PPPD Persistent Postural-Perceptual Dizziness

PPPD is a functional vestibular disorder — not a structural one

Persistent Postural-Perceptual Dizziness (PPPD) is characterised by persistent dizziness, unsteadiness or non-spinning vertigo despite there being no requirement for ongoing structural damage to the vestibular system.

The term was formally defined by the Bárány Society in 2017, but the clinical presentation had been recognised for decades under labels such as phobic postural vertigo, visual vertigo and chronic subjective dizziness.

Calling PPPD a functional disorder is important. It does not mean the symptoms are imagined or purely psychological. It means that the nervous system is functioning differently despite the absence of a structural lesion that fully explains the symptoms.

Psychiatric conditions such as anxiety can coexist with PPPD, but they are not required for the diagnosis.

Diagnosis requires a specific pattern

PPPD should not be used as a label for any patient with chronic dizziness.

All five Bárány Society criteria must be satisfied.

Symptoms of dizziness, unsteadiness or non-spinning vertigo must be present on most days for at least three months, usually lasting for prolonged periods rather than short isolated attacks.

Symptoms are characteristically worsened by three situations:

• upright posture

• active or passive movement

• visually complex or moving environments

Patients may therefore report difficulty in supermarkets, crowded streets, traffic, scrolling on screens, large open spaces or environments containing substantial visual movement.

There must also be a precipitating event capable of producing dizziness, imbalance or significant fear around balance. Common examples include vestibular neuritis, BPPV, vestibular migraine, concussion, panic episodes or autonomic disorders.

Finally, symptoms must produce meaningful functional impairment and must not be better explained entirely by another condition.

Importantly, PPPD is not simply a diagnosis of exclusion. A patient can have PPPD and another vestibular disorder at the same time.

The original vestibular problem can disappear while the symptoms remain

One of the most useful models for understanding PPPD is the maladaptive postural strategy model.

During an acute vestibular problem, changing how balance is controlled is appropriate.

The nervous system may temporarily increase reliance on visual and somatosensory information, stiffen the trunk and consciously monitor balance more closely.

These are useful protective strategies during the initial event.

In PPPD, however, the strategies remain active after they are no longer needed.

A cycle can develop:

vestibular event → threat → rigid postural control → increased visual dependence → heightened symptom perception → avoidance → reduced tolerance

Over time, normal movement and sensory information begin to feel threatening.

The problem therefore becomes less about the original vestibular injury and more about how the nervous system is continuing to process movement and balance information.

Visual dependence is a major feature

Many patients with PPPD become unusually dependent on visual information to maintain orientation.

This helps explain why environments such as supermarkets, crowds, moving traffic or scrolling screens can become particularly provocative.

The vestibular system normally combines information from vision, the vestibular organs and somatosensory input.

In PPPD, this balance can shift excessively toward vision.

When the visual environment becomes complicated or moves unpredictably, symptoms increase because the system has become less flexible in how it weighs sensory information.

Treatment therefore needs to progressively restore sensory flexibility, rather than simply teaching the patient to avoid visually demanding environments.

Conscious balance control can actually make balance worse

Another characteristic feature is attentional hypervigilance.

Patients may constantly check:

“Am I swaying?”

“Am I going to fall?”

“Why does my head feel strange?”

“Is the dizziness starting again?”

This increased attention can interfere with automatic postural control.

Balance normally operates largely outside conscious awareness. Constantly monitoring body position pulls attention toward a system that functions best automatically.

Patients may consequently develop a stiffened trunk, shortened stride, reduced arm swing and guarded walking pattern.

The rehabilitation goal is therefore not to teach increasingly complicated conscious balance strategies.

It is to gradually help the nervous system return to automatic, relaxed postural control.

Anxiety can perpetuate the cycle without being the original cause

Anxiety is frequently present in PPPD, but it should be understood carefully.

The condition is not simply anxiety presenting as dizziness.

However, anticipatory anxiety can reinforce symptoms.

If a patient expects a supermarket, escalator or busy street to make them dizzy, the threat response increases before exposure even begins. This may increase bodily monitoring, postural stiffness and avoidance.

Avoidance then prevents the nervous system from learning that the environment can be tolerated.

The cycle becomes self-reinforcing.

This is why psychologically informed rehabilitation is particularly important in PPPD.

Assessment must still look for other vestibular conditions

A PPPD diagnosis should never replace a proper vestibular examination.

Conditions such as BPPV, vestibular neuritis, unilateral vestibular hypofunction, vestibular migraine, Ménière's disease, concussion and orthostatic hypotension can produce overlapping symptoms.

They can also coexist with PPPD.

For example, a positive Dix-Hallpike test means BPPV is present and should be treated.

A positive head impulse test may indicate persistent vestibular hypofunction.

Neither finding automatically excludes PPPD.

The clinician therefore needs to ask two questions:

Is another vestibular or neurological condition still active?

and

Has a persistent functional dizziness pattern developed alongside it?

Both problems may require treatment.

The examination should test sensory and attentional behaviour

The physical examination can include peripheral vestibular testing, oculomotor testing, balance assessment and gait observation.

Particular attention should be paid to sensory reweighting.

Patients may struggle disproportionately when visual information is reduced, such as standing on foam with the eyes closed.

Dual-task testing can also be valuable.

Walking while performing a cognitive task may expose how much attentional capacity is being used to consciously control posture.

Psychological screening tools such as the GAD-7 and PHQ-9 can help identify anxiety or depressive symptoms that may influence the rehabilitation strategy.

These measures are used to inform the clinical formulation, not to suggest that the dizziness is “all psychological.”

Rehabilitation starts with an explanation

The first stage of treatment is psychoeducation and formulation.

Patients need a clear explanation of why their symptoms persist.

Simply saying “all your tests are normal” can be unhelpful because it gives the patient no model for understanding why they still feel dizzy.

Instead, rehabilitation should explain how an originally protective strategy became persistent:

threat → increased monitoring → stiffened movement → increased symptoms → avoidance → increased sensitivity

Understanding this cycle is itself part of the intervention.

Exposure should provoke some symptoms

Vestibular rehabilitation for PPPD should use graded exposure, not complete symptom avoidance.

Movement, upright posture and visually complex environments are progressively reintroduced.

Treatment may begin below the symptom threshold before gradually increasing speed, amplitude, duration and environmental complexity.

Some symptom provocation is expected.

The guide proposes approximately 3–5/10 symptom intensity during exposure as an acceptable rehabilitation target.

The important distinction is between controlled exposure and overwhelming the patient.

Very high symptom provocation can reinforce the belief that movement is dangerous, while insufficient exposure provides little opportunity for adaptation.

Visual rehabilitation should become increasingly realistic

Visual desensitisation can progress from simple stimuli toward increasingly complex environments.

Examples include:

simple visual movement → optokinetic stimuli → busy videos → dual-task visual exercises → shops, streets and crowded environments

The purpose is not simply to tolerate a screen in the clinic.

The goal is to restore normal participation in the environments that the patient has begun avoiding.

Retrain normal movement, not defensive movement

Rehabilitation should also address the characteristic stiffened postural strategy.

Walking can be retrained toward:

• normal stride length

• relaxed trunk movement

• natural arm swing

• reduced conscious monitoring

• improved balance with reduced sensory input

Dual-task exercises become especially useful here.

Adding a cognitive task while walking or balancing is not simply a way of making the exercise harder.

It intentionally reduces the attention available for conscious postural monitoring, encouraging balance control to become more automatic again.

Daily short exposures are preferable to occasional large sessions

The rehabilitation programme should generally rely on frequent, manageable exposure rather than occasional exhausting sessions.

Short sessions of approximately 5–10 minutes performed two or three times per day can provide repeated opportunities for habituation.

Progress is then based on decreasing symptom response, reduced avoidance and improved functional confidence rather than simply completing a predetermined number of weeks.

Medication and psychological treatment may complement rehabilitation

For some patients, physiotherapy alone is not enough.

Where significant anxiety or avoidance persists, cognitive behavioural therapy may be appropriate alongside vestibular rehabilitation.

The guide also discusses SSRIs and SNRIs as potential pharmacological options managed by an appropriate medical specialist.

The important principle is that treatment should address the whole self-perpetuating system, rather than separating vestibular symptoms, psychological factors and behaviour into unrelated problems.

Avoid vestibular suppressants in chronic PPPD

Long-term use of vestibular suppressants such as antihistamines or benzodiazepines is discouraged in chronic PPPD.

These medications can suppress the vestibular signals required for adaptation and may reinforce avoidance of symptoms rather than helping the nervous system relearn normal movement.

Likewise, passive interventions alone are unlikely to address the core problem.

PPPD rehabilitation requires active exposure, sensory retraining and behavioural change.

Know when the presentation does not fit

New neurological or otological findings require further investigation before attributing symptoms to PPPD.

Important warning signs include:

• new spontaneous nystagmus

• unilateral hearing loss with tinnitus

• diplopia

• dysarthria or dysphagia

• limb ataxia

• pulsatile tinnitus

• orthostatic presyncope with measurable blood-pressure change

• rapid progression or new focal neurological signs

These findings may indicate a different or additional disorder requiring medical investigation.

The aim is to make balance automatic again

The central rehabilitation goal in PPPD is not simply to reduce dizziness.

It is to change the patient's relationship with movement and sensory information.

Successful rehabilitation progressively reduces visual dependence, postural rigidity, hypervigilance and avoidance, while restoring automatic movement and confidence in increasingly complex environments.

PPPD is therefore best understood not as a damaged vestibular organ, but as a nervous system that has remained stuck in an overly protective strategy.

Treatment works by gradually teaching that system that movement, visual complexity and normal postural variation are safe again.