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Review Article
Dizziness and neuro-otologic findings in neurodegenerative disorders: a review
Seunghee Na1orcid, Yun Jeong Hong2orcid, Seong-Hoon Kim2orcid, Eek-Sung Lee3orcid
Research in Vestibular Science 2025;24(2):68-78.
DOI: https://doi.org/10.21790/rvs.2024.026
Published online: June 15, 2025

1Department of Neurology, Incheon St. Mary’s Hospital, the Catholic University of Korea, Seoul, Korea

2Department of Neurology, Uijeongbu St. Mary’s Hospital, the Catholic University of Korea, Seoul, Korea

3Department of Neurology, Soonchunhyang University Bucheon Hospital, Bucheon, Korea

Corresponding author: Eek-Sung Lee Department of Neurology, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Bucheon 14584, Korea. E-mail: eeksung@schmc.ac.kr, eeksung@gmail.com
• Received: December 17, 2024   • Revised: March 10, 2025   • Accepted: April 11, 2025

© 2025 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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  • Eye movement abnormalities can provide valuable diagnostic insights across various neurodegenerative disorders. This review summarizes the characteristic oculomotor findings in different neurodegenerative conditions, focusing on cognitive disorders and parkinsonian syndromes. The neural control of eye movements involves complex networks across multiple cortical regions, including the frontal eye field, supplementary eye field, and dorsolateral prefrontal cortex, functioning in coordination with subcortical structures. In Alzheimer disease, patients exhibit impaired fixation with large saccadic intrusions, prolonged saccadic latency, and increased antisaccade errors, which correlate with cognitive decline. Frontotemporal dementia shows variant-specific patterns of oculomotor dysfunction, with behavioral variant particularly affecting antisaccade performance while maintaining the ability to self-correct errors. In parkinsonian syndromes, distinctive eye movement abnormalities aid in differential diagnosis. Idiopathic Parkinson disease typically presents with hypometric saccades and increased saccadic intrusions during fixation, which correlate with disease severity. Progressive supranuclear palsy characteristically shows early vertical saccade abnormalities and frequent macro–square-wave jerks. Multiple system atrophy demonstrates various central nystagmus patterns and perverted head-shaking nystagmus, while corticobasal degeneration presents with saccadic apraxia and asymmetric oculomotor abnormalities. While eye movement abnormalities can be nonspecific and overlap between conditions, careful evaluation of oculomotor function can provide important diagnostic clues, particularly for differentiating parkinsonian syndromes. Understanding these distinct patterns of oculomotor abnormalities provides critical insights into the underlying pathophysiology and serves as a valuable tool for differential diagnosis of neurodegenerative disorders.
  • Keywords: Neurodegenerative disorders; Oculomotor abnormalities; Dizziness; Parkinsonian syndromes; Dementia
Neurodegenerative disorders are characterized by progressive damage or death of neural cells. These conditions involve the aggregation and accumulation of abnormal proteins, leading to neuronal dysfunction and death, synaptic deterioration, and neuroinflammation, resulting in various symptoms [1]. As time progresses, neural cell function gradually deteriorates, affecting various bodily functions, typically following an irreversible course. Notable examples include Alzheimer disease, frontotemporal dementia (FTD), and Parkinson disease. Each major neurodegenerative disorder typically affects specific brain regions. For instance, Parkinson disease primarily involves the brainstem and basal ganglia, while Alzheimer disease progressively spreads from the entorhinal cortex and limbic system to the neocortex [1]. Since ocular motor control involves multiple brain regions, including the brainstem, basal ganglia, cerebellum, and cerebral cortex, patients may experience dizziness or balance disorders and show abnormalities in various vestibular function tests related to the affected brain regions [2,3].
Therefore, patients presenting with dizziness may ultimately be diagnosed with neurodegenerative disorders such as Parkinson disease. Additionally, dizziness may develop during the progression of neurodegenerative diseases. Various vestibular function test parameters can be used to differentiate specific diagnoses of neurodegenerative disorders, assess disease severity, or predict prognosis.
The neural circuits controlling eye movements involve complex and distributed networks across multiple cortical regions, working in concert with the brainstem, basal ganglia, and cerebellum [2,4]. At the cortical level, three main frontal regions play crucial roles: the frontal eye field (FEF), supplementary eye field (SEF), and dorsolateral prefrontal cortex (DLPFC). The FEF is primarily involved in the preparation and triggering of voluntary saccades, while the SEF and DLPFC are critical for higher-order control processes such as inhibiting unwanted reflexive saccades, maintaining spatial memory for eye movements, and producing sequential eye movements. In the posterior regions, the posterior parietal cortex is essential for visuospatial integration and attention, providing crucial sensory-motor transformations for eye movement control (Fig. 1).
Different types of saccadic eye movements help evaluate specific aspects of this cortical control network [2,4]. Prosaccades, which are reflexive eye movements toward a suddenly appearing target, primarily involve parieto-collicular pathways and require minimal frontal involvement. In contrast, memory-guided saccades, where subjects must make eye movements to remembered target locations, require additional activation of the DLPFC and FEF for spatial working memory maintenance. Antisaccades, where subjects must suppress a reflexive saccade to a visual target and instead look in the opposite direction, are particularly complex, requiring coordinated activity across the entire frontal network: the DLPFC for inhibiting the reflexive response, the SEF for motor preparation, and the FEF for generating the voluntary saccade in the opposite direction. The initiation and maintenance of smooth pursuit eye movements begins with visual processing in the extrastriate cortical regions, specifically the middle temporal visual area (MT/V5) and medial superior temporal visual area (MST) [4] (Fig. 1). These regions send ipsilateral projections to brainstem structures, including the nucleus reticularis tegmenti pontis and dorsolateral pontine nucleus, which then project to multiple cerebellar regions including the vermis, fastigial nucleus, flocculus, and paraflocculus.
This cortical control network is hierarchically organized, though recent findings suggest more complex interactions than previously thought. Understanding this cortical control system and its expression through different types of saccadic movements and temporal paradigms is essential for interpreting the oculomotor disturbances observed in neurodegenerative disorders, as these conditions often affect multiple nodes within this network, leading to characteristic patterns of eye movement abnormalities that can aid in diagnosis and disease monitoring.
Voluntary eye movements are complex neurophysiological phenomena requiring the integration of reflexive mechanisms and higher cognitive processes [5]. Within this system, top-down intentional and bottom-up reactive eye movements interact to enable environmental exploration and adaptive responses to visual stimuli [5]. The cognitive control mechanisms of eye movements are based on sophisticated neural circuit synchronization between frontal and parietal cortices and subcortical structures. This forms the core element enabling context-optimized responses.
Alzheimer Disease
Alzheimer disease, the most common cause of dementia, is a representative neurodegenerative disorder characterized by amyloid deposition leading to tau phosphorylation, neuronal loss, and cognitive decline [6]. The tau pathology, associated with cognitive status in Alzheimer disease, progresses from the entorhinal cortex to the limbic system and then to the neocortex [7,8]. In Alzheimer dementia, eye movement functions such as fixation, saccades, and smooth pursuit are impaired, while the vestibulo-ocular reflex is preserved.
When patients attempt to fixate on a target, large saccadic intrusions are observed due to peripheral stimuli that interfere with attention (Fig. 2A). These large saccadic intrusions differ from square-wave jerks, which are small-amplitude movements commonly seen in elderly individuals. Not only in amplitude but unlike saccadic intrusions in normal elderly individuals that typically occur in the horizontal plane, they appear obliquely in patients with mild cognitive impairment (MCI) and Alzheimer dementia [9]. The frequency of these saccadic intrusions and the duration of fixation showed a correlation with the Mini-Mental State Examination (MMSE) scores [10]. Fixation abnormalities may be attributed to brainstem dysfunction responsible for saccades [11]. However, considering that Alzheimer disease only affects the brainstem in advanced stages, fixation abnormalities in Alzheimer dementia may result from impairment of cognitive functions such as attention or working memory.
Regarding saccades, there are tendencies toward prolonged latency [10,12-14], slower saccadic velocity [12], hypometric saccades [12,14], and increased error rate in antisaccade tasks [12-17] (Fig. 2B). The prolonged latency and saccadic velocity showed correlation with MMSE scores [10] and intelligence quotient [12], respectively. Neuroimaging studies showed that prolonged saccadic latency predicted reduced parietal and occipital lobe volume [13], possibly because the parietal lobe is both commonly affected in Alzheimer disease [18] and crucial for visual attention [2]. In antisaccade tasks, patients show prolonged latency and multiple errors due to inability to suppress reflexive saccades toward visual stimuli, known as visual grasp reflex [12,14,17,19]. These antisaccade abnormalities are thought to result from impaired inhibitory control related to the DLPFC [20], and the volume of the right FEF showed a positive correlation with antisaccade accuracy, while pre-supplementary motor area (pre-SMA) and SEF volumes negatively correlated with antisaccade latency [18]. Additionally, the frequency of antisaccade errors showed a correlation with MMSE scores and neuropsychological test results including working memory [14-16,21].
In Alzheimer dementia patients, smooth pursuit movements either appear normal [22] or show reduced gain with corrective catch-up saccades [13,16,23]. These corrective saccades worsen with cognitive decline and have shown a correlation with the MMSE and dementia rating scales [23]. Thus, saccades and smooth pursuit movements show varying degrees of abnormality from normal to various levels of impairment across studies, and considering their correlation with MMSE and neuropsychological test results, these heterogeneous findings may be attributed to differences in dementia severity.
While the vestibulo-ocular reflex is preserved in Alzheimer dementia, normal responses in cervical and ocular vestibular evoked myogenic potentials (VEMPs) are reduced [24,25]. Evidence suggests a dose-response relationship between vestibular function and cognitive status, with MCI patients showing an intermediate level of vestibular impairment between controls and Alzheimer dementia patients [25]. This relationship may be explained by the well-established vestibular-hippocampal connections, as the hippocampus is a major site of pathology in Alzheimer disease [24].
Mild Cognitive Impairment
Patients with MCI and Alzheimer dementia demonstrate increased latency in prosaccadic tasks and higher error rates in antisaccade tasks compared to control groups, with antisaccade tasks showing particularly marked abnormalities with the highest diagnostic accuracy (area under the curve, 0.79) [19]. VEMPs also show reduced responses compared to normal controls, with MCI showing an intermediate level of impairment between controls and Alzheimer dementia [25].
MCI patients with dizziness show poor executive function performance and reduced blood flow in the left temporal and frontal lobes [26]. MCI patients with wayfinding difficulties demonstrate lower activities of daily living capabilities and more severe bilateral fusiform gyrus atrophy [27], suggesting that dizziness and spatial perception abnormalities may be related to the involvement of specific brain regions.
Frontotemporal Dementia
FTD consists of three distinct variants: behavioral variant FTD (bvFTD), nonfluent variant FTD (nfvFTD), and semantic dementia (SD) [28]. Neuroimaging studies reveal characteristic patterns of atrophy and metabolic reduction in each variant: bvFTD predominantly affects the frontal and anterior temporal lobes, nfvFTD involves the Sylvian fissure-frontal region and surrounding insula, and SD shows focal atrophy centered on the temporal poles [29]. These distinct patterns of brain involvement can lead to variant-specific oculomotor abnormalities, although research findings on eye movement disorders in FTD have not been entirely consistent.
Compared to healthy controls, bvFTD patients exhibited a higher frequency of small square-wave jerks, which negatively correlated with the volumes of the orbitofrontal cortex, ventromedial prefrontal cortex, and striatum. They also demonstrated shorter periods of stable fixation, which correlated with both disease severity and orbitofrontal cortex volume [30]. FTD patients demonstrate significant abnormalities in saccadic tasks. Patients with bvFTD show increased saccadic latencies [31-33], which correlate with their reduced decision-making speed [31]. While saccadic velocity remains normal compared to control groups [16,30,31], this distinguishing feature differentiates FTD from progressive supranuclear palsy (PSP), where these parameters are typically abnormal. FTD patients show pronounced deficits in antisaccade performance [13,16,30-33]. The antisaccade task reveals increased latencies, which correlate with atrophy in the pre-SMA and SEF [16]. Notably, both bvFTD and nfvFTD variants demonstrate higher error rates in antisaccade tasks compared to control groups [13,16,30-33]. However, an interesting distinguishing feature of FTD is that patients retain the ability to spontaneously correct their antisaccade errors, which differs from patients with Alzheimer dementia or corticobasal degeneration (CBD) who typically lack this ability [13].
Findings regarding smooth pursuit eye movements in FTD have been somewhat contradictory. Some studies report normal smooth pursuit function [30], while others describe variant-specific impairments: normal pursuit in language variants but impaired performance in behavioral variants [13,16]. This inconsistency likely reflects the heterogeneous nature of cortical involvement across FTD variants and suggests that smooth pursuit performance may depend on the specific pattern of cortical damage in individual cases.
In summary, bvFTD is characterized by increased saccadic latencies, higher error rates in antisaccade and memory-guided saccade tasks, and potential smooth pursuit abnormalities. SD shows relatively preserved oculomotor function with performance similar to control groups. The nonfluent variant primarily demonstrates increased error rates in antisaccade tasks. These variant-specific patterns of oculomotor dysfunction provide valuable insights into the differential involvement of frontal-subcortical circuits across FTD subtypes and may serve as useful diagnostic markers.
Creutzfeldt-Jakob Disease
Creutzfeldt-Jakob disease (CJD) is a rare and fatal prion disease. The condition is characterized by rapidly progressive dementia, ataxia, visual/cerebellar symptoms, and extrapyramidal signs [34]. Most patients’ survival time was less than one year after symptom onset [35].
Multiple studies investigating CJD have documented diverse oculomotor abnormalities, suggesting the involvement of multiple brain structures. In the early stages of CJD, patients may exhibit various eye movement abnormalities including slow vertical saccades and reduced smooth pursuit gain [36]. They may also demonstrate periodic alternating nystagmus and ocular dipping movements [36,37]. The presence of these abnormalities indicates involvement of the cerebellar nodulus and uvula, as well as the brainstem reticular formation. Additionally, CJD can present with high cortical visual dysfunction and progressive visual impairment due to occipital lobe involvement, which may precede cognitive decline [38]. Therefore, CJD should be considered in the differential diagnosis of patients presenting with unexplained visual disturbances. This early visual involvement makes oculomotor and visual assessment particularly valuable in the early detection and diagnosis of CJD.
Parkinson disease is a neurodegenerative disorder characterized by resting tremor, rigidity, bradykinesia, and postural instability [39]. Beyond classical Parkinson disease, the spectrum of parkinsonian disorders includes several Parkinson-plus syndromes, which present with additional symptoms beyond classical parkinsonism. These include multiple system atrophy (MSA) [40], PSP [41], CBD [42], and Lewy body dementia (LBD) [43].
In these disorders, eye movement abnormalities can manifest from the early stages of disease and progressively worsen with disease progression, as the cerebral control of the oculomotor system projects to the brainstem via the basal ganglia, and these conditions affect the basal ganglia, brainstem, and corticobasal circuits [44]. These oculomotor abnormalities carry significant diagnostic value in distinguishing between different parkinsonian subtypes [45,46]. For example, PSP patients characteristically demonstrate vertical gaze abnormalities from early in the disease course, providing an important diagnostic clue that distinguishes it from other variants. MSA can be differentiated from idiopathic Parkinson disease by the presence of autonomic dysfunction along with cerebellar ataxia and central nystagmus. CBD may present with asymmetric oculomotor abnormalities. We will now discuss the characteristic eye movement abnormalities in each of these conditions.
Idiopathic Parkinson Disease
Idiopathic Parkinson disease develops due to the loss of nigrostriatal dopaminergic neurons extending from the substantia nigra to the basal ganglia, resulting in dopamine deficiency [39]. The cardinal eye movement abnormalities in Parkinson disease include saccadic hypometria and increased saccadic intrusions during fixation, even though eye abnormalities are often subtle or absent in early disease stages [47].
Parkinsonian patients demonstrate increased saccadic intrusions during fixation [47,48]. While square-wave jerks are more frequent compared to controls, they are significantly less pronounced than in MSA or PSP patients [47]. Notably, Parkinsonian patients who exhibit fixation abnormalities with more than 10 square-wave jerks per minute show more severe falls, freezing of gait, and postural instability, suggesting that these oculomotor abnormalities correlate meaningfully with impairments in daily activities related to gait and posture maintenance [47,48].
Saccadic impairments in Parkinson disease result from hyperactivity of inhibitory projections from the substantia nigra to the superior colliculus [45,49]. Hypometric saccades appear from the early stages of the disease [40,49-51] and saccadic latency is preserved [40,52] or slightly prolonged compared to controls [49,51,53]. The latency prolongation tends to worsen as disease severity progresses [49] and disease duration increases [51], likely reflecting the development of non-dopaminergic neural dysfunction and cognitive decline [45]. Interestingly, while volitional saccades show these abnormalities, reflexive saccades remain relatively normal in early disease stages, suggesting that the frontal-basal ganglia-collicular pathway is more critically involved in volitional saccade control [44]. Additionally, paralleling the characteristic bradykinesia of Parkinson disease, repeated saccades show progressive deterioration in velocity and amplitude over time, a phenomenon termed ‘saccadic bradykinesia’ [54]. Patients also demonstrate increased error rates in antisaccade tasks compared to controls [40,52], and the antisaccade error rate correlates with symptom severity [40].
Smooth pursuit movements in patients with Parkinson disease show reduced gain [55,56]. The decreased smooth pursuit gain correlates with motor symptom severity [57], and smooth pursuit gain improves after administration of dopamine agonists [55] or levodopa [57]. Convergence insufficiency is commonly observed in Parkinson disease [58] and can lead to blurred vision during near viewing, impacting the quality of life [51]. Furthermore, Parkinsonian patients demonstrate abnormal visual search patterns compared to controls, likely resulting from a combination of reduced saccadic amplitudes and impaired visual information processing [51].
Progressive Supranuclear Palsy
PSP is a tauopathy affecting the basal ganglia, brainstem, cerebellum, and cortex [41]. It is characterized by oculomotor dysfunction, postural instability, cognitive impairment, and freezing of gait. The classical variant, PSP-Richardson syndrome (PSP-RS), presents early with supranuclear gaze palsy and vertical eye movement abnormalities, accompanied by falls, dysarthria, dysphagia, and cognitive impairment. The PSP-P (parkinsonism) variant shows asymmetric parkinsonian features with tremors, and compared to PSP-RS, demonstrates a relatively delayed onset of falls and cognitive impairment [41].
During visual fixation, patients with PSP demonstrated more frequent and larger amplitude saccadic intrusions with markedly reduced vertical components, particularly in macro–square-wave jerks [59-61]. Furthermore, the frequency of square-wave jerks was significantly higher in PSP patients compared to those with idiopathic Parkinson disease [47,48,62]. The feature of frequent macro–square-wave jerks is one of the ocular motor dysfunction domains in the PSP diagnostic criteria [41]. In Richardson syndrome, the earliest oculomotor abnormality is slow vertical saccades, with horizontal saccades becoming affected later in the disease course [45,59,63-65]. As the disease progresses, all voluntary eye movements except the vestibulo-ocular reflex are lost, ultimately resulting in supranuclear gaze palsy [45]. Notably, downward saccades are especially affected, leading to the characteristic “dirty-tie sign” where patients spill food while eating due to impaired downward gaze [66]. During vertical saccades, the eyes follow a curved trajectory deviating from the midline, known as the “round the houses” sign [46,65]. PSP patients show prominent hypometric saccades due to reduced firing of excitatory burst neurons in the brainstem [65]. They demonstrate markedly increased error rates in antisaccade tasks [13,33,64], and volitional saccades show reduced accuracy and velocity compared to reflexive saccades, likely reflecting frontal lobe dysfunction affecting the FEF network [46].
Smooth pursuit movements show significantly reduced gain [13,56], with greater impairment than that observed in Parkinson disease [56]. Optokinetic nystagmus showed reduced slow phase gain and quick phase abnormalities characterized by slower vertical components, increased horizontal square-wave jerks, and an oblique trajectory pattern that was more pronounced than in Parkinson disease or healthy controls [67]. Torsional vestibulo-ocular reflex testing may reveal loss of quick phases, a finding rarely seen in other parkinsonian syndromes and thus serving as a useful diagnostic marker [68]. Additional features include reduced blink rate and lid retraction from early in the disease course [62], with the potential development of eye-opening and eye-closing apraxia as the disease progresses [41]. These characteristic oculomotor abnormalities play a crucial role in the diagnosis of PSP.
Multiple System Atrophy
MSA is a synucleinopathy characterized by degeneration affecting the autonomic nervous system, pyramidal tract, and presenting with parkinsonian and cerebellar symptoms [69]. It is classified into two main subtypes: MSA-P (parkinsonian type), which predominantly shows parkinsonian features, and MSA-C (cerebellar type), where cerebellar ataxia is the primary manifestation. The distinctive oculomotor abnormalities observed in MSA can be attributed to pathology in both the olivopontocerebellar system and the striatonigral area [70].
MSA patients often display more frequent square-wave jerks, sometimes presenting as macro–square-wave jerks with large amplitude [47,48,71,72]. On saccadic tasks, patients with MSA frequently show abnormal saccadic findings: mild hypometric saccades [70,72], hypermetric saccades (which are more frequent in MSA-C type) [51,72], increased prosaccade latency [73], and frequent error rates and increased latency in antisaccade tasks [73]. Prosaccade velocity typically remains normal [70]. Smooth pursuit gain is decreased in patients with MSA compared to those with Parkinson disease and normal controls [70,72,74]. Impaired visual suppression of the vestibulo-ocular reflex is also observed in patients with MSA [70].
Various central nystagmus can be seen in patients with MSA; during gaze-holding tasks, gaze-evoked nystagmus is frequently observed in these patients [70,72]. Both perverted head-shaking nystagmus (pHSN) and positional downbeat nystagmus (pDBN) occur more frequently in patients with MSA compared to Parkinson disease, and pHSN is more commonly documented in patients with MSA-P (absence of overt cerebellar signs) than in those with Parkinson disease [75]. Head-impulse tests can help distinguish MSA from Parkinson disease by demonstrating reverse or perverted catch-up saccades [76]. When these oculomotor abnormalities appear in combination, MSA should be considered as the primary diagnosis before Parkinson disease; however, if slow saccades or prominent supranuclear gaze palsy are present, other conditions should be considered before diagnosing MSA.
Corticobasal Degeneration
CBD presents with a complex combination of symptoms including akinesia, rigidity, dystonia, myoclonus, apraxia, and alien limb phenomenon, manifesting as asymmetric parkinsonian symptoms alongside cortical signs [42]. A characteristic finding in CBD is saccadic apraxia [13,45,64,77]. Patients demonstrate marked difficulty initiating saccades toward target locations, with significantly prolonged latencies during testing. This latency prolongation may be more pronounced in the direction ipsilateral to the patient’s apraxia [64,77]. Distinctively, unlike in Parkinson disease and PSP, saccadic velocity remains normal [64]. In antisaccade tasks, patients show both increased latency and error rates, with an inability to self-correct errors [45,64]. While smooth pursuit movements may show reduced gain, the impairment is typically less severe than in PSP [45]. Eye-opening apraxia can be observed in patients with CBD [77-79]. Moreover, involvement of higher-order visual processing cortical areas in CBD can manifest as Bálint syndrome, which is characterized by ocular apraxia, optic ataxia, and simultanagnosia [79].
Lewy Body Dementia
LBD is recognized as the second most common cause of dementia after Alzheimer disease, characterized by parkinsonism, dementia, REM sleep behavior disorder, and visual hallucinations [43]. Well-formed, detailed, and recurrent visual hallucinations serve as a core clinical feature for diagnosis. Cognitive impairment particularly affects attention and visuospatial function, manifesting early as wayfinding difficulties and impaired pentagon copying on MMSE [80,81]. In cases of familial diffuse LBD, pathological changes in vertical gaze control areas with Lewy body deposits were observed, accompanied by parkinsonism-dementia complex and vertical gaze abnormalities, making this condition clinically similar to PSP [46,82].
As our understanding of the neural circuits controlling eye movements in the cerebral cortex, basal ganglia, and brainstem has advanced, there have been continued efforts to utilize eye movement abnormalities and visual symptoms for early diagnosis, differential diagnosis, and monitoring of disease progression in neurodegenerative disorders [2,45,46]. However, just as clinical symptoms often overlap among various degenerative diseases, eye movement abnormalities can manifest non-specifically, reflecting both the brain regions damaged by the disease and associated cognitive dysfunction. Therefore, their role as meaningful biomarkers for disease status and diagnosis has not yet been convincingly established.
Nevertheless, oculomotor evaluation in patients suspected of having neurodegenerative disease can provide important diagnostic clues, particularly for conditions with characteristic eye movement abnormalities such as PSP, CBD, and MSA. To enhance the diagnostic potential of oculomotor assessment, future developments must focus on clinically applicable evaluation techniques and more accurate interpretation through machine learning approaches.

Funding/Support

None.

Conflicts of Interest

No potential conflict of interest relevant to this article was reported.

Availability of Data and Materials

The datasets are not publicly available but are available from the corresponding author upon reasonable request.

Authors’ Contributions

Conceptualization: Na S, Lee ES; Data curation, Project administration: Na S; Investigation: Na S, Hong YJ, Kim SH; Validation: Hong YJ, Kim SH, Lee ES; Writing–original draft: Na S; Writing–review and editing: Hong YJ, Kim SH, Lee ES.

All authors read and approved the final manuscript.

Fig. 1.
Main supratentorial areas involved in eye movement control. DLPFC, dorsolateral prefrontal cortex; FEF, frontal eye field; MST, medial superior temporal visual area; MT, middle temporal visual area; PPC, posterior parietal cortex; SEF, supplementary eye field.
rvs-2024-026f1.jpg
Fig. 2.
Videonystagmography findings in a patient with Alzheimer dementia. (A) Frequent saccadic intrusions observed during visual fixation. (B) Random saccade testing revealed increased saccadic latency and hypometric saccades. RH, right horizontal.
rvs-2024-026f2.jpg
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        Dizziness and neuro-otologic findings in neurodegenerative disorders: a review
        Res Vestib Sci. 2025;24(2):68-78.   Published online June 15, 2025
        DOI: https://doi.org/10.21790/rvs.2024.026
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      Dizziness and neuro-otologic findings in neurodegenerative disorders: a review
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      Fig. 1. Main supratentorial areas involved in eye movement control. DLPFC, dorsolateral prefrontal cortex; FEF, frontal eye field; MST, medial superior temporal visual area; MT, middle temporal visual area; PPC, posterior parietal cortex; SEF, supplementary eye field.
      Fig. 2. Videonystagmography findings in a patient with Alzheimer dementia. (A) Frequent saccadic intrusions observed during visual fixation. (B) Random saccade testing revealed increased saccadic latency and hypometric saccades. RH, right horizontal.

      Fig. 1.

      Fig. 2.

      Dizziness and neuro-otologic findings in neurodegenerative disorders: a review
      Res Vestib Sci : Research in Vestibular Science
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