# Differential diagnosis of orthostatic dizziness with persistent postural-perceptual dizziness and its underlying mechanisms

**Authors:** Zhang Dao Pei, Zhang Yong Hui, Liu Bing Yang, Zhang Huai Liang, Zhao Min

PMC · DOI: 10.3389/fneur.2025.1642869 · Frontiers in Neurology · 2025-10-01

## TL;DR

This paper discusses how to differentiate persistent postural-perceptual dizziness from other causes of orthostatic dizziness and explores possible underlying mechanisms.

## Contribution

The paper provides a comprehensive overview of differential diagnoses and potential mechanisms for orthostatic dizziness in PPPD.

## Key findings

- PPPD symptoms worsen when standing or walking, often mimicking other forms of orthostatic dizziness.
- Key differential diagnoses include hemodynamic OD, POTS, and vestibular syncope, among others.
- Underlying mechanisms may involve altered brain activity, vestibular-autonomic dysfunction, and sensory-perceptual issues.

## Abstract

Persistent postural-perceptual dizziness (PPPD) is characterized by one or more symptoms of dizziness, unsteadiness, or non-spinning vertigo, which persist on most days for at least 3 months. The most common symptom of PPPD worsens when standing or walking, often leading to confusion with other forms of orthostatic dizziness (OD). There are some main differential diagnosis as follows: hemodynamic OD, postural orthostatic tachycardia syndrome, vestibular syncope, BPPV, bilateral vestibulopathy, primary orthostatic tremor, sensory neuropathy, neurodegenerative disorders, cerebral small vessel disease associated with gait disorders, dizziness due to cardiac problems, orthostatic cerebral hypoperfusion syndrome, intracranial hypotension, and the possible mechanisms by which these diseases are associated with OD are briefly elaborated. However, the mechanism underlying OD in PPPD patients remains unclear. There are some impact factors of OD with PPPD, including sex and age, anxiety state and neurotic personality, comorbid vestibular disorders. There are some underlying mechanisms of OD with PPPD, such as altered activity and connectivity of cerebral cortical networks, vestibular-autonomic dysfunction and sensory-perceptual dysfunction, hemodynamic changes, changes in postural control, otolith dysfunction, visual and somatosensory dependence, neurotransmitter abnormalities. For patients with established PPPD, it is important to distinguish the etiologies of OD from other relevant diseases, enabling early intervention and preventing adverse effects on workability, and evaluate responses to therapies to reduce diagnostic errors and missed diagnoses.

## Linked entities

- **Diseases:** postural orthostatic tachycardia syndrome (MONDO:0011479), BPPV (MONDO:8000018), primary orthostatic tremor (MONDO:0016546), intracranial hypotension (MONDO:0006811)

## Full-text entities

- **Diseases:** orthostatic cerebral hypoperfusion syndrome (MESH:D006261), gait disorders (MESH:D020233), confusion (MESH:D003221), vestibular syncope (MESH:D013575), BPPV (MESH:D065635), OD (MESH:D004244), neurodegenerative disorders (MESH:D019636), vestibular disorders (MESH:D015837), postural orthostatic tachycardia syndrome (MESH:D054972), intracranial hypotension (MESH:D019585), sensory neuropathy (MESH:D009477), vertigo (MESH:D014717), anxiety (MESH:D001007), vestibular-autonomic dysfunction (MESH:D000160), primary orthostatic tremor (MESH:C536418), cerebral small vessel disease (MESH:D059345), cardiac problems (MESH:D006331)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

138 references — full list in the complete paper: https://tomesphere.com/paper/PMC12520903/full.md

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Source: https://tomesphere.com/paper/PMC12520903