Impact of Prolonged Screen Use on Vestibular Function: A Case Study

Impact of Prolonged Screen Use on Vestibular Function: A Case Study | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Impact of Prolonged Screen Use on Vestibular Function: A Case Study Nishanth G, Abhijith M, Reshma R This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9071693/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 7 You are reading this latest preprint version Abstract Background : Prolonged screen exposure is increasingly prevalent among young adults and may influence visual–vestibular integration. While symptoms such as visual fatigue, dizziness, and imbalance are frequently reported in individuals with high digital exposure, objective evidence of vestibular pathway involvement remains limited. Case presentation : Two young adult males (Patient 1; Patient 2) with more than six years of daily screen use exceeding four hours underwent comprehensive audiological, vestibular electrophysiological, and cranio-oculography. Peripheral hearing and middle-ear function were normal in both individuals. oVEMP testing demonstrated prolonged P1 and N1 latencies with reduced amplitudes relative to laboratory normative values, suggesting subtle utriculo-ocular pathway involvement. Cranio-oculography revealed normal saccadic parameters, optokinetic responses, gaze stability, positional testing, and VOR function in both participants. However, smooth pursuit testing demonstrated reduced gain with compensatory catch-up saccades, more pronounced in Patient 1 (particularly vertical pursuit), and mild bilateral gain reduction in both horizontal and vertical planes in Patient 2. Both participants reported intermittent dizziness, visual fatigue, and imbalance, with mild functional impact reflected in Dizziness Handicap Inventory scores. Conclusion : The combined electrophysiological (oVEMP) and oculomotor (pursuit) findings suggest early functional strain within visual–vestibular integration pathways despite otherwise normal vestibular reflexes. Prolonged screen exposure may be associated with subtle adaptive or maladaptive changes in vestibulo-ocular processing, supporting the need for larger, controlled studies. screen time vestibular function oVEMP cranio-oculography visual fatigue dizziness smooth pursuit Figures Figure 1 Figure 2 Figure 3 Background The rapid expansion of digital technology has fundamentally transformed daily life, particularly among adolescents and young adults, leading to unprecedented levels of prolonged screen exposure [ 1 , 2 ]. Activities such as online learning, gaming, social media engagement, and multimedia consumption require sustained visual attention, continuous visual tracking, and prolonged fixation on dynamic visual environments [ 3 ]. These conditions impose high demands on the visual system and promote visual dominance in sensory processing, often at the expense of vestibular and somatosensory inputs essential for spatial orientation and postural control [ 10 , 11 ]. The vestibular system plays a central role in balance, gaze stabilization, and spatial perception through its integration with visual and proprioceptive systems [ 10 ]. Visual–vestibular integration is essential for maintaining perceptual stability during head and body movements. Prolonged exposure to visually dominant environments may disrupt this balance, leading to sensory reweighting in which visual input is prioritized over vestibular information [ 11 ]. Such maladaptive sensory reweighting has been implicated in symptoms including dizziness, visual fatigue, cybersickness, motion sensitivity, and imbalance [ 1 , 3 , 7 ]. Increasing reports of screen-related dizziness and visually induced motion sickness suggest that chronic digital exposure may influence vestibular processing even in individuals without overt vestibular pathology [ 3 , 6 ]. Despite growing clinical recognition of these symptoms, objective physiological evidence demonstrating vestibular system involvement in chronic screen exposure remains limited [ 4 ]. Traditional clinical vestibular assessments often fail to detect subtle functional changes within vestibular pathways. However, advanced vestibular assessment techniques, such as ocular vestibular evoked myogenic potentials (oVEMP) and cranio-oculographic analysis, provide sensitive measures of otolith organ function, vestibulo-ocular pathways, and higher-order visual–vestibular integration [ 4 , 5 , 10 ]. These tools enable detection of subclinical dysfunctions that may precede overt vestibular disease. Understanding the neurophysiological impact of prolonged screen exposure is therefore of increasing clinical relevance. Investigating early functional changes within visual–vestibular integration networks may provide important insights into the mechanisms underlying screen-related dizziness and visual fatigue, and may support the development of preventive strategies, early diagnostic protocols, and targeted rehabilitation approaches for individuals with chronic digital exposure [ 8 , 9 , 12 , 15 ]. Case Presentation Two healthy young adult males with a history of intensive digital screen exposure were evaluated. Patient 1, aged 19 years, was a habitual gamer with more than six years of daily screen use exceeding four hours per day. Patient 2, aged 20 years, also reported high daily screen exposure for more than six years. Both individuals experienced intermittent dizziness, transient imbalance following prolonged screen use, and significant visual fatigue, particularly after exposure to high-motion digital content. Neither participant had a history of otological disease, neurological illness, migraine, vestibular disorders, or head trauma. Comprehensive audiological assessment including otoscopy, pure tone audiometry, speech audiometry, and immittance measures revealed normal peripheral hearing sensitivity, normal speech recognition, and normal middle-ear function in both participants, excluding peripheral auditory pathology as a contributing factor. Vestibular electrophysiological assessment using oVEMP testing with 500 Hz tone bursts at 105 dBnHL revealed present and replicable responses in both patients. However, both individuals demonstrated prolonged P1 and N1 latencies and reduced response amplitudes relative to laboratory normative values. These findings indicate delayed neural conduction and reduced excitability within the utricular–superior vestibular nerve–vestibulo-ocular pathway, suggesting early subclinical involvement of otolith-mediated vestibular pathways. Parameter Participant 1 Participant 2 Interpretation P1 Latency (ms) 17 16 Prolonged conduction N1 Latency (ms) 12 11 Prolonged conduction Amplitude (µV) 3.06 3.12 Decreased excitability Table I: Summary of the electrophysiological findings Cranio-oculographic evaluation demonstrated conjugate and symmetrical horizontal and vertical saccades with normal latency, velocity, and precision in both patients, with no evidence of hypometria, hypermetria, initiation delay, or slowing. Optokinetic testing elicited normal conjugate nystagmus responses in both horizontal and vertical directions, reflecting preserved optokinetic reflex integrity. Gaze testing under fixation and non-fixation conditions demonstrated stable ocular alignment in all gaze positions, with no gaze-evoked nystagmus, no rebound nystagmus, and no skew deviation, indicating intact gaze-holding mechanisms. Positional testing using Dix–Hallpike maneuvers showed only transient physiological nystagmus during head movement, with no nystagmus in static head positions, effectively ruling out benign paroxysmal positional vertigo or peripheral positional vestibular pathology. Clinical chair rotation, vestibulo-ocular reflex testing, VOR suppression, and sinusoidal rotation paradigms demonstrated preserved vestibulo-ocular reflex integrity, normal visual suppression of VOR, and symmetrical responses without asymmetry or pathological findings in both participants, indicating preserved semicircular canal and brainstem vestibular reflex function. Smooth pursuit testing revealed functionally relevant abnormalities. In Patient 1, horizontal pursuit demonstrated reduced gain with compensatory catch-up saccades during rightward tracking, and vertical pursuit showed reduced gain during upward tracking, reflecting impaired pursuit efficiency and increased reliance on corrective saccades. In Patient 2, smooth pursuit tracking remained conjugate but demonstrated bilaterally reduced gain in both horizontal and vertical planes, indicating mild but consistent pursuit inefficiency. These findings suggest altered cortical–vestibular–visual integration mechanisms rather than primary vestibular reflex pathology. Discussion The integration of vestibular electrophysiology and cranio-oculographic findings provides a coherent neurophysiological profile of early visual–vestibular system strain in both patients. Despite normal peripheral hearing, intact semicircular canal reflexes, preserved vestibulo-ocular reflex (VOR) function, and normal oculomotor reflex pathways, both individuals demonstrated objective abnormalities in utriculo-ocular electrophysiology and higher-order oculomotor control. This dissociation between preserved reflexive vestibular pathways and altered integrative vestibular processing highlights the presence of early functional changes rather than overt vestibular pathology [ 4 , 10 , 11 ]. Such a pattern supports the concept that higher-order sensory integration networks may be affected before primary vestibular reflex circuits become clinically involved [ 7 , 13 ]. The prolonged oVEMP latencies and reduced amplitudes indicate delayed neural conduction and reduced excitability within the utricular–superior vestibular nerve–vestibulo-ocular pathway, suggesting early subclinical otolith pathway involvement [ 4 , 5 , 10 ]. The utricular system plays a crucial role in linear acceleration detection, gravitational orientation, and spatial perception, and subtle dysfunction within this pathway may not produce classical vestibular signs but may contribute to perceptual instability and spatial disorientation [ 10 , 13 ]. These electrophysiological abnormalities therefore provide objective evidence of early otolith system vulnerability in individuals with chronic visual dominance and prolonged digital exposure. The smooth pursuit abnormalities provide complementary evidence of central visual–vestibular integration strain. Smooth pursuit eye movements depend on distributed cortical networks, including visual motion processing areas, frontal eye fields, cerebellar circuits, and vestibular integration centres, making them particularly sensitive to visual overload and prolonged visual dominance [ 10 , 11 , 13 ]. Reduced pursuit gain and compensatory catch-up saccades reflect inefficiency in continuous visual tracking and impaired integration of visual motion information, suggesting functional strain within cortical–cerebellar–vestibular networks [ 11 , 14 ]. Chronic exposure to high-motion digital environments may reinforce visual dominance and induce maladaptive adaptations in these networks, reducing the efficiency of multisensory integration mechanisms [ 3 , 6 , 14 ]. These findings support a model of sensory reweighting and adaptive neuroplasticity, in which prolonged digital screen exposure promotes visual dominance and alters the balance between visual and vestibular inputs [ 1 , 2 , 3 , 6 ]. Sensory reweighting models propose that persistent reliance on one sensory modality leads to central reorganization of multisensory processing networks, potentially resulting in maladaptive plasticity when environmental demands change [ 13 , 14 ]. Over time, this imbalance may lead to subtle neurophysiological changes in utricular pathways and higher-order visual–vestibular integration networks, producing symptoms such as visual fatigue, intermittent dizziness, motion sensitivity, and imbalance without classical vestibular disease [ 1 , 3 , 7 , 8 ]. The preservation of semicircular canal reflexes, vestibulo-ocular reflex integrity, gaze stability, and optokinetic responses indicates that these changes represent early functional adaptation rather than structural vestibular pathology, supporting the interpretation of subclinical functional vestibular strain rather than established vestibular disorder [ 4 , 9 , 12 ]. This pattern is consistent with models of early-stage functional vestibular dysfunction, in which central integration mechanisms are affected prior to measurable peripheral vestibular damage [ 7 , 10 , 13 ]. Clinically, this distinction is critical, as early functional changes may be potentially reversible through behavioral modification, visual hygiene strategies, controlled screen exposure, and targeted vestibular rehabilitation interventions [ 9 , 12 , 15 ]. Early identification of such changes may therefore play a key role in preventing progression to chronic vestibular disorders and persistent dizziness syndromes in populations with high digital exposure. Conclusion This case study demonstrates that prolonged screen use may be associated with subtle but measurable neurophysiological changes within visual–vestibular integration pathways. Objective evidence from oVEMP testing indicates early utriculo-ocular pathway involvement, while cranio-oculography reveals higher-order oculomotor integration deficits, particularly in smooth pursuit function. These abnormalities occur despite preserved peripheral hearing, intact semicircular canal function, normal vestibulo-ocular reflexes, and stable gaze mechanisms. The combined electrophysiological and oculomotor findings support the concept of early functional vestibular strain driven by prolonged visual dominance and sensory reweighting rather than overt vestibular disease. Subjective symptoms of visual fatigue, dizziness, and imbalance further reinforce the clinical relevance of these objective findings. As digital exposure continues to increase globally, understanding its impact on visual–vestibular neurophysiology is essential, and larger controlled studies with longitudinal follow-up are required to validate these observations and develop preventive and rehabilitative strategies for screen-related vestibular dysfunction. Abbreviations DHI – Dizziness Handicap Inventory oVEMP – Ocular Vestibular Evoked Myogenic Potential PTA – Pure Tone Audiometry VOR – Vestibulo-Ocular Reflex µV – Microvolt ms – Milliseconds Hz – Hertz dBnHL – Decibels normalized hearing level Declarations Ethics approval and consent to participate Ethical approval for this study was obtained from the Institutional Ethics Committee of Sri Devaraj Urs Academy of Higher Education and Research, Tamaka, Kolar SDUAHER/R&D/CEC/FAHP-F/61/NF/2025-26. Written informed consent was obtained from all participants prior to their inclusion in the study. Consent for publication Written informed consent for publication of anonymized clinical data and findings was obtained from all participants. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Author Contribution  Authors contribution in the studyMr. M Abhijith- Interpretation of both behavioural and physiological Audiological tests- Revision of the manuscript which is drafted by the student clinician- Supervision of the whole process during data acquisition and interpretation of data for diagnosis.Ms. Reshma R- Revision of the manuscript which is drafted by the student clinician- Supervision of the whole process during data acquisition and interpretation of data for diagnosis.Mr. Nishanth G- Acquisition of data by administering Behavioural test, Physiological tests andvestibular evaluation.- Manuscript drafting Acknowledgement The authors sincerely thank the Department of Speech Pathology and Audiology, Sri Devaraj Urs Academy of Higher Education and Research, for providing the infrastructure and clinical facilities required for this study. References Bertolini, G., & Straumann, D. (2016). Moving in a moving world: A review on vestibular motion sickness. Frontiers in Neurology, 7 , 14. Golding, J. F. (2016). Motion sickness susceptibility. Autonomic Neuroscience, 129 , 67–76. Keshavarz, B., Riecke, B. E., Hettinger, L. J., & Campos, J. L. (2015). Visually induced motion sickness: Causes, characteristics, and countermeasures. Human Factors, 57 (4), 761–789. Shepard, N. T., & Telian, S. A. (2019). Vestibular testing in clinical practice: Clinical and electrophysiological perspectives. Journal of the American Academy of Audiology, 30 (5), 399–416. Yagi, R., Sugiura, S., Kaga, K., & Suzuki, M. (2009). Age-related changes in ocular vestibular evoked myogenic potentials. Clinical Neurophysiology, 120 (4), 781–785. Zhang, J., Li, B., & Song, Q. (2021). Effects of visual overload on postural control and vestibular function. Journal of Vestibular Research, 31 (3), 233–244. Brandt, T., & Dieterich, M. (2017). The dizzy patient: Don’t forget disorders of the central vestibular system. Nature Reviews Neurology, 13 (6), 352–362. Staab, J. P., Eckhardt-Henn, A., Horii, A., Jacob, R., Strupp, M., & Brandt, T. (2017). Diagnostic criteria for persistent postural-perceptual dizziness (PPPD). Journal of Vestibular Research, 27 (4), 191–208. Lacour, M., & Bernard-Demanze, L. (2014). Interaction between vestibular compensation mechanisms and vestibular rehabilitation therapy. Frontiers in Neurology, 5 , 285. Angelaki, D. E., & Cullen, K. E. (2008). Vestibular system: The many facets of a multimodal sense. Annual Review of Neuroscience, 31 , 125–150. Bronstein, A. M. (2016). Multisensory integration in balance control. Handbook of Clinical Neurology, 137 , 57–66. Pavlou, M., Kanegaonkar, R. G., Swapp, D., Bamiou, D. E., Slater, M., & Luxon, L. M. (2012). The effect of virtual reality on visual vertigo symptoms. Brain, 135 (4), 1320–1333. Dieterich, M., & Brandt, T. (2015). The bilateral central vestibular system: Its pathways, functions, and disorders. Annals of the New York Academy of Sciences, 1343 (1), 10–26. Balaban, C. D., & Thayer, J. F. (2001). Neurological bases for balance–anxiety links. Journal of Anxiety Disorders, 15 (1–2), 53–79. Whitney, S. L., & Rossi, M. M. (2000). Efficacy of vestibular rehabilitation. Otolaryngologic Clinics of North America, 33 (3), 659–672. Additional Declarations No competing interests reported. Supplementary Files CAREchecklistImpactofProlongedscreenusage.docx Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 18 Apr, 2026 Reviewers agreed at journal 18 Apr, 2026 Reviewers agreed at journal 18 Apr, 2026 Reviewers invited by journal 18 Apr, 2026 Editor assigned by journal 12 Mar, 2026 Submission checks completed at journal 12 Mar, 2026 First submitted to journal 09 Mar, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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of digital technology has fundamentally transformed daily life, particularly among adolescents and young adults, leading to unprecedented levels of prolonged screen exposure [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Activities such as online learning, gaming, social media engagement, and multimedia consumption require sustained visual attention, continuous visual tracking, and prolonged fixation on dynamic visual environments [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. These conditions impose high demands on the visual system and promote visual dominance in sensory processing, often at the expense of vestibular and somatosensory inputs essential for spatial orientation and postural control [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe vestibular system plays a central role in balance, gaze stabilization, and spatial perception through its integration with visual and proprioceptive systems [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Visual\u0026ndash;vestibular integration is essential for maintaining perceptual stability during head and body movements. Prolonged exposure to visually dominant environments may disrupt this balance, leading to sensory reweighting in which visual input is prioritized over vestibular information [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Such maladaptive sensory reweighting has been implicated in symptoms including dizziness, visual fatigue, cybersickness, motion sensitivity, and imbalance [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Increasing reports of screen-related dizziness and visually induced motion sickness suggest that chronic digital exposure may influence vestibular processing even in individuals without overt vestibular pathology [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eDespite growing clinical recognition of these symptoms, objective physiological evidence demonstrating vestibular system involvement in chronic screen exposure remains limited [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Traditional clinical vestibular assessments often fail to detect subtle functional changes within vestibular pathways. However, advanced vestibular assessment techniques, such as ocular vestibular evoked myogenic potentials (oVEMP) and cranio-oculographic analysis, provide sensitive measures of otolith organ function, vestibulo-ocular pathways, and higher-order visual\u0026ndash;vestibular integration [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. These tools enable detection of subclinical dysfunctions that may precede overt vestibular disease.\u003c/p\u003e \u003cp\u003eUnderstanding the neurophysiological impact of prolonged screen exposure is therefore of increasing clinical relevance. Investigating early functional changes within visual\u0026ndash;vestibular integration networks may provide important insights into the mechanisms underlying screen-related dizziness and visual fatigue, and may support the development of preventive strategies, early diagnostic protocols, and targeted rehabilitation approaches for individuals with chronic digital exposure [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e].\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eTwo healthy young adult males with a history of intensive digital screen exposure were evaluated. Patient 1, aged 19 years, was a habitual gamer with more than six years of daily screen use exceeding four hours per day. Patient 2, aged 20 years, also reported high daily screen exposure for more than six years. Both individuals experienced intermittent dizziness, transient imbalance following prolonged screen use, and significant visual fatigue, particularly after exposure to high-motion digital content. Neither participant had a history of otological disease, neurological illness, migraine, vestibular disorders, or head trauma.\u003c/p\u003e\n\u003cp\u003eComprehensive audiological assessment including otoscopy, pure tone audiometry, speech audiometry, and immittance measures revealed normal peripheral hearing sensitivity, normal speech recognition, and normal middle-ear function in both participants, excluding peripheral auditory pathology as a contributing factor.\u003c/p\u003e\n\u003cp\u003eVestibular electrophysiological assessment using oVEMP testing with 500 Hz tone bursts at 105 dBnHL revealed present and replicable responses in both patients. However, both individuals demonstrated prolonged P1 and N1 latencies and reduced response amplitudes relative to laboratory normative values. These findings indicate delayed neural conduction and reduced excitability within the utricular\u0026ndash;superior vestibular nerve\u0026ndash;vestibulo-ocular pathway, suggesting early subclinical involvement of otolith-mediated vestibular pathways.\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"606\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eParameter\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eParticipant 1\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eParticipant 2\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eInterpretation\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eP1 Latency (ms)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e17\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e16\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eProlonged conduction\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eN1 Latency (ms)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eProlonged conduction\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eAmplitude (\u0026micro;V)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e3.06\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e3.12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eDecreased excitability\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cstrong\u003eTable\u003c/strong\u003e \u003cstrong\u003eI:\u003c/strong\u003e Summary of the electrophysiological findings\u003c/p\u003e\n\u003cp\u003eCranio-oculographic evaluation demonstrated conjugate and symmetrical horizontal and vertical saccades with normal latency, velocity, and precision in both patients, with no evidence of hypometria, hypermetria, initiation delay, or slowing. Optokinetic testing elicited normal conjugate nystagmus responses in both horizontal and vertical directions, reflecting preserved optokinetic reflex integrity. Gaze testing under fixation and non-fixation conditions demonstrated stable ocular alignment in all gaze positions, with no gaze-evoked nystagmus, no rebound nystagmus, and no skew deviation, indicating intact gaze-holding mechanisms.\u003c/p\u003e\n\u003cp\u003ePositional testing using Dix\u0026ndash;Hallpike maneuvers showed only transient physiological nystagmus during head movement, with no nystagmus in static head positions, effectively ruling out benign paroxysmal positional vertigo or peripheral positional vestibular pathology. Clinical chair rotation, vestibulo-ocular reflex testing, VOR suppression, and sinusoidal rotation paradigms demonstrated preserved vestibulo-ocular reflex integrity, normal visual suppression of VOR, and symmetrical responses without asymmetry or pathological findings in both participants, indicating preserved semicircular canal and brainstem vestibular reflex function.\u003c/p\u003e\n\u003cp\u003eSmooth pursuit testing revealed functionally relevant abnormalities. In Patient 1, horizontal pursuit demonstrated reduced gain with compensatory catch-up saccades during rightward tracking, and vertical pursuit showed reduced gain during upward tracking, reflecting impaired pursuit efficiency and increased reliance on corrective saccades.\u003c/p\u003e\n\u003cp\u003eIn Patient 2, smooth pursuit tracking remained conjugate but demonstrated bilaterally reduced gain in both horizontal and vertical planes, indicating mild but consistent pursuit inefficiency. These findings suggest altered cortical\u0026ndash;vestibular\u0026ndash;visual integration mechanisms rather than primary vestibular reflex pathology.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThe integration of vestibular electrophysiology and cranio-oculographic findings provides a coherent neurophysiological profile of early visual\u0026ndash;vestibular system strain in both patients. Despite normal peripheral hearing, intact semicircular canal reflexes, preserved vestibulo-ocular reflex (VOR) function, and normal oculomotor reflex pathways, both individuals demonstrated objective abnormalities in utriculo-ocular electrophysiology and higher-order oculomotor control. This dissociation between preserved reflexive vestibular pathways and altered integrative vestibular processing highlights the presence of early functional changes rather than overt vestibular pathology [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Such a pattern supports the concept that higher-order sensory integration networks may be affected before primary vestibular reflex circuits become clinically involved [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe prolonged oVEMP latencies and reduced amplitudes indicate delayed neural conduction and reduced excitability within the utricular\u0026ndash;superior vestibular nerve\u0026ndash;vestibulo-ocular pathway, suggesting early subclinical otolith pathway involvement [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. The utricular system plays a crucial role in linear acceleration detection, gravitational orientation, and spatial perception, and subtle dysfunction within this pathway may not produce classical vestibular signs but may contribute to perceptual instability and spatial disorientation [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. These electrophysiological abnormalities therefore provide objective evidence of early otolith system vulnerability in individuals with chronic visual dominance and prolonged digital exposure.\u003c/p\u003e \u003cp\u003eThe smooth pursuit abnormalities provide complementary evidence of central visual\u0026ndash;vestibular integration strain. Smooth pursuit eye movements depend on distributed cortical networks, including visual motion processing areas, frontal eye fields, cerebellar circuits, and vestibular integration centres, making them particularly sensitive to visual overload and prolonged visual dominance [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. Reduced pursuit gain and compensatory catch-up saccades reflect inefficiency in continuous visual tracking and impaired integration of visual motion information, suggesting functional strain within cortical\u0026ndash;cerebellar\u0026ndash;vestibular networks [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. Chronic exposure to high-motion digital environments may reinforce visual dominance and induce maladaptive adaptations in these networks, reducing the efficiency of multisensory integration mechanisms [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThese findings support a model of sensory reweighting and adaptive neuroplasticity, in which prolonged digital screen exposure promotes visual dominance and alters the balance between visual and vestibular inputs [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Sensory reweighting models propose that persistent reliance on one sensory modality leads to central reorganization of multisensory processing networks, potentially resulting in maladaptive plasticity when environmental demands change [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. Over time, this imbalance may lead to subtle neurophysiological changes in utricular pathways and higher-order visual\u0026ndash;vestibular integration networks, producing symptoms such as visual fatigue, intermittent dizziness, motion sensitivity, and imbalance without classical vestibular disease [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe preservation of semicircular canal reflexes, vestibulo-ocular reflex integrity, gaze stability, and optokinetic responses indicates that these changes represent early functional adaptation rather than structural vestibular pathology, supporting the interpretation of subclinical functional vestibular strain rather than established vestibular disorder [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. This pattern is consistent with models of early-stage functional vestibular dysfunction, in which central integration mechanisms are affected prior to measurable peripheral vestibular damage [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. Clinically, this distinction is critical, as early functional changes may be potentially reversible through behavioral modification, visual hygiene strategies, controlled screen exposure, and targeted vestibular rehabilitation interventions [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. Early identification of such changes may therefore play a key role in preventing progression to chronic vestibular disorders and persistent dizziness syndromes in populations with high digital exposure.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case study demonstrates that prolonged screen use may be associated with subtle but measurable neurophysiological changes within visual\u0026ndash;vestibular integration pathways. Objective evidence from oVEMP testing indicates early utriculo-ocular pathway involvement, while cranio-oculography reveals higher-order oculomotor integration deficits, particularly in smooth pursuit function. These abnormalities occur despite preserved peripheral hearing, intact semicircular canal function, normal vestibulo-ocular reflexes, and stable gaze mechanisms.\u003c/p\u003e \u003cp\u003eThe combined electrophysiological and oculomotor findings support the concept of early functional vestibular strain driven by prolonged visual dominance and sensory reweighting rather than overt vestibular disease. Subjective symptoms of visual fatigue, dizziness, and imbalance further reinforce the clinical relevance of these objective findings. As digital exposure continues to increase globally, understanding its impact on visual\u0026ndash;vestibular neurophysiology is essential, and larger controlled studies with longitudinal follow-up are required to validate these observations and develop preventive and rehabilitative strategies for screen-related vestibular dysfunction.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eDHI \u0026ndash; Dizziness Handicap Inventory\u003c/p\u003e\n\u003cp\u003eoVEMP \u0026ndash; Ocular Vestibular Evoked Myogenic Potential\u003c/p\u003e\n\u003cp\u003ePTA \u0026ndash; Pure Tone Audiometry\u003c/p\u003e\n\u003cp\u003eVOR \u0026ndash; Vestibulo-Ocular Reflex\u003c/p\u003e\n\u003cp\u003e\u0026micro;V \u0026ndash; Microvolt\u003c/p\u003e\n\u003cp\u003ems \u0026ndash; Milliseconds\u003c/p\u003e\n\u003cp\u003eHz \u0026ndash; Hertz\u003c/p\u003e\n\u003cp\u003edBnHL \u0026ndash; Decibels normalized hearing level\u003c/p\u003e"},{"header":"Declarations","content":"\u003ch2\u003eEthics approval and consent to participate\u003c/h2\u003e\n\u003cp\u003eEthical approval for this study was obtained from the Institutional Ethics Committee of Sri Devaraj Urs Academy of Higher Education and Research, Tamaka, Kolar SDUAHER/R\u0026amp;D/CEC/FAHP-F/61/NF/2025-26. Written informed consent was obtained from all participants prior to their inclusion in the study.\u003c/p\u003e\n\u003ch2\u003eConsent for publication\u003c/h2\u003e\n\u003cp\u003eWritten informed consent for publication of anonymized clinical data and findings was obtained from all participants.\u003c/p\u003e\n\u003ch2\u003eFunding\u003c/h2\u003e\n\u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\n\u003cp\u003e Authors contribution in the studyMr. M Abhijith- Interpretation of both behavioural and physiological Audiological tests- Revision of the manuscript which is drafted by the student clinician- Supervision of the whole process during data acquisition and interpretation of data for diagnosis.Ms. Reshma R- Revision of the manuscript which is drafted by the student clinician- Supervision of the whole process during data acquisition and interpretation of data for diagnosis.Mr. Nishanth G- Acquisition of data by administering Behavioural test, Physiological tests andvestibular evaluation.- Manuscript drafting\u003c/p\u003e\n\u003ch2\u003eAcknowledgement\u003c/h2\u003e\n\u003cp\u003eThe authors sincerely thank the Department of Speech Pathology and Audiology, Sri Devaraj Urs Academy of Higher Education and Research, for providing the infrastructure and clinical facilities required for this study.\u003c/p\u003e"},{"header":"References","content":"\u003col start=\"1\" type=\"1\"\u003e\n \u003cli\u003eBertolini, G., \u0026amp; Straumann, D. (2016). Moving in a moving world: A review on vestibular motion sickness. \u003cem\u003eFrontiers in Neurology, 7\u003c/em\u003e, 14.\u003c/li\u003e\n \u003cli\u003eGolding, J. F. (2016). Motion sickness susceptibility. \u003cem\u003eAutonomic Neuroscience, 129\u003c/em\u003e, 67\u0026ndash;76.\u003c/li\u003e\n \u003cli\u003eKeshavarz, B., Riecke, B. E., Hettinger, L. J., \u0026amp; Campos, J. L. (2015). Visually induced motion sickness: Causes, characteristics, and countermeasures. \u003cem\u003eHuman Factors, 57\u003c/em\u003e(4), 761\u0026ndash;789.\u003c/li\u003e\n \u003cli\u003eShepard, N. T., \u0026amp; Telian, S. A. (2019). Vestibular testing in clinical practice: Clinical and electrophysiological perspectives. \u003cem\u003eJournal of the American Academy of Audiology, 30\u003c/em\u003e(5), 399\u0026ndash;416.\u003c/li\u003e\n \u003cli\u003eYagi, R., Sugiura, S., Kaga, K., \u0026amp; Suzuki, M. (2009). Age-related changes in ocular vestibular evoked myogenic potentials. \u003cem\u003eClinical Neurophysiology, 120\u003c/em\u003e(4), 781\u0026ndash;785.\u003c/li\u003e\n \u003cli\u003eZhang, J., Li, B., \u0026amp; Song, Q. (2021). Effects of visual overload on postural control and vestibular function. \u003cem\u003eJournal of Vestibular Research, 31\u003c/em\u003e(3), 233\u0026ndash;244.\u003c/li\u003e\n \u003cli\u003eBrandt, T., \u0026amp; Dieterich, M. (2017). The dizzy patient: Don\u0026rsquo;t forget disorders of the central vestibular system. \u003cem\u003eNature Reviews Neurology, 13\u003c/em\u003e(6), 352\u0026ndash;362.\u003c/li\u003e\n \u003cli\u003eStaab, J. P., Eckhardt-Henn, A., Horii, A., Jacob, R., Strupp, M., \u0026amp; Brandt, T. (2017). Diagnostic criteria for persistent postural-perceptual dizziness (PPPD). \u003cem\u003eJournal of Vestibular Research, 27\u003c/em\u003e(4), 191\u0026ndash;208.\u003c/li\u003e\n \u003cli\u003eLacour, M., \u0026amp; Bernard-Demanze, L. (2014). Interaction between vestibular compensation mechanisms and vestibular rehabilitation therapy. \u003cem\u003eFrontiers in Neurology, 5\u003c/em\u003e, 285.\u003c/li\u003e\n \u003cli\u003eAngelaki, D. E., \u0026amp; Cullen, K. E. (2008). Vestibular system: The many facets of a multimodal sense. \u003cem\u003eAnnual Review of Neuroscience, 31\u003c/em\u003e, 125\u0026ndash;150.\u003c/li\u003e\n \u003cli\u003eBronstein, A. M. (2016). Multisensory integration in balance control. \u003cem\u003eHandbook of Clinical Neurology, 137\u003c/em\u003e, 57\u0026ndash;66.\u003c/li\u003e\n \u003cli\u003ePavlou, M., Kanegaonkar, R. G., Swapp, D., Bamiou, D. E., Slater, M., \u0026amp; Luxon, L. M. (2012). The effect of virtual reality on visual vertigo symptoms. \u003cem\u003eBrain, 135\u003c/em\u003e(4), 1320\u0026ndash;1333.\u003c/li\u003e\n \u003cli\u003eDieterich, M., \u0026amp; Brandt, T. (2015). The bilateral central vestibular system: Its pathways, functions, and disorders. \u003cem\u003eAnnals of the New York Academy of Sciences, 1343\u003c/em\u003e(1), 10\u0026ndash;26.\u003c/li\u003e\n \u003cli\u003eBalaban, C. D., \u0026amp; Thayer, J. F. (2001). Neurological bases for balance\u0026ndash;anxiety links. \u003cem\u003eJournal of Anxiety Disorders, 15\u003c/em\u003e(1\u0026ndash;2), 53\u0026ndash;79.\u003c/li\u003e\n \u003cli\u003eWhitney, S. L., \u0026amp; Rossi, M. M. (2000). Efficacy of vestibular rehabilitation. \u003cem\u003eOtolaryngologic Clinics of North America, 33\u003c/em\u003e(3), 659\u0026ndash;672.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"the-egyptian-journal-of-otolaryngology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [The Egyptian Journal of Otolaryngology](https://ejo.springeropen.com/)","snPcode":"43163","submissionUrl":"https://submission.springernature.com/new-submission/43163/3","title":"The Egyptian Journal of Otolaryngology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"screen time, vestibular function, oVEMP, cranio-oculography, visual fatigue, dizziness, smooth pursuit","lastPublishedDoi":"10.21203/rs.3.rs-9071693/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9071693/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e: Prolonged screen exposure is increasingly prevalent among young adults and may influence visual–vestibular integration. While symptoms such as visual fatigue, dizziness, and imbalance are frequently reported in individuals with high digital exposure, objective evidence of vestibular pathway involvement remains limited.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase\u003c/strong\u003e \u003cstrong\u003epresentation\u003c/strong\u003e: Two young adult males (Patient 1; Patient 2) with more than six years of daily screen use exceeding four hours underwent comprehensive audiological, vestibular electrophysiological, and cranio-oculography. Peripheral hearing and middle-ear function were normal in both individuals. oVEMP testing demonstrated prolonged P1 and N1 latencies with reduced amplitudes relative to laboratory normative values, suggesting subtle utriculo-ocular pathway involvement. Cranio-oculography revealed normal saccadic parameters, optokinetic responses, gaze stability, positional testing, and VOR function in both participants. However, smooth pursuit testing demonstrated reduced gain with compensatory catch-up saccades, more pronounced in Patient 1 (particularly vertical pursuit), and mild bilateral gain reduction in both horizontal and vertical planes in Patient 2. Both participants reported intermittent dizziness, visual fatigue, and imbalance, with mild functional impact reflected in Dizziness Handicap Inventory scores.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e: The combined electrophysiological (oVEMP) and oculomotor (pursuit) findings suggest early functional strain within visual–vestibular integration pathways despite otherwise normal vestibular reflexes. Prolonged screen exposure may be associated with subtle adaptive or maladaptive changes in vestibulo-ocular processing, supporting the need for larger, controlled studies.\u003c/p\u003e","manuscriptTitle":"Impact of Prolonged Screen Use on Vestibular Function: A Case Study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-28 00:19:52","doi":"10.21203/rs.3.rs-9071693/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2026-04-18T18:25:36+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"93978399179168845607658792493499175179","date":"2026-04-18T17:14:59+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"36440045894365752887887793378274007834","date":"2026-04-18T17:00:28+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-04-18T16:50:35+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-03-12T04:48:18+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-03-12T04:47:40+00:00","index":"","fulltext":""},{"type":"submitted","content":"The Egyptian Journal of Otolaryngology","date":"2026-03-09T10:26:24+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"the-egyptian-journal-of-otolaryngology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [The Egyptian Journal of Otolaryngology](https://ejo.springeropen.com/)","snPcode":"43163","submissionUrl":"https://submission.springernature.com/new-submission/43163/3","title":"The Egyptian Journal of Otolaryngology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"562c9aba-2319-4b7d-a598-fabbacdff8ca","owner":[],"postedDate":"April 28th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-04-28T00:19:52+00:00","versionOfRecord":[],"versionCreatedAt":"2026-04-28 00:19:52","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9071693","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9071693","identity":"rs-9071693","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}