perception.

It is a common clinical observation that individuals suffering from peripheral vestibular impairment do not experience any perception of motion when undergoing caloric irrigation or rotary chair testing during the assessment of the vestibulo-ocular reflex. This occurs as a function of the loss of peripheral vestibular system sensitivity (i.e., in much the same way that we lose sensitivity to sound as we accumulate hearing loss as we age). Interestingly, it is not uncommon to encounter patients in the clinic who have normal vestibular end-organ function but do not experience any perception of motion during testing designed to provoke vertigo. Thus, these patients will show normal and robust caloric responses, but, unlike normal patients who will report a sensation of rotation (i.e., vertigo), these patients do not have any sensation of self-rotation.

Several electrophysiologic studies have been conducted to examine this phenomenon. These studies suggest that a lack of motion perception, referred to by some as “nystagmus-sensation dissociation” or “vestibular neglect,” is related to both increased age and postural instability and may represent an impairment in the central integration of vestibular input.9,10 Prior research implicates both the parietal and temporal lobes as regions of the brain that contribute to the perception of self-motion. Studies have shown that pathological changes in these regions, including ischemia, age-related cell loss, and white matter damage, may be the source of altered motion perception during caloric stimulation.9 So, while the peripheral end organ may be intact, pathological changes in the central nervous system that are implicated in vestibular perception may explain altered perception of motion in some individuals. In our clinic at Vanderbilt University Medical Center, it has been observed that patients who do not perceive motion during caloric testing are older and report impairments in postural control and visuospatial impairment. These findings have clinical implications for treatment but also highlight the need for the development of better methods to evaluate the vestibular system from the end organ, through brainstem processing, and up to subcortical and cortical areas of the brain where motion perception and visuospatial recognition occur.

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REFERENCES

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