PPPD persistent postural perceptual dizziness

Timothy C. Hain, MD • Page last modified: February 7, 2021

Also see: brainfogpsychological causes of dizzinesscommittee diagnoses

Definition of PPPD

PPPD is an abbreviation for functional (i.e. psychological) dizziness. 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 this is a recent development. This acronym was developed by Dr. Jeffrey Staab, a psychiatrist. Dr. Staab, however, states that it 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, with "psychiatric" words being 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". Bittar et al (2015) defined PPPD as "dizziness that lasts for over three months with no clinical explanation for its persistence." PPPD is a symptom inventory, and requires both endorsement of these symptoms as well as exclusion of alternatives.

The World Health Organizations new classification, ICD-11, contains a code for this condition. 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 his definition of PPPD.

  • 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 ?rst, and then consolidate into a persistent course.
    • 2. When the precipitant is a chronic syndrome, symptoms may develop slowly at ?rst 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. "

Extracting the salient features, what it takes to have PPPD from this definition is

  1. Dizziness at least 50% of the time (but no spinning) for 3 months. This is a time/severity criterian.
  2. Worse upright (this excludes most BPPV)
  3. Worse while in motion and with vision (the motion criterian excludes mal de debarquement syndrome which usually gets better while driving)
  4. No other diagnosis. (this makes it a "wastebasket syndrome")

These criteria are very inclusive, and not at all specific. For example, one might imagine a person with a visual disturbance, perhaps due to a change in glasses, who had met all of these criteria. One might also imagine an anxious person taking too much of a blood pressure pill.

In Staab et al (2017), it is stated that "Individuals who respond to the precipitating event with a high level of anxiety and body vigilance appear likely to progress to PPPD". Thus these words -- "anxiety" and "body vigilance" are often used when discussing PPPD. Hufner and Sperner-Unterweger (2019) commented that "Persistent-postural perceptual dizziness (PPPD)-Yes, it is a psychosomatic condition!"

Differential Diagnosis of PPPD

PPPD is a "wastebasket" syndrome, meaning that it depends on exclusion of diagnoses that have objective findings. Or another way to put this -- anyone who reads this web page could have "PPPD", because they would know how to answer questions about symptoms. It usually takes a committee to define a wastebasket syndrome.

There are several other dizzy wastebasket syndromes, each having a different symptom inventory. The most popular of these is vestibular migraine. Another is called "non-motion triggered mal de debarquement".

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." They furthermore found "The most prevalent comorbidities were hypercholesterolemia (31%), migraine headaches (26%), carbohydrate metabolism disorders (22%) and cervical syndrome (21%).

There is no "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 by simply endorsing the symptoms. Practically, if you can't identify what you are developing a test to start with, it is unrealistic to think that you will be able to confirm that your new procedure is accurate.

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.

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).

Woll et al (2019) also found that patients with the PPPD symptom complex performed differently on a postural control task than healthy subjects.

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."

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 a proxy for anxiety, accounting for this finding.

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%). In essence, this is another study comparing one questionaire to another. .

There are a many 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 find this difficult to comprehend.

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 in 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 psychiatric disorder should have atrophy of their brains.

Treatment of PPPD

The consensus criteria document concerning PPPD provides no direction concerning treatment.

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) suggested 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 is a combination of patient education, vestibular physical therapy, psychotherapy, and medication (usually an antidepressant such as an "SSRI" or SNRI/SSRI).

Studies of treatment of PPPD that seem reasonable:

Studies that don't seem very reasonable.