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In 1986, German neurologists Thomas Brandt and Marianne Dieterich first described a condition that they called phobic postural vertigo (PPV). Symptoms included postural dizziness without vertigo and fluctuating unsteadiness provoked by environmental or social stimuli (e.g. crowds), which could not be explained by some other neuro-otologic disorder. Triggers included a pre-existing vestibular disorder, medical illness or psychological stress.
Behavioral criteria of PPV included the presence of an obsessive-compulsive personality, mild depression, and anxiety. Studies on PPV showed that it was NOT a psychiatric disorder, but rather a neuro-otologic condition with behavioral elements.
In the early 2000s, the American team of Jeffrey Staab, Michael Ruckenstein, & their colleagues performed studies to update the concept of PPV and described the clinical syndrome of chronic subjective dizziness (CSD). The symptoms of CSD included non-vertiginous dizziness and unsteadiness that was increased by a person’s own motion, exposure to environments with a complex or moving stimuli (e.g., stores, crowds), and performance of tasks that required precise visual focus (e.g., reading, using a computer).
Other vestibular experts described space-motion discomfort and visual vertigo, symptoms that overlapped to some extent with PPV and CSD.
In 2010, scientists from around the world began a process of identifying the most important features of these syndromes. In early 2014, they reached a consensus on the key symptoms and defined a diagnosis of Persistent Postural-Perceptual Dizziness (PPPD).
The World Health Organization has included PPPD in its draft list of diagnoses to be added the next edition of the International Classification of Diseases (ICD-11) in 2017.
Other medical problems, such as dysrhythmias and adverse drug reactions that manifest with acute bouts of vertigo, unsteadiness or dizziness are less common triggers of PPPD.
PPPD rarely starts slowly and gradually without a triggering event, although it is not always possible to sort out the cause.
Anxiety or mild depression may be present as comorbidities. However, they are not symptoms of PPPD, as they were with PPV.
PPPD may coexist with other vestibular disorders, which can confuse the diagnosis since patients may exhibit other symptoms, including vertigo.
Patients with PPPD may have a history of vertigo, suggesting a previous vestibular dysfunction. Patients typically exhibit chronic symptoms due to accumulated exposure to motion stimuli, making them more susceptible to recurrence of symptoms.
Patients with PPPD avoid situations that may exacerbate symptoms because they don’t want to feel worse physically. Some patients also avoid these situations because they are afraid that something terrible might happen. Thus PPPD is a physiological disorder that can have psychological consequences.
Physical exams, laboratory tests, and neuroimaging are NOT used to diagnose PPPD itself, but to identify potentially comorbid conditions, which can lead to a suspected diagnosis of CSD. Physical examination and laboratory testing are often normal or may show a current or previous vestibular problem that does not fully explain the patient’s symptoms.
Behavioral assessment of PPPD patients may be normal and/or show low levels of anxiety and depression. Other psychiatric disorders may also present.
Behavioral factors contribute to PPPD in three ways:
High anxiety intensifies postural instability and reactivity to motion stimuli during acute vestibular trauma and slows recovery by preventing the patient from developing adaptive strategies.
Anxiety and depression can increase the likelihood of developing PPPD.
By 2014, no large scale, randomized, controlled trials of therapeutic interventions for CSD had been conducted, but several smaller studies have been completed around the world.
In clinical trials for the use of SSRIs (selective serotonin reuptake inhibitors) and SNRIs (serotonin norepinephrine reuptake inhibitors) on patients with CSD:
Patients who do not respond to one SSRI have a good chance of responding to another one. Increased dizziness was rarely observed, and comorbid anxiety and depression were improved. Treatment must be maintained for at least one year or more to minimize relapse.
Benzodiazepines and other vestibular suppressants are NOT effective as a primary treatment for PPPD.
Vestibular/balance rehabilitation therapy works to desensitize or habituate patients to motion stimuli.
In 2014, the first small study on the efficacy of VBRT specifically for PPPD patients was completed. Its results support previous clinical experience and suggest the following:
Psychotherapy is not a very successful treatment for fully established, longstanding PPPD, but it may be able to reduce the chances of developing PPPD if used early. Older trials showed that cognitive behavioral therapy (CBT) had a moderate effect for reducing dizziness in patients with PPPD, but, unfortunately the benefits did not last after therapy was finished. More recent trials showed that just three CBT sessions resulted in significantly reduced dizziness and dizziness-related avoidance symptoms when treatment was started within 8 weeks of the triggering event (i.e., as PPPD symptoms were starting, but before they were fully established). Under those circumstances, the benefits seemed to last.
Research studies are beginning to uncover physiologic processes associated with PPPD. Investigations have provided hints about alterations in postural control, visual perception of space, and processing of vestibular and visual stimuli in the brain. More details should be forthcoming over the next few years.
Staab JP. Chronic Subjective Dizziness. Continuum (Mineapp.Minn.). 2012 Oct; 18(5 Neuro-otology):1118-41.
World Health Organization, International Classification of Diseases, ICD-11 beta draft, http://apps.who.int/classifications/icd11/browse/l-m/en#/http%3a%2f%2fid.who.int%2ficd%2fentity%2f2005792829