Review

Pract Neurol: first published as 10.1136/practneurol-2017-001809 on 5 December 2017. Downloaded from http://pn.bmj.com/ on November 12, 2020 by guest. Protected by copyright.
Persistent postural-perceptual
dizziness (PPPD): a common,
characteristic and treatable cause of
chronic dizziness
Stoyan Popkirov,1 Jeffrey P Staab,2 Jon Stone3

1
Department of Neurology, Abstract of distraction and may flare fleetingly
University Hospital
Persistent postural-perceptual dizziness (PPPD) is without apparent provocation. PPPD
Knappschaftskrankenhaus
Bochum, Ruhr-University a newly defined diagnostic syndrome that unifies is precipitated by episodes of vertigo or
Bochum, Bochum, Germany key features of chronic subjective dizziness, unsteadiness of vestibular, neurolog-
2
Department of Psychiatry phobic postural vertigo and related disorders. ical or psychiatric origin. These triggers
and Psychology and
Otorhinolaryngology – Head
It describes a common chronic dysfunction of appear to induce involuntary utilisation
and Neck Surgery, Mayo the vestibular system and brain that produces of high-demand postural control strate-
Clinic Minnesota, Rochester, persistent dizziness, non-spinning vertigo and/ gies and an over-reliance on visual stimuli
Minnesota, USA or unsteadiness. The disorder constitutes a for spatial orientation. An initial period of
3
Centre for Clinical Brain
Sciences, University of
long-term maladaptation to a neuro-otological, high anxiety and excessive vigilance about
Edinburgh, Western General medical or psychological event that triggered the acute physical symptoms appears
Hospital, Edinburgh, UK vestibular symptoms, and is usefully considered to perpetuate these reflexive processes,
within the spectrum of other functional which are then inadequately mollified
Correspondence to
Dr Stoyan Popkirov, Department neurological disorders. While diagnostic tests and by top-down interactions among cortical
of Neurology, University Hospital conventional imaging usually remain negative, vestibular, visual and threat assessment
Knappschaftskrankenhaus patients with PPPD present in a characteristic networks.2–4 Maladaptive cognitive-be-
Bochum, Ruhr-University
Bochum, 44892 Bochum,
way that maps on to positive diagnostic criteria. havioural responses commonly add
Germany; ​popkirov@​gmail.​com Patients often develop secondary functional secondary psychological and functional
gait disorder, anxiety, avoidance behaviour and morbidity, such as fear of falling, anxiety
Accepted 15 October 2017 severe disability. Once recognised, PPPD can or depressive disorders, and functional
Published Online First
5 December 2017 be managed with effective communication gait abnormalities. However, PPPD
and tailored treatment strategies, including persists independently of any lesional or
specialised physical therapy (vestibular structural disease.
rehabilitation), serotonergic medications and Different aspects of the disorder can
cognitive-behavioural therapy. dominate the clinical presentation, such
as the primary symptoms of dizziness,
unsteadiness and hypersensitivity to
Introduction self-motion or complex visual stimuli, or
Persistent postural-perceptual dizziness the secondary complications of phobic
(PPPD) is a chronic functional disorder avoidance of provocative situations and
of the nervous system, characterised functional gait abnormalities. This can lead
by non-spinning vertigo and perceived patients to different medical specialties
unsteadiness (see box 1 for diagnostic (otolaryngology, psychiatry, neurology).
criteria1). The symptoms are exacerbated Historically, the varied presentations
►► http://dx.doi.org/10.1136/ when patients assume upright postures resulted in the definitions of various
​ 2017-
practneurol- ​ ​ 001817
​ ​ ​ and in situations with complex or moving overlapping nosological predecessors of
​ ​ PPPD, such as phobic postural vertigo,
visual stimuli (figure 1). The most
common provocations are benign circum- space–motion discomfort, visual vertigo,
stances such as standing, walking, looking chronic subjective dizziness, psychogenic
at traffic or sitting in a busy restaurant, gait disorder and others.3 5 Arguments for
To cite: Popkirov S, Staab JP, which may be perceived as noxious or differentiation of these disorders remain
Stone J. Pract Neurol threatening. Symptoms of PPPD may valid, but PPPD has recently emerged as a
2018;18:5–13.
be alleviated transiently in moments unifying and diagnostically unambiguous

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Box 1  Bárány Society diagnostic criteria for
persistent postural-perceptual dizziness1

A. One or more symptoms of dizziness, unsteadiness

or non-spinning vertigo on most days for at least
3 months.
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 provo-
cation, but are exacerbated by three factors: upright
posture,  active or passive motion without regard to
direction or position, and exposure to moving visual
stimuli or complex visual patterns.
C. The disorder is triggered by events that cause vertigo,
unsteadiness, dizziness,  or problems with balance,
including acute, episodic or chronic vestibular
syndromes, other neurological or medical illnesses,
and psychological distress.
Figure 1  Complex visual stimulation such as patterned 1. When triggered by an acute or episodic precipi-
carpets (above) or busy streets (below). Above images are tant, symptoms settle into the pattern of crite-
from the personal archive of Jeffrey P Staab. Photo below is rion A as the precipitant resolves, but may occur
Busy Street in Causeway Bay by edwin.11, licensed under the intermittently at first, and then consolidate into a
Creative Commons Attribution 2.0 Generic licence, cropped.
persistent course.
2. When triggered by a chronic precipitant, symptoms
may develop slowly at first and worsen gradually.
disorder that has been recognised by the WHO and will D. Symptoms cause significant distress or functional
be included in the upcoming 11th edition of the Inter- impairment.
national Classification of Diseases6 and the recently E. Symptoms are not better accounted for by another
established International Classification of Vestibular disease or disorder.
Disorders.7 The new name, PPPD (best pronounced
‘triple PD’ or ‘three PD’ to avoid confusion with
BPPV (benign paroxysmal positional vertigo)), aims common diagnosis, accounting for about 15%–20%
to provide an aetiologically neutral but positive diag- of all patient presentations.4 Prospective studies of
nostic term that avoids jumping to conclusions about patients who were followed for 3–12 months after
whether the symptoms have arisen from a structural acute or episodic vestibular ailments such as vestibular
lesion or a purely ‘phobic’ or ‘psychogenic’ process. neuritis or BPPV suggest that persistent dizziness of
This review will provide a neurobiologically the type seen in PPPD will develop in one out of four
informed clinical guide to recognising, diagnosing and individuals,1 making the incidence of PPPD in this
treating PPPD as a common functional disorder in situation much higher than widely appreciated.
neurological practice.
Diagnosing PPPD
Epidemiology Core symptoms and commonly associated clinical features
It is difficult to obtain validated data on incidence The diagnosis of PPPD requires all Bárány Society
and prevalence for a recently redefined disorder criteria to be fulfilled. Thus, making the diagnosis
that is seen by general practitioners, otolaryngolo- relies on the patient history (Box 11). Dizziness,
gists, neurologists and psychiatrists. A UK popula- unsteadiness and vertigo are notoriously difficult
tion-based study of primary care found that 4% of all to describe and patients will offer various reports of
patients registered with a general practitioner expe- symptoms, including non-spinning vertigo (“I feel
rience persistent symptoms of dizziness, and most of a sense of motion – it’s not whirling – even though
those were incapacitated by their symptoms.8 In UK I'm still”; “I feel as if my body is swaying like I’m
neurology outpatient clinics, 2% of all secondary on a boat”), unsteadiness (“I feel I’m about to fall”),
referrals were diagnosed primarily with vertigo or light-headedness (“I feel as if I might pass out”) and
dizziness, half of which were deemed psychological/ mild dissociation (“I feel spaced out/as if my legs are
functional.9 In tertiary dizziness centres, either phobic spongy/as if I'm floating”). Unsteadiness and non-spin-
postural vertigo or chronic subjective dizziness, two ning vertigo tend to dominate the clinical picture.
conceptual predecessors of PPPD, is the second most Symptoms are exacerbated by upright posture, moving

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about actively or being moved passively (eg, standing, adequately the presence or absence of conditions in the
walking or riding in a vehicle), or being immersed in differential diagnosis of PPPD. These include periph-
environments with complex or moving visual stimuli eral or central vestibular deficits, autonomic disorders,
(eg, a hallway with complex patterned carpet, a super- head injuries, or cardiac conditions. Historical enquiry
market aisle, looking at traffic). This visual hypersensi- should be extended to symptoms of migraine, panic
tivity, which can occur in isolation as the symptom of attacks and generalised anxiety, the three conditions
‘visual vertigo’,10 is a characteristic feature of PPPD, that most commonly coexist with PPPD. Side effects of
and often one of its most impairing features, especially medications from many classes can mimic some symp-
in the modern world with its ever-growing intensity of toms of PPPD. Consider temporal associations between
visual stimulation. symptoms of PPPD and initiation or changes in doses
Symptoms usually wax and wane (partially in accor- of prescription and non-prescription medications.
dance with introspection and distraction, alertness and
exhaustion), but are generally described as persistent.
Patients’ account of symptom intensity, persistence Secondary psychiatric morbidity
and impairment in daily activities might appear at Screening for psychiatric morbidity may be accom-
odds with their relatively benign appearance on casual plished easily using short, standardised, self-report
observation in the clinic or testing in the vestibular questionnaires, such as the seven-item Generalised
laboratory. However, as in many functional neurolog- Anxiety Disorders Scale for anxiety disorders12
ical disorders, clinical ‘inconsistencies’ (eg, reports of and the nine-item Patient Health Questionnaire for
persistent symptoms, but retained abilities to manage depression13 (available free online at http://www.​
complex tasks intermittently when necessary) are a phqscreeners.​com/). Fear of falling is more common
typical feature of attention-modulated disorders, and among patients with PPPD than the conventional fear
not signs of inauthenticity or malingering. of panic attacks. A neurologist could usefully ask basic
Patients will usually volunteer a triggering episode questions about whether the patient is avoiding situa-
of vertigo or unsteadiness. In a quarter of cases the tions where falls may occur. If fear of falling arouses
precipitating event is a peripheral or central vestibular excessive distress or avoidance behaviours, then inter-
disorder (eg, BPPV or vestibular neuritis), and in a vention for this specific phobia is warranted.
further 20% of cases an attack of (vestibular) migraine
can be identified.1 11 Panic attacks or generalised Secondary functional gait abnormality
anxiety disorders account for 15% of triggers each. Most patients with PPPD as their only active diagnosis
Trauma to the head associated with mild traumatic will perform routine tests of posture and gait normally
brain injury or whiplash injury is a trigger in up to or with minimal difficulty due to mild caution. Some
15%, and autonomic disorders account for 7%. Less patients, however, will show increased body sway
common are dysrhythmias or adverse drug reactions and amplified compensatory movements of the arms
(3%). PPPD will usually develop as the immediate during tests of stance (ie, Romberg test). Some patients
effects of the incipient event begin to fade. may develop secondary features of a functional gait
Patients may give accounts of avoiding provocative disorder with a slow or hesitant gait and/or a ‘walking
situations with resultant impairment in social and on ice’ gait pattern.14 Unlike Parkinsonian freezing,
occupational activities. Patients with PPPD may be this slowness remains unchanged after gait initiation.
quite consumed by their problem and present at their Distraction techniques during standing and walking
‘wits end’. They may describe anticipatory anxiety can provide positive evidence that the unsteadiness
or incapacitation in situations where dizziness would has a broadly functional basis.15 16 During standing,
be particularly problematic such as stairs or roads. this can be achieved by asking the patient to name a
When these secondary phobic thoughts and avoid- number written on their back or with a motor task such
ance behaviours reach a distressing or disabling level, as using a phone or testing eye movements.17 18 These
they warrant the additional diagnosis of a specific are usually more effective than mental distraction such
phobia such as fear of dizziness, fear of falling or as serial sevens or listing months backwards.16 Coun-
agoraphobia. PPPD does not include recurrent falls terintuitively, more demanding postural tasks, such as
or gait impairment, so a history of frequent falls or standing in tandem position or walking backwards, can
near falls or clinical signs of significant alterations in also normalise body sway and gait.19 There may also
gait or stance merit consideration of gait diagnoses be sudden knee buckling without falls; when present,
(see below). this may have specific features of functional leg weak-
PPPD is a diagnosis made by collecting a sufficient ness such as a positive Hoover’s sign or hip abductor
history to find that patients fulfil the diagnostic criteria sign. These examination ‘tricks’ provide a positive
for the disorder. It is not a diagnosis of exclusion. Phys- diagnosis of a functional gait disorder, and can be used
ical examination, clinical laboratory testing, vestib- to explain the diagnosis to patients, demonstrate the
ular evaluation and diagnostic neuroimaging may be potential for reversibility and provide a starting point
needed, not to ‘rule out everything else’, but to assess for therapy.20 21

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Table 1  Related disorders and previous incarnations
Complex symptoms Clinical syndromes
Episodic and Chronic with
Longitudinal course Episodic chronic Fluctuating Chronic fluctuations
Triggering event Medical condition Phobic postural Chronic Persistent postural-
Psychological stress Space–motion vertigo subjective perceptual dizziness
discomfort dizziness
Vestibular syndromes Visual vertigo
Primary symptoms Dizziness, unsteadiness,
non-spinning vertigo
Provocative factors Visual stimuli
Motion of self
Upright posture
Phobic symptoms Minor Space phobia Anxiety
Major disorders

Red flags in the differential diagnosis of PPPD consider carefully the time course of vestibular and
Like other functional disorders of the nervous system, associated symptoms to disentangle often interwoven
PPPD usually has a relatively acute onset, typically on aetiologies. The practical purpose of undertaking this
the heels of its precipitating events, so an insidious task is to identify potentially reversible components
symptom development should raise doubts about the of the presentation, which may be treatable through
diagnosis. In typical cases, patients do not experience different therapies from those indicated for structural
symptom-free intervals, but rather a transition from disorders or PPPD alone.
acute to chronic symptoms (eg, acute spinning vertigo PPPD should not be used as a ‘wastebasket’ diagnosis
of vestibular neuritis to persistent unsteadiness of for patients who present with non-specific or enigmatic
PPPD). In cases of episodic precipitants such as BPPV dizziness without fulfilling all criteria for the diagnosis.
or vestibular migraine, symptoms of PPPD may remit In our clinical experience, these patients are more likely
and then return with recurrences of the triggering to have another problem, such as a slowly developing
condition before settling into a persistent pattern. A neurodegenerative disorder (eg, cerebellar degener-
more difficult diagnostic dilemma arises when the ation) or evolving episodic disorder (eg, vestibular
precipitating events themselves are insidious illnesses, migraine). Prospective monitoring and reconsideration
such as degenerative disorders of the central nervous of the differential diagnosis is warranted for patients
system or vestibular labyrinth. In these cases, clinicians with insidious symptoms, short bouts of functional dizzi-
may need to follow up patients prospectively with ness and multiple chronic complaints.
careful serial examinations to complete the diagnostic Finally, as with all functional disorders, it is a mistake
assessment. to make a diagnosis of PPPD based on a history of
Another possible pitfall is the co-occurrence of childhood trauma or adulthood adversity (eg, physical
comorbid disorders. The presence of structural, or sexual abuse or neglect in childhood, relationship or
metabolic or psychiatric disorders does not preclude employment struggles in adulthood). In a study of 546
the diagnosis of PPPD. On the contrary, PPPD can patients with vestibular symptoms, rates of lifetime
and does co-occur with many of the conditions in its adversity were equally common among patients with
differential diagnosis. For example, BPPV or vestibular structural and functional/psychiatric comorbidities.24
migraine can trigger PPPD and then coexist with it,
causing recurrent attacks of vertigo superimposed on Precursors of PPPD
the chronic symptoms of PPPD. Patients with Parkin- The history of this area is of evolving and overlapping
son’s disease and other structural gait disorders can clinically described syndromes (table 1). In 1986 Brandt
develop functional dizziness.22 In this situation, PPPD and Dieterich first described stance-dependent and
is suggested most strongly by the presence of sensi- gait-dependent dizziness and unsteadiness as phobic
tivity to visually challenging stimuli when patients postural vertigo. An obsessive–compulsive personality
are seated.1 Panic disorder and generalised anxiety was included in the diagnostic criteria.25 Jacob and
disorder may be causes or sequelae of PPPD. They colleagues26 described space–motion discomfort as a
may also predate the onset of PPPD without causing clustering of uneasiness about spatial orientation and
dizziness, but then worsen when PPPD is triggered by increased awareness of motion stimuli in some patients
another condition. This circumstance is easily miscon- with dizziness in an anxiety clinic. In 1995 Bronstein10
strued as ‘psychogenic dizziness’, with resultant failure described visual vertigo, which saw patients who had
to properly identify all conditions contributing to the otherwise recovered from acute vestibular disorders
patient’s morbidity.23 Hence, the clinician needs to reporting dizziness when confronted with complex or

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Figure 2  The normal physiological reaction to strong dizziness or dysequilibrium (1) is to activate alternative and additional
systems of movement control (2) that do not rely on vestibular information. Once the acute trigger has subsided, instead of
returning to normal function, a vicious cycle of maladaptation can arise (3), driven in part by excessive self-observation and anxiety.
Somatosensory information about body position is thus amplified and distorted, which in turn produces subjective dizziness and
leaves movement control on ‘red alert’. Secondary effects like stiffening of gait, phobic avoidance and mental fatigue can develop.
The aim of therapy (4) is to readapt the system to normal function by reducing anxiety and self-monitoring, habituating to provoking
factors, and promoting automatic movement control until recovery (5) is achieved. SNRI, serotonin norepinephrine reuptake
inhibitors; SSRI, selective serotonin reuptake inhibitors.

moving visual stimuli. In a series of studies starting in slippery surfaces (figure 2).27 28 Normally, these strate-
2004 Staab and Ruckenstein11 defined chronic subjec- gies are abandoned when the postural threat subsides.
tive dizziness, which overlapped significantly with In patients who develop persistent dizziness following
phobic postural vertigo, but separated the physical acute vestibular syndromes, however, failure of symp-
symptoms from coexisting or premorbid psychopa- tomatic recovery is predicted by an acute behavioural
thology. PPPD was conceived in a collaborative effort response comprising high anxiety, excessive vigilance
among many of these researchers. about vestibular and balance sensations,29–31 and
persistent high dependence on visual cues for spatial
Pathophysiology orientation compared with those who recover well.31
Although the exact pathophysiology of PPPD remains Pre-existing anxiety23 32 or neurotic personality traits33
to be elucidated, data from physiological investiga- appear to predispose patients to this problematic
tions and rapidly emerging advanced structural and reaction. High-risk postural control strategies have
functional neuroimaging studies of patients with been measured in patients with long-standing phobic
phobic postural vertigo, chronic subjective dizziness postural vertigo34 and chronic subjective dizziness,35
and PPPD itself have revealed three key mechanisms and persistent visual dependence has been found in
by which this disorder is thought to develop.1 3 4 These patients with chronic dizziness and visual vertigo.31 36
are stiffened postural control, a shift in processing So why is there a failure to readapt after a precip-
spatial orientation information to favour visual over itating event? Two hypotheses have been offered.
vestibular inputs, and failure of higher cortical mecha- The first is based on well-established processes of
nisms to modulate the first two processes. The normal Pavlovian conditioning as incorporated into cogni-
physiological response to the onset of dizziness, tive-behavioural formulations of anxiety and func-
vertigo or the threat of falling is to activate high-risk tional disorders. Brandt and Dieterich25 suggested
postural control strategies (eg, stiffened stance, shorter this for phobic postural vertigo, as did Staab5
strides) and to rely more on visual or somatosensory initially for chronic subjective dizziness. In particular,
inputs than vestibular signals, as can be observed Brandt and Dieterich (see ref 4 for review) proposed
in healthy individuals exposed to great heights or that patients with phobic postural vertigo became

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consciously sensitised to transient discrepancies Treatment
between predicted and actual postural movements Communicating the diagnosis
(ie, to differences between feedforward efferent Treatment starts with education of the patient about
copies of planned movements and feedback afferent the diagnosis. As with other functional disorders, some
measurements of actual motions). Normally, these clinicians might feel the temptation to start the conver-
signals are used to make instinctive (ie, unconscious sation with the last diagnostic criterion: listing negative
or preconscious) corrections of movements, but test results and structural disorders the patient does not
Brandt and Dieterich suggested that patients who have.43 Instead, once the diagnosis of PPPD is suspected
became consciously aware of these signals exert more or ascertained, we recommend giving patients the diag-
conscious effort into maintaining control of posture. nostic name and explaining that it is a well-known,
These circumstances were thought to stand in the way common and potentially treatable cause of chronic
of normal readaptation and, instead, set in motion dizziness. In our experience, it is particularly helpful to
a vicious cycle of maladaptation. In this model of explain the nature of the disorder using a typical ‘case
illness, the expectation of dizziness and unsteadiness, history’ (see box 2). Even if all the elements do not apply
which might be called an ‘experiential engram’ from to particular patients, we usually find that it resonates
the triggering episode, is awarded disproportionate well enough to give confidence that they have met a clini-
predictive strength and can then distort and even cian who has seen this disorder before and understands
it. The process of going through the typical case history
over-ride bottom-up sensory input at the preconscious
leads naturally to an explanation of potential mecha-
level of sensory integration.37 This leads to subjective
nisms wherein a review of figure 2 can be very infor-
sensations of dizziness during everyday vestibular and
mative. In particular, the figure illustrates the dynamic
visual stimulation (eg, moving about, encountering
course of PPPD from the triggering event to persistent
complex visual inputs), which reinforces stiffening of
symptoms, highlighting the critical interplay of structural
stance and gait.15 The increased burden of abnormal
and psychological processes. This provides the back-
self-monitoring could explain the common occur-
ground needed to introduce treatment options such as
rence of dissociation and fatigue as results of mental
physiotherapy (to desensitise the vestibular and balance
overload38; neck stiffness and functional gait disorder
system), medications (which may alter the tone of inter-
could develop secondary to the abnormal postural actions among vestibular, visual and threat systems in
control39; and a cycle of fear and avoidance could the brain) and psychological therapy (cognitive-be-
give rise to secondary phobic disorders such as agora- havioural ‘reprogramming’ to reduce heightened vigi-
phobia.23 Distraction from heightened attentiveness lance about dizziness and lessen worry/demoralisation
to postural control can temporarily restore healthy about its consequences). In those patients with secondary
function15 and can be used in therapy to facilitate functional gait disorder, temporary improvements of
functional rehabilitation.40 standing or walking during distraction on examination
However, it is simplistic to assume that PPPD can be used to demonstrate potential reversibility to
results solely from anxiety-driven interference with the patient.20 21 43
natural postural control and spatial orientation. The In order to reinforce patient education, it is quite
first neuroimaging studies of visual vertigo,41 chronic helpful to provide a printed fact sheet about PPPD (avail-
subjective dizziness2 and PPPD42 suggest that there may able at www.​neurosymptoms.​org/​dizziness/​453319731;
be an additional pathophysiological mechanism under- figure 3) as well as a copy of the clinic letter to the
lying PPPD, namely a deficiency in cortical processes general practitioner. This written information will offer
that subserve locomotion and spatial orientation at the patient a chance to digest a diagnosis that may be
the highest levels. Although the research paradigms hard for them to get their head round.
differed from one another and the use of imaging
techniques for studying PPPD is just getting started, a Individualised treatment
pattern of results is beginning to take shape. Activity Having communicated the diagnosis with sufficient
and connectivity appear to be greater in visual versus clarity, the next step for the consulting neurologist is to
vestibular regions of the cortex, in keeping with phys- recommend appropriate therapy tailored to the needs
iological data on visual dependence, but activity and of the patient with PPPD. For functional dizziness, as
connectivity between key cortical regions that process in PPPD, vestibular exercises promoting habituation
space–motion information (eg, posterior insula, are most apt.44 45 These differ from treatments used
hippocampus) and modulate threat responses (eg, to promote recovery from structural vestibular disor-
anterior cingulate cortex) are reduced. These results ders. Exercises for PPPD must be started more gently
suggest that underactive and insufficiently interactive and increased more slowly. Techniques aim at fatiguing
cortical networks may fail to suppress the bottom-up abnormal reflexive responses to movement tasks and
influences of instinctive threat on postural control and reducing sensitivity to visual stimuli have shown long-
spatial orientation leading to sustained use of the acute term clinical benefit in PPPD.46 Patients can be provided
high-risk strategies. with self-help material from a variety of sources (eg,

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Box 2  A typical case history of persistent postural-perceptual dizziness (PPPD) with some secondary features
of anxiety that may be useful to share with a patient during explanation of the diagnosis (adapted from http://
www.neurosymptoms.org)

A 24-year-old woman gave a history of persistent dizziness for the previous 2 years. She had an initial bout of spinning vertigo,
where she felt sick and could hardly get out of bed for a week. A diagnosis of vestibular neuritis was made.
Core symptoms of PPPD
As she recovered, her vestibular symptoms changed from spinning vertigo to a feeling of dizziness that she found really hard
to describe. It was not the spinning sensation any more. Rather, she felt light-headed, with a sensation of swaying present
mainly on standing and walking, but also noticed it when lying in bed at night if she was extremely tired. She found that she
had become really sensitive to objects moving in her environment, even when she was still. It was difficult for her to use a
computer or be in busy environments such as supermarkets.
Secondary dissociative and anxiety symptoms
Every now and then she also felt ‘spaced out’ as if she was floating and people seemed far away, which she found fright-
ening. She thought quite often about the possibility of falling. She had only ever fallen once but had some ‘near misses’. The
thought of being embarrassed by falling in public made her avoid busy places. Despite her best efforts, she found that the
dizziness had started to take over her life. Initially she was anxious about possible sinister diseases and found herself looking
up possible causes on the internet. She then saw doctors who had carried out detailed balance tests and performed an MR
scan of brain that was normal.
Resolution of anxiety but persistence of PPPD with migraine
After her medical consultation, she became more confident that she did not have a life-threatening condition. Her anxiety dimin-
ished, but she found it very hard to cope with her continuing dizziness. She developed fatigue and poor concentration and had
various periods of time off work. The whole thing was made worse by regular migraines, which exacerbated her dizziness. She now
felt at her wits’ end.

instructional materials from the Vestibular Disorders started with one SSRI, followed by a second SSRI trial
Association are available online at http://​vestibular.​org/​ if the first was ineffective or poorly tolerated. After
sites/​default/​files/​page_​files/​Vestibular_​Rehabilitation_​ that, a switch to an SNRI is recommended. Clinical
0.​pdf). However, patients must be instructed to start response is usually seen after 8–12 weeks, and, if
the exercises gradually and increase them slowly, but effective, medication should be continued for at least
steadily. An exercise programme that is too aggressive 1 year. Clinical experience with other classes of antide-
may exacerbate symptoms, causing patients to stop far pressants has not been promising.
before they can achieve any benefit. Oversight of the There is limited experience with cognitive-behavioural
habituation programme by an experienced vestibular therapy (CBT) for treating functional dizziness. In a study
therapist is recommended to ensure that it is properly on 39 patients with phobic postural vertigo, adding CBT to
designed and paced. self-administered vestibular rehabilitation exercises had a
Selective serotonin reuptake inhibitors (SSRI) and positive short-term effect that was not sustained at 1-year
serotonin norepinephrine reuptake inhibitors (SNRI) follow-up.47 48 Newer investigations, fortunately, have
showed promise in reducing dizziness and unsteadiness been more promising. In a waiting-list controlled study
in a majority of patients with chronic subjective dizzi- on 41 patients with chronic subjective dizziness, just
ness, a previous incarnation of PPPD.5 Treatment with three sessions of CBT led to significant improvements
medications from these two classes of serotonergic in 75% of patients,49 which persisted at 1 and 6 months
antidepressants is supported by multiple prospec- post-treatment.50 A small study on patients with func-
tive, open-label clinical trials, but no randomised tional dizziness showed that a psychotherapeutic inter-
controlled trials as yet. A positive response seems not vention using CBT approaches led to a normalisation
to depend on the presence of psychiatric symptoms as of postural behaviour as measured by static posturog-
treatment may help patients with PPPD but without raphy.51 Although there is little direct evidence, CBT
psychiatric comorbidity. As expected, comorbid symp- would be expected to help patients with pronounced
toms of depression and anxiety, where present, also fear of falling or fear of dizziness, since it can reduce
improved. Dosing needs to start slowly and effects are similar avoidance and safety behaviour in patients with
usually seen with doses in the lower half of the ranges other anxiety disorders.40 In case of a secondary func-
recommended for depression. As in many functional tional gait disorder, CBT-informed physiotherapy that
disorders, patients may be particularly sensitive to focuses on illness beliefs and attention allocation can
side effects, which led to one in five patients stopping help.52 53 A recent report backed clinical experience
during trials. In clinical practice, treatment is usually in supporting the use of combinations of these three

Popkirov S, et al. Pract Neurol 2018;18:5–13. doi:10.1136/practneurol-2017-001809 11

Review

Pract Neurol: first published as 10.1136/practneurol-2017-001809 on 5 December 2017. Downloaded from http://pn.bmj.com/ on November 12, 2020 by guest. Protected by copyright.
beliefs. Undiagnosed or untreated patients can suffer for
many years on end, which is why neurologists need to
be familiar with functional dizziness and PPPD, must
not shy away from a firm diagnosis and be aware of
the treatment options summarised above. The presence
of long duration symptoms does not preclude a good
outcome with treatment.

Contributors  SP wrote the first draft of the article, and all

authors were involved in rewrites.
Funding  This work was supported in part by a scholarship for
SP from the FoRUM Forschungsreferat (research office) of the
Medical Faculty of the Ruhr-University Bochum, Germany.
JeS is supported by research funding from the US National
Institute on Deafness and Other Communication Disorders
and Mayo Clinic. JoS is supported by an NHS Scotland NRS
Career Fellowship.
Competing interests  None declared.
Provenance and peer review  Commissioned; externally peer
reviewed. This paper was reviewed by Adolfo Bronstein,
London, UK.
© Article author(s) (or their employer(s) unless otherwise stated
in the text of the article) 2018. All rights reserved. No commercial
use is permitted unless otherwise expressly granted.

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