Abstract
To the Editor:
Kim and Crimmins’ recent article in the Journal of Applied Gerontology provides important evidence that persistent dizziness in older adults is associated with accelerated cognitive decline and an increased risk of dementia (Kim & Crimmins, 2025). These findings are clinically relevant, but the epidemiological nature of the article does not allow potential mechanisms underlying this association to be addressed. In this letter, we will bring evidence suggesting that the observed relationship between dizziness and cognitive decline is best understood in terms of cerebral small vessel disease–related disruption of brain connectivity, particularly within frontal–subcortical networks.
In the last 10–15 years, large-scale studies in the elderly population have shown it is not labyrinthine disease that is prominently associated with dizziness but rather psycho-social and cardio-vascular factors, hypertension in particular (Maarsingh et al., 2010). Although hypertensive patients can experience dizziness via multiple mechanisms, the fact that hypertension and age are the two most important contributors to the development of microangiopathy (Markus and Joutel, 2025) places small vessel disease (SVD) as a potential underlying mechanism creating imbalance and dizziness. SVD is a well-established cause for the cognitive decline, imbalance and falls experienced in old age (Erkinjuntti et al., 2011). Careful interrogation of the elderly dizzy patient often establishes that the ‘dizziness’ is in fact a feeling of unsteadiness and patients with both cognitive impairment and postural instability experience worse dizziness than those without postural instability (Lee et al., 2020).
In later life, chronic dizziness is frequently labelled ‘idiopathic’ once neuro-vestibular disorders and postural hypotension have been excluded. However, clinical imaging demonstrates that older adults with unexplained dizziness show greater white matter abnormalities consistent with SVD than patients whose dizziness is underpinned by alternative vestibular or haemodynamic diagnoses (Ahmad et al., 2015).
More recent work has extended these observations beyond structure to network-level physiology. Using EEG during postural tasks, older adults with unexplained dizziness exhibit disrupted postural brain networks consistent with SVD-related disconnection (Ibitoye et al., 2021). Further, postural experiments found abnormalities of the protective stepping response in these patients, a fall-preventive reaction mediated by fronto–basal ganglia mechanisms known to be disrupted by SVD (Castro et al., 2024).
More directly, structural analyses further demonstrate that this dizziness is associated with reduced frontal white matter integrity and greater SVD burden (Ibitoye et al., 2022). Notably, these frontal–basal ganglia circuits are well recognised as critical substrates for executive function, gait control, attentional regulation and cognitive resilience.
From this perspective, in agreement with Kim and Crimmins, chronic dizziness may represent an early clinical marker of network vulnerability arising, in my view, from SVD-mediated disconnection. Frontal–subcortical circuits are particularly susceptible to microvascular injury, and their disruption is a well-established contributor to executive dysfunction, gait disturbance and progression to vascular and mixed dementias (Wardlaw et al., 2013). Given the intricate relationship between white matter damage and hippocampal atrophy (Fiford et al., 2017), however, it should be acknowledged that the association between dizziness, cognitive decline and dementia may also depend on grey matter loss (Felfela et al., 2024). We hope that the paper by Kim and Crimmins, and the additional mechanistic input provided here, will make geriatricians consider persistent dizziness as a potential sentinel symptom of cerebral network pathology, particularly SVD, rather than an isolated sensory complaint.
Yours sincerely,
Prof Adolfo M. Bronstein MD PhD FEAN FANA FRCP
