Vestibular‐related dizziness duration and cognitive deficits in older adults

Abstract

OBJECTIVE

The objective of this study is to investigate the relationship between symptom duration of vestibular‐related dizziness/vertigo and cognitive function in elderly patients, and to establish clinical guidance for assessing and intervening in vestibular‐related cognitive impairments.

METHODS

This study included 100 elderly patients with vestibular dysfunction presenting dizziness, vertigo, or balance disorders, categorized into short‐duration (n = 64) and long‐duration (n = 36) groups based on symptom duration. A control group of 21 healthy elderly individuals was included. Cognitive assessments comprised P300 event‐related potentials (latency/amplitude) and Montreal Cognitive Assessment (MoCA) with domain‐specific analysis.

RESULTS

Significant between‐group differences in P300 latency were observed (control vs short‐duration vs long‐duration: p < 0.001), whereas amplitude showed no difference (p  =  0.817). MoCA total scores differed significantly across groups (p  =  0.001), although abnormality rates were comparable (p  =  0.093). Domain analysis revealed significant differences in visuospatial (p < 0.001) and abstract abilities (p  =  0.005). Symptom duration correlated with: MoCA total (R ²  =  0.113), visuospatial ability (R ²  =  0.181), attention (R ²  =  0.068), and orientation (R ²  =  0.157). P300 latency correlated with: MoCA total (R ²  =  0.141), visuospatial ability (R ²  =  0.090), delayed recall (R ²  =  0.112), and orientation (R ² = 0.082).

CONCLUSION

Prolonged vestibular‐related dizziness/vertigo in elderly patients is associated with cognitive deficits, particularly in visuospatial and executive functions. P300 latency demonstrates greater sensitivity than both P300 amplitude and MoCA screening, suggesting that combined electrophysiological and neuropsychological assessment enhances early detection of vestibular‐related cognitive impairment.

Highlights

• Long‐duration vestibular‐related dizziness or balance disorders are associated with a higher risk of cognitive impairment in elderly patients.

• Among early assessment tools, P300 latency proves more sensitive than both P300 amplitude and the Montreal Cognitive Assessment (MoCA) questionnaire.

• A combined evaluation using P300 latency and MoCA provides a more effective measure of how dizziness affects cognitive function in this population.

1. BACKGROUND

Vestibular‐related symptoms such as dizziness, vertigo, and balance disorders are common among the elderly. In the United States, the prevalence of vestibular dysfunction is 35.4% among adults 40 years or older, ¹ 58% in those 60 years or older, and significantly increases to 85% in individuals 80 years or older. ² , ³ Multiple studies have shown a correlation between vestibular dysfunction and cognitive impairment. ⁴ , ⁵ , ⁶ , ⁷ A report from the U.S. National Health and Nutrition Examination Survey (1999–2002) indicated that 14.3% of patients with vestibular dysfunction experience cognitive deficits. ² The 2008 National Health Interview Survey (NHIS) reported that individuals with vestibular dysfunction were eight times more likely to experience severe attention deficits or memory difficulties, and four times more likely to have activity limitations due to memory difficulties or confusion. ⁸ The severity of vertigo can affect cognitive function, with higher degrees of vertigo being associated with a greater incidence of cognitive impairment. ⁵ , ⁹ Bilateral vestibular dysfunction leads to more severe cognitive impairment than unilateral damage. ⁹ , ¹⁰ Even acute unilateral vestibular dysfunction can also result in cognitive impairment. ⁴ In addition, Pineault et al. examined the relationship between lesion location and cognitive impairment, finding that saccular damage was associated with deficits in executive function, attention, non‐verbal memory, and visuospatial skills, whereas semicircular canal dysfunction was linked to non‐verbal memory and visuospatial skills. ¹¹

Subjective questionnaires can be used to assess cognitive impairment. ¹² The Montreal Cognitive Assessment (MoCA), developed by Nasreddine and colleagues, is a quick and simple test that is widely used to screen for mild cognitive impairment (MCI). ¹³ Its sensitivity exceeds 90%, and its specificity ranges from 70% to 90%. ¹⁴ Objective electrophysiological tests can also assess cognitive impairment. Event‐related potentials (ERPs) are objective electrophysiological tests that measure cognitive function, involving both endogenous and exogenous components, which reflect different stages of cognitive processing during task performance. ¹⁵ P300 is an endogenous component of ERPs, representing the brain's initial cognitive processing of information. P300 consists of two components: P3a and P3b. P3a is related to the orienting response of attention, whereas P3b is associated with the allocation of attention resources for updating working memory, reflecting the activity of the frontal and temporoparietal regions. ¹⁶ , ¹⁷ P300, as an important tool in the field of neuroscience, is widely used to assess cognitive function in various diseases. Its latency and amplitude are key neurobiological indicators for evaluating cognitive function. ¹⁸ , ¹⁹ , ²⁰ , ²¹

Although an increasing number of studies have begun to explore the potential link between vertigo and cognitive impairment, specific evidence on the relationship between the duration of vertigo and cognitive dysfunction remains limited. This study aims to investigate the effect of the duration of vestibular‐related dizziness or vertigo on cognitive impairment in elderly individuals. We aim to reveal how cognitive function changes in relation to vertigo duration. By examining the relationship between disease duration and cognitive impairment, we hope to provide theoretical guidance for vestibular‐related cognitive function assessment, early detection, and intervention in elderly patients.

2. METHODS

2.1. Subjects

We selected elderly patients 60 years or older who visited our dizziness and balance disorders clinic between January 2023 and January 2024. Patients were divided into two groups based on the duration of their symptoms: the short‐duration group (less than 1 year, n = 64) and the long‐duration group (1 year or longer, n = 36). ¹ In addition, 21 healthy elderly individuals were included as the control group, making a total of 121 participants (58 male, 63 female, mean age ± SD: 66.8 ± 6.0 years). All participants gave informed consent.

Each participant underwent routine vestibular function and audiological assessments to confirm vestibular‐related dizziness or vertigo. A detailed medical history and physical examination were also conducted. Vestibular tests included oculomotor exams, caloric testing, video head impulse test (vHIT), subjective visual vertical, and vestibular evoked myogenic potentials (VEMPs). Audiological tests included tympanometry, pure‐tone audiometry, auditory brainstem response (ABR), and P300 ERPs.

Inclusion criteria: (1) Diagnosed with vestibular‐related dizziness or vertigo, including vestibular neuronitis (VN), benign paroxysmal positional vertigo (BPPV), vestibular migraine (VM), benign recurrent vertigo (BRV), persistent postural‐perceptual dizziness (PPPD), vestibular paroxysmia (VP), or bilateral vestibular hypofunction (BVH). (2) Normal pure‐tone hearing thresholds or mild hearing loss. (3) Able to communicate in Mandarin and actively cooperate with tests and questionnaires. Exclusion criteria: (1) Peripheral vestibular disorders commonly accompanied by hearing loss, such as labyrinthitis, sudden sensorineural hearing loss with vertigo, and third window syndrome. (2) Patients with cerebellar infarction or hemorrhagic disorders. (3) Patients previously diagnosed with dementia or mild cognitive impairment. (4) Patients with a history of psychiatric disorders. (5) Patients with severe visual or auditory impairments that prevent normal communication and the ability to complete tests or questionnaires.

The final study included 121 participants: Control group: 21 participants (9 male, 12 female; mean age 65.9 ± 5.1 years), 17 with less than 12 years of education and 4 with 12 years or more of education. Their pure‐tone hearing threshold was 22.4 ± 4.3  decibels hearing level (dB HL). Short‐duration group: 64 participants (33 male, 31 female; mean age 67.3 ± 6.2 years), 58 with less than 12 years of education and 6 with 12 years or more. Their pure‐tone hearing threshold was 24.5 ± 7.1 dB HL. Long‐duration group: 36 participants (16 male, 20 female; mean age 66.4 ± 6.1 years), 28 with less than 12 years of education and 8 with 12 years or more. Their pure‐tone hearing threshold was 23.7 ± 5.3 dB HL.

RESEARCH IN CONTEXT

1. Systematic review: We searched electronic databases such as PubMed and Google Scholar for studies examining the relationship between vestibular dysfunction and cognitive impairment. Although emerging evidence suggests an association between vestibular disorders and cognitive decline in older adults, few studies have focused specifically on the impact of symptom duration. Moreover, the integration of electrophysiological and neuropsychological measures in this context remains limited.

2. Interpretation: Our findings support the notion that prolonged vestibular‐related dizziness is associated with cognitive deficits, particularly in the visuospatial and executive domains. We also demonstrate that P300 latency is more sensitive than MoCA total score or P300 amplitude in detecting early cognitive changes. The combined use of neurophysiological and cognitive assessments enhances the clinical evaluation of vestibular‐related cognitive risk.

3. Future directions: Future studies should employ larger, more diverse cohorts and adopt longitudinal designs to determine the trajectory of cognitive change in vestibular patients. In addition, stratifying participants by vestibular pathology and lesion laterality will help clarify disorder‐specific cognitive patterns and mechanisms.

There were no significant differences between the groups in terms of gender, education, age, hearing threshold, cardiovascular disease, or the distribution of different vestibular disorders (p > 0.05) (see Table 1).

TABLE 1.

Demographic characteristics of different groups.

Variables	I (N = 21)	II (N = 64)	III (N = 36)	p‐value
Age, y, mean (SD)	65.9 ± 5.1	67.3 ± 6.2	66.4 ± 6.1	0.614
Gender, n (%)
Male	9 (42.9%)	33 (51.6%)	16 (44.4%)	0.694
Female	12 (57.1%)	31 (48.4%)	20 (55.6%)
Education, n (%)
<12 y	17(81.0%)	58(90.6%)	28(77.8%)	0.187
≥12 y	4(19.0%)	6(9.4%)	8(22.2%)
Hearing threshold, mean (SD), dB HL	22.4 ± 4.3	24.5 ± 7.1	23.7 ± 5.3	0.488
With tinnitus, n (%)	3(14.3%)	7(10.9%)	5(13.9%)	0.874
With cardiovascular disease, n (%)	18(85.7%)	56(87.5%)	27(75.0%)	0.259
VN, n	/	6	7	0.820
BPPV, n	/	10	4
VM, n	/	12	5
BRV, n	/	14	9
PPPD, n	/	19	9
VP, n	/	2	1
BVH, n	/	1	1

Note: Group I: Control; Group II: Short‐duration; Group III: Long‐duration.

Abbreviations: BPPV, benign paroxysmal positional vertigo; BRV, benign recurrent vertigo; BVH, bilateral vestibular hypofunction; PPPD, persistent postural perceptual dizziness; VM, vestibular migraine; VN, vestibular neuritis; VP, vestibular paroxysmia.

This study was approved by the ethics committee of Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine (Approval No. XHEC‐D‐2024‐151). This is a single‐center clinical study, and all patients were evaluated by an otologist with over 10 years of experience in treating vestibular‐related inner ear disorders.

2.2. Objective cognitive function assessment

All patients underwent cognitive function assessment using the MoCA Beijing Version, ²² administered by trained professionals through face‐to‐face interviews. MoCA covers seven different dimensions: visuospatial/executive function, naming, attention, language, abstraction, delayed recall, and orientation. Cognitive function is evaluated based on educational attainment. The maximum MoCA score is 30 points. For participants with fewer than 12 years of education, 1 point is added. A total score below 26 indicates cognitive impairment. ¹³ , ²³

2.3. P300 latency and amplitude of event‐related potentials

The evoked potentials (EP) module of the Interacoustics Eclipse (Denmark) was used in a soundproof room, with the ground electrode placed on the forehead (Fpz), the recording electrode on the vertex (Cz), and reference electrodes on the left and right mastoids (M1 and M2). Inter‐electrode impedance was maintained at ≤5 kΩ. The window length was set to 700 ms, with a high‐pass filter of 1 Hz and a low‐pass filter of 17 Hz. The repetition rate was 0.6 s per stimulus, with more than 100 repetitions. Stimuli were delivered via ER‐3A insert earphones at an intensity of 70 dB nHL.

Throughout the test, patients remained awake and comfortably supine on the testing bed. They were instructed to keep their eyes open, avoid eye movements, and count the target stimuli amidst the standard stimuli. The frequencies of the standard and target stimuli were 1000 and 2000 Hz, respectively, presented in an oddball paradigm with probabilities of 80% and 20%. Participants lay supine on the testing bed in a standard soundproof room—background noise <20 dB (A)—remaining relaxed and avoiding blinking or swallowing while maintaining focus. Before the test, participants were informed that they would hear two different frequencies: a 1 kHz short pure tone as the standard stimulus and a 2 kHz short pure tone as the deviant stimulus. These tones were presented randomly at intervals, and participants were instructed to mentally count the occurrences of the 2 kHz (target) tone and ignore the 1 kHz (non‐target) tone. Before the formal test, two to three practice trials were conducted to familiarize participants with the procedure. During the formal test, participants reported the number of target stimuli. Each participant underwent two tests with a 5‐min interval, and the error margin between the two tests had to be less than 10%. The P300 amplitude was defined as the peak‐to‐peak difference between the average baseline voltage and the largest positive ERP peak between 250 and 500 ms after stimulus onset, measured in microvolts (µV). Within this time window, the P300 component was defined as the earlier and larger peak elicited by the deviant stimulus. ¹⁷ , ²⁴

2.4. Statistical analyses

Statistical analyses were performed using SPSS version 26.0, and graphical illustrations were created with Prism 9 Version 9.4.1. Descriptive statistics for continuous data were expressed as mean $\pm$ SD ($\overline{\mathrm{x}}\pm \mathrm{s}$). Independent data with normal distribution and homogeneity of variance were compared using t‐tests, and multiple independent samples were analyzed using analysis of variance (ANOVA) with Bonferroni correction. For data not following a normal distribution or with unequal variances, the rank‐sum test was used. Multiple independent samples were analyzed with the Kruskal–Wallis test, followed by Bonferroni correction. Paired t‐tests were used for non‐independent data with normally distributed differences. Spearman's correlation analysis was used to assess parameter correlations, with r > 0.5 and p < 0.05 indicating significant correlations.

3. RESULTS

3.1. Comparison of P300 latency and amplitude across different groups

The P300 latencies for the different groups were 301 ± 41, 332 ± 42, and 342 ± 32 ms, respectively. The differences in P300 latencies between the groups were statistically significant (F = 9.026, p < 0.001). Further pairwise comparisons revealed significant differences between Groups I and II (t = −3.447, p = 0.002) and between Groups I and III (t = −4.242, p < 0.001). However, no significant difference was found between Groups II and III (t = −1.549, p = 0.369). The P300 amplitudes were 4.80 ± 7.59, 6.15 ± 8.13, and 8.41 ± 11.11 µV, respectively, with no statistically significant difference (F = 0.202, p = 0.817) (see Figure 1).

FIGURE 1.

Comparison of P300 latency and amplitude across different groups. (A) Comparison of P300 latency between groups; significant differences were observed between Group I and Group II, and between Group I and Group III. (B) Comparison of P300 amplitude between groups; no significant differences were found. (C) Schematic of P300 waveforms across groups.

3.2. Comparison of MoCA scores across different groups

The MoCA scores were 25 ± 2, 24 ± 3, and 21 ± 5 for the groups, with a statistically significant difference between them (F  =  8.197, p  =  0.001). There was no significant difference between Groups I and II (t  =  1.414, p  =  0.485), but significant differences were observed between Groups I and III (t  =  3.886, p  =  0.001) and between Groups II and III (t =  3.061, p  =  0.009). The abnormal MoCA rates for the three groups were 50%, 65.8%, and 81.8%, with no statistically significant difference (χ ² = 4.750, p  =  0.093). Comparisons across different dimensions revealed statistically significant differences in visuospatial (H  =  16.424, p < 0.001) and abstract abilities among the three groups (H  =  10.785, p  =  0.005). For visuospatial: Group I versus II (U  =  0.756, p  =  0.450), Group I versus III(U  =  3.643, p < 0.001), and Group II versus III (U  =  3.466, p  =  0.01), For abstract abilities: Group I versus II (U  =  2.559, p  =  0.010), Group I versus III (U  =  3.180, p  =  0.001), and Group II versus III (U  =  1.033, p  =  0.302), (see Figure 2).

FIGURE 2.

Comparison of Montreal Cognitive Assessment (MoCA) scores across different groups. (A) Comparison of MoCA scores; significant differences were observed between Group I and Group III, and between Group II and Group III. (B) Comparison of abnormal rates across groups; no significant differences were found. (C) Comparison of visuospatial/executive function between groups; significant differences were observed between Group I and Group III, and between Group II and Group III. (D) Comparison of abstraction between groups; significant differences were found between Group I and Group II, and between Group I and Group III.

3.3. Comparison of the correlation between disease duration and MoCA

There was a significant correlation between disease duration and the MoCA score, visuospatial ability, attention, and orientation (p < 0.05), with regression coefficients of R ²  =  0.113, R ²  =  0.181, R ²  =  0.068, and R ²  =  0.157, respectively. No significant correlation was found between disease duration and naming, language, abstraction, or delayed recall (p > 0.05), (see Figure 3).

FIGURE 3.

Correlation between disease duration and MoCA. (A) Negative correlation between MoCA and disease duration. (B) Negative correlation between visuospatial/executive function and disease duration. (C) Negative correlation between attention and disease duration. (D) Negative correlation between orientation and disease duration.

3.4. Comparison of the correlation between P300 latency and MoCA

There was a negative correlation between P300 latency and the MoCA score, visuospatial ability, and orientation (p < 0.05), with regression coefficients of R ²  =  0.141, R ²  =  0.090, and R ²  =  0.082, respectively. P300 latency was positively correlated with delayed recall (p < 0.05, R ²  =  0.112). No significant correlation was found between P300 latency and naming, attention, language, or abstraction (p > 0.05), (see Figure 4).

FIGURE 4.

Correlation between P300 latency and MoCA. (A) Negative correlation between MoCA and P300 latency. (B) Negative correlation between visuospatial/executive function and P300 latency. (C) Positive correlation between delayed recall and P300 latency. (D) Negative correlation between orientation and P300 latency.

4. DISCUSSION

Vestibular dysfunction is recognized increasingly as a significant risk factor for cognitive impairment. Several studies have established that vestibular dysfunction is not only associated with cognitive deficits, ²⁵ , ²⁶ but may also contribute to hippocampal atrophy. ²⁷ , ²⁸ This atrophy, in turn, is implicated in the development of MCI, ³ , ²⁹ and patients with vestibular dysfunction face a threefold higher risk of developing Alzheimer's disease (AD) compared to healthy individuals. ²⁹ Given that MCI can serve as an early clinical manifestation of AD—with patients typically not showing impairments in daily functioning at this stage ³⁰ —it becomes critical to identify and intervene early. Indeed, studies have indicated that many patients with MCI progress to AD each year, ³¹ underscoring the importance of early screening to improve cognitive function and potentially slow the progression of dementia. ³²

One objective method to detect cognitive deficits is through the P300 ERP, which reflects post‐stimulus information processing, including classification speed and various executive functions such as attention and memory. ²⁴ , ³³ , ³⁴ Numerous studies have reported that patients with MCI exhibit prolonged P300 latencies and reduced amplitudes relative to healthy controls. ³⁵ , ³⁶ , ³⁷ Our study supports these findings, showing statistically significant differences in P300 latency between the healthy control group and both the short‐duration (p = 0.002) and long‐duration groups (p < 0.001). Of interest, there was no significant difference between the short‐duration and long‐duration groups (p = 0.369), suggesting that vestibular dysfunction leads to an early prolongation of P300 latency, which does not continue to extend with disease progression. These results also indicate that P300 latency is highly sensitive to the presence of vertigo, even in its early stages. In contrast, although a systematic review of 29 studies reported mixed findings regarding P300 amplitude in MCI patients, ³⁸ our study found no statistically significant differences in amplitude among groups. This discrepancy might be due to differences in the type of stimuli used, as many studies demonstrating amplitude differences employed visual stimuli, whereas our study used auditory stimuli with different intensity parameters. ³⁵ , ³⁷ , ³⁹ , ⁴⁰ , ⁴¹ , ⁴²

In addition to electrophysiological measures, cognitive screening tools like the MoCA play an important role. In our study, MoCA scores did not differ significantly between the healthy control group and the short‐duration group (p = 0.485), but significant differences emerged between the healthy control group and the long‐duration group (p = 0.001), as well as between the short‐ and long‐duration groups (p = 0.009). These findings suggest that although MoCA may not be sufficiently sensitive to detect cognitive impairment in the early stages of vestibular dysfunction, it becomes increasingly effective as the disease progresses. Consequently, P300 latency might offer greater clinical value for the early assessment of cognitive deficits associated with vestibular dysfunction.

Beyond these measures, previous studies have also linked vestibular dysfunction with impairments in various cognitive domains. For example, some research on patients with chronic vertigo has demonstrated that lower MoCA scores were associated with significantly reduced vestibular function, as assessed by vHIT and caloric tests. ⁴³ Other studies have found that vestibular dysfunction is linked to declines in executive function, visuospatial ability, attention, and short‐term memory, ⁹ , ⁴⁴ , ⁴⁵ whereas some suggest that spatial orientation and memory are particularly affected. ⁴⁶ Although some studies did not find significant associations between vestibular function and certain cognitive domains—such as executive function or verbal memory—they did observe poorer visuospatial ability in the elderly with vestibular dysfunction ⁴⁴ and impaired topographical memory. ⁴⁷ Our results further contribute to this body of evidence by revealing statistically significant differences in visuospatial/executive function and abstraction across the three groups (p < 0.001 and p = 0.005, respectively). Notably, although visuospatial/executive function deficits appeared only as the disease progressed, abstraction deficits were evident even in the early stages of vestibular dysfunction. In contrast, no significant differences were observed in naming, attention, language, delayed recall, or orientation, which is consistent with some earlier studies using the Wechsler Memory test ⁴⁶ and the Corsi Block Tapping Test. ⁹

The duration of vestibular symptoms also appears to be an important factor. Research by Li et al.³³ and Dobbels et al. ⁴⁵ indicates that chronic vestibular disorders, such as PPPD and Meniere's disease, are more likely to result in cognitive impairment than acute conditions like BPPV. Our analysis showed that disease duration is correlated with declining MoCA scores and deterioration in specific cognitive domains, including visuospatial/executive function, attention, and orientation. Although some studies ⁹ did not find a significant correlation between vestibular dysfunction duration and certain cognitive abilities, our findings—possibly influenced by the higher sensitivity of the MoCA and a larger sample size—suggest that cognitive impairment may indeed progress with longer disease duration.

Finally, our study explored the relationship between P300 latency and MoCA scores. We found a negative correlation between P300 latency and both overall MoCA scores and specific cognitive domains such as visuospatial/executive function and orientation, implying that prolonged P300 latency corresponds to poorer cognitive performance. Of interest, a positive correlation was observed between P300 latency and delayed recall (memory), which was unexpected. This finding, which might be attributable to our limited sample size, warrants further investigation in future studies. Supporting our results, Demirayak et al. ³⁴ reported similar associations between P300 latency and various cognitive tests, although inconsistencies remain regarding the relationship between P300 amplitude and cognitive function. Although Wang et al. ⁴⁸ observed a correlation between P300 amplitude and certain cognitive domains, Another study reported no such relationship. ³⁸ These discrepancies could arise from differences in stimulus type, intensity, or sample sizes, suggesting that further research is needed to clarify the role of P300 amplitude in assessing cognitive deficits related to vestibular dysfunction.

In summary, our findings underscore the complex relationship between vestibular dysfunction and cognitive deficits. They highlight the potential of P300 latency as an early, sensitive marker of cognitive impairment, while also emphasizing the need for further studies to refine our understanding of how stimulus parameters and disease duration impact both electrophysiological and cognitive assessments.

This study has several limitations. (1) We did not differentiate between types of vestibular dysfunction. Since different conditions may involve damage to different areas of the vestibular system, the location of the damage could result in varying cognitive impairments. (2) We did not distinguish between the affected side of the vestibular dysfunction (left, right, or bilateral). Unilateral and bilateral vestibular dysfunction may present different patterns of cognitive impairment. (3) Uneven group distribution (short‐duration, n = 64 vs long‐duration, n = 36) may reduce statistical power for subgroup analyses. In future studies, we aim to increase the sample size and refine groupings to explore the differences between various vestibular conditions and sides in more detail. (4) We did not employ a full neuropsychological test battery, which may limit the scope and depth of cognitive domains assessed beyond those captured by the MoCA.

The study is from one center in China with 121 participants. Like many similar studies, this limits generalizability, especially across different ethnic, linguistic, or health care populations. Additional, long‐term longitudinal follow‐up would be insightful to see if the cognitive deficits is progressive, reversible, and so on. Other confounders that should be considered include depression and anxiety, as well as medication use for chronic dizziness (benzodiazepines).

5. CONCLUSIONS

This study highlights the significant impact of vestibular dysfunction on cognitive function, particularly in elderly patients. Our findings suggest that P300 latency is a sensitive marker for early cognitive deficits in vestibular dysfunction, even before changes in MoCA scores become evident. By combining P300 latency with traditional cognitive assessments like MoCA, clinicians could more effectively identify and intervene in the early stages of cognitive impairment associated with vestibular dysfunction. Future studies with larger, more balanced sample sizes and detailed subgroup analyses will further elucidate the role of vestibular dysfunction in cognitive deficits and improve diagnostic accuracy.

AUTHOR CONTRIBUTIONS

X.M. was responsible for data interpretation and manuscript preparation. J.S. collected the clinical data. W.W. contributed to data analysis. L.W. helped to optimize the auditory test, Y.J. was responsible for vestibular tests. M.D. contributed to statistical consultation. Q.Z. reviewed and revised the manuscript. J.Y. and J.C. were responsible for the research design and manuscript revision. All authors contributed to the article and approved the submitted version.

CONSENT STATEMENT

All participants provided written informed consent prior to study enrollment.

CONFLICT OF INTEREST STATEMENT

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Author disclosures are available in the supporting information.

ETHICS STATEMENT

This study was approved by the ethics committee of Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine (Approval No. XHEC‐D‐2024‐151).

Supporting information

Supporting Information

Ma X, Shen J, Wang W, et al. Vestibular‐related dizziness duration and cognitive deficits in older adults. Alzheimer's Dement. 2025;11:e70153. 10.1002/trc2.70153

DATA AVAILABILITY STATEMENT

The authors confirm that the data supporting the findings of this study are available within the article.