Chronic dizziness in older adults: disrupted sensorimotor EEG beta oscillations during postural instability
File(s)
Published version
Author(s)
Type
Journal Article
Abstract
Objective
Chronic dizziness is common in older adults, yet frequently occurs without a clear cause (‘idiopathic dizziness’). Patients experience subjective unsteadiness with minimal objective imbalance, potentially related to small vessel disease. Here we examine the hypothesis that this syndrome is associated with disrupted cortical processing of postural instability.
Methods
EEG and postural sway were recorded in 33 older adults with chronic, idiopathic dizziness (Age, Mean = 77.3 years, SD = 6.4, 61 % female) and 25 matched controls (Age, Mean = 76.9 years, SD = 6.0, 56 % female). EEG was time-locked to spontaneous instances of postural instability and analysed via time–frequency decomposition.
Results
Significant between-group differences in EEG were observed during the early phase of postural instability (p < 0.05, cluster-corrected). Whilst controls exhibited broadband increase in EEG power across sensorimotor areas, dizzy patients displayed suppressed beta activity (19–24 Hz). Contrary to predictions, these differences did not relate to small vessel disease markers (rs < 0.05, ps > 0.720) but to fear of falling (r = -0.44, p = 0.001).
Conclusions
Previous work implies that suppressing cortical beta enhances the relay of sensory information. We therefore propose that the modulation in beta EEG observed in patients reflects an anxious, top-down strategy to increase sensitivity to instability, which paradoxically causes persistent feelings of subjective imbalance.
Significance
These results identify associations between idiopathic dizziness and disrupted sensorimotor beta activation during postural instability. Cortical beta during imbalance may be a possible biomarker of chronic, idiopathic dizziness in older adults and/or fear of falling.
Chronic dizziness is common in older adults, yet frequently occurs without a clear cause (‘idiopathic dizziness’). Patients experience subjective unsteadiness with minimal objective imbalance, potentially related to small vessel disease. Here we examine the hypothesis that this syndrome is associated with disrupted cortical processing of postural instability.
Methods
EEG and postural sway were recorded in 33 older adults with chronic, idiopathic dizziness (Age, Mean = 77.3 years, SD = 6.4, 61 % female) and 25 matched controls (Age, Mean = 76.9 years, SD = 6.0, 56 % female). EEG was time-locked to spontaneous instances of postural instability and analysed via time–frequency decomposition.
Results
Significant between-group differences in EEG were observed during the early phase of postural instability (p < 0.05, cluster-corrected). Whilst controls exhibited broadband increase in EEG power across sensorimotor areas, dizzy patients displayed suppressed beta activity (19–24 Hz). Contrary to predictions, these differences did not relate to small vessel disease markers (rs < 0.05, ps > 0.720) but to fear of falling (r = -0.44, p = 0.001).
Conclusions
Previous work implies that suppressing cortical beta enhances the relay of sensory information. We therefore propose that the modulation in beta EEG observed in patients reflects an anxious, top-down strategy to increase sensitivity to instability, which paradoxically causes persistent feelings of subjective imbalance.
Significance
These results identify associations between idiopathic dizziness and disrupted sensorimotor beta activation during postural instability. Cortical beta during imbalance may be a possible biomarker of chronic, idiopathic dizziness in older adults and/or fear of falling.
Date Issued
2025-06-01
Date Acceptance
2025-03-09
Citation
Clinical Neurophysiology, 2025, 174, pp.31-36
ISSN
1388-2457
Publisher
Elsevier
Start Page
31
End Page
36
Journal / Book Title
Clinical Neurophysiology
Volume
174
Copyright Statement
© 2025 The Author(s). Published by Elsevier B.V. on behalf of International Federation of Clinical Neurophysiology. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
License URL
Identifier
10.1016/j.clinph.2025.03.032
Publication Status
Published
Date Publish Online
2025-03-27