PPPD is a functional vestibular disorder characterized by chronic non-rotatory dizziness, unsteadiness, and postural instability. In 2017, the Bárány Society (International Society for Vestibular Disorders) established diagnostic criteria (ICVD), and it was included in ICD-113).
PPPD was named by integrating multiple preceding concepts.
The prevalence in specialized dizziness clinics is reported to account for approximately 10–20% of outpatient dizziness cases, and about 14% of dizziness consultations in general internal medicine. In German specialized facilities, it is reported as the most common cause of dizziness (17%), making it by no means a rare disease.
PPPD is triggered by acute vestibular disorders or psychological events. The main triggers and their frequencies are as follows1).
| Trigger | Frequency |
|---|---|
| Acute peripheral vestibular disorders (BPPV, vestibular neuritis, etc.) | Approximately 25% |
| Vestibular migraine | 15–20% |
| Panic attack | 15–20% |
Other triggers include head trauma and psychological stress.
Acute vestibular event → maintenance of high-risk postural control strategy → anxiety and balance hypervigilance → increased visual dependence → rigidity of postural control → decreased cortical integration → chronicity, forming a cycle1).
Individuals with anxiety-related personality traits (such as neuroticism) or a history of anxiety disorders or depression have a higher risk of developing PPPD. Approximately 46–49% of PPPD patients are reported to have comorbid anxiety disorders. PPPD often develops after acute vestibular disorders such as BPPV or vestibular neuritis, panic attacks, or vestibular migraine.
PPPD is diagnosed when all of the following 5 criteria are met3).
PPPD is not a diagnosis of exclusion but an active diagnosis (rule-in diagnosis) based on positive clinical features 2). Examples of positive features include onset after a triggering event, symptoms present on most days, exacerbation in visually complex environments, and postural misperception.
The Niigata PPPD Questionnaire (NPQ) can be used to assess symptom severity and functional impairment.
It is important to differentiate PPPD from diseases with similar symptoms.
| Disease | Key points for differentiation from PPPD |
|---|---|
| Vestibular migraine (VM) | Recurrent vertigo attacks lasting 5 minutes to 72 hours with migraine features. VM is episodic, PPPD is persistent3) |
| Phobic postural vertigo (PPV) | Vertigo lasts seconds (PPPD lasts hours), associated with obsessive-compulsive personality traits |
| Orthostatic hypotension | Differentiated by blood pressure measurement. Systolic blood pressure drops ≥20 mmHg within 3 minutes of standing8) |
| Bilateral vestibular hypofunction | Vestibular hypofunction confirmed by vHIT and caloric testing8) |
| Postural orthostatic tachycardia syndrome (POTS) | Diagnosed by a heart rate increase of ≥30 bpm upon standing8) |
| Primary orthostatic tremor | Tremor at 14–18 Hz while standing; diagnosed by surface electromyography and Fourier analysis8) |
The basic treatment strategy is a multidisciplinary approach combining vestibular rehabilitation therapy (VRT), pharmacotherapy, and cognitive behavioral therapy (CBT)2).
At the start of treatment, it is important to explain to the patient that PPPD is “a common and treatable condition” and “a problem with the brain’s software”2).
Vestibular Rehabilitation
Goal: Reduce visual dependence and reintegrate multisensory input.
Content: Combine habituation training (repeated exposure to stimuli) with postural stability training2).
Efficacy: A meta-analysis (8 studies, 522 cases) showed significant improvement in DHI-total score (WMD=21.84, 95%CI: 10.97–32.71)6).
Pharmacotherapy (SSRI/SNRI)
First-line: SSRIs or SNRIs such as sertraline, escitalopram, and fluoxetine4).
Duration: Usually recommended for 1 year. Effective even without comorbid depression or anxiety.
Starting dose: Start at a lower dose than that used for depression treatment2).
Cognitive Behavioral Therapy (CBT)
Target: Psychological intervention for fear of falling, health anxiety, and avoidance behavior2).
Effect: Meta-analysis (6 RCTs, 406 patients) showed that adding CBT to conventional therapy significantly improved DHI-total (MD=−8.17, 95%CI: −10.26 to −6.09)5).
Note: Additional CBT was significantly superior to control groups of VRT alone, SSRI alone, and VRT+SSRI5).
Advantage of combination therapy: Meta-analysis of conservative treatments (22 studies, 1764 patients) showed that combination therapy with SSRI and VRT was significantly superior to monotherapy in improving DHI and HAMA scores4).
CBT subgroup analysis (Zang 2024): The effect sizes of additional CBT for each treatment are as follows5).
Non-recommended drugs: Antihistamines, benzodiazepines, and betahistine are not recommended for PPPD2).
Meta-analyses have shown that combining vestibular rehabilitation therapy (VRT) or cognitive behavioral therapy (CBT) with medication is more effective than medication alone. However, placebo-controlled RCTs of SSRIs/SNRIs have not yet been conducted, and evidence is still accumulating. A multimodal approach is recommended.
The pathophysiology of PPPD involves a complex interplay of persistent maladaptive postural control strategies, increased visual dependence, abnormal predictive coding, and structural and functional brain changes1).
High-risk postural control strategies (stiffness, shortened stride) required after an acute vestibular event may persist even after the threat has resolved 1). In patients with PPPD, low-amplitude, high-frequency postural sway and co-contraction of leg muscles are characteristic, and the perceived sway significantly exceeds actual sway (postural misperception) 1).
A state of excessive reliance on visual information over vestibular and somatosensory cues for spatial orientation (visual dependence) develops 1). fMRI has confirmed a positive correlation between visual cortex activity and dizziness disability 1).
The brain overestimates the mismatch between actual sensory input and prediction. The “broken escalator phenomenon” is used as an analogy 2). Hypervigilance for balance creates a vicious cycle by consciously sensing and trying to control even minor sensory discrepancies 1).
The main neuroimaging findings confirmed by research are summarized below.
| Imaging Method | Key Findings |
|---|---|
| Structural MRI | Gray matter volume reduction in the dorsolateral prefrontal cortex, anterior cingulate cortex, hippocampus, cerebellum, etc.1) |
| fMRI | Decreased PIVC activity during vestibular stimulation, increased visual cortex activity during visual stimulation1) |
| SPECT | Decreased cerebral blood flow in the frontal lobe and insula, increased cerebral blood flow in the cerebellum1) |
| Magnetoencephalography | Increased neuromagnetic activity in the 1–4 Hz band at the temporoparietal junction (TPJ), positively correlated with DHI score1) |
Anxiety-related neural networks: Neuroticism is associated with hyperactivity of the inferior frontal gyrus (IFg) and increased functional connectivity (FC) between the IFg and visual association areas 1). Networks involving the insula, anterior cingulate cortex, prefrontal cortex, and amygdala are also altered 1).
Impaired multisensory integration: Abnormal sensory weighting leads to excessive reliance on visual input 1).
Spatial navigation deficits: In a virtual Morris water maze task, the PPPD group shows non-strategic and disorganized search behavior 1).
Altered vestibular perceptual thresholds: Reduced rotational motion perception thresholds (motion hypersensitivity) correlate with disease duration 1).
In PPPD, there is maladaptive stiffening of postural control, excessive reliance on visual information, and “abnormal predictive coding” where the brain overestimates sensory discrepancies. Neuroimaging studies have confirmed reduced gray matter volume in the prefrontal cortex, anterior cingulate cortex, and hippocampus, as well as decreased activity in the vestibular cortex and increased activity in the visual cortex.
Transcranial Direct Current Stimulation (tDCS): Significant therapeutic effects on regional cerebral blood flow (rCBF) in patients with PPPD have been reported, with changes confirmed in the right superior temporal region and left hippocampus1). However, the Cochrane SR includes only one RCT (24 cases), and the current evidence is considered insufficient10).
Repetitive transcranial magnetic stimulation (rTMS): Mentioned as a potential treatment for PPPD, but sufficient clinical trial data are not yet available1).
Non-invasive vagus nerve stimulation (nVNS): There are reports of significant improvement in QOL in patients with PPPD1).
A meta-analysis of VR-based VRT confirmed improvement in DHI-total scores (WMD=23.77), and it is expected to be at least as effective as conventional VRT6). Customized VRT also showed a favorable improvement effect with WMD=21.066).
Oxidative stress: Elevated oxidative stress parameters and decreased antioxidant activity have been confirmed in patients with CSD, making it a potential future therapeutic target, but clinical studies have not yet been conducted1).
Impairment of spatial navigation ability and changes in vestibular perception thresholds are expected to be useful as novel diagnostic biomarkers and tools for evaluating rehabilitation efficacy1).
Qin C, Zhang R, Yan Z. Research Progress on the Potential Pathogenesis of Persistent Postural-Perceptual Dizziness. Brain Behav. 2025;15:e70229.
Özdemir HN, Charlton J, Cortese E, et al. Persistent Postural-Perceptual Dizziness: A Practical Approach to Diagnosis and Patient Communication. Eur J Neurol. 2026;33:e70494.
Moreno-Ajona D. Persistent postural-perceptual dizziness versus vestibular migraine: A narrative review. Headache. 2026;66:298-306.
Zheng Y, Guo Z, Liu X, et al. Effect of conservative therapy for persistent postural-perceptual dizziness: a systematic review and meta-analysis. Front Psychiatry. 2025;16:1676218.
Zang J, Zheng M, Chu H, Yang X. Additional cognitive behavior therapy for persistent postural-perceptual dizziness: a meta-analysis. Braz J Otorhinolaryngol. 2024;90:101393.
Li Y, Pei X, Ding R, et al. Effect of vestibular rehabilitation therapy in patients with persistent postural perceptual dizziness: a systematic review and meta-analysis. Front Neurol. 2025;16:1599201.
Piatti D, De Angelis S, Paolocci G, et al. The Role of Vestibular Physical Therapy in Managing Persistent Postural-Perceptual Dizziness: A Systematic Review and Meta-Analysis. J Clin Med. 2025;14:5524.
Dao Pei Z, Yong Hui Z, Bing Yang L, et al. Differential diagnosis of orthostatic dizziness with persistent postural-perceptual dizziness and its underlying mechanisms. Front Neurol. 2025;16:1642869.
Webster KE, Harrington-Benton NA, Judd O, et al. Pharmacological interventions for persistent postural-perceptual dizziness (PPPD). Cochrane Database Syst Rev. 2023;3:CD015188.
Webster KE, Kamo T, Smith L, et al. Non-pharmacological interventions for persistent postural-perceptual dizziness (PPPD). Cochrane Database Syst Rev. 2023;3:CD015333.
