Timothy C. Hain, MD • Page last modified: September 30, 2022
PPPD is an abbreviation for a functional (i.e. psychological) dizziness with certain characteristics (that are rather broad). As of 2020, there were 36 references in PubMED with either "PPPD" or "persistent postural perceptual dizziness" in their title. The first paper was written in 2015, so PPPD is a recent development. This acronym was developed by Dr. Jeffrey Staab, a psychiatrist. Dr. Staab states that PPPD is not a psychiatric condition -- in particular quoting his article, "Thus, PPPD is classified as a chronic functional vestibular disorder. It is not a structural or psychiatric condition." (Staab et al, 2017). There are many who differ with the "not a psychiatric condition" statement, however. "Psychiatric" words are used varying from anxiety, somatization syndrome, neurosis, and psychosomatic. (Passamonti et al, 2018; Hufner 2019, Yan et al, 2017).
The full acronym is "Persistent postural perceptual dizziness", PPPD, or "triple-P D". PPPD is a symptom inventory, and requires both endorsement of certain symptoms as well as exclusion of alternatives. You can check to see if you have the required symptoms here.
The World Health Organizations new classification, ICD-11, contains a code for PPPD. Thus PPPD is official ! There is currently no ICD-10 code for PPPD. The closest you can do is to combine two codes: F45.9 (psychosomatic disorder), and R42 (vertigo).
Staab et al (2017) in the "Consensus document of the committee for the Classification of Vestibular Disorders of the Barany Society." provided the currently accepted definition of PPPD. They are as follow:
- A. One or more symptoms of dizziness, unsteadiness, or non-spinning vertigo are present on most days for 3 months or more.
- 1. Symptoms last for prolonged (hours-long) periods of time, but may wax and wane in severity.
- 2. Symptoms need not be present continuously throughout the entire day.
- B. Persistent symptoms occur without specific provocation, but are exacerbated by three factors:
- 1. Upright posture
- 2. Active or passive motion without regard to direction or position, and
- 3. Exposure to moving visual stimuli or complex visual patterns.
- C. The disorder is precipitated by conditions that cause vertigo, unsteadiness, dizziness, or problems with balance including acute, episodic, or chronic vestibular syndromes, other neurologic or medical illnesses, or psychological distress.
- 1. When the precipitant is an acute or episodic condition, symptoms settle into the pattern of criterion A as the precipitant resolves, but they may occur intermittently at first, and then consolidate into a persistent course.
- 2. When the precipitant is a chronic syndrome, symptoms may develop slowly at first and worsen gradually.
- D. Symptoms cause significant distress or functional impairment.
- E. Symptoms are not better accounted for by another disease or disorder.
According to Staab et al (2017), " There are no findings on physical examination, laboratory testing, or diagnostic imaging that are pathognomonic of PPPD. "
These criteria are inclusive, and in the author's opinion, not at all specific. For example, one might imagine a person with a visual disturbance due to a change in glasses or after cataract surgery, who saw their doctor for some reason within the last 6 months, who had met all of these criteria. One might also imagine an anxious person taking too much of a blood pressure pill.
Staab et al (2017) states "PPPD is not a diagnosis of exclusion.
It should not be given to patients who report only
non-speciﬁc chronic vestibular symptoms or those
who have enigmatic complaints that do not fulﬁll its deﬁnition. " OK. It does seem rather broad.
PPPD is based on symptoms and absence of other diagnoses- -thus a normal person who reads this web page (or the 2017 paper) could meet the diagnostic criteria for "PPPD", because they know the answers to questions about symptoms and have no other diagnoses. This is a problem.
There are several other dizzy syndromes based entirely on symptoms, each having a different symptom inventory. The most popular of these is vestibular migraine. Another is called "non-motion triggered mal de debarquement". Understandably, there is overlap. Considering migraine, Sarna et al (2021), reported that of 36 subjects with PPPD, "A total of 19 (53%) patients met the International Classification of Headache Disorders criteria for migraine headache, and 6 of those (17%) met the criteria for definite VM. Of the patients who did not meet full migraine headache criteria, 6 (17%) patients met 4 of 5 criteria, and 5 (14%) patients met 3 of 5 criteria. " In other words, the overlap is nearly complete between PPPD and migraine.
Bittar et al (2015) felt that patients with PPPD could also have migraine, meaning that it is not an "either or". In particular, they stated "Persistent postural-perceptual dizziness affects more women than men, with a high associated prevalence of metabolic disorders and migraine."
A discussion of how PPPD/vestibular migraine/MdDS are differentiated (or not) is found on our "rocker" page:
There are a lot of "rule out" diagnoses for PPPD, which may be a motivation to see a specialist.
One would not want to be treated for a psychiatric condition if one actually had something that can be "fixed" such as BPPV or perhaps vestibular migraine. A list of the "rule out" tests that might be considered for a PPPD patient is on our "rocking" page.
There is no "rule in test" for PPPD other than enumerating symptoms.
The main problem with developing a test for PPPD, is that anyone who reads this page can have PPPD diagnosed by simply endorsing the symptoms. Practically, if you can't identify what you are developing a test for to start with, it is unrealistic to think that you will be able to confirm that your new procedure is accurate. You can check to see if you meet the symptom criteria here.Examples of papers suggesting that they might have a "rule in test"
Yagi et al (2019) stated that "We developed a questionnaire that exhibited high reliability and validity in evaluating PPPD severity." The problem here is that using one symptom inventory to evaluate another symptom inventory is meaningless.
On the other hand, procedures that have a subjective component to them, can be modified by the subject, and might reasonably be different in people who meet these criteria. These studies are probably accurate, they just aren't very useful (in our opinion of course).
For example, moving platform posturography. According to Sohsten, Bittar and Staab, 2016, ". These patients have nearly identical subtest scores as do patients who have "recovered" from vestibular deficits." In other words, moving platform posturography does not diagnose PPPD (Sohsten, Bittar and Staab, 2016). Morisod et al (2018) differed and in their study of the related condition of CSD, stated "Patients with CSD have a high rate of abnormal posturography, but without a specific pattern." They also commented "We included 114 patients, of whom 74% had known anxiety disorders and 33% a history of past vestibular disorder. 62% of the assessment posturographies were abnormal. The most affected sub-items were limit of stability, composite score of sensory organization tests and condition 5 in respectively 34%, 23% and 20% of the cases." They did not report out the "aphysiologic score" of the Cevette analysis. We ourselves think that because CDP is sensitive to PPPD, and vestibular disorders can be ruled out with conventional VHIT and rotatory/VENG testing, one can often detect a higher probability of PPPD when CDP is abnormal, but vestibular testing is normal.
Woll et al (2019) found that patients with the PPPD symptom complex performed differently on a postural control task than healthy subjects. OK, makes sense.
Testing of "brain network functional connectivity" -- i.e. Functional MRI, of course is different in people who are selected to have PPPD symptoms as opposed to people who don't, because PPPD is associated with a different pattern of brain functioning. Thus Li et al (2020) found " At the whole brain level, through enhancement of functional activities of the visual network, the integration of multiple sensations and the regulation of posture and movement are primarily driven by visual information." Doesn't help with diagnosis.
Holle et al (2015) reported that people with PPPD were slower to get used to painful shocks causing a blink. These are called "Nociceptive blink reflex". We think that PPPD may be (sometimes) a proxy for anxiety, accounting for this finding. Not very practical.
Yan et al (2016) reported in 43 subjects that women were in the majority, the usual age of onset was middle-age, sleep-quality was reduced, and anxiety was higher than in normal subjects. In their Chinese population, they reported that "neurotic personality may be the risk factor for developing PPPD". In particular, they noted that "neurotic patients were in the majority in the PPPD group (67.4%), and this was significantly higher than in the control group (37.8%). This is another study comparing one questionnaire to another. Hm.
There are a many other studies claiming to find abnormalities in PPPD that we find rather dubious.
Na et al (2019) reported using SPECT that 'PPPD patients showed a significantly decreased rCBF in the insula and frontal lobe, mainly in the left posterior insula, bilateral superior frontal gyrus, right inferior frontal gyrus, right precentral gyrus, and left medial orbital gyrus." We wonder if this is a cause or effect.
Similarly, Nigro et al (2019) reported structural anomalies in the cortex of patients with PPPD. They claimed "These findings demonstrate abnormal cortical folding in vestibular cortices and correlations between dizziness severity and cortical folding in visual and somatosensory spatial association areas in PPPD patients," This is extremely difficult to comprehend -- we do not see why a collection of symptoms should be associated with structural brain anomalies.
RIcelli et al (2017) stated that fMRI (a method of assessing blood flow) was different in patients with "PPPD" exposed to virtual reality roller coaster simulations than people who didn't claim to have PPPD. We think this is a "straw man" experiment -- people who get more excited about visual motion are likely to have different blood flow in parts of their brain when exposed to roller coasters.
Cui et al (2019), suggested that there was a gene associated with PPPD. They stated: "Our findings indicate that the DRD2 TaqIA A1 allele is possibly the susceptibility polymorphism for PPPD, and that the A2/A2 genotype has a potentially protective role for PPPD. " We find this very dubious given that there is no "gold standard" in terms of an objective abnormality for this collection of symptoms. We would wonder if they found a gene associated with anxiety in their study group.
Breinbauer et al (2019), suggested that "While all patients suffering a vestibular disorder had poorer navigational abilities than healthy controls did, patients with PPPD showed the worst performance, to the point that this variable allowed the discrimination of PPPD from non-PPPD patients." We think that patients who were selected for their symptoms of being dizzy all the time would logically also have poor navigational abilities, and this is a "straw man" type experiment.
Wurthmann et al (2017), stated that ""PPPD patients showed gray matter volume decrease in the temporal cortex, cingulate cortex, precentral gyrus, hippocampus, dorsolateral prefrontal cortex, caudate nucleus and the cerebellum." This is almost the entire brain. It doesn't make sense to us that a person with a psychiatric disorder should have atrophy of their brains.
The Barany society "consensus" criteria document concerning diagnosis of PPPD provides no direction concerning treatment. (Staab et al, 2017)
Dieterich and Staab (2017) stated "Treatment plans that include patient education, vestibular rehabilitation, cognitive and behavioral therapies, and medications substantially reduce morbidity and offer the potential for sustained remission when applied systematically." Trinidade and Goebel (2018) similarly suggested that "Cognitive behavioral therapy, vestibular rehabilitation, selective serotonin uptake inhibitors (SSRIs), and serotonin-norepinephrine reuptake inhibitors (SNRIs) all seem to have a role in its management. "
Popkirov et al (2018) wrote in a review article, that "In PPPD and related disorders, vestibular rehabilitation combined with CBT, and possibly supported by medication, can help patients escape a cycle of maladaptive balance control, recalibrate vestibular systems, and regain independence in everyday life".
Thus, the recommended treatment of PPPD based on the references above is a combination of patient education, vestibular physical therapy, psychotherapy (CBT), and medication (usually an antidepressant such as an "SSRI" or SNRI/SSRI).
Our thought is that the "PPPD" acronym is sometimes useful to identify persons with undiagnosed chronic dizziness. We think it commonly overlaps with other symptom inventories for dizziness, such as vestibular migraine and "non motion triggered mal de debarquement". We don't think it is very meaningful to discuss whether or not these collection of symptoms can be distinguished from each other, as the assumption is that they represent an "disease", which is not at all clear.
When one assigns the PPPD diagnosis to a patient, one must be aware that perhaps there is an underlying medical condition (not based on symptom inventories) that will eventually be identified, as well as being flexible about assigning treatments from vestibular migraine or perhaps MdDS. "PPPD" provides a framework for advocating for treatment with vestibular or visual rehab, SSRI or SNRI drugs, and psychotherapy (Popkirov et al, 2018). If these patients get better with treatment, that is really what matters.