ReviewFrontiers in neurology2026
Attentional dysfunction in persistent postural-perceptual dizziness: a narrative review of mechanistic evidence.
Review in Frontiers in neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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3 authors.
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Abstract
Persistent postural-perceptual dizziness (PPPD) is a common chronic functional neuro-otological disorder characterized by persistent non-spinning dizziness, unsteadiness, and heightened sensitivity to upright posture, motion, and visually complex environments. Several conceptual models have been proposed to explain its persistence, including failure of readaptation after a destabilizing event, maladaptive multisensory integration with excessive visual or somatosensory weighting, and prediction-actual sensory mismatch with amplified prediction errors. This narrative review synthesizes neuroimaging, behavioral, psychophysical, and clinical evidence to examine attentional dysfunction as a candidate organizing mechanism that may link these partly overlapping pathways. Structural and functional alterations involving the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), posterior insula, precuneus, visual cortex, vestibular cortical regions, and large-scale attention, salience, sensorimotor, visual, and default-mode networks suggest distributed functional reorganization rather than a single lesional substrate. Behavioral studies indicate that postural control and self-motion perception may become excessively attention-dependent in subsets of patients, with dual-task effects, altered visual exploration, stiffened postural strategies, and abnormal sensory-perceptual scaling. Clinical studies further show balance vigilance, attentional bias, and heterogeneous symptom phenotypes, including visual intolerance, quiet standing or sitting intolerance, passive motion intolerance, and active motion intolerance. We propose a revised active-inference model in which attention contributes to dysregulated precision weighting across visual, vestibular, somatosensory, interoceptive, and postural prediction-error signals. This model is hypothesis-generating rather than definitive. It accommodates patients with or without a clear preceding vestibular disorder and patients whose symptoms occur without overt body motion. The framework highlights testable targets for future studies using event-related potentials, computational modeling, dual-task paradigms, and phenotype-stratified treatment trials.
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