The review, led by Moyan Wang of Changchun University of Chinese Medicine and colleagues at the Jilin Academy of Chinese Medicine Sciences, dissects the biology of vestibular compensation, the brain’s first-line recovery strategy. After unilateral vestibular injury, neurons in the ipsilateral vestibular nucleus lose their resting drive—a state of deafferentation that produces spontaneous nystagmus and postural deviation. Within hours, however, the intrinsic membrane properties of certain medial vestibular nucleus cells begin to change. B-type neurons, identifiable by their narrow action potentials and biphasic afterhyperpolarization, recover spontaneous firing as early as four hours after denervation through a compensatory increase in excitability, driven partly by bidirectional regulation of large-conductance calcium-activated potassium channels by CAMKII and PKC.

Static compensation—the rebalancing of resting discharge between the bilateral vestibular nuclei when the head is still—typically completes quickly. Dynamic compensation, the recovery of the vestibulo-ocular and vestibulospinal reflexes during head movement, is slower and often incomplete. During this later phase, long-term potentiation of synapses and commissural sprouting restore the sensitivity of deafferented neurons to head velocity and acceleration. Imaging studies using voxel-based morphometry and resting-state functional MRI reveal corresponding gray matter changes in the somatosensory cortex, superior temporal gyrus, insula, inferior parietal lobule, and posterior hippocampus, while animal work shows that brevican, a component of the perineuronal net in the superior vestibular nucleus, undergoes expression changes indicating extracellular matrix remodeling around neurons.

Yet this recovery carries a hidden cost: increased visual dependence. Sensory reweighting is the central nervous system’s dynamic adjustment of the relative contributions of vestibular, visual, and proprioceptive inputs to postural control. After a vestibular lesion, the weight of visual input rises while vestibular weight falls. Patients with bilateral vestibular dysfunction show markedly increased postural sway during visual or proprioceptive deprivation, yet perform nearly normally when both channels are intact. This dependence renders patients vulnerable to visual motion in complex environments—supermarket aisles, moving crowds, vehicular travel—producing visual vertigo in susceptible individuals.

Neural sensitization, the review’s first key mechanism, describes an abnormal increase in the processing gain of the vestibular system and its associated networks, causing normal stimuli to be perceived as abnormal vertigo. Synaptic remodeling provides the structural basis. Degradation of perineuronal nets may release constrained synaptic plasticity, promoting compensation while potentially permitting aberrant synaptic connections. Brain-derived neurotrophic factor, signaling through its TrkB receptor, drives remodeling of excitatory markers in the brainstem within the early window after vestibular neurectomy, balancing GABAergic neurons and GABA-A receptor expression between lesioned and intact sides—yet BDNF can also increase nervous system sensitivity by activating microglia. Glutamatergic synaptic strength in the ipsilateral medial vestibular nucleus, reflected by a decreased AMPA/NMDA ratio, reverses within twenty-four hours after labyrinthectomy, though presynaptic glutamate release probability remains incompletely compensated.

Neuroimaging in patients with persistent postural-perceptual dizziness and vestibular migraine substantiates these mechanisms. PPPD patients show significantly reduced gray matter volume in the inferior parietal lobule and hippocampus, negatively correlated with disease course—suggesting progressive structural depletion of key multisensory integration regions. Surface-based morphometry reveals reduced local gyrification in the bilateral posterior insular cortex, supramarginal gyrus, and posterior superior temporal gyrus, critical hubs for vestibular-somatosensory-visual convergence. During simulated vertical self-motion, activation of the parieto-insular vestibular cortex is markedly weaker in PPPD patients, while primary visual cortex activation intensity correlates positively with Dizziness Handicap Inventory scores—compensatory overactivation of the visual cortex. In vestibular migraine, regional homogeneity in the left middle temporal gyrus and middle occipital gyrus declines with increasing attack frequency.

Psychological sensitization, the second mechanism, operates through the fear-avoidance model, originally developed to explain chronic pain persistence. After a vertigo attack, patients develop catastrophic thinking about provoking movements—rapid head turns, turning around—believing these will inevitably cause a fall. Avoidance follows, and long-term avoidance alters proprioceptive input patterns from the neck, trunk, and lower limbs, making postural control more difficult and confirming the patient’s concern about instability. Neurobiologically, vestibular dysfunction activates the stress axis: upregulation of arginine vasopressin and corticotropin-releasing factor-immunoreactive cells in the paraventricular nucleus, and increased dopamine-β-hydroxylase in the locus coeruleus. The amygdala, detecting threat signals, sends excitatory projections to the locus coeruleus, which releases norepinephrine throughout the brain—including the vestibular nuclei—enhancing the spontaneous firing rate of medial vestibular nucleus neurons and their sensitivity to peripheral input. In chronic anxiety states, persistent amygdala overactivation keeps this system at high output, chronically elevating baseline vestibular excitability and reducing sensory thresholds.

Individual differences shape who descends this path. Neuroticism, assessed in a clinical observational study of 247 patients with chronic dizziness using the Eysenck Personality Questionnaire, was the only independent variable significantly predicting Dizziness Handicap Inventory scores, irrespective of diagnostic category and symptom duration. Neuroticism is associated with increased task-dependent functional connectivity between the amygdala and hippocampus and dorsolateral prefrontal cortex, and with altered coupling between the basolateral amygdala and anterior insular cortex—suggesting high-neuroticism individuals are more prone to hypervigilance after acute stress. Adverse childhood experiences produce long-term alterations in HPA axis function, while genetic variants including the BDNF Val66Met polymorphism, COMT Val158Met, and 5-HTTLPR short allele each modulate stress responsiveness, fear extinction learning, and anxiety susceptibility.

Crucially, the two sensitization processes do not operate independently. Neural sensitization lowers the brain’s processing threshold for vestibular, visual, and somatosensory information, increasing the frequency and salience of bodily signals—the subtle sway of normal posture and natural variations in visual scenes may be perceived as abnormal. Excessive bodily signals trigger hypervigilance and catastrophic appraisal. Psychological sensitization, in turn, enhances sensory processing gain through descending facilitatory pathways, modulated by limbic and autonomic systems. Patients who over-rely on visual input for spatial orientation experience longer-term vestibular symptoms; anxious patients show reduced proprioceptive thresholds and heightened sensitivity to body posture perception. Attentional orienting to proprioceptive stimulation alters processing in the primary sensorimotor cortex, decreasing beta wave power and increasing motor evoked potential amplitude.

The review proposes comprehensive interventions targeting sensory reweighting, fear-avoidance behavior, and psychiatric comorbidity to interrupt this process. Vestibular rehabilitation training, through repeated exposure to motion and visual stimuli that provoke dizziness, gradually reduces neural input sensitivity while breaking avoidance behaviors. Selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors activate descending inhibitory pathways, reducing neural sensitivity. Transcranial alternating current stimulation of the dorsolateral prefrontal cortex effectively reduces vestibular responses and cortical excitability, while transcranial direct current stimulation targeting the parieto-insular vestibular cortex alleviates vestibular-related symptoms such as motion sickness. Antiepileptic drugs including pregabalin and topiramate inhibit calcium influx, reducing neural excitability. Cognitive behavioral therapy may benefit patients with pronounced fear-avoidance behavior and high Dizziness Handicap Inventory scores. The dual sensitization model remains a theoretical simplification—some individuals with severe health anxiety develop chronic dizziness-like symptoms without clear peripheral vestibular lesion, and most cited neuroimaging studies are cross-sectional with small samples—but it reframes chronic dizziness as a disorder of central processing gain rather than peripheral damage alone, offering a mechanistic bridge between the inner ear and the anxious brain.

Subject of Research: Mechanisms of the transition from acute vestibular events to chronic dizziness through neural and psychological sensitization

Article Title: Chronic dizziness: neuro-sensitization and psycho-sensitization

Article References: Chronic dizziness: neuro-sensitization and psycho-sensitization. (n.d.). https://doi.org/10.3389/fnint.2026.1929481

Image Credits: AI Generated

DOI: 10.3389/fnint.2026.1929481

Keywords: chronic dizziness, neural sensitization, psychological sensitization, PPPD, vestibular migraine, vestibular compensation, sensory reweighting, fear-avoidance model, visual dependence, BDNF, amygdala, vestibular rehabilitation

The study, led by Huseyin Nezih Ozdemir, Iryna Klopotovska and Diego Kaski of the SENSE Research Unit in UCL’s Department of Clinical and Movement Neurosciences, was conducted at the National Hospital for Neurology and Neurosurgery in London between April 2025 and April 2026. Consecutive patients aged 18 and over arriving at the dizziness clinic underwent a structured ten-question interview before their clinical consultation. Crucially, the interviewer recorded answers about symptom timing, triggers, avoidance behaviours and behavioural responses before any diagnosis had been established. The final diagnoses were then made independently by a vestibular neurologist who was blinded to the interview responses, using established criteria from the Bárány Society and the International Classification of Headache Disorders. This design ensured that the behavioural data could not be contaminated by knowledge of the diagnosis.

The cohort of 109 patients had a mean age of 55.3 years, and 71.5 percent were female. Thirty-three patients were diagnosed with vestibular migraine, thirty-three with persistent postural-perceptual dizziness, fourteen with benign paroxysmal positional vertigo and fifteen with orthostatic dizziness. Smaller groups included patients with central structural disorders such as posterior circulation stroke and other peripheral vestibular conditions including bilateral vestibular loss. When the researchers applied logistic regression to the interview data, four clear behavioural profiles emerged, each mapping closely onto the known biology of the underlying disorder.

The strongest single predictor belonged to vestibular migraine. Patients who reported that reading while travelling as a passenger in a vehicle brought on their dizziness were more than twenty times more likely to have vestibular migraine than any other diagnosis, with an odds ratio of 20.99. This finding fits with the idea that vestibular migraine reflects a heightened vulnerability to sensory conflict, the discordance between visual motion signals and vestibular input that occurs when the eyes track a page while the inner ear registers the movement of a car. It also builds on earlier work from the same group showing that motion sickness while reading in a moving car is highly predictive of the condition. For patients with persistent postural-perceptual dizziness, visually stimulating environments such as crowded, busy or visually complex settings were the strongest precipitating factor, carrying an odds ratio of 12.45, consistent with the disorder’s characteristic over-reliance on visual cues for spatial orientation.

The two remaining diagnoses produced equally distinctive patterns. For benign paroxysmal positional vertigo, head movements and positional changes were the dominant trigger, with an odds ratio of 11.51, exactly what would be expected from the abnormal movement of displaced calcium carbonate crystals, or otoconia, within the semicircular canals. Patients with orthostatic dizziness, by contrast, pointed to standing up quickly as their principal trigger, reflecting the transient drop in cerebral blood flow that occurs during orthostatic stress. In each case, the reported precipitant was not an arbitrary preference but a direct behavioural echo of the underlying mechanism: sensory conflict in vestibular migraine, visual dependence in persistent postural-perceptual dizziness, otoconial displacement in positional vertigo and cerebral hypoperfusion in orthostatic dizziness.

Avoidance behaviours proved just as diagnostic as triggers. Patients with vestibular migraine disproportionately avoided bright or noisy environments and sought refuge by resting in dark, quiet rooms, mirroring the visual and auditory hypersensitivity that characterises migraine more broadly. Those with persistent postural-perceptual dizziness avoided visually busy places such as supermarkets, crowded streets or scrolling screens, and notably reported trying to maintain their activity despite the symptoms, an effort to push through the persistent, physically non-disabling dizziness that defines the condition. Patients with benign paroxysmal positional vertigo reported deliberately avoiding quick head movements and staying still during attacks, an understandable strategy to prevent the violent, brief episodes of rotational vertigo that position changes provoke. Orthostatic dizziness patients avoided sudden standing and tended to sit or lie down slowly, a sensible countermeasure against orthostatic intolerance, although this particular association did not reach statistical significance, likely because of the smaller size of that subgroup.

Temporal patterns added a further layer of discrimination. Episodic dizziness was significantly associated with vestibular migraine, while patients with persistent postural-perceptual dizziness were far more likely to report continuous dizziness lasting days or longer, in keeping with the chronic nature of that disorder. Patients with benign paroxysmal positional vertigo characteristically reported brief episodes lasting seconds to minutes, matching its paroxysmal presentation. Although patients with positional vertigo and orthostatic dizziness tended to describe dizziness that comes and goes, these associations did not reach statistical significance, a limitation the authors attribute to the relatively small numbers in those diagnostic groups.

The clinical implications of the work are considerable. Because neuroimaging has limited utility in most cases of dizziness and definitive tests are lacking for many vestibular syndromes, diagnosis rests heavily on history taking, and patients’ descriptions of symptom quality are notoriously imprecise. Structured questions about avoidance and coping could capture dimensions of the patient’s experience that conventional symptom questions miss. Asking simply whether a patient avoids supermarkets, refrains from turning their head quickly, or retreats to a dark room when dizzy may sharpen diagnostic accuracy, shorten the long delays many patients experience before correct treatment, and potentially prevent progression to chronic dizziness. Beyond diagnosis, recognising these behaviours may help clinicians understand how the disorders impair daily and occupational functioning, since triggers such as bright environments or awkward head positions have been shown to interfere with work tasks and contribute to reduced productivity and absenteeism.

Perhaps the most intriguing aspect of the findings is that patients developed these behavioural signatures without any formal knowledge of disease mechanisms. The researchers argue that such adaptations arise intuitively through repeated symptom experience, which is precisely what makes them informative: they represent the body’s own experiment on the disorder, conducted over months or years. The behaviours therefore function as natural biomarkers, reflecting pathophysiology rather than clinical teaching. The authors also caution that avoidance behaviours can themselves contribute to disability, and identifying them may open the door to rehabilitation strategies that prevent deconditioning and fear-driven withdrawal from activity.

The study is not without limitations. The structured interview was not a validated instrument, several diagnostic subgroups were small, limiting statistical power for some response categories, and the single-centre design in a specialised London clinic may constrain generalisability. Larger cohorts will be needed to confirm the diagnostic value of these behavioural markers and to quantify their impact on patients’ functioning. Even so, the message is clear and potentially transformative for routine practice: when a patient says they feel dizzy, the clinician should ask not only what it feels like and when it happens, but what the patient does about it. The answers, this research suggests, may point directly to the diagnosis hiding behind one of medicine’s most vague and common complaints.

Subject of Research: Behavioural signatures as diagnostic clues in common vestibular disorders causing dizziness

Article Title: What patients do when they feel dizzy: behavioural signatures reveal diagnostic clues in common vestibular disorders

Article References: Ozdemir, H. N., Klopotovska, I., & Kaski, D. (2026). What patients do when they feel dizzy: behavioural signatures reveal diagnostic clues in common vestibular disorders. Journal of Neurology, 273(10), Article 587. https://doi.org/10.1007/s00415-026-14133-0

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14133-0

Keywords: dizziness, vestibular disorders, vestibular migraine, PPPD, BPPV, orthostatic dizziness, avoidance behaviour, coping strategies, behavioural adaptation, diagnosis, vertigo, neurology