Ross Hauser, MD

Persistent postural-perceptual dizziness, commonly called PPPD, can feel like rocking, swaying, floating, imbalance, or non-spinning dizziness. Symptoms are often worse when standing, walking, moving the head or body, riding in a vehicle, scrolling on a screen, or entering a visually busy environment such as a supermarket.

For many patients, the most frustrating part is being told that testing is “normal” or that the diagnosis means the symptoms are psychological. PPPD is classified as a functional vestibular disorder, but functional does not mean imaginary. It means that the brain’s processing and use of balance information have become persistently altered, sometimes after a vestibular illness, migraine, concussion, medical event, or period of intense stress.

New research adds an important qualification: PPPD can coexist with measurable abnormalities in the peripheral vestibular system. A PPPD diagnosis therefore should not automatically end the evaluation of a patient whose history suggests an inner-ear, neurologic, visual, autonomic, or cervical contributor.

At Caring Medical, we are especially interested in the subgroup of patients whose dizziness is accompanied by neck pain, headache, a history of whiplash or concussion, a sense that the head is difficult to support, or symptoms that are reproducibly aggravated by neck position. These findings do not prove cervical instability, but they may justify a careful cervical assessment alongside—not in place of—appropriate vestibular and neurologic care.

Article summary

• PPPD causes persistent dizziness, unsteadiness, or non-spinning vertigo that is typically aggravated by upright posture, movement, and complex visual stimulation.
• A 2026 study found evidence of otolith dysfunction in 9 of 23 patients with PPPD, or 38%.
• The vestibular abnormalities did not predict short-term improvement after medication and vestibular rehabilitation.
• PPPD and peripheral vestibular dysfunction can coexist; an abnormal vestibular test does not rule out PPPD, and a PPPD diagnosis does not rule out another contributor.
• The 2026 study did not investigate the cervical spine and cannot be used as evidence that cervical instability causes PPPD.
• Patients with neck pain, trauma, headache, or dizziness reproducibly provoked by neck motion may warrant a separate evaluation for cervicogenic dizziness or cervical instability.
• Treatment should be individualized and may include education, vestibular rehabilitation, cognitive-behavioral strategies, medication, migraine management, and treatment of confirmed contributing disorders.

What is persistent postural-perceptual dizziness?

The Bárány Society diagnostic criteria describe PPPD as one or more symptoms of dizziness, unsteadiness, or non-spinning vertigo occurring on most days for at least three months. The symptoms are present for prolonged periods and are aggravated by upright posture, active or passive movement, and exposure to moving or visually complex surroundings. PPPD usually begins after an event or condition that causes vertigo, imbalance, dizziness, or disruption of balance. It may follow a peripheral vestibular disorder, vestibular migraine, concussion, another medical illness, or psychological distress. The symptoms must cause meaningful distress or functional impairment and must not be better explained by another diagnosis. (1)

Patients may describe:

• Rocking, bobbing, floating, or swaying
• A sensation similar to being on a boat
• Imbalance without true spinning vertigo
• Visual motion sensitivity in stores, crowds, traffic, or on screens
• Symptoms triggered by standing, walking, turning, or riding in a vehicle
• Fatigue, brain fog, nausea, headache, or anxiety that accompanies the dizziness

The diagnosis is based primarily on the pattern of symptoms and the clinical history. Vestibular tests can help identify a coexisting disorder, but there is no single laboratory or imaging test that confirms PPPD.

New 2026 research: Peripheral vestibular abnormalities were found in some PPPD patients

In 2026, Goto, Kaneda, and Wasano published a retrospective study of 23 patients with PPPD. The patients underwent video head-impulse testing, known as vHIT, as well as cervical and ocular vestibular-evoked myogenic-potential testing, known as cVEMP and oVEMP. (2)

These tests examine different parts of the peripheral vestibular system:

• vHIT evaluates the vestibulo-ocular reflex generated by the semicircular canals during brief head movements.
• cVEMP is used primarily to assess pathways associated with the saccule and inferior vestibular nerve.
• oVEMP is used primarily to assess pathways associated with the utricle and superior vestibular nerve.

The researchers identified otolith dysfunction in nine patients, or 38% of the cohort. The otolith organs—the utricle and saccule—help the nervous system detect gravity and linear acceleration. Dysfunction in these structures can contribute to sensations of tilting, rocking, movement, or imbalance.

This finding supports a clinically important point: a functional vestibular diagnosis and a peripheral vestibular abnormality are not mutually exclusive. Some patients may have PPPD while also retaining measurable dysfunction from a preceding or coexisting vestibular disorder.

The abnormalities did not predict short-term improvement following medication and vestibular rehabilitation. This means the tests may help characterize a patient’s vestibular function, but this small study did not establish them as reliable predictors of treatment response.

What this study does—and does not—show

The study suggests that neuro-otologic testing can identify peripheral vestibular abnormalities in a subset of patients with PPPD. It does not show that otolith dysfunction is the sole cause of PPPD, that every PPPD patient needs every vestibular test, or that an abnormal VEMP result identifies the best treatment.

The study was retrospective, included only 23 patients, and had no healthy control group. Its results therefore need confirmation in larger prospective studies. Most importantly for this article, the researchers did not evaluate cervical instability. The paper cannot be cited as evidence that cervical instability caused the vestibular abnormalities or the patients’ PPPD.

The 2026 findings build on earlier otolith research

The new results are not isolated. A 2023 study used VEMP and vHIT testing to classify 43 patients with PPPD. Isolated otolith dysfunction was the largest subgroup, found in 44.2%, while 37.2% had normal findings on both types of testing. The authors cautioned that otolith dysfunction was unlikely to be the only driver of PPPD and that larger studies were needed. (3)

An earlier study of 21 patients also identified isolated otolith dysfunction in nine patients, but symptom questionnaires and postural measures did not clearly distinguish that subgroup from other PPPD patients. (4)

Together, these studies suggest a layered model. A peripheral vestibular injury or deficit may initiate dizziness in some patients. Persistent changes in visual dependence, threat assessment, postural control, and sensory processing may then help perpetuate symptoms. Finding one component does not necessarily explain the entire illness.

Why visual motion can make PPPD worse

Visual dependence is a prominent feature of PPPD. Patients may feel worse when watching traffic, scrolling, walking through patterned aisles, or observing people moving around them.

In a 2022 study, researchers compared 27 patients with PPPD, 12 with unilateral vestibular hypofunction, and 14 healthy controls. After exposure to moving visual stimuli, the PPPD group showed a significant increase in gaze instability. The change correlated with visually provoked dizziness but not with standard vestibular tests or symptom-scale scores. (5)

This helps explain why a patient can experience severe symptoms even when some conventional tests are normal. It also explains why carefully graded visual-motion and balance exercises may be useful, while overly aggressive exposure can be difficult to tolerate.

Neck disorders were present in a meaningful minority of PPPD patients

An older clinical study of 81 patients with persistent postural-perceptual dizziness reported that visual stimuli aggravated symptoms in 74%, body movement in 52%, and sleep deprivation in 38%. Migraine occurred in 26% and “cervical syndrome” was recorded in 21%. (6)

This finding shows that neck disorders were present in a meaningful minority of that cohort. It does not establish that the neck disorder caused PPPD, and “cervical syndrome” is not the same as radiographically confirmed cervical instability.

In our clinic, a cervical contribution becomes more plausible when dizziness occurs with several of the following:

• Persistent neck pain or upper-cervical pain
• A history of whiplash, concussion, repetitive neck trauma, or connective-tissue laxity
• Headache beginning in the neck or occipital region
• Dizziness consistently provoked by neck position or sustained head posture
• A feeling that the head is heavy or difficult to support
• Neck clicking, clunking, muscle guarding, or restricted motion
• Symptoms that began with a neck injury and have not followed a typical vestibular recovery

These features should prompt a differential diagnosis, not an automatic conclusion. Vestibular migraine, benign paroxysmal positional vertigo, Ménière’s disease, unilateral vestibular loss, medication effects, orthostatic intolerance, neurologic disease, and other causes may need evaluation.

For further discussion, see our articles on Cervical Vertigo and Cervicogenic Dizziness, Vestibular Migraine and Spontaneous Vertigo, and Mal de Débarquement Syndrome.

How cervical instability could contribute to dizziness in selected patients

The cervical spine contains dense proprioceptive input that helps the brain integrate information from the eyes, vestibular organs, and body. Injury, pain, muscle guarding, or abnormal motion in the neck may distort cervical sensory input and contribute to dizziness or imbalance in some patients.

Ligament injury is one proposed cause of excessive cervical motion. A 2014 review from our group discussed capsular ligament laxity as a potential contributor to cervical instability, chronic neck pain, headache, tinnitus, and dizziness. (7) This was a narrative review and hypothesis-generating clinical discussion, not a controlled PPPD treatment trial.

That distinction matters. The current evidence supports considering the neck as one possible contributor in a clinically selected patient. It does not support treating every person with PPPD for cervical instability.

When cervical instability is suspected, the goal of the evaluation is to determine whether the history, physical examination, and appropriate imaging or motion assessment converge on the same explanation. The presence of dizziness alone is not enough.

 

The cervical ligaments are strong bands of tissues that attach one cervical vertebra to another. In this role, the cervical ligaments become the primary stabilizers of the neck. When the cervical ligaments are healthy, your head movement is healthy, pain-free, and non-damaging. When the ligaments are suffering from degenerative wear and tear or excessive looseness or laxity that prevents the ligaments from holding the vertebrae together, the ligaments lose their ability to control the proper motion of your head. The head begins to move in a destructive, degenerative manner on top of your neck.

Treatment of PPPD is usually multimodal

PPPD treatment commonly combines a clear explanation of the diagnosis with individualized vestibular rehabilitation, cognitive-behavioral strategies, and medication when appropriate. Migraine, anxiety, autonomic symptoms, and a preceding vestibular disorder may require parallel management.

A 2025 systematic review and meta-analysis of eight studies found improvement in Dizziness Handicap Inventory scores with vestibular rehabilitation. The authors also emphasized the need for additional randomized controlled trials because the available studies varied in design and quality. (8)

This caution is important. A 2023 Cochrane review applying strict diagnostic and follow-up criteria found too little high-quality randomized evidence to draw firm conclusions about non-pharmacologic interventions. (9) The apparent difference between reviews reflects different inclusion criteria and illustrates why treatment evidence should not be overstated.

For some patients, vestibular rehabilitation needs to begin slowly. Exercises may address gaze stability, balance, habituation to movement, and tolerance of visually complex environments. If neck pain or suspected instability limits head movement, the therapist and treating physician should coordinate the program rather than simply pushing through escalating symptoms.

Small preliminary studies have also investigated non-invasive vagus nerve stimulation. One prospective study reported improvements in quality of life and depression in treatment-refractory PPPD, but the sample was small and the intervention remains investigational for this indication. (10)

Where Prolotherapy may help

Prolotherapy is not an established treatment for PPPD or for inner-ear otolith dysfunction. We do not use a PPPD label alone as an indication for cervical injections.

In selected patients, however, a separate evaluation may identify painful ligament laxity or cervical instability that appears to be contributing to neck pain, headache, motion intolerance, or cervicogenic dizziness. In that situation, treatment is directed at the documented musculoskeletal problem, not at PPPD as a whole.

Evidence directly testing Prolotherapy for patients who meet Bárány Society criteria for PPPD is currently lacking. Patients should understand this limitation when considering treatment. Appropriate vestibular, neurologic, otologic, migraine, and autonomic evaluation should continue when indicated.

Summary: PPPD should not become a diagnostic stopping point

The most useful message from the 2026 Goto study is not that PPPD is an inner-ear disease. It is that a functional vestibular diagnosis can coexist with measurable peripheral vestibular dysfunction.

For patients, this means that an abnormal vestibular test does not invalidate a PPPD diagnosis, and a PPPD diagnosis does not automatically make further investigation unnecessary. The clinical history should guide the search for relevant contributors.

For a patient with rocking dizziness, visual motion sensitivity, and no neck symptoms, a vestibular-centered treatment plan may make the most sense. For a patient whose dizziness began after whiplash and is accompanied by neck pain, occipital headache, and reproducible symptoms with neck motion, a cervical evaluation may be appropriate in addition to vestibular care.

The responsible approach is not to force every patient into one explanation. It is to identify the combination of vestibular, visual, neurologic, autonomic, migraine, psychological, and musculoskeletal factors that best fits the individual case.

If you would like our team to review whether your history suggests a possible cervical contribution, you may contact the Hauser Neck Center. We cannot accept every case, and an initial review is used to determine whether our diagnostic approach may be appropriate.

References

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