Review

Functional (psychogenic) movement disorders: merging

mind and brain
Mark J Edwards, Kailash P Bhatia

Lancet Neurol 2012; 11: 250–60 Functional (psychogenic) movement disorders (FMD) are part of the wide spectrum of functional neurological
Sobell Department of Motor disorders, which together account for over 16% of patients referred to neurology clinics. FMD have been described as
Neuroscience and Movement a “crisis for neurology” and cause major challenges in terms of diagnosis and treatment. As with other functional
Disorders, UCL Institute of
disorders, a key issue is the absence of pathophysiological understanding. There has been an influential historical
Neurology, London, UK
(M J Edwards PhD, emphasis on causation by emotional trauma, which is not supported by epidemiological studies. The similarity
Prof K P Bhatia MD) between physical signs in functional disorders and those that occur in feigned illness has also raised important
Correspondence to: challenges for pathophysiological understanding and has challenged health professionals’ attitudes toward patients
Prof K Bhatia, Sobell with these disorders. However, physical signs and selected investigations can help clinicians to reach a positive
Department, UCL Institute of
diagnosis, and modern pathophysiological research is showing an appreciation of the importance of both physical
Neurology, Queen Square,
London WC1N 3BG, UK and psychological factors in FMD.
k.bhatia@ucl.ac.uk
Introduction directly affects case definition, diagnosis, treatment,
Functional (psychogenic) movement disorders (FMD) research agenda, and explanations of illness that we give
are part of the spectrum of functional neurological to patients.
disorders, some of the most prevalent disorders seen in Some terms, such as psychogenic, conversion, or
neurological practice.1 In common with other functional somatisation, directly suggest that the cause of physical
disorders, there is an absence of appropriate health- symptoms is psychologically mediated. Conversion and
service provision and research interest for FMD, despite somatisation are operationalised diagnoses that specif-
their prevalence. These disorders occupy a grey area ically need the presence of a psychological triggering
between neurology and psychiatry—often with neither factor and exclusion of feigning. However, for most
specialist group willing to take charge—which has movement disorder clinicians, the presence of a
resulted in what has been described in relation to FMD psychological triggering factor is not a requirement for
as a “crisis for neurology”.2 diagnosing a patient with FMD,3 and the difficulties of
There are three rationales behind this Review. First, routinely excluding feigning in clinical practice are
there have been notable developments in diagnostic complex.4 We also show later that recent epidemiological
techniques, pathophysiological understanding, and treat- studies question the relevance of psychological triggers
ments in FMD, which together represent a substantial in most patients with FMD.5 However, other terms also
advance in knowledge. Second, we wish to highlight an have their difficulties. For example, does a disorder
important shift that has taken place in approaches to that is medically unexplained simply mean that we
functional disorders in general: the historically influential have not yet found the medical explanation, and with
explanation for symptoms triggered by emotional trauma advancement of medical knowledge it will become a
(and the research and treatment agendas that emerge medically explained disorder? What level of medical
from this explanation) has been challenged. Third, explanation do we need for a disorder to be medically
because of the enormous health-care and social-care explained? The term hysteria comes with substantial
costs associated with functional symptoms such as FMD, historical baggage, but some movement disorder
health professionals and medical scientists need to take specialists, including the most eminent of recent times,
an active interest in keeping up to date with best practice David Marsden, have argued passionately that the term
in diagnosis and management. FMD have traditionally should be retained.6 The term functional also has a
been thought of as the most difficult of the functional long and distinguished neurological history, but some
neurological disorders to diagnose and manage, but we argue that it has lost its meaning over time and is now
will show that they need not always carry such a too broad a term to be helpful.7
reputation. Patients are directly affected by the diagnostic labels we
give them. Stone and colleagues8 explored this issue with
Terminology and definition unselected neurology outpatients and found that many
When experts cannot agree on a unified terminology for terms were judged by patients as suggesting that the
a disorder, there is likely to be a fundamental problem doctor thought their symptoms were “put on” or “all in
with understanding the underlying pathophysiology. the mind”. Hysteria came out badly on this assessment,
This difficulty in understanding is certainly present for but so did the term medically unexplained. The term
psychogenic disorders, including FMD, for which there psychogenic was not specifically assessed, but psycho-
are many descriptive terms to choose from (panel 1). somatic was and was rated negatively. Functional was the
The choice of term is not a trivial issue, because it term most acceptable to patients.

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We use the term functional in this Review. The origins
and chequered history of this term have been discussed
in detail by Trimble.7 He argues that the original
physiological use of the term as a disturbance of
functioning of the nervous system where the cause has
yet to be defined has value, in contrast to its use as a
“polite eponym” for a psychiatric disorder.7 We accept
that there are difficulties in using this term as a
replacement for other terms such as psychogenic.
Although in our view this term accurately reflects the
state of the evidence regarding the pathophysiology of
psychogenic disorders, this use does also mean that the
word functional is used to apply to the functional
disturbance that occurs in this patient group only,
and not in patients with, for example, headache.
Unfortunately, this debate cannot be solved in this
Review, and we recognise the insufficiency of present
terminological options. In clinical practice, we use the
term functional, because it is the term most acceptable
to patients and does not presuppose a cause for
symptoms that is unproven. We specifically define this
disorder by its clinical appearance, rather than by any
causative speculation as a movement disorder that is
significantly altered by distraction or non-physiological
manoeuvres (including dramatic placebo response) and
that is clinically incongruent with movement disorders
known to be caused by neurological disease.
Epidemiology, quality of life, and cost
The subject of this Review represents an important
issue because of its prevalence and effect on quality of
life and health-care economics. FMD are part of the
wide spectrum of functional or psychogenic neurological
symptoms, which together account for 16% of new pa-
tients attending neurology outpatients’ clinics.1 Accurate
estimates of prevalence of FMD are hampered by case
definition and the setting of the clinic from which
cases are ascertained, and range between 2 and 20% of
patients attending movement disorder clinics.9,10 These
disorders cause an impairment in quality of life that
is similar to, and in some aspects worse than, that
experienced by patients with Parkinson’s disease.11 No
studies have specifically addressed the economic
burden of FMD but, given the level of disability reported
by patients in the long term (see Prognosis section),
there are probably substantial associated health and
social care costs. In a large study of patients with
functional neurological symptoms (n=1144) who were
followed up for 1 year, at least 50% had stopped working
and more than one-quarter were receiving illness-
related financial benefits;12 the economic burden for
those with FMD is unlikely to differ from this. UK
estimates for the yearly costs associated with working-
age patients with “medically unexplained symptoms”
are approximately £18 billion,13 slightly more than the
annual cost associated with dementia for patients of all
ages in the UK.14 Women are more often affected by
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Review
Panel 1: Terms commonly used to describe psychogenic
disorders and their implications
Psychogenic
• Suggests psychological causation
Conversion disorder
• Operationalised within DSM: requires an identified
psychological triggering factor for diagnosis
Somatisation disorder
• Operationalised within DSM: requires presence of
multiple physical symptoms including one conversion
neurological symptom
Medically unexplained symptoms
• Suggests that a medical explanation might one day
be apparent
• Could refer to many medical symptoms that are not
thought to be psychogenic, but still are not of a
known cause
Functional
• Broad term suggesting a functional rather than a
structural deficit, which could apply to several
neurological disorders not regarded as psychogenic but
where structural pathology is absent, eg, migraine
Hysteria
• Historical term that carries substantial stigma in society
and implies a link between symptoms and the uterus
Non-organic
• Defines the condition by what it is not; the term organic is
itself not well defined
DSM=Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, American
Psychiatric Association.
FMD than men, and mean age at onset in different
studies ranges from 37 to 50 years.9,10 FMD are also
reported, but not commonly, in children15 and in the
elderly.9,10
Clinical features
Several historical features and examination findings
are commonly noted in patients with FMD regardless
of the movement disorder phenomenology. These
features are not diagnostic of FMD, but can be helpful
as part of the diagnostic process. Patients often describe
the sudden onset of symptoms, which might be
precipitated by a physical event (eg, injury or illness).9,10
Symptoms can rapidly progress to become severe—a
pattern that is unlike the slow progressive course of
most movement disorders.9,10 Patients might report
marked variability in symptom severity, including
complete remissions and sudden recurrences. The
phenomenology of the movement disorder might shift
over time. Patients might have a history of other
functional symptoms. Neurological signs apart from
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the movement disorder can be consistent with
functional illness, for example Hoover’s sign (leg
paresis), give-way weakness, and non-anatomical
patterns of sensory loss.9,10 The co-occurrence of
functional and organic movement disorders might be
expected, given the common co-occurrence of other
functional disorders with organic disorders, for example
epilepsy and non-epileptic seizures.16 However, hard
evidence for the prevalence of this phenomenon is
limited.17,18
Functional tremor
Functional tremor (FT) is the commonest presentation of
FMD, accounting for at least 50% of patients.9 Commonly,
the historical features are as outlined earlier, with sudden
onset, variability in severity with remissions, and variability
in the body part affected. Most patients have a tremor that
is present (or at least can be present at different times) at
rest, in posture, and during action, which is an unusual
pattern for organic tremor. Tremor can occur in any body
part; the hands and arms are most frequently involved,
but tremor of the head, legs, or even palate can also occur.
By contrast with patients with organic tremor, patients
with FT often direct clear visual attention towards their
affected limb during examination.19
The key clinical feature that helps to differentiate
FT from organic tremor is that FT changes with the
level of attention towards the affected limb. This can be
appreciated during history taking as fluctuation in
tremor severity (or even presence) while the patient’s
attention is engaged. Conversely, FT commonly worsens
during examination. Specific examination manoeuvres
can be used to distract attention away from the
tremoring limb; some formal assessments of specificity
and sensitivity have been done on these manoeuvres
clinically,20 and more extensively with electrophysiological
tremor recordings.21–25 Thus, tremor may change with
cognitive distraction tasks or tapping at different
frequencies (it may entrain to the tapping frequency,
shift in frequency, or stop altogether; or the patient
might inexplicably be unable to undertake the required
tapping movement correctly);21,22 pause with ballistic
movement of the other limb (figure 1);23 or paradoxically
worsen with loading.24 The specificity and sensitivity of
some of these tasks have been investigated (without
tremor recordings) in patients with FT compared with
those with essential tremor; tapping tasks had the
highest sensitivity and specificity (72·7% and 73·3%,
respectively).20 In a head-to-head study, we compared
these techniques with tremor recordings in FT and a

–0·04
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AccZL

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0
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0·050
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0
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0
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Ballistic movement
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0
–0·025
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1372 1374 1376 1378 1380 1382 1384 1386 1388 1390 1392 1394 1396 1398 1400 1402 1404 1406 1408 1410 1412
Time (s)

Figure 1: Tremor recordings in a patient with functional tremor

Tri-axial accelerometry recordings from an accelerometer attached to the tremoring hand (top three traces) and to the unaffected hand (bottom three traces). The
patient is undertaking rapid reaching movements to a target with the unaffected hand, which produces brief pauses in the tremor in the other hand.
Acc=acceleration. X=x axis. Y=y axis. Z=z axis. R=right. L=left.

252 www.thelancet.com/neurology Vol 11 March 2012


range of organic tremor disorders (Parkinson’s disease,
essential tremor, dystonic tremor, and neuropathic
tremor).25 We found that no single measure had
sufficient specificity and sensitivity to differentiate FT
from organic tremor. This finding is probably due to
the different mechanisms for tremor generation in FT,
with some patients generating tremor primarily by co-
contraction, which is not readily distractible by tapping
tasks.24 Cognitive distracter tasks were poor dis-
criminators between organic tremor and FT. A cutoff
score was devised by combining several of these
measures, which, if validated in a prospective study,
could provide a laboratory-supported level of diagnostic
certainty (table).
Functional dystonia
Functional dystonia is the second most common
presentation in patients with FMD.9 There are
substantial differences of opinion between experts
regarding the diagnosis of functional dystonia. These
differences are not helped by the history of dystonia in
general: patients now classified as having organic
dystonia were, until the 1980s, commonly classified as
having hysteria. Advances in genetics have led to
recognition of the phenotypes of primary idiopathic
dystonia, which have typical ages of onset, courses, and
distributions of dystonia. For example, DYT1 gene-
related primary dystonia starts before age 25 years,
often affects the legs at onset, and can spread over a few
years after onset to cause generalised dystonia.26 By
contrast, late-onset primary dystonia affects the cranio-
cervical region (spasmodic torticollis is the most
common form) and tends to remain focal.26 This
identification of distinct phenotypes has made easier
the recognition of secondary dystonic (including
functional) disorders, which have presentations
incongruous with primary dystonia phenotypes.
Patients with functional dystonia typically present with
fixed abnormal postures accompanied by severe pain
similar to that noted in chronic regional pain syndrome
type 1 (CRPS1). Most patients with functional dystonia
are young women and the usual trigger is a minor
peripheral injury, but the disorder is sometimes
spontaneous. Such patients (who might also be classed
as having “causalgia-dystonia”27 or “tonic dystonia of
chronic regional pain”28) may experience spread of
symptoms to other body parts without further injury.
Limbs are usually involved, but fixed dystonia affecting
the neck or jaw has also been reported.29
Physical examination manoeuvres can be used to
show with certainty whether attention is playing a key
part in symptom generation in functional tremor;
however, to show the same level of certainty in fixed
dystonia is difficult. One might argue that this difficulty
occurs because fixed dystonia is not a functional
disorder, but to state that maintenance of postures does
not need a similar level of attention as maintenance of
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Review
tremor would also be reasonable. However, in some
patients a brief give way of muscle activity in the
affected limb will be felt when the patient is distracted.
In support of the functional label for fixed dystonia,
symptoms may resolve with multidisciplinary re-
habilitation with an emphasis on cognitive-behavioural
therapy,30 the disorder may co-exist with other more
clearly defined psychogenic disorders,29,30 and marked
(curative) placebo responses have been reported.31
However, some,32 but not all,33 research electro-
hysiological tests suggest similarities between patients
with fixed dystonia and those with organic dystonia,
although these tests are all subject to confounding from
muscle activity, attention, and anxiety. Maintenance of a
fixed posture has been hypothesised to produce
secondary changes in central body schema,34 and these
changes might contribute to pain and other unusual
features, such as the seeking of limb amputation by
some patients.35
Functional myoclonus
Functional myoclonus is reported in about 20% of
patients with FMD.9 As might be expected in patients
with intermittent movements, distractibility can be
difficult to demonstrate on examination. Electro-
physiological tests can therefore be of substantial
diagnostic help to clinicians.36 Simple electromyography
(EMG) recordings can be used to assess EMG burst
duration: consistent EMG bursts of less than 75 ms do
not occur in functional myoclonus. However, the
converse is not true, because some forms of organic
myoclonus are associated with long-duration EMG
bursts. Electrophysiological features associated with
cortical myoclonus (giant somatosensory evoked
potentials, electroencephalogram [EEG] spike 20 ms
Points
Incorrect tapping performance at:
1 Hz 1
3 Hz 1
5 Hz 1
Entrainment, suppression, or pathological frequency shift at:
1 Hz 1
3 Hz 1
5 Hz 1
Pause or 50% reduction in amplitude of tremor with ballistic 1
movements
Tonic activation before tremor onset 1
Coherence of bilateral tremors 1
Increase of TP (as surrogate of tremor amplitude) 1
Cutoff score for functional tremor ≥3
TP=total power of the spectra between 1 and 30 Hz. Data from Schwingenschuh
and colleagues.25
Table: Suggested electrophysiological test criteria for diagnosis of
functional tremor
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 Review
20
10
Potential (μV)
–10
–20
–2500 –2000 –1500
Latency (ms)
Figure 2: Electroencephalogram recordings from a patient with functional myoclonus
A slow rising potential can be seen, which starts around 1 s before movement.
before jerks) would not be expected in functional
myoclonus. The most useful diagnostic test in patients
with suitable symptoms (see below) is EEG–EMG back-
averaging—a method for assessing cortical activity
shortly before movement (figure 2). In healthy people
undertaking a self-paced voluntary movement, a slow
rising potential is seen in the EEG starting about 1·5 s
before movement and peaking just before movement:
this is the pre-movement potential, or Bereitschafts-
potential.36 This potential can be recorded in patients
with functional myoclonus and is not seen in people
with organic myoclonus. There are technical limitations
to this test: at least 30 jerks need to be recorded, so
patients must have a reasonable number of jerks within
the recording time; and pre-movement potentials are
often difficult to record in patients with very rapid jerks
(more than one every 3–5 s), although distractibility is
often easy to indentify in such patients clinically. Pre-
movement potentials have been reported in patients
with tics,37 but not consistently.38 Two groups have inde-
pendently reported that most patients diagnosed with
idiopathic spinal segmental or propriospinal myoclonus
(the latter characterised by flexion jerks of the abdomen)
have pre-movement potentials before jerks and are
therefore best characterised as functional.39,40
Other functional movement disorders
Pure functional gait disturbance accounts for about 6%
of patients with functional movement disorders, but an
abnormal gait is a common feature in patients with
other FMD.41 Various gait patterns are described, but a
key feature of most of these patterns is that the patient
does not seem to adapt to the gait problem they
complain of in an optimum way.42–44 For example,
patients who complain of unsteadiness might walk with
a narrow base or might adopt uneconomic postures,
which are apparently compensatory for the gait
disturbance but would seem objectively to make it
worse.41 Some patients have objectively very good
balance while subjectively complaining of poor balance;
such patients shift their centre of gravity by pivoting
from side to side at the waist on a narrow base without
254
Onset of movement
–1000 –500 0
falling, thus showing excellent balance. This pattern
has been termed the “walking on ice” gait.44 Another
common pattern of functional gait disturbance is a
monoplegic dragging gait, where the affected leg is
dragged behind the patient, typically with the medial
surface of the foot in contact with the floor and the leg
externally rotated.45 This is quite different from the
circumducting gait typically seen in patients with
organic hemiplegia. So-called bizarre patterns of gait
are seen in organic movement disorders such as
Huntington’s disease and generalised dystonia, and
care needs to be taken in reaching a diagnosis with
regard to unusual gait disturbance.
Functional parkinsonism, chorea, and tics are rarely
reported.9 Most patients diagnosed with functional
parkinsonism actually have a functional resting tremor
rather than other features (such as slowness of move-
ment) that mimic parkinsonism.46 Dopamine trans-
porter scans can be helpful to a limited extent if
diagnostic uncertainty exists. Dopamine transporter
scans are normal in patients with functional
parkinsonism but also in organic parkinsonism due to
postsynaptic dopaminergic deficit, such as drug-
induced parkinsonism. Paroxysmal functional move-
ment disorders are rarely reported but do occur.9 They
may be under-recognised because patients might
instead be diagnosed with functional non-epileptic
seizures. Clinicians need to be familiar with the range
of triggers, attack durations, and attack frequencies that
occur in organic paroxysmal movement disorders to
help them to differentiate patients with functional
attacks with confidence and to exclude epilepsy by EEG
measurement during an attack if necessary. There is no
substitute for seeing an attack, and the video facility
available on many modern mobile phones makes it
easier for patients’ relatives to record an attack for
viewing by the physician.
Diagnostic criteria
We emphasised earlier that the diagnosis of FMD
should as much as possible be a positive diagnosis. It
should not be a diagnosis of exclusion, nor a diagnosis
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made on the basis of co-existence of a movement disorder
with psychological disturbance. Co-existent psychological
disturbance is common throughout organic neurological
disease and is not an adequate symptom on its own to
diagnose a psychogenic disorder.47
Operationalised diagnostic criteria for functional
movement disorders include the Fahn-Williams
criteria48 (the most widely used), the Shill-Gerber
criteria,49 and a recent revision of the Fahn-Williams
criteria proposed by Gupta and Lang (panel 2).47 All
these criteria have as a key element a gradation of
certainty of diagnosis; for example, in the Fahn-Williams
criteria the gradation is documented, clinically
established, probable, and possible. Various alterations
to the Fahn-Williams criteria have been suggested,
including a merging of documented and clinically
established categories into one category of clinically
definite; the removal of the possible category; and the
addition of laboratory tests to produce a category of
laboratory supported.47 The Shill-Gerber criteria have
been criticised for being so heavily weighted towards
historical information that the diagnosis of FMD could
possibly be made with little reference to the clinical
characteristics of the movement disorder.50 These
criteria also place weight on the notion of disease
modelling, in which experience of a disease in a family
member, acquaintance, or via work provides a model
for patients to produce functional symptoms. This
notion is difficult to investigate (eg, the quantification
of all potential disease models to which a person has
been exposed would seem to be very difficult), and
therefore its place in diagnostic criteria seems
questionable according to the available evidence.
The Fahn-Williams and Shill-Gerber criteria have
recently been subjected to assessment of inter-rater
reliability.51 There was only poor (Shill-Gerber) to
moderate (Fahn-Williams) inter-rater reliability for
probable and possible categories, with good agreement
for the clinically definite category.
Pathophysiology
The earlier discussion of terminology shows a historical
emphasis on psychological causation in FMD, as with
other functional disorders. Psychiatric formulations
based on late 19th and early 20th century concepts of
conversion, somatisation, and dissociation still form
the basis for psychiatric diagnoses in these disorders
and, by extension, ideas regarding pathophysiology.52
However, patients with psychogenic disorders in
general, including those with FMD, do not have the
expected rates of psychological trauma, either at the
onset of physical symptoms or in the past.5,53 This
finding presents a problem for those who emphasise
such factors as important pathophysiologically. This
problem has traditionally been solved, in a rather
circular argument, by suggesting that recall of such life
events is repressed by patients and therefore is not
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Review
Panel 2: Fahn-Williams and Gupta-Lang criteria for
diagnosis of psychogenic movement disorders
Fahn-Williams criteria48
Documented
Persistent relief by psychotherapy, suggestion, or placebo has
been demonstrated, which may be helped by physiotherapy;
or the patient was seen without the movement disorder
when believing himself or herself unobserved.
Clinically established
The movement disorder is incongruent with a classical
movement disorder or there are inconsistencies in the
examination, plus at least one of the following three: other
psychogenic signs, multiple somatisations, or an obvious
psychiatric disturbance.
Probable
The movement disorder is incongruent or inconsistent with
typical movement disorders or there are psychogenic signs
or multiple somatisations.
Possible
Evidence of an emotional disturbance.
Laboratory supported definite
Not included in this classification.
Gupta and Lang proposed revisions47
Clinically definite
Includes Fahn-Williams documented and clinically
established categories, and also includes movement
disorders that are incongruent with a classical movement
disorder or for which there are inconsistencies in the
examination, without the need for the additional presence
of psychogenic signs, multiple somatisations, or an obvious
psychiatric disturbance.
Probable
Not included in this classification.
Possible
Gupta and Lang question the utility of this category. They
suggest it could be used to include those with movement
disorders congruent or consistent with a classical
movement disorder but where there are additional
psychogenic signs, somatisations, or evidence of emotional
disturbance. However, they suggest that this category may
then include patients who are different
pathophysiologically from those with true psychogenic
movement disorders.
Laboratory supported definite
Presence of data from electrophysiological tests that prove
the presence of a psychogenic movement disorder
(primarily evidence of pre-movement potentials before
jerks or data from tremor studies).
available for report. Although this repression may
occur in some patients, the suggestion is largely
untestable.
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The key clinical feature that separates patients with
FMD from those with organic movement disorders is
that the movements have features that one would
usually associate with voluntary movement
(distractibility, resolution with placebo, and presence of
pre-movement potentials), but patients report them as
being involuntary and not under their control. There
seem to be just two logical explanations for this feature:
either movements are deliberately feigned or there must
be a brain mechanism that allows voluntary movement
to occur but to be experienced subjectively as involuntary.
Understanding this mechanism would seem to be key
to understanding the development of symptoms and
their treatment.
Although study of subjective experience of movement
might seem impossible, cognitive neuroscience has
revealed the existence of mechanisms within the
brain that confer a sense of intention and a sense of
agency to movement, and examples of organic brain
disease in which such processes are disrupted.54
Functional imaging recorded in patients during an
episode of functional tremor or when the same patients
were voluntarily mimicking their tremor showed
hypoactivation of the temporoparietal junction during
the psychogenic tremor.55 This area is thought to be an
important comparator region, comparing actual with
predicted sensory feedback. The suggestion is that
hypoactivity might represent a failure to match the actual
and predicted sensory feedback, producing a feeling of
involuntariness associated with movement.55 Linked
with this finding, we have reported that patients with
functional tremor do not have the normal sense of
intention that is associated with voluntary movement.56
Another functional imaging study in FMD noted
abnormally strong amygdala–supplementary motor area
connectivity when patients were presented with
emotionally valent stimuli and abnormally weak
supplementary motor area–prefrontal cortex connectivity
in a reaction time task.57 A hypothesis arising from this
work and a further functional imaging study in FMD58 is
that emotionally arousing events might trigger
movement controlled by the supplementary motor area
that is functionally disconnected from top–down control
by the prefrontal cortex.
In a recent study that compared patients with
functional tremor to those with organic tremor, we
compared self-completed diaries in which patients rated
the amount of the waking day they felt they had tremor
with the results of continuous tremor recordings from
a wrist-worn actigraph.59 Patients were all aware of the
purpose of the study, as confirmed in a post-study
questionnaire. Patients with organic tremor tended to
over-rate their tremor (by about 20%) in diaries
compared with the tremor watch recordings. Patients
with functional tremor over-rated their tremor by a
significantly higher amount (more than 65%; p=0·0001),
and had on average only 30 min of tremor per day. We
256
have interpreted this finding within a Bayesian
framework as a dominance of prior expectancy over
sensory data.59
These studies all provide results that would be
unexpected in patients feigning symptoms, although
they do not amount to an aid to diagnose feigning of
symptoms. However, these studies do provide examples
of research in functional disorders that look beyond the
rigid framework that has provided a causal model for
symptoms on the basis of emotional trauma alone.
There has been a wider rebalancing of attitudes toward
functional disorders, so that they are considered within
a biopsychosocial model, not just a psychosocial one.
This change in attitude might prompt a search for
psychological factors of causative importance that are
not solely related to emotional trauma. This type of
search has been underway for some decades in other
disorders (eg, schizophrenia) once regarded as mental
disorders but in which great importance is now given to
understanding the biological basis of the disorder. The
old dichotomy between mental and brain disorders has
increasingly been swept away by the progress of
cognitive neuroscience and, although long overdue,
this process is now affecting views of functional
neurological disorders. To regard FMD and other
functional disorders as just brain disorders would also
be incorrect, and so a combined approach is necessary
that integrates societal and psychological factors with
our present knowledge of the biology of brain function.
This process might not just lead to better understanding
of FMD, but might also improve our understanding of
the human brain.
Management
There are limited studies available on which to base
management decisions in FMD. It seems reasonable to
presume that treatment of FMD can be informed by data
regarding treatment of other functional neurological
conditions, in particular those that involve motor
symptoms.
In our view, the most important first steps in a
successful treatment approach are effective commu-
nication of the diagnosis and the provision to patients
and their families of a rational model within which
to understand the physical symptoms. In light of the
earlier discussion regarding diagnosis, we emphasise
the positive ways in which the diagnosis has been made
rather than falling back on explanations based on
normal test results. We try to introduce the role of
psychological factors in their proper context and do not
insist on extensive exploration for underlying psycho-
logical trauma. Patients with FMD are vulnerable to
unscrupulous medical and health practitioners, par-
ticularly over the internet.60 There are some useful web
resources that can help to support understanding of the
diagnosis for patients with functional symptoms, and we
direct patients towards these.61
www.thelancet.com/neurology Vol 11 March 2012

There is no evidence to support the use of drugs
traditionally used for the treatment of organic
movement disorders in patients with FMD. Medical
and surgical interventions are often harmful to patients
with FMD,30,35 and part of successful treatment is
removal of unnecessary medications and avoidance of
unnecessary tests and surgical treatments. The only
exception to this is provided by studies of intrathecal
baclofen in patients with fixed dystonia and CRPS1, but
these results carry important caveats. An initial
controlled study in a small group of patients gave
impressive results,62 but a follow-up study of a larger
group of patients63 found treatment-related com-
plications to be high, although a beneficial effect was
seen in many patients. The difficulty with both studies
is that the systemic effects of intrathecal baclofen
cannot be adequately controlled, and therefore patients
are systematically unmasked to the intervention. We
would urge caution with the use of this invasive
treatment given evidence of dramatic placebo response
of patients with fixed dystonia to other treatments.31 We
have highlighted earlier the difference of specialist
opinion regarding the nature of the disorder in patients
with fixed dystonia. Despite this difference in opinion,
there is no need to delay effective management, because
delay is associated with worse outcome and, in some
patients, the development of irreversible contractures.30
The key component of treatment is rapid early mobil-
isation with suitable holistic management of pain (with
emphasis on techniques used in CRPS1 such as
desensitisation). Surgical intervention and prolonged
immobilisation should be avoided.
There is some evidence that psychological intervention,
in the form of either psychodynamic psychotherapy64 or
more pragmatic symptom-based cognitive-behavioural
therapy,65 might be helpful for patients with functional
motor symptoms, including FMD. These techniques are
only applicable to those patients who accept that
psychological or behavioural interventions are valid
methods of treatment for their physical symptoms. Like-
wise, there is evidence that a subset of patients who are
willing to take antidepressants (in this study, those
diagnosed with primary conversion disorder and not
those with somatisation disorder) can benefit from this
treatment.66
Physical rehabilitation has face validity as a treatment
to manage motor symptoms, but there are few trials
upon which to base opinion. There is evidence that a
multidisciplinary approach combining physical and
psychological treatment can be effective for some
patients.30 This intensive (often inpatient) treatment is
expensive and will always have limited availability. In a
retrospective, case-control study, a brief (5 day) intensive
inpatient physical therapy programme produced major
self-rated improvement in symptoms in more than 60%
of participants (n=48) compared with 22% of control
individuals (n=32) after 2 years of follow-up.67 This
www.thelancet.com/neurology Vol 11 March 2012
Review
study used an explanatory model of symptoms that was
deliberately physical (abnormal motor learning) and,
although psychological factors were addressed, the
focus was maintained on physical symptoms and
treatment. Benefit has also been reported from a simple
12-week programme of supervised low-to-medium
intensity walking in patients with FMD.68 Such findings,
if confirmed by further studies, suggest that physical
interventions (perhaps combined with symptom-
focused cognitive-behavioural techniques65) may provide
an effective and acceptable means of symptom
management.
Placebo interventions can have strong effects in patients
with FMD,31 but evidence for long-term benefit is absent
and the ethics of such treatments are hotly debated.69 In
this vein, transcranial magnetic stimulation has been
reported to be of benefit in patients with FT, with
investigators suggesting a possible real effect of
stimulation.70 However, the unmasked nature of the
intervention makes a placebo effect likely.
Prognosis
Long-term follow-up studies are confounded by the
manner in which cases are diagnosed—typically by
tertiary movement disorder clinics where patients with
brief transient symptoms will be missed. In these
studies, about half of patients report some improvement
in symptoms at long-term (3–5 years) follow-up,
although most patients remain out of work due to
illness.71,72 Good prognostic features include a short
duration of illness, perception by the patient of effective
management by the clinician, and the presence of
depression or anxiety (which is therefore amenable to
psychiatric treatment).71,72
Future work
This Review reports several areas in which evidence-
based knowledge is limited. With specific reference to
FMD, we wish to highlight the following areas and
important questions.
Diagnostic tests and criteria
The discussion of FT shows how clinical (and simple
electrophysiological) tests can be used to make a
positive diagnosis. This process urgently needs to be
extended to other movement disorders, in particular to
patients with abnormal postures. If successful, use of
this process could lead to new diagnostic criteria, which
would be based on these positive clinical features and
rely less on associations with psychological factors or
with the notion of (unspecified) incongruity with
organic movement disorders.
Research
By contrast with some functional disorders in which
symptoms are subjective (pain, sensory loss, or disturb-
ance), functional motor disorders such as FMD provide
257
 Review
Search strategy and selection criteria
For the purposes of this Review, we searched Medline
between 1975 and December, 2011, for articles with the
keywords “psychogenic”, “functional”, “conversion”,
“movement disorder”, “parkinsonism”, “tremor”,
“dystonia”, “myoclonus”, “chorea”, “tics”, and “gait”. We
selected papers relevant to diagnosis, treatment, and
pathophysiology.
researchers with a measurable entity that reflects the
underlying symptom. We suggest, therefore, that patients
with functional motor disorders, in particular FMD, are
the natural group to include in future research studies.
Research studies such as those reviewed herein show
that such patients can participate in research and that
informative results can be obtained.
Treatment
There is a clear and urgent need for treatment studies
in FMD and other functional neurological disorders.
The acceptability of treatment approaches and the
availability of those who might deliver treatment should
be considered when planning clinical trials. In this
regard, patients with FMD may not accept that there is
an important psychological dimension to their symp-
toms, and therefore they might be less likely to accept
treatments based solely on psychotherapy or cognitive-
behavioural therapy. However, research on symptom-
focused cognitive-behavioural therapy approaches and
simple physical interventions point towards workable
interventions which, if given early in the course of the
illness, could produce benefit in these patients.
Education
None of the aforementioned suggested changes is likely
to happen unless concerted efforts are made to increase
interest and knowledge about FMD among movement
disorder specialists. Through this process, patients will
be most likely to receive early positive diagnoses, avoid
iatrogenic harm by unnecessary investigations and treat-
ments, benefit from world-class research, and receive
effective treatment in a timely manner.
Conclusions
We have described here how the correct diagnosis of
FMD should rely on positive clinical characteristics and
not on the presence of psychological trauma. The
historical emphasis on psychological trauma as a
triggering factor has perhaps skewed research agendas
and neurological interest in these patients, and has
certainly alienated many patients who cannot believe
that their physical symptoms are related to psycho-
logical trauma. We do not aim to minimise the
importance of psychological factors (anxiety, depression,
arousal, and attention) in such patients, but rather to
258
point out that a dogmatic and relentless search for a
clear triggering psychological trauma may be misguided
and unhelpful.
One additional benefit of rebalancing the approach to
FMD and functional disorders in general is that it might
allow us to reconsider some of the symptoms that are
present in our patients with organic neurological dis-
orders. Any practising neurologist would recognise that
patients with the same organic disease of apparently
similar severity manifest symptoms in differing ways,
which can have a dramatic effect on disability and quality
of life. This phenomenon, often called functional overlay,
is, we would suggest, often ignored as a non-symptom
that interferes with the neurological management of
patients. However, understanding the pathophysiology
of this overlay and knowing how to treat it—knowledge
that is likely to come from research into pure functional
disorders—could be of substantial benefit to patients
with organic disease. The common occurrence of
physical triggering events such as illness or injury in
patients with pure functional symptoms is itself a pointer
towards an important overlap between organic and non-
organic illness.5
Although we agree that FMD and other functional
disorders do represent a crisis for neurology, it is not
an unsolvable one. We believe that now is the time for
the movement disorder and wider neurological
community, in cooperation with psychiatry, psychology,
and physical therapy services, to lead the search for
solutions.
Contributors
MJE and KPB generated an outline for the paper. MJE wrote the first
draft and MJE and KPB revised this draft.
Conflicts of interest
MJE is supported by a National Institute for Health Research (NIHR)
Clinician Scientist Fellowship; has received funding from the UK
Dystonia Society and Parkinson’s UK; receives royalties from The
Oxford Specialist Handbook of Parkinson’s Disease and Other
Movement Disorders (Oxford University Press, 2008); and has received
honoraria for speaking engagements from the Movement Disorders
Society and UCB. KPB has received funding for travel from
GlaxoSmithKline, Orion Corporation, Ipsen, and Merz
Pharmaceuticals; serves on the editorial boards of Movement Disorders
and Therapeutic Advances in Neurological Disorders; receives royalties
from the publication of The Oxford Specialist Handbook of
Parkinson’s Disease and Other Movement Disorders (Oxford
University Press, 2008); received speaker honoraria from
GlaxoSmithKline, Ipsen, Merz Pharmaceuticals, and Sun
Pharmaceutical Industries; and has received research support from
Ipsen and the Halley Stewart Trust through the Dystonia Society UK
and the Wellcome Trust MRC strategic neurodegenerative disease
initiative award (reference number WT089698).
Acknowledgments
MJE is supported by an NIHR Clinician Scientist Grant. NIHR had no
involvement in the writing of the paper or in the decision to submit for
publication.
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