revue neurologique 174 (2018) 203–211

Available online at

ScienceDirect
www.sciencedirect.com

Frontiers between neurology and psychiatry

Motor functional neurological disorders: An update

B. Garcin a,b,*
a
Neurology department, Memory Center, Avicenne University Hospital, AP–HP, 125, route de Stalingrad, 93009
Bobigny, France
b
UPMC UMRS 1127, Inserm U 1127, CNRS UMR 7225, Institut du cerveau et de la moelle épinière (ICM), 75013 Paris,
France

info article abstract

Article history: Motor functional neurological disorders (FNDs) are motor symptoms not explained by a
Received 11 October 2017 lesion or related to a known dysfunction of the central nervous system, yet functional
Received in revised form imaging studies suggest the presence of a genuine brain dysfunction. With this common
28 November 2017 disabling condition, there is a particular need for collaboration between neurologists and
Accepted 29 November 2017 psychiatrists. Neurologists can search for positive clinical signs to make the diagnosis,
Available online 31 March 2018 which can then be followed by an explanation of the disease, whereas psychiatrists can look
for psychological factors and psychiatric comorbidities in order to deliver appropriate
Keywords: treatment. Such a multidisciplinary approach is important, particularly with the participa-
Functional neurological disorder tion of neurologists, psychiatrists, physiotherapists and psychologists. If necessary, addi-
Conversion disorder tional treatments such as transcranial magnetic stimulation (TMS), hypnosis and sedation
Psychogenic may be proposed.
Functional movement disorder # 2018 Elsevier Masson SAS. All rights reserved.
Functional deficit
Treatment

1. Introduction ‘‘conversion’’ itself reflects Sigmund Freud’s theory that

Functional neurological disorders are neurological symptoms
that cannot be explained by a lesion or related to an identified
dysfunction of the central nervous system (CNS). The name
that should be given to these symptoms has been the subject
of debate for decades [1,2]. The term ‘‘hysteria’’, proposed in
the first three editions of the Diagnostic and Statistical Manual of
Mental Disorders (DSM-I–III), suggests the disorder is the
consequence of uterine dysfunction. For this reason, it was
abandoned in the fourth edition (DSM-IV) published in 1994
and replaced by ‘‘conversion disorder’’ [3]. However, the term
unconscious conflicts are converted into neurological symp-
toms, an idea that has never been scientifically demonstrated.
Other terms frequently used by clinicians include ‘‘psycho-
genic disorders’’, ‘‘somatization disorders’’, ‘‘non-organic
symptoms’’ and ‘‘medically unexplained symptoms’’. The
term ‘‘functional neurological disorders’’ (FNDs) is relatively
acceptable to patients and is now widely accepted by
physicians. It appears in DSM-V and best reflects the current
knowledge of the pathophysiology [4,5]. The term has also
been proposed for the 11th revision of the International
Classification of Diseases (ICD-11), which should be available

* Correspondence. Neurology department, Memory Center, Avicenne University Hospital, AP–HP, 125, route de Stalingrad, 93009 Bobigny,
France.
E-mail address : beatrice.garcin@aphp.fr.
https://doi.org/10.1016/j.neurol.2017.11.003
0035-3787/# 2018 Elsevier Masson SAS. All rights reserved.
204 revue neurologique 174 (2018) 203–211
in 2018 [6]. For these reasons, this is the term used in the
present review.
The clinical presentation of FNDs is heterogeneous and
includes motor deficits, movement disorders, sensory deficits,
non-epileptic seizures, language disorders and/or swallowing
impairment. The present report mainly focuses on FNDs
presenting with motor symptoms (mFNDs), such as motor
deficits and movement disorders.
2. Epidemiology and Challenges
Studying the epidemiology of FNDs is especially difficult most
notably because of the changes in diagnostic criteria for FNDs
over the past several decades [7]. According to epidemiological
studies, the incidence of FNDs varies from 5 to 12/100,000
population [8]. Their prevalence, calculated from population
registries, is approximately 50/100,000, yet in clinical practice,
FNDs are frequently observed. In a consecutive series of 3781
patients seen in Scottish outpatient neurological clinics, 30%
had medically unexplained symptoms and 6% met the criteria
of conversion disorder according to DSM-IV. These figures are
similar to those described in eight smaller patient series [9],
thereby demonstrating the high prevalence of FNDs in
neurology clinics.
Thus, FNDs represent an important socioeconomic
challenge, and there is now clear evidence that their
economic burden is considerable. In the above-mentioned
Scottish cohort of 3781 patients, those with medically
unexplained symptoms were more likely to not be able to
work because of their health issues, and they also received
more health benefits for their handicap than patients with
‘‘organic’’ neurological diseases [10]. In the present author’s
experience at the Salpêtrière University Hospital in Paris,
more than half of the 482 patients with mFNDs received
disability-related benefits because of their symptoms [11],
while a UK study estimated that the annual cost of
somatization disorders represents 10% of public health
expenses, translating to a total annual sickness cost of
£ 14 billion [12]. FNDs also constitute a human challenge:
given the similar severe motor problems, the quality of life of
an FND patient is as altered as in an ‘‘organic’’ disease such as
Parkinson’s [13].
The management of these disorders is also challenging.
First, there is no consensus or recommendations on how to
manage FNDs. Second, there is a lack of training of
neurologists and psychiatrists, partly due the position of
FNDs at the boundary between neurology and psychiatry. In a
survey to assess how much neurologists like to manage
specific neurological diseases, FNDs came out last in a list of 20
of them. This ranking reveals how uncomfortable neurologists
feel with a diagnosis of FND [14,15]. Moreover, as there is no
identified lesion in the CNS, the prognosis of patients with
FNDs is generally poor. A meta-analysis involving 2069
patients with mFNDs found that symptoms persisted or
worsened in 50% of cases at the 1-year follow-up. After 7 years
of follow-up, only 24% were in remission [16]. In that meta-
analysis, the best predictors of a good outcome were short
duration of disease, early diagnosis and high patient satisfac-
tion with their care.
3. Pathophysiology considerations
Patients suffering from FNDs have motor symptoms that often
mimic organic deficits, making it logical to wonder such
symptoms are not real, but being feigned by patients instead.
However, if they are considered ‘‘real’’ experiences for
patients and not being voluntarily produced, it then becomes
reasonable to suspect that a cerebral dysfunction is underlying
these symptoms. The emergence of functional imaging
techniques has allowed both hypotheses to be tested, and
an increasingly large number of such studies have been
performed over the past 20 years (for a review, see Aybek and
Vuilleumier [17]).
3.1. Functional imaging
Functional imaging studies show that cerebral activation in
patients with mFNDs differs from the cerebral activation in
patients simulating the same deficit or movement disorder
[18–21]. These results suggest that the symptoms are not
voluntarily produced, but in fact reflect genuine brain
dysfunction. Although functional imaging studies are hete-
rogeneous in terms of their experimental paradigms
and patients’ characteristics, some results remain relatively
constant. In particular, patients with mFNDs consistently
show hypoactivation in both cortical and subcortical motor
pathways, with no recruitment of the prefrontal regions
usually associated with voluntary motor inhibition; in
contrary to what is observed with simulated deficits [19].
In addition, some authors have evidenced hypoactivation
of the right temporoparietal junction [18,22], a region
often fsassociated with the sense of agency. This is in
agreement with theories that place disruption of the sense of
agency as a key triggering factor [23]. Furthermore, some
authors have noted greater amygdala activity in arousing
stimuli [24] and abnormal recruitment of the ventromedial
prefrontal cortex (PFC) [25], possibly in relation to emotion
dysregulation.
3.2. Theories of pathophysiology
Why FND symptoms arise has been a source of debate since
antiquity [26]. Until recently, it was accepted that psycho-
logical factors are the main causes of symptoms [27].
However, such a causal relationship between psychological
factors and symptoms has never been demonstrated, and
psychological factors have recently been removed from the
diagnostic criteria of FNDs. However, recent functional
magnetic resonance imaging (fMRI) studies have suggested
a dysregulation of emotional processing in patients with
FNDs [25,28,29]. New cognitive theories have also recently
emerged: most notably, Edwards et al. [30] proposed that
psychological or physical trauma might induce the forma-
tion of an abnormally strong predisposition. In such cases,
the conjunction of an individual’s beliefs and expectations
about how the brain and body can go wrong, a disrupted
sense of agency for movement and an abnormal switching of
attention to the body/symptoms could lead to functional
symptoms.
 revue neurologique 174 (2018) 203–211
4. Clinical characteristics and diagnosis
4.1. Demographic characteristics of mFND patients
The experience of the present author is that, between 2008
and 2016, 482 patients were seen for exploration of a possible
mFND by the neurophysiology department of the Salpêtrière
University Hospital in Paris. Half of these patients (n = 241)
were suffering from motor deficits, while the other half had
movement disorders. The mean age of these patients was 40
years (range: 8–77 years), and 74% were female. Symptoms
were of sudden onset (within < 24 h) in 93% of cases and had a
mean duration of 4.3 years [11]. These demographic data are
consistent with other published cohorts, which reported that
mFND is more frequent in women, with proportions ranging
from 60% to 79%, and has an age of onset of 39–50 years
[9,13,31–34]. A few studies have assessed the sudden onset in
functional movement disorders as ranging from 54% to 92% of
patients [9].
4.2. FND diagnostic criteria
The diagnosis of an FND relies on fulfillment of the following
DSM-V criteria [4]: (A) one or more symptoms of altered
voluntary motor or sensory function; (B) clinical findings
offering evidence of incompatibility between the symptom
and a recognized neurological or medical condition; (C) the
symptom or deficit is not better explained by another medical
or mental disorder; and (D) the symptom or deficit causes
clinically significant distress or impairment in social, occu-
pational or other important areas of functioning, or warrants
medical evaluation.
It is worth noting that the above criteria list reveals three
significant changes in DSM-V, modifications that merit some
discussion as they illustrate a progressive evolution in the
perception, understanding and management of FNDs by
neurologists and psychiatrists over the past 10 years [27].
Indeed, in this latest edition of the DSM, two criteria
mentioned in the previous version (DSM-IV-R) have been
removed: psychological factors are adjudged associated with
the symptom or deficit if conflicts or other stressors precede
the initiation or exacerbation of the symptom or deficit; and
the symptom or deficit is not intentionally produced or
feigned.
The first criterion was removed because psychological
factors are not always found. In fact, most studies found more
life events and previous emotional disorders in patients with
FNDs compared with controls [32,35,36], but this does not
mean that stress and emotional symptoms are a necessary
prerequisite for the diagnosis (see also ‘‘psychological factors’’
below). In addition, there is evidence that physical factors
such as pain, injury and surgery can also trigger FNDs in ways
that may be physiological as much as psychological [37,38].
The second criterion was removed for two main reasons:
first, it is difficult to verify in clinical practice that a patient is
not simulating a symptom, and any discrepancy between the
patient’s complaint and observations of the preserved per-
formance does not necessarily mean that the patient is faking
it [39]. Moreover, this criterion implies that the physician does
205
not trust the patient, which can then alter the doctor–patient
relationship [1].
Finally, criterion B was added to the DSM-V list. This
criterion highlights the diagnostic value of the positive clinical
signs showing incompatibility between symptoms and orga-
nic disease. This is a major evolution in the management of
FNDs, as it emphasizes that FND is not only a diagnosis of
exclusion, but a genuine diagnosis in itself. Indeed, some of
the clinical signs that can be used for a positive diagnosis of
mFNDs are described below.
4.3. Positive signs of motor deficit
There are 24 positive clinical signs described in functional
motor deficits. The diagnostic validity of each one has been
recently reviewed [40], and seven of them have been validated,
each with excellent specificity (97–100%; Table 1). Identifying
these signs is of significant diagnostic value, but they can be
sought for only if there is a deficit in the muscle(s)/limb(s)
assessed by the sign.
The other 17 signs, while not validated, still constitute
diagnostic tools that can be used for clinical diagnosis (for a
full listing, see Daum et al. [40]). Also, a sensorimotor scale has
recently been validated for positive diagnosis of functional
sensorimotor deficit [48]. In its validation study, the scale
showed excellent diagnostic value, with a sensitivity of 95%
and a specificity of 90% with a cutoff score of  4 (Table 2).
4.4. Positive signs of functional movement disorders
(FMDs)
FMDs can present with tremor, dystonia, myoclonus, chorea,
Parkinsonism, tics or any other type of movement disorder. In
a cohort of 88 patients, most (74%) exhibited two or more types
of movement disorder [49]. Among published cohorts, tremor
or dystonia is the main clinical presentation of an FMD, noted
in70–90% of patients [49–51]. In our cohort of 241 FMD patients,
102 presented with tremor and 98 with dystonia, accounting
for 83% of all such patients [11].
4.4.1. Functional tremor
The most common presentation of an FMD, this represents
around 50% of cases [49–51]. Tremor is usually observed at
rest, posture and action [52]. Distractibility, entrainment and
variability are the three main positive clinical signs for
diagnosing functional tremor [53]. Distractibility is a common
positive clinical sign of FMDs in general: it refers to reduction
or resolution of an FMD during a mental or motor task, and can
be demonstrated by, for example, asking the patient to
perform a quick movement with the unaffected arm [54].
Entrainment is evinced by asking the patient to make a
rhythmical (preferably 3-Hz) tapping movement with the
unaffected hand. Tremor in the affected hand then either
‘‘entrains’’ to the rhythm of the unaffected hand or the patient
is not able to make a simple rhythmical movement at all [55].
Variability refers to changes in frequency and intensity
observed during clinical examination.
Additional clinical signs can be found in the current
diagnostic criteria proposed by Gupta and Lang [53]. Also,
the diagnosis can be further documented electrophysiologi-
206 revue neurologique 174 (2018) 203–211

Table 1 – Description of the 7 validated positive clinical signs in functional motor deficit.
Clinical sign Reference Sensitivity (%) Specificity (%) Description
Hoover’s sign [41] 63 99 Hip extension weakness that returns to normal with
contralateral hip flexion against resistance
Abductor sign [42] 100 100 Hip abduction weakness that returns to normal with
contralateral hip abduction against resistance
Abductor finger sign [43] 100 100 Synkinetic abduction finger movements of paretic
hand during abduction finger movement against
resistance with healthy hand
Spinal injury test [44] 100 98 Patient in supine position is asked to lift his knees. If
not possible, examiner lifts them up. The sign is
positive if the patient keeps them up, negative if legs
drop in abduction
Collapsing/give-way [45] 63 97 A position is maintained, and limb collapses with a
weakness light touch. During muscle strength testing: a
normal strength is developed and then collapses
suddenly
Co-contraction of [46] 17 100 During muscle strength testing: simultaneous
antagonist contraction of agonist and antagonist muscles,
muscles resulting in no or very little movement
Motor inconsistency [47] 13 98 Impossibility to do a movement while another
movement using the same muscle is possible
Reference is the first article for validation. Sensitivity and specificity have been estimated in a recent meta-analysis with the help of different
existing validation studies [40].

Table 2 – Sensorimotor scale (adapted from [48]).

Clinical sign Scale points
Give-way weakness 2
Drift without pronation (arms stretched out, palms up in supinated position, fingers adducted, eyes 2
closed for 10 seconds: positive if downward drift with NO pronation)
Collapsing weakness 1
Co-contraction 1
Spinal injury test 1
Hoover’s sign 2
Splitting the midline (positive if exact splitting of sensation in the midline) 2
Splitting of vibration sense (positive if the sensation of a tuning fork is different when applied over left or 1
right side of the sternum or frontal bone)
Non-anatomical territory (diminished sensation that does not fit dermatomal or other neural lesion) 1
Systematic failure (Positive if patient always fails in a discriminative task) 1
Total score 14
A cutoff of 4 or more shows good diagnostic value for the diagnosis of a functional deficit.

Table 3 – Laboratory-supported criteria for the diagnostic

cally through electromyography (EMG) and accelerometry [56]. of functional tremor, adapted from [57].
Finally, laboratory-supported criteria have recently been Criteria Points
validated for functional tremor (Table 3) [57].
Incorrect tapping performance
1 Hertz 1
4.4.2. Functional dystonia 3 Hertz 1
Making this diagnosis is a challenge because of the lack of 5 Hertz 1
positive clinical signs. Moreover, electrophysiological studies Entrainment, suppression or pathological frequency
have proved unhelpful [56]. However, a fixed dystonic posture shift at
1 Hertz 1
characteristically of the hand (flexion of fingers, wrist and/or
3 Hertz 1
elbow) or ankle (plantar flexion and dorsiflexion) [58] 5 Hertz 1
associated with pain is suggestive of the diagnosis. Pause or 50% reduction in amplitude of tremor with 1
ballistic movement
Tonic activation before tremor onset 1
5. Psychological factors Coherence of bilateral tremors 1
Increase of total power (as surrogate of tremor 1
amplitude)
As discussed above, the presence of psychological factors has
Cutoff score for functional tremor 3
been removed from the diagnostic criteria listed in DSM-V [4].
Sensitivity of 90% and specificity of 96% for the diagnosis of
While it may seem contrary to the Freudian idea that
functional tremor at a cutoff score > 3/10.
functional symptoms originate from psychological conflict,
 revue neurologique 174 (2018) 203–211
the main reason for this removal was that it is extremely
difficult to prove that a psychological event has a causal
relationship with the onset or exacerbation of a symptom.
Indeed, what evidence does the scientific literature provide
regarding psychological factors in mFNDs?
5.1. Prevalence of traumatisms
Recent studies have shown that patients with mFNDs have
higher rates of childhood trauma, including sexual abuse,
physical trauma and emotional neglect, compared with so-
called organic patients and healthy controls [35,36,59]. Other
studies have also revealed that mFND patients have expe-
rienced more physical and psychological trauma in the 3
months prior to symptom onset than do their organic controls
[32,36–38,60]. In those studies, the rate of significant trauma
preceding FND onset ranged from 20% to 80%.
To summarize, there is a higher rate of trauma in early
childhood and in the months preceding symptom onset in
patients with mFNDs and, returning to Freud’s theory, several
recent neurobiological models have included trauma as a key
factor in the pathogenesis of FNDs [28,29,61].
5.2. Psychiatric comorbidities
While it seems obvious that trauma are more frequent in FND
patients than in organic patients, there is more controversy
regarding psychiatric comorbidities. Some authors have found
more depression and/or anxiety disorders in FND than in
organic patients [31,32], but others have not [36,62]. Similarly,
some authors have observed more personality disorders [32] in
FND than in organic patients, whereas others have not [36,62].
Overall, however, it is important to highlight that 39% of FND
patients have no psychiatric comorbidities at all [62].
Although psychological factors are often associated and
may play a role in the development of FNDs, they are not
always found. In a survey of 512 neurologists, 82% considered
that emotional disorders are not necessary for a diagnosis of
FMD [63]. This means that, while psychiatric comorbidities
and trauma should be looked for and treated, they are not
essential for a positive diagnosis.
6. Treatment
6.1. Crucial role of neurologists and psychiatrists
It is widely accepted that both neurologists and psychiatrists
play important roles in the diagnosis and treatment of FNDs,
and two recent studies have demonstrated the positive effect
of such a combined consultative approach on outcomes of
patient care [64,65]. Also, guidelines have been proposed by a
Scottish team for the management of FND patients by both
neurologists and psychiatrists [66,67]. Neurologists play a
crucial role in giving a positive diagnosis followed by an
explanation of the disorder, which could also include
emphasizing that the symptoms are genuine, common and
potentially reversible, while also discussing the diagnosis, and
advising on distraction and self-help techniques. Specific
treatment and an outpatient review may also be offered [68].
207
Self-help resources have been developed to aid communica-
tion, including an online web resource (www.
neurosymptoms.org) that has been translated into many
languages, including French. Moreover, a randomized control-
led trial (RCT) is currently assessing the effect of Internet-
based education on patients’ symptoms and functioning
(https://clinicaltrials.gov/ct2/show/NCT02589886). In addition,
depending on the symptoms and context, the following
treatments may also help to improve patients’ conditions.
6.2. Physiotherapy
A growing number of studies have shown the efficacy of
physiotherapy in mFND patients [69–71], including two RCTs
demonstrating the benefits of inpatient physiotherapy deli-
vered as a 5-day [72] or 3-week program [73]. Open access
recommendations have also been published by a consortium
of experts [74]. Physiotherapy for mFNDs should include
education about the disorder and correction of mistaken
beliefs about the condition, while showing its reversibilit, . It
should show the effects of attention on symptoms and correct
abnormal habitual movement patterns.
6.3. Transcranial magnetic stimulation (TMS)
In the present author’s experience, repeated low-frequency
(0.25–0.5 Hz) supra-threshold (120–150% of the motor thres-
hold) TMS can significantly improve patients with FMDs
[75,76]. Six observational TMS treatment studies and three
RCTs have so far been reported for mFNDs (Table 4) [77,78], and
it is worth noting that five of the six studies with supra-
threshold TMS intensity showed beneficial effects, whereas
both of the two studies using infra-threshold TMS intensity
showed negative results.
In general, TMS can improve symptoms, yet the mecha-
nisms behind its efficacy are still unknown. To test whether
TMS efficacy in FMD patients is due to cortical neuromodula-
tion, TMS was compared with root magnetic stimulation (RMS),
a control condition that induces a similar movement without
direct stimulation of the cortex. The study included 33 FMD
patients and had a crossover design. Patients were improved by
61% after both TMS and RMS sessions, and remained stable
over the 1-year follow-up. More important, no significant
difference was found between TMS and RMS [76], thereby
suggesting that the efficacy of TMS is not due to neuromodula-
tion, but rather a combination of placebo effect and motor
relearning with the help of TMS-induced movement.
In summary, TMS appears to be a treatment of interest in
addition to a multidisciplinary approach. A currently ongoing
trial (TONICS) aims to determine the impact of different
stimulation intensities (supramotor vs. submotor threshold
stimulation), while a recently completed trial [rTMS and
functional paralysis (PARALYSTIM)] has looked at the role of
the placebo effect on TMS efficacy by comparing repetitive
TMS (rTMS) with sham rTMS.
6.4. Psychological treatment
Two main types of psychotherapy have been proposed for
FNDs: cognitive behavioral therapy (CBT); and psychodynamic
208 revue neurologique 174 (2018) 203–211

Table 4 – Transcranial magnetic stimulation (TMS) as treatment for motor functional neurological disorders (FNDs).
Observational treatment studies

Reference Population TMS protocol Target Results Time laga

[79] 11 tremor (8 bilateral) 0.2 Hz, 30 pulses, > MT cMC Positive (97% mImpr) NA
[75] 24 MD (15 bilateral) 0.25 Hz, 20 pulses, > MT cMC Positive (66.5% mImpr) 24 h
[80] 1 paraplegia Single pulses, > MT cMC Positive (full recovery) 1 week
[81] 4 paresis (1 bilateral) 15 Hz, 4000 pulses, > MT cMC Positive (3/4 Impr) 4–12 weeks
[82] 70 paresis (42 bilateral) 0.25 Hz, 30 pulses, > MT cMC Positive (62/70 Impr) Immediately after TMS
[83] 6 bilateral MD 0.33 Hz, 50 pulses, < MT dMC, then dPMC Negative (Impr slight) 2 weeks

Randomized controlled trials

[84] 11 paresis 15 Hz, 4000 pulses, < MT cMCb Negative (Impr slight in objective strength, 24 h and day 10
(2 bilateral) Control: sham but not subjective strength)
[78] 10 unilateral 46–70 single pulses, > MT cMC Negative (Impr slight immediately) Immediately after TMS
paresis Control: waiting list (and after 3 months)

Hz: hertz; > or < MT: above/below motor threshold; mImpr: mean improvement (assessed by movement disorder scale); NA: not available; MD:
movement disorders; dMC: dominant motor cortex; dPFC: dominant premotor cortex.
a
Between treatment and assessment of clinical improvement (Impr).
b
TMS applied only to motor cortex contralateral (cMC) to most symptomatic side for bilateral symptoms; otherwise, applied to cMC (or
bilaterally for bilateral symptoms).

therapy. Over the past few years, data from RCTs have
emerged to reinforce the role of psychotherapy in the
treatment of FNDs.
6.4.1. Cognitive behavioral therapy
CBT is a form of psychotherapy that encourages patients to
change the behaviors and beliefs thought to be obstacles to
symptomatic improvement by focusing on perpetuating
factors rather than on predisposing factors. Sharpe et al.
[85] showed the benefits of brief (4  30 min) guided self-help
based on CBT in 127 patients with a variety of FND symptoms
[odd ratio (OR): 2.4 for improved outcome; P = 0.02], and a
recent pilot study observed beneficial effects with CBT in FMD
patients (90 min/week for 12 weeks) compared with standard
medical care on its own [86].
6.4.2. Psychodynamic therapy
This form of treatment aims to help patients see their
symptoms in the context of interpersonal relationships and
their life narrative. In a case series of 10 patients, eight
improved with interpersonal therapy [87]. Reuber et al. [88]
also reported efficacy with tailored psychodynamic therapy in
91 patients with FND symptoms, including FMDs and paresis:
49% improved by at least 1 standard deviation (SD) on
measures of health status. However, a subsequent RCT of
early psychodynamic therapy vs. 3 months of monitoring by a
neurologist failed to show any differences between the two
groups; this, however, may have been due to the study’s lack of
sufficient power [89].
6.5. Other treatments
Other treatments have been proposed for mFNDs, including
suggestion [90,91], hypnosis [92], neurofeedback [93] and
sedation [94]. A step-by-step approach has also been proposed
by the Scottish healthcare system (http://www.
healthcareimprovementscotland.org/our_work/long_term_
conditions/neurological_health_services/neurological_
symptoms_report.aspx), which may provide guidance for
other countries, including France, towards better manage-
ment of mFND patients. This proposal comprises the
following: (step 1) the neurologist provides the diagnosis
and initial management; (step 2) a brief intervention is
delivered, usually by a physiotherapist with the support of a
neurologist and specialist psychiatrist; and (step 3) more
complex multidisciplinary care is delivered by the full
rehabilitation team together with psychiatric/psychological
treatment.
7. Conclusion
mFNDs are commonly seen, and cause distress and disability
with a poor prognosis. Unfortunately, such patients are often
not adequately addressed by the current medical system
because of the clinicians’ lack of knowledge and the absence of
dedicated clinics. Given this context, there is a particular need
for collaboration between neurologists and psychiatrists. The
former should be aware of the positive clinical signs to make a
positive diagnosis, followed by an explanation of the disorder,
while the latter should then search for psychological factors
and psychiatric comorbidities, and treat them accordingly. A
multidisciplinary approach is especially important, and
should include neurologists, psychiatrists, physiotherapists
and psychologists. If necessary, additional treatment can be
proposed, such as TMS, hypnosis and/or sedation.
Disclosure of interest
The author declares that she has no competing interest.
Acknowledgments
This work was supported by the Foundation for Medical
Research [grant number: FDM20150632801]. I am grateful to Pr
Bertrand Degos for revising this article.
 revue neurologique 174 (2018) 203–211
references
[1] Stone J, LaFrance WC, Brown R, Spiegel D, Levenson JL,
Sharpe M. Conversion disorder: current problems and
potential solutions for DSM-5. J Psychosom Res
2011;71:369–76. http://dx.doi.org/10.1016/j.jpsychores.2011.
07.005.
[2] Edwards MJ, Stone J, Lang AE. From psychogenic movement
disorder to functional movement disorder: it’s time to
change the name. Mov Disord 2014;29:849–52. http://
dx.doi.org/10.1002/mds.25562.
[3] American Psychiatric Association. Diagnostic and
statistical manual of mental disorders. 4th ed. DC:
American Psychiatric Publishing; Washington; 1994.
[4] AP Association. Diagnostic and statistical manual of mental
disorders: Dsm-5. 5th revised edition. Washington, DC:
American Psychiatric Publishing; 2013.
[5] Stone J, Wojcik W, Durrance D, Carson A, Lewis S,
MacKenzie L, et al. What should we say to patients with
symptoms unexplained by disease? The ‘‘number needed
to offend.’’ BMJ 2002;325:1449–50.
[6] Stone J, Hallett M, Carson A, Bergen D, Shakir R. Functional
disorders in the Neurology section of ICD-11: a landmark
opportunity. Neurology 2014;83:2299–301. http://dx.doi.org/
10.1212/WNL.0000000000001063.
[7] Kanaan RA, Carson A, Wessely SC, Nicholson TR, Aybek S,
David AS. What’s so special about conversion disorder? A
problem and a proposal for diagnostic classification. Br J
Psychiatry 2010;196:427–8. http://dx.doi.org/10.1192/
bjp.bp.109.073981.
[8] Akagi H, House A. The clinical epidemiology of hysteria:
vanishingly rare, or just vanishing? Psychol Med
2002;32:191–4.
[9] Carson A, Lehn A. Epidemiology. Handb Clin Neurol
2017;139:47–60. http://dx.doi.org/10.1016/B978-0-12-801772-
2.00005-9.
[10] Carson A, Stone J, Hibberd C, Murray G, Duncan R, Coleman
R, et al. Disability, distress and unemployment in neurology
outpatients with symptoms ‘‘unexplained by organic
disease.’’. J Neurol Neurosurg Psychiatry 2011;82:810–3.
http://dx.doi.org/10.1136/jnnp.2010.220640.
[11] Villain N, Mesrati F, Naccache L, Marie V, Roze E, Bertrand
D, et al. Caractéristiques cliniques et démographiques des
patients ayant un trouble moteur fonctionnel. Rev Neurol
(Paris) 2017;173(Supplement 2):S178. http://dx.doi.org/
10.1016/j.neurol.2017.01.346.
[12] Bermingham SL, Cohen A, Hague J, Parsonage M. The cost
of somatisation among the working-age population in
England for the year 2008-2009. Ment Health Fam Med
2010;7:71–84.
[13] Anderson KE, Gruber-Baldini AL, Vaughan CG, Reich SG,
Fishman PS, Weiner WJ, et al. Impact of psychogenic
movement disorders versus Parkinson’s on disability,
quality of life, and psychopathology. Mov Disord
2007;22:2204–9. http://dx.doi.org/10.1002/mds.21687.
[14] Evans RW, Evans RE. A survey of neurologists on the
likeability of headaches and other neurological disorders.
Headache 2010;50:1126–9. http://dx.doi.org/10.1111/j.1526-
4610.2010.01708.x.
[15] Carson A, Stone J, Warlow C, Sharpe M. Patients whom
neurologists find difficult to help. J Neurol Neurosurg
Psychiatry 2004;75:1776–8. http://dx.doi.org/10.1136/
jnnp.2003.032169.
[16] Gelauff J, Stone J, Edwards M, Carson A. The prognosis of
functional (psychogenic) motor symptoms: a systematic
review. J Neurol Neurosurg Psychiatry 2014;85:220–6. http://
dx.doi.org/10.1136/jnnp-2013-305321.
209
[17] Aybek S, Vuilleumier P. Imaging studies of functional
neurologic disorders. Handb Clin Neurol 2017;139:73–84.
http://dx.doi.org/10.1016/B978-0-12-801772-2.00007-2.
[18] Voon V, Gallea C, Hattori N, Bruno M, Ekanayake V, Hallett
M. The involuntary nature of conversion disorder.
Neurology 2010;74:223–8. http://dx.doi.org/10.1212/
WNL.0b013e3181ca00e9.
[19] Cojan Y, Waber L, Carruzzo A, Vuilleumier P. Motor
inhibition in hysterical conversion paralysis. Neuroimage
2009;47:1026–37. http://dx.doi.org/10.1016/
j.neuroimage.2009.05.023.
[20] Stone J, Zeman A, Simonotto E, Meyer M, Azuma R, Flett S,
et al. FMRI in patients with motor conversion symptoms
and controls with simulated weakness. Psychosom Med
2007;69:961–9. http://dx.doi.org/10.1097/
PSY.0b013e318156c14.
[21] Spence SA, Crimlisk HL, Cope H, Ron MA, Grasby PM.
Discrete neurophysiological correlates in prefrontal cortex
during hysterical and feigned disorder of movement.
Lancet 2000;355:1243–4. http://dx.doi.org/10.1016/S0140-
6736(00)02096-1.
[22] van Beilen M, de Jong BM, Gieteling EW, Renken R, Leenders
KL. Abnormal parietal function in conversion paresis. PloS
One 2011;6:e25918. http://dx.doi.org/10.1371/
journal.pone.0025918.
[23] Stenner M-P, Haggard P. Voluntary or involuntary? A
neurophysiologic approach to functional movement
disorders. Handb Clin Neurol 2016;139:121–9. http://
dx.doi.org/10.1016/B978-0-12-801772-2.00011-4.
[24] Voon V, Brezing C, Gallea C, Ameli R, Roelofs K, LaFrance
WC, et al. Emotional stimuli and motor conversion
disorder. Brain 2010;133:1526–36. http://dx.doi.org/10.1093/
brain/awq054.
[25] Vuilleumier P. Brain circuits implicated in psychogenic
paralysis in conversion disorders and hypnosis.
Neurophysiol Clin 2014;44:323–37. http://dx.doi.org/
10.1016/j.neucli.2014.01.003.
[26] Trimble M, Reynolds EH. A brief history of hysteria: from
the ancient to the modern. Handb Clin Neurol 2017;139:3–
10. http://dx.doi.org/10.1016/B978-0-12-801772-2.00001-1.
[27] Demartini B, D’Agostino A, Gambini O. From conversion
disorder (DSM-IV-TR) to functional neurological symptom
disorder (DSM-5): when a label changes the perspective for
the neurologist, the psychiatrist and the patient. J Neurol Sci
2016;360:55–6. http://dx.doi.org/10.1016/j.jns.2015.11.026.
[28] Voon V, Brezing C, Gallea C, Hallett M. Aberrant
supplementary motor complex and limbic activity during
motor preparation in motor conversion disorder. Mov
Disord 2011;26:2396–403. http://dx.doi.org/10.1002/
mds.23890.
[29] Aybek S, Nicholson TR, Zelaya F, O’Daly OG, Craig TJ, David
AS, et al. Neural correlates of recall of life events in
conversion disorder. JAMA Psychiatry; 2014;71:52–60.
http://dx.doi.org/10.1001/jamapsychiatry.2013.2842.
[30] Edwards MJ, Adams RA, Brown H, Pareés I, Friston KJ. A
Bayesian account of ‘‘hysteria.’’. Brain J Neurol
2012;135:3495–512. http://dx.doi.org/10.1093/brain/aws129.
[31] Stone J, Warlow C, Sharpe M. The symptom of functional
weakness: a controlled study of 107 patients. Brain J Neurol
2010;133:1537–51. http://dx.doi.org/10.1093/brain/awq068.
[32] Binzer M, Andersen PM, Kullgren G. Clinical characteristics
of patients with motor disability due to conversion
disorder: a prospective control group study. J Neurol
Neurosurg Psychiatry 1997;63:83–8.
[33] Stone J, Carson A, Duncan R, Roberts R, Warlow C, Hibberd
C, et al. Who is referred to neurology clinics? – the diagnoses
made in 3781 new patients. Clin Neurol Neurosurg
2010;112:747–51. http://dx.doi.org/10.1016/
j.clineuro.2010.05.011.
210 revue neurologique 174 (2018) 203–211
[34] Nazir FS, Lees KR, Bone I. Clinical features associated with
medically unexplained stroke-like symptoms presenting to
an acute stroke unit. Eur J Neurol 2005;12:81–5. http://
dx.doi.org/10.1111/j.1468-1331.2004.01010.x.
[35] Roelofs K, Spinhoven P, Sandijck P, Moene FC, Hoogduin
KAL. The impact of early trauma and recent life-events on
symptom severity in patients with conversion disorder. J
Nerv Ment Dis 2005;193:508–14.
[36] Kranick S, Ekanayake V, Martinez V, Ameli R, Hallett M,
Voon V. Psychopathology and psychogenic movement
disorders. Mov Disord 2011;26:1844–50. http://dx.doi.org/
10.1002/mds.23830.
[37] Stone J, Carson A, Aditya H, Prescott R, Zaubi M, Warlow C,
et al. The role of physical injury in motor and sensory
conversion symptoms: a systematic and narrative review. J
Psychosom Res 2009;66:383–90. http://dx.doi.org/10.1016/
j.jpsychores.2008.07.010.
[38] Pareés I, Kojovic M, Pires C, Rubio-Agusti I, Saifee TA,
Sadnicka A, et al. Physical precipitating factors in
functional movement disorders. J Neurol Sci 2014;338:174–
7. http://dx.doi.org/10.1016/j.jns.2013.12.046.
[39] Pareés I, Saifee TA, Kassavetis P, Kojovic M, Rubio-Agusti I,
Rothwell JC, et al. Believing is perceiving: mismatch
between self-report and actigraphy in psychogenic tremor.
Brain J Neurol 2012;135:117–23. http://dx.doi.org/10.1093/
brain/awr292.
[40] Daum C, Hubschmid M, Aybek S. The value of ‘‘positive’’
clinical signs for weakness, sensory and gait disorders in
conversion disorder: a systematic and narrative review. J
Neurol Neurosurg Psychiatry 2014;85:180–90. http://
dx.doi.org/10.1136/jnnp-2012-304607.
[41] McWhirter L, Stone J, Sandercock P, Whiteley W. Hoover’s
sign for the diagnosis of functional weakness: a prospective
unblinded cohort study in patients with suspected stroke. J
Psychosom Res 2011;71:384–6. http://dx.doi.org/10.1016/
j.jpsychores.2011.09.003.
[42] Sonoo M. Abductor sign: a reliable new sign to detect
unilateral non-organic paresis of the lower limb. J Neurol
Neurosurg Psychiatry 2004;75:121–5.
[43] Tinazzi M, Simonetto S, Franco L, Bhatia KP, Moretto G,
Fiaschi A, et al. Abduction finger sign: a new sign to detect
unilateral functional paralysis of the upper limb. Mov
Disord 2008;23:2415–9. http://dx.doi.org/10.1002/mds.22268.
[44] Yugué I, Shiba K, Ueta T, Iwamoto Y. A new clinical
evaluation for hysterical paralysis. Spine 2004;29:1910–3
[discussion 1913].
[45] Gould R, Miller BL, Goldberg MA, Benson DF. The validity of
hysterical signs and symptoms. J Nerv Ment Dis
1986;174:593–7.
[46] Knutsson E, Mårtensson A. Isokinetic measurements of
muscle strength in hysterical paresis. Electroencephalogr
Clin Neurophysiol 1985;61:370–4.
[47] Chabrol H, Peresson G, Clanet M. Lack of specificity of the
traditional criteria for conversion disorders. Eur Psychiatry
1995;10:317–9. http://dx.doi.org/10.1016/0924-
9338(96)80314-2.
[48] Daum C, Gheorghita F, Spatola M, Stojanova V, Medlin F,
Vingerhoets F, et al. Interobserver agreement and validity
of bedside ‘‘positive signs’’ for functional weakness,
sensory and gait disorders in conversion disorder: a pilot
study. J Neurol Neurosurg Psychiatry 2015;86:425–30. http://
dx.doi.org/10.1136/jnnp-2013-307381.
[49] Hinson VK, Cubo E, Comella CL, Goetz CG, Leurgans S.
Rating scale for psychogenic movement disorders: scale
development and clinimetric testing. Mov Disord
2005;20:1592–7. http://dx.doi.org/10.1002/mds.20650.
[50] Factor SA, Podskalny GD, Molho ES. Psychogenic movement
disorders: frequency, clinical profile, and characteristics. J
Neurol Neurosurg Psychiatry 1995;59:406–12.
[51] Thomas M, Vuong KD, Jankovic J. Long-term prognosis of
patients with psychogenic movement disorders.
Parkinsonism Relat Disord 2006;12:382–7. http://dx.doi.org/
10.1016/j.parkreldis.2006.03.005.
[52] Hallett M. Functional (Psychogenic) movement disorders –
clinical presentations. Parkinsonism Relat Disord
2016;22:S149–52. http://dx.doi.org/10.1016/
j.parkreldis.2015.08.036.
[53] Gupta A, Lang AE. Psychogenic movement disorders. Curr
Opin Neurol 2009;22:430–6. http://dx.doi.org/10.1097/
WCO.0b013e32832c169.
[54] Kumru H, Valls-Solé J, Valldeoriola F, Marti MJ, Sanegre MT,
Tolosa E. Transient arrest of psychogenic tremor induced
by contralateral ballistic movements. Neurosci Lett
2004;370:135–9. http://dx.doi.org/10.1016/
j.neulet.2004.08.009.
[55] Zeuner KE, Shoge RO, Goldstein SR, Dambrosia JM, Hallett M.
Accelerometry to distinguish psychogenic from essential or
parkinsonian tremor. Neurology 2003;61:548–50.
[56] Hallett M. Physiology of psychogenic movement disorders. J
Clin Neurosci 2010;17:959–65. http://dx.doi.org/10.1016/
j.jocn.2009.11.021.
[57] Schwingenschuh P, Saifee TA, Katschnig-Winter P,
Macerollo A, Koegl-Wallner M, Culea V, et al. Validation of
‘‘laboratory-supported’’ criteria for functional
(psychogenic) tremor. Mov Disord 2016;31:555–62. http://
dx.doi.org/10.1002/mds.26525.
[58] Schrag A, Trimble M, Quinn N, Bhatia K. The syndrome of
fixed dystonia: an evaluation of 103 patients. Brain J Neurol
2004;127:2360–72. http://dx.doi.org/10.1093/brain/awh262.
[59] Roelofs K, Pasman J. Stress, childhood trauma, and
cognitive functions in functional neurologic disorders.
Handb Clin Neurol 2016;139:139–55. http://dx.doi.org/
10.1016/B978-0-12-801772-2.00013-8.
[60] Nicholson TR, Aybek S, Craig T, Harris T, Wojcik W, David
AS, et al. Life events and escape in conversion disorder.
Psychol Med 2016;46:2617–26. http://dx.doi.org/10.1017/
S0033291716000714.
[61] Aquino CC, Fox SH. Understanding conversion disorders:
back to Freud’s theory. Mov Disord 2014;29:720. http://
dx.doi.org/10.1002/mds.25907.
[62] van der Hoeven RM, Broersma M, Pijnenborg GHM, Koops
EA, van Laar T, Stone J, et al. Functional (psychogenic)
movement disorders associated with normal scores in
psychological questionnaires: a case control study. J
Psychosom Res 2015;79:190–4. http://dx.doi.org/10.1016/
j.jpsychores.2015.06.002.
[63] Espay AJ, Goldenhar LM, Voon V, Schrag A, Burton N, Lang
AE. Opinions and clinical practices related to diagnosing
and managing patients with psychogenic movement
disorders: an international survey of movement disorder
society members. Mov Disord 2009;24:1366–74. http://
dx.doi.org/10.1002/mds.22618.
[64] Aybek S, Hubschmid M, Mossinger C, Berney A,
Vingerhoets F. Early intervention for conversion disorder:
neurologists and psychiatrists working together. Acta
Neuropsychiatr 2013;25:52–6. http://dx.doi.org/10.1111/
j.1601-5215.2012.00668.x.
[65] Hubschmid M, Aybek S, Maccaferri GE, Chocron O,
Gholamrezaee MM, Rossetti AO, et al. Efficacy of brief
interdisciplinary psychotherapeutic intervention for motor
conversion disorder and nonepileptic attacks. Gen Hosp
Psychiatry 2015;37:448–55. http://dx.doi.org/10.1016/
j.genhosppsych.2015.05.007.
[66] Stone J, Carson A. Functional neurologic disorders. Contin
Minneap Minn 2015;21:818–37. http://dx.doi.org/10.1212/
01.CON.0000466669.02477.45.
[67] Stone J, Carson A, Hallett M. Explanation as treatment for
functional neurologic disorders. Handb Clin Neurol
 revue neurologique 174 (2018) 203–211
2016;139:543–53. http://dx.doi.org/10.1016/B978-0-12-
801772-2.00044-8.
[68] Stone J. Functional neurological disorders: the neurological
assessment as treatment. Pract Neurol 2016;16:7–17. http://
dx.doi.org/10.1136/practneurol-2015-001241.
[69] Nielsen G, Stone J, Edwards MJ. Physiotherapy for
functional (psychogenic) motor symptoms: a systematic
review. J Psychosom Res 2013;75:93–102. http://dx.doi.org/
10.1016/j.jpsychores.2013.05.006.
[70] Nielsen G, Ricciardi L, Demartini B, Hunter R, Joyce E,
Edwards MJ. Outcomes of a 5-day physiotherapy
programme for functional (psychogenic) motor disorders. J
Neurol 2015;262:674–81. http://dx.doi.org/10.1007/s00415-
014-7631-1.
[71] McCormack R, Moriarty J, Mellers JD, Shotbolt P, Pastena R,
Landes N, et al. Specialist inpatient treatment for severe
motor conversion disorder: a retrospective comparative
study. J Neurol Neurosurg Psychiatry 2014;85:895–900.
http://dx.doi.org/10.1136/jnnp-2013-305716.
[72] Nielsen G, Buszewicz M, Stevenson F, Hunter R, Holt K,
Dudziec M, et al. Randomised feasibility study of
physiotherapy for patients with functional motor
symptoms. J Neurol Neurosurg Psychiatry 2016;88:484–90.
http://dx.doi.org/10.1136/jnnp-2016-314408.
[73] Jordbru AA, Smedstad LM, Klungsøyr O, Martinsen EW.
Psychogenic gait disorder: a randomized controlled trial of
physical rehabilitation with one-year follow-up. J Rehabil
Med 2014;46:181–7. http://dx.doi.org/10.2340/16501977-1246.
[74] Nielsen G, Stone J, Matthews A, Brown M, Sparkes C,
Farmer R, et al. Physiotherapy for functional motor
disorders: a consensus recommendation. J Neurol
Neurosurg Psychiatry 2014. http://dx.doi.org/10.1136/jnnp-
2014-309255 [jnnp-2014-309255].
[75] Garcin B, Roze E, Mesrati F, Cognat E, Fournier E, Vidailhet
M, et al. Transcranial magnetic stimulation as an efficient
treatment for psychogenic movement disorders. J Neurol
Neurosurg Psychiatry 2013;84:1043–6. http://dx.doi.org/
10.1136/jnnp-2012-304062.
[76] Garcin B, Mesrati F, Hubsch C, Mauras T, Iliescu I, Naccache
L, et al. Impact of transcranial magnetic stimulation on
functional movement disorders: cortical modulation or a
behavioral effect? Front Neurol 2017;8:338. http://
dx.doi.org/10.3389/fneur.2017.00338.
[77] Nicholson TRJ, Voon V. Transcranial magnetic stimulation
and sedation as treatment for functional neurologic
disorders. Handb Clin Neurol 2017;139:619–29. http://
dx.doi.org/10.1016/B978-0-12-801772-2.00050-3.
[78] McWhirter L, Ludwig L, Carson A, McIntosh RD, Stone J.
Transcranial magnetic stimulation as a treatment for
functional (psychogenic) upper limb weakness. J
Psychosom Res 2016;89:102–6. http://dx.doi.org/10.1016/
j.jpsychores.2016.08.010.
[79] Dafotakis M, Ameli M, Vitinius F, Weber R, Albus C, Fink GR,
et al. Transcranial magnetic stimulation for psychogenic
tremor – a pilot study. Fortschr Neurol Psychiatr
2011;79:226–33. http://dx.doi.org/10.1055/s-0029-1246094.
[80] Jellinek DA, Bradford R, Bailey I, Symon L. The role of motor
evoked potentials in the management of hysterical
paraplegia: case report. Paraplegia 1992;30:300–2.
[81] Schönfeldt-Lecuona C, Connemann BJ, Viviani R, Spitzer M,
Herwig U. Transcranial magnetic stimulation in motor
conversion disorder: a short case series. J Clin Neurophysiol
2006;23:472–5. http://dx.doi.org/10.1097/
01.wnp.0000219004.69158.1e.
211
[82] Chastan N, Parain D. Psychogenic paralysis and recovery
after motor cortex transcranial magnetic stimulation. Mov
Disord 2010;25:1501–4. http://dx.doi.org/10.1002/mds.23187.
[83] Shah BB, Chen R, Zurowski M, Kalia LV, Gunraj C, Lang AE.
Repetitive transcranial magnetic stimulation plus
standardized suggestion of benefit for functional
movement disorders: an open label case series.
Parkinsonism Relat Disord 2015;21:407–12. http://
dx.doi.org/10.1016/j.parkreldis.2015.01.013.
[84] Broersma M, Koops EA, Vroomen PC, Van der Hoeven JH,
Aleman A, Leenders KL, et al. Can repetitive transcranial
magnetic stimulation increase muscle strength in
functional neurological paresis? A proof-of-principle study.
Eur J Neurol 2015;22:866–73. http://dx.doi.org/10.1111/
ene.12684.
[85] Sharpe M, Walker J, Williams C, Stone J, Cavanagh J, Murray
G, et al. Guided self-help for functional (psychogenic)
symptoms: a randomized controlled efficacy trial.
Neurology 2011;77:564–72. http://dx.doi.org/10.1212/
WNL.0b013e318228c0c7.
[86] Dallocchio C, Tinazzi M, Bombieri F, Arnó N, Erro R.
Cognitive behavioural therapy and adjunctive physical
activity for functional movement disorders (conversion
disorder): a pilot, single-blinded, randomized study.
Psychother Psychosom 2016;85:381–3. http://dx.doi.org/
10.1159/000446660.
[87] Hinson VK, Weinstein S, Bernard B, Leurgans SE, Goetz CG.
Single-blind clinical trial of psychotherapy for treatment of
psychogenic movement disorders. Parkinsonism Relat
Disord 2006;12:177–80. http://dx.doi.org/10.1016/
j.parkreldis.2005.10.006.
[88] Reuber M, Burness C, Howlett S, Brazier J, Grünewald R.
Tailored psychotherapy for patients with functional
neurological symptoms: a pilot study. J Psychosom Res
2007;63:625–32. http://dx.doi.org/10.1016/
j.jpsychores.2007.06.013.
[89] Kompoliti K, Wilson B, Stebbins G, Bernard B, Hinson V.
Immediate vs. delayed treatment of psychogenic
movement disorders with short term psychodynamic
psychotherapy: randomized clinical trial. Parkinsonism
Relat Disord 2014;20:60–3. http://dx.doi.org/10.1016/
j.parkreldis.2013.09.018.
[90] Shamy MCF. The treatment of psychogenic movement
disorders with suggestion is ethically justified. Mov Disord
2010;25:260–4. http://dx.doi.org/10.1002/mds.22911.
[91] Rommelfanger KS. The role of placebo in the diagnosis and
treatment of functional neurologic disorders. Handb Clin
Neurol 2016;139:607–17. http://dx.doi.org/10.1016/B978-0-
12-801772-2.00049-7.
[92] Moene FC, Spinhoven P, Hoogduin KAL, van Dyck R. A
randomized controlled clinical trial of a hypnosis-based
treatment for patients with conversion disorder, motor
type. Int J Clin Exp Hypn 2003;51:29–50. http://dx.doi.org/
10.1076/iceh.51.1.29.14067.
[93] Espay AJ, Edwards MJ, Oggioni GD, Phielipp N, Cox B,
Gonzalez-Usigli H, et al. Tremor retrainment as therapeutic
strategy in psychogenic (functional) tremor. Parkinsonism
Relat Disord 2014;20:647. http://dx.doi.org/10.1016/
j.parkreldis.2014.02.029.
[94] Stone J, Hoeritzauer I, Brown K, Carson A. Therapeutic
sedation for functional (psychogenic) neurological
symptoms. J Psychosom Res 2014;76:165–8. http://
dx.doi.org/10.1016/j.jpsychores.2013.10.003.