What is the difference between PPPD (Persistent postural‑perceptual dizziness) and BPPV (benign paroxysmal positional vertigo)?

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PPPD vs BPPV: Key Distinguishing Features

BPPV and PPPD are fundamentally different disorders: BPPV is a mechanical inner-ear problem causing brief episodes of spinning vertigo triggered by head position changes, while PPPD is a chronic functional vestibular disorder characterized by persistent non-spinning dizziness lasting months to years that worsens with upright posture and visual motion.


Duration and Temporal Pattern

  • BPPV episodes last less than 1 minute (typically 5–60 seconds), with sudden onset and resolution when the head returns to neutral position 1, 2.
  • PPPD symptoms persist continuously for at least 3 months, with waxing and waning intensity but never complete resolution between episodes 3, 4.
  • BPPV presents as discrete, paroxysmal attacks separated by symptom-free intervals, whereas PPPD produces constant background dizziness that fluctuates in severity 5, 3.

Quality of Dizziness

  • BPPV produces true rotational vertigo—patients describe the room spinning or themselves spinning 1, 2.
  • PPPD causes non-spinning vertigo, unsteadiness, or a sensation of rocking/swaying without the illusion of rotation 3, 4.
  • The American Academy of Otolaryngology-Head and Neck Surgery emphasizes that BPPV does not cause constant severe dizziness unaffected by position or movement 2.

Triggers and Exacerbating Factors

BPPV Triggers

  • Specific head position changes relative to gravity: rolling over in bed, looking up, bending forward, or lying down 1, 2.
  • Symptoms begin 5–20 seconds after the provocative movement (latency period) and resolve within 60 seconds 1, 6.

PPPD Exacerbating Factors

  • Upright posture or active walking (symptoms improve when lying down) 3, 4.
  • Active or passive self-motion (riding in a car, turning the head while walking) 3, 4.
  • Exposure to complex or moving visual stimuli (grocery store aisles, scrolling screens, busy patterns) 3, 4.

Diagnostic Testing

BPPV

  • Dix-Hallpike maneuver is diagnostic, producing characteristic torsional upbeating nystagmus with 5–20 second latency, crescendo-decrescendo pattern, and fatigability on repeat testing 1, 6.
  • Supine roll test identifies lateral canal BPPV with horizontal nystagmus 1, 6.
  • Positive findings on these maneuvers confirm the diagnosis; no imaging is needed 2, 6.

PPPD

  • Conventional vestibular tests (Dix-Hallpike, caloric testing, VNG) are typically normal or show only nonspecific findings 5, 4.
  • Head roll-tilt subjective visual vertical test may reveal somatosensory-dependent spatial orientation (a characteristic feature) 4.
  • Gaze stability testing after exposure to moving visual stimuli can demonstrate visually-dependent spatial orientation 4.
  • PPPD is a clinical diagnosis based on symptom pattern, not test results 5, 3.

Pathophysiology

  • BPPV results from dislodged otoconia (calcium carbonate crystals) in the semicircular canals—most commonly the posterior canal (85–95% of cases)—causing abnormal endolymph flow and false motion signals 1, 2.
  • PPPD represents a chronic maladaptation of vestibular, postural, and cognitive networks following an initial trigger (often BPPV, vestibular neuritis, or psychological stress), with neuroimaging showing shifts toward visual dominance over vestibular inputs and stiffened postural control 3, 4.

Associated Features

BPPV

  • No hearing loss, tinnitus, or aural fullness (these suggest Ménière's disease instead) 1, 2.
  • No constant dizziness between episodes (though 50% report subjective imbalance between attacks) 6.
  • Nausea and vomiting may occur during acute episodes 1.

PPPD

  • High comorbidity with anxiety, avoidance behavior, and functional gait disorder (patients develop cautious, stiff gait patterns) 5, 3.
  • Severe disability and quality-of-life impairment despite normal structural testing 5, 4.
  • Often triggered by a prior vestibular event (BPPV in 25–30% of cases), medical illness, or psychological distress 3, 4.

Treatment Approaches

BPPV

  • Canalith repositioning procedures (Epley maneuver) are first-line therapy, with 80% success after 1–3 treatments and 90–98% success with additional maneuvers 6.
  • Vestibular suppressant medications should NOT be prescribed for BPPV, as they prevent central compensation 6.
  • No imaging or laboratory testing is needed for typical cases 2, 6.

PPPD

  • Multimodal treatment combining vestibular rehabilitation, cognitive-behavioral therapy (CBT), and serotonergic medications (SSRIs/SNRIs) 7, 5, 3, 4.
  • Vestibular rehabilitation must be specially adapted to address visual dependence and postural stiffness 7, 4.
  • CBT targets maladaptive balance strategies, anxiety, and avoidance behaviors 7, 5.
  • SSRIs/SNRIs facilitate rehabilitation, though mechanisms remain unclear 7, 3.

Critical Diagnostic Pitfalls

  • Do not assume PPPD is "just anxiety"—it is a distinct functional vestibular disorder with specific diagnostic criteria, though anxiety is a common comorbidity 5, 3.
  • PPPD can coexist with BPPV or other structural vestibular diseases—successfully treating BPPV does not automatically resolve PPPD if both are present 8, 4.
  • PPPD is NOT a diagnosis of exclusion; it has positive diagnostic criteria and should be recognized when the symptom pattern fits, even if other conditions are also present 4.
  • Failure to respond to canalith repositioning procedures in a patient with "BPPV" should raise suspicion for PPPD or another central cause 6.

When to Suspect PPPD After BPPV

  • Dizziness persists for more than 1 month after successful Epley maneuver (negative Dix-Hallpike) 6, 8.
  • Patient reports constant unsteadiness rather than episodic spinning 5, 3.
  • Symptoms worsen in visually complex environments (supermarkets, crowds) despite negative positional testing 3, 4.
  • Development of cautious, stiff gait pattern and avoidance of head movements 5, 4.

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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