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Review Article
Exploring the nexus: unilateral vestibulopathy and visuospatial cognitive impairments
Sun-Young Oh1,2orcid, Thanh Tin Nguyen1,3orcid, Marianne Dieterich4,5,6orcid
Research in Vestibular Science 2024;23(4):132-146.
DOI: https://doi.org/10.21790/rvs.2024.014
Published online: December 15, 2024

1Department of Neurology, Jeonbuk National University Hospital, Jeonbuk National University Medical School, Jeonju, Korea

2Research Institute of Clinical Medicine, Jeonbuk National University-Jeonbuk National University Hospital, Jeonju, Korea

3Department of Pharmacology, Hue University of Medicine and Pharmacy, Hue, Vietnam

4Department of Neurology, University Hospital, Ludwig-Maximilians-University, Munich, Germany

5German Center for Vertigo and Balance Disorders, University Hospital, Ludwig-Maximilians-University, Munich, Germany

6Munich Cluster for Systems Neurology (SyNergy), Munich, Germany

Corresponding author: Sun-Young Oh Department of Neurology, Jeonbuk National University Hospital, Jeonbuk National University Medical School, 20 Geonji-ro, Deokjin-gu, Jeonju 54907, Korea E-mail: ohsun@jbnu.ac.kr
*These authors contributed equally to this work as co-first authors.
• Received: July 31, 2024   • Revised: December 9, 2024   • Accepted: December 11, 2024

© 2024 The Korean Balance Society

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • The interplay between vestibular disorders and visuospatial impairments has long captured scholarly attention. While evidence robustly supports visuospatial deficits in bilateral vestibulopathy, findings regarding unilateral vestibulopathy remain equivocal. Recent studies, both animal-based employing vestibular deafferentation models and human-based involving spatial cognitive tasks, hint at potential visuospatial cognitive impairments in individuals with acute and chronic unilateral vestibulopathy. Nevertheless, these results are preliminary and necessitate further rigorous investigation. The posture-first principle is evident in cognitive-motor dual tasks among patients with vestibular disorders. This review synthesizes these emergent insights, aiming to lay a groundwork for future studies that seek to elucidate this complex relationship further.
  • Keywords: Vestibular disease; Cognition; Posture
Traditional views have predominantly recognized the vestibular system as crucial for gaze stabilization and balance maintenance, primarily through reflexive pathways. However, recent research has begun to uncover a broader role for the vestibular system, particularly in spatial cognitive functions—an indispensable faculty for perceiving, understanding, remembering spatial configurations, and navigating environmental spaces in daily activities for both humans and animals [1-4]. The hippocampal formation, pivotal in spatial processing, has emerged as a key neural substrate in the study of vestibular dysfunctions [2,5-12]. While bilateral vestibulopathy (BVP) has been consistently linked to these deficits and hippocampal atrophy, the impacts of unilateral vestibulopathy (UVP) remain controversial, underscoring the need for additional research [1,4,13,14]. Currently, there is growing interest in determining whether unilateral vestibular disorders significantly influence visuospatial abilities in orientation and navigation.
Research on spatial cognitive impairments in UVP has intensified, underpinned by both animal and human studies [10,15-17]. Our investigations using rodent models have highlighted acute deficits in short-term and long-term visuospatial memory and navigation following unilateral chemical labyrinthectomy, with more severe cognitive deficits observed when lesions affected the dominant vestibular side [15,16]. Furthermore, patients with chronic UVP exhibit spatial memory and navigational challenges, the severity of which varies depending on the lesion’s side [9,18]. Variability in spatial strategies, such as allocentric versus egocentric approaches, and attentional deficits across studies may reflect differences in assessment tools and patient-specific factors [1,19,20]. Notably, structural changes such as atrophy in the motion-sensitive area MT/V5 and in parietal-temporal regions ipsilateral to the vestibular lesion have been documented, adding a structural dimension to the observed functional impairments [21]. Such changes appeared also to depend on the extent of the damage, complete or incomplete.
The role of the vestibular system transcends sensory processing to include postural control, acting as a dual sensory and motor mediator [22]. Recent studies suggest that maintaining posture, particularly in challenging or disrupted conditions, requires more attentional resources than previously recognized [23-25]. This is especially apparent in the interactions between the basal ganglia and cerebellum with the brainstem and cortex, which are essential for both automatic and cognitive aspects of postural control [25]. The concept of limited attentional capacity, both structurally and energetically, underlies various hypotheses that posit a competition for resources between postural control and spatial cognitive tasks [26-28]. Kerr et al. [29] observed that while balance tasks impacted spatial memory, they did not affect non-spatial memory, highlighting this resource competition. Given the interactions between visual, vestibular, and proprioceptive systems in maintaining postural control [30], body balance performance could theoretically reflect cognitive function.
This review explores the interplay between visuospatial cognitive functioning and postural control in vestibulopathy patients. It particularly focuses on how cognitive demands and postural control might compete for attention, especially in situations involving unstable posture. This concept adheres to the ‘posture-first’ principle, which prioritizes postural stability over other cognitive tasks when resources are limited [29,31,32]. The aim of this review is to synthesize recent findings in this area, providing interpretative insights and guiding future research endeavors. It highlights the need to consider the attentional limitations in patients with UVP, especially in understanding how these limitations might influence cognitive processing in contexts demanding postural control.
Vestibular Role in Postural Control
Postural control, essential for independent standing and walking abilities, emerges from the complex interplay between the nervous and musculoskeletal systems [22,32]. This control mechanism, illustrated in Fig. 1, involves biomechanical and neurophysiological processes working in tandem to facilitate stability [32,33]. Effective postural control depends on the integrated sensory feedback from the vestibular, visual, and somatosensory systems; the collective interpretation of these signals is essential for precise body orientation and equilibrium in the three-dimensional (3D) space [22,33]. The vestibular system, integral to both sensory and motor functions, plays a pivotal role in the nervous system’s postural control mechanisms (Fig. 1) [22]. Serving as an inertial sensor, it detects head accelerations, capturing translational and rotational movements [22,34]. The system’s afferents remain vigilantly active, swiftly identifying even subtle head motions, even during rest [34]. Central processing of vestibular information is characterized by its extensive convergence and robust multimodal integration, involving interactions among vestibular (canals and otoliths), vision, and proprioceptive inputs—all indispensable for effective regulation of posture and gaze [22,34]. Vestibular inputs trigger various reflexes: the vestibulo-ocular reflex, vestibulocollic reflex (VCR), and vestibulospinal reflex (VSR) (Fig. 1) [22,35]. The VCR, via the medial vestibulospinal tracts, counters head movement by eliciting compensatory head motions, while the VSR modulates lower limb postures, intensifying extensor activity on the head tilt’s side and flexor activity contrarily [22,35].
A comprehensive systematic review and meta-analysis of neuroimaging studies on human postural control identified numerous brain regions implicated in this process, including the cerebellum, brainstem, basal ganglia, thalamus, and cortical areas [36]. Dijkstra et al. [36] discerned that static postural control activates distinct neural regions like the brainstem (midbrain, pons [lateral vestibular nucleus, lateral reticular formation] and pontomesencephalic junction), thalamus (anterior thalamic radiation), cerebellum, basal ganglia (caudate nucleus, putamen, and pallidum), hippocampal formation (anterior hippocampus, parahippocampal cortex, and fusiform gyrus) and the cortex, while dynamic control involves the red nucleus, cerebellar vermis, and striatal and cortical regions (frontal, cingulate and parietal lobules). Structural brain metrics revealed a stronger correlation between the frontal cortex and dynamic postural control outcomes compared to static control outcomes [37]. During actual stance, brain activations are noted in the occipital, anterior cingulate, and paracentral lobule, while deactivations occur in the occipital and frontal cortex. Connectivity analysis revealed an integrated dynamic postural control network, characterized by enhanced coupling between the thalamus and globus pallidus, and between the supplementary motor area and the mesencephalic locomotor region [38].
The interaction of the vestibular system, postural control, and spatial cognition becomes evident through the involvement of the basal ganglia and hippocampus [36,39]. Notably, enhanced hippocampal volume has been correlated with reliance on vestibular and proprioceptive input for postural stability in older adults, suggesting a hippocampal role in processing sensory information essential for upright posture [36,40]. Furthermore, disruptions in basal ganglia activity, particularly within the putamen and caudate, are implicated in the postural instability and fall risk seen in Parkinson disease, highlighting the influence of these structures on postural regulation [25,36]. This points to the potent inhibitory signals from basal ganglia outputs to brainstem nuclei that orchestrate postural muscle tone [25]. Connections between the vestibular system and the striatum are well-established. The dorsal striatum, comprising the putamen and the caudate nucleus, plays a crucial role in learning and memory, interacting with the hippocampus to process cognitive information [41]. Potential pathways for transmitting vestibular information to the striatum involve the pedunculopontine tegmental nucleus, which has been shown to exhibit plasticity following bilateral vestibular loss [42]. Moreover, the pedunculopontine tegmental nucleus, known to project to the striatum, is also connected to the vestibular nucleus.
Illustrating the role of vestibular signals in postural control presents challenges under normal conditions, such as standing on a stable surface with eyes open, where proprioceptive and visual inputs likely predominate. However, the importance of vestibular function in postural control becomes notably evident in situations with limited proprioceptive information and unclear visual inputs [43,44]. Vestibular signals may contribute in two ways: through reflex responses to imposed displacements and through conscious perception of postural displacement [45]. The vestibular system, signaling the direction of gravity, plays a significant role in aligning the head and trunk in animals [22]. Vestibular dysfunction often leads to a postural misalignment, characterized as a vestibular syndrome, which includes both static and dynamic posturo-locomotor deficits, as observed in numerous studies [15,16,46]. In rodents, unilateral vestibular lesions result in static deficits like asymmetrical muscle tone in limbs (hypertonic on the intact side, hypotonic on the lesioned side), an enlarged support surface, nystagmus, and head tilting towards the lesion side [46]. Dynamic deficits are evident in behaviors like retropulsion, tumbling, and circling [46]. Vestibular compensation over time reduces asymmetrical posturing and restores normal alignment [22]. In humans, the impact of unilateral vestibular lesions on postural alignment is more variable and transient compared to rodents [22]. Acute UVP may cause lateral head flexion and gait deviation toward the affected side, but within weeks, postural alignment and control often become indistinguishable from those without vestibular impairment [22], especially when compensation is not restricted by additional lesions at the cerebellar or cortical level [47-49].
Vestibular Role in Visuospatial Cognition
The vestibular system is recognized for its critical role in cognitive processes such as self-motion perception, bodily self-consciousness, spatial orientation, navigation, learning, memory, and object recognition, as evidenced by extensive research [1,2]. Through the integration of peripheral vestibular signals with other sensory inputs, this system cultivates multisensory pathways, enhancing perception and navigation efficacy [50]. Current studies delineate five key pathways where vestibular signals might project to structures linked with spatial cognition: thalamocortical, cerebellocortical, hippocampal theta rhythm, head-direction, and basal ganglia pathways (Fig. 2) [2]. Spatial cognition is a fundamental capability in humans and animals, underpinning the ability to perceive, understand, remember, and interact with the spatial dimensions of the environment [1]. It involves comprehending attributes such as size, shape, scale, and spatial relationships among objects, including distance and orientation [3]. These spatial constructs are integral to a breadth of cognitive functions, from attention and perception to memory and language, and they are deeply embedded in various psychological processes [3]. Impairments in spatial cognition are on one hand recognized as precursors to mild cognitive impairment and Alzheimer disease [51]. On the other hand, spatial impairments can also occur in peripheral vestibular failure [52].
Two primary strategies in spatial navigation are identified: egocentric and allocentric navigation [53]. Egocentric navigation, or body-centered, enables individuals to pinpoint a destination using their own position as a reference. This strategy often involves mastering stimulus-response associations, which might include sequences of bodily turns, route details, path integration, or proximate cues linked to the goal [53]. Conversely, allocentric navigation, world-centered, is a more intuitive approach that employs a map-like strategy, drawing on distal visual landmarks [53]. These two navigational strategies are associated with distinct neural underpinnings: allocentric navigation is supported by the hippocampal formation, whereas egocentric navigation is supported by the caudate nucleus [53]. Intriguingly, beyond age-induced modifications in spatial navigation, gender also influences preference: males typically favor allocentric methods, whereas females are inclined towards egocentric ones [54]. Patients with cognitive impairment employed more egocentric 3D pointing strategies while patients with BVP but normal cognition and healthy controls used more world-based solutions [52]. This suggests that despite decreased allocentric navigation, BVP patients may adopt world-based strategies, leveraging visual and proprioceptive cues to compensate for vestibular deficits.
Brandt and Dieterich [55] postulated that the vestibular system’s involvement in spatial orientation might differ depending on whether an individual is in dynamic (motion) or static (stationary) conditions. In dynamic scenarios, otoliths and semicircular canals function in an “allocentric mode” for orientation and navigation. Contrastingly, during stationary states, with only minimal vestibular stimulation from slight head movements, otoliths are believed to function in an “egocentric mode” [51,55]. In light of this, one might discern variations in spatial cognitive performance in a virtual Morris water maze (MWM) when comparing a walking-based (dynamic) approach to a screen-based (static) one [51,55]. Generally, spatial orientation and navigation gain enhanced benefits from the rich data in a dynamic mode, offering a comprehensive depiction of motion in a 3D space, than from a limited two-dimensional static perspective. Recent animal research by El Mahmoudi et al. [10] revealed that unilateral vestibular neurectomy causes significant, enduring deficits in egocentric and allocentric spatial memory. While allocentric memory shows partial long-term recovery—possibly due to visual sensory substitution—egocentric memory challenges often persist despite vestibular compensation [10]. Similarly, Zheng et al. [17] reported that recovery of egocentric spatial memory functions is protracted, with improvements seen at 6 months after lesion, as opposed to allocentric memory. These findings underscore the profound impact of vestibular inputs on egocentric spatial representation [56,57]. In UVP, the observed reduction in egocentric navigation likely stems from asymmetrical vestibular input, which impairs body-centered spatial representations crucial for this strategy. Allocentric navigation, however, may remain less affected due to the compensatory role of contralesional vestibular nuclei and visual substitution, which supports distal landmark-based orientation. Following unilateral vestibular loss, the vestibular nuclei adapt over time, increasing the compensatory role of the contralesional side for vestibular function restoration [58]. The role of visual inputs is also paramount in reestablishing both navigation strategies, with distal cues aiding allocentric and proximal cues assisting egocentric memory functions [10].
Asymmetry in Vestibular Function: Comparative Analysis of Lateralization Effects in Humans and Rodents
The vestibular systems, while is bilaterally organized with parallel ascending pathways, demonstrate an inherent asymmetry known as vestibular lateralization [59]. In humans, there is often a correlation between the dominant hand and the dominant side of the vestibular system, suggesting that vestibular input on the dominant side might be processed by a more complex interplay of cortical and subcortical networks [59-61]. This lateralization can lead to discrepancies in the effects of vestibular lesions; damage on the dominant side can result in more pronounced motor and visuospatial cognitive deficits, as well as a protracted and less complete recovery [16,21,62]. This was evidenced by our previous study, we found that right-handed individuals with right-sided unilateral vestibular neuritis scored lower on tests of visuospatial perception and memory than those with left-sided lesions [62]. Furthermore, Hüfner et al. [9] showed that patients with chronic right-sided UVP faced greater challenges in spatial memory and navigation compared to those with left-sided UVP in a virtual MWM task. Becker-Bense et al.’s utilization of positron emission tomography imaging [63] highlighted that the signal changes indicative of vestibular deficits, notably between acute and chronic stages, were more substantial in patients with right-sided vestibular neuritis than in those with left-sided lesions.
Contrasting with human patterns, rodents generally exhibit left-sided vestibular dominance [59,61]. Our previous research utilizing a unilateral labyrinthectomy model in mice, with Y maze and MWM assessments, demonstrated that those with left-sided lesions had greater impairments in both short-term and long-term visuospatial memory and navigation than those with right-sided lesions [16]. This distinction between species underscores the complexity of the vestibular system and its integrative role in spatial orientation and cognition.
Attentional Demands and Postural Control
Healthy adults maintain balance seemingly effortlessly, without overt conscious attention. This apparent simplicity masks an intricate process where the central nervous system constantly integrates sensory inputs, predominantly from visual, vestibular, and somatosensory sources, to monitor and adjust the body’s center of gravity [24,25]. Steady stepping movements, involving postural reflexes that encompass head-eye coordination along with the proper alignment of body segments and the maintenance of an optimal level of postural muscle tone, are orchestrated by descending pathways originating in the brainstem and projecting to the spinal cord [25]. Notably, the reticulospinal pathways from the lateral mesopontine tegmentum significantly influence this process [25]. Recent insights suggest that postural control, especially under challenging conditions or when system disruptions arise, requires more attention than traditionally believed (Fig. 3) [23-25]. In unfamiliar settings, walking requires cognitive postural control based on body schema and spatial motion awareness [25]. The elderly’s increased gait variability might arise from added cognitive networks, including structural changes, modified proprioceptive feedback, and heightened cognitive control for posture stability [64]. The temporoparietal association cortex provides essential cognitive input for upright posture and motor planning [25]. Motor cortical areas then make anticipatory adjustments for intentional movements [25]. The basal ganglia and cerebellum, through connections with the brainstem and cortex, might affect both automatic and cognitive aspects of posture and gait [25]. As postural tasks become more complex—for instance, in tandem Romberg stances, external balance disturbances, or navigating obstacles—the demands on attentional control increase [65]. Given the inherent limits of attentional capacity, encompassing both structural and energetic facets [66], several assumptions have arisen regarding the concept of competition for attentional resources between postural control and cognition [26-28]. This competition becomes more evident in multitasking scenarios compared to isolated postural tasks, especially in the elderly.
Dual-Task Interference: Balancing Cognition and Motor Function
In daily life, dual-task postural control—maintaining stability while concurrently executing a cognitive task, such as conversing while standing—is commonplace [26]. Therefore, it is assumed that, in cognitive-motor dual tasks, attention will be allocated to both sensorimotor and cognitive activities. In such cognitive-motor dual tasks, attention must be judiciously divided between sensorimotor and cognitive endeavors. Several models have been proposed to explain the effects of dual tasks on human performance; however, consensus on which theory best predicts these effects remains elusive. Widely recognized theories include (Fig. 4) [26,67,68]: (1) capacity sharing theories, which suggest that a limited pool of cognitive resources exists, requiring tasks to compete for these resources; (2) bottleneck theories, which propose that dual-task interference occurs because certain cognitive processes must be completed sequentially, creating a “bottleneck” where tasks converge and are processed serially, potentially delaying task execution [69]; and (3) cross-talk theories, which predict a facilitation effect when two tasks utilize similar domains and neural populations, as they would not interfere with each other [70]. Such dual-task scenarios can affect the primary task’s proficiency, reflecting the impact of the concurrent secondary task [26]. Specifically, the effectiveness of postural control may decrease under dual-task conditions compared to single-task conditions, depending on the cognitive load of the simultaneous task.
Recent investigations have delved into the intricate interplay between cognitive endeavors, particularly spatial cognition, and postural control functions within cognitive-motor dual-task paradigms [26,29,71,72]. In such scenarios, where the brink of one’s information-processing capacity is tested, judicious attention distribution between concurrent tasks becomes paramount. A study by Li et al. [73] revealed that elderly participants often decelerate their gait when faced with demanding memory tasks, underscoring an inclination in the aged to prioritize ambulation and balance over memory engagement. Contrastingly, Siu and Woollacott [65] discerned that, within a dual-task milieu, diverting attention to an ancillary task does not compromise postural regulation. It appears that an ample degree of attention spontaneously gravitates toward ensuring balance, even when individuals are directed to concentrate on a secondary cognitive endeavor [65]. Some authors have proposed a U-shaped relationship between cognitive demand and postural sway [72,74,75]. Within this framework, minimal cognitive stress augments arousal in a manner beneficial for postural regulation, whereas intensive cognitive demands amplify arousal to levels that are counterproductive, culminating in performance declines [72,74].
Evidence indicates that challenging balance tasks can diminish cognitive performance. However, the influence of cognitive tasks on balance remains inconsistent [76]. A U-shaped relationship has been suggested by some authors to depict the effect of cognitive demand (serving as a secondary task) on postural sway, which in this context is the primary task of postural control [72,74,75]. The descending part of the U-shaped curve suggests that a basic, low-demand cognitive task might enhance attention, improving postural performance and reducing sway [72,74]. In contrast, the ascending segment of the U-shaped curve signifies that intricate, high-demand cognitive tasks may disrupt postural control due to resource competition between domains, resulting in greater postural sway [72,74]. The association between postural control and spatial cognition is largely postulated based on evidence suggesting a mutual reliance on vision. Difficulties in postural maintenance or observed disruptions in those with visual impairments highlight the paramount importance of vision in postural control. Concurrently, visual input is pivotal for visuospatial perception and navigation.
Dual-task walking has been found to be associated with changes in the activation of both the indirect locomotor pathway and the frontoparietal network, which are linked to attention, working memory, and executive function [64]. A recent hypothesis suggests a connection between the mechanisms governing postural control and spatial cognition, emphasizing interactions within the basal ganglia pathways, particularly the vestibulo-striatal connections [39]. Though initially tied mainly to postural control, these connections have been increasingly acknowledged for their involvement in learning and memory, and their synergy with the hippocampus in cognitive information processing [39]. Importantly, the dorsal striatum, encompassing the putamen and caudate nucleus, plays a pivotal role in these functions [39].
Visuospatial Cognition in Unilateral Vestibulopathy
Pathophysiological evidence has increasingly underscored the link between UVP and cognitive impairments. Numerous studies report cognitive deficits, particularly in visuospatial cognition, in individuals with UVP. Our previous study, using a rodent model of unilateral labyrinthectomy and employing Y maze and MMW tasks, has revealed impairments in both short-term and long-term visuospatial memory and navigation [15,16]. Zheng et al. [17] demonstrated that rats subjected to unilateral labyrinthectomy faced challenges in performing the dead reckoning task in darkness 3 months after lesion, though interestingly, these impairments showed recovery by the 6-month mark. This study provided important insights into the potential for cognitive recovery post-UVP. El Mahmoudi et al. [10] contributed significantly with their comprehensive study using various cognitive tasks, including the T-maze, 8-arm radial maze, object recognition task, and continuous navigation task. Their research on rats post-unilateral vestibular neurectomy revealed significant and enduring deficits in various facets of both egocentric and allocentric spatial memory, lasting up to 3 months postoperation. These behavioral deficits were accompanied by persistent alterations in hippocampal plasticity, as evidenced by a marked decrease in cell proliferation (monitored with 5-Bromo-2’-deoxyuridine) and an increase in N-methyl-D-aspartate receptor GluN2B subunit expression, particularly in the ipsilesional dorsal hippocampal formation [10]. This study underscored the profound and lasting impact of UVP on brain plasticity and memory function. However, conflicting findings regarding hippocampal structural changes in UVP have been reported. While some studies show significant volume reductions in the ipsilesional hippocampus, others fail to detect such changes, possibly due to variability in imaging techniques, sample sizes, or compensatory neural plasticity. These discrepancies highlight the need for standardized protocols and longitudinal studies to elucidate the relationship between vestibular dysfunction and hippocampal morphology.
In a human study, Oh et al. [62] utilized the Visual Object and Space Perception battery and the block design and Corsi block-tapping tests to illuminate moderate visuospatial memory impairments during the acute phase of UVP, with a notable recovery observed by a 1-month follow-up. Notably, these deficits were more pronounced in those with vestibular lesions on the vestibular dominant side than in those with lesions on the opposite side [62]. Guidetti et al. [14] found that patients with UVP showed significantly lower scores in the Corsi block test compared to healthy controls across all age groups, suggesting a pervasive impact of UVP on spatial memory. Péruch et al.’s work [77] in a virtual environment further reinforced the idea that asymmetrical vestibular peripheral loss leads to comprehensive impairment of internal spatial representation, impacting complex spatial processing tasks. This was particularly evident in Ménière’s disease patients who underwent unilateral vestibular neurectomy, as they exhibited notable disruptions in both direction and distance components of spatial tasks. Ayar et al. [78] detected visuospatial functional impairments during the acute phase using the cancellation test, Benton’s Judgment of Line Orientation test, and Rey–Osterrieth Complex Figure test. Deroualle et al. [79] evidenced that UVP negatively impacted embodied spatial cognition, especially in tasks requiring a third-person perspective. In a study involving 16 chronic UVP patients, Popp et al. [18] revealed significant visuospatial ability impairments, evidenced by lower scores on the visual scanning test and the Corsi block-tapping test, compared to healthy controls. Notably, neither the lesion’s side nor the disease’s duration influenced cognitive performance. Hüfner et al.’s investigation [9] in patients with chronic UVP due to vestibular schwannoma removal was particularly enlightening. Using virtual MWM testing, they observed spatial memory and navigation deficits exclusively in patients with right-sided UVP, while left UVP patients did not exhibit such deficits. Thus, the extent of vestibular lesion—complete or incomplete—also seems to play a crucial role. Furthermore, manual volumetric analysis revealed no hippocampal atrophy in either patient group [9]. Subsequent voxel-based morphometry (VBM) analysis also did not detect gray matter atrophy in the hippocampus or insular cortex. However, they identified ipsilateral atrophy in the motion-sensitive area MT/V5 and parietal-temporal regions, integral parts of the cortical vestibular network [21]. In contrast, zu Eulenburg et al. [80] found in their VBM analysis in 22 patients 2.5 years after the onset of vestibular neuritis, volume increases in the medial vestibular nuclei, the right gracile nucleus and the area of the pontine commissural vestibular fibers whereas a relative atrophy was observed in the left posterior hippocampus and right superior temporal gyrus. Patients with residual canal paresis further showed a volume increase in MT/V5 bilaterally. These findings indicate that the process of central compensation after vestibular neuritis occurs in three different sensory systems, the vestibular, somatosensory, and visual. Furthermore, Conrad et al. [20] provided a different perspective with respect to neglect signs, finding that unilateral vestibular lesions did not lead to spatial hemineglect, but rather were associated with mild attentional deficits across both visual hemifields. This collective research underscores the multifaceted impact of UVP on cognitive functions, particularly visuospatial abilities, offering invaluable insights for clinical approaches and rehabilitation strategies.
Attentional Dynamics in Postural Control in Unilateral Vestibulopathy
A solid body of experimental evidence distinguishes between controlled and automatic attentional processes [66]. Contention scheduling, the lower attentional level, manages familiar and routine situations, while the supervisory attentional system, a higher level, addresses more intricate and demanding scenarios [66]. In the general population, postural control is often achieved without the need for decision-making or invoking complex cognitive processes indicative of automatic attention. Yet, for UVP patients, tasks requiring executive attention disrupt this automaticity, necessitating controlled attentional engagement [66]. Research indicates that individuals with chronic vestibular disease need to allocate more attention to maintain postural stability compared to healthy individuals [27,31]. Sprenger et al. [81] found increased postural instability (measured by sway speed) in UVP patients during cognitive-motor dual tasks, such as arithmetic calculations while balancing. This highlights the need for cognitive control over posture in those with compromised vestibular function. Similarly, Nascimbeni et al. [82] observed a decline in the ability to count backward while walking in subacute UVP patients, compared to performing the task while seated. This suggests a higher demand for attentional resources to compensate for the disrupted vestibular input during movement, impacting motor-sensory integration [82]. Employing a cognitive-motor dual-task paradigm, Redfern et al. [28] assessed patients who had effectively compensated for vestibular lesions without evident dizziness or postural deficits. They found these patients, even in seated postures, had slower reaction times—pointing to a need for enhanced attention. This indicates that compensating for vestibular deficiencies isn’t merely automatic but demands consistent heightened attentional commitment [28]. Broadly, it’s posited that attention can modulate the temporal dynamics of postural control [28]. Attention’s role in gait initiation, requiring more focus than steady-state walking, is marked by anticipatory postural shifts, influencing step preparation and execution [27].
Balancing Cognition and Posture in Vestibular Disorders
Through cognitive-motor dual tasks in patients with vestibular disorders, Andersson et al. [31] illuminated the link between postural sway (under both stable and unstable conditions) and cognitive function, characterized by backward counting. Notably, dual-task interference is primarily manifested in cognitive performance rather than balance, reinforcing the idea that balance often takes precedence in unstable postural situations—echoing the posture-first principle observed in cognitive-motor dual tasks [29,31,32].
Drawing on Kahneman’s capacity model of attention, Lacroix et al. [83] suggested that patients with UVP might suffer cognitive deficits even when they successfully compensated for postural imbalances (Fig. 5). This theory proposes that cognitive resources are diverted to maintaining balance due to vestibular loss, which could explain cognitive impairments observed in these patients. Interestingly, the model suggests that UVP patients without postural compensation might experience challenges in cognitive function, potentially clarifying the observed cognitive dysfunctions reported in various clinical vestibular studies [39]. In their study on compensated UVD patients using motor-cognitive dual tasks, Redfern et al. [28] observed increased postural sway and decreased sway velocity during reaction time tasks. Importantly, reaction times fluctuated based on the postural challenge, especially during the translational platform condition. Their findings indicate an interference in spatial orientation updating when attention is split due to simultaneous information processing. Additionally, this research unveiled a pattern of shifting attention between postural control tasks and secondary information processing during postural disturbances. These UVP patients, even after compensating for vestibular lesions, demonstrated a higher attentional demand than their healthy counterparts. This heightened attention potentially stems from sensory integration levels, where various sensory signals converge for spatial orientation [28].
Given the accumulating evidence highlighting the role of attention in postural control for UVP patients, it’s conceivable that the allocation of limited cognitive resources, particularly in the visuospatial domain, might be negatively impacted (Fig. 5) [39,83]. Kahneman’s capacity model of attention provides a foundational hypothesis for grasping these findings in UVP patients, and continued research is vital to refine this conceptual framework. Emphasizing the interplay between cognition and motor function, especially when adhering to the posture-first principle in UVP patients, should motivate scholars to judiciously choose suitable visuospatial cognitive tasks. Considering the patients’ postural states during experimentation will facilitate more consistent cross-study results, fostering a robust understanding of visuospatial cognitive deficits in UVP and developing adequate and individual rehabilitation strategies to further improve compensation processes in the visuospatial domain. The latter is especially important in the elderly with reduced resources for compensation and incipient cognitive decline.
Beyond the potential oculomotor and postural dysfunctions, UVP is emerging as a possible contributor to cognitive deficits. Yet, the exact nexus between UVP and a decline in visuospatial cognition remains to be delineated. The advent of advanced virtual experimental methodologies offers a more refined approach to research, fostering thorough investigations. As we factor in elements like gender, age, and lesion localization, understanding the intricate balance between postural control and visuospatial cognition becomes paramount. This is especially true when contemplating the postulated posture-first principle observed in UVP patients. These revelations have profound implications for diagnostic procedures, therapeutic interventions, and the conceptualization of tailored rehabilitation plans.

Funding/Support

None.

Conflicts of Interest

Marianne Dieterich is a member of the Editorial Board of Research in Vestibular Science and was not involved in the review process of this article. The authors declare no other conflicts of interest.

Availability of Data and Materials

All data generated or analyzed during this study are included in this published article. For other data, these may be requested through the corresponding author.

Authors’ Contributions

Conceptualization: SYO; Supervision: MD; Writing–Original Draft: SYO, TTN; Writing–Review & Editing: MD.

All authors read and approved the final manuscript.

Acknowledgments

This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Korean government (Ministry of Science and ICT) (No. 2022R1A2B5B01001933) and by the Biomedical Research Institute Fund, Jeonbuk National University Hospital. MD’s work was supported by a grant of the German Foundation for Neurology (Deutsche Stiftung Neurologie, No. 80721017).

Fig. 1.
Roles of vestibular system in postural control. This figure illustrates the integration of sensory inputs (vision, vestibular, and somatosensation) and motor outputs required for maintaining postural stability. Key components include the vestibulo-ocular reflex, vestibulospinal reflexes, and anticipatory postural responses, all of which work together to stabilize gait and control posture.
rvs-2024-014f1.jpg
Fig. 2.
Schematic distribution of central vestibular pathways. This schematic highlights the anatomical connections between the vestibular system and cortical, subcortical, and spinal regions, emphasizing their role in sensory integration and motor control. Pathways linking the vestibular nuclei to the temporoparietal cortex, brainstem, cerebellum, and limbic structures are depicted. Adapted from the article of Hitier et al. [2], according to the Creative Commons License.
rvs-2024-014f2.jpg
Fig. 3.
Hypotheses of the cognitive process of posture-gait control. This figure proposes a framework distinguishing cognitive and automatic processes in postural and gait control, emphasizing the interaction between sensory input transmission, bodily cognition, motor programming, and control. SMA, supplementary motor area; PM, premotor cortex.
rvs-2024-014f3.jpg
Fig. 4.
The main theories of dual-task. This diagram summarizes key dual-task theories, including capacity-sharing, bottleneck models, and time-sharing hypotheses, providing insights into how attentional resources are distributed between cognitive and motor tasks. Reproduced from the article of Bayot et al. [26] with the permission of Elsevier.
rvs-2024-014f4.jpg
Fig. 5.
Proposed overview of the visuospatial cognitive performance following unilateral vestibulopathy. This model outlines potential outcomes of vestibular compensation, from normal to slightly abnormal visuospatial function in compensated individuals, to persistent abnormalities in those with incomplete compensation. It also highlights the role of attentional resource allocation in cognitive-motor dual-task scenarios.
rvs-2024-014f5.jpg
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        Exploring the nexus: unilateral vestibulopathy and visuospatial cognitive impairments
        Res Vestib Sci. 2024;23(4):132-146.   Published online December 15, 2024
        DOI: https://doi.org/10.21790/rvs.2024.014
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      Exploring the nexus: unilateral vestibulopathy and visuospatial cognitive impairments
      Image Image Image Image Image
      Fig. 1. Roles of vestibular system in postural control. This figure illustrates the integration of sensory inputs (vision, vestibular, and somatosensation) and motor outputs required for maintaining postural stability. Key components include the vestibulo-ocular reflex, vestibulospinal reflexes, and anticipatory postural responses, all of which work together to stabilize gait and control posture.
      Fig. 2. Schematic distribution of central vestibular pathways. This schematic highlights the anatomical connections between the vestibular system and cortical, subcortical, and spinal regions, emphasizing their role in sensory integration and motor control. Pathways linking the vestibular nuclei to the temporoparietal cortex, brainstem, cerebellum, and limbic structures are depicted. Adapted from the article of Hitier et al. [2], according to the Creative Commons License.
      Fig. 3. Hypotheses of the cognitive process of posture-gait control. This figure proposes a framework distinguishing cognitive and automatic processes in postural and gait control, emphasizing the interaction between sensory input transmission, bodily cognition, motor programming, and control. SMA, supplementary motor area; PM, premotor cortex.
      Fig. 4. The main theories of dual-task. This diagram summarizes key dual-task theories, including capacity-sharing, bottleneck models, and time-sharing hypotheses, providing insights into how attentional resources are distributed between cognitive and motor tasks. Reproduced from the article of Bayot et al. [26] with the permission of Elsevier.
      Fig. 5. Proposed overview of the visuospatial cognitive performance following unilateral vestibulopathy. This model outlines potential outcomes of vestibular compensation, from normal to slightly abnormal visuospatial function in compensated individuals, to persistent abnormalities in those with incomplete compensation. It also highlights the role of attentional resource allocation in cognitive-motor dual-task scenarios.

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      Fig. 2.

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      Fig. 4.

      Fig. 5.

      Exploring the nexus: unilateral vestibulopathy and visuospatial cognitive impairments
      Res Vestib Sci : Research in Vestibular Science
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